Zagazig University Faculty of Veterinary Medicine

Department of Avian and Rabbit Medicine

Avianand Rabbit Diseases

STAFF MEMBERS OF AVIAN AND RABBIT MEDICINE

DEPARTMENT

ContentsPreface....................................... 3 -

Newcastle Disease (ND)........................................ 4 -

Avian Influenza............................................................................ .......................-17 -

Infectious Bronchitis (IB).................................. ..- 29 -

Infectious Bursal Disease (IBD).................................................... - 37 -

Chicken Infectious A nem ia......... ........................................................... 47 -

Infectious Laryngeotracheitis.......................................................................... - 53 -

Avian Encephalomyelitis................................................................................. ..- 58 -

Avian Reovirus In fections............................................................. ................... - 64 -

Avian Neoplasms................................................................................ ...............- 68 -

Avian Leukosis............................................... ................................................ ...... 69 -

Marek's Disease....................................................................................................- 7 7 -

" Avian Reticuloendotheliosis................................................................................- 88 -

Lymphoproliferative Diseases o f Turkeys................................................ - 91 -

Avian Pox................................................................................................................ - 95 -

Avian Adenovirusesjnfection..........................................................................-107 -

M ycosis.......................................................................... 123

^ Avian Salmonellosis........................................................................................... 147

^ Avian Coliform In fection........ .............................................................................. 163

Avian M ycoplasm osis...........................................................................................174

_ Infectious Coryza...................................................................................... 188

—• Avian Chlamydiosis........................................................... !97

— Avian Tuberculosis................................................................ 205

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Avian Spirochaetosis.................................... ........................................................ 210

Avian Pasteurellosis................................... .......................................................214

Clostridial Infections.......................................................................................... 224

Avian Bordetellosis................................................................................... ........241

Ornithobacterium rhinotracheale........................................ 251

Staphylococcosis.................................................................................................255

Streptococcus in fec tion ................................................................................... 258

PARASITIC DISEASES....................... ........................................... ......................260

N utritional Diseases...................................................................... 292

Duck Diseases.................................................................................. ...320

Rabbit Diseases........................................................... 345

References........................................................................................................ ...387

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Preface

In order to have the opportunity to become a member in the veterinary medicine field, the student should understand the key elements in poultry diseases diagnosis. This book brings together some of the Egyptian experts in their respective field of poultry disease diagnosis, prevention and control. I do believe that this text book will be an important guidance during your scholar and practical life. This book is intended to be precisely such as the authors convinced to be useful to the study of veterinary practice. This new edition of the book includes two novel sections that discuss the goose parvovirus and omithobacterium rhinotracheale infection in birds. In addition, it contains many new interactive images compared to the previous editions. I take this opportunity to acknowledge all the authors for their efforts and contributions to have this book in this shapev Moreover, I hereby confirm and declare that the contents of this book are from the author’s composition.

Prof. Dr. Mohamed Mahrous Megahed

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Newcastle Disease (ND) (pneumoencephalitis)

ByProf. Dr. Ahmed M. El-sadek Hegazy

Def:Acute or subacute infectious highly contagious and destructive disease of birds of all ages, characterized by respiratory manifestation or nervous signs or both.

ND is caused by a paramyxovirus (rubula virus), RNA, enveloped ss non-segmented with helical symmetry and

diemagglutinate red blood cells of chickens, some birds and mammals. There are nine distinct serotypes of paramyxoviruses (PMV-l to PMV-9). NDV is serotype 1 (PMV-1). The virus is sensitive being destroyed by most disinfectants, ether chloroform, formalin and direct sunlight. The virus is inactivated by temperatures (56°C for 5 minutes or 30°C for l/2 hour).

Cause:

Paramyxovirus serogroups are:1- Serotype 1 (in all birds).2- Serotype 2 in chicken and turkey (n respiratory signs and troubles in production).

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3- Serotype 3 in turkey and pet birds (mild respiratory signs and egg problems).4- Serotype 4 in ducks and geese (no signs).5- Serotype 5 in budgerigar.6- Serotype 6 in ducks and geese (mild respiratory signs and elevated mortalities in turkeys).7- Serotype 7 in pigeon, doves, turkey and ostriches (mild respiratory signs in turkey).8- Serotype 8 in ducks and geese (no signs).9 - Serotype 9 in duck (no signs).

The ND viruses are classified into 3 strains: a -According to pathogenicity:1~ Lentogenic; mild pathogenicity, e.g. Hitchner-Bi, F and

La Sota (used for vaccine production).2- Mesogenic; moderate pathogenicity, e.g. Komarov.3- Velogenic; highly pathogenic, e.g. Herts, GB-Texas and

Milano.b- According to clinical signs:1- Doyle’s form:Acute lethal infection of all ages. Hemorrhages of the digestive tract W N D .2 - Beach’s form:Acute often lethal infection of all ages. Respiratory and neurological signs NVND.3 - Beaudette’s form:

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Less pathogenic form of NVND. It is characterized by deaths in young birds due to mesogenic pathotype and used as secondary vaccine.

4 - Hitchnerfs form:Mild respiratory or inapparent caused by lentogenic pathotype and used as live vaccine.5 - Asymptomatic form:Enteric form is chiefly gut infection with lentogenic virus.

Susceptibility:- All birds of all ages are susceptible but young birds

are more seriously affected.- Chickens, turkeys, pheasants, guinea fowl, ducks, geese,

pigeons, Sparrows, partiridge and caged birds as well as free living and migratory birds are susceptible.

- Mammals, dog, cat, rat, ferret, G. pig and hamester can be infected.

- Infection \n man appears as conjunctivitis (eye infection).

Transmission and spread of infection:- Airborne spread (droplets, dust or dried faeces).- Contaminated feed, water, meat, feathers, blood, bones

and vaccines. Also visitors and contaminated shoes, crates, equipment, feed sacs and wild birds.

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- Incubated eggs laid by infected hens m ay contain the . virus and when brocken contaminate the hatcher and the chicks may be exposed.

- Cage birds and fighting cocks (imported) is the main source o f velogenic Newcastle virus.

- Feeding infected viscera, eggs or egg shell.- The virus is shed in body fluids, secretions and

droppings during the viremic stage and spread by direct contact or contaminate houses, equipments, litter and environment.

- Animals as dogs, cats, rat and blood sucking insects play a role in transmission of infection.

Severity of infection depends upon:1- Virulence o f the virus (virulant virus more pathogenic).2- Dose and age (some strains needs high doses o f the

virus) and young ages are more seriously affected.3 - General health condition during exposure to infection

and presence o f stress factors (malnutrition, parasitism and dampness leads to severity of disease with long course).

4 - Immune status o f birds as presence o f specific antibodies prevent introduction o f infection.

Incubation period:1- Natural 2-15 days (average 5 days).

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2- Experimental 2-4 days.

Clinical signs:• In velogenic viscerotropic ND (VVND) symptoms often

begin with listlessness, increased respiration and weakness ending with prostration and death.

• Respiratory signs: Gasping, coughing, nasal and ocular watery discharge with dark odema around the eyes.

• Conjunctivitis and cyanosis of comb and wattles.• The respiratory signs may be followed by nervous signs

in birds that don’t die early in the form of tremors, convulsions and torticolis, opisthotonous with leg and

- wings paralysis. Movement in circles and twisting o f the head and neck (star gazers). Mortality frequently reaches 100 %_in susceptible chickens.

• In neurotropic velogenic ND (NVND) may start by respiratory signs followed by nervous signs one or two days later. Morbidity may reach 100 % and mortality ranges from 50 % (in adult) and 95 % (in young)

• Mesogenic strains of NDV usually cause respiratory signs, nervous signs may follows with drop in egg production in adult birds

• In both respiratory and nervous forms affected flocks show general signs as depression, loss o f appetite, ruffled feather and decrease in water Consumption. Green yellow diarrhea, lentogenic viruses cause no signs

in adults while respiratory signs occurs in young susceptible birds

• In laying hens sudden drop in egg production (40%) or may drop to zero % with soft shelled or rough shelled eggs, misshaped eggs, low egg quality and hatchability and pigmentation of egg shell. Production may return to normal levels from the fourth week up to 12 week postinfection.

• Signs in turkeys are respiratory' and nervous manifestations.

• In ducks and geese no specific symptoms but in young age group nervous signs and leg paralysis and variable mortalities.

• In pigeon also paralysis and nervous signs are observed• In young ostrich may show depression and nervous

signs.

Lesions:1- Facial swelling (odema), severe congestion and

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hemorrhages in all tissues' (skin, musculature, coronary and body fat).

2- Dark muscles.3- Catarrhal conjunctivitis, rhinitis and sinusitis.4- Peticheal hemorrhages on mucous membranes of

respiratory passages (trachea and pharynx).5- Airsacculitis and odema o f the lungs.

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6- Peticheal hemorrhages in mucosa of proventriculus at the junction with esophagus or at proventriculus-gizzard junction.

7- Lymphoid follicles of the intestine are swollen and inflamed with necrotic red raised areas or ulcers with elevated edges (pathognomic for W N D ). Caecal tonsils swollen with peticheal hemorrhages and or necrosis.

8- Catarrhal inflammation of the intestine and the contents are gray green.

9- Liver, spleen and kidneys are congested and swollen, ovary congested with inflamed follicles.

10- Brain congested with hemorrhages in the inner side of the skull.

Histopathology:Microscopically CNS involvement, neuronal degeneration, perivascular cuffing with lymphocytic cells and endothelial hypertrophy.

Diagnosis:1- Case history, signs and lesions can serve as

a preliminary field diagnosis.2- Immunoflourescenec and Immunoperoxidase thin

sections from trachea for rapid antigen detection3- Isolation of ND virus through inoculation of chick

embryos and identification by: Hemagglutination and

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hemagglutination inhibition test’s, neutralization test (in embryos and on tissue culture) and Immunoflourescene test.

4- Inoculation of susceptible and immune chickens and observe symptoms.

5- Serology For detection of serological response by ELISA, AGPT and HI test.

6- PCRtest.

Differential diagnosis:ND must be differentiated from other respiratory diseases, vitamin E deficiency, IB, ILT, and Avian influenza.

Control and prevention:A-Control measures:1- Prevent the spread of infection by isolation of infected

(sanitation).2- Burning or burying of diseased and dead birds.3- No visitors and prevent movement of persons.4- Cleaning and disinfection of infected premises and

utensils.5- Emergency vaccination of apparently healthy birds with

suitable vaccine according to immune status, age and severity of infection and numbers of birds via drinking

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water or by spray vaccination especially at the beginning o f the infection.

B-Prevention:Sanitary measures and good management. Prevent all methods o f transmission of the disease by strict isolation, quarantine measures and periodical cleaning and disinfection of buildings and surroundings.

Prophylactic vaccination:- Lentogenic ND vaccines (Hitchner-Bl, F and LaSota

vaccines) through drinking water, eye drops, nasal drops, beak dipping and spray.

- Oil emulsion killed vaccine by S/C or I/M injection.

Vaccination pro fir am :A- Fattening flocks (50-55 day):

-1- In the first week Hitchner-Bl vaccine by one method spray, drinking water, eye drops applications.

2- Revaccination at 20 day by La Sota vaccine (spray or drinking water) revaccinate again in some cases at 35 day with La Sota vaccine. •••■

B- For breeders and laying hens:1- As mentioned above and continue to vaccinate every

30-40 days along the production period. Other program is to vaccinate with HB1 vaccine in the

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first week and inject inactivated oil emulsion vaccine i.m. at 14 day of age followed by HB1 vaccine in drinking water at the second day of injection (15 day) and this is -enough for fattening flocks- in endemic areas.

2- In layers vaccinate again with killed vaccine I/M two weeks before egg production.

Precautions:A- For drinking water vaccine1- Birds should be thiristen for 4 hours in winter and 2

hours in summer.2 - Allow sufficient water equipments.3- Vaccination should be in the early morning to avoid

high temperature in summer.4- Water used for vaccination should be free from

deliterious substances.5- Stop any drug given through drinking water one day

before vaccination and ensure that water devices are clean.

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B- For spraying method of vaccination1- Birds should be free from respiratory troubles.2- Birds should be placed in tightly closed room and

kept for 30 minutes after spraying.3- Choose the suitable nozzle diameter for spraying.

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Small number of birds which come to the clinic must be vaccinated according to age:Under one month as eye drops or drinking water while birds, over one month vaccinated with Komarov i.m injection and revaccinated every 3-4 months.1- Generally follow the directions of the vaccine producer

with regard to preservation, dilution and dose.2- Should not vaccinate birds under stress and bad

management.3- Normally mild post vaccinal reaction may be developed

(Komarov).4- Avoid natural infection 3 weeks post vaccination.5- Good management.

4- Spray directly one meter over the level of chicks.

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In viscerotropic velogenic NDV, hemorrhagic and necrotic lesions in the intestines tend to be concentrated in areas with lymphoid tissue, such as the cecal tonsils.

Severe hemorrhages on the cecal tonsils and the mucosa o f the

rectum.

There is hemorrhagic proventriculitis. Often, these hemorrhagic lesions cluster around the esophageal- proventricular junction.

Some viscerotropic strains can produce severe lesions in the lungs. In this bird, there is pulmonary edema and extensive hemorrhages.

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Avian Influenza (Fowl Plague)

ByProf. Dr. Ahmed M. El-sadek Hegazy

Def:

Acute highly infectious fatal septicemic disease characterized by sudden onset, rapid spread, short course and high mortality. From 187Q - 198, the disease was known as fowl plague after 1981 known as highly pathogenic avian influenza (HPAI).

Classification is according to pathogenicity which based on genetic features and/or severity of disease in poultry.

■ Low pathogenic avian influenza (LPAI): These include HI to H4, H6, H8-H16 subtypes.

■ Highly pathogenic avian influenza (HPAI): These include some H5 or H7 subtypes. Some low pathogenic avian influenza H5 and H7 subtypes may mutate into HPAI.

\Cause:

The Influenza virus is caused by Orthomyxoviruses which are single strand segmented (8 segments) RNA viruses. They are assigned to the types A, B or C. Orthomyxoviruses of birds are

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restricted to influenza A type viruses. Influenza type B is only infective for human while type C is infective for both human and swine. There are different subtypes according to H “haemagglutinins” and N “neuraminidase” antigens.

Subtypes of avian influenza isolated from different species:j

In chickens: In turkeys: In ducks: In caged

H5N2 h 5n 2 H3 N8 birds: i)

HsN, . . h 5n 8 H4 N6 H^N, .

h 7n 7 H5N9 h 5 n 8 h 3 n 6

i i7n 3 , a n , ; H5N1 h 3 n 8 ■ • *

HsNj i i4 n 6•

H4 N 8. • 1

At present there are 16 “H” “haemagglutinins” and 9 “N” “neuraminidase” subtypes. Each virus possesses one surface antigen of each subtype in any combination.

- The H antigens are the most important in induction of protective immunity in the host.

- Propagation in chicken embryos leading to death of embryos within 36 hours, which appears dark and congested.

I

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- Agglutinate RBCs.

- Highly infectious even in minute doses 1/1,000,000 from one ml enough to cause outbreak in susceptible birds.

- Destroyed by disinfectants as formalin, iodine, sunlight, heat, PH 2.

- HPAI subtypes could propagate on T.C and produce CPE which differ in size and time o f its production according to the virulence of the virus. While Mild pathogenic (MP) and low pathogenic (LP) avian influenza subtypes needs trypsin to produce the CPE.

Susceptibility:

- Chickens, turkeys and pheasants are highly susceptible.

- All ages are susceptible but semi-mature showed more severe infection.

- Ducks, geese and pigeons are refractory to influenza infection while youngs are susceptible.

- Other avian species may show no symptoms, others show mild symptoms (caged birds) wild bird, migratory birds, while human and pigs act as reservoir.

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Transmission:

- f Direct contact o f infected with susceptible birds (contaminated food or water).

- Indirect contact through aerosol droplets or exposure to contamionated fomits.

- Faecal-oral route especially in ducks “water fowl” or faecal-cloacal route.

- Blood sucking insects.

- Migratory, wild and caged birds (carriers).

- Mammals, pigs, man, and utensils act as mechanical means.

- Through injured skin.

- Inoculation by any route.

- Infected brocken eggs in incubators.

- Vertical transmission in turkey.

- Eggs laid from infected birds 3-4 days post infection showed marked embryo mortality.

- AI virus is excreated from the nares, mouth, conjunctiva and cloaca o f infected birds into the environment (because virus replication in the respiratory, intestinal renal and reproductive systems).

- Live poultry production markets (LPM) system posseses a significant risk to the introduction o f MPAI and HPAI subtypes into the commercial integrated poultry systems.

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Sources of infection: ,

■ Other domestic poultry

■ Migratory water fowl

■ Domestic pigs

■ Pet birds ...

N.B) Experimentally The AI virus replicate, and is excreated from ducks up to 30 days, in chickens up to 36 days and in turkeys up to 72 days post infection.

Incubation period:

1 - Naturally 4 days.

2- Experimentally from few hours up to 36 or 48 hours.

Clinical signs:

Depend upon age, host and stresses.• Sudden onset, dullness, inappetance, weakness, short

course, rapid spread and birds may die without any symptoms.

• High morbidity and high mortality (near f 00%) 50-70% in moderate virulence. 80% in young chicks less than one month of age.

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• Respiratory signs: gasping, coughing, sneezing, nasal discharge, tracheal rales, lachiymation, sinusitis and laboured breathing.

• Wet eyes and swollen red eye.Cyanosis of comb and wattles.

• Oedema of the head, neck and face, around eyes and earlobes.

• Dark skin.• Swelling and discolouration of the hocks and feet. .• Watery diarrhoea and may be greenish in colour and

birds appear thirst and water running on side o f the neck during drinking as a result of sleep condition.

• Comatized condition appears and birds lie on ground lifeless and end with death.

• Birds which do not died early show nervous signs as rolling, movement in circles, and paralysis, torticollus, opisthotonous, tremors of head and neck.

• In laying birds: drop of egg production with low egg quality and hatchability or cessation of egg production within 6 days.

• Depigmentation of egg shell in turkey (white shell).• In ostrich, reduced activity and appetite, depression,

ruffled feather, sneezing and open mouth breathing. Some birds had paralysis of the wings, incoordenation and tremors of the head and neck.

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• MPAI viruses show high morbidity and low mortality (less than 5 %) in young poults H7N1 produce 97% mortality when accompanied with secondary pathogens in birds less than 4 week of age.

• HPAI viruses shows high mortality and morbidy (50 - 89%) and can reach 100 % in some flocks.

• In ostrich moderate morbidities and low mortalities and may be high in young birds less than 3 months with mortalities 30%.

Lesions:1- In peracute outbreaks birds die suddenly with no' gross lesions.2- Haemorrhages (peticheal) allover the serous

membranes', abdominal fat, coronary fat of the heart. Peticheal haemorrages on the inner surface of the keel bone, on the pectoral muscles, proventriculous, under the cuticle of the gizzard and on the mucosa of duodenum with cattarrhal enteritis

3- Serous fluid under the skin due to oozing of plasma to subcutaneous tissue.

4- Fibrinous exudate in peritonium which clots directly after opening the abdomen.

5- Fibrinous exudate in the pericardial sac and on air sacs with air sacculitis and congestion of lungs.

6- Tracheal oedema and caseous tracheal exudate.

7- Congested subcutaneous blood vessels, dark red skin and dark red flesh.

8- Necrotic area on comb and wattles.9- Also foci of necrosis in liver, spleen, kidney or lung.10- Conjunctiva red and swollen.

11- In layers: congested ovary with large follicles and its blood vessels engorged and congested.

12- Fibrinous exudate in oviduct.

13- In ostriches HPAI viruses produced edeiiia of head and neck, severe hemorrhagic eneteritis, enlargec and firm' pancrease, mild to severe airsaculitis and splenomegally.

Histopathology: <Congestion, oedema, haemorrage and perivascular lymphoid cuffing at many sites. Foci of necrosis in spleen, liver, kidney, pancreas and lung.

Diagnosis:

1- Case history, signs and lesions.

2- Virus isolation on 10-day old embryonated chicken eggs.

3- Identification: HA-test and Hi-test, Nt, ellisa test, AGII and electron microscope examination.

4- PCR and DNA probing.

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Differential diagnosis: ‘Differentiation from similar conditions: ND, F. cholera (acute

wattle form) and mycoplasmosis.and

ontrol and prevention:■ Prevention of exposure to likely carriers o f ATV (water

fowls, exotic pet b irds,........ etc.).■ No birds should be introduced to started flocks.■ All wild, migratory and exotic birds should be

prevented.•. Quarantine measures for imported caged and exotic

birds.■ Quarentine. zone implementation, official notification

systems in places for positive areas.■ Depopulation.■ Vaccination.

phase 1: during outbreak for eradicationof the disease.Phase 2: post outbreak to prove freedom from disease.Jphase 3: survillanceand monitouring (long term monitoring).

accmes1. Inactivatd vaccines (need booster dose)

■ Heterologous■ Homologous

2. Vectored vaccines(recombinant)

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Using ILT or Pox (not used in old birds) gives solid immunity.

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Vaccination programSpecies Age Dose(ml)/routeBroiler lor 12 day 0.25 S/C

Saso 1 week 0.25 S/C6 weeks 0.5 S/C

Layers 1 day 0.25 S/C4-6 weeks 0.5 I/M

14-18 weeks 0.5 I/M35-40 weeks 0.5 I/M

Ducks 0-1 week 0.5 S/C2-3 weeks 1 S/C6-8 weeks 1 I/M

14-18 weeks 1 I/M35-40 weeks 1 i/m ’

Turkeys s 1 weeks 0.5 S/C4-7 weeks 0.5 S/C

10-13 weeks 0.5 S/C24-26 weeks 0.5 S/C40-50 weeks 0.5 S/C

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T he subcutanous tissu e o f the co m b , w attles and face is extrem ely sw o llen . There are large dark purple areas on both the com b and w attles.

T hese tw o legs are from tw o different birds. The right leg leg show s m inim al sw ellin g o f the foot. In the left leg, there is more extensive hem orrhage over the intertarsal jo in t,'th e skin overlying the tarsometatarsus, digital and metatarsal pad.

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Infectious Bronchitis (IB)By

Prof. Dr. Ahmed M. El-sadek Hegazy

Def:

IB is an acute, highly contagious airborne disease of chickens. It affects respiratory tract, urinary system and reproductive tract.

Cause:

Coronavirus, RNA virus, cultivated on embryonated chicken eggs causing curling, dwarfing and death o f embryos. Also, the virus cultivated on tissue culture producing syncytia and plaques. • :

- Ether sensitive virus.

- The virus does not haemagglutinate RBCs (the hemaggultination can be demonstrated by antigen concentration and treatment with phospholipase (C).

- Most strains are inactivated at high temperature (56°C for 15 minute) and by ultraviolet irradiation.

- IB virus is stable at pH 7.8.

- 10% glucose and 50% glycerin used as stabilizers to the IB virus.

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Antigenic properties:- At least 8 different serotypes are detected: Massachusetts

(M41, H), Connecticut (Florida, Arkansas 99, Georgia, Delaware (Holte, Gray), Iowa 97, 609, New Hampshire and Australia-T-strain.

- All IB Vs contain common antigen detected by AGID and ELISA, also showed variable cross-reactions with (VN, HI and plaque reduction test). Hi-test is more sensitive and shows greater number of antigenic types.

Susceptibility:

The virus can infect chickens and all ages are susceptible 6ut the disease is more severe in early ages. Also, IBV was isolated from pheasants, racing pigeons and guinea fowl.

Transmission:

Through:

- Inhalation, aerosoL

- Lateral, direct or indirect contact of infected chickens with susceptible chickens.

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- By carriers which shed the virus for longer periods due to latency and infect susceptible birds and contaminate premises.

- Spread from farm to farm within 1-2 days and faster when air movement increases.

- Infected eggs up to 50 days post infection.

- Infected semen up to two weeks post infection.

Incubation period:

1- Naturally: 3-10 days naturally.

2- Experimentally: 18-48 hours. _

Clinical signs:

Signs of IB depend upon age, virulence, immunity and general health condition.

I- In baby chicks (up to one month of age):• Rapid spread, 100% infection.• Gasping, coughing, rales, sneezing, nasal and ocular

nasal discharge and chilling.• Weakness, inappetance, depression and chicks huddle

together under the heat source with laboured breathing and sleepy.

• Some birds die suddenly and mortality increased (about 25% or more) in complicated outbreaks (E. coli, mycoplasma, adenovirus and hemophilus).

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• Retarded growth and the course 5-7 days:• In less virulent strains accumulation of white sticky

exudate around the vent (pasting).

2- In chicks over one month up to maturity:• Mild respiratory signs, coughing, sneezing and rales,

retarded growth with low mortality (5-10%) and the. course about 10 days.

3- In laving chickens:• Slight respiratory signs, coughing and rales with decline

in food and water consumption.• Marked drop in egg production (up to 60%) from 4-6

weeks.• Thin shelled eggs and rough shelled (shell with

calcareous deposits, depressions and ridging). Misshapened eggs with thin watery albumen with blood spots in yolk and low egg quality.

• False layers 8-10 weeks after an outbreak (in pullets) due to shortening and narrowing of oviduct and layers visit the nest but lay no eggs (trap nests used for diagnosis).

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Lesions:

1- Catarrhal tracheitis, bronchitis, pneumonia and air saculitis (thickening and opacity).

2- Conjunctivitis, nasal discharge and cheesy exudate in the trachea, bronchi, lungs and air sacs.

3- Caseous plugs at the end of trachea blocks air flow leading to death.

4- In laying birds: congested ova, ruptured ova with free yolk in the abdominal cavity (peritonitis), reduction in

' oviduct weight and length (shortening and narrowing) egg ovulate into abdominal, cavity (egg pretonitis). Soft shelled or complete eggs or egg yolk are found in the abdominal cavity.

Diagnosis:1- Rapid onset, symptoms, lesions, positive fluorescent

antibpdy test, positive virus isolation with positive serology. Two samples 2 weeks apart if IB is present the second sample will show marked antibody-titer increase.

2- Isolation of the virus from respiratory tissue (air sacs, turbinate), spleen, oviduct and faeces.

3- Inoculation of 9-11 day old embryonated eggs through Allentoic route.

4- IB adapted strains cause dwarfing, curling, stunting and death of embryos 24-48 hoursf post inoculation.

5- Inoculation of susceptible day old chicks.

6- AGPT: precipitating antibodies 10-14 days p.i up to 30- 40 days.

7- Neutralizing antibodies 7 day p.i for months (for detection of antigenic groups and sub-groups by cross neutralization test).

8- HI antibodies 5-7 day for months p.i. and Hi-test confirms the antigenic differences shown by VN tests and suggests that many antigenic subtypes exists within the major groups.

9- Elisa test also rapid and sensitive for detecting IB antibodies.

Differential diagnosis:

Other respiratory diseases: ND, ILT, Avian Influenza,Pasteurella, coryza or aspergillosis.

Control and prevention:

1- Raise the temperature 2°C.

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2- Use antibiotic to overcome secondary bacterial infections. Provide good management, fresh feed and water.

3- Obtain chicks from immune breeders against IB, IBD.

4- No visitors and birds of same age.

Vaccination:

* In broilers:

1- Vaccination with H I20 via drinking water or spray at 1 day old.

2- H I20 at 6 weeks of age.

* In layers and breeders:

1 - H I20 at 1 day by spray.

2 - H I20 at 6 weeks by spray.

3- Killed vaccine M41+ D274 at 16-20 week i.m injection.

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Egg material, yolks and or partially formed eggs may be found

in the abdominal-cavity.

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Wrinkled egg shells as the result o f infectious bronchitis in a laying hen.

Infectious Bursal Disease (IBD) Gumboro disease (GD)

ByProf. Dr. Ahmed M. El-sadek Hegazy

Eef:IBD was first recognized in Gumboro, Delaware, USA in1962. The virus belongs to Bimaviridae family.

Cause:

IBD belongs to genus Avibima virus of the familyBimaviridae. It is a double stranded RNA vims

'

Virus characteristics:

1- The vims is resistant to ether and chloroform, pH2 and to high temperature (56°C for 5 hours, 60°C for 30 min.).

2- The vims has survived in a house for 122 days after removal of infected birds, and in contaminated feed, water and faeces for at least 52 days.

3- The vims has inactivated or killed by some disinfectants 2% chloramine solution, formalin, formaldehyde, gtutaraldehyde and iodophore.

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4- Two serotypes; serotype 1 isolated from chickens and serotype 2 isolated form turkeys.

5- About 30% relatedness between several strains. Further subdivision occurs variant IBD viruses are classified as subtypes of serotype 1 and there are at lest 6 subtypes.

6- The same are present in serotype 2.

7- Both serotypes 1 and 2 viruses share a group antigen detected by IFT or AGID. The virus does not haemagglutinate RBCs.

8- CAM is the more sensitive route for cultivation

9- Propagated on CEF cells (plaques production)

Susceptibility:

1- Serotype 1 mainly infects fowl (also isolated formducks and turkeys).

2- Serotype 2 viruses are widely distributed in turkeys (also isolated from fowl and antibodies detected in ducks).'

3- Pheasants are susceptible.

4- Quails are susceptible.

- 38-

5- Antibodies are present in water fowl (ducks, geese, gulls). All ages of birds are susceptible to infections but clinical disease not <3 week.

Transmission:

- The disease is highly contagious and spreads by direct contact (for up 2 weeks post infection, virus is present

in faces and considered the main source).

- Wild birds and rodents act as mechanical vectors. Also meal-worms and mosquitoes.

- Transmission appears to be by contaminated feed, water, litter, droppings or equipments.

Incubation period:

Incubation period is very short and clinical signs occurs 2-4 days post infection.

Pathogenesis:

- The natural infection is usually via oral route, virus can be detected 4 hours p.i. in the macrophages and lymphoid cells of the caecum and 5 hours post infection in macrophages and lymphoid cells of duodenum and jejunum and in kupffer cells of liver.

-39-

- The virus reaches the blood steam and is distributed in other organs including the bursa Fabricius in which massive virus replication takes place 11 hours p.i. and leads to second viraemia with lesions in most organs.

- The virus can be isolated from bursa, thymus, spleen, kidney and caecal tonsils 2-8 days p.i.

Blood changes:

- Lymphocytes decreased sharply (lymphopaenia) up to 2 days p.i. (due to destruction of bursal lymphocytes).

- Increase in heterophils count (hetrophilia). These changes returned to normal, again.

Clinical signs: • Slight tremors of head and body one to two days before

outbreaks of GD. ;

• Chicks appear sleepy with inappetance, depression, anorexia, ruffled feathers.

• Some birds has a tendency to pick at their vents and watery diarrhea with soiled vent feathers,.

• High temperature but dropped below 35°C before death.

• Trembling, reluctant to move and inability to stand

before death.

- 4 0 -

• Some chickens showed yellowish mucoid diarrhoea or greenish with white or haemorrhagic threads, followed by death or rapid recovery.

• The disease appears suddenly and morbidity is usually high 30-50% (80%), mortality may be zero (subciimcal inf.) or high ranging from 1-25% in most outbreaks. In some outbreaks may reach up to 50% and usually begins from the third day of infection and the disease will peak and end within 5-7 days with a characteristic course of mortality.

• Infected birds at 2 weeks of age or less with maternal antibodies show no signs. Immunosuppression is present in susceptible flocks and subclinical infection leads to decreased growth rate and poor productivity.

t

Lesions:Birds dying in acute stage 3-4 days P.I showed:

1- Dehydration with dark muscles.2- Multiple haemorrhages in the leg and thigh muscles,

and pectoral muscles.3- Bursa Fabricius are enlarged 2-3 times than theI

normal size, oedematous and contained flaky deposits and internal haemorrhages with necrosis. Bursa may be creamy yellow coloured. Enlargement of bursa from 2-4 days after infection, return to

' normal size at 5 days and atrophy occurs after 8 days

-41 -

of infection (one third the normal' size) and becomes grey in colour with necrosis of the centers o f the lymphoid follicles.

4- Kidneys in about 5% of infected birds are enlarged with pronounced tubules, pale or congested and ureters filled with urates.

i 5- Increased mucous content of the intestine and haemorrhages in the proventriculus-gizzard junction.

6- Spleen may be slightly enlarged and pigmented with white pinheaded foci in many outbreaks.

Histopathologicai changes:In case of IBD infection, lymphoid structures are affected bursa Fabricius, thymus, caecal tonsile, spleen, and. Harderian glands. In bursa there is hypraemia, haemorrhages heterophilic infiltration, atrophy and necrosis of lymphocytes which soon replaced by heterophils, pyknotic debris, anc reticuloendothelial cells, in addition to oedema of the interfollicular connective tissue.

Immunosuppression:- The importance of IBD is due to its effect on

lymphoid elements in bursa Fabricius, thymus, spleen, caecal tonsils and Harderian glands. Degeneration as well as necrosis of lymphocytes give rise to a condition known as “immunosuppression”

- 42-

which leads to vaccine failure (ND vaccine....) in addition to early infected chickens with IBD virus were more susceptible to inclusion body hepatitis, coccidiosis, Salmonella, E. coli, ILT, MD, IB and gangrenous dermatitis.

- Also, IBD virus suppress the secretory immunoglobulin A (IgA), which is responsible for production of local immunity, a reduction in synthesis of IgA leads to increase in local enteric and respiratory infections.

Diagnosis:1- Sudden onset.in 3-6 week old birds and characteristic

course of mortality (3rd day to 9th day) also enlarged, oedematous and haemorrhagic bursae.

2- Virus isolation: ,,,- Isolation from bursa, spleen or faeces.- Some strains (virulent) require bird inoculation

(instillation of suspension into the conjunctival sac of3-4 week old birds).

- Isolation, on CAM of 9-11 days old embryonated chicken eggs, is the more sensitive route for initial isolation, inoculated embryos will die within 3-7 days (may need some blind passages). Died embryos appeared oedematous, abdominal distention, cutaneous congestion, peticheal

- 43 -

haemorrhage along feather tracts and on toe joints. Haemorrhage and necrosis in the liver. Kidneys congested, CAM odematous with area of haemorrhage only.

- Strains o f low pathogenicity needs tissue culture . (CEFc) for isolation.

' 3- Identification for detection of vims: NT, IFT, IPOX, AGPT, ID and direct EM.

4- Serological identification:- NV-test; for detection of antibodies (N. antibodies).- Pricip. Antibodies (AGPT or ID test).- ELISA test., ■ r : '-

5- Histopathology for diagnosis, sections from bursa, spleen, thymus.

Differential diagnosis:Enlarged bursa, gelatinous and haemorrhagic not present in related conditions coccidiosis, IB infection (variant strains) haemorrhagic syndrome and mycotoxines.

Prevention and control:1- Good hygiene.2- Vitamin-electrolyte therapy is helpful and molasses in water.3- Fumigation with formaldehyde and iodine (iodophore).

-44-

4- Apply insecticide to the floors and wall floor junctions for control of beetles and meal worm.5- Prevent mosquitoes from entering poultry houses.

Vaccination:Three types of IBD vaccines:1- Attenuated mild vaccines.2- Intermediate vaccine used with success in chicks with maternal antibodies.3- Killed or inactivated vaccine.

*In broilers:- Eye drop M- days old.- Drinking water 22 days old.

*In layers and breeders:- 11 days eye drops.- 22 days DW.- Killed vaccines I.M 6-8 weeks of age and at 18-20 week of age.

Enlargment and hemorrhage in bursa o f fabricious.

Hemorrhagic streaks on the lateral aspects ot the thigh muscle.

46

Chicken Infectious Anemia CIA By

Prof. Dr. Ahmed M. El-sadek Hegazy

Def:This disease was firstly isolated in 1979 infect young chickens between 2-4 weeks o f age with retarded growth and mortality between 10-20%. Constitutes serious economic importance. Have no public health importance.

Cause:'.. ;CIA virus is 'the only member of the genus Gyrovirus of the Circoviridae family, Non enveloped, single stranded, circular and DNA virus.

• Resistant to most disinfectant, ether and chlorophorm resistant.

• 5% phenol for two hours is ineffective to kill the virus• 5% formaldehyde for 24 hour at room temperature

inactivate the virus completely,

• No antigenic differences have been recognized among virus isolates.

• The virus resist heating at 56 or 70 C for 1 hour and 80 C for 15 minutes

• The virus can be propagated in tissue culture, 1 day old chicks and chicken embryo. In inoculated chicks it

•• . • 4 7 -

produce anemia and lesions in the lymphoid tissues as well as lesions in bone marrow within 12-28 days post inoculation, low and rarely exceeded 30 %. While chicken embryo inoculated with the virus via yolk sac show hemorrhagic and edematous embryo within 14 days post inoculation. Mortality after 16-20 days.jof inoculation (50 %) embryos are small, hemorrhagic mnd edematous.

Susceptibility:- Chickens are the only natural host.- All ages are affected, 2-4 week old are more and severly

affected.- The virus isolated from geese arid from intestinal

contents of ostrich suffering from enteritis, while antibodies detected in quails only.

Transmission:• CIAV spreads both horizontally and vertically within 8-

14 days post infection (when antibodies negative hens were infected). Field observation indicated that egg transmission occur during a period o f 3-9 weeks post exposure.

• Direct and indirect contact and via oral route as aresul of virus shedding in the feces o f chickens for 5-7 week:

- 4 8 -

post infection and contaminate food, water and environment.

Incubation period:1- Experimentally the incubation period ranged from 10-14

days up to 21 days. 2- Naturally in congenitally infected birds shorter

incubation period 10-12 days.

Clinical signs:1- Anemia (specific signs) with a b e a k ; 14-16 days post

infection, chicks are depressed, pale with retarded growth and pale mucus membrane. ;

2- The secondary bacterial infection in form of skin lesions with gangrenous dermatitis, pododermatitis and subcutaneous haemorrhage o f shank and toe.

3- The secondry bacterial infection leads to increase in the signs and mortalities which may reach 30% in field cases.

Hematology:Blood o f severely affected chickens is watery, the clotting tie is- increased and blood plasma is paler than nomal. Haematocrite value begin to drop below 27% at 8-10 days' after infection, 10-20% at 14-20 days may drop to 6% and return to normal (29-35%) within 28-32 days post infection.

- 4 9 -

Mortality and morbidity:Depending upon viral, host and environmental factors. Uncomplicated horizontal transmission produces no-morbidity with slight mortality or go unobserved. Morbidity and mortality increased when infection with CIAV complicated

..with immunosuppressive vinises (MD, IBDV, Reticuloendotheliosis).

Lesions:Depend upon route of infection, age at exposure, viral dose and immune, status of the host.

1- Thymic atrophy (complete or the reminant showed dark reddish colour.

2- Bone marrow atrophy is the most characteristic lesion (in the femur) becomes fatty and yellowish or pink or dark red.

3- Bursal atrophy is less common.4- Hemorrhage in the proventriculous mucosa with

subacutaneous and muscular hemorrhage (thigh, pectoral with severe anemia).

5- Outbreaks are mostly associated with the so called hemorrhagic syndrome CIAV is also involved in the . etiology of a plastic anemia associated with IBH and IBD. The characteristic lesions are punctuate hemorrhage in proventriculus, S/C hemorrhage of the

wings with severe edema, subcutaneous hemorrhage of shanks and feet result in formation of ulcers.

Histopathology:• Bone marrow atrophy, aplasia, necrosis and the

haemopiotic cells replaced by adipose tissue.• Severe lymphoid depletion in the thymus (repopulation

with lymphocytes 20-24 days, normal at 32-36 days of infection)

• Mild to severe atrophy of the lymphoid follicle in the bursa o f fabricius.

• Small eosinophilic intranuclear inclusions in the thymus and bone marrow 5-7 days post infection.

Diagnosis:1- Isolation on TG for cytopathic effect. Isolation from

liver and spleen, microscopic examination 36-48 hour after passage for CPE.

2- Bioassay by I/M or intraperitoneal inoculation of suspension in 1-2 day old chicks is the most specific method for primary isolation o f CIAV.

•3- Hematological examination, hematocrit values below 27 % indicative for CIAV.

4- PCR or imunohistochemistery (confirmatory)

- 5 1 -

5- Detection o f CIAV by- antibodies , by immunofluorescence and immunoperoxidase thymus stained tissue sections.

6- Serological tests for detection o f antibodies 7-12 days post infection using ELISA, indirect IF and VNT.

Differential diagnosis:• ' f rom Marek’s disease and IBD (atrophy o f bursa and

thymus but do not cause anemia).• In acute IBD (aplastic anemia syndrome, disappear

earlier than that of CIAV).• Adenovirus (IBH) at 5-10 week (not produce a plastic

anemia after a single infection o f exposed chicken);, .

Vaccination:1- Artificially exposure of young breeder flocks by transfer

of infected litter or providing drinking water with infected homogenate tissue.

2- Commercial live vaccine at 13-15 weeks o f age in drinking water or by injection, (safe)

3- Inactivated vaccines.

- 5 2 -

Infectious Ldryngeotracheitis ILT

ByProf. Dr. Mohamed A. El Sisi

Def:Infectious laryngeotracheitis (ILT) is a viral respiratory disease which affects chickehs that may result in severe production losses due to mortality and /or decreased egg production. Severe forms of the disease are characterized by respiratory signs e.g. depression, gasping and expectoration of bloody stained mucous and high mortality. There is no evidence that the virus is transmissible to human beings.

cause:The causal agent is a virus of the family herpesviridae. Antigenically the vims strains appear to be homogenous. Strains vary in vimlence. It can survive outside the host for several weeks under farm conditions. The vims grows well on the CAM of the chicken embryo.

Susceptibility:Under natural conditions the vims infects only the jowl and occasionally the pheasants. All ages of fowl are susceptible.

Males are more susceptible than females. H eav ier b reed s a re more susceptible than light breeds.

Mode o f infection and transmission:The virus is present mainly in the exudates fro m th e respiratory tract and conjunctiva and infection is tra n sm itte d by aerosol. It enters the body through the u p p er re sp ira to ry tract and conjunctiva. Carriers or infected b irds e x c re te th e virus for long periods. The living bird is the m o st im p o rtan t source o f infection and spread o f the disease. B ec a u se o f th e survival o f the vim s outside the host fom ites can b e tra n sm itte r o f the vims.Transmission through the egg is not know n.

Incubation period:Under natural conditions is about 6-12 days.

Clinical signs:A. Peracute form- The bird may be found dead without previous symptoms.B. A cute form

- Characterized by dyspnea, rales, gasping with a wide opened beak, some birds show nasal discharge and conjunctivitis. Death usually occurs in 3-4 days.

- 5 4 -

C. In mild formD. Slight coughing, head shaking, nasal exudate, moist

rales and conjunctivitis.- Egg production is affected and cease entirely for a time

however egg production returns to normal and there is no loss o f egg quality.

Lesions:Vary with the severity of the disease.

1- Lesions mainly are restricted to the upper respiratory tract, hemorrhagic tracheitis, trachea is filled with blood stained mucous.

2- The primary bronchi may also be affected.3- The tracheas are often congested, caseous, diphtheritic

excudate and some hemorrhages.4- In mild forms, there may be excess mucous.5- The nares .may show an inflammatory response with

caseous exudate and conjunctivitis.6- The lungs and air sacs are rarely affected.

Histopathology:The mucosa of the respiratory tract shows inflammation, necrosis and presence of intranuclear inclusion bodies in

. \ f V A G

epithelial cells before desquamation of cells.

-.55-

Diagnosis:1- History of the disease, clinical signs and lesions2- Isolation of the virus or an increase in titer between

acute and convalescent sera.3- Detection of intranuclear inclusion in tracheal sections.4- Examination of tracheal exudate for ILT virus by agar

gel diffusion or by immunofluorescence.5- Examination of exudate with DNA probes.6- Isolation in the CAM of chicken embryos or cell

cultures identification by gel diffusion, neutralization test.

7- Antibodies to ILT virus may be demonstrated by agaigel diffusion or ELISA which is sensitive, specific anc rapid. 1

Control:Live vaccines'are used. In high risk areas vaccination may b< adopted at 1-3 days of age. In other areas vaccination may b< delayed between 3-18 weeks. Method of vaccination include eye drop, spray, drinking water or rarely cloacal scarification Vaccination in the face of an early stage of outbreak may b adopted. i

-56-

H em orrhagic tracheitis due to in fectio u s laryngotracheitis in a ch icken .

5 7

Avian Encephalomyelitis AE

Prof. Dr. Mohamed A. El-Sisi

Def:AE is an infectious viral disease affecting young chickens, pheasants, quails and turkeys. It is characterized by ataxia and tremors in chicks, reduced egg production o f temporary nature and lowered hatchability o f fertile eggs.

cause:AE is a member o f the picomaviridae family. It is an RNA * vims. The vims is resistant, to chloroform, trypsin and pepsin. Susceptible to formaldehyde fumigation and Beta- propriolactone field strains are mainly enterotropic.

Susceptibility:• A natural infection occurs in chickens, pheasants, quails

and turkeys.

• Laboratory animals are refractory to experimental infections.

• Clinical manifestations are only seen in . birds aged 1-6 weeks.

, - 5 8 -

Modes of infection and transmission:Natural infections occurs both horizontally and vertically. Horizontal infection, takes place by direct contact. The oral route is the main way of infection among immature and adult birds.Chicks become infected mainly through the egg from infected hens to the progeny vertically. Chicks may also be infected in the incubator or in the brooder by contact with infected chicks.

Incubation period:After vertical transmission (1-7) days and after horizontal infection (9-16) days.

Clinical signs:1- Young birds show depression,' inappetance,

incoordination of movement, paresis of pa~alysis of the legs, tremors of head and neck, prostration and death.

2- Mortality ranges from 5-20% up to 50-60%. Some of the survivors in chickens may develop blindness as result of opacity of the pupil of one or both eyes. . . -

' 3- Semimature and adult birds develop no neurological signs.

4- In layers there is a drop in egg production (10-15%) which lasts 10-14 days.

5- Egg's laid by infected hens show low hatchability due to embryonic mortality during the last 3 days of inoculation, chicks which hatch from these eggs develop ataxia and leg paralysis.

Lesions:No gross lesions are observed in AE and pathological changesare mainly microscopic.

Diagnosis:1- History of the flock and clinical manifestation frequently

allow a tentative diagnosis.2 - Absence of gross lesions and the finding of the

histopathological changes in the CNS and some visceral organs are characteristic. Neuronal degeneration in the brain, gliosis and perivascular round cell infiltration. Peripheral nerves are not involved visceral organs, namely proventriculous, gizzard and pancreas show hyperplasia of lymphoid follicles.

3- Isolation of virus in embryonated chicken eggs via yolk sac inoculation. The embryos are examined 10-12 days

post inoculation for the presence of paralysis and muscular dystrophy. However for these changes to be detected as many as 5 blind passages may be required for slow egg adapting field strains to induce these changes.

The isolated virus is identified by serum neutralization test using known AE antiserum.

4- Infected birds develop neutralizing antibodies, which can be detected in sera. Eggs laid by these birds. A passive haemagglutination test and ELISA test also have been developed and compare favorably with the VN test. Because of the specificity and rapidity of performance

the ELISA has replaced other tests for antibodyscreening.

5- Egg susceptibility test was used in epidemiological and immunological studies of the disease. From breeder flocks to be tested, 30-40 eggs are used to test AE susceptibility or immunity status. Eggs are incubated. After, incubation for 6 days the fertile eggs are inoculated via yolk sacs with 10'2 EID50 of an egg adapted strain of AEV. Ten to twelve days post inoculation the embryos are examined for the specific AE lesions. If all embryos show AE lesions, the breeder flock is considered susceptible. If 70-100% of the embryos show no lesions the flock is regarded adequately immune.

6- For differential diagnosis, it is necessary to consider other causes of neurological disorders as ND, Marke’s disease, encephalomalaecia and riboflavin deficiency.

Prevention and control:1- Hatching from flocks known to be immune.

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I - Vaccination o f breeder chickens at the age o f 14-16 weeks with live enterotropic vaccine via drinking water affords a satisfactory immunity to the progeny.

S- Also inactivated vaccines are available and may be used.

- 6 2 -

C om eal opacity o f the pupil o f chicken survived from AEinfection

Nervous m anifestation o f baby chicks suffered from AE

infection.

63

Avian Reovirus InfectionsBy

Prof. Dr. Mohamed A. El-Sisi

Def: Avian Reoviruses have been isolated from a variety of tissues •from chickens affected, with arthritis, stunting syndrome, malabsorption syndrome, enteric disease, respiratory disease as well as from chickens that were clinically normal. Infections following, reoyiras is very much dependant upon host age, virus pathogen, route of exposure and immune status. In broilers, losses related to- the infection are increased

-mortalities, vital arthritis, poor feed conversion, uneven growth and reduced marketability.Breeder flocks, develop viral arthritis, decreased egg production, reduced fertility, hatchability and egg transmission of virus.

cause:RNA virus, replicate in the cytoplasm, there is no envelope. The virus is resistant to chloroform, trypsin and Ph3. lacks haemagglutination.

- 6 4 -

The virus grows well in ECE via yolk sac & CAM routes of inoculation as well as in tissue cultures. Avian reoviruses have a common group antigen as detected by gel diffusion. There are at least 11 serotypes. There are considerable variations in virulence between antigenically similar isolates.

Modes of the infection and transmission:The virus present mainly in exudates from upper respiratory tract, conjunctiva and faeces of affected as well as carriers. A movement of such birds is a potent method o f spread. Transmission through the egg is not known. Because o f the survival of the virus outside the host fomites as infected crates, equipments and buildings and mechanical carriers such as man, free birds, cat's and dogs can be transmitters o f the virus.

Signs and lesions:1 - Avian reoviruses have been associated with entire

conditions, cloacal pasting, ulcerative enteritis, respiratory troubles, anemia, hydropericardiium and inclusion body hepatitis.

2- The viruses may be involved in syndromes as runting in broilers, proventirculitis, diarrhea and skeletal changes, However other agents been implicated.

3- Avian reoviruses are associated with tenosynovitis or viral arthritis in meat producing birds characterized by bilateral swelling of the digital flexors and

- 65-

transometatarsal tendons. Articular erosion may be recorded.

4- Morbidity is variable; mortality is usually under 1 % but can reach 10%.

Diagnosis:1- Case history.2- Signs and lesions.3- Isolation in chicken embryos or tissue cultures (chick

embryo, lung or liver kidney cells) faeces and spleen are good sources o f virus.If arthritis is present synovial fluids should be included in the inoculum.

4- In high virus concentrations rapid death o f embryos with congestion and hemorrhages o f skin and internal organs. I f the embryos live longer, become dwarfed and show necrotic focci in spleen, liver and hearts

5- Group antibody can be detected by gel diffusion test and neutralization tests.

- 6 6 -

R u p tu re o f th e g a s tr o c n e m iu s te n d o n d u e to v ira l arthritis.

Poor feathering as a result o f m alabsorption syndrom e.

Avian Neoplasms By

Prof. Dr. Abd El-Shakor Ismail

Def:

A variety group o f related and unrelated diseases possessing a single common character ‘"Neoplasms” these are:

I. Virils induced tumors: (Tum or v iruses) com prise f iv e

d ise a se s co n d itio n s

• Marek’s disease: Lymphoprolifrative disease affecting peripheral nerves and visceral organs.

• Leukosis sarcoma group: Are related neoplasm (Leukosis, Sarcoma).

• Reticuloendotheliosis: Antigenically related neoplastic disease in ducks, turkey and reticuloendotheliosis in chickens.

• Lymphoprolifrative disease of turkey.

• Myeloid leukosis (subgroup ALV - J)

NB: These are transmissible tumors of mesodermal origin.

- 6 8 -

II. Tumors of unknown etiology: Described on basis of morphological characters.

Classification of transmissible tumors is difficult due to:

1- Many virus strains have multi-potent characteristics.

2- Sometimes pathogenic lesions are difficult to distinguish.

Prevalent diseases in poultiy are Leukosis and Marek’s disease.' The problem is that flocks may be infected with more than one agent.

Avian Leukosis

Def:Included in this group of diseases is wide range of neoplasm of mesenchymal origin characterized by irreversible, progressive autonomous proliferation of essential blood forming cells or other types of cells.

Economic importance:Losses from ALV induced diseases are attributed to:

1- Mortalities around 1-2 % with occasional losses up to 20%or more.

2- Subclinical infection produces depressive effect on important performance trait including egg production and quality.

3- Immunosuppressive effect.

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Cause:Oncoviruses belonged to family Retroviridae, they are multipotent viruses inducing variety of neoplastic diseases, They are grouped:

1- Avian leukosis sarcoma group includes.• Exogenous viruses (infective viruses) which produce

neoplastic changes in hemopioetic system and cause inapparent infection in CEF-cells, (sub-group A,B,C and D, AL viruses) and sarcoma viruses which produce neoplastic changes predominantly in connective tissue proper and transfer CEF-cells to tumor cells

• Endogenous viruses, integrated gene do not produce infective virai’ particles, with little or no pathogenicity (Subgroup E).

2- Reticuloendotheliosis viruses,' exogenous viruses causing lymphoma and ranting disease syndrome3- Lymphoprolifrative disease of turkey.4- AL- viruses (Subgroup J). Associated with myeloid leucosis, occasionally other types of tumors are also seen (meat type of chicken) appear as a new virus as a result of genetic recombination between exogenous virus of subgroup k , B and endogenous virus (subgroup E).

Susceptibility:D om estic poultry is the natural host, turkey, ducks, geese p igeon and some other birds may be affected.

• r

Transmission:1- Exogenous viruses are transm itted in 2 w aysa. Vertical transm ission through eggs.

b. Horizontal transm ission from bird to b ird b y direct and indirect contact (o f little importance).

c. Congenitally infected embryo develop immune] tolerance to virus and make up V +A- class v/ith high level o f virus in blood and tissues and absence ofantibodies. V irus shedding into egg album en isassociated w ith virus production by album en secreating glands o f the Oviduct.

2- Endogenous leucosis -viruses usually transmittedgenetically in germ cells o f both sexes. M any ate genetically defective and incapable o f g iv ing infective viruses.

Incubation period: Depend on virus strain, dose, route, age at exposure and genetic constitution o f the host. In the field cases can occur after 14 w eeks o f age, w hen infection occur genetically or at early age.

- 71 -

Rous Sarcoma (RS)RS- doesn’t occur, frequently as a cause o f spontaneous neoplasia in fowl, it 's importance is a laboratory tool for tumor research.

Clinical features and pathology of avian leukosis:From standpoint o f clinical disease, leukosis include a number o f distinct entities in domestic fowl. Pathological features are basically sim ilar in that from cellular —stand point o f view at least. They are comprised o f blood cells or their precursors. The site o f specific lesions however varies considerably.

Clinical Leukosis* can be divided into:• Leukemic leukosis, manifested by abnormal cell content

in the peripheral circulation.• A leukem ic leucosis, manifested by neoplastic growth in

which the basic cells are lymphocytes or its precursor.

Clinical Pathology of the disease:I- Lym phoid leukosis (visceral leukosis, Big Liver disease) this is the commonest form o f leucosis and observed in birds over 14 weeks. Females are affected more than males. Pale com b and wattles, progressive emaciation, enlargem ent o f liver w ith either diffuse grayish red marbled appearance o r nodular and bird is anemic. Neoplastic lesions in the visceral organs beside liver are spleen, kidney, ovary, heart and lung. Lesions are either diffuse

.. - 7 2 -

enlargement o f the parenchymatus organs or localized (nodular) or both.

II- Erythroid leukosis: Sporadic disease usually seen in birds o f 6months, characterized by progressive weakness, anemia, appearance o f immature erythrocytes (erythroblasts) in blood. Blood is often pale, w atery and clots slowly. HB is reduced. Lesions include diffuse enlarged liver, spleen and kidneys with bright cherry red discoloration. Petecheal hemorrhage in the m ucosa o f intestine and liver capsule. Bone marrow is grayish red and jelly like, rare rupture o f paranchematous organs especially liver.

III- Myeloblastosis: Sporadic cases o f mature birdscharacterized by extravascular proliferation of granulocytes. Symptoms are those o f anemia leading to progressive weakness and death. Lesions are diffuse enlargement o f liver, spleen and kidneys with grayish: mottling and granular appearance. Bone marrow appear pale or pink.

IV- Myelocytomatosis: occur sporadically in grower birds. Lesions are small yellowish-white solid tumo rs are usually present along the ribs or inside the keel bone or on the

cranium. Occasionally muscular invasion and metastasis in visceral organs.

V-Osteropetrosis: Sporadic infection affect male and female birds, characterized by jerky gait associated with bilateral, irregular thickening of the diaphysis of long bones, followed by marked thickening of legs, which exhibit a boot-like appearance. Anemia as a result of progressive reduction of bone marrow.

VI- Avian leucosis virus subgroup-J (ALV- J): Wide spread poses a serious economic importance for broiler integrators. The virus cause Myeloid leucosis in broiler breeders. It beloilged to Retrovirus family as genetic recombination of an exogenous ALV with non functional env- gene from endogenous retroviral gene. It can spread both vertically and horizontally. Virus isolation and identification is more difficult. Commercially available AC-ELISA kits detect the (GS) antigen of all ALV including endogenous ALV.

Differential diagnosis:MD, TB, Pullorum disease, Coli granuloma, Aspergellosis,Rickets and osteopetrosis.

- 7 4 -

Diagnosis:The diagnosis of AL for most part has been based on:

1- PM, Histopathology and Hematological changes.2- Induction of the disease in susceptible birds.3- IF, RIF and COFAL tests.

Prevention:1- Complete isolation of susceptible chickens for at least 1st weeks of life.2- Hygienic measures.3- Breeding of resistance breeds.4- No recommended vaccination.

- 75-

L ym p h oid L . E rythroblastosis M yelob lastosis M ylocytom atosis

I n c i dence 5-8 M - 3-16 W 3-16 W

ClinicalEnlarged liver,

weaknessAnaem ia and

em aciationAnaem ia and

emaciationAnaem ia and

emaciation

PathologicalTumor,diffuse,

nodular

D iffuse Nodular

Liver

Greatly enlarged

D iffuse, focal

D iffuse cherry

redD iffuse grayish M ahogny color

Y ellow ish , white

nod.

|SpleenD iffuse, nod Enlarged, diffuse

cherry softD iffuse tumor Nodular

BF Nodular N o . Tumor Nodular

B m arrow Focal diffuse C h en y d iff D if f Tum or nodules

TCytology Lym phocyte Erythroblast M yeloblast M yelocyte

BloodLeukem ia . A nem ia

Erythroblastosis: M . leukem ia N o

|Others K idney, ovary ' ' K idney, ovary Surface bone

.. - 76 -

Marek's DiseaseFowl paralysis, polyneuritis, neural lymphomatosis.

By

Prof. Dr. Abdelshakor Ismail

Def:

Ml!) is acommon lymphoprolifrative disease o f domestic fowlsaffecting the peripheral nerves and visceral organs. The mainforms o f the disease are:

• Classical MD, in which the peripheral nerves areprimarily involved and in which only small proportion o f ! cases have lymphoid tumors o f visceral organs.

• Acute MD, in which neural lesions are less predominant. and lymphoid tumors are common. ~

• Acute cytolytic disease and transient paralysis are less common.

The absence o f control measures can cause devastating losses in commercial layers and broiler flocks with MD.

Jr

Cause:

MDV is cell associated herpes virus with lymphotropic properties similar to those o f Gama-herpesviruses. Three

serotypes of the virus exist. Serotype-1 strains are further divided into pathotypes, which are often referred to as mild (m) MDV, virulent (V) MDV, very virulent (W ) MDV and very virulent plus (W +) MDV. Strains, the two additional groups of non oncogenic herpesvirus are SB1, HPRS-24 and HVT (FC126),respectively.

For virus isolation from affected organs cells suspension and not cell free filtrate, whole blood with anticoagulant is useful for isolation. The virus replicate in the epithelial cells of feather follicle maturates and release of infectious virion occurs.

Factors for establishment of disease are

1 - Pathogenicity of MDV.

2- Age

3- Genetic constitution

4- Sex, mAb (maternal antibodies) and interference

5- Virus infections, coccidiosis, helminthes, andbacterial infection.

6- ’ ‘Nutrition, Housing, Water, Light, ventilation.

N.B: I n f e c t i o n i n t h e 1 st d a y s o f l i f e r e s u l t i n :

Increased rate of disease condition.

Long term viremia

Skin form (skin leukosis).

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• k • ‘

-•'I

Transm ission:

M D V is transm itted readily by direct and indirect contact betw een chickens apparently by airborne route. Epithelial cells in kera tin ized layer o f the feather follicle replicates fully-in fectious virus. V irus associated w ith feathers and dander is,' • uin fectious and contam inate poultry house. D ust remains infectious for at least several m onths at 20 — 25°C and for years at 4°C. In lym phoid lesions cells the infection is not productive, b u t accom panied by proliferation o f these cells and eventual developm ent o f tumors.

R esp irato ry tract infection is the natural route o f virus entry. A fte r inhalation exposure to infectious feather m aterial, high incidence o f infection was established. M DV is taken up by phagocytic a lveolar cells where it m ultiplies. During substantial v irus replication in the viscera , in the 1st week of exposure, a persistent infection o f the w hite b lood cells was found. The signs o f infection subsided briefly in the 2nd weed post exposure, followed by progressive lym phoproliffation and spread o f infection to an increasing num ber o f tissues.

Turkeys reared in commercial environm ent are commonly infected w ith turkey herpesvirus (HVT) a potentially transm itted non-pathogenic herpesvirus w hich share some antigens w ith M DV. W hen inoculated in chickens prevent

• Immune depression.• *’i

Im m une depression.

neoplastic disease caused by super infecting MDV. Darkling beetles were shown to passively carry the virus.

MD infection under field conditions may occur as early , as 1st. week after hatching and the incidence o f infection often approaches 100% by eight weeks. Infection persists for long periods both in flocks and individual chickens. Although the development o f microscopic lesions and the presence of virus are closely related infection seldom result in clinical disease.

Pathogenesis:

MDV infects birds through the respiratory route via inhalation of cell-free virus in the feather dander. The alveolar

| macrophage cells present in the lung act as transporters for ;j MDV from the respiratory tract to different organs. They carry ij MDV through the blood stream to the lymphoid organs, i especially the spleen. After MDV particles are delivered to the I lymphoid organs, the virus undergoes cytolytic infection in B-

lymphocytes o f these organs 4-6 dpi. After the establishment o f lytic infection in B-lymphocytes, MDV becomes latent inside T-lym phocytes,This mainly starts at 6-7 dpi. After the 2nd or 3rd week o f infection, some virus particles reactivate from latency state and a lytic infection appears in different epithelial tissues (Feather follicle.. epithelium). The transformation in MDV is defined as the neoplastic changes of the latently infected lymphocytes to lymphoblastoid tumour

- 8 0 -

cells. Three to four weeks post infection;, latently infected ,, lymphocytes migrate into different visceral organs and peripheral nerves, where they differentiate to form lymphoma.

N.B:- Latent infection is a phase in certain viruses' life cycles in which after initial infection, virus production stop. However, the virus genome is not fully eradicated. The result of this is that the virus can reactivate after a while and begin producing large amounts of viral progeny without the host being infected by new outside virus.

Clinical signs:1-The classical form Usually occurs birds aged 12-24

. weeks and affects primarily the peripheral nerves or nerve plexuses resulting in varying degrees: of paralysis of particular or several parts of the body. Involvement of

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sciatic results in : progressive lameness of one or both legs, the birds lies on the ground with a tendency to hold one leg stretched forward and the other backward, paralyzed bird is unable to reach food and water, usually die from starvation or dehydration. Involvement of the brachial plexus is indicated by droopiness of the wings. Affection o f the vagus and intercostal nerves lead to difficult breathjpg (gasping) while affections of nerves supplying the digestive tract may be manifested by digestive disturbances as flacid croup and diarrhea.

•Occasionally when the cervical nerves are involved there is torticollis locomotors disturbances are often associated with loss of weight paleness of the comb and wattles and diarrhea although the appetite may remain good.

2- Lymphomatosis (Visceral lymphomas) There is a few clinical signs appeared on the birds ranged from general depression to totally comatose.

3- O cular form Characterized by depigmentation or diffuse grayish fading of the iris of one or both eyes and irregular pupil (serration, slight or pinheaded like) which show progressive loss of light accommodation (blindness).

4- Skin form (Skin leukosis) Nodular lesion appear on many areas of the bird skin.

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5- Early mortality syndrome and acute cytolytic formOccurs in young birds raised intensively at the age, o f 3- 6 weeks up to 12 weeks, with rapid course and high morbidity and mortality up to 50%. In this form only small proportion o f birds show symptoms o f paralysis, others appear depressed and many birds die suddenly without preceding symptoms. j

6- Transient paralysis MDV infection o f the central j nervous system (CNS) usually results in cases o f general flaccid paralysis called transient paralysis. It is temporary flaccid paralysis in the bird neck which disappears after 2-4 days. Birds recover from the paralysis may have other neurological signs, such as ataxia and torticollis, appear and persist.

Lesions:

1- In classical form, affected nerves show localized or diffuse swelling as a result o f edema and infiltration with mononuclear cells together with loss o f cross striation. Mortality rarely exceeds 10 - 15%, occurring over few weeks or may months. A proportion o f birds with nerve lesions may show lymphoid tumors in visceral organs.

2- In acute form, lymphoid tumors, involving the visceral organs; gonads, spleen kidney, lung, heart, liver and sometimes the digestive tract mesentery, skeletal

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muscles and skin are present with or without nerve lesion. Lymphomas in visceral organs with frequency of 10 - 30% and major outbreaks can go up to 70%, depression, weight loss, anorexia and diarrhea.3- Acute cytolytic disease, infection with VYMDV with sever atrophy of lymphoid organs is recognized results in high mortality between 10-14 days the disease is also described as early mortality syndrome.

4- Transient paralysis, associated with edema of the brain in some cases it can be fatal.

Diagnosis:■ 1-History, clinical, postmortem and histopathological

examination.

2- Virus isolation has no value in the diagnosis, as infection usually result in persistent viremia with or without clinical disease.

3- Antigen detection in feather tips FFE, lymphoid tissues immunohistochemistry, Fluorescent antibody test, Agar precipitation tests, ELISA.

4- Detection of the viral genome in the FFE and tumor tissues via using PCR and DNA Probe.

5- Electron microscopy.

6- Ab demonstration.;

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Prevention and control:1. Sanitation and isolated rearing which o f value o f

minimizing but riot preventing outbreaks o f the disease.

2. Selective breeding for resistance is relative but not absolute.

3. All in all out policy.

4. Possible break of infection cycle by disinfection, removal of used litter & control o f arthropod.

Vaccination:Live vaccines are used to day old chickens at hatcheries or inovo vaccination to provide protection against naturalchallenge. Vaccines are usually used at dose o f 103 PFU.

• Serotype-1 vaccines: Attenuated HPRS-16 and CVI- 988 (Rispens vaccines) which is able to protect against challenge with w MDV and w + MDV pthotype.

• Serotype-2 vaccines: Naturally non pathogenic strain of MDV (SB- 1& 301 B/a) strains. They are protective in cell associated form against challenge with virulent viruses but less against W M D .

• Serotype-3 vaccine: FC-126, wide used commercially,' low cost, available in cell free form. .

• Polyvalent vaccines: Combination o f two vaccines result in protective synergism.

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Although MP vaccines are successful in controlling major losses, vaccine failure may be due to:

1- Emergence of vMDV that can break vaccine-induced immunity2- Exposure to vMDV before development of immunity.3- Interferance with maternal antibody.4- Improper vaccination and use of non-protective vaccines.5- The current vaccine does not provide sterilizing immunity, meaning the bird remains as a potential source for viral infection.

• Recombinant vaccines: Using FPV vector.

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Distinguishing features o f Avian Leukosis and' M arek's diseaseFeature MD ALEtiology Alpha herpesvirus Retroviru

PropertiesRIF activity - +

COFAL activity +„ Cell association + -i 1 ,• Antiodies +

Epidem iology_______________ .Agg__________ > 6 weeks >16 weeks

Sex V1OfA2 - c?

Incidence <50%In non-vaccinated

Flocks

< 5 %

Latent period Short LongEgg transmission ? ■ +++Contagiousness +++ +

Immunity + +Developm ental disturbances + +

W eakness and anemia + +Respiratory manifestation Rare NoLocomotors disturbances Yes No

Tumor development Yes YesPathology

CNS Yes No11 Peripheral nerves Yes No

Lymphoid cell prolifration Yes NoSkin and feather follicle Yes No

Liver tumors Perivascular Focal or diffusOrigin of neoplastic cells T-Cells B-Cells j

Avian Reticuloendotheliosis By

Prof. Dr. Abd Elshakor Ismail

Def:Designates group of pathological syndromes caused by a group of retroviruses .that are distinct from those causing AL/Sarcoma group. Natural infection occurs in turkey, chicken ducks pheasants and quails.

The disease syndromes include:

1- Runting disease syndromeThe clinical signs with .runting disease syndrome may be notably stunted and pale birds. Weight reduction may be 20- 50% lower than 'normal birds by 3-5 weeks after infection. Some chickens may have abnormal feather development, termed Nakanuk in which wing feather have adhesions of barbules to part of the feather shaft.Culling is more than 50% between 5 and 8 weeks. Sometimes infiltration of peripheral nerves by lymphocytes and plasma ceils, leading to nerve enlargement and sometimes lameness and paralysis. These may be accompanied by lymphoma in other organs. Proventriculifis may also occur. The syndrome is due to infection with non defective REV.

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2- Chronic lymphoid neoplasm fThe non defective strains of REV induce two types of chronic lymphoma in chickens. The 1st is bursa-dependant (B-Cells Lymphoma) indistinguishable from LL occur iri chicken after long latent period (4-10months). The 2nd is T-Cell lymphoma

shave been induced experimentally composed of large uniform Hymphoreticular cells in various visceral organs and peripheral nerves 3 weeks after inoculation. Grossly these tumors are some what similar to those of Marek's disease. Birds developing chronic lymphoma becomes depressed prior to death but show specific signs.

*. . . y - v

3- Acute reticular cells neoplasiaThe disease manifestation is not common, although infection appear to be wide spread. Laboratory derived strain T is a defective; for replication it requires non defective RE- helper virus. Newly hatched chicks or turkey that develops acute reticulum cell neoplasm following inoculation with defective strain T become depressed prior to death.

,<b

.

Pathology:1- Runting disease syndrome

, Atrophy of thymus & bursa enlargement of peripheral nerves, abnormal feathering, development, proventriculitis, enteritis, anemia and necrosis of liver and spleen. These are often

'i

i t- 89-

Iccompanied by depression of cellular and humeral immune Response.

I- Acute reticular cells neoplasiaeffected birds develop large liver and paleness with

Infiltrative focal or diffuse lesions is common in pancreas, gonads, heart and kidneys. Blood shows low heterophils and Increased lymphocytes.

Chronic lymphoid neoplasia)eve!ops B-cells lymphoma of liver, bursa producing nodular jr diffuse lesions in liver bursa and other visceral organs.

)iagnosis:1- No pathognomonic lesions.2- Histopathology.3- Virus detection, viral antigen could be detected in sera of

viremic birds using AGPT, COFAL, ELISA and PCR.

Control:LEV infections are sporadic and often not associated with dinical; signs. No control procedures have been developed.

Lymphoproliferative Diseases of Turkeys By

Prof. Dr. Abd Elshakor Ismail

Def: ■ •••*

The disease is mainly seen in growing turkeys between 7-18 weeks of age and occasionally adults. Affected birds die suddenly, Sometimes after preceding depression. Up to 20% of; the flock could be affected..

cause:; i r, «,j

Retrovirus distinct serologically and antigenically from other*' avian retroviruses. The disease may be reproduced by* inoculating turkey poults with tissue extract and plasma from'* infected affected birds.LPD is characterized by marked enlargement of spleen which is usually pale pink in color with marble appearance. Liver may be moderately enlarged with military grayish-white foci 'which may occur also in kidneys, gonads, intestinal wall,' / ' ‘ .. • ' $;■ pancreas, lung, and myocardium. Peripheral nerves may beslightly enlarged. Anemia could be occurred. Leukocytosis orleukocytopenia have been observed proliffative lesions aresimilar in all organs.

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piagnosis:1- Gross and microscopic lesions.

2- Detection of the reverse transcriptase enzyme in the serum.

Control:No; specific measures.

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Typical presentation o f paresis o f legs in a chicken with Marek's d isease.

Eye in vo lv em en t w ith n eop lastic cell infiltration into the iris resulting in an irregular pupil in a ch ick en w ith M arek's d isease.

Lymphoid l iv e r tu m o r c o m p a t i b l e w ith both l e u k o s i s and M a r e k s d i s e a s e .

Avian leukosis

94

Avian Pox

ByProf. Dr. Mohamed A. Lebdah

Def:Fo>vl pox is a slow spreading viral disease o f chickens, turkeys, pigeons and other birds characterized by appearance of prolifrative skin lesions (cutaneous lesions) on unfeathered portions o f the body and/or diphtheritic lesions in the upper digestive and respiratory tracts, that often occurs in late summer. It is worldwide in distribution.

Cause:Avian poxes are a member of the Avipox genus, of the family poxviridae. These members are fowl pox, turkey pox, pigeon pox, sparrow pox, canary pox and quail pox which are closely related but distinguishable. Fowl pox is the largest virus known. It is brick-shaped, with dimensions of 300 x 250 x lOOnm. It have tubular structures which are wound round the surface p f . the virion giving the virus its characteristic appearance. Fowl pox is DNA virus contained within internal structure known as a core, it have an oval structure in the concavity of the core, known as lateral bodies, which contains the viral enzymes. The viral enzymes use the DNA as jr._

- 9 5 -

a template to initiate the cycle o f replication which produces all the necessary viral proteins, enzymes and DNA for new infectious virions. Fowl pox virus is resistant to ether. It is inactivated by 1% caustic potash when separated from its matrix. It withstands 1% phenol and 1% formaline for 9 days. It can survive in dried scabes for months or even years. Fowl pox virus usually replicate intracytoplasmic o f the cells, forming inclusion bodies, which composed o f amorphous material surrounded by an outer membrane and known as Bollinger’s bodies, which contains elementary bodies known as Borrel bodies. Recovery from poxvirus infection usually results in a strong, enduring immunity to later exposure o f the same virus.

Incidence:Fowl pox is world - wide in distribution and the disease is endemic in tropical and subtropical regions. The disease is a

relatively common disease.

Susceptibility:Domestic and most wild birds o f ail ages except the recently hatched are susceptible to infection with pox virus. Pox occurs frequently in chickens and turkeys. Among other birds pigeons, canaries and psittacines are frequently infected.

, I

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T ran sm ission :

Routes of infection1- Cutaneous route injured or abrasions of the skin either through direct contact or through blood - sucking insects especially mosquitoes and sometimes from contact with contaminated litters.2- Respiratory route through inhalation of contaminated aerosols.

Routes of transmission1- Insect transmission through mechanical or biological

transmission of the pox virus by biting the susceptible chickens.

2- Lateral transmission occurs through direct contact of diseased birds to non-ififected birds.

3 - Mechanical transmission through cannabilism of infected birds.

N.B) Bad hygienic and sanitary measure aids in more and rapid spread of the infection.

Pathogenesis:Virus enters an epithelial cell and then spreads from cell to cell locally, helped by the induction of epidermal growth factor which causes proliferation of cells. Some virus enters the blood to cause a viraemia. Although there is spread to internal

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organs, no gross pathological changes are evident. However,' there is some viral replication in liver and spleen and secondary viraemia occurs and then the virus relocalize in the; epithelium.

Clinical findings:Fowl pox classified according to the site o f pox lesions.into:

a- Skin or cutaneous or dry form: In which wart-like nodules either reddish-brown or blackish in colour, appears on the unfeathered skin o f the head (comb and wattles, com er of the mouth, around the eyelids, and angle o f the beak), neck, legs, ventral surface of wings, vent, and feet. The cutaneous lesions can vary in appearance. First there is a papule, which rapidly progresses through the vesicle to pustule and finally to the crust or scab stage, after two weeks the scab will drop off and may or may not leaving a scar (papule - vesicle - pustule - crust or scab). A mild form of the disease may remain unnoticed with only small focal lesions, usually on the comb and wattles. . ;i:

. l ib- Mucous membrane or diphtheritic or wet form : In which the diphtheritic lesions either white or yellow in colour on the

. mucous membranes of upper respiratory and digestive tracts ; (mouth, nares, pharynx, larynx, oesophagus, or trachea)^iThe

disease begins as small white nodules, then coalesces to form

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raised yellow plaques. M ost diphtheritic lesions are present in the m outh that interfere with feeding but others are present in

the larynx, trachea and oesophagus. These lesions leads to inappetance and/or difficulty in breathing (dyspnoea). Lesions in the nares can give rise to nasal discharges, whilst those on

the conjunctiva give rise to ocular discharges and in rare cases result in blindness.

c- M ixed fo rm : Both cutaneous and/or diphtheritic lesions are present. The disease usually spreads slowly through the flock, this m ay last several weeks. Sometimes, the disease may only show as m ild reduction in the rate o f weight gain or a lack of vigour in the flock. Fowl pox in layers can cause a drop in egg

production and in young chicks, it reduces growth. The mortality rate is as high as"50% reported with the diphtheritic form but it is usually low.

D iagnosis:Fowl pox diagnosis depends on:

• 1 - Case history: slow spreading o f either cutaneous lesions ordiphtheritic membrane lesions.

2- C linical findings: cutaneous form of pox can be

diagnosed w ith the clinical findings but the diphtheritic form is confused with others e.g. avitaminosis A and candidiasis.

3- Laboratory diagnosis o f fowl pox depends on:

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a. Histological examination of cutaneous lesions or diphtheritic lesions to detect the esinophilic intracytoplasmic inclusion bodies (Bolinger’s bodies).

' • 'j

b. Isolation of poxvirus.

Sample collectionPox viruses are readily isolated from the nodular lesions of infected . birds. Tissues with lesions-preferably recently developed lesions - can be removed with sterile scissor, and forceps by cutting deep into the epithelial tissue. The material is ground with sterile fine sand in a sterile mortar and with saline make a 10% suspension is centrifuged for 10 minutes at about 700 rev/min to remove large tissue particles. Antibiotics (Penicillin and streptomycin) are added to the supematent fluid and then the suspension is held at room temperature for 30 minutes to 60 minutes before inoculation. A piece of tissue should also be collected (in 10% neutral formaline) for histopathological examination to reveal cytoplasmic inclusion bodies. Serum samples may be collected to determine previous exposure by serological tests.

'Laboratory hostsECE, susceptible birds and cell culture.

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ECE inoculationECE, 9- to - 12 day - old, about 0.1 ml of virus suspension is inoculated on the CAM. Inoculated embryos are incubated at 37°C for 5 to 7 days and then examined for pocks on the CAM. Pox lesions appear either as focal white opaque pocks or as a generalized thickening of the CAM. Then histological examination of pock lesions of CAM to detect the intracytoplasmic inclusion bodies.

c. Experimental infection of susceptible chickens with lesion material by inoculation either in wing web or

’ with scarification of the comb or into the feather follicles. The characteristic lesions should be present 5to 7 days after inoculation.

\ N

d. Serological examination: Serological tests have been used to detect fowl pox specific antibodies. These

include the agar gel precipitation test, passive haemagglutination test, serum neutralization and

ELISA.

Agar gel diffusion test

Skin, CAM, or diphtheritic lesions can be used for preparation of antigen to be tested against known antisera. Lines of precipitation may appear in 24 to 48 hours after incubation of positive sera with viral antigen at room temperature:

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Passive haemagglutination test

Antibodies against fowl pox virus can be measured by a'

passive haemaglutination test using tanned horse or sheep

erythrocytes coated with fowl pox virus antigen partially

purified by fluorocarbon treatment. Passive haemagglutiriating '

antibodies are detectable in some sera o f infected birds as early

as 1 week after inoculation and may persist for 15 weeks, i.e.

longer than precipitating antibodies.■■ ■ i

Differential diagnosis: • :

The diphtheritic form o f fowl pox must be differentiated from

Avitaminosis A and candidiasis.

a. Difference between pox and Avitaminosis A:C riterion Pox A vitam inosis A

1-Cause P oxvirus Vit. A deficiency

2-Incidence Moderate to high in

incidence

Low in incidence

3-Susceptible age Any age M ostly young ages

4-Lesions W hite or yellow plaques

are difficult to be

removed from its

underlying tissue and on

detaching, leave o ff

bleeding surface

W hite pustule-like lesion j

on m.m. o f buccal cavity !

extended to oesphageal

membrane and are easily

to be detached and not'

leaving bleeding surface. !

5-Therapy diagnosis w ith

administration o f vit. A.

N o response Good response j

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b. Difference between pox and candidiasis (thrush):1 -C ause P o x viru s C andida alb icans2 -In cid en ce M od erate to high L o w in in c id en ce3 -S u sc ep tib le a g e A ll . d o m e stic birds

e x c e p t w ater fo w lA ll d o m estic birds

4 -L esio n s W h ite or y e llo w p laq ues are d iff icu lt to b e rem o v ed from its u n d er ly in g tissu e and o n d etach in g , lea v e o f f b le e d in g su rface

W h ite ulcerations c o a le sc e s togeth er form ing T urkish to w e lin g and e a s ily to b e rem oved

5-R apid sm ear S h o w n oth in g S h o w sp ores and hyphae.

Control:The control o f avian p ox depends on:

1- A doption o f good biosecurity measures to prevent the spread o f the d isease w ithin the affected flock.

2 - Strict iso lation o f d iseased birds from healthy birds and then apply the fo llow ing:

3- Treatment o f d iseased birds by:a. R em oval o f all pox lesions.b . Then, touching the b leeding surface o f the skin with

tincture iodine-glycerine (1:4), tw ice daily till its drying or b leed ing m ucous surface w ith gentian violet 2-4% .

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c. Administration of vit. K3 (vit. K320%R) via drinking: water with a dose of 10 mg/bird/day for 3-5 successive

. days.d. Administration o f vit. AD3E, especially vit A to

repairing cutaneous or mucous membrane healthy condition and increases vitality of birds.

e. Administration of broad spectrum antibiotic, especially that of high-effect on respiratory tract, to compensate or prevent secondary bacterial invaders.

4- Emergency Vaccination of apparently healthy birds using pigeon pox vaccine.

Prevention:

Avian pox can be prevented in chickens, turkeys and pigeons by vaccination, but there, is no effective vaccine against canary pox. Vaccination is usually done when the birds are well started but can be done at any age if necessary. Pullets should be vaccinated well before production begins. There are three live pox vaccines (fowl pox vaccine, pigeon pox vaccine and turkey pox vaccine). There are two methods of pox vaccination, the wing web stick method, in which, the vaccine is inoculated into the skin of the wing web, usually using a bifurcated needle, which has a groove that holds the vaccinal fluid and by which chickens and pigeons are usually vaccinated. Turkeys should not be vaccinated by the wing web stick method but are vaccinated by a thigh stick method in

- 1 0 4 -

which the feathers are removed from the thigh and vaccine brushed into the resulting follicles. Whichever method is used, the skin is examined 7 to 10 days later for the existence o f pox lesions (vaccinal take). I f more than 10% o f the birds do not have any lesions, then the vaccination has been unsuccessful. The wing web stick method o f pox vaccination in turkeys is not practised as the turkeys sleep with their head under their wing and hence lesions on the head could be produced. Fowl pox vaccines used in chickens and turkeys while turkey pox vaccine used in turkeys only, whereas, the pigeon pox vaccines are widely used in turkeys, chickens and pigeons. Vaccination

•is usuaLly done in areas where fowl pox is endemic or there have been outbreaks in the last season. M ost layers and breeders are vaccinated before they become lay, ideally 3 to 5 weeks before egg ^production starts. It is best to vaccinate chickens when they at least 6 weeks o f age. It is very important to follow the instructions given by the vaccine manufacturer. Do not vaccinate birds which are in poor condition or which are affected with any other condition. Precautions should be taken to minimize the spread o f the vaccine virus, both on the birds and in the environment.

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Scab-like lesion on the unfeathered portion o f the skin due to fowlpox on a broiler-breeder.

Scab-like lesion on the unfeathered portion o f the skin due to fowlpox on a turkey.

106

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Avian Adenoviruses Infection By

Prof. Dn Mohajned A.Lebdah Def: Adenoviruses' Infection' in poultry are variable greatly, either acute, sub acute or chronic infections of many kinds-of birds. Adenoviruses infection manifested in several clinical forms, differs according to the affected species of birds. The adenovirus infection appears in the following forms or diseases:A- Adenovirus infections of chickens: in the form of:

1- Inclusion body hepatitis. (IBH)2- Respiratory disease.

nn.3- Falls or drops in egg production.4- Viral arthritis or tenosynovitis.5- Diarrhea.6- Poor growth and reduction of food conversion.7- Pancreatitis, anaemia and severe lymphoid depletion of . > the bursa and spleen.

B- Adenoviruses infection of birds other than chickens: inthe form of:1- Egg Drop Syndrome 1976 (EDS-76).2- Turkey Haemorrhagic Enteritis (THE).

. 3- Marble spleen disease of pheasants. (MSD)'

Cause:

Adenoviruses are members of aviadenoviridus genus, which are] members of adenoviridae family. They are DNA viruses, with] icosahedral symmetry, ranged between 74 to 80 nm in diameter, i They have a characteristic morphology as they composed of 252 structural units (capsomeres), which are arranged into 20

triangular faces, with 12 vertices, from each vertex projects a pin-shaped projection, known as a fibre.- They posses no envelope and they replicates in the nucleus, inducing characteristic intranuclear inclusions. Avian adenoviruses characterized into:

1- Conventional avian adenovirus o f fowls with FI type species.

2- Haemagglutinating virus (EDS-76 with 127 subtypes).3- Viruses associated with Turkey Haemorrhagic Enteritis

(THE) and Marble spleen disease (MSD) with THE as type species.

1- Conventional avian adenovirus of fowls: They possess common group antigen, detected by AGPT. There are at least 12 serotypes of conventional fowl adenovirus, i serotyped using the neutralization test. Only serotype 1 (CELO) haemagglutinates only rat erythrocytes. They are the adenoviruses inducing the following diseases in

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chickens; Inclusion body hepatitis (IBH), Respiratory disease, Drops in egg production, Viral arthritis, and Anemia w ith severe lymphoid depletion of the bursa and spleen.

Haemagglutinating adenoviruses or adenoviruses of birds o ther than fowls: There are at least three adenovirus serotypes in turkeys, at least three adenovirus serotypes in geese and one adenovirus serotype in Muscovy ducks. Also, conventional fowl adenoviruses serotypes have been isolated from ducks, guinea fowl, pheasants, pigeons, quail and budgerigars. They differ from conventional fowl adenoviruses in that, they agglutinates avian but not mammalian erythrocytes. They are natural adenoviruses of ducks and geese which infect the fowl. They grows best in ducks and gesse cell cultures but also well in chick embryo liver and chick kidney cells. They grow to very high titres in embryonated duck eggs but poorly in fowl embryos. They are the avian adenovirus inducing Egg Drop Syndrome-76 in turkeys, ducks, geese and fowls.

I- Viruses associated with Turkey Haemorrhagic Enteritis (THE) and m arble spleen disease (MSD) of pheasants: \They are differ from conventional fowl adenoviruses in some respects, were isolated from turkeys, chickens and pheasants. They possess a common group antigen which differs from that of conventional fowl adenoviruses. These

viruses have not been grown in cell culture o r embryonated eggs. Variation in virulence occurs among isolates and antibody to THE virus is widely distributed in turkeys without signs o f the disease. They are the avian adenoviruses inducing both turkey haemorrhagic enteritis and Marble spleen disease o f pheasants. -

FOWLS AVIAN ADENOVIRUS INFECTIONS

Transmission:A- Routes of infection

1 - Egg - borne infection through congenital infection.2- Oral route, through ingestion o f contaminated food and

water.3- Respiratory route, through inhalation o f contaiminated

aerosol droplets.

B-Routes of transmission f1- Vertical transmission, through the ermbryonated eggs. ,:2- Lateral transmission, through direct c o n t a c t w i t h

infectious droppings, through aerial spread especially if complicated with other respiratory pathogens. . .

3- Mechanical transmission through contaminated fomites and visitors.

..r

■■ } i

■ J i

’I

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Susceptibility:

Chickens are the main natural host and the young aged

chickens are m oreresistan t than adult birds. The chicks hatching from infected hens, will have maternal antibody and a percentage o f embryos will also have virus, when maternally derived antibodies .is. lost, usually between 2 and 4 weeks of life, the virus is .reactivated and the chicks excrete vims. The chicks in contact ;will be infected and as most commercial flocks are made up o f progeny of a number of parent flocks, there is a considerable exchange of serotypes. It is not uncommon to isolate two serotypes from the same bird and a flock o f birds may well have four or more serotypes present. By the time bird- reaches sexual maturity, it may well have been infected with most o f the 12 recognized serotypes. - Clinical findings and forms of fowl adenovirus infection:

1-Inclusion body hepatitis (IBH): It is an adenoviral infection, characterized by sudden increase in mortality (vary from 2% up to 10%) and lasts for 3 to 4 days, beside the deaths, the other birds o f the flock either healthy and bright or depressed with either paleness or icterus of the skin. It is more recorded in meat - producing chickens (Broilers) aged 4 to 9 weeks, also recorded in older birds and in replacement pullets. The affected dead chickens on postomortem examination reveals: Liver swollen and haemorrhagics and presence of anaemia, icterus o f the skin and subcutaneous tissue. There are haemorrhages o f various organs, especially the museles and

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bone marrow, with presence of degeneration, with variable

severity. In some outbreaks, the bone marrow lesions are the

most obvious and thus suggested that the disease called

hepatomyeloporetic disease. 'fc

2- R espiratory disease: Adenoviruses are frequently isolated from airsacs, lungs and tracheas of birds with respiratorydisease. Adenoviruses usually represent as secondary

>

pathogens and this is usually with birds immunosuppressed by IBD. 4

' ' m

. , n

3- Drop in egg production: The drop in egg production is a sequallae of fowl avian adenovirus infection and this falls in

' -Cegg production would appear to be relatively unimportant.}

1

4- V iral a rth ritis or tenosynoitis: The adenovirus infection may be produced arthritis or tenosynovitis in combination with other viral pathogens e.g. Reovirus infection. -.ob

i J t

rf

i n

a d e n o v i r u s e s o f b i r d s o t h e r t h a n f o w l s o r

HAEMAGGLUTINATING ADENOVIRUS INFECTIONS OR EGG DROP SYNDROME-1976 (EDS-76)

v . r : !■ ' '■

Transmission:

According to the transmission or spread of the infection thereare three types o f EDS-76:

Classical, endem ic and sporadic EDS-76 ' /

Thus, there are three patterns o f disease spread:

1- The classical EDS-76 followed the introduction of vims into prim ary breeding stock, probably through a” vaccine grown in duck cells. Then, the spread of infection was

. through the embryo and the resulting reactivation of virus at around peak egg production gave an apparent breed and age susceptibility.

2- The endem ic EDS-76, the lateral spread is occurred betw een flocks': This is primarily due to contaminated eggs or egg trays and usually occurred in commercial layers. A ny age o f laying flock may be affected.

3- The sporadic EDS-76, which is seen in any age or breed o f birds. It results from infection from ducks, geese or any infected w ild birds. The contact can be direct or indirect through contam inated drinking water. Although faeces do no t contain virus, droppings do, because o f the exudate from oviduct. M echanical transmission between flocks via contam inated people or fomites can occur. Also, through

. contam inated needles and possibley, biting insects.

-in.

ir

Pathogenesis: A1- The virus particles are enters the body and grows poorly

in nasal mucosa, this followed by viraemia and grows of virus in lymphoid tissue.

2- Eight days post infection, the virus reaches the oviductand grows excessively in the oviduct (shell - gland region), this leads to egg shell changes. Both normal and affected eggs contain virus both externally and internally for the next two weeks. 7

3- Chicks hatched from those eggs, often do not develop antibody, but they are latently infected.

4- The resulted latently infected chickens or birds, at the beak of egg production, the virus reactivated and the cycle recommences.

Clinical signs:

. The first feature of the EDS-7 6 infection in the affected flock is the loss of shell strength and pigmentation and then quickly followed by thin - shelled, soft - shelled and shell - less eggs. Egg shells may show mineral deposits. It is not clear whether there is an actual depression in egg numbers, or the apparent fall or drop is due to affected eggs being eaten or lost in the; litter. The birds are normally healthy but sometimes theyj appear slightly depressed for 48 hours or so. Diarrhoea is found, but this is probably an excess o f oviduct secretion in the droppings. The classical EDS-76 is manifested either by a sudden drop in production around peak egg production (this

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flock has been devoid o f detectable antibodies before the drop) or by failure to achieve or hold expected or predictedV > *production (This flock is with small percentage of the flock have developed antibodies during the growing period). The antibodies act as a damper and slow the spread of the virus down.

Control:

The classical form of EDS-76 can be controlled by:

' 1-Vaccination by inactivated oil adjuvant vaccines, by 1/m injection between 14 and 18 weeks - old and usually accompanied with other vaccines e.g. ND or IBD vaccines. It is commercially known as trivalent or quadrivalent vaccine. (ND + IB + EDS76 or ND + IB + EDS 76 + TRT)

2- Adoption o f all sanitary and hygienic measures to prevent the lateral transmission of the infection through the eggs, egg-trays or plastic trays.

The sporadic form of EDS-76 can be controlled b y :

1- Segregation o f fowl from ducks and geese, i.e adoption of All In All Out system of breeding.

3- Providing the fowl with freshly bore hole derived water and not from the lakes or damp water.

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Adenoviruses Associated with THE and Marble spleen disease (MSD)

1- Turkey Haemorrhagic Enteritis(THE):

It is an adenoviral infection of turkeys, characterized by sudden deaths, either acute, subacute or chronic infections. The disease outbreaks may be exaggerated by overcrowding, chilling and low plane of nutrition. The mortality of the disease increased with the previous predisposing factors reaching up to 50%. The younger turkeys, under 4 weeks of age, appear to be resistant or protected by maternal antibodies.

Transmission:1- The agent is spread in the faeces and is similar, if not

identical, to that causing marble spleen disease in pheasants.

2- There is no evidence of egg transmission.

Clinical signs:

They are1 varying gfeatly from flock to flock depending greatly on:

1- Variation in the virulence of the agent.

2- Variation in the predisposing factors.

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Acute TH E: in which, sudden deaths may occur over 5 to 10 days period. The tail feathers are often stained with blood and the whole carcass may appear pale.

Subacute TH E: in which, the birds may be depressed- and show wet droppings. There is very little mortality.

Chronic TH E: in which, the birds may be depressed and sitting back on their hocks, disinclined to move and have dark tarry droppings that white birds look dirty.

I Lesions:1- The intestine is full with blood and mucosal debris,

invariably involving the duodenum, but extending as far as the caeca in severe cases.

2- The intestinal mucosa of the duodenum has a velvety appearance and show sometimes necrotic areas.

3- The survivors, sometimes, show a thickening of the duodenal wall and mild catarrhal enteritis. The spleen is enlarged and mottling. I I

I Control:

■ There is no specific treatment, Hygienic corrections of theI house with electrolyte and vitamins therapy may be useful.

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Prevention:

Phenolized convalescent serum use, No available vaccines inh Egypt till now, Good management practices, ensuring optimal ! nutrition, avoidance,of overcrowding and chilling. J

THE virus infection of fowl: * ]* If fowls are inoculated with THE virus, they developed ) ,enlarged, mottled spleen. ? J

2- MARBLE SPLEEN OF PHEASANTS:It is the adenoviral infection in pheasants and is characterized 1

by sudden deaths and appeared in pheasants aged 2 to 8

months and the affected bird die from asphyxia as a result of acute pulmonary oedema. The dead bird reveals in P.M. examination severe, enlarged, spleen with grey necrotic foci, j

Diagnosis:-

The adenoviruses infection depends onI- Clinical diagnosis depends on history o f the flock, clinical

signs and P. M. lesions.II- Laboratory diagnosis: The laboratory diagnosis depends on:

A- Isolation of the adenoviruses:

Sample collection•# i* J .V r l U_

The main sites o f replication o f conventional adenoviruses of fowls are the alimentary' tract and the upper respiratory passage, thus the samples should include feaces or large

- 1 1 8 -

intestine with feaces, and also the affected organ e.g. livers in cases o f inclusion body hepatitis. 10% suspensions are made in cell-culture media or bacteriological broth with 10.000 IU penicillin and lOmg streptomycin/ml. They are then frozen and after thawing, the fluid is centrifuged at 1500 rev/min for 20 minutes, and the supematent fluid is removed for inoculation. Because adenoviruses are resistant to cold, the supematent can be stored at 4°C or -20°C until it is inoculated.

Cultural media

Embryonic liver cells, embryonic kidney cells, and kidney cells from 1 to 4 week-old birds are suitable cell systems from the homologous species should be used. The viruses associated with EDS-.76 are best isolated in duck cell cultures, although chicken embryonic liver .cells or, to a lesser degree, chick kidney cells can be used instead. Embryonated eggs are not a sensitive medium for isolating most strains of adenoviruses. Recently, it has shown that yolk sac inoculation permits the growth o f adenoviruses o f fowls especially serotypes 1 and 5.

The EDS-76 viruses produce very high titers of haemagglutinin when inoculated into the allantoic cavity of embryonated duck or geese eggs, but they do not produce haemagglutinin or cause death in embryonated chicken eggs.

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B-Identification of Adenoviruses:1- R eco g n itio n o f grow th in ce ll culture: A d en o v iru ses cause c e lls to b eco m e round and retractile and detach from glass. T h e E D S -7 6 v iru ses agglutinate avian eryth rocytes but not m am m alian erythrocytes.2 - S ero lo g ic identification o f adenovinruses using:

Agar gel precipitation (double immunodiffusion) test (AGPT)

'This is the test u sed m ost com m on ly for d etectin g in fection o f con ven tion a l adenoviruses o f fo w ls as detected com m on group antigen.

Virus neutralization test (NY)V irus neutralization is the standard m ethod for detecting type antibod y and for typ ing adenoviruses iso la tes . A n tib od ies to con ven tion a l avian adenoviruses m ay occu r in chickens, turkeys, quail, p ig eo n s, and other avian sp ec ies . A n tib od ies to con ven tion a l avian adenoviruses, and duck adenoviruses have b een foun d in ducks and ch ickens. A n tib od ies to adenoviruses o f other sp ec ies have been described o n ly in hom ologous

sp ec ies .

Haemagglutination inhibition (HI) testHI test is u sed o n ly for detecting in fectio n w ith the virus associated w ith E D S -7 6 . It is not su itab le for other

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adenoviruses. B irds do not usually develop antibody until after they have the disease.

Frnk hemorrhaging into the intestinal lumen o f a turkey with

hemorrhagic enteritis.

MycosisMycotic diseases

ByProf. Dr. Ibrahim A. Ghanem

Def:Disease problems associated with fungal infection.

AspergillosisBrooder pneumonia, mycotic pneumonia or

? pneumomycosis

Def:Mycotic disease caused by aspergillus spp characterized by respiratory manifestation, conjunctivitis and emaciation.

cause:Aspergillus Fumigatus, Aspergillus Flavus and other aspergillus.

Susceptibility:All species of birds (inbred strains more than crossbred (newly hatched chicks are more susceptible) showing acute form (brooder pneumonia) with high mortality up to 50% survivors develop chronic form (chronic pulmonary insufficiency, ascites, blindness, neural signs and or sever emaciations).

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Source and route of infection:1- Feed and litters (in bad ventilated poultry houses).2- In the hatchery, Asp. Fumigatus penetrate egg shells

infect embryo which hatch with well developed lesions. Brocken infected eggs release large number o f spores and contaminate the hatchery environments that responsible for outbreaks of aspergillosis in very young chicks.

Pathogenesis and disease manifestations:I- Primary infections:

By inhalation of large numbers of spores from heavily contaminated feed, litter or environments. Inducing pneumonic aspergillosis and or superficial ocular infection by external exposure.

II- Secondary infection (systemic aspergillosis)By rapid haematogenouns dissemination to other tissues e.g. brain, posterior chamber of the eye, pericardium, bone marrow, Kidney and other soft tissues.

Sequelle:1- Encephalitis

Caseous necrotic lesions in brain ----- > nervousmanifestation.

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2- OphthalmitisIn posterior eye and intra-ocular structure or via direct external exposure of the conjuctival sac.

3- Osteomycosis'Deformity of vertebrae leads to partial paralysis of young chicks due to spinal cord compression.

4- DermatitisNecrotic granulamatous dermatosis.

Clinical signs:1- Dyspnea, gasping, cynosis, diarrhea, anorexia and

increased thirst2- Nervous signs in the form of ataxia, falling, pushing over

backwards, opisthotonus and paralysis.3- Gray white opacity in eyes, ocular discharge and large

mass of excudate at the medial canthus under the 3rd eyelidS.

Lesions:Lesions depend on the site of infection (localized or generalized).

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1- Lesions o f caseous mucopurulent exudate w ith fungal mycelial masses in the syrinx, trachea and bronchi.

2- Fungal hyphae may invade tracheal and bronchial epithelium and cartilage.

3- Pulmonary lesions vary from miliary to large nodules and may be localized hepatization.

4- Air sac may develop generalized involvem ent with circular,disk-shaped necrotic mass with concave surface loosely attached to thoracic and abdominal air sacs were greatly' distended with thickened wall that sometimes covered with a fur like growth o f mold.

5- Pin headed to pea size yellow soft nodules in the lungs, thoracic, abdominal cavities and for serosal surface of liver, kidneys and or mesentery.

6 - In neonate chicks (diffuse yellow greenish infiltration in the lungs).

7- Brain lesions as white to yellow circumscribed area’s.

H istopathology:Lesions o f granuloma are central area o f necrosis containing heterophils surrounded by macrophages, giant cells, lymphocytes and fibrous tissues. Fungi can be seen in the necrotic area. ; «

i126

D ia g n o s is 1- Case history.2- Signs, lesions and microscopical examination.

3- Isolation and identification: Isolation on SabouraudDextrose Agar (Fungal growth of aspergillus. (blue greenA.fumigatous and yellow green A s p e r g i l l u s f l a v u s ) .

4 - Serology ELISA and PPT.

Differential Diagnosis:Associated with CRD,. Dactylaria gallopava, Salmonella pullorum (baby chicks), T.B and E.coli granulomatous lesions.

Prevention arid control:1- No current satisfactory treatment2- Control depend on

a. Clean, selected, disinfected hatching eggs.b. Hatching equipment sanitation and periodical

disinfection.c. Use o f dry, clean litter and freshly mold free feedsd. Destroy affected birds and contaminated feed and

littere. Clean and disinfection of the house with 1:2000

cupper sulphate.f. Use mold inhibitors (on ration) to feed to control

fungus growth e.g. gentian violet, propionic acid, calcium propionate and thiabendazole.

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Treatment:• Usually not worth ,• Nystatine, amphotericin B, micronazol and hamycin.

CandidiasisMoniliasis - Thrush - Digestive mycosis - Sour crop

Def:Mycotic disease of birds involving the upper digestive tract.

Cause: sC a n d i d a a l b i c a n s (yeast like fungus) is normal digestive tract saprophytes and under debilitation it invade the mucosa and produce lesions.

Susceptibility:- All birds and animals affected. - Young more susceptible.

Common predisposing factors:1- Parasitism. 2- Nutritional deficiency.3- Infectious diseases. 4- Lack of good sanitation and over treatment with

antibiotics.

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Clinical signs:1- Retarded growth.2 - Listlessness.3- Ruffled feather and / or diarrhea.4- Over distension of crop (pendulous crop).

Lesions:1- Common in mouth, pharynx, esophagus, crop,

proventriculus and intestine in the form of diffuse and or focal mucosal thickening with white to gray pseudomembranous patches (towel - like appearance).

2- Raised focal lesions may be sloughed off into the lumen as mass of soft cheesy materials.

Histopathology:- Destruction o f crop mucosa.- Penetration of pseudomycelia to the submucosa.

Diagnosis:1- History o f fermented food and long term use of

antibiotics.2- Gross lesions.3- Histopathology confirms pseudomycelia invasions.

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4- Culture on Sabouraud's dex trose a g a r r e v e a l w hitish l

creamy convex colonies (under m ic ro s c o p e show ed

' oval-budding yeast cells).

Prevention:1- Sanitation and sound m anagem ent.

2- Avoid fermented food.

3- Avoid over treatment w ith an tib io tics a n d p re v e n t other

diseases. • - i

4- Routine addition o f antifungal and p ro p e r d is in fe c tio n of

houses by 2 % form aldehyde and 5% io d in e so lu tio n in drinking water.

Treatment: !1- Gentian violet or ketoconazole o r c u p p e r sulphate

1/2000 in drinking water.

2- Nystatin 62.5 m g/ liter 3-5 days.

3- Supportive treatm ent w ith v itam in A a n d C . j

Dactylariosis TDef:M ycotic disease o f young ch ickens a n d tu rk e y poults characterized by nervous m anifesta tion a n d o r pulmonarj

lesions.

cause:pactylaria gallopava.It is thermophilic fungus grow on sabouraud’s dextrose agar as brown hyphae w ith two celled brown conidia.

Epidemiology:1 - It grow w ell in high temperature (> 43 c) and at low pH (

< 5) such condition o f wet shaving as poultry litter.2- Inhalation o f spores and haematogenous spread to the

CNS is the m ain w ay o f infection.3- Chickens m ore susceptible between (1-5) weeks of age

w ith (3-10% ) m ortality.

Clinical signs:1 - N ervous m anifestation.

2- O cular lesions.

Lesions:1 - P u lm onary granulom ous.

2- G rey and ye llow necrosis in brain tissue.

Histopathology:- N ecrosis in brain tissue with large number of giant cells

and brow n hyphae o f D a c ty la r ia g a llo p a v o are seen in

histopathology o f brain tissues.

Diagnosis:... 1- Case history.

2- Clinical signs and gross lesions.3- Histopathology (brain sections reveals brow n hyphae

large number of giant cells and brain necrosis).4 - Isolation and identification: Culture from brain andl

pulmonary lesions on Sabouraud's dextrose agar at 45J reveal brown colonies with brown surrounding pigments and the hyphae show characteristic two celled conidia.

Differential diagnosis:1- Vitamin E deficiency.2- Aspergillosis (hyphae wider in diameter than dactylarial

which is brown hyphae bear two celled).3- ND.

Control:1- No treatment.2- Avoid exposure to mouldy litter.

FavusDermatomycosis - Ring worm

Def:Chronic dermatomycosis of birds and animals w ith comb t skin lesions.

1 3 2

cause:Trichophyton megninii (T. gallinae) and Microsporumgypseum.

Pathogenesis and disease description:1- The fungus grows on unfeathered skin with white scaly

crust as sprinkled with white flour.2- Feather follicles are depressed (Favus cups ) and

feathers fall out in patches.3- Skin becomes wrinkled and crusty.

' 4- Birds appear depressed, emaciated and anaemic.

Diagnosis: *i 1- Gross lesions.

2 - Histopatholdgical lesions.3- Domenstration o f hyphae and spores.4- Isolation on Sabouraud's dextrose agar (demonstration

of fungal growth as small, round white velvety disks with small central cups and radial grooves with reddish pigment diffuse through the media).

Treatment1- Tincture iodine glycerine or dipping in 0.5 %

pentachlorophenol2- Micronazol nitrate is highly effective.

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M y c o to x ic o s e s

Def:Pathological condition. resulting from ingestion o f fungal

metabolites (mycotoxins)

’ r Thousands of different mycotoxins are existed but only

hundreds are recognized.

=> Each mycotoxin has characteristic toxicogenic action

e’g- •• Aflatoxin — hepatotoxic

• Ochratoxin — ► nephrotoxic

• Trichothecene — ► caustic and radio-m im etic effects

Some mycotoxins interrupt protein synthesis and othersinterfere with carbohydrate or fat metabolism .

Forms of mycotoxicoses:1- Acute form: high dose o f toxin causes sudden onset

o f death.

2- Chronic form: low level o f toxin causes decrease the

production and performance.

* Very low 'levels o f different m ycotoxins interact with

each other and magnify their harm ful effects.

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Impact of mycotoxins on poultry production■ Reduce feed intake, conversion rate and body

weight gain.■ Reduce egg production, poor egg shell quality and

reduced egg size.■ Erosive ulcers and necrosis in the oral mucosa (T-

2 toxin).■ Enteritis.■ Impaired fertility and hatchability.* Immuno-suppression lead to vaccination failure

and increase susceptibility to infectious diseases.■ Adverse effects of some drug-kinetics.■ Impaired hepatic and pancreatic functions.■ Ascites, poor pigmentation (shank, skin and poor

feathering). ,

■ Bruising increase carcass condemnation during processing.

■ Leg weakness and poor skeletal development.

Aflatoxicoses

Natural occurrence:• Aflatoxins are produced by A. flavus and A.

parasiticus in wide variety of agriculturalcommodities at any stage of production, processing,transportation, and/or storage.

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• Drought, insect damage and creaked kernels enhance

fungal growth and totfin production. *

• Relative humidity (80-85%) m oisture (17% ) and

temperature o f (24-35C) are the optim al condition for

their production.

• They are extremely stable.

Chemistry and Types:Difuro-coumarin derivatives, there are aflatoxin B l , B2, G l, G2. Aflatoxin B l is the most predom inant and highly toxic.

Toxicity and susceptibility:• Aflatoxin B l interact with D N A and RNA synthesis.

• LD50 (1-50 mg/kg)

• D uckling—► turkey p o u lts—► pheasant chicks—» Chicks.

••i

• Wide variation among breed, age and sex.

• The toxic effect are both dose and time j dependant.

• Acute from : (depression, anorexia, hemorrhages, periportal necrosis o f hepatocytes associated with bile duct proliferation.

136

• • Chronic form : Reduced body weight gain, feed

hepatic steatosis (fatty liver).• Residues- In egg and edible tissues.- It would require 72 hours to significantly reduce

residues.

Clinical signs of Aflatoxicoses in chickens:

1- It impairs production parameters (body weight gain, feed intake conversion,-egg production, egg size, hatchability and fertility, male and female reproduction performances).

2- Depression, ataxia, recumbency and death.3- Stunting, poor appearance, nervous signs, leg

weakness and dropping of wings.4- Chicken looked paler than normal.

1- Yellow, friable enlarged liver with multi focal haemorrhages and reticular pattern on capsular surface.

2- Then atrophy of liver, bursa of fabricus, spleen and thyroid.

intake and conversion with bile duct hyperplasia and

Lesions

• 137

1 3- By time liver develop white focci as hepatic lip^ content increase.

Effect on the immune system:Immimo-suppression due to

1 - Atrophy of bursa of fabricus, thymus, spleen. .2- Suppression of interferon production3- Delay hypersensitivity, lymphoblastogenesis, leukocyte

migration, impairs chemotaxis and phagocytosis.

Prevention:

Detoxification1- Adsorbents (physical) 2-5kg/ton Prevent absorption of Aflatoxin in GIT.

a- Activated charcoal.b- Hydrated sod. Cal. Aluminium silicate (HSCAS) good

mixing and left 72hr before use. c- Other adsorbents (clay, soil, zeolites).

2- Chemical (ammoniation) could reduce 99% of aflatoxins levels.

3 - Biological methodsBacteria (L- form Lactobacillus) by its enzyme able to digest and destroy the toxic ring of aflatoxin.

138

treatment:1- Remove toxic feed.2- Treatment of concurrent infection.3- Good management.4- Antioxidant, vitamin, selenium and amino-acids

(increase level of protein) could be helpful.

Ochratoxicosespef: Ochratoxins are isocoumarin compounds, produced by Aspergillus ochraceus. They are ochratoxin A, B, C, D, and their methyl and ethyl esters. Ochratoxin is the most toxic, widespread in cereal grains and potent nephrotoxic metabolite.

'■ / .

Natural occurrence:Levels ranging from 300-16000 ppb were recorded in feed associated with ochratoxicoses in chickens.

Residues:In chicken tissues for only 4 days after withdrawal of contaminated feed. .

Toxicity and susceptibility:- Interfere with DNA, RNA and protein synthesis also

with gluconeogenesis in the kidney cortex.

LD50 of Ochratoxins varies with the age and sex. Duckling— ►chicks— ►turkey poults —quails.

Pathogenesis and clinical signs:- Damage to proximal convoluted tubules— ► osmotic

duresis —► dehydration —► hemoconcentartion increase PCV.

- Decrease egg production, weight, specific gravity, increase shell stain and blood spots.

- Delayed sexual maturity, increase incidence of embryq mortality due to embryonic gout.

- Increase uric acid level in blood.- Reduce feed intake, weight gain and conversion Acute toxicity

• Birds appear listless, huddle, diarrhea dehydration, tremors and prostration leading to death.,

Lesions1- Dehydration with dry firm gizzard, proventricular

mucosal haemorrhages and catarrhal enteritis. ,2- Kidneys are pale, swollen and enlarged. , ,i3- Liver, enlarged, pale and friable or hemorrhagic with

distended gall bladder.4- Extensive accumulation of urates on the serosal surface

of several organs.

140

5- Reduction o f breaking strength and diameter of tibiotarsal bones.

6 - Increase intestinal fragility and its lipid content leads to intestinal ruptures and carcass contamination rates.

7- Less carcass pigmentation.

Effects of ochratoxins on the immune systemLead to immune-suppression due to

1- Regression and lymphocytic depletion of lymphoid organs leading to humeral immunity impairment.

2- Impairment o f heterophil phagocytic and locomotory activities.

3- Reduction in cell-mediated immunity.4- Impairment o f vaccinal response.

Prevention and treatment:1- Increasing dietary protein levels could improve feed

efficiency.2- Vit C counter acts the adverse effect of ochratoxins.3- Vit E (anti-oxidant) partially ameliorates the adverse

effect o f ochratoxin.4- Adsorbant o f no value.

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TrichothecenesDef:They are group of over 100 fungal metabolites produced by fiisarium spp e.g. T-2- toxin and HT-2 toxin, diacetoxyscirpenol (DAS), deoxynivalenol (DON) and

nivalenol (NTV).f > . •• • .• .

t Natural occurrence: nThey are associated with different disease problem e.g. alimentary toxic aleukia (ATA) stachybotrytoxicosis and refusal-vomitoxin syndrome.

Mode of action:They inhibit protein synthesis in the actively dividing cells as those lining the gastrointestinal tract, skin; lymphoid and erythroid cells. This result in extensive necrosis o f oral mucosa and skin in contact also depression of bone marrow and immune system function.

Signs and lesions:1- Circumscribed yellow proliferative caseaous plaques at

the beak margin, mucosa of hard palate, angle of the mouth and tongue.

2- Growth retardation.3- Abnormal feathering.4- Regression of bursa of fabricius and anaemia.5- Decrease egg quality and quantity.

142

prevention and control:1- No specific therapies are currently available.2- The only effective treatement is removal of the source

of toxin.3- Anti-oxidants and vitamin E have proven to be

effective.

Fuminisin' • Produced by Fusarium moniliforms.• They are Al, A2, Bl, B2, B3 and B4.

Mode of action:• Interfere with the bio'synthsis of sphingeolipids which

important for cell membrane physiological activities specially those of nervous tissues leading to neural degeneration.

• Fuminisn not represent a threat to poultry health where the minimum effective dose of 75 ppm is about 150 times higher than the highest level of contamination Fuminisn Bl in poultry feed.

Other types of mycotoxins

• Cyclopiaonic acid (Penicillium commune) leads to GIT inflammation.

143

• Oosporein (C h e a t o m i u m t r i l a t e r a l ) leads to renal damage and gout.

• Citrinin (P e n i c i l l i u m c i t r i n u m ) leads to renal damage and diarrhea.

• Ergot alkaloids (C l a v i c e p s p u r p e r a e ) leads to necrosis of peripheral tissue (gangrene).

• Zearalenone (F u s a r i u m g r a m i n e a r i u m ) has estrogen like action.

My cotoxin diagnosis:

Definitive diagnosis should involves > ^1- History of seasonal association with specific feed.2- Isolation, identification and quantification of

mycotoxins.3- No response to antibiotic and no transmissibility.4- Signs of feed refusal.5- Evidence of fungal activity.

Detection of mycotoxin in feed by:• Analytical techniques but multiple sampling (sample

size, numbers and representativeness) are indicated.• Sample of 500 gm submitted in separate, labeled , in

clean paper bags/

144

analytical techniques include:1- Thin layer chromatography and gas liquidchromatography.2- ELISA.3- Bright greenish yellow fluorescence.

145

M u ltifo c a l g ra n u lo m a s in th e lu n g s o f a ch ic k en in fec ted w ith

A sp erg illu s .

146

Fatty d e p o s itio n in th e liv e r o f a b ro ile r c h ic k en w ith a f la to x ico sis .

Avian Salmonellosis , By

Prof. Dr. Mohamed A. El-Sisi

There are two main salmonella infections in poultry.- Infection with salmonella gallinarum pullorum.- Paratyphoid infections.

1 - Salmonella pullorum gallinarum (Pullorum disease; Fowl typhoid)

Def:This infection causes serious economic losses in poultry as a result o f high mortalities in baby chicks, adverse effects on growth, adverse effects on egg production of affected layer birds and low fertility and hatchability of eggs laid by carrier birds.

Cause:Non motile, gram negative rods. The somatic antigenic structure is 1,9,12. Antigen 12 can be further differentiated into 12], 122, 123 antigen factors.Some antigenic fractions are shared with other members of salmonellae. So occasionally fowls infected with certain other

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salmonellae may react to the routine whole blood agglutination test.

Susceptibility:Chickens and turkeys are the main natural hosts. The disease was diagnosed in guinea fowl, pea fowl, pheasants , pigeons and other wild birdsLight breeds are generally more resistant than heavy breeds and males more resistant than females,. Chickens can be infected at any age, most outbreaks occur in chicks during the | first 3 weeks of age, and in growing birds from 3 months to point of lay.

Mode of infection and spread:Infected eggs from carrier hens. About 10 % of eggs laid by carriers are infected and chicks hatched from these eggs are infected.Incubator infection, when non infected eggs are hatched with eggs from carriers. Infection occurs at hatching time by inhalation and direct contact of healthy and infected baby chicks.Contaminated incubators if not thoroughly cleaned and disinfected is a source of infection to non infected eggs. Ingestion of food or water contaminated with dropping of infected chicks in the brooders.

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Attendants may transmit the infection in brooders on their hands, feet and clothes. Infection may occur during sexing, contaminated chicks boxes or brooder equipment improperly cleaned and disinfected.Adult birds may be infected by ingestion of contaminated feed or water. Rodents, dogs, cats, and flies can transmit infection

Clinical signs:- Mortality may vary from 2-3 % to over 50 % according

to virulence of stain and sanitary conditions.- When infection occurs in incubator from infected eggs,

chicks may be found dead within a day or of hatching and the disease spreads rapidly within subsequent few days, reaching a peak mortality about the 7th day.

- When infection occurs in the brooder, losses are recorded between the second or third week, symptoms are more prolonged and mortality lower.

- Acute cases show no signs before death. Subacute cases, appear sleepy, huddle together with closed eyes and

• • droopy wings. Loss, of appetite and sometimes a white chalky diarrhea. Labored breathing and gasping may be observed. Chicks which survive on outbreak reveal a high percentage of carriers at mortality.

- Outbreaks- have been observed in broiler chicks, the recorded, symptoms were lameness as a result of swelling ,of the hock joint. Poor feathering and under

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development. Deaths occurring mainly between 2-5 weeks of age.

- In adults, acute outbreaks are usually rare. The cause of the disease is rapid and deaths occur within 48 hours of the onset of symptoms. In subacute outbreaks, symptoms may last as long as 5-6 days. Mortalities varies from 4 % up to 30% or more - symptoms reported include increased thirst, loss of appetite. Ruffled feathers, watery foetid diarrhea accelerated respiration and high temperature.

- Chronic carriers, usually show no symptoms, egg production is 'lower 10-20 % than in normal birds and the fertility and hatchability of their eggs is reduced (20%). Sporadic deaths may occur among carrier birds.

Lesions:In chicks

- Chicks dying from acute infection during the first week of age may not reveal gross lesions, or at the most enlargement and congestion of the liver which may be streaked with hemorrhages and the other internal organs may show hyperemic changes.

- The lungs may be congested. The yolk sac may reveal slight or no alternations. Protracted cases with increasing of age of the affected chicks the absorption of the yolk may be poor and the contents o f the yolk sac

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may be creamy and blood stained or form cheesy mass. White or grayish necrotic focci are seen in the liver, lungs, heart, gizzard and caeca. The spleen may be enlarged, kidneys congested and the ureters distended with urates and the caeca may contain a cheesy core.

- In the chronic arthritis form in broilers, orange colored gelatinous, exudates is found in the hock joints, often with necrotic focci in myocardium and liver.

In adults: - Acute form, both sexes show pericarditis, heart show

grayish white nodule, yellowish green granular liver. Enlarged spleen with focal necrosis and a fibrinous

. peritonitis. In layers the ovary showed marked• degeneration,, ruptured ovules and yolk material may be

present in peritoneal cavity.- Chronic form, lesions are seen in the ovary ovules are

discolored, misshapen, pedunculated with prominent thickened stalks. Ovules may become detached and found free or adherent to the peritoneal lining causing

• . peritonitis. The oviduct may be impacted with eggmaterial. Pericarditis is present. In males pericarditis and myocarditis are common. The testes may be atrophied and may reveal small abscesses.

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Diagnosis:- In acute cases in chicks and adults; a tentative diagnosis

may be achieved on the basis of history, clinical manifestation and lesions.

- A definite diagnosis is by isolation and identification of the causative agent in carrier birds by demonstrating antibodies in blood samples by agglutination tests.

Control and eradication:- When an outbreak occurs in a breeding flock. The entire

flock should be depopulated, followed by thorough cleaning and disinfection of brooders and all equipments and utensils. When chicks are to be used for meat, the prompt removal and disinfection of dead and culling chicks. Hygienic measures are adopted. Administration of furazolidone for 10 days in ration at a concentration of 0.04 %. This drug can be used prophylactically in broilers at 0.01 % level.

- In acute outbreaks in adults, furazolidone may be used as mentioned before. Treated birds should not be kept for breeding some treated birds remain carriers to infection.

- The eradication of salmonella gallinarum pullorum infection depends on the detection and elimination of carriers from the breeding flocks by means of agglutination test. The test is carried out when birds are

16 week old. There are two methods for application of the test.

> The whole blood, stained antigen agglutination test.

> The standard serum tube test. Certain factors must be taken in consideration when

doing the test.A. When positive reactors are detected in a flock retesting

must be carried out at 3-4 weeks intervals until we obtain at least two consecutive negative tests of the tested flock. During retesting, single reactors should be submitted to bacteriological exam.

B. All reactors should be removed from premises and slaughtered immediately. These reactors should not be sold alive. •

C. It is advisable to cull the whole flock if the percentage of reactors exceeds 10 %

D. It is preferable, whenever possible, to transfer the non reactors to clean disinfected premises.

E. Thorough cleaning and disinfection of premises and equipments should be done

F. Day old chicks and fertile eggs for hatching should be purchased from pullorum free flocks

G. Eggs used for preparation of live virus vaccines should be from SPF flocks

H . Hatcheries should be disinfected by fumigation with formaldhyde gas after thoroughly cleaning

I. Biosecurity measures in tested flocks should be strictly followed

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2- Paratyphoid infections

Def:Infections with any organisms of the salmonellae other than S. gallinarum pullorum. Besides its economic importance due to mortality in young birds and low hatchability, paratyphoid of poultry is of public health importance.

Cause:Any of the various species of salmonella other than S. gallinarum pullorum. The organisms are motile, Gram negative, non sporing bacilli.

Susceptibility:All avian species, the acute form is only during the-first month at hatching. Adults may be infected and commonly serve as intestinal carriers with little or no evidence of infection. These birds seldom develop acute symptoms, especially when exposed to stress factors.In canaries, pigeons and parakeets infection may cause acute form in adults. Human beings and most animals are susceptible to infection and may act as carriers.

Mode of infection and transmission:> Transovarian transmission occurs particularly in relation

to S. typhimurium especially in ducks and occasionally

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in turkeys Carriers are intermittent faecal excretors and the organism contaminates the outside of the shell either during the passage of the egg through the cloaca or after the eggs is laid by soiling with faeces in the nest box.: The organism can then penetrate the pores of the shell.

> Infection at hatchihg from contaminated egg shell and debris as well as contaminated down. Spread of infection can also occur during brooding by ingestion of feed and water contaminated with faeces of infected chicks

> Animal protein supplement in current use may be contaminated and constitute a potent sources of infection.

> Rats, mice and most animals, wild birds and flies are frequently carriers and constitute sources of infection for poultry.

> Human excretors are also possible sources.

Clinical signs:In chick and turkey poultsSymptoms are similar to those ofS. gallinamm pullorum infection.In duckling and goslingsAffected duckling show swelling of eyelids and keeling over.Wings drooping. The vent may be pasted with urates.

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Tn pigeonsSquabs show arthritis in wing and leg joints and result in inability to move or fly. Nervous symptoms are sometimes recorded as result o f localization of infection in brain. Diarrhea and conjunctivitis were recorded. Carriers birds show no symptoms. Mortality up to 20 % and may reach in severe outbreaks in young birds 80 % or higher.

Lesions:More or less similar to those pf gallinarum pullorum infection in chicks.In pigeons, subcutaneous swelling of the wings or leg joint is common V i c ■:

Degeneration o f ovaries in carrier chickens is comparatively rare but common in adult ducks and turkey.

Diagnosis:Definite diagnosis c a n 'b e made only by bacteriological examination and identification by biochemical and serological tests.Treatment:

• Sulphonamides and antibiotics have been used to control chick mortality with variable resultsFurazolidone and furaltadone at level of 0.04 % for 10-14 days are highly effective in reducing mortality in chicks. Some of these drugs can completely eliminate the organisms from

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infected birds but the majority of treated birds become carriers. Therefore treated birds should not used for egg production or for breeding purposes.Prophylactic medication with suitable drugs in the feed during the first few weeks after hatching has been used with beneficial results.

Prevention and control:hatching egg hygiene

• Clean egg should be used for hatching. Eggs should be collected and stored in a cool place. Clean and disinfected containers should be used. Early fumigation o f the eggs at the commencement o f incubation as well as in the farm after collection for 20 minutes is highly recommended

• Dipping duck eggs in germicidal solutions has been shown to be effective. The dipping fluid must be at higher temperature than that o f the egg throughout the operation (at least 80 F) for 15 minutes and then hung

up to drip day before setting.

Sanitation during brooding• Young birds should be isolated from sources of

infection (man, animals and flies). Feed and water

containers should be cleaned and disinfected. Sick and

dead birds should sent to the laboratory for diagnosis

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flock sanitationMice, rats and flies should be controlled. Animals should be kept away from poultry. Mechanical spread by persons, contaminated equipments, visitors should be given special consideration. Samples of animals protein supplements should be sent to the laboratory for bacteriological examination. Serological testingSpecific. antigens for the salmonella type involved must be prepared in the laboratory for the tube agglutination test In Denmark, the swelling of duckling, gosling and turkey poults hatched in incubators is allowed only when the hatching eggs originated, from breeders in which no reactors to the S. typhimurium and S. enteritidis tube agglutination tests.

3,t Avian Arizona infections

Def:Infection are caused by a group of bacteria belonging to the family enterobacteriacae, infections are seen most often in chicks less than one month old.

Cause:Arizonas are Gram negative flagellated bacilli. Grow in ordinary media at 37c. Two serotypes are the most frequently isolated from turkeys in North America. The disease has been described in chicks and ducklings.

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Clinical signs:Affected birds are listless, tend to huddle and have pasty faeces stick to vent feathers. Various nefvbus signs, ataxia, trembling, leg paralysis, torticollis and convulsions. Visual j impairment can be seen in eyes due to opacity. Signs are seen j in poults under 5 weeks of age. Adult birds show no clinical signs and can excrete the organisms from long periods.

' ‘ • \

Lesions:A mottled yellow liver, a discolored heart, peritonitis and an

unabsorbed yolk sac. Eye lesions are common in turkeys.

Diagnosis:Clinical signs, PM, By cultural examination, the isolation and

identification of the organisms.

Treatment:Suiphonamides, furazolidone for 5-7 days.

Prevention and control:'Hie same methods used in the control o f paratyphi

infections are useful to control arizonosis.

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Enlarged and bronze greenish tint of liver due to fowl typhoid infection.

* >x?*-

^welling o f the joint and synovitis are common features of pullorumdisease.

/

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Avian Coliform Infection (Colibacillosis)

ByProf. Dr. Ibrahim A. Ghanem

Def:

Colibacillosis refers to any localized or systemic infection caused by avian pathogenic Escherichia coli (APEC). Collectively, infections cause economic losses due to:

1- High mortalities (young birds).2- Poor food conversion and increase down-graded

carcasses.3- Reduce hatchability and the hatched chicks may suffer

omphalitis.

Cause:Avian pathogenic E s c h e r ic h ia c o l i e.g. Oj, O2, Og, O35,O36 andOn.

Susceptibility:- Chicken, turkey and ducks.

Mode of transmission:1- Ingestion of contaminated feed and water.2- Inhalation of contaminated dust.

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3- Through faecal contaminated egg shells.4- M.O could transmit through equipment, incubators,

hatcheries and/or brooders.5- Rodents, flies and free-living birds may spread the

disease.

Pathogenesis:1- Pathogenic serotypes o f E.coli are common inhabitants,

in lower part o f small intestine, ceca, throat and upper trachea o f apparently healthy poultry. The pathogenic E.coli probably invade the birds from the respiratory tract and produce septicemia and other characteristic condition, also through fecal contamination of egg shells, E.coli can infect embryos and may cause death during incubation.

2- Infected chicks or poults may:a. Hatch and die with omphalitis during the first

week of age. ^ jb. Show yolk infection that results in slower growth.

3- E.coli from dust (dried fecal material) may infect birds j causing respiratory form.

4- In laying birds salpingitis and peritonitis may folldiv air sac infection or as ascending infection from the cloaca, j

5- Panophthalmitis usually follow colisepticaemia. ;

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Forms of colibacillosis

Forms of colibacillosis

Systemic forms

. Respiratory origin coli- Enteric origin coli- Neonatal colisepticemia- Colisepticemia o f layer- Colisepticemia in ducks

Localized forms

- Yolk sac infection- Cellulitis- SHS- Acute vaginitis- Hjarr's disease Arthritis- Meningitis- Osteomylitis- Panophthalmitis- Salpingitis

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1- System ic fo rm s o f colibacillosis

A. C oli-septicaem ia

Def:

It is the most serious m anifestation o f co lib ac illo sis causing

acute infection o f chickens characterized b y sep ticaem ia and

high mortality.

Epidem iology:

Susceptibility

- Chickens (broilers) 2 -4 -1 2 . w eeks are commonly

affected. V .

- Ducks - turkeys.

Pathogenesis

The developm ent o f broiler industry w ith m assive production

broiler flocks w ere may be infected b y mycoplasma

gallisepticum that predisposed or exacerbated colisepticaemia, coccidiosis, also, viral infection e.g. (N D and IB ), even live j

vaccine, IBD and nutritional deficiencies all predispose the disease.

j . t

N.B: E.coli will persist for long periods ou tside th e birds in dry, dusty condition. It has been show n that w etting the litter can reduce the incidence o f colisepticaem ia.

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Clinical signs1- General signs o f illness (off food, inactive, listless,

sleepy)2- First signs is drop in food consumption (in broilers)3- Respiratory manifestation4- Greenish diarrhea.5- Ip baby chicks, the disease usually associated with yolk

sac infection (severe depression and diarrhea).6 - Mortality from colisepticaemia may exceed 5%

although high mortality rate can occur.7- Poor conversion rate, retarded growth with poor carcass

quality.

Lesions:1- Picture o f septicaemia (congestion of liver, spleen, lung,

/kidney and muscles)

2- Fibrinous airsacculitis (air sacs are thickened, opaque with adhered caseous deposits).

3- Fibrinous pericarditis (the pericardial sac thickened, white adhering to myocardium)

4- Fibrinous perihepatitis (the surface of the liver is covered by sheath of fibrinous material)

5- In baby chicks unabsorbed inflamed yolk sac.

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Colisepticemia Sequelae:Death is the usual fate, but some birds may recover with residual sequelae and E. coli can localize in brain, eyes, synovial tissues (joints, tendon sheaths, sternal bursa) and bones.Colisepticemia results in:

1- Meningitis.2 - Panophthalmitis3- Osteoarthritis and synovitis 4- Arthiritis •5- Salpingitis (juvenile) |

B. Coli-granuloma (Hjarre’s)

Def:Characterized by multiple granulomas in the caeca, duodenum,! mesentry and liver.

Susceptibility:- Chickens and turkeys. It occurs poradically in old birds

Clinical signs: • Emaciation and poor condition.

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Lesions: _• Granulomatous nodules in caecum, duodenum,

mesentry and liver.

Differential diagnosisT.B and tumors.

2- Localized forms of colibacillosisA. CoJiform omphalitis/ yolk sac infection

• Follow, contamination of the unhealed navel with virulent strains of E.coli.

• Translocation of bacteria from intestine or blood.• E.coli was present in yolk sacs of about 70 % of chicks

with (mushy chick disease) other types of bacteria (Proteus spp., Bacillus spp., Pseudomonas, Clostridium perffingens etc.).

Clinical signs and PM:1- Swelling, edema, redness and inflammed navel.2- Distended abdomen, with lysis of skin which become■ wet and dirty with bad smell.3- Unabsorbed yolk sac with abnormal color, consistency

and smell.

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B. Coliform cellulitis (Inflammatory Process)

Def:An inflammation of the subcutis that extends beneath the normal skin.

e.g) Swollen-head syndrome (SHS)Acute to subacute cellulitis with inflammatory exudates involve the periorbital and adjacent subcutaneous tissues resulting in swelling of the head. Also, SHS may be predispoded by some viruses such as coronavirus, pneumovirus &IB or ammonia gas.

C. Diarrheal diseasePrimary enteritis in poultry caused by E.coli with pale distended intestine with fluid.

D. Venerial colibaciilosis (Acute vaginitis)Acute, often fatal, vaginitis that affected turkey breeder hens shortely after first insemination which characterized by thickened, ulcerated mucosa covered with diphtheratic, caseonecrotic membrane.

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£. Salpingitis/peritonitis (Adult)

Def:Inflammation o f the oviduct caused by E. coli results in decreased egg production and sporadic mortality in laying chickens and breeders.Pathogenesis:

1- Ascending E. coli infection to the oviduct from the cloaca. .

2- Heavy egg produce estrogenic activity predispose to salpingitis by relaxing the sphincter between the vagina and cloaca.

3- Mucosal infections with vimses (e.g., infectious bronchitis vims) or mycoplasmas. The oviduct is distended markedly with masses of caseous exudates.

4- Concurrent peritonitis also occurs due to free yolk in the body cavity.

5- Abdominal laying and misovulated ova may accompany salpingitis and contribute to peritonitis.

.Diagnosis:1- Case history.2- Clinical signs.3- Gross lesions.4- Isolation and identification: Culture on MacConkeys

agar (pink colonies-lactose fermenter).

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Treatment:1- Antibiotic sensitivity test. -I

2- E. coli may be senstive to many drugs such asampicillin, chloramphenicol, chlotetracycline, neomycin, gentamicin, streptomycen, sulpha drugs and flouroquinolones.

3- Correct the managemental errors.4- Control other accompanied diseases.

Subacute pericarditis in 4 weeks old turkeys due to E. coli infection.

Fibrinous pericarditis and Fibrinous perihepatitis due to CRD infection in

chickens.

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Avian Mycoplasmosis By

Prof. Dr. Mohamed M. Megahed

Def:The infection causes reduced feed conversion efficiency, downgrading of broilers and turkeys at slaughter and suboptimal egg production in layers, production losses of between 10 and 20 % have been reported in layers. In breeders the infection may necessitate slaughter of valuable flocks, and even suspicion of infection in such flocks may result in export, restrictions for eggs and progeny. Other costs, include treatment, laboratory diagnosis and control measures such as increased biosecurity or vaccination.Mycoplasma share with viruses in many prosperities as the following

1. Small size. .2. Filterability.:3. Ability to haemadsob.4. Ability to haemagglutinate.5. Morphology in electron microscopy.6. Interference.7. Ether-chloroform sensitive.

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8. Antibiotic resistant (Penicillin).9. Neutralization of homologous serum! • lO.In-vitro cytopathic effect.

Role of Mvcoplasmas in disease At least 25 species of mycoplasmas have been reported in

birds the avian mycoplasma pathogens include 4 species1 M. gallisepticum2 M. synoviae3 M. meliagredis4 M. iowae

M. gallisepticum

Responsible for the following lesions• CRD in chicken

• Infectious sinusitis in turkeys• Keratocongunictivitis in chicken• Salpingitis in chicken• Losses in egg production j• Upper respiratory disease in game birds Susceptible birds

Chicken, Turkeys, Ducks, Geese, Parrots, Quails, Falcons, Ostrich, Pheasants, Song birds, House sparrows

M. SynoviaeIt has two forms1 - Arthritic form2 - Respiratory form

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Responsible for the following lesions• Infectious Synovitis associated with

o Hepatomegaly o Splenomegaly o Swollen pale kidney o Atrophy of bursa and thymus

• Exudative synovitis, tenosynovitis and bursitis• Airsaculitis espicially in broiler

Susceptible birdsChicken, Turkeys, Ducks, Geese, Parrots, Quails, Falcons,

Ostrich, Pheasants, Pigeon, House sparrows, Partridges and Guinea fowls. -- •

M. meleagridis Responsible for the.following lesions

• Airsaculitis in young pullets• Poor growth and Poor feathering• Ascitis• Infection of embryo followed by osteodystrophy and airsaculitis• Skeletal deformities■ Perosis■ Deviation of cervical vertebral column

Susceptible birdsTurkeys (main host), Japanese quails, Pigeon, Peacocks

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M. iowae " .*i>: v

Responsible for the following lesions

• High embryo mortalities

• Moderate sirsaculitisi

• Reduce hatcliability in turkeys

• Tenosynovitis

• Bursal atrophy and poor growth

• Leg and joint abnormalities

• Rupture of digital flexor tendon

• Chondrodystrophy

Susceptible birds j

Turkeys (natural host), chickens, Geese, Parrots, and wild

birds.

M. Anseries (Geese) :

Responsible for the following lesions (

• Airsaculitis and Peritonitis

• Embryo motalities and drop of egg production

Susceptible b i r d s G e e s e

M. Species (1220)/Geesse

Responsible for the following lesions

• Inflammation and necrosis o f phallus and atrophy oftesticules

• Infertility problem and embryo mortalities

• Airsaculitis and Peritonitis

• Reduce egg production

• Inflammation o f cloacae

• Lack o f weight gain in hatched geese Susceptible b i r d s G e e s e

Mycoplasma spp transmitted through:1. Vertical Transmission: the highest shed takes place 2 -

3 weeks post infection' 2. Venereal transmission: from males to females thought

mating or artificial insemination with infected semen3. Horizontal transmission: By direct contact between

infected carriers and healthy susceptible birds the transmission o f MG is slowly in the house also between houses,is slowly. Good biosecurity can stops spread to adjacent farm s.: Transmission could occurred through indirect contacts including: dust, contaminated feeds, water or litter.. .etc::

4. Biological Carrier: All avian species - especially gallinaceous birds - should be considered potential carriers

,5. Mechanical carriers: Human, flying birds, rodent and other mammals

6 . Contaminated live vaccines7. Use o f raw processed immune - egg yolk

Causal agent1 Mycoplasmosis are distinguished phenotypically from

other bacteria by their minute- size (125-150 mill microns).

2 Lack o f cell wall this make them :-

• Sensitive to Osmotic shock and D etergent -

• Resistant to penicillin ; 3. Formation o f fried eggs shape colonies

4. Mycoplasma belong to Mollicutes (soft skin)

Laboratory diagnosis of Mycoplasmosis1. Primary isolations

• Culture media . ,

• Chicken embryo ~

• In- Vivo bio assay in susceptible chicken or,turkey

• In-contact turkey sentinels '2. Colony confirmation by Biene’s stain3. Purification4. Maintainace of prim ay isolates5. Genus identification

• Sferal requirments by Digitonin test+ Mycoplasma - Ureaplasma

• Urea Utilization + Ureaplasma

• Biochmicl grouping6. Serological Monitoring (SPA test, HI, IF, MI)

A - Serum plat agglutination test (SPA or RSA)• Agglutination test is the first step screening a flock

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• Serum that react within 2 minute with stained Ag of I Mycoplasma gallisepticum is heated at 56C and retested

after dilution.j • Serum still react even after dilution in saline (1/8 or

greater) considered positive this is useful in decreasing | the nonspecific reaction.I • Positive sera frozen and confirmed by HI and ELISA I test

• The infected birds may react 5-10 days PI• False positive result may occurred due to cross reaction

between MG and MS or even other species or other bacteria as Staph, aureus

• Oil-emulsion vaccines can give false positive result so the status o f the flock should be determined prior to vaccination.

B - Haemagglutination inhibition test (HI)• Diluted sera is mixed with a haemagglutinating

Mycoplasma broth culture, then fresh chicken red blood cells are added. T he inhibition indicates the presence of specific antibodies.

• The test caould be performed with serum samples or extracted yolk from fresh eggs

• Very specific test measures IgG.• Some times gives false negative results due to antigenic

variability among MG strains.• Disadvantages: delayed development o f HI antibodies (3

weeks PI).

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Interpretation of HI test• < 1:20 Negative

• 1:20 to 1:40 Suspicious• >1 :180 Positive

The Use off SPA and HI test gives im portant information• Low positively in SPA below 30% and 3-10% positively

in HI, indicate fresh MG infection|

• High positively in both tests , indicates infection whichstarted in the flock 3-8 wk previously. I

• Low SPA positively and high in HI positively indicates an infection that started 3-6 months previously

C - Enzyme linked immunosorbent assay ELISA• Less sensitive but more specific.• Seroconversion is more slower than SPA. I

• Used for detection of Ab in serum and yolk. 1• Detect IgG for long period post infection

D - Metabolic inhibition test : Not suitable for large scale* detection of antibodies 1

E - Microimmunoflorscence (MIF) test• Estimate IgG, IgM and IgA• Used to measure antibodies• Not used at larg scale monitouring

7- Species identificationA - Immunological Methods

A - Growth inhibition test B - Growth precipitation test

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C - Immunofluorescent p - Immunoperoxidase E - Metabolic inhibition test

B - Molecular assayA - D N A prob

• Detect mycoplasmal DNA in tissues and detect thestrain

• H ighly specific• Relatively rapid® D etect the organism in clinical samples or even in

m ixed cultures B - P C R

« H ighly sensitive (theoretically 1, organism but practically 100 organism)

• Rapid (24-36 hour)* H ighly specific• Can detect D N A in clinical samples.

* Can distinguish between field and vaccinal strainsCRD

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Control of avian Mycoplasma infections 1 - Eradication programme

• Birds should kept in small flocks and complete isolation• Positive groups should be eliminated as soon as possible• Negative flocks should reared in strict isolation to avoid

introduction of the disease• Improve hygiene• Medication reduce the vertical transmission• Treatment of hatching eggs either by heating (46C for

12-14 hours) or by antibiotic via injection or dipping• Regular flock monitoring

2 - Biosecurity• Proper housing• Standard qualities of air, litter and water• Application of all in all out systemHighest standards of biosecurity is important to avoid

horozontal introuduction of the disease after the recent establishment of relatively longer survivals of avian mycoplasma outside the bird 3 - Chemotherapy

• Mycoplasma resistant to antibiotic inhibit cell wall formation as penicillin or inhibiting membrane synthesis aspolymexinBSensitive to those inhibit protein synthesis ■. J,

Effective antibiotics include:-

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, Tetracycline (oxy tetracyclines, chlorotetracyclines and : doxycycline) as bacteriostatic effect and time dependant

. Macroloides (erythromycin, tylosin, spiramycin, lincomycin and kitasamycin) bacteriostatic effect and time dependant

. Aminoglycosides; (Spectinomycine) Bactericidal and concentration dependant.

• Quinolones as (Norofloxacine, enerofloxacin and danofloxacin) Bactericidal and concentration dependant.

• Pleuromutilins as (Tiamulin) bacteriostatic effect and time dependant.

Some instruction for medicatione MG, Ms, MM and MI is the order of sensitivity of

Mycoplasma species sensitivity for avilable antibiotics (Tiamulin, danofloxacin, enerofloxacin and loncomycin)

• Tiamulin and enerofoxacine reach 500 to 100 time than their MIC in tissues of respiratory mucosal membrane.

® Combination of tetracyclines and timulin have good synergestyic effect in controling respiratory pathogen in addition to their antimycolpasmal effect

Prophylactic medications are recommended at :- * • 1st 3 weeks of life

• 3-5 weeks of age for broiler• At expected stress periods (vaccination, transportation)

4 - Treatment of Hatching Eggs1. Pre incubation heating 45-46 c

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2. Antibiotic treatments o f eggs• Injection (via air sac or rounded small bottom of turkey

eggs).• Egg dipping using temperature differential method or

pressure differential method.• Double egg treatment: - dipping followed by injection.

Methods for Mycoplasma susceptibility testing• Broth dilution• Agar dilution• Agar gradient diffusion• Disc diffusion• Metabolism inhibition test : using broth medium in

which the antibiotic inhibit the growth of the organism and inhibit its metabolism

(MIC) in mycoplasmology defined as the lowest concentration that inhibit any visible growth or metabolism of mycoplasma

5 - Vaccination

• Live vaccines (F-strain, 6/85, ts-11 strain and Nev K5054 strain)

Advantages• Less expensive• Protect against most egg losses• Mass application

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♦> Spread help in immunization of missed birds during vaccination

^ a d v a n ta g e s♦> D isrupt serological survey❖ V irulence for turkey and mild virulence for chicken

❖ In a c tiv a ted vaccines advantages

❖ D on’t spread❖ Reduce egg losses❖ Reduce egg transmission❖ Could be used when live vaccine are not available

Disadvantages❖ Individual application❖ Expensive❖ M issed birds not protected❖ Sever tissue reaction❖ Tw o doses before sexual'maturity

❖ R ecen t vaccines❖ Recom binant Vaccines ♦♦♦ Subunit vaccines

Objectives o f vaccination ' I . Prevent clinical disease2. Prevent egg production losses3. R educe egg transmission4. A void cost o f medication5. Eradication o f field virulent strains

Ideal vaccine prosperities1. Safe, not produce disease2. Not revert to virulent strain3. Produce life-long immunity4. Single dose administration5. Economical, high potency6. A long shelf life

The strategy of prevention program summarized as:-

1. Genetic improvement2. Eradication program3. Strict hiosecurity '4. Maintaining immunocompotence in birds5. Good quality vaccines6. Good management practice• All in all out• Hatchary sanitation• Proper housing• Optimum stock denisty• Proper feeding

7. Proper medication and vaccination program

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Infectious Coryza Fowl Coryza

ByProf. Dr. Mohamed M. Megahed

Coryza firstly means a disease of upper respiratory tract which characterized with slight respiratory manifestation.Coryza can be classified according to the causative agent into, infectious coryza, nutritional coryza and environmental • coryza.

Infectious CoryzaDef:It is highly contagious and produces an acute disease of upper respiratory tract of-chickens, which can turn into a chronic respiratory disease when complicated by other pathogens. The disease occur world wider and causes economic losses due to an increase of the culling rate in meat chickens and significant reduction in egg production in laying and breeding fowl. The disease is limited to chickens and has no public health importance.

Cause:Haemophilus paragallinarum. The caustive organism of this disease belongs to the the bacterial strains of genus Pasteurella than to other genera in the family Pasteurellaceae. It is Gram-

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negative, non motile, non spore form ing and capsu la ted rode

shaped bacterium (0.3-0.6 pm X 1-3 pm ) w ith a ttendance to

morphological degeneration after incubation- period o f more

than 24 hours.Complex media, m icroaerobic conditions and h igh hum idity

are used to obtain dense growth on solid m edia. Chicken

serum, (1%) is required for the grow th o f som e strains. All

strains required V-factor (nicotinam ide adenine dinucleotide)

for growth in artificial media. W hile V -facto r independent pathogenic Haemophilus paragallinarum strains have been isolated recently from chickens.Two different serotyping schemes have been m ain ly used - the

page and the kume schemes. Recently, B lackall has proposed

an alternative nomenclature for the kum e haemagglutinin scheme.Variation from very high to low virulence occurs and although little is known about virulence factors, it is know n that the presence o f the capsule and the specific haem agglutination antigens are necessary for the pathogenicity ofH.paragallinarum. It is delicate bacterium w hich dies quickly outside the host tissues. Survival outside the body under farm conditions is probably no more than 48 hour at 18-24 C. Many drugs known to have bacteriostatic than a bactericidal effect on the organism. However the second generation, of fluoroquinolones have been shown to be bactericidal under the

in vivo conditions and effective therapeutic agents.

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Mode of infection and spread:The disease cause economic losses in many parts of the world due to increased number of culls in growing chickens and reduced egg production in layers, particularly multi age farms. The disease is limited to chickens but the organism has been rarely isolated culturally from pheasants, japans quails, and guinea fowl. Chickens of all ages are susceptible but older birds tend to react more severely. The main source of infection is clinically affected and carriers birds, especially from replacement flocks. Because only few viable organisms are necessary for the infection, it can be transmitted by drinking

I water contaminated by nasal discharges as well as by air bom means over a short distance. Lateral transmission occurs readily by direct contact; spread between batteries with nipple drinkers occur more slowly.

I ' _ .Predisposing factors:• Old ages more severely affected.

• Intercurrent infection with other pathogen especially which affect the upper respiratory tract.

’ • ‘ Bad environmental condition i.e. increase ammonia, cold and dust.

• A vitaminosis A.

• Immune state o f birds.

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Pathogenesis:Adherence of the micro-organism to the ciliated mucosa of upper respiratory tract seems to be the first step o f infection. The capsule and haemagglutination antigens play an important. role in the colonization. Toxic substances released from organism during proliferation are associated with production of lesions in the mucosa and the appearance o f the clinical , signs., The capsule might act as a natural defense substance against the bactericidal power o f complement through the alternative pathways. H.paragallinarum is non-invasive ; bacterial agent with strong tropism for ciliated cells and : migrates into the lower respiratory tract (lungs and airsacs) ; only after synergistic interaction with ether infectious agents and/or encouraged by immuno-suppression. Factors that i predispose to more sever and prolonged disease (chronicn

respiratory disease) include intercurrent infections withD infectious bronchitis virus, ILT virus, M.gallisepticum orE.coli, Pasteurella species and unfavorable environmental condition. ' •

Incubation period:Usually 1-3 days and depending upon the stresses and immune., state o f birds.

Clinical signs:The d isease in flocks on floor management is characterized by

rapid spread, h igh m orbidity and low mortality the period of

incubation 1-3 days after contact infection and all susceptible

birds show signs w ithin 7-10 days. If not complicated with

other d iseases the course o f the disease is not more than about

10 days in the m ild form and approximately 3 weeks in the

more sever form. The 1st typical signs include seromucoid

nasal and ocular discharges and facial edema. In sever cases

marked conjunctivitis with closed eyes, swollen wattles (wattle

disease) and difficulty breathing can be seen. Feed and water

consum ption is usually decreased resulted in drop of egg

production o f more than 2 0 % indicates multifactorial disease.

If com plicated w ith other infectious agents a more sever and

prolonged disease may develop with the clinical picture of chronic respiratory disease. Swollen head like syndrome

associated w ith H.paragallinarum has been reported in the

absence o f pneum ovirus but in the presence of other pathogens such as virulent E.coli.

Lesions:1- Catarrhal to fibrino-pumlent inflammation of the nasal

passages and infraorbital sinuses and conjunctiva.2- Subcutaneous edema o f the face and wattles.3- The upper trachea may be involved but the lungs and

airsacs only affected in case of complicated cases.

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Histopathology:Loss o f cilia and microvilli, cell edema, degeneration and

desquamation o f mucosal and glandular epithelium , infiltration

of leukocytes, and deposition o f purulent like substance can be

seen and are followed by infiltration o f m ast cells into the

lamina propria o f the mucus membranes.

Diagnosis:1- History o f rapid spreading.

2 - Clinical signs.

.3- Lesions.

4- Isolation o f the causative agent through swabbing the

nasal passage from 2 or 3 acutely diseases birds onto blood agar plates cross streaked with feeder organism

such as Staphylococcus epidermidis. A fter incubation

for 24-48 hours at 37 C in a candle ja r or in an

atmosphere o f 5% CO2. Tiny translucent colonies o f 0.3-

1 mm in diameter appear on the culture plates adjacent

to the feeder culture.

5- Confirmatory test using PCR following efficient

isolation.

6 - Inoculation o f culture suspension or the exudates into 2

or 3 susceptible chickens. The organism present in the

inoculum the clinical signs appear w ithin 1 -3 days.

7 - Serological tests include Flurouscent “antibody

techniques, ELISA, and HI test.

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Differential diagnosis:The disease should be differentiated from other disease showing the same symptoms like, myoplasmosis chronic fowl cholera, environmental coryza and viral diseases such as fowl pox, paramyxovirus infectious, infectious bronchitis and infectious laryngotracheitis.

Control:1- Improved management measures such as depopulation,

good sanitation, traffic control, and avoiding birds of

multiple ages; may help in the break of the disease cycle. To eliminate the agent from a farm it is necessary to depopulate the infected or recovered flocks because such birds remain reservoir of the bacterial agent. After cleaning and disinfecting, resting the building for 1

week, new birds'may be introduced, only one day old chicks or older birds known to be free frown the micro­organism should be used for restocking.

2- Vaccination using inactivated whole culture of the organism containing adjuvant can protect chickens against the disease. Such vaccines protect provide specific immunity but no protection across serogroups. At present it is not clear weither antigenic differences of the strains within a serogroup also have specific immunologic differences. An autogenus bacterin should

194

be used. Two doses of vaccines each of which should contain 108 CFU, given S/C 3-6 weeks .apart with the first at 16 weeks of age. Live vaccines could stimulate; more cross serogroup immunity but give rise to carriers and may cause a disease. ,

3- Therapeutic control using various sulphonamides, trimethoprim and tetracycline combination as well as the second generation quinolones drevatives (enerofloxacin and norofloxacin) for 5-7 days treatment, the clinical sighs diappear but relapse-may occur if the treatment discontinued.

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swollen sinuses with nasal exudate in a hen with infectious coryza.

Avian Chlamydiosis (Psittacosis, Ornithosis)

ByProf. Dr. Ahmed M. El-Sadek Hegazy

Def:It caused by bacteria Chlamydophila psittaci, systemic infection occasionally fatal. In human & birds called psittacosis or parrot fever. The disease called ornithosis in man & other non psittacine birds. The disease from turkey ornithosis is more severe in man. Human infection is common following handling or processing of infected turkeys or ducks. Most infections in human are through, inhalation of infectious aerosols (l.P . 5-15 d) systemic & pneumonia.

Cause:- Intracellular gram- negative bacteria infecting both

human & animals. Morphologically present in three forms.• Elementary bodies (EB) 0.2 - 0.3 pm• Reticulate bodies (RB) 0.5-2pm• Intermediate body (IB) 0.3-1 pm

Divides by binary fission & matures into EB- F. chlamydiaceae has two genera Chlamydia (3sp.) and

Chlamydophila (6 sp.) (C. psittaci, C. abortus, C. felis, C.caviae, C. peamoniae,7 C. suis).

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- Using DNA sequence analysis of phylogenetic markers provide a rapid & reproducible method for identifying grouping, and classifying Chlamydia strains Chlamydia are large enough to be seen with Light microscope using special optics or with selective stains, Bright-field optics and field illumination.

' . ! • • .. : : . I

Staining:Chlamydia may be seen in touch impression smears of infected tissues by staining with Castaneda, Giemsa, Gimenez, Macchiavello, or stamp methods after appropriate fixation. • They appear:1 -dark purple with Giemsa.2- Blue with Castaneda.3- Red with Macchiavello; Gimenez and stamp stains.Gimenez is preferred for staining (yolk sac, air sacs, spleens, pericardium), of naturally infected birds. Tetracycline, chloramphenicol & erythromycin inhibit activity.

Sensitivity to chemical compounds:- Quaternary ammonium compounds & Lipid solvents.- Resistant to Cresol & lime.- Destroyed by alcoholic iodine solution, 3% hydrogen

peroxide. ■ A

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gtrain classification:Chlamydophila psittaci includes 8 known serotypes (A, B, C,

p,E, F, M 56 & W C). 6 o f them could infect birds naturally.

A) From psittacine birds

B) PigeonsC) W ater fowl

I D)Turkey ( B & E also)E) Ducks , pigeons and ostriches.

F) Psittacine birds.Recognized by monoclonal antibodies (MAbs) that detect

LPS, PCR.

[ Pathogenicity:1- H ighly virulent acute 5-30% in turkey mortality.

2- Less virulent, pigeons & ducks. Mortalities below 5% cause slowly progressive epidemics.

- Serotype (D) called toxigenic as it produces rapidly fatal disease (extensive vascular congestion & inflammationo f vital organs).

- Chlamydiosis in pigeons & ducks accompanied by concurrent infections with salmonellae, the mortality is

, high.

Incidence & distribution:Avian Chlamydiosis Occurs worldwide psittacine birds harbor one serotype o f Chlamydia that is endemic & many

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psittacine birds are chronically infected, under stress may become clinically ill or shed the organism, spread o f infection to human occurs .Turkey , ducks, geese*, swan, pigeons. Younger domestic birds generally are more susceptible than older birds to infection, clinical disease & mortality.

- Laboratory hosts (mice & Genia pigs) rabbits for production of polyclonal antibodies.

Transmission:1- Caniers shed the organism C.psittaci (under stress)

psittacine birds shed serotype "A" while pigeons & doves shed serotypes Bor E.

2 - Other infected birds.3- Transmission by inhalation or ingestion o f contaminated

material.4- Direct aerosol transmission (respiratory exudates)

primary method o f transmission during outbreaks. Mites act as vectors.

5- Vertical transmission in ducks, chickens, turkeys & wild

birds.

Incubation period:Varies according to virulence & number o f Chlamydia inhaled

in young turkey 5-10 days & longer in older birds.

2 0 0

Turkeys Clinical signs:In turkey infected with virulent strain are cachexia, anorexia, elevated body temperature, conjunctivitis and respiratory signs. Yellow -green or gelatinous droppings. Egg production declines rapidly to 10-20% temporarily cease (50-80% morbidity) signs in case o f infection with low virulent strains, anorexia, loose, green droppings in some birds with less effect on egg production. (5-20% morbidity) mortality 10-30% & 1- 4% respectively.

Lesions:Lungs showed diffuse congestion with fibrinous exudates in pleural cavity, in fatal cases dark transudate may fill the thoracic cavity.The pericardial membrane is thickened , congested & coated with fibrinous exudates. The heart may be enlarged and covered w ith thick fibrin plaques (or yellowish flaky exudates).Liver is enlarged & discolored & covered with thick fibrin. Air sacs are thickened & heavily coated with fibrinous exudates. The spleen is enlarged, dark & soft & may be covered with gray white spots.Peritonitis, mesentery show vascular congestion and coated with foam y white fibrinous exudates.

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Ducks & geese Clinical signs:I n v o u n z : anorexia, imbalanced gait cachexia , serous to purulent discharge from eyes & nostrils emaciation & die in convulsions. Morbidity 10-80%, mortality 0-30%, of public health importance.

PigeonsSigns:In a cute disease are anorexia unthrifty and diarrhea, conjunctivitis, . swollen eyelids, rhinitis. Weakness & emaciation. 30-90% mortality.

Lesions:1- Fibrinous exudates on thickened air sacs, peritoneal

serosa & epicardium.2- Liver swollen, soft and discolored.3- Spleen, enlarged soft & dark.

Chickens1- Chickens are resistant to many strains.2- Inapparent & transient signs may occur.3- Conjunctivitis, pericarditis, perihepatitis and ®

sacculitis in young birds.

Diagnosis:1- Direct detection of C.psittaci by staining techniques.2- Isolation on:

a. Cell culture monolayer's.b. Yoik sac of ECE (vascular congestion).c. Mice.

The preferred method to demonstrate the chlamydia spp inclusion is the direct or indirect immunofluorescence using monoclonal antibodies. Yolk sac touch impressions for staining, IF seems to be the most specific & sensitive direct antigen detections, test. PCR for detection of C.psttaci specific genes (easy, simple, rapid, high sensitivity & specificity) but cross contamination can occur & false negative as well as positive PCR sometimes reflect a carrier status and needs specialized laboratories.Diagnosis can be made by serology. CFT high titers > 64 in poultry are indicative' of recent infection if lower (needs retesting after 10-14 day & detect change in titer 4-fold or greater increase is considered diagnostic for the presence of Chlamydia infection.■ • Latex Agglutination (LA): detect IgG & may be (lgM).

• Elementary body agglutination test (EBA): detect only lgM.

• Direct (CF): detect lg G only.Differential Diagnosis:- Pasteurellosis in turkeys which may be similar.

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- Mycoplasmosis, colibacillosis and avian influenza.

Prevention & control:1- Avoid contact with contaminated equipment or

premises, contact with carriers or vectors.2- General sanitation.3- Movement of people should be restricted.4- Vaccination: needs further studies.

Treatment:Chlortetracycline’s (CTC) medicated feed for 2 weeks is effective for poultry & pet birds at a concentration of 400gm/ton o f pelleted feed. Not give calcium during treatment.Alternative treatment with antibiotics is effective as well as alternative periods. Treatment may not be effective in eliminating the carrier status.

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A v ia n T u b ercu losis

ByProf. Dr. Ahmed M. El-Sadek Hegazy

Def:Tuberculosis is a contagious disease caused by Mycobacterium avium and characterized by

• Its chronicity• Persistent in the flock• Decreased the egg production• Emaciation ended by death.

Serotypes o f Mycobacterium avium isolated from humans are usually different from those commonly isolated from chickens.

cause:• Mycobacterium avium• Serotypes 1 and 2 in USA.• Serotype 3 in Europe• 1,2, and 3 serotypes occur mainly in animals.

, • Serotypes 4-20 are commonly found in humans.• Highly resistant acid fast bacilli, it resist heat, cold

dryness and PH changes also resist many disinfectants and survives in soil for months.

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• The organism grows slowly in culture at temperati ranges from 39-45 C and growth is enhanced by atmosphere of 5-10 % Co2.

• Initial isolation on media containing whole egg or ej yolk with glycerin gives larger colonies (smooth, raisi grayish white colony). After 3-4 weeks incubation.

• Smooth transparent colonies were virulent for chickeiin contrast to rough colonies. -

■

■

Pathogenesis and EpizootiologySusceptibility:

• All species of bird are susceptible• Captive exotic birds are affected more than those livin

in a wild state.• May occur in ducks, geese, swans, peacock, pigeon!

turkeys, parrots and canaries.• Mammals, cattle, sheep, rabbit and swine.• Less prevalent in young fowl; not due to resistance, bi

due to longer periods of exposure in older birds.

Transmission:• Infected fecal material with tubercle bacilli exuded fror

tuberculous lesions of the intestine, liver,: and ga bladder.

• Contaminated environment, soil and litter.• Infected carcasses, offal, shoes. Equipments, sacs.

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• W ild birds, pigeons and sparrows,

finical signs:1- The affected fowl fatigues easily and apperars

depressed.

2 - The appetite remains good, but the birds become emaciated.

3 - Atrophy o f pectoral muscles and the keel bone deformed, the face appears smaller than normal.

4- Anemic comb, wattles and ear lobes.5- Ruffled feathers and dull birds.6 - Severe diarrhea.7- Lameness . due to tuberculus involvement of bone

marrow. 8 - Birds may die suddenly due to hemorrhage from rupture o f liver and spleen.

Lesions:The lesions are seen most frequent in liver, spleen, intestines and bone marrow. The lesions characterized by irregular grayish yellow or grayish white nodules of varying sizes. Large nodules has irregular contour. Lesions near the surface of liver and spleen are enucleated easily from the adjacent tissues. On cross sections o f the nodules, showed fibrinous nodules containing number of small yellowish foci or softyellow region which may be caseous. Internal hemorrhage due

/to rupture o f liver and spleen may occur. Bone marrow

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affection may occur easily and characterized by hypertrophy and end with tuberculous nodules formation in the marrow Tubercles nodules may appear in other organs as heart, ovary lung, testes and skin.Diagnosis:

1- Gross lesions2- Smear from the infected liver, spleen or other organs

and then stained with Ziehl-Neelsen is very helpful in diagnosis of the acid fast bacilli.

3- Tuberculin test: injection of tuberculin into the dermal layer of one wattle and the other left as a control for comparison.

Reaction: after 48 hours the positive reaction includes softness, swelling of tissues and thickening of the wattles to five times.

4- Serological tests• Rapid serum agglutination test

P r o c e d u r e s

Drop from antigen (10% suspension of M. avium in 85% sodium chloride contain 0.5% phenol) + drop of fresh blood on warm plate.R e s u l t s I

; Agglutination within 1 minute indicates positive result. IELISA for detection of antibodies in serum of infected I

birds or captive birds and exotic birds without wattles. I

Differential Diagnosis:F.cholera, neoplasia.

Treatment:• O f no value in chickens

& -• In captive birds or exotic birds (rifampicin "45mg/Kg")

for 18 months.

prevention and control:1- All chickens should be marketed after their first laying

season.2- Thoroughly clean and disinfect buildings betw een

broods.3- Standard sanitation at all times.4- Regular tuberculin testing aids in removal o f reactors.5- V accination (serotype 6) live orally.6 - Q uarantine 60 days for exotic birds.

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Avian SpirochaetosisB y

Prof. Dr. Mohamed M. MegahedDef:It is usually an acute infectious disease of poultry characterized by fever, locomotory disturbance and progressive paralysis.

Cause:Borrelia anserina, a spirochaete which is difficult at present to be cultured on artificial media or cell culture A suitable, mini-definition of the genus Borrelia is: a spirochete that causes a relapsing feverlike condition in man or animals and is transmitted by lice or ticks.The daily observation is necessary because Borrelia quickly disappears from blood. Six-day-old embryonating chicken eggs can also be used in isolation B.anserina. Samples are inoculated by the yolk-sac route. After 2-3 days o f incubation, allantoic fluid should be examined for Borrelia.Borrelia can be observed either by dark-field microscopy or in stained samples. Smears of blood or tissue can be stained with Wright’s stain, Giemsa stain. Other stains that can be used are Ziehl-Neelsen carbol fuchsin, methylene blue.

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Avian Spirochaetosis By

Susceptibility:- Naturally: chickens, turkeys, geese, ducks, grouse, and

canaries.- Pigeons are refractory to natural infection.- Birds o f all ages m ay become infected but young birds

are more susceptible.

Mode o f infection and transmission:By the bites o f avian ticks (Argus persicus, A .m iniatus, A.reflexus), red m ite or mosquitoes. Fowl tick (A .persicus) is infective by all stages (eggs, nymph, larva) and transovarian transmission o f the organism occurs in the tick. B irds m ay be infected by ingesting infected ticks, their eggs, or food contaminated w ith infected droppings. ‘

Incubation period:- 3-9 days.

Symptoms and course:A. acute form:

1- Fever and swelling o f the feet and claws.2- The birds becom e listless and droopy, with cyanotic

heads and ruffled feathers.3- Infected .individuals stop eating, and then the comb

becomes pale.

2 1 1

. 4- Greenish diarrhoea and paralysis is usually seen beforedeath. - Average duration of the disease is about 5 days, •

:and mortality may reach up to 90%.

.

B. chronic form:1- Prolonged course of the disease (about 21 days) with

marked anaemia.2- Emaciation and stupor.3- The temperature drops to subnormal a day or two before

death.4- Mortality may reach 60%.

• r

Lesions:1- Enlarged and mottled of the spleen, with ecchymotic

haemorrhages. ' ; • o2- Liver enlarged and studded with numerous pinpoint

necrotic foci. :■ j3- Fibrinous pericarditis and myocarditis.4- A greenish-yellow mucoid enteritis.

Diagnosis:The finding of the organism in peripheral blood smears taken during the febrile stage and stained with Giemsa is diagnostic.In freshly dead birds the organism can be demonstrated in smears made from the pericardial fluid or heart blood and in sections from the liver, or spleen.

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Control: *1- Check ticks, mites, and other biting insects on the

birds and in the houses by suitable insecticides.2 - Treat with ? * specific drugs as .penicillin, atoxyl

(sodium arsenilate), arsenobenzol drugs, and oxytetracydine. A single dose of penicillin at the rate of 10-15,000 units per bird, or oxytetracydine at the rate of 40 mg/kg body weight is highly effective under field conditions. Recovered birds are solidly immune.

Prevention:1- Clean and hygienic poultry houses.2- Eradication of ticks and other insects.3- Using the chick embryo vaccine produced locally. The

vaccine used I/M inoculation at 2 weeks in between 7-8 weeks of age and you have to twice see fine orders of producers.

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Avian PasteureilosisBy

Prof. Dr. Ibrahim A. GhanemDef:It is a general term used to cover a variety of infectious diseases caused by pasteurella, of which Fowl cholera and infectious serositis are of economic importance.

Fowl choleraDef:It is contagious acute or chronic infectious disease affecting, domesticated and wild birds, characterized by rapid course and high mortality in acute septicaemic form and localized affections in chronic one.

Epidemiology:Cause:P asteurella has been divided into 3 subspecies (subspecies multocida, septica and gallicidia).

1- Gram -ve , non motile , non spore forming and capsulated rounded end rods, capsule is associated with pathogenicity

2- It appears bipolar in blood or tissues stained with methylene blue or Giemsa stain and can be propagated in blood agar.

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Avian Pasteurellosis By

3- There are 5 capsular types of pasteurella multocida are recognized (A,B,D,E and F ) where capsular type A and D were isolated from fowl.

Incidence, resistance and susceptibility:1- Fowl cholera is more prevalent in late summer, autumn

and winter seasons.2- It can survive for few weeks in yard, 1 month in manure

and 3 months in infected dead carcasses.3- Humidity (15%), temperature (15-18c) and pH (7) o f the

environment play a great role in viability o f pasteurella multocida.

4- Chicken, turkey, duck, geese, pigeons and other wild birds are susceptible.

5- W ater fowl more susceptible than turkey and turkeys more than chickens.a. M ature chickens than young one.b. Young turkeys than mature.c. Heavy breed than light one.d. Fatty chicks than normal.e. Rabbits and mice are very susceptible but not guinea

pig or ratf. M an m ay get a localized infection through wounds.

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Source, mode and route of infection:1- It lives in the upper respiratory tract o f birds and under

stress as bad management etc..., it become invasive and

cause the disease.

2- Carrier birds (survivors o f natural outbreaks).

3- Clinically diseased birds, their excretions and carcasses.4- Newly purchased birds.

5- Rats, wild birds, attendants and insects.6- Air and water may facilitate transmission.7- Route o f transmission (oral, nasal, conjunctiva and

wound)8- Orally through nasal cleft, pharynx or mouth but not

. esophagus, crop nor proventriculus.9- Spread o f infection in flock is by excretion o f the

organism from the mouth o f infected birds which

contaminate food and water.

Incubation period:1 - Naturally 4-9 days.

2- Experimentally 2 days.

Symptoms:• Peracute form:

Death without any symptoms, where large number of

birds are found dead in good bodily condition.

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0 Acute form :1- General symptoms with marked depression and

anorexia. -»

2- Picture o f septicemia (cynosis o f comb and wattles and elevated temperature, greenish-yellow diarrhea)

3- Difficult breathing with mucous discharge of beak4- Death in few days5- Mortalities are 10-50% in chickens, 20-70%. in

turkeys and 50-80% in water fowls.• C hronic form :

Characterized by localized infection and this form usually follow an acute stage o f the disease or result from infection with low virulent M.O.

Localized infections includeA- W attle form (swelling o f wattles)B- C a ta rrh a l o r roup form.

Rales- dyspnoea -. conjunctivitis

swelling o f sinusescatarrhal discharge from the nose and beak.

; C -A rth r it ic form.Lameness with enlargement o f joints (legs, wings, foot pad and sternal bursae).

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D- Nervous form or otitis media formTorticollis due to localization o f M .O in ear base

o f the brain and air spaces o f bone o f head (turkey, chicken, geese and ducks).

E- Ovarian form or peritonitis (no clinical signs).

Lesions:

• Peracute:

No PM lesions.

• Acute:

1- Congesion o f carcasses and dehydration, hydropericardium (straw yellow in color).

2- Swollen liver with peticheal haem orrhages and streaked with light areas.

3- Multiple petichation on mycocardium , coronary fat, serosa o f gizzard, proventriculus, abdom inal fat, serous and mucous membranes.

• Subacute form:

1- Pin point necrotic focci o f coagulative necrosis. Grayish in color are evenly distributed on the liver surface.

2- Haemorrhagic duodenitis.3- Ovaries (mature follicles appear flaccid with less

evidence o f thecal blood vessels, im m ature follicles

and ovarian stroma are hyperemic).4- Free yolk in abdominal cavity.

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5- Odema in lungs with pneumonia, serofibrinousperihepatitis, pericarditis and catarrhal tracheitis.

• Chronic form: *a

1- Wattle form (fluid or caseous exudates in wattles).

2- Catarrhal or roup form (caseous exudate in nasal passages, infraorbital sinuses, trachea, air sac and conjunctival sacs.

3- Arthritic form (caseous exudate in joints, tendon sheath, food pad and sternal bursae)

4- Nervous form or otitis media form (caseous exudate in middle ear and air spaces o f cranial bone).

5- Ovarian or peritonitis form (caseous exudate in abdominal cavity, around ovary and in oviduct).

Diagnosis- Case history.- C linical signs.- Gross lesions.- Peracute and acute:

L iver im pression smears and blood smears stained w ith G iem sa o r m ethylene blue show bipolar organism with rounded end rods.

- Iso lation from liver, heart blood or bone m arrow on

b lood agar (dew drop like colonies) and follow ed by

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Gram stain which reveals Gram negative coccobacillj (no bipolarity in artificial media).

- Biochemical reaction. Serological reaction (serum plate agglutination, Rapid whole blood agglutination).

- In decaying carcasses, the best site for isolation is bone marrow.

- Chronic cases (localized lesions)Inoculation in mice or rabbit with 0.2ml o f 18 hours ground tissue or broth culture I/P will induce death within 24-48 hr then blood smear to detect the bipolarity or reisolation on blood agar culture.

Treatment:- It is better to carry out sensitivity test- Sulphonamides

Sulphadimidine- sulphamerazin and sulphaquinoxaline Dose 0.33% in water for 5-7 days.

Disadvantage of sulphonamideso It is bacteriostatic instead o f bacteriocidal

• In ability to cure localized abscess

• Toxic effect on birds (decrease egg production and j

- AntibioticsOxytetracycline, Streptomycin, chlorotetracycline and Chloramphenicol, quinolones (ehrofluxacin,

f ■■■ i ‘

danofluxacin and ofluxacin)

egg shell quality)

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N.B reccurent of infection on stop of treatment is common, so, the use of autovaccination is a must for effective control of infection.

prevention and control:1- Good management.2- Avoid adverse environmental conditions.3- Do not rear more than one species in the same yard.4- New birds should be quarantined for 2 weeks before

being introduced.5- Prevent entrance o f wild birds and combat rodents.6- Thoroughly disinfect utensils and equipments.7- VaccinesA. Bacterin (killed or inactive)■ In chicks 80-100 day of age 1st dose 0.5 ml -S/C

followed by 2nd dose after 4 weeks■ In ducks 1 month of age or before 0.5ml S/C followed

by 2nd dose 1ml after 4 weeksN.B:

> Bacteria must be the same serotypes of the field outbreaks, so periodical serotyping of the field isolates is very important.

> Perfect S/C inoculation is very important (faulty in vaccine injection in neck muscles may lead to abscesses and emaciation followed by the death of the vaccinated birds)

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B. Live vaccine as CU strain used via eye installation or wing web sticking (which is avirulent strain it could be used as emergency vaccine.

Sw ollen wattles in a broiler breeder male as the result o f a chronic fc

cholera infection.

Petechial hemorrhages on the coronary fat.and swollen liver wit

point necrotic foci o f Fowl cholera infected chickens.

Clostridial InfectionsBy

Prof. Dr. Ibrahim A. Ghanem

s j Clostridia are large, anaerobic Gram positive bacteria, most of i f which produce spores that are resistant to high temperatures

and many disinfectants. They are ubiquitous worldwide, being found in soil, dust, animals, insect larvae and they are frequently found in low numbers in the intestinal tract of normal birds. Some are opportunistic pathogens and for these there are factors which predispose to outbreaks of disease in a flock. Management, particularly associated with feed, overcrowding and inadequate hygiene. In addition perhaps genetic constitution.The most important clostridial infections in poultry are:

1 - Clostridium colinum )* Ulcerative enteritis

2 - Clostridium perfringens Necrotic enteritisGangrenous dermatitis

Yolk sac infection

3 - Clostridium botulinum - > Botulism (Limber neck)4 - Clostridium novyi5 - Clostridium septicum

Gangrenous dermatitis

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Ulcerative enteritis (UE)(Quail disease )

Def:Acute bacterial infection in young chickens, turkeys and game

birds characterized by sudden onset and rapidely increasing mortality.

cau se:Clostridium colinum

• Anaerobic Gram positive rods.

• Grow on tryptose- phosphate agar with addition o f 0.2 % glucose and 0.5 % yeast extract.

• Produce white, circular,... convex and semitranslucent colonies with filamentous margins.

Susceptability:1- Quail is the most susceptible species e.g. bobwhite

quail, turkey and chickens.

2- Young chicks and quails (4-12) weeks old and (3-8)

weeks old turkey.

3- Light breeds o f chickens (balady, layers) are more

susceptible than heavy breeds.

4- Outbreaks in chickens often occurs along with or after

period o f stress or coccidiosis, CIA, IBD. . :

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Transmission :Ingestion o f contam inated feed, water or litter.

• . *

Clinical signs:1- Depression.2- Anorexia. ;;3- Dullness.4- Humped up.5- Partially closed eyes. ■ ■6- Ruffled feathers.7- Shrinked comb and wattles.8- In quail dropping is white watery.9- In acute cases death of well muscled individuals with

feed in the crop.10- * In young, mortality reaches 100 % in a few days -

but typical range (2-10%).

lesions:1 - Ulcers may be lenticular or circular sometimes

coalescing to form large necrotic, diphtheritic patches. U lcers in ceca may have central depression filled with dark staining material that cannot be rinsed off.

2 - U lceration may be extensive enough to erode through intestineal wall and perforate it, resulting in peritonitis and adhesive ulcers appear gray in centre and red in peripheral through the serosal surface.

226

3- Small punctate hemorrhages may be visible through the serosa in the intestinal wall.

4- Liver, Lesions vary from light yellow mottling to large

irregular yellow areas along the edges. Disseminated gray focci or small yellow circumscribed foci sometimes surrounded by a pale yellow halo.

5- The spleen is enlarged, congested and hemorrhagic.6 - Acute lesions in quail are characterized by marked

hemorrhagic enteritis in the duodenum.

Diagnosis:1 - Case history. -2- Clinical signs.3 - Gross lesions.4- Crushing o f necrotic liver tissue between 2 slides, fixed

by heat followed by staining using Gm. stains reveal Gm+ rods o f subterminal spores.

5- Flourescent antibody technique.6- Agar gel immunodiffusion test.7- Isolation and identification (Liver is recommended for

sampling than intestine).

Differnetial diagnosis:1- Coccidiosis (Lesions restricted to intestinal tract).2- Necrotic enteritis (Swelling o f the intestinal tract).3- Histomoniasis (Smear from caecum).

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Treatment: ‘> Ampicillin, chlorotetr-acycline and tylosin were used in drinking water. Bacitracin methylene disalycilate 200g / ton and penicillin 50-100 gm / ton feed for the control o f ulcerative enteritis.

prevention and control:1- Because the MO produce spores and persist in

dropping. Rem ove the contaminated litter and use clean litter.

2- Control o f coccidiosis and other viral diseases e.g, IBD, CIA that induce immunosuppression

3- Avoid crowdness.4- Practise a high standard o f hygiene.

Necrotic enteritis (NE)

Def:Necrotic enteritis is sever disease of avian species. It ischaracterized by necrosis of intestinal mucosa.cause:C l o s t r i d i u m p e r f r i n g e n s Gram +ve bacilli, type-A produces alpha-toxins while type C produces beta-toxin both toxins are responsibel for intestinal mucosal necrosis.C l o s t r i d i u m p e r f r i n g e n s could isolated on blood agar under anaerobic condition and. colonies surrounded by double zone of haemolysis.C l o s t r i d i u m p e r f r i n g e n s importance:

1 - Necrotic enteritis2- Yolk sac infection3- Gangrenous dermatitis

Predisposing factors:1- High energy-high protein ration.2- Damage of intestinal mucosa (high fibre).3- Litter of coccidiosis.

Susceptibility:1- Chickens (2-5 week in broilers and 3-6 months 111

layers).

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2- Turkeys (6-11 week).3- Fattening breeds more susceptible than light one.

Pathogensis:The disease associated with proliferation of Clostridium perfringens in large intestine and caecum, migration to small intestine. Where the toxin is produced and destroy the epithelial cells o f the gut.

Clinical signs:1- Severe depression.2- Decreased appetite.3- Relactance to move.

. 4- Diarrhea.5- Ruffled feathers. '6- Clinical illness is very short, often birds are just found

acutely dead.

Lesions:1- Friable intestine distended with gases and excessive

mucous.2- Small intestine primarily jejunum and ileum also cecal

mucosa lined by losely to tightly adherent yellow or green pseudomembrane.

3- Flecks o f blood have been reported but haemorhages is

not a prominent features.

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4- Necrosis of intestinal mucosa progress .overtime to severe fibrinonecrotic enteritis with formation of diphtheritic membrane.

5- Hepatitis characterized by swollen, tan colored liver with necrotic focci.

Differnetial diagnosis:• Ulcerative enteritis

• Coccidisosis

Control and prevention:1- Virginimycin, tylosin, penicillin, ampilcillin, bactitracin

and lincomycin.2- Removal o f fish meal and control o f coccidiosis3- Using o f probiotic lactobacillus acidophilus and

enterococcus faecium help in prevention and reduce the severity of necrotic enteritis.

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BotulismL im berneck - Western duck sickness

Def:is intoxication caused by exotoxins produced by clostridium botuilinum

cause:Neurotoxins produced by Clostridium botuilinum, which is a gram positive, spore forming bacilli, grow under anaerobic conditions. They are 8 types(A-G) type C associated with most outbreaks in poultry.

Susceptibility:Chickens, turkey, duck, pheasant and ostrich. It is relatively

rare in dom estic poultry kept under good standards o f hygiene.

Source of toxins:- Feeding o f carcasses, maggots or decaying plants.

Clinical signs:1- F laccid paralysis o f , legs, wings, neck and eyelids.

Signs progress cranially from legs to neck and

eyelids.

2 - In itia lly affected birds reluctant to move and if

coaxed to walk they lame, followed by paralysis and

death due to cardiac and respiratory failure.

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3- Mortality in severe cases up to 40%.

Lesions:1 - Lack of gross lesions.2- The presence of beetles and maggots in the crop

which may be contain the preformed C l o s t r i d i u m

b o t u i l i n u m toxins.

Pathogensis:Toxin of type C acts as a neurotoxin at the peripheral chologenic nerve terminus, resulting in blocking the releases o f acetylcholine leading to muscle paralysis.

Diagnosis:1- Case history2- Clinical signs3- Gross lesions4- C l o s t r i d i u m b o t u l i n u m is widely distributed in gut,

liver and spleen o f clinically and normal chickens so that isolation o f the organism from bird o f little help in diagnosis

5- Detection o f toxin in serum or crop and GIT wash using mouse bioassay

2 3 3

Treatment:

p a c im c in cblom tetracycline and in valuable birds can use specific antitoxin. • use

234

Prevention and control:1- Removal of potential sources of the organism and its

toxin from the environment (the litter).2- Hygienic disposal of dead birds and culling of sick

birds.

235

Gangrenous dermatisis (GD)

(Wing rot disease)Def:Cutaneous infection characterized by necrosis of skin, S/C tissue and underlying musculature, mostly seen in broilers, layers and breeders.

cause:C l o s t r i d i u m p e r f r i n g e n s

Susceptibility:• Chickens and turkeys• 17 day to 20 week of age• Mostly in 4-8 weeks of age broilers• In commercial layers 6-20 week old• In broiler breeders 20 week old

Predisposing factors:1 - Immunosuppressive agentsA- viral agents

1. Infectious bursal disease2. Chicken infectious anaemia3. Reticuloendotheliosis4. Avian adenovirus infection5. • Inclusion body hepatitis6. Reo virus

7. M,arke’s disease.B- Mycotoxin C- Nutritional deficiency

• Inadequate protein to feather and skin growth

• Vitamin E deficiency (responsible for immunity and antioxidant)

cause:C l o s t r i d i u m s e p t i c u m

Also C l o s t r i d i u m p e r f r i n g e n s type A and S t a p h y l o c o c c u s

a u r e u s w e r e isolated.

Route of infection:Direct contact with skin lesions.

Clinical signs:1- Depression

2- Incoordination

3- Anorexia

4- Ataxia and weakness

5- Disease is acute and short bird found dead within 24

hours

6- Mortality ranged from 1-60 %.

7- Rapidly decomposed carcasses w ith foul odour.

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Lesions:1- Dark and moist skin, usually devoid of feathers under

wings, breast, abdomen, or between thighs.2- Extensive bloody tinged odema with or without gas

(emphysema) which present beneath affected skin.3- The underlaying masculature is discolored gray or

tan and may contain odema and gas in between muscle bundles.

4- In some cases, emphysema and serosanguineous fluid are present in subcutaneous tissue.

Diagnosis:1- Case history.

2- Clinical signs.3- Gross lesions.4- Bacterial culture (misleading, since staphylococcus

aureus is normal skin flora and clostridial organisms

are present on the litter and contaminate normal skin).

Treatment:1- Adminstration o f chlorotetracycline,

oxytertacycline, erythromycin or penicillin in

water

2- Chlorotetracycline in feed.

3- Failure o f treatment usaully is attributed to the

underlaying etiology, usually viral which is not controled by antibiotics.

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Mucosal surface o f the intestine affected by necrosis in laying hen.

Dark and moist skin o f the breast - broiler 5 weeks of age.

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Avian Bordetellosis By

Prof. Dr. Amal A. M. EidIn tro d u c tio n :

Avian bordetellosis is a highly contagious bacterial disease affecting the upper respiratory tract o f birds mainly in turkeys. (Turkey coryza) and cockatiels (Lockjaw), while in chickens the disease is less severe, also avian bordetellosis was recorded among many other avian species (ostrich, pheasants, ducks, geese and quails).Bordetella avium is the etiological agent. Although B. avium is considered a definite pathogen and has the potential virulence factors. It is suggested that management factors might be instrumental in inducing the incidence of the disease. Concurrent bacterial, viral and or fungal infections were recorded in several outbreaks.The new species o f B ordetella (B. hinzii) has been isolated

from the respiratory tracts o f chickens and turkeys in various parts o f the world. Human isolates have been recorded. Bordetella bronchiseptica was also recorded in turkeys.In Egypt there are lim ited studies on the disease because the turkey production was lim ited to backyard and few scattered farms. Now there is development in commercial turkey flocks, which require more awareness o f turkey diseases.

241

Background and taxonomy of bordetella species:In the past, various members of the genus have been classified with other bacterial species, including Haemophilus, Brucella, and Alcaligenes. In the 1984 edition of Bergey’s Manual of Determinative Bacteriology, both Bordetella and Brucella species are listed as genera of uncertain affiliation. In 1986, De Ley and coworkers proposed a new family, called Alcaligenaceae to include Alcaligenes and Bordetella genera. The genus Bordetella contains seven species.

Genus Bordetella-bacterial nomenclature up to-date (DSMZ, 14 December 2000).Species AuthorsBordetella avium Kersters et al. 1984Bordetella bronchiseptica (Ferry 1912) Moreno-Lopez 1952Bordetella hinzii Vandamme et al. 1995Bordetella holmesii Weyant et al. 1995Bordetella parapertussis (Eldering and Kendrick 1938)

Moreno-Lopez 1952Bordetella pertussis (Bergey et al. 1923) Moreno-

Lopez 1952Bordetella trematum Vandamme et al. 1996

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Disease synonyms:■ Adenovirus-associated Rhinotracheitis.■ Turkey Coryza.■ Turkey Bordetellosis.* Alcaligenes rhinotracheitis (ART).* Acute respiratory disease of turkey.

Bacterial synonymsB . a v i u m B . h i n z i i

A l c a l i g e n e s f a e c a l i s B . a v i u m - l i k e

B . b r o n c h i s e p t i c a - l i k e A l c a l i g e n e s f a e c a l i s t y p e I I

T C ( t u r k e y s c o r y z a )

B a c t e r i u m t y p e I I

A l c a l i g e n e s s p . S t r a i n C 2 T 2

Physical properties of brodetella avium:Gram-negative rod (0.4-0.5 pm x 1-2 pm).Strict aerobe

Motile.

Capsulated.

Fimbriated (2 nm diameter)

Colonies, 0.2-1 mm at 24 hr; round, glistening, convex (some strains dissociate* to larger colonies).

Hemagglutination of guinea, pig erythrocytes, and

erythrocytes of other species. . ,

Growth temperature, optimal at 35°C, killed at 45°C.

243

• Generation time, 35 to 40 minutes at 35°C.• Strict tropism for ciliated epithelium.• Guanine+cytosine composition of DNA, 61.6 - 62.6

mol%.

Preferred culture media and substrates:B . a v i u m grows well on a wide variety of solid media, although use of selective media such as Macconkey’s and modified peptone agar may inhibit other bacterial species. Also medium 220 (CASO agar) used for isolation of Bordetella species.

Resistance to chemical and physical agents:Although the B. avium is very resistant in nature the organism appears to be susceptible to most commonly used disinfectants at levels recommended by the manufacturers. Survival of B. avium is prolonged by low temperatures, low humidifies, and neutral pH.

Virulence factors:Major virulence factors of B. avium can be divided into those involved in a adhesion, local mucosal injury, or systemic effects. Motility and chemotaxis are important virulence factors in turkeys, beside hemagglutination (HA) o f guinea pig erythrocyte correlates closely with virulence.

244

Toxins:1- Dermonecrotic (heat labile) toxin.2- Heat stable toxin.3- Osteotoxin.4- Tracheal cytotoxin.5- Pertussis toxin.

Susceptibility:Bordetellosis is an acute, persistent, contagious upper respiratory disease of turkeys. However, Bordetella avium (B. avium) also infects cockatiels, chickens and other birds. Most commonly occurs between 1-6 weeks of age in turkeys and more commonly in summer and fall, while in cockatiels as early as 3 days and as late as 4 weeks.

Transmission:Recovered older flocks and wild birds serve as carriers. Transmission between flocks occurs as a result of human activity. Contaminated water, feed or litter are the most common ways of in house spread and carry over the successive flocks. There is no egg transmission.

Incubation period:Approximately 1 week, the course of the disease may run from 3 to 6 weeks.

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Clinical signs:More severe in young poults. Abrupt onset, high morbidity, low mortality, and decreased growth rate. If there is another respiratory disease agent (E. coli is the most common), mortality may be high. Sneezing, snicking, and flicking of the head. Loss of voice. Frothy ocular discharges and clear mucoid nasal discharge. Exudates become progressively thicker. Sinusitis and upper respiratory signs are more common in turkeys 4 weeks of age or younger. In older turkeys the most typical sign is tracheal rales. Because the bacteria attach to the trachea lining, the clearance from the respiratory tract is impaired allowing secondary infections. The role of B. avium as a primary pathogen in chickens in less obvious than in turkeys. But its presence in chickens has been associated with increased severity of respiratory disease. In cockatiels the disease is characterized by respiratory manifestations and locked jaw.

Lesions:1- Lesions occur in the upper third of the trachea.2- Deciliation o f the trachea occurs in 6-10 days PI.3- Tracheal ring collapse occurs in severe infections

usually about 1 week PI.4- Regeneration o f the tracheal mucosa can occur in the

less severe and uncomplicated infections.

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5- Small bacilli associated with cilia are commonly seen on histological examination.

Diagnosis:- Isolation and identification of B. avium from the

trachea, tracheal swabs obtained early in the infection provide the best opportunity for isolation.

- Hemaggluatination of Guinea pig RBCs. Also chicken, rabbit and turkey RBCs.

- Serology such as microagglutination and enzyme-linked immunosorbent assay (ELISA).

Control and prevention:Daily biosecurity:Wash and sanitize water fountains daily. Restrict human contact. , , _ ,Traffic should always move from younger to older flocks without backtracking. Prevent contact with wild birds. Between flocks:Flush water lines with disinfectant.Clean out and disinfect the brooder house and all equipment.

VaccinationThe following points should be kept in mind in vaccination against bordetellosis.1- Local immunity of primary importance.

247

2- Vaccinated birds can act as carriers of field strains.3- B. avium can be isolated from 100% of the lower

tracheas by 10 days post-exposure.4- Seroconversion begins 10-14 days post exposure and

peaks about 28 days post-exposure.5- Bacteria persist in presence of humoral antibody.A- Live vaccine is available for use in poults:1- Eye drop and spray are better than drinking water.2- Turkeys were immunized at 2 days of age then at 14

days.B-Oil-emulsion bacteria for use in breeder hens: .

1 - In drinking water.2 - Given at 7 and 21 days of age.3- This will provide maternal immunity for up to 4 weeks,

the interval when infection may be most severe.C-Recombinant vaccines (still under investigation). T reatm ent:

• Improve ventilation and increase house temperature.• Encourage the birds to move, eat and drink.• The effectiveness of antimicrobial agents in the

treatment of turkey coryza remains a continuous issue despite a series of studies performed in several countries.

• Since antibiotic sensitivity o f B. avium is controversial, any empirical treatment programs for turkey coryza outbreaks in any country should be based on the results of sensitivity test o f the native isolates among available

248

antibiotics, taking in considerations the vaccination and management pillars in combating the disease.

n e w t r e n d s i n t r e a t m e n t o f b r o d e t e l l o s i s

I- L-tryptophan and niacin (dietary supplement): L-tryptophan (precursor of niacin)

Increase dietary L-tryptophan (0.34%) and niacin 110 mg/kg improved the body weight and minimized the clinical signs o f avian bordetellosis.II- Oxy-halogen formulation (OHF):It is a combination o f chlorine materials that have antimicrobial activity.0.016% o f an OHF continuously in the drinking. OHF leads to decrease B. avium colonization and signs and im proves the body weight.

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Flattened upper third o f the trachea in a turkey poult infected w ith B.avium.

O rn ith o b a c te riu m rhinotrachealeO R T

ByD r. O la Hassanin

Def:Ornithobacterium rhinotracheale (ORT) is a re< encountered bacterium which has been associated respiratory disease in poultry. Certain bacteriologic pathologic aspects of the organism and disease have recently been investigated.

Cause:O. rhinotracheale is a pleomorphic Gram negative rod w grows well (but slowly) on blood agar plates. After 24 horn incubation at 37 C in 7.5% C02, OR colonies are pinpoii size and show no hemolysis. No growth is observed MacConkey agar plates.

S u sce p tib ility :

O. rhinotracheale has been isolated from broiler (2-3 wee and layer chickens, turkey and chicken breeders, meat turke game birds, pigeons, pheasants, partridges, and chit Isolates are most frequently obtained from respiratory si such as the trachea, sinuses, and lungs. Occasionally, systeff

in vo lve m e n t is indicated by iso la tions from the heart, spleen, liver, bone, and jo in t.

predisposing factors:1- Bad management.2- Concurrent v ira l and bacterial in fection .3 - Vaccines.

Rout of Infection and Transmission:1- Respiratory route via aerosol.2- Vertical.3- Animal vectors.4- Wild birds act as a po ten tia l reservoir.

Clinical s ig n s:

1- Mild respiratory signs are m ost frequently observed with only a s ligh t increase in m o rta lity (0.5 - 2 %) but may reach to 30-40 % w ith concurrent in fec tion and morbidity ranged fro m (5 - 90%).

2- Birds may experience m ore severe resp ira tory signs with gasping, m arked resp ira to ry e ffo rt, rales, head edema, decrease d a ily gain, Increase the condem nation rate due to a ir sacculitis.

2 5 2

Lesions:

1 - Mild sinusitis, tracheitis, or unilateral or bilateral lung consolidation may be observed.

2- Serofibrinous bronchopneumonia and fibrinous inflammation of the air sacs are noted.

3- A foamish, white, “yoghurt like” exudates can be seen in the air sacs, commonly accompanied by unilateral pneumonia.

Diagnosis:

1- Bacterial culture is required to demonstrate.2- O. rhinotracheale’s involvement in respiratory disease.

3- Signs and PM.4- API 20 trips.5- PCR.6- Differentiation from fowl cholera and other respiratory

diseases.

T reatm ent:Treatments with tetracycline and amoxicillin have been reported in Europe. Limited success has been reported with enrofloxacin and trimethoprim/sulfa.

253

Abdominal air sac filled with froamish white-yoghurt like exudates due to ORT infection.

254

StaphylococcosisBy

Dr. Emad AzmiDef:Staphylococcus aureus is Gram-positive! cocci, normally inhabitant o f skin and mucous membrane and in inviroment. Damaged skin or mucus membrane will enable staph. Aureus to enter to internal location to cause one of the following forms.

cause:Staphylocuccus aureus which contains 32 species. Staphylococcus aurous is the most common isolate from lesions in diseased birds.

Forms of staphylococci:1- Septicaemia

- Bird may be found dead.- Lameness.- Signs o f septicaemia.

2- Arthritis and tenosynovitisSigns occur in birds of any age. The affected joints, usually the hocks, are hot, swollen and painful. The affected birds are depressed and unable to walk.

255

In tenosynovitis, the synovial membrane of tendon sheath (commonly in the region of the hock and feet) become thickened and odematous.

3- Bacterial chondronecrosis and osteomyelitisThis disease is the most common cause of lameness in broiler chickens. The disease is often associated with green liver in turkeys,The disease sometimes called femoral head necrosis but the proximal end. of the tibiotarsus may be affect.

4- Gangrenous dermatitisCommonly in broiler chickens. The wing Tips and back are most affected. Skin is darkned of tenmcist Or weeping, and the underlying tissue may be oedematous. Staphylococci have been recovered together with Clostridium spp.

5 - Subdermal abscessesAffect the feet (Bumble foot) and sternal bursa. They occur most frequently in mature birds, particularly those of heavy breeds. Caseous material accumulates and there is swelling, heat and pain.

6 - Endocarditis and granulomaVegetative endocarditis may also be a result of septicaemic infection, and particularly affects the left atiouventricular

256

valves. Small granulomatous lesions may occur in liver, and sometimes in spleen and kidney.

7- Yolk sac infection (omphalitis)It is the com m onest cause o f mortality in chicks during the first w eek after hatching. Y olk sac infection can be associated with a thickened inflamed, prominent and necrotic navel. The affected chicks appear depressed, distended abdomens and tendency to handle. Unabsorbed yolk sac with the yolk abnormal in colour and consistency.

Diagnosis:1 - History, clinical signs and PM lesions.2 - Laboratory diagnosis depends on the isolation and

identification o f staphylococcus aureus.

Differential diagnosis:Staphylococcosis must be differentiated from any disease causing lamoness and leg disorders in poultry which either Bacterial (E. coli, Pasteurellosis, mycotlase, or viral (viral arthritis/tonosynovitis). Also, Nutritional disorders such as (Cal-P-Vit. D. def.).

Control and Treatment:Administration o f Tetracyclins or Streptomycin/penicillin combination especially at early stage of infection.

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Streptococcus infectionBy

Dr. Emad Azmi1- SepticaemiaIn chickens, septicaema is most common in adults, but may

occur at any age.

Clinical signs:Birds may be found dead. There is marked depression with

ruffled feathers, cyanosis o f the face and comb. Blood -

staining o f feathers around the head. Mortality can vary but

may reach 50%. Decrease in egg production and late

embryonic mortality.

Lesions:- Congested carcass splenomegaly and hepatomegaly.

- Hydropericardium - pin-point necrotic foci on the liver.

- In late stage, fibrinous pericarditis, perihepatis and

pneumonia.

2 - Cellulitis: ? \f ...A 1 7 i f

- Caseous plaques found under the skin.

- Skin may appear thickened or discolored.

258

3- EncephalomaleciaAffected chicks may be found closed or exhibit nervous signs. (Torticollis is common).

4

4- EndocarditisIt causes vegetative endocarditis in young and older birds.

5- Amyloid arthrophy

Diagnosis:1- Clinical signs.2- PM. Lesions.3- Isolation & identification o f the pathogenic cause.

Control:- Quinolones, Pencillins and tetracyclines.

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PARASITIC DISEASESBy

Dr. Emad Azmi

Diseases caused by parasites play an important role in domesticated birds and lead to extensive losses in poultry industry in Egypt.I - Internal parasites A- Helminthes1- Ascaridiasis (Intestinal or large round worm)Ascaridia are the largest nematode of birds.Cause:

• Ascaridia galli c = ^ > Inhabit the small intestine of chickens, less frequency turkeys, geese and ducks.

• Ascaridi coiumbae t=C> Inhabit the small intestine of pigeons.

Transmission:Contaminated food and water.

Clinical signs:Severely affected birds showing emaciation with persistent diarrhea.

260

Lesions:• Affected birds showed lesions of emaciation.• Opened intestine filled with the adult worms.• Enteritis or intestinal impaction.

Diagnosis:1- Clinical signs and PM lesions.2- M icroscopic examination of the droppings which reveal

the Ascaridia eggs.Treatment:Piperazin salts (0.3 -0.5gm/bird) as a single dose for chickens w hile for pigeon (0.25 gm/bird).

Prevention of Ascaridiasis:.1- Prophylactic administration of piperazin salts at 2-

months of age and repeated every 2 months.2- Sanitary and hygienic measures to prevent

contamination of food and water.3-

2-Hetrakis spp. (Caecal worm)Cause:

• Hetrakis gallinarum t= > Inhabit the caecum of chickens and turkeys.

• It is probably never pathogenic but it is important because its role in transmission of Histomoniasis.

• Hetrakis isolonche caeacl mucosa of pheasant.

261

• Hetrakis disper inhabits the caecum of ducks and g*

Transmission:Through contaminated food and water.

Clinical signs:N o specific clinical signs.

Lesions:Typhlitis and yellow caecal core.

Diagnosis:1- Clinical signs and P.M.2- M icroscopic examination of direct smear to detec

» * % . .

Hetrakis eggs.

T re a tm e n t:Levamisol 0.7 ml/Kg L.B.W.

P re v e n tio n :Cleaning and good managment in poultry houses.

3 - C a p il la r ia Spp. ( H a ir w o rm )

Cause. Capillaria annulata < = > inhabit the crop of chick®

and turkeys

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• Capillaria Columbae c=£> inhabit small intestine of chickens and pigeons

Clinical signs:No specific signs (general signs).

Postmortem examinationThickening o f the intestinal mucosa.

Diagnosis:1- Clinical signs and P.M.2- Microscopic examination to detect the capilaria eggs

(lemon shape).

Treatment:Phenothiazine

❖ 0.5 - lgm / chicken❖ and l-2gm/turkeys❖ 0.25 gm for pigeon

4-Tracheal worm (G apcworm )

CauseSyngamus tracheae

Signs:

• Respiratory signs in the form of dyspnoea /cough / violent inspiration.

• Extended neck and opened beak with shaking o f head.

Lesions:Opened trachea showed dark red worms and tracheitis with blood tinged exudates. v

Diagnosis: — ,Clinical signs and P.M.

Treatment:Lugol's solution in glycerin (1:5) or tincture iodine in water (1:9) and sprayed via the nasal opening. ■ j

Prevention:Sanitary and hygienic measures

5 - Cestodiasis (Tape worm infestation)Susceptibility:All domesticated birds are susceptible especially chickens, ducks geese and others.

Clinical signs:Emaciation, weakness and yellow pigmentation o f legs.

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Lesions:• V elvety appearance o f the intestinal wall.• Tubercle like nodules.• Segm ented / band like worms inside the intestine.

Diagnosis:Clinical signs and P.M.

Prevention and control:• Control o f the intermediate host.• Yomasan, M ansonil or Tapinex bolus 500 mg/bird.

B — Protozoal diseases 1 — Avian Coccidiosis

Coccidiosis is one o f the most important diseases o f poultryworld wide. It is caused by protozoan parasites o f the genusEimeria.Life Cycle:

• Com prises a parasitic and non-parasitic phase. The sporulated oocyst is ingested and the action o f m echanical and chemical factors in the gut (bile salts and trypsin) leads to release o f sporocysts and then sporozoites in the duodenal lumen. The sporozoites invade the mucosa/sometimes passing down the whole length o f the alimentary tract before doing so. There

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follow phases of intracellular growth and a sexual multiplication with periodic releases of merozoites back into the gut lumen. After a number of such schizogonous cycles (the number is primarily a genetically determined characteristic of a given species or strain), sexual forms, the gametocytes develop intracellular. These differentiate into macro and micro gametocytes. The micro gametocytes release many micro gametes, which are flagellated and motile and migrate to the microgametocyte. The micro gametocytes develop into a single macrogamete which after fertilization, develops into a zygote and then an oocyst. During this processes, large intracytoplasmic granules appear peripherally and eventually coalesce to form the oocyst wall. This cycle is quite, rapid with a prepatent period of about 4-5 days.

• These oocysts only become potentially infective after undergoing sporulation. This entails subdivision into four sporocysts each of which contains tow sporozoites).

• Sporulation required three conditions (warmth, moisture and oxygen). Under optimal conditions, around 25-30 C this takes 1-2 days. Sporulated oocysts, protected by the thick oocyst wall.

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Chicken Coccidiosiscause: ,Nine species o f Eimeria causing chicken coccidiosis :

1- E. acervulina, E.mivati, E. Hagni and E.praecox these species parasited the anterior part of small intestine.

2- E.maxima, and E.necatrix these species parasited the middle part o f the small intestine.

3- E.brunetti, E.mitis and E.tenella these species parasited the posterior part o f small intestine and caecum.

Susceptibility:All types o f birds are susceptible to infestation with Eimeria genus. All ages and breeds o f chickens are susceptible to the disease the younger are severely affected than older chickens. There are some factors influencing susceptibility and severity of infections.

• Age resistance: chickens kept free from infection, its susceptibility increased with age.

• Previous exposure to infection resulted in resistance to reinfection.

• The severity o f the diseases. Depends on the number of oocysts ingested and the frequency of ingestion of oocysts.

• Certain vitamins and amino acids (B l, B2 & B6 ) affect susceptibility and severity of infestation.

• Bad management, concurrent infections with either bacterial or immunosuppressive diseases.

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Transmission:Ingestion of contaminated food and water with millions of viable sporulated oocysts.

Incubation period:The prepatent period of Eimeria species infested chickens varied from 4-6 days according to the infected species. Clinical signs:

❖ Caecal coccidiosisInfected birds showed general signs of an illness (huddle together, inactive and sleepy, ruffled feathers with droopy wings) and bloody diarrhea

❖ Intestinal coccidiosisAffected chickens showed both general signs of an illness and specific signs in the form of (dropping mixed with blood or brownish-red diarrhea). Uneven growth, emaciation, paleness of visible mucus membranes, comb and wattles. Also drop in egg production in layers is also observed. Morbidity rate is usually high but mortality is varied from 5 to 50%.

Lesions:Caecal coccidiosis showed swollen cecai with pin point hemorrhagic and whitish spots on serosal surface and sometimes caeca resemble sausage in shape. Thickening of the cecal wall and filled with fluid or clotted blood, later with

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pieces of cecal mucosa and nectrotic material forming cecal cores. Birds suffer from intestinal coccidiosis, showed pale and emaciated breast musculature, ballooned un open intestine with either whitish and/or hemorrhagic spots on serosal surface or gray whitish discrete small round or elongated lesions. In dead birds, the gray or whitish and red spots petehiae will be white and black giving the appearance of (salt and pepper).

Diagnosis:1- Flock history, clinical signs and lesions.2- Microscopic examination, .

prevention and Control:I - Control

1- Application of hygienic and sound management to destruct the oocyst.

2- Raising of the vitality of the affected chickens by administration of both vitamins a(AD3E and Vit. K3) via drinking water.

3- Destruction or inhibit the development of the Eimeria inside the host using anticoccidial drugs as

• Amprol 20%• Mixture of amproliun, sulphadimidine &

. f sulphaquinoxaline at ratio 2 : 1 : 1 added by2gm/L drinking water.

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• Patent preparations (Vetacox, cocciplus, Esb3).II - Prevention

1- Application of hygienic measures and sound managements (avoid over crowding, disinfection ..........etc.).

2- Use of coccidiostatic vaccines to induce the immunity.3- Prophylactic therapy as anticoccidial drugs.

The coccidioststics used in Egypt• Stenerol (1-2 kg/Ton)• Avatec (500 - 850 gm /Ton)• Coxistac (1 Kg/Ton)]• Amprolium plus (0.5 Kg/Ton)• Elancoban (100-120 gm/Ton)• Pegicoccin (0.5 kg/Ton)• Cycostate (0.5 kg/Ton)• Cygro (0.5 kg/Ton)• Clinacox (200 gm/Ton)

Coccidiosis in Turkeyscause:Seven species o f Eimeria but the pathologenic species are E. adenoids, E. dispers, E. meligrimitis and E. gallopovanis.

E. adenoids inhabit caeca and may extend to the intestine and

cloaca. E. dispers inhabits the small intestine. E. meligrimitis

inhabits upper small intestine, while E. gallopovanis

parasitized posterior portion o f small intestine. E. dipersa is the

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only Eimeria species in chickens and turkeys known to infect more than species. And it is more pathogenic in quails.

Susceptibility:Turkeys o f a ll ages are susceptible to infection and birds older than 6-8 weeks are more resistant to the disease.

Signs and Lesions:Caecum or intestine is swollen and edematous with congestion, edema, hemorrhagic petechiae and mucus. Caeca contains white caseous cores.

Prevention and control:Dmg used in chicken are effective in Turkey.

Treatm ent:Amprolium 0.025% in drinking water or sulphonamides for successive two days withdraw for 3 days and given for another 3 days.

Coccidiosis in water fowlCoccidiosis in water fowls (duck and geese) is sporadic.

Cause:13 species o f Eimeria could infect domestic and wild ducks. Coccidia in ducks may be o f Eimeria or Tizzeria pemiciosa.

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Oocysts of Eimeria species have 4 sporocyst each contain 2 sporozoites, while Tyzzeria species contained 8 sporozoites without sporocysts.

Clinical signs:Affected ducks and geese showed anaroxia, loss of body weight, weakness and distress. Mortality and morbidity reach up to 70%.Lesions:Hemorrhagic areas in the anterior portion of intestine that filled with bloody or cheesy exudates.

Coccidiosis in PigeonsCharacterized by general signs of illness, marked dehydration and emaciation with the bloody droppings accompany enteritis.

• Young pigeons suffer from high losses / but mortality may occur in birds as old as 3-4 weeks caused by Eimeria labbeana.

• Mortality of 15-70 % in young pigeons.• Affected pigeons showed anorexia, greenish

diarrhea, marked dehydration and emaciation.

• Droppings may be blood tinged and enteritis.

« Coccidiosis in pigeon treated by sulphonamides in drinking water as in chickens.,

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HistomoniasisBlack head, Infectious enterohepatitis, Typhlohepatitis) Def:Acute infestation of turkeys characterized by typhlitis, focal hepatitis and sulpher colored diarrhea.

Cause:• Histomonas meleagridis with E.coli or with other

intestinal bacteria work synergistically to produce the disease.

• . Histomonas meleagridis is pleomorphic in intestinallumen, but in tissues, it is rounds up and losses its . flagellum.

• Histomonas is sensitive to disinfectants and drying , unless protected within earth worms or within the

ova o f Hetrakis gallinarum.Susceptibility:• Turkeys are highly susceptible host of the disease.

• Chickens, pheasants and quail contract the disease.

• Young turkey poults are highly and commonly affected Transmission:

1 - Ingestion o f eggs of Hetrakis gallinarum containing theprotozoon.

2 - Cannibalism of recently dead birds.

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3 - Ingestion o f earth worms containing Histomonas meleagridis within Heterakis gallinarum.

In c u b a t io n p e r io d (7-14) days in turkeys.

C lin ic a l signs:1- General signs o f illness and sulpher yellow colored

diarrhea with droopy wings.2- Rarely, birds showed bluish-black coloration of the skin

o f the head, finally the affected turkey is depressed and stands with its wings droppings, eyes closed, head drawn close to the body followed by death.

3- Mortality may reach (80 — 100) % in turkey poults.

Lesions:1 - The caeca appear enlarged with thickening of caeca!

wall. Ulceration and necrosis of caecal mucosa and contain large caecal cores.

2- The liver reveals circular or irregular round- cream colored necrotic areas surrounding a darker hemorrhagic depressed central area.

3- These areas are 1-2 cm in diameter and may coalesce to produce larger lesions.

Diagnosis:I - History o f c h ic k e n s a n d tu r k e y b r e e d in g to g e th e r , c l in ic a l

signs, and l e s io n s .

2 - M icroscop ic e x a m in a t io n o f p a r a s it e .

3 - H is to p a th o lo g ica l s e c t i o n f r o m l iv e r o r c a e c a l t i s s u e .

Treatment:Several d ru g s a r e e f f e c t i v e i n c l u d i n g f u r a z o l id o n e ,

carbasone, em tr y l a n d f l a g y l .

Prevention a n d c o n t r o l :

1- Hygienic measures to prevent infection.2- Preventive drugs to inhibit the parasite development.3- Preventive medication of caecal worms in chickens

and turkeys.4- Chickens must be reared separately from turkeys.

Trichomoniasis (Canker in pigeons)

Def:Important infection caused by Trichomonas gallinae characterized by foul-smelling fluid drilling from the mouth with raised yellow necrotic foci or profuse caseous exudates in the mouth, esophagus, pharynx and crop.

Causes:Flagellated protozoa (Trichomonas genus)1 - Trichomonas gallinae

Inhabits the upper digestive tract (mouth, crop and oesophagous)

2 - Trichomonas gallinarumInhabits the lower digestive tract (caeca). It isn’t

pathogenic.

Susceptibility:Pigeons, doves, raptors and rarely occurs in chickens and turkeys

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Transmission:Ingestion, o f contaminated crop milk incase of squabs andcontaminated food and water in chicken, turkey andpigeons.

Clinical signs:1- O ff food, ruffling feathers and foul-smelling fluid

drilling from the mouth with caseous yellow necrotic focci in the mouth and pharynx. Watery eyes, rare cases show signs of nervous manifestation (loss of balance).

2- Affected chickens showed both general signs and some clinical signs of pigeons.

Lesions:1- Yellow necrotic focci or profuse caseous exudates on

the mucosa of mouth and esophagus.2- Ulceration o f crop.3- Yellow necrotic focci in the liver and on the other

viscera.

Diagnosis:Clinical signs, gross lesions and microscopic examination.

Differential diagnosis:Pox, deficiency o f vit. A and candidiasis.

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Treatment:1 - Flagyl (metronidazole) in drinking water 60mg / kg B. Wt

over five days.2 - Enheptin (0.05-0.1 %) for squabs.

Prevention and control:1 - Sanitary and hygienic measures.2 - Strict breeding o f chickens and turkeys separately from

pigeons and doves.

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pef:

Infection o f young turkeys and characterized by foamy watery diarrhea, nervous signs and progressive emaciation.

cause:Hexamita melegridis is flagellated protozoa.It forms cysts which facilitate transmission.Transmission:Oral route through contaminated food and water.

Clinical signs:1- Progressive emaciation.2- Foamy watery diarrhea and nervous signs (torticollis

and opisthotonous).

Lesions:Dry and dark red carcass, catarrhal or hemorrhagic enteritis.

Diagnosis:1- Case history.2- Clinical signs.3- PM lesions.4- Microscopic examination.5- Histolopathology.

Hexamifiasis

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Hexamitiasis

Treatment:1- Furazolidone 400 gm / ton 5-7 successive days.2- Tetracycline and or chlortetracycline 1 kg / ton for 5

successive days or drinking water in dose o f 20-30 mg / bird / day.

3- Flagyl 200mg / bird for 5-7 days.

LeucocytozoonsisDef:It is arthropode transmitted protozoa related to plasmodium

spp- -

Etiology:

• Leucocytozoon affected more than one type o f poultry.

• Gametes usually are seen in distorted RBCs, leucocytes or both types.

Susceptibility:1- Turkeys, geese and ducks but usually is subclinical.2- Most outbreaks occur during the warmer seasons of the

year when black flies are numerous and some outbreaks usually are in birds housed near slow steams.

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Transmission:Mechanical transmission through insects (black flies and midges) which act as vectors and transmit leucocytozoons to young susceptible birds on which they feed.

Clinical signsThe disease characterized by sudden onset and numerous birds soon show clinical signs which are in the forms of:

1- Depression, anorexia, thirst, loss of equilibrium, weakness and anaemia.

2- There is rapid labored breathing.3- The course of the disease is short and affected birds die

or improve within a few days. Mortalities vary but often are high.

Lesions:1- Enlargement of spleen and liver with evidence of

anemia.2- Microscopically, megaloschizonts are apparent in the

brain of many birds that show loss of equilibrium. Schizonts often apparent in the liver.

diagnosis:1- History, clinical signs and gross lesions.2- Microscopic examination.3- Histopathologic examination.

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Prevention and Control1- Hygienic measures.2- No effective treatment is known.

Haemoproteus infestation

Def:It is the infestation o f birds with different species of haemoproteus and it's a sexual multiplication occurred in the endothelial cells o f the internal organs and transmitted through sucking pigeon fly.

No clinical signs and postmortem lesions

Control:Control o f ectoparasites.

Treatment:Atebrin and plasmochin s/c.

AegyptianellosisDef:It is either an acute or chronic blood protozoal disease of

chickens, ducks, geese and turkeys.

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Cause:Aegyptianella Pullorum (found in blood erythrocytes)

Transmission:Biting of infected ticks to non infected birds

Incubation Periods:- 12-15 days or more

Clinical signs:1 - Acute form seen in young ages . ..

• Anemia, fever and jaundice2 - Chronic form:

• Seen in adult birds marked depression, inability to walk, paresis followed by paralysis of extremities with pale, yellow discoloration of the visible mucous membranes.

Lesions:1- Spleen is severely enlarged.2- Liver appeared grayish- yellowish color.

Diagnosis:1 - Clinical signs and PM lesions2 - Microscopic examination(trophozoites and schizonts in the cytoplasm of bird'

erythrocytes).

. < 2 8 3

Treatment:1- Dagrinol.2- Flagyl.

Prevention and control:1- Hygienic measures.2- Control of ectoparasites especially ticks.

Avian MalariaDef:Blood protozoal disease of avian species, transmitted by mosquitoes.

Cause:Plasmodium species.

Susceptibility:Ducks, geese and chickens.

TransmissionBiting of infected mosquitoes.

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Clinical signs:Affected birds showed non specific clinical signs, but the affected birds showed anemia, fluctuating temperature and paralysis.Lesions:Carcass appears pale in color, v/ith marked enlargement of spleen.

Diagnosis:Identification of the plasmodium in blood films.

Treatment:1 - Dagrinol 100 mg / kg B.wt.2- Flagyl 7.5 or 3.25 mg/ kg B. wt for 5 successive days.

Prevention and control:1- Hygienic measures.2- Control of ectoparasites.

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Ectoparasites of Poultry1- U c e ; ./'•*' /'■’

• Several species o f biting (chewing) Lice (Oder Mallophaga) may infect poultry.

• They spend their entire life cycle on the host and cause irritation by feeding on skin and feather.

• Menocanthus stramineus is probably the commonest in chickens and it may also infect turkeys.

• It is found on the skin, especially around the cloaca and on the breast and thighs, laying eggs on the base of the feathers.

2- MitesA-Two species o f non-burrowing mite can be serious pests due to their blood-sucking habits:1- Dermanyssus gallinae (red mite).2- Liponyssus (omithonyssus) Sylviarum (northern fowl mite)

- Heavy infestations, especially o f Dermanyssus, can cause reduced egg production and anaemia. Dermanyssus can also transmit Borrelia anserine. D. gallinae is widely distributed and infests chickens and

other birds.B-Burrowing mites o f genus Cnemidocoptes may cause

feather loss (Deptuming itch mite, Cnemidocoptes gallinae. Or

excessive scaliness o f the skin, leading to thickening and even

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deformation o f the legs (scaly log mite, Cnemidocoptes mutans).

Diagnosis:Cleared in 10 skin scooping potassium or sodium hydroxide.

Treatment of scaly leg mite:1- Clip o f the shanks in warm water and soap for minutes or paint with glycerol or oil and leave for several hours, and then wash with wa rm water and soap this is followed by dipping the shanks in one o f the following preparations:

- crude peteroleum or kerosene.- 1 part heated tar + 1 part teresine.

2- Soak the shanks in soapy warm water, then remove the scales with a brush, then dry the legs and then apply pheno/ointment 2% or sulpher ointment is-20%.3- Use potent preparation e.g. diazenun.

3- Ticks• The most important tick is the soft fick (Argas persicus)

which is widely distributed in tropical and subtropical areas.

• Spend most o f their time off the host.

• Cause (anemia/anorexia, weight loss and depressed egg

out put.

• It transmits Borrelia.

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Control of ectoparasitesA-Use o f insecticides on the host1- Wet dipping (diozenon, malathicn).

-dilution 1/10.000 and must supply early enough to allow the birds to dry.

2- Wet spraying.3- Dusting.

e.g. Gamaxane.4- Greasing.

e.g. sulpher oinment.5- Fumigation.

e.g. nicotine sulphate 40%.B- Control o f ectoparasite on the host surroundings and houses.

e.g. Diazenon, malathion 1/1000 (1 Liter/30m2).

Precautions:1- B irds should be removed from house and allowed to

return only after complete dryness.2- All cracks should be closed and may be burned.3- Litter and all necessary equipments should be removed.4- Birds must be provided with fresh and clean drinking

water before insecticides application.

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Ascaridiasis: opened intestine filled with the adult worms.

Histomoniasis: liver contains bulls-eye lesions on the surface of the live (irregular-round depressed lesions, usually grey in color).

Trichomoniasis: Yellow necrotic focci or profuse caseous exudates on the mucosa o f the mouth.

p cal c°ccidfosis: chicken cecum impacted with cecal bloody core due to tteneJ<a infestation.

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Intestinal coccid iosis: chicken intestine contains pin point hemorrhagi spots due to E. necatrix infestation.

Nutritional DiseasesRy

Prof. Dr. Amal A. M. Eid • *

There are more than 36 nutrients are absolutely essential and must be in the diet in appropriate concentrations and balance in order to maximize the ability of poultry' to express their genetic potential to grow and reproduce.

A. Adequate supply of nutritious food and water- Normal growth.- Reproduction.- Liavability.

B. Deficiency of any nutrient- Serious deficiency is usually expressed by specific

signs, preceded and/or accompanied by non-specific signs.

- Partial deficiency induces non-specific signs and leads to confusion on diagnosis.

C. Non-specific signs- Retarded uneven growth.- Rough feathers.- Decreased egg production.- Lowered hatchability.

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I- Proteins and amino acidsThere are 10 absolutely essential A.A; Arginine, histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophane and valnine.

- Cysteine & tyrosine are synthesized from essentialA.A..

- Glycine & proline plus essential A.A are essential for young chicks.

- Ration which is formulated from com and soyabean meal, methionine and lysine should be supplemented.

Signs of protein deficiency:1 - The effects of essential A.A.deficiencies are non­

specific:- Reduced growth.- Reduced feed consumption.- Decreased egg production and egg size.- Loss ofbody v/eight in adults.

2- Marginal A. A. deficiencies often result in:- Increased food intake or maintenance of food intake.- Reduction of body weight gain and lean tissue

growth leading to increased body fat.3- Severe deficiencies result in altering in the body

composition:- Decreased methionine exacerbates choline or vit.

B12 deficiency.

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- Decreased lysine impaires pigmentation of Bronze turkey poults and causes stunting and retarded development in chicks.

- Decreased arginine leads to upward curling of wing feather.

Increased dietary protein:May cause hyperuricemia and articular gout, particularly in

birds that are genetically susceptible.

Protein in rations (requirements):Broilers: starter (1 -3 w k) 23% , grower (3-6 w k) 20% and

fin ish er (6 -8 w k ) 18%. ;

Layers'. = 1-3 w k (20% ), 4-8 w k (18% ) and 12-14 w k (15%).

II-Carbohydrates- T h ere is n o d efic ien t ration in carbohydrate.

- T h ere is lo w activ ity o f lactose in avian intestine.

- W h e y is a g o o d source o f v it. B and unidentified

g ro w th factor and although ben eficia l at low levels,

e x c e s s iv e le v e ls in d iet cause growth depression and

se v e r e diarrhea.

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IH-FatsA. Source of energy:L in o le ic a c id co n ta in s 2 u n sa tu ra ted b o n d s o n e o f th e m c a n not

b e sy n th esized b y p o u ltry b u t ca n b e c o n v e r te d to arch id o n ic acid b y pou ltry . T h e s e fa tty a c id s are im p o rta n t c o n s t itu e n ts o f

the c e ll o rg a n e lls , m em b ra n e an d a d ip o s e t i s s u e a ls o as precursors o f p ro sta g la n d in es .

B. Fat Deficiency:- S u b o p tim a l g ro w th in y o u n g c h ic k s .- E n larged fa tty liv e r s .

- E ssen tia l fa tty a c id d e f ic ie n c y in la y in g h e n s r e su lts

in lo w e r e d e g g p r o d u c tio n , e g g s iz e a n d h a tc h a b il ity .

2 9 5

£, Unsaturated fatty acids:

The addition o f synthetic antioxidants provides further

pro tection o f v itam ins A , D, E and biotin and other essential

nutrients.

IV-VitaminsThe term v itam in refers to a heterogeneous group o f fat

so lub le and w ater soluble chemical compounds essential in

nutrition that bear n o .. structural or necessary functional

relationship to each other. A ll vitamins are dietary essentials

for p ou ltry ex cep t (vit. C).

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A. Functions:T h ey are integral parts o f v ita l en zy m es. P la y variou s catalytic

ro les in m an y ch em ica l reaction con cern ed in digestion,

in term ed iary m eta b o lism , an ab o lism and ca tab o lism within

an im al b od y .

B. Poultry ration:S h o u ld b e form u la ted as co n ta in in g v ita m in s in quantities

m o re th an a d eq u a te , that p ro v id in g m arg in s o f safety to

c o m p e n sa te p o s s ib le , lo s s e s durin g p r o c e ss in g , transportation,

s to r a g e an d v a r ia tio n s in fe e d c o m p o s it io n and environm ental

c o n d it io n s .

C. Note:Fat soluble vitamins A, D, E, also thiamin and pantothenic acid are destroyed by bad storage.D. Factors affecting vitamins Requirements of poultry:

1 - Genetic factors (breed and type of production).2- System of rearing as battery system increase the

vitamin requirments.3- High enviromental temperature will increase the

requirements o f vit. C.4- Factors hindering absorption from the gut.

a. Enteritis.b. -Hepatitis.

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c. -High fat content in ration.d. -Enteric parasites.e. -Mycotoxins.

5- Damage of nutrients during storage.a. -Excessive temperature.b. -Lack of antioxidants.c. -Direct exposure to light or UV.

• » ' * >’ i

6- Presence of substance in the. feed or water that interferes with the absorption of specific elements.

a. -Anticoccidial drugs compete with vit.K.b. -Amprolium competes with vit.B.c. -Raw fish (thiamerase enzyme) destroys vit.B.d. -Nitrites and sulfite destroy vit. A and B1.

7- Disease affections in general increase the vitamin requirements.

8- Excessive usage of antibiotics kills intestinal M.o. and reduces vit. synthesis.

Vitamin AVitamin A is essential in poultry diets for growth, optimal vision and integrity of mucous membranes.

Signs of deficiency:A. Adult chickens or turkeys

Fed on severely deficient diet in vitamin A. signs and lesions usually develop within 2-5 M.o.

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1- Emaciation, weakness and ruffed feathers.2- Egg production decreases sharply, and the length

between clutches increases and the hatchability is decreased the incidence of blood spots in eggs is increased.

3- A watery discharge from the nostrils and eyes is noted and eye lides are often stucked together.

4- As deficiency continues, milky white caseous material accumulates in the eyes which fill the eyes and birds can not see in many cases the eye is destroyed.

B. Chicks and poults1- Partial deficiency- Cessation of growth.- Drowsiness, weakness incoordination, emaciation

and raffled plumage.2- Severe deficiency- Birds may show ataxia look like vit. E deficiency.- Lacrimation and a caseous material may be seen

under eye lids.- Xerophathalmia (pathognomic) but may be not in all

birds because in acute deficiency birds may die before this sign be exhibited.

- Periorbital edema may occur.

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- Increased testes weight, decreased sperm count andmotility. - ? • • '

Lesions:1- The first lesions appear in the pharynx then down to

esophagus and may crop also buccal cavity and upper respiratory tract may be affected.

2- The original epithelium is replaced by keratinized epithelium that blocks ducts of the mucous glands, causing them to become distended with secretions and necrotic materials.

3- Small white pustules are found in the nasal passages mouth, esophagus and pharynx and may extend into the crop (~ 2mm) in diameter. As the deficiency progresses,’ lesions enlarge, are raised a bone the surface of the mucous membrane and have depression in the center, small ulcers surrounded by inflammatory products may appear at the site of these lesions ~ (resemble certain stages of fowl pox). Also bacterial, viral affections may show similar lesions.

Respiratory signs:- It is difficult to differentiate this condition from

infections coryza, fowl, pox, and IB.

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- In vitamin A. thin membranes and nasal plugs are usually limited to the cleft palate and its adjacent epithelium.

- They may be removed easily without bleeding. „,- Exudates may also fill sinuses and other nasal

cavities causing swelling of one or both sides of the face.

- Small nodule like particles may be found in or beneath the mucous membrane in the upper part of trachea.

Chronic Vit. A deficiencyDamage to the kidney tubules, which leads to azotemia and visceral gout in severe cases.

Hyper vitaminosis A~ 200 mg retinyl acetate / kg B.W/day for growing chicks lead to

- skeletal deformity and unsteady gait.- Ventricular dilation.- Brain swelling.

Treatment of deficiency:- 10,000 IU vit. A/kg of ration.- Absorption of vit. A is rapid = birds should response

except advanced blindness which may be permanent.

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Vitamin D(cholecalciferol)

Function:1- Vit. D is required for proper metabolism of Ca & P

in formation of normal bone, hard beak, claws strong eggshell.

2- Vit. D stimulates gastrointestinal absorption of Ca.3- Control serum phosphatase that increase serum

phosphatase indicates border line of rickets.

Activation:Vit. D3 (cholecalciferol) Hydroxylatlon ? . 5 , hydroxy

Liver cholecalciferoll,25,hydroxycholercaliferol < Hydroxylation 1

kidney

Signs of deficiency of vit. (D):

Growing broilers (rickets) Laying hens (osteomalacia), s . + J in egg production

Signs of hypervitaminosis (D):

Renal damage

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- Calcium “Ca” and phosphorus “P” are clc associated in metabolism, particularly in l formation.

- Utilization of Ca & P depends on presence of adequate amount of vit. D in the diet.

- In vit. D deficiency, the deposition of these mineral bones of growing chicks and poults is reduced quantity of Ca in egg shell decreased.

C a function:1- T he m ajor po rtion o f d ie tary Ca is used for bone

form ation in grow ing chicks o r pou lts and for egg shell form ation in m ature hens.

2- It is essential for b lood clotting.3- It is required along w ith N a & K for norm al heart

beating. /4- It is an im portant factor in the regulation o f cellular

metabolism.

P function:1- P. is an essential com ponent o f purine n u c l e o t i d e s ,

and other phosphorylated compounds.2- Essential in metabolism o f carbohydrates and fa ts .3 - Enters in the composition o f living cells. I4- Essential for acid-base balance.

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Causes of deficiency:J vit. D/ iC a / impairement of Ca, P ratio (2:1) (1%_ 0 .6%)

A. Chicks and poults (Rickets):Signs:

1- Retarded growth.2- Severe bone weakness.3- Fed from hatchery to 2-3 wk beaks, claws -> soft

pliable.4- Unsteady steps, and then squat on their hocks.5 - Poor feathering.6- Increase serum phosphatase.7- Chronic def. -> narrow thorax.

Lesions:1- Curved keel bone:

r 2- Bending o f ribs at their junction with spinal column - downward and posteriorly -> narrow thorax->

pressure on vital organs.

• ■ 3- W ell defined knobs on the inner surface of ribs at

costochordinal junction rachitic rosary.

4- Poor calcification at epiphysis of tibia or femor.

5- W idening o f the epiphyseal plate hypertrophy

softening o f the bone.

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B. In laying hens (osteomalacia / cage layer fatigue):Signs appear after 2-3 months.

1- Marked increase of thin shelled and soft shelledeggs.

2- Marked decrease in egg production.3- Marked decrease in hatchability.4- Pengnin-type squate.5 - Beak claws, keel soft and pliable.6- Sternum bent, ribs lose rigidity and curve.

Lesions:1 - Enlarged parathyroid gland. WT u ■ .2- Soft easily breaking bones. . -3- Rachitic rosary.4- Narrow thorax.5- Widening of ephysial cartilage.

Note: The withdrawal of Ca from medullary bone then cortica bone leading to sponge bone (osteomalacia and cage layer fatigue).

Signs of hyper-vitaminosis D:1- Renal damage due to dystrophic calcification of

kidney tubules (visceral gout).2- Calcification in aorta and other arteries.

305

Treatment:Single massive dose 15,000 IU vit. D3. 'Note: the dose should be scaled for the degree of def., avoid increased levels.

Vitamin EFunction:

1- , Vit. E is required for normal embryonic growth(development) in chickens, turkeys and probably

y, ducks.2- Alcoholic form of vit. E is antioxidant, that protect

essential fatty acids, unsaturated fatty acids, vit. A and D3 carotenes and xanthophyles.

3- Selenium 0.04-0.1 ppm prevent and cure -> exudative diathesis in chicks and 0.1-0.2 ppm myopathies of gizzard and heart in young poults.

4- Vit. E is required for normal repoduction.5- Vit. E prevents encephalomalacia (antioxidant).6- Vit. E + S e t cystine -> prevent muscular dystrophy.

Forms of Vit. E deficiency:A. Chicks

- Encephalomalacia.- Exudative diathesis.- Muscular dystrophy = white muscle striations. 4

306

B. Turkeys- Enlarged hocks.- Dystrophy of gizzard Ms.

C. Ducks:- Muscular dystrophy (enzootic muscular dystrophy).

N.B: in mature chickens and turkeys thers is no no specific signs. However, the birds suffered from marked decrease in hatchability, embryonic death in 4th day o f incubation, bilateral cataract,, blindness (in turkeys) testicular degeneration.

1 - Encephalomalacia in chicks (Crazychick disease)

Clinical signs: (15-30 d or as early as 7 d as late as 56 d).1- It is a nervous dearrangement ch. by ataxia.2 - Backward or downward retraction o f head with

lateral twisting.3- Forced movement increasing incoordination, rapid

contraction and relaxation o f legs.4- And finally complete prostration and death.

Lesions:1- Cerebellum is softened and swollen.2- The meninges are edematous.3- Minute hemorrhage on the surface o f cerebellum.

307

4- N ecrotic areas present as green yellow opaque appearance.

2- Exudative diathesis1- It is an edema in the s/c associated with abnormal

prem ability in the capillary walls.2- G reen blue viscus fluid is easily seen through the

skin (containing blood components, hemorrhage in keel and thigh Ms, also intestine.

3- D istention o f pericardium leads to death.4- N ote Se-containing enzyme (Glutathione peroixidase

enzyme) which protects the capillary membrane against oxidative damage.

- 3- M uscu lar dystrophy- M uscular dystrophy in chickens and ducks, turkeys due

to vit. E + Sulfur containing AA deficiency- C hicks: breast muscle (4 wk) has light colored streaks

easily distinguished from normal bundles.- D ucks: throughout all skeletal muscle o f the body

(inability to walk, nervous tremores).- T u rk ey s: gizzard and heart myopathy (vit. E + Se).

4- E n la rg e d hock disorder in turkeys 2-3 weeks- V it. E decrease + Fat. rancidity destroy biotin

308

- Hock enlarged then disappear by time 6 week and repear severe 14-16 weeks.

Treatment:1- Add BHT/sintoquin (antoxidant).2- Encephalomalacia Vit. E 5-10 mg/bird 2-3 d.3- Exudative diathesis vit. E 5-10 mg/bird + Se 0.01

mg/ton.4- Muscular dystrophy Vit. E + 0.3% cystine, 10.4%

methionine.5- Enlarged hock, vit. E, Zinc 30 g/ton, 1200/2000

mg/kg choline. ^

Thiamin (vitamin Bi) deficiency Polyneuritis gallinarum .Thiamin (Bi) deficiency

Function:Thiamin pyrophosphate (activated thiamin) is a cofactor in oxidative decarboxylation, its deficiency leads to extreme anorexia, polyneuritis and death in some cases.

Signs of deficiency:1- Signs are variable according to age, in young chicks2- (>2 week) of age, sudden polyneuritis and deaths are

possible, growing birds (3 wks and up) exhibit gradual polyneuritis while in adult thiamin deficiency accompanied blue comb syndrome.

3 0 9

3- A norexia, loss o f body weight, ruffled feathers, leg - w eakness and unsteady gait.

4- W ith deficiency, progress o f signs occurred and resem bled by apparent paralysis o f muscles which begin w ith flexors o f Foes and progressing upward affecting extensors o f legs, wings and neck.

5- The chick has a characteristic sit on its flexed legs and draw back the head in a “stargazing position” re traction o f the head backw ard is due to paralysis o f an terio r m uscles o f the neck.

6- L oses the ability to stand and decreased body tem perature (35.6 C), in addition to decreased resp iration w hich m ay lead to deaths in some cases.

Treatment:Thiam in 2-5 m g/kg on diet, or 2-5% yeast extract on ration.

Riboflavin deficiency Vit. B2 def.

Curled toe paralysisFunction:R iboflav in is a cofactor in m any enzym e systems in the body (N A D -N A D P-cytochrom e reductase and m any others). Some o f w h ich are v ita ly associated w ith oxidation-reduction reactions invo lved in the ce ll respiration.

310

Signs and pathology of vit. B2 deficiency:When birds fed on a diet deficient in riboflavin, birds exhibit the following signs.

A. Chicks1- Slow growth, weakness, emaciation o f birds.2- Good appetite, diarrhea (1st to 2nd week).3- No walk except forced to walk on hocks.4- Toes are curled inward when both walking and

resting.5 - Droopy wings.6- Atrophied leg muscles and flappy.7- Dry harsh skin.8- In severe cases: sciatic nerves and brachial nerves are

softened swollen (5 times).

B. Hens1- Decreased egg production.2- Increased embryonic mortality. .3- Increase o f fat in liver.

4- Decreased hatchability (dwarfed, edema, defective down) clubbed.

C. Young turkeys1- Poor growth.

2- Incrustation in the comers o f the mouth and on the eye lids and around cloaca.

311

3- Severe dermatitis of the feet and shanks (marked edema, desquamation a deep fissures) death may - occurs after 3 weeks.

D. DucksDiarrhea and poor growth

T reatm en t:100 jig riboflaviin dose each bird or 4.5-5 mg/kg diet.Note: pancreatic and duodenal lesions (thiamin, pantothenic acid riboflavin and niacin).

Pyridoxine (vit. B6def.)

Function:Vit. B6 is required for several enzymes particularly these concerned in transamination and decareboxylation of amino acids.Signs an d pathology of deficiency:

A. Chicks1 - Depressed appetite2- Poor growth3- Perosis4- Characteristic nervous signs (Jerky nervous

movements o f legs when walking, spasmodic

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convulsions, run aimlessly flappying wings followed by death.

B. Adult1- Marked reduction in egg production and hatchability.2- Decreased food consumption, loss of weight.

Note: High protein contents in diet required increased B6 as coenzyme in amino acids metabolism. 1

Treatment:4-6 mg/kg diet.

Nicotinic acid (Niacin)Function:It is a component of coenyzmes (NAD), NADP in carbohydrate, fat and protein metabolism.Note: Tryptophan requires vit. B6 as a cofactor to give Niacin. So niacin requirements depends on the tyrptophan levels in diet and B6.Signs and pathology of deficiency.

1- Enlarged hock, perosis (differs from manganese, choline def.) that there is no slipping of the tendon.

2- Poor feathering.

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3- Drop in egg production and hatchability.

Treatment:lm g niacin, bird /day.

Pantothinic acidFunction:It is a com ponent o f co-enzyme A and is involved in citric acidsynthesis and oxidation o f fatty acids and other reactions.

Signs and pathology of deficiency:Signs in chicks are difficult to differentiate from biotin def.

1- Perosis.2 - Poor growth, dermatitis broken feathers emaciation

and crusty scabs in the comers o f the mouth eyelid

margins = stucked together = restricted vision and

toes show ed (keratinization), cracks, fissures. While

in layers (wartlike balls o f feet) decreased egg

production and hatchability.

• 314

BiotinFunction:It is a cofactor in carboxylation and dearboxylation reactions.

Signs and pathology of deficiency:1- Poor growth dermatitis in feet, skin around beak, eyes as

in pantothenic acid (examine the composition of the diet).

2- Perosis and slipped tendon.3- Drop in egg production and hatchability, birds parrot

shape beak).4- It has a role in acute sudden death syndrome.

Folk acidIt is a part of the enzyme system -> nucleic acid, A.A and nucleoproteins.

Signs and pathology of deficiency:A. Chicks- Poor featehring, anemia and perosis.

Note: Folic acid, lysine, copper, iron -> decrease pigmentation of feathers.

B. Layers / breeders- Marked increase in embryonic mortality.

315

Treatment:Single IM injection 50-100 gg pure pteroylglutamic (folic) acid.

Vit. B12 (Cobalamin)It is required in carbohydrate and fai metabolims

Signs and pathology:1- Slow growth, mortality, reduced egg size and

hatchability, hemorrhage on embryos, muscle atrophy in legs and death o f embryos (14-17 d) of incubation.

2- Perosis-edema and fatty liver.

Treatment:2 pg vit B12/IM/hen.

CholineIt is essential in acetylcholine in phospholipids and A.A synthesis.

Clinical signs:1- Perosis.2- Pin point hemorrhages, puffiness o f hock joint

metatarsus twisting.3- Deformed articulator cartilage slipped tendon.4- Increased fat in liver and drop in egg production.

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Essential inorganic elements (mineral elements)Elements Function Signs Treatm ent

Ca, P 2:1

normal bone

formation

Rickets osteom alacia an d thin

egg shell

(1) 1 gm C a

carbonate 2-3

d./bird

(2) + viL D

(3) Correct

Ca, P in diet

Magnesium

Mg

Carb.

metabolism

bone

formation

egg shelh

Deficiency: poor growth -

convulsions gasping

coma=death

Excess poor growth diarrhea

thin egg shell

Nacl Fluid and

ionic balance

Deficiency: poor growth, soft

bone corneal kerat, drop in egg

prod, and nervous signs.

Excess: 4 g/kg B .w (lethal)

inability to stand, intense thirst

and m uscle weakness

convulsions = death

Congested liver, heart, lung and

intestine hemorrhages and

ascitis.

K. Normal heart

beat

W eakness in m uscles o f

intestine cardiac and tetanic

seizures<tr.

Manganese

(Mn)

Activator o f

several

enzym es

normal

growth,

reproduction.

Perosis = slipped tendon (2-10

wk) thin egg shell drop in

hatchability em bryo deaths

chondrodystrophic

Zinc Enzym e

activation

D eficiency: poor growth

enlarged hocks dermatitis

(crusts) excess: increased m olt.

30 gm/ton

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Encephalomalacia: Cerebellum is softened and swollen. The meningesj are edematous.

Muscular dystrophy: light colored streaks easily distinguished from normal bundles.

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Rickets-OsteomaladVCage$ layer Fatigue: Beading or swelling of the rib costochondral junctions.

Perosis: slipping o f Achilles tendon. Malposition o f leg distal to the hock.

Duck DiseasesBy

Prof. Dr. Mohamed M. MegahedI. Viral Diseases of Ducks

Duck virus hepatitis (DVH)

ByProf. Dr. Abd-Elshakor Ismail

Def:DVH is an acute, highly contagions disease of duckling characterized by sudden onset, rapid spread and . high mortality. Survivors recover very rapidly.Most losses occur on the 3‘ a 4. days of clinical disease onset. These can be close to 100% in a flock7 up to 2 weeks old. Thereafter an age resistance develops that gradually mortality until after 4tk week, ducks die only rarely. Age resistance is complete at about 5-6 weeks of age.Cause:Three antigenically distinct viruses have been described, which can cause similar clinical signs and lesions. They have been called duck hepatitis. Type I, the originally described classic duck hepatitis is Picomavirus the more wide spread and more virulent than type II, III, while type II is an Astrovirus Type III is an picomavirus. DHV type II & III were 1st

320 •

recognized as separate entites because they induced hepatitis in DH type I among ducklings.

Susceptibility:

Natural disease occur throughout the world have been recognized only in ducks. Duck, 2 to 3 weeks old, but 3 days old birds may be affected. Other birds and mammals are resistant to natural infection.

DVH-Type I

Epidemiology:

The virus is excreted by latent infected and recovered birds up to 8 weeks after infection. The virus can be transmitted through food, water and air bom infection can occur.

Incubation period:

1- Naturally: infection takes about 2-5 days.2- Experimentally: 1 -3 days.

Transmission:

Natural infection occurs by direct & indirect contact, oral and

respiratory routs are the main pass ways o f infection. Mechanical spread is also possible. There is no evidence of egg transmission.

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• In susceptible duckling less than 2 weeks old the disease

is sudden with possible high daily mortality (65%).

• Duckling 1st become dull depressed and show droopiness and inapetance. They soon stop moving and fail to keep with the others, within short time the duckling lies on their sides with spasmodic paddling leg movements and die with the head drown backwards (opisthotonus) position.

• The disease run very rapid course, duckling may die within an hour o f the onset of symptoms.

• Mortality may reach over 90% of the flock, although in endemic areas a 5 to 10% loss is mqre common.

• Mortality in a brood depends on the virulence of the virus, physical and immures status of duckling and the presence or absence o f concurrent or secondary infection (Salmonella, Pasturella, Aspergillus and E-coli).

Lesions:

1- Punctuate or echymotic hemorrhages on swollen livers are pathognomonic.

2- Swilling o f the kidneys and spleen may be also seen.

Diagnosis:1- Case history.

Clinical signs:' 1

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Clinical signs:

2- Clinical symptoms and PM picture.3- Virus isolation and identification.4- Artificial infection of susceptible day old duckling,

which die as early 16 how post inoculation.5- Sero-diagnosis "SN, PPT, ELISA. ,

Differential diagnosis:ND, DVE, Duck Influenza, salmonellosis, Duck Cholera,intoxication and mycotoxicosis.

Prevention and control:

1- Prevent introduction of infection (sanitation and a management).

2- Breeder vaccination with attenuated or field (virulent) virus before breeding at 16- 18 weeks of age. Hatched offspring acquire challengeable passive immunity which protects them in the susceptible period of life.

3- Exposure of day old antibody free duckling using live attenuated vaccine via (foot-web, I.M., S/C), Virus strains and degree of attenuation are important.

4- Inactivated vaccines5- Therapy:Passive immunization using of convalescent serum of birdsthat are survive infection or hyperimmune serum protectduckling at 1-3 days old as a prophylactic measures in

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endemic areas when the 1st mortalities from disease are noticed. Serum from breeder ducks gives the same results.

DVH-Type II

Although similar to DVH-type I as pathologic entity, it caused by entirely different agent. Outbreaks were often sporadic affecting some batches of ducks. Most reliable diagnostic method is E.M examination of liver homogenate for the detection of Astrovirus particles.

DVH- Type IIIFor isolation of DVH virus, inoculation of blood or tissue Suspension following inoculation of susceptible day old duck, cell culture and serological tests have been proved not useful diagnosis.

Control:Immunization with attenuated live vaccine provides maternal Ab that prevents high mortality in young ages.

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E n la r g e d l iv e r w ith p e t e c h ia l o r e c c h y m o t i c h e m o r r h a g e .

3 2 5

Duck plague Duck virus Enteritis

(DVE)B y

Prof. Dr. Abd-Elshakor IsmailDef:Is an acute, contagious Herpesvirus infection o f Duck, geese and swans characterized by:

~ • Vascular damage, with tissue hemorrhages and free blood in body cavities.

• D igestive mucosal eruptions (Enthanthemetous lesions).• Lesion o f lymphoid organs.• Degenerative changes in-parenchymatus organs. .

Economic importance:In Duck producing areas where the disease has been reported, DVE has produced significant economic losses

1- High mortality.2- In breeders associated with loss o f egg production.3- High carcass condemnation.

Cause:Herpesvirus, w hile differences in virulence among DVE- strains have been noted, all appear immunologically identical.

326

Cultivation on DEF- culture, CAM 9-14 day old embryonated duck eggs. The virus can be adapted to grow on embryonated chickens eggs. However they are unsatisfactory for primary isolation.

Susceptibility:Although the virus has been adapted to grow in ECE and chicks under 2 weeks o f age, natural infection has been limited to anseriforms, wild and free flying water fowl, and migratory water fowl.Transmission:

1- Direct contact between infected and susceptible birds.2- Indirectly by contact with contaminated environment,

water appears to be the natural means of virus transmission, population densities encourage rapid spread with high mortality.

3- Carrier state has been suspected in wild ducks, contact between domestic and wild anseriforms is common and frequently mediated by use of open bodies of water for duck production. Experimentally stressed carriers shed more viruses.

Incubation period:3-7 days, death usually follow within 1-5 days, deaths Natural infection has been observed in ages ranging from 7 days old duckling to mature breeders.

/ 327 -

Clinical signs:• In domestic breeder, sudden, high persistent mortality is

often the 1st observation.• Mature ducks die in good fleshy condition.• Prolapsed penis may be evident in dead mature S

breeders.• . Drop in egg production o f 25- 40% may be noted during

the period o f greatest mortalities.• A s the disease progress {prolonged course) within a

flock more signs are observed:a- Photophobia, associated with half closed pasted

eyelids.b- Inappetence, extreme thirst, droopiness, ruffled

feathers, nasal discharge, soiled went and watery diarrhea appears.

c- Ataxia, affected bird are unable to stand they maintain a posture with drooping out-stretched wings and head down, Suggested weakness and depressions.

d- When forced to move may have tremors, e- Young market duckling (2-7 weeks o f age) show

dehydration, loss o f weight, blue beaks, and often blood stained vents. -

Mortality:In domestic ducks range from 5-100%, morbidity, based on the observation that sick birds usually die, closely approaches 100% mortality. Adult breeders tend to experience greater mortality than young ducks.Lesions:Depend age, sex, virulence, susceptibility (the collective lesions when present are diagnostic).

1- Petecheal, ecchymootic or large extravasations o f blood may be found on or in the myocardium and other visceral organs and their supportive structures including mesentery and serous membranes. On the visceral pericardium of the heart especially within coronary grooves, closely packed petechiae give the surface a red paintbrush print appearance.

2- Surfaces o f liver, pancreas, intestine, lung and kidney may be covered with petechiae. Annular hemorrhagic bands on the mucosa of the intestinal tract.

3- Mature layers , deformed, discolored ovarian follicles massive hemorrhage from the ovary may fill the abdominal cavity, lumen of intestine and gizzard are often filled with blood esophageal- proventricular sphincter appear as hemorrhagic ring.

4- Specific digestive mucosal lesions are found along the alementy canal (oral cavity, esophagus, caeca, rectum and cloaca). Each of these lesions undergoes progressive

329

alteration during the course o f the disease. Initially, macular surface hemorrhage, appears, which, later- covered by elevated yellow- white crusty plaque. Subsequently the lesions become organized into a green superficial scab. In esophagus and cloaca, lesions m ay,... becom e confluent. In esophagus maculas occur parallel to longitudinal fold.

5- In young ducklings individual lesions in the esophagus are less frequent. Stuffing o f the entire mucosa is more common.

6- In caeca macular lesions are singular separated and well defined bet and mucosal folds.

7- Rectal lesions are usually few in number with greatest concentration adjacent to the cloacae.

8- A ll lymphoid organs are affected, spleen tends to be normal and smaller in size dark and mottled, thymus has m ultiple petechiae. Bursa o f Fabric is intensely redden, becom e surrounded with clear yellow fluid that discolors adjacent tissues.

9- During early stage o f infection, entire liver surface is pale copper color with an admixture o f irregularly distributed pin point hemorrhages with white foci, late stages o f infection are characterized by dark brown or b ile stained liver without hemorrhage.

330C,

Immunity:Recovered birds are immune to infection.

Diagnosis: ;

1- Clinical signs and PM picture.2- Histopathology, Intra nuclear inclusion bodies in the

epithelial cells.3- Isolation and characterization of the causative agent.4- Infectivity tests using susceptible birds.5- Serological tests NT, ELISA.

Differential Diagnosis:DVH, Duck cholera, Intoxication, parvovirus myocardites and anatipestifer syndrom.

Prevention:1- Vaccination (chicken embryo adapted) for breeders 2

weeks o f age attenuated or inactivated virus.2- Hygiene.

Control:1- Hygiene (sanitation and management).2- Depopulation o f infection flock.

331

Diphtheritic membrane in the oesophagus.

Diphtheritic cloacitis and diphtheritic membrane in the rectum.

332

Goose parvovirus infection

Derzsy's Disease

GPV

Def:It is a highly contagious and fatal disease of goslings and Muscovy ducklings. Goose parvovirus has been reported from all the major goose-farming countries of Europe and the Far East where the disease is of serious economic significance.

Cause:Goose parvovirus is a member of the family P a r v o v i r i d a e and has recently been shown to be related to the human dependovirus genus. Apart from the Muscovy duck parvovirus, to which it is closely related, goose parvovirus shows no similarity to the other avian or mammalian parvoviruses. Following primary infection, the virus replicates in the intestinal wall and after a short virernic phase reaches the heart, liver, and other organs.

Susceptibility:1 - GPV can infect all breed of domestic goose and

Muscovy ducks.2- Muscovy duck parvovirus reported in Muscovy ducks

only.

333

3- Young age more susceptible (especially less than one week old). Resistance to infection occurs so that by the time the birds are 4-5 weeks old negligible losses occur.

Transmission:1- Horizontal: The virus is excreted in large amounts in the

feces of infected birds, resulting in rapid spread by direct ' and indirect means.

2- Vertical: Outbreaks are often initiated in susceptiblegoslings or ducklings following transmission of the virus via eggs laid by infected or carrier breeder geese and , ducks. ' ..

Diagnosis:1- A presumptive diagnosis is based on the characteristic

clinical course, age incidence, and gross and lesions.,2 - Isolation of the parvovirus in cell cultures or

embryonated eggs derived from susceptible geese and Muscovy ducks.

3- Presence of the virus can be confirmed by electron microscopic examination of infected cultures and neutralization with specific goose parvovirus antiserum.

v 4- Direct detection of antigen or virus in tissues from infected birds, by immunofluorescence, or by the use of PCR.

334

5- Serologic tests for goose parvovirus include virus neutralization, agar gel precipitation, and ELISA.

Differential Diagnosis:- A lthough goose parvovirus causes disease in both geese

and M uscovy ducks, recent studies have shown that M uscovy ducks are also infected with another antigenically related parvovirus (Muscovy duck parvovirus). This virus causes serious disease in M uscovy ducklings but not in goslings and can be detected and differentiated using molecular methods.- Differential diagnoses should also include duck viral enteritis, duck viral hepatitis^Riemerella anatipestifer and P multocida.

Prevention and Treatment:1- Goslings and ducklings should be hatched together only

from flocks that are known to be free o f goose parvovirus, as many outbreaks are attributed to the practice o f custom hatching eggs from various sources.

2- Eggs should be imported only from countries that canguarantee freedom from goose parvovirus.

3- Geese and ducks that have survived an outbreak should not be used for breeding purposes.

4 - Vaccination:

. 3 3 5

Both live and inactivated oil emulsion vaccines are available and are widely used in countries where the disease is endemic. Vaccination o f breeding flocks induces high levels of maternal antibody in the progeny.

336

I I . Bacterial Diseases of Ducks Infectious Serositis

Rimerella Anatipestifer (RA)Duck Septicaemia, Pasteurelia Anatipestifer Infection,

New Duck Disease By

Prof. Dr. Ibrahim A. GhanemDef:It is contagious acute septicemic or chronic disease of growing ducklings, characterized by

- H igh mortality and morbidity in acute form. Serofibrinous inflammation.

The disease is usually associated with bad hygienic measures.

C ause:• P a s t e u r e l i a a n a t i p e s t i f e r

> Gm —ve non motile, capulated non spore forming rods, .may stain bipolar, cultured on chocholate and blood agar. About 20 serotypes have been reported based on agglutination reaction.

Susceptibility:1- Growing duckling, 1-8 weeks old.2- Water fowl, pheasants, quail and turkeys.3- Chickens only under experimental infection.

,337

4- This disease is usually associated with bad environmental conditions and other diseases may predispose the outbreak as Mycoplasma anatis, influenza virus or E.colii ^

Mode of infection and transmission:1 - Direct and indirect contact '2 - Respiratory route3 - Wound or skin (of the feet) - .. .4- M.O live in upper repiratory tract and under: stress, out breaks may start. - . .

Clinical signs: ^1- Ocular and nasal discharge.2- Mild coughing and sneezing.3- Greenish diarrhea, ataxia, tremors of head and neck

- followed by coma and death 5-75%.4- Affected ducks become rapidly emaciated and the

survivors may be stunted.

Lesions:1 - Fibrinous pericarditis, perihepatitis and airscaulitis.2- Caseous salpinsitis, arthritis and sinusitis.3- Fibrinous meningitis.4- Enlargement, mottling of liver and spleen with focal

necrosis.

338

Diagnosis:1- Case history.2- Clinical signs.3 - Gross lesions.4- Isolation and identification.

Treatment:1 - Sanitation and sound managment (avoid wet litter).2- Chlortetracyclin, streptomycin, suphadimidine. ;3- Sulphamethazine 0.2-0.25 % in drinking water or feed

sulphaquinoxaline at level of 0.025 or 0.05 % in feed.4- Penicillin-streptomycin combination or lincomycin-

sepectinomycin combination' by injection S/C is effective. Half the dose every 12 hours is preferable.

5- Florofenicol.

Duck choleraDuck cholera is caused by Pasteurella multocida and affectsbirds above 4 weeks of age.

Clinical Signs:1- The birds show loss of appetite, increased thirst,

ruffled feathers.2- Mucous discharge from mouth, high body

temperature.

339.

3- Diarrhea first with mucous droppings followed by light greenish types.

Prevention and control:1- Antibiotics are effective in controlling the disease and

reducing mortality. They can be given either in feed or in water.

2- Where there is possibility of the outbreak of the disease the birds should be vaccinated against the disease at least twice: first at the age of 2 months and the second at 4 to 5 months later.3- Proper sanitation, avoiding overcrowding, proper

ventilation.

SalmonellosisDef:Paratyphoid is an acute or chronic disease of poultry, many other birds, and mammals caused by any one of a large group of salmonellae that are not host specific.

Causes:1 - Over 200 species of Salmonella.2- Approximately 10-20 species of Salmonella cause most

outbreaks in poultry. Frequent isolates include: S. enteritidis, and S. typhimurium.

340

Mode of infection and transmission:1- Transovarian transmission2- Infection at hatching from cont. egg shell.3- Animal protein.4- Rats, mice and most animals

I Clinical signs:I 1- Ducklings have dropping wings raffled feathers,

anorexia, increased thirst and watery diarrhea.

2- .Swelling and edema of the eyelids.

3- Keeling over with head backwards and paddling of legs

following by death.

Lesions:1- Ducklings: Septicemia- enteritis- necrotic foci on liver

surface.

2- Adults: bronze color liver and pin point necrotic foci.3- Air sacculitis and pericarditis.4- Arthritis with orange gelatinous exudate.

Prevention and control:1- The eggs should be disinfected with formalin solution to

prevent egg-shell contamination.2- Pelleting the feed is a solution to feed contamination;

because during pelleting the feed is heated and the Salmonella organisms die.

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3- Besides all these maintaining proper sanitation frequent and regular disinfection are very important for the control of this disease. Infected birds should \ not be used as breeding stock.

OrnathosisIt is caused by Chlamydia psittaci. The young ducks are more susceptible to this disease which is transmitted through the eggs as well as direct contact.

Clinical signs:1- Symptoms are observed usually in duckling less than 3

weeks old.2- Purulent conjunctivitis, blindness, general weak-ness,

stunted growth, watery diarrhea and emaciation are the visible symptoms.

3- Mortality may be up to 30 percent.4- In layers there will be a drastic reduction in the egg - production and in breeding flock increased mortality of

day old duckling are also noticed.

Prevention and control:Broad spectrum antibiotics like chlorotetracyclin 500 ppm mixed with feed can control the disease effectively but the recovered birds may remain as carriers.

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ColibacillosisT h is d isea se is u su ally affect the ducklings from 2-3 weeks of

a g e and is caused b y 2 serotypes o f E. C oli. M ost o f the

sym ptom s are sim ilar to infectious serositis but without

n ervou s sym ptom s. U se o f Sulpham ides and antibiotics are

u sefu l to control the disease. G ood management and hygiene

are n ecessary for its prevention.

Ill, Fungal Diseases of Ducks Mycotoxins

• A. Aflatoxicosis

Aflatoxins are a group of closely related toxic compounds produced by the fungi Aspergillus flavus and A. parasiticus. Four types of aflatoxins are - commonly found in grains contaminated by fungi; Bl, B2, G1 & G3, Domestic ducklings are quite sensitive and the effect of aflatoxin exposure has been studied extensively in this species.

Clinical Signs; (young duckling)1- Inappetance and reduced growth 2 weeks after initial

consumption of toxic food.2- Ducks picked at their feathers.3- Leg and feet become discolored.4- Lameness, convulsion, opisthotonos and death.

Lesions:1- Enlargement and paleness of liver and kidney. Later,

liver became shrunken, firm and nodular with distended gallbladder.

2- Hydropericardium and ascites.3- Hemorrhage on kidney, pancrease and S/C.

B.OchratoxicosisOchratoxins, mainly ochratoxin A, are.. nephrotoxic mycotoxins produced mainly by Penicillium vindication and Aspergillus ochraceus on com, other grains and feedstuffs. Mainly cause retarded growth but no other clinical signs.

Lesions:1 - Liver is enlarged, increased weight; hepatocytes

contained misshapen mitochondria and accumulations of glycogen.

2- Kidney is enlarged, increased weight, thickening.3- Thymus has regression and decreased weight.

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Rabbit DiseasesI. V IR AL DISEASES OF RABBITS

ByDr. Abeer Shaheen

V IR A L HEMORRHAGIC DISEASE (VHD)RABBIT HEMORRHAGIC DISEASE (RHD)

Def:Acute -highly contagious fatal disease of rabbit characterized by sudden onset, rapid spread, short course and heavy losses.

Cause:Cacli virus

Susceptibility:1- Rabbit above 8 weeks old are more susceptible to

infection.2- All young rabbit survive after infection become immune

and resistant to infection.3- All breeds are susceptible.4- Both sex are susceptible.

Route of infection:■ Respiratory.

■ Oral.

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■ Skin scratches.

Source of infection:■ Infected animal■ Contaminated environment■ Insects.

Incubation period:From 1 to 3. days.

Clinical signs:1- Epistaxis.

Y 2- Some rabbit died suddenly.3- Respiratory distresses.4- Pyrexia, fever.5- Mortality exceeds 90% in some affected units.

Lesions:1- Hemorrhagic rhinitis with frothy bloody stained muffle.2- Trachea, bronchi and bronchioles showed congestion

and hemorrhages.3- Lung shows punctuate hemorrhage o f various sizes.4- Pleurisy and blood tinged fluid in thoracic cavity.5- Heart show hydropericardium with hepatitis and

distended gall bladder. > - ;

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6 - Spleen and kidney are enlarged, congested and hemorrhagic.

7- Lymph node show swelling and peticheal hemorrhages.8- Gastrointestinal mucous membrane shows congestion

and hemorrhage.9- Brain show congestion and hemorrhage.

Diagnosis:1- History, clinical signs and gross lesions.2- Hemagglutination test (HA test) from infected organs

------- which could agglutihate-humas-RBG-(Q),------------------------

N.B: On the other hand other HA viruses must be propagated on ECE or tissue culture firstly' and then can agglutinated chicken RBC.

3- HI test using specific antisera.4- Virus isolation on tissue culture but not on ECE.5- Virus neutralization test by injection of Rabbit by virus

and known antibody show the lesion on the specific host.

Differential diagnosis:From bacterial hemorrhagic septicemia by culture on specific media.

Prevention and control:1- Strict hygienic measures.

,34?

2- Control of insects parasites using insecticide.3- All sick rabbits should be isolated.4- Disinfectionwith formalin and sodium hydroxide (8%).5- Vaccination using oil adjuvant vaccine (1 ml) S/C at (1)

month old followed by booster dose which must be given after 15 days and revaccinate every 6 months.

2 - MYXOMATOSISDef:It is viral disease of rabbits, causing high economic losses due to high mortality and skin lesions.

Cause:Myxomavirus (member of pox virus group).

Transmission:1- Virus transmitted mainly by vectors as mosquitoes and

rabbit fleas.2- Oral and respiratory routes not play a role in viral

transmission.

Signs and lesions:1- Typical odema of head, eye lids and external genitalia

and base of ear.2- Mucopurulent nasal discharge.3- Normal appetite until before death.

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4- Nodular form heals leaving scales which disappear later.

Diagnosis:■ I/D inoculation of young rabbit with fresh tissue

collected from lesions will develop lesions at site of inoculation.

■ The virus isolated on CAM at 11-13 days ECE for 6

days leading to development of focal pocks and plaque formation on tissue cultures, intracytoplasmic inclusion

. bodies can be detected on cut section.

Prevention and control:1- Control o f insects parasites using insecticides.2- All sick rabbits should be isolated.3- Quarantine of newly introduced rabbit.4- Disinfection with formalin and sodium hydroxide (8 %).

P revention:By vaccination S/C by live homologous strain 162 which produce long lasting immunity.

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IT. BACTERIAL DISEASES OF RABBITS By

Dr. Abeer Shaheen

1- PASTEURELLOSIS (Bacterial hemorrhagic septicemia)

(Snuffles)Def:It is an acute, subacute or chronic disease of rabbit characterized by respiratory distress in acute and subacute forms and subcutaneous abscesses in chronic form.

Cause:Pasteurella multocida

Mode of infection and transmission:1- P a s t e u r e l l a m u l t o c i d a normally inhabitants in upper

respiratory tract, when animals are subjected to stress factors, the organism may produce the disease, these factors are■ Pregnancy* Heavy lactation* Parturition■ Enteritis specially during the period of lactation

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■ Improper hygienic measure■ Change in diet■ Change in temperature

2 - Other bacterial agents are also involved in the production of the disease such as E.coli, streptococcus species, staphylococcus and Pseudom onas aeroginosa.

3- The respiratory route with wet or dried nasal discharge fromdiseased rabbits is the main source of transmission of the disease.'

4- Infection from mother to offspring after birth.5- Mechanical transmission by rats, flies and rodents play

important role in the transmission of the disease from diseased to healthy rabbit.

Susceptibility:- All ages are susceptible.- Young animals usually develop acute form with high

mortality.- Semimature and adult rabbit develop subacute or

chronic forms with low mortality.

Clinical signs:A —acute

■ General signs of diseaseOff food, depressed, sleepy with rough fur and fever.

■ Respiratory symptoms

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Catarrhal nasal discharge.

Coughing and sneezing.

Animal shake his head to get ride o f nasal discharge

■ Conjunctivitis

Excessive lacrimation.

■ Course o f the disease 3-7 days B - Subacute form

■ Respiratory signs in the form o f mucopurulent discharge.

■ Progressive emaciation■ Course of the disease 3-5 weeks

C - Chronic form■ Subcutaneous abscess in belly and back regions.■ Abscess in middle ear and brain causing nervous

manifestation.* Sterility in some cases.

Lesions:A - Acute

Hemorrhages on serous and mucous membranes (catarrhal rhinitis, tracheitis and bronchitis).

B - Subacute formPurulent rhinitis, tracheitis and bronchitis and Cropus pneumonia (lung).

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C - Chronic formLocalized abscesses in belly, back regions, brain, lung and middle ear.

Pyometra with chessy sticky pus.

Diagnosis:1- Case History

2- Clinical signs.

3- Gross lesiops

4- Isolation and identification o f m.o on blood agar as

specific media for pasteurella multocida.

5- Mice inoculation.

Treatment:1- Treatment should • be restricted in early stage

streptomycin 100 mg /kg b.wt. I/M for 3 days.

Tetracycline 0.4 % in ration for 7 days.

2- Badly affected one should be destroyed.

Prevention and control:1 - Control

• Isolation o f diseased rabbit

• Hygienic disposal o f dead one

• Cleaning and disinfection o f hatches and equipments

2 - Treatment• Streptomycin 100 mg / kg

• Oxytetracycline 0.4% in ration

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• • Sulphonamides

3 - Emergency Vaccination

Apparently healthy rabbits by locally prepared vaccines

which formalized monovalent, autogenous vaccine (broth

culture).

Age o f vaccination

At 2 monthS; S/C 0.5ml and booster vaccination after 15

days and revaccination every 6 months.

Prevention:

1 - Sanitation and sound management

> Daily cleaning o f rabbit houses

> Avoid stress factors.

> Rearing young rabbit away from adult

2 -- Use prophylactic dose o f antibiotic.

3 - Vaccination at 2 month o f age.

2- SALMONELLOSISDef:

it is uncommon enteric infection o f young rabbits

characterized by septicemia, rapid death with diarrhea.

Cause:• Salmonella typhimurium

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• ' Salmonella enteritidis

• Salmonella pullorum

Salmonella are gram negative bacilli, non spore forming, non lactose fermenting rods.

Susceptibility:A ll ages may be affected, but young and pregnant are more

susceptible.

Mode of infection and transmission:1 - Ingestion o f contaminated food and water.2 - Faeces o f carriers and diseased rabbits are the main source

' o f infection.

3 - Direct contact with an infected animals.

4 - Rodents are susceptible to be a source o f infection.

Clinical signs:1- Peracute form

Rabbit are found dead

2- Acute form■ Anorexia

.■ Depression

* Fever . ..

■ Diarrhea

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■ Abortion and mucopurulent vaginal discharge in

pregnant rabbit.

Lesions:1- Hemorrhages on surface o f abdominal and thoracic

organs and other serosal surface.2- Pinpoint focal areas o f necrosis on the liver.3- Suppurative metritis in pregnant rabbits.

Diagnosis:Isolation o f M.G fromllver, spleen, heart blood on salmonella shigella agar or MacConkey’s agar.

Control:1 - Isolation o f diseased rabbit.2- Hygienic disposal o f dead rabbit.3- Cleaning and disinfection.4- Treatment by using specific drugs as neomycin.

Prevention:1 - Daily cleaning o f hutches.2 - Prevent food and water contamination3 - Eradication o f rodents4 - Use o f prophylactic dose o f antibiotic.

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3 - E.COLI INFECTIONS

The clinical diseases caused by E.coli

A- neonatal diarrhea

Def:It is a disease of neonatal and unweaned rabbits and cause severe losses among rabbits caused by E.coli 0109.

Mode of infection:1- Oral route is the main route of infection.2- Lateral transmission by direct contact with diseased

mother.

Clinical signs:1- Watery diarrhea of 1-14 days old rabbits.2- Belly and posterior are soiled with yellowish diarrhea

and rabbits are found dead in nest.

Lesions:1- Watery content of intestine.2- Complete wet of young rabbit.3- Septicemia in the carcasses.4- Abscesses can be detected in liver.

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Diagnosis:1- History, signs and gross lesions.2- Bacterial examination and histopathology examination.3- Differential diagnosis from the disease causing diarrhea

in young rabbits.

Treatment:U sing specific antibiotic.

B — E.coli diarrhea in weaned rabbits

Definition:It is an important intestinal disease in large scale allover the

w orld o f rabbit farms.

cause:E .co li 0 1 5 , 0 1 0 3 , 0 1 0 9 and 0 1 3 2 .

Susceptibility:N e w ly w eaned rabbit (4 -12 w eeks).

Mode of infection and transmission:1- Contam inated food and water.

2 - Stress factors as sudden change in ration, cold climate,

and im proper care, this cause E .coli which normally

inhabitant in intestine to produce disease.

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Clinical signs:1 - Peracute form (Sudden death)2 - Acute form

* Loss o f appetite.■ Watery diarrhea.■ Faeces contain mucous tinged with blood.■ Animal appear dehydrated and weakened

• * Mortality reach 50%.

Lesions:1- Caecum and large intestine are filled with watery fluid.

. 2 r Catarrhal or hemorrhagic inflammation o f intestine.

3- Food filled stomach.

Diagnosis:1- History, signs and gross lesions.2- Isolation o f M.O on MacConkey’s agar.3- Histological examination.

Differential diagnosis from other diseases causing diarrhea:

■ Intestinal coccidiosis

■ Salmonellosis■ Other E.coli infection

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Treatment:By using specific and effective antibiotic

4-LISTERIOSISDef:It is a septicemic disease o f adult rabbits characterized by

sudden death, abortion, delayed parturition and nervous

disorder.

Cause:Listeria monocytogens

Gram +ve, difficult to isolate on artificial media, M.O has

public health importance which cause abortion, endocarditis

and m eningeoencephalitis.

Susceptibility:

1- Adult rabbits more susceptible.

2- Stress factors make doe much more susceptible to

listeriosis.

Mode of infection and transmission:1- Ingestion o f contaminated food and water.

2- Stress help in the producing the d isease as poor nutrition

and pregnancy.

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3- Respiratory routes and venereal transmission have been suggested.

Clinical signs:1- Symptoms are non specific as depression, anorexia and

death.2- Pregnant does may abort and vaginal blood tinged

exudates.3- Nervous disorder.

Lesions:1 - Peracute casesSepticemia, congesion of visceral and thoracic organs .2 - Acute cases

■ Enlargement and odema of cervical and mesenteric lymph nodes

■ Clear fluid in thoracic cavity pericardial sac, abdominal cavity.

■ Liver and spleen show numerous pinpoint gray foci ■ through parenchyma.

■ Suppurative meteritis in pregnant does.

Diagnosis:- Neither signs nor gross lesions are specific for diagnosis diagnosis depend on isolation of M.O from blood, brain and visceral organs, vaginal exudates

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Prevention and control:- Vaccination with both killed and live vaccine is not

successful.- Treatment wit tetracycline and streptomycin are

effective.

m . PARASITIC DISEASES

ByProf. Dr. Mohamed A. Lebdah

III. 1. Mange

Mange is a contagious disease affecting rabbits with rapid spread. It is one o f the major problems facing rabbiteries in Egypt and causes high economic losses:

Economic importance:

1- It causes a lo ss o f meat due to (severe emaciation).

2 - It cau ses dam age o f rabbit skin leading to loss in fur

production.

3. It is o f public health importance.

T here are tw o types o f m ange according to the affecting site.

Ear m an ge and b ody m ange.

m .l.a . EAR MANGE

(Ear canker, psorptic mange, psorptic scabies)

It is one of the most common diseases in backyard rabbits, rarely in industrial rabbit farms, contagious disease

characterized with rapid ,spead, itching ears and presence o f a

dry whitish - gray to tan crusty exudate inside the ear.

Economic importance:

1- It causes high econom ic losses among affected rabbits.

2 - It has public health significance.

Cause:

A small mite, Psorptes cunicuii, just v isib le to the naked eye. It

is oval-shaped mites with w ell developed legs bearing jointed

pedicels. At the end o f the pedicels are bell-shaped suckers or

caruncles. The pedicel o f the tarsal suckers too are long and

are com posed o f three segments. The anus is terminal. The

mite spends its entire life cycle on the affected hosts i.e. all

developmental stages may be found (egg, larvae, nymph and

adult). Psorptes cunicuii is found almost on the inner epithelial

surface o f the pinna and concha o f the ear. A lso , it has lesions

on the face, neck and limbs in the absence o f any pathogenic

agent.

Infection and transmission:

V ia direct and indirect contact w ith diseased rabbits or

contaminated utensils, vehichles etc.

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1- The parasite attacks the skin of the inside of the ear, causing severe irritation and inflammation associated with a brownish, sticky, sour-smelling discharged which fills the inside of the ear then becomes a dry whitish- gray to tan crusty exudate.

2- The animal itching or scratching at its head and ears and shake the head to get rid of the discharges.

3- Self mutilation may lead to secondary infection with bacterial pathogenes in or about the head and neck.

4- As the disease progresses the crusty dry bran-like material thickens to’ as much as three -fourths of an inch or more and consists of desquamated epithelial cells.

5- In severely affected rabbits, ulcers may develop.

6- If the diseased rabbit is left without treatment, the parasite may cause severe damage to the middle and internal ear and may extend to the brain tissue. In this condition, affected rabbits show lateral deviation of the head, moves in circles.

7- If the crusts and exudae are removed, the skin surface is found to be moist and red. There may be an offensive odor emanating from the ears and are very painful when touched.

Clinical Signs:

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Clinical Signs:

8- Also, affected rabbits show general symptoms in the form of ruffled fur, emacciation, off food and dullness.

Diagnosis:

It depends on the presence or observation of the clinical findings in the form of inflammation and itching of ears which fills with bad-smelling, whitish-gray to bran exudate and may be observed. Fur loss-areas on other parts of the body. Definite diagnosis by microscopic examination of the exudate and detection of Pserotpes cuniculi or its developmental stages.

Treatment:

Treatment of severely affected rabbits is usually of no value, but moderately or slightly affected rabbits treatment is advisable as the following

1-Topical or local treatment: Clean the inside of the eargently with cotton swabs soaked in hydrogen peroxide (H20 2), glycerol or mild detergent solution. Then, sv abing the inside of the ear with one of the following dressings once or twice daily for 5-6 successive days : phenol-glycerine (1:20), Iodine - ether - liquid paraffin (1:10:20) mixtures or using patent preparation e.g. Neguvon watery solution (0.15%) or Diazenon watery solution (0.15%).

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N.B. In presence o f secondary bacterial invaders, the use of antibiotic is recommended and antinflammatory is advisable.

2.Systemic treatment (injection): Ivermectin (Ivomec)® 400 pg/kg b.wt.or lml/50 kg. b.wt. via subcutaneous injection and must be repeated once, 6 days later.

Prevention and control:

Control o f ear mange depends on:

1- Application o f biosecurity measures inside the rabbituries to prevent the spread of infection to other healthy rabbits.

2- Treatment o f diseased rabbit either with local treatment and or systemic treatment.

Prevention o f ear mange depends on:

1- Application o f good sanitation and hygiene to prevent introduction o f the infestation by using the suitable

insecticide (Diazenon) to thorough cleaning and disinfection.

2- Prophylactic use o f Ivomec® at a month-old and then

every 2 months by subcutaneous injection.

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in .l .b . BODY MANGE (Sarcoptic mange, itch or scab mites)

It is a contagious, rapidly spread parasitic disease affecting rabbits and a wide variety of mammalian hosts, including man.

Economic importance:

1- It causes high losses among affected rabbits by reduction of meat production damage of skin and loss of fur.

2- It has public health significance.

Cause:

Sarcoptic mite, Sarcoptes scabiei, the mites are small, globose or round with short legs. They possesses two pairs of legs do not project beyong the margins of the body. Female sarcoptes is about twice as large as the male sarcoptes or all of the legs. The pedicels of the tarsal suckers are not segmented. The anus of sarcoptes is terminal.

Infection and transmission:

Through direct and indirect contact with diseased rabbits or mammals and/or infected utensils, equipments etc.

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1- Sarcoptic mange usually first appear on the nose and lips extending to the eyes, forehead, face, belly and occasionally the external genital organs. Sometimes, it . may observe on the lateral surface of the ears.

2- Firstly, the parasite cause an intense pruritis which leads the rabbit to rub and scratch at the infected areas leading to partial alopecia and a serous exudate develops followed by the formation of a whitish - yellow and later brownish scales or crusts of dried serum and epidermal debris. Then, affected rabbit scratching the affected areas with legs resulting in spread of the infection to legs, belly, face", forehead.

3- The continual self-mutilation leads to the appearance of skin lesions and open wounds.

4- Affected rabbits show complete loss of fur in affected area, progressive emaciation and death within a matter o f weeks.

5- f Secondary bacterial infection is common.

Clinical Signs:

Diagnosis:

It depends on observation of itching and scratching of affected rabbits to affected area, presence, of yellowish-white to

369.

Clinical Signs:

brownish exudate or scales, loss of fur and emacciation. M icroscopic examination to detect the sarcoptes mite from the lesion, a deep skin scraping is usually necessary to obtain specim ens for examination. All stages of the life cycle of mite may be observed in clinical specimens.

T rea tm en t:

Scverelly affected rabbit treatment is of no value but m oderately or slightly affected treatment is of great value as following:

1-L o ca l treatm en t:

- Clipping o f the fur at and around the affected areas.

- Removal o f crusts or scales using stiff brush with warm w ater and soap.

- Dry well and apply one o f the following preparations.

- Sulpher oint (10-15%)., Neguvon watery solution (0.15%) and Diazenon watery solution (0.15)

II -S y stem ic treatm en t (injections):

Ivomec® lm l/50kg. b.wt via s/c injection and must be repeated once, 6 days later.

3 7 0

Prevention and control:

Depends on sanitation and sound management and periodical use of anti-mange drug, with thorough and periodical cleaning and disinfection with the suitable insecticide. Quarantine of newly introduced rabbits to the flock par at least three weeks

IU.2. COCCIDIOSIS

It is an acute, subacute or chronic fatal disease of rabbits, characterized by diarrhoea, salivation and bloat. It is a major problem facing rabbit industry in Egypt. There are two forms of rabbit coccidiosis, hepatic coccidiosis and intestinal coccidiosis.

Economic Importance:

1- It causes high loses among affected rabbits especially youngs.

2- It causes downgrading carcasses due to emacciation and hepatic lesions.

Susceptibility:

Rabbits are the only susceptible host. Young rabbits up to 8 weeks-old are more seriously and commonly affected. The frequency of the disease in rabbits over 9 weeks-old decrease

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and this may be due to either age resistance or formation o f some degree of immunity due to previous mild infestation.,

Infestation and transmission:

Routes of infection and spread mainly through ingestion of contaminated food and water with infective stage.

III.2.A. HEPATIC COCCIDIOSIS

Cause:

Eimeria stiedae, infects the bile duct epithelium, E. stiedae oocyst ovoid or ellipisodal in shape, one pole is flattened and contains a rnicropyl. The wall is smooth and yellow-orange. The sporuiated occyst contain 4 sporocysts, the sporcyst with terminal knob (stiedae body), each sporocyst containing 2 sporozoites.

Pathogensis and life cycle of E. Stiedae:

The sporocysts are ingested by the rabbit and excyst in the duodenum, the sporozoites penetrate the intestinal mucosa, but how they are transported to the liver is not yet known, but may be via hematogenous spread or lymphatogenous spread. The sporozoites invade the epithelial cells of the bile ducts and begin schizogony. Numerous merozoites are produced which

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infect contagious epithelial cells. The exact number of asexual generations is not known for E. stiedae. In gametogony,. microgametes are formed and after fertilization they develop ocyst. The unsporulated oocytes breadkout of the host cells, pass into the lumens of the bile ducts and exit the body in the faeces. Sporulation takes place outside the host’s body.

Prepatent period: The time which elapses from exposure to infection until the appearance of the first oocysts in the faeces is approximately 15 to 18 days.

Clinical Signs:

1- The acutely affected rabbits showed both general symptoms in the form of off food, paleness of visible mucus membranes and emaciation and specific symptoms in the form of ultemative constipation and diarrhoea with severe emacciation.

2- Deaths are rare except in young rabbits with extremely heavy infection. These signs are observed due to the interference of hepatic function and blockage of bile ducts.

3- Meanwhile, the subacutely and/or chronically affected rabbits showed both general symptoms and specific symptoms in the form of either consipation or diarrhoea,

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emacciation, hepatomegaly resulting in an enlarged, pendulous abdomen and icterus in advanced phases of. the disease (the enlarged liver may be 20% of the total body weight in comparison with healthy uninfected 3- 7%).

4 - The enlarged liver may be palpated in severely emacciaed rabbits.

Lesions:

The hepatic coccidiosis lesions are confined to the liver.

1- The liver enlarged with yellowish-white or grayish- white circumscribed swellings or lesions of varying size, to size of a pea on hepatic surface and embedded in the parenchyma. These lesions are dilated bile ducts that contain a yellow exudate.

2- The gall bladder may be enlarged and contain a yellow exudate.

3- In heavily infected rabbits, the liver is cirrhosed and difficult to be cut. Ascitis may be found.

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Diagnosis: It depends on:

1- History and clinical findings of diarrhoea and/or constipation with progressive emacciation and severely enlarged liver.

2- Postmortem examination to detection of liver lesions.3- Microscopic examination of faeces for detection of

oocysts also, exudate from dilated bile ducts and gall bladder also be examined for E. striedae oocysts.

III.2.b. Intestinal coccidiosis Cause:

Many Eimeria species occur in the intestinal tract of rabbits but the most important species are E. intestinalis, E. magna, E. media, E. perforans ' and E. irresidua. Eimeria and developmental stages occurs in the epithelial cells of the intestinal mucosa.

Pathogenesis and life cycle:

There are 3 phases in the life cycle of Eimeria: Schizogony, gametogony and sporogony. Generally, oocysts are ingested and sporozoites are librated in the intestinal tract, where they enter the epithelial cells and multiply by schizogony. Usually 2 generations of 8 to 32 merozoites develop by schizogony. The next phase is gametogony which involves the formation of a large number of male microgamets, which are comma-shaped

375

bodies, and females macrogametes. After fertilization of macrogametes by the microgametes, sporogony begins. Oocysts develop and are extruded into the intestinal lumen and. passed in the faeces. Freshly voided unsporulated occysts are not infective. They become infective after the formation of 4 sporocysts, each containing 2 sporozoites.

Prepatent period:

The time which elapses from exposure to infection until the appearance of the first oocysts in the faeces differs from parasite species to another. Prepatent period ranged between 5- 12 days.

Clinical Signs:

Affected rabbits showed clinical symptoms varied greatly according to:

1. Age of the affected rabbit.

2. Relative susceptibility.

3. Degree of the infection.

4. Causative organism or organisms.

The acutely affected rabbits showed both general symptoms in the form of depression, ruffled fur, off food and specific symptoms in the form of intermittent to profuse watery faeces

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admixed with mucus and blood. In addition, affected rabbits, showed intense thirst and deaths due to dehydration and secondary bacterial infection. The course of the disease is short 2-3 days. Mortality rate is high with an average 75-90%. Meanwhile, the subacutely affected rabbits showed general symptoms and specific symptoms in the form of watery diarrhoea soaked on the hind quarters and posterior part of affected-rabbits, bloat or so called “pot-belly” rabbits and salivation. Moreover, the chronically affected rabbits showed either diarrhoea or constipation with severe emacciation. Paresis or paralysis of fore or hind legs may be observed.

Lesions:

Intestinal coccidiosis lesions are seen in the small and large intestine depending on the causative agent.

The postmortem examination of both freshly dead and sacrificed rabbits affected with intestinal coccidiosis revealed gross lesions in the from of:

• Catarrhal enteritis and presence of multiple white or grayishareas in the wall of the intestinal tract, this is due to the parasitized epithelial cells usually died, resulting in ulceration and admixed with mononuclear andpolymorphonuclear exudate.

• The caecum contains a milk-like fluid.

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Diagnosis:

It depends on:

1 - History and clinical signs of watery diarrhoea souled the hind quarters, bloat and salivation.

2- Postmortem examination reveals the white spots on intestinal wall, enteritis, milk-like content of caecum.

3- Microscopic examination of faeces or intestinal smear to detect occysts.

Treatment:1. The most effective drugs are the sulfonamides administrated

either via drinking water or via s/c or 1/m injection for three consecutive days..

a. S.’dimethoxine or S. monomethoxine (S. methoxine) is effective in a dose of 75mg/kg. b. wt. on 3 courses, each of 3 days, with 7 days interval via drinking water.’Also. S. methoxine fed in the diet for 7 consecutive days to ensure a dose of 75mg/kg. b. wt.

b. S. Quioxaline sodium is effective at a dose of 0.05% in drinking water and 0.03% in the feed for 7 successive days.

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II

c . S . m e ra z in e so d iu m or S . d im idine sod ium adm inistered as.

0 . 02% in d rin k in g w ater and 0 .04% in th e ration .for 7

s u c c e s s iv e d ays.

d . S . th ia z o le in a d o se o f 4 0 0 m g/k g . b . w t. for 4 days

f o l lo w e d b y d o s e s o f 1 00 m g /k g . b . w t. o n th e 5th day.

W h a tev e r th e su lp h o n a m id e u sed , th e ad dition o f v itam in s

A , k 3 . D 3 , E to th e ration or drink ing w ater d u rin g th e

th era p eu tic co u r se s or in b e tw ee n th em is o f great

im p o rta n ce .

Prevention and control:Control depends on:

1- Isolation of diseased from apparently healthy rabbits.

2- Hygienic disposal of dead rabbits. •

3- Thorough cleaning and disinfection of rabbit hatches using suitable insecticide and ammonia solution 3% for destruction of oocyst.

4- The use of sulphonamides in therapeutic doses for diseased animals and' in prophylactic doses for apparently healthy ones.

Prevention: depends on:

1. Application of sanitation and sound management including:

379

• Daily thorough cleaning of the rabbit hatches and removal of faecal material.

• Feeders and waterers must be raised above the floor of the hatches to minimize food and water contamination.

• Isolation of youngs from adult directly after weaning.

• Rabbits manure is not to be used as soil fertilizer, especially in Barsem fields.

II. The use of sulphonamides in a prophylactic doses greatly reduce the incidence of the disease. In field use trisulfa for 3 days via drinking water, every month.

III. 3. Cysticercosis

It is the infestation of rabbits with the cysticercus stage of the adult tape worm (taenia pisiformis) which inhabits the small intestine of dogs.

Economic Importance:

1. It causes losses among affected rabbits and downgrading carcasses due to emacciation and liver lesions.

2. The rabbit act as an intermediate host for the infestation.

3 8 0

Cause:

Larval stage (cysticercus pisiformis) of adult tape worm of dogs (Taenia pisiformis)..

Infection and transmission:

Oral route through ingestion of contaminated food and water from faeces of infested dogs, which containing the eggs of the adult tapeworms.

Pathogensis:

After ingestion of contaminated food and water with eggs. The eggs hatch in the intestine of the rabbit and the embryos become free. The embryos penetrate the intestinal wall and reach the liver in which they migrate, usually in zigzag lines, causing damage of liver cells. The destroyed cells are replaced by connective tissue. The embryos leaves the liver to the peritoneal cavity and lodge on the omentum in which they develop to cysts in groups resembling grapes.

Clinical Signs:

The mildly affected rabbit showed no specific clinical symptoms. Meanwhile, the heavily affected rabbits showed sudden deaths of good bodily condition rabbit.

3 8 1 -

Lesions:

Postmortem examination of freshly dead or sacrificed affected rabbit revealed gross lesions in the form of:

• Enlarged liver and show grayish-white zigzag lines.

• Omentum revealed lodged grapes-like cysts.

ffl. 4. COENUROSIS

It is the infestation of rabbits with larval stages (coenurus serialis cysts) of Multiceps serialis tape worm or (Coenurus cerebralis cysts) of Taenia coenurus adult tape worm of dogs.

Economic Importance:

1: It causes losses among affected rabbits and down-grading carcasses of broiler rabbits.

2. It is an intermediate host of Taenia coenurus and Multiceps serialis of final host (dogs).

382

Cause:

Coenurus cyst or larval stage of Taenia coenurus of dogs, (coenurus serialis cyst Multiceps serialis) and (coenurus cerebralis cyst of Taenia coenurus).

Intestation and transmission:

Oral route through ingestion of contaminated food and water with the faeces of infested dogs which containing the eggs.

Pathogenesis:

The embryos become free in the intestine after ingestion of contaminated food and water with eggs. Then, migrate to its predilection site (in case of C. serialis subcutaneous tissues) of the back region. Then, the embryos develop to cysts. A fully developed cyst is bladder-like, in the size of a lemon or more, with more than one envaginated scolex. Occasionally, the cysts developed in the brain and under the eyeball, resulting in nervous symptoms and blindness respectively. Meanwhile, coenurus cerebralis cysts predilection site is the brain and usually the affected rabbits shown nervous manifestations.

Clinical Signs:

In case of coenurus serialis cysts, affected rabbits manifested with subcutaneous swellings (bladder-like swellings), some swellings with one or more envaginated scolex with or without

383

nervous symptoms and/or blindness. In case of coenurus cerebralis cysts, affected rabbits manifested with torticolis, incoordination and lateral deviation o f the head.

Lesions:

Bladder-like cysts, lemon-sized in the back region. Cysts either in the brain or under the eyeball.

Diagnosis:

Depends on Clinical symptoms and P.M. lesions.

Differential diagnosis:

Subcutaneous parasitic cysts should be distinguished from subcutaneous abscesses, haematoma and tumors.

Treatment:

Surgical removal o f cysts in valuable breeds.

in.5. ECHINOCOCCOSISIt is the infestation o f rabbits with the larval stage (Echinococcus cyst) o f dog’s and cat’s tape worm (Taenia

echinococcus)..

384

Economic importance:

1. It causes losses among affected rabbits and downgrading

carcasses.,: j ......

2. It is act as an Intermediate host of adult tapeworm of dogs and cats.

Cause:»

Echinococcus polymorphic or Echinococcus cyst or granulosus cysts of adult tape worm. T. echinococcus.

Infestation and transmission:

Ingestion of contaminated food and water with faeces of dogs and cats containing eggs.

Pathogenesis:

After ingestion of parasite’s egg, the hexacanth embryos liberated in the intestine, then migrating through blood and lymph streams and many of them reach to the liver through the portal vein, resulting in cyst formation. In the same time, some embryos escape through hepatic capillaries into heart and lungs, where they also develop to the cyst (Hydated or echinocccous cyst).

•v 385

Clinical Signs:

Clinical examination of affected rabbits showed general and without symptoms of an illness specific clinical symptoms.

Lesions:

Postmortem examination of both freshly dead and sacrificed rabbit revealed gross lesions in the form of cyst in either liver, heart and/or lungs.

Prevention and control: It depends on:

i. Prevent dogs and cats from gaining entrance to rabbiteries and to green foods.

ii. Hygienic disposal of dead rabbits.

References

1- Saif, y. M. (2008); Disease of poultry (Ed, 12) Blackwell Publishing, Iowae Univeristy Press.2- Saif, y. M. (2006); Disease of poultry (Ed,l 1) Blackwell Publishing, Iowae Univeristy Press.3- Saif, y. M. (2006); Disease of poultry (Ed,10) Blackwell Publishing, Iowae Univeristy Press.4- Jordah,F. T. T and Pattison, M. (1996); Poultry diseases (Ed,4) W.B.Saunders Company Ltd, London.5- Davison, F. and Nair, V. (2004); Marek’s disease an evolving problem, Elsevier, Oxford.

D isease causes Signs an d P .M T rea tm en t

6-M uscular

dystrophy

Vit. E, cystine

m ethionin def.

C hicks white m uscle striations in breast ms.

D ucks: white M all skeletal m uscles o f die body +■ inable to walk and nervous signs.

T u rk ey s: gizzard, heart muscles.

V it.E 25-45

m g/kg diet

cystine, 0.3%

m ethionin 10.4%

7- Enlarged hocks

o f turkey

Vit. E + Zn def.

choline

Enlarged hocks (2-3 wk) disappear 6 wk reappear severe at 14-16 wk V i t E

Zinc 30 g/ton

Choline 1200-

2000 m g/kg wt.

8-Polyncuntis

gallinarumThiam in

(vit. B l)d e f .

Inappitance, loss o f body w e ig h t, emaciation, paralysis o f legs and w ings starts from the

flexors o f toes upto extensors o f legs and wings, (stargazing position) hypotherm ia-death.

B1 2-5 m g/kg

2-5% yeast

extract

9-C urled toe

paralysis

Vit. B2 d e f

riboflavin

C hicks: slow growth, diarrhea, emaciation, walk on hocks, droopy wings toes curled in

ward, atrophied leg m uscle, enlarged sciatic nerved.

Adult drop in egg production and hatchability, em bryo deaths.

B2 100 pg/bird

or

4.56- m g/kg d iet

10- Dermalitis

■

A-Vit. B2

3-Biotin,

Jantothcnic acid.

T u rk e y s incrustation around the com ess o f m outh eye l id s , toes, fissures, drop egg

production and hatchability

C h ick s : incrustation around the com ess o f m outh eye l id s , toes, fissures, drop egg

production and hatchability

B2

Biotin 0.1-0.3

mg/kg

panthothenic 12-

15 mg/kg

11-P erosis

slipped tendon.

vln, choline

liacin, biotin, folic

icid, Ca, P, vit. E,

312, Zinc (B6)

Pin point hem orrhages, puffing o f hock jo in t, tw isting o f m etatarsus, deform ed articulator

cartilage and slipped tendon. -

A ll elem ents

included.

Table 2: Summarize the disease caused by nutritional deficiencies.

D isease causes • Signs and P.M treatm ent

1-Nutritional

roup

Vit. A. def. Chicks: poor growth, ruffled feathers, inappitance, incoordination

xerophthalmia stucked eye lids, milky while caseous material accumulates in

eyes,: and nasal sinuses, and ataxia.

Adult: pustule like lesions in oesophagus, acc. Of caseous material in

pharynx, mouth, accumulation of mates in kidneys and ureters, drop in egg

production, hatchabiliyt,, hemorrhagic spots in eggs.

5000-30,000

IU/kg diet +

BHT

2- Rickets

3- Osteo­

malacia

Vit. D3 def.

Ca, P def. Or

incorrect

ratio (2:1)

Chicks: 2-4 wk soft pliable beak and claws, green stick like long bones and

rachtic rosary (cartilaginous knobs in ribs and bending.

Adult: drop in egg production and hatchability, soft egg shell

1- Vit. D3

2000 IU/bird

2- 4 d.

2- 15,00011!/

one dose

3- 1-2 gm/liter

Cacl2.

4- Correct Ca,

P ratio in diet

4- Crazy

chick disease

Vit. E def. Chicks 2-3 wk-ataxia, nervous dearrangement backward and downward head

retraction with lateral twisting and walking in circles-rapid contractions and

relaxations of MS, soft brain, h. spots, edema in meninges and necrotic areas

in the brain.

Vit. E 5-10

mg/bird 2-5

d.

5- Exudative

diathesis' 1,1 —

Vit. E + Se

def.

Green-blue viscus fluid accumulated under the skin of breast, distention of

pericardium -> death *.

Vit. E + Se

0.01 mg/ton.

الكلية رؤية

فى بارزا عضواا تكون ان الى البيطرى الطب كلية تتطلع

ها معترف مؤسسة العليا والدراسات للتعليم متميزة وقيادة ب

المعرفة وتطبيق الكتشاف المستدامة والتنموية البيئية والخدمات

الغذاء وسالمة والحيوان اإلنسان صحة اجل من

الكلية رسالة تهدف البيطرى الطب كلية رسالة فان الجامعة رسانة هع تمشيا

والمجاالت البيطرى مجال.الطب فى الجودة عالى. تعليم توفير إلى الكلية تهتم كما والبينة. الغذاء سالمة و إلذساث١ بصحة الصلة نات.

أ خدصات تقديم إلى باإلضافة والتطبيقية األكاديمية البحوثة ؤبإجراء

ب مي ت ة ۶لئمجتئ ب و ث ب ب م تاهيأ ب جي رب إ١ م ۶قادري ب ث ت ل

ة . إ ك ا