Avian coccidiosis.dr mahmoud sedeek

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Avian coccidiosis By: Dr :Mahmoud Sedeek

Transcript of Avian coccidiosis.dr mahmoud sedeek

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Avian coccidiosis

By:

Dr :Mahmoud Sedeek

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Some important notes:

Coccidiosis :–  Infection by sufficient numbers of Eimeria.– Produce clinical manifestations, macroscopic lesions,

economic losses.– It has self-limiting nature.

 Coccidiasis:– Light infection, does not produce clinical signs or

macroscopic lesions. Sub-clinical Coccidiosis:

– Infection that reduce body weight, cause poor F.C.

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Coccidia characterized by

Host specific

Tissue specific

Immune specific

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Why Coccidia is worldwide disease

Direct life cycle.

Short incubation period (4-7 days).

Resist environmental conditions and disinfectant.

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introduction

Coccidia are almost universally found wherever chickens are raised.

Coccidiosis remains one of the most expensive and common diseases of poultry production in spite of advances in chemotherapy

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Economic Importance:

Broiler growth and weight are reduced. feed conversion rate is reduced by 5-10%. increase in condemnation rate at processing. increase in mortality rates. increase the susceptibility to other disease agents. Costs of treatment and prevention($ 300 Million/ year

(1991) Subclinical Coccidiosis cost 4.7Cents/broiler. A survey in Russia ( 1990 ) revealed that :

Mortality of 15%, loss of 100-270 Grams/broiler

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Etiology:

Eimeria species (intracellular parasite) , host-specific protozoa

Nine species of Eimeria been identified in chickens:

Seven of these species are frequently encountered in broiler E.acervulina, E. brunette , E. maxima , E. mitis, E. necatrix, E. praecox and E. tenella.

Oocyst survive for years. Dryness and direct sun are lethal.

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Mode of infection

Ingestion of sporulated oocyst.

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Mode of transmission

Mechanical transmission through persons and equipements.

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Life Cycle of Eimeria:

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Infection occurs when susceptible chicks ingest a sporulated oocyst(contain four sporocysts each contain two sporozoites) .

Liberation of sporozoites in digestive tract by mechanical and biochemical actions .

The liberated sporozoites invade epithelial cells, transformed into Trophozoite ( 12-48 hours ).

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Trophozoites enlarge,divides transforme to Schizont which contain merozoites .

Trophozoites mature, rupture ( day 3 ) releasing merozoites which invade other epithelial cells to repeat development of Trophozoites and Schizonts .

Merozoites of second generation Schizont either invade other epithelial cells ( 3 rd. generation ), or transforme into Gametocytes.

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• Male gametocyt mature, rupture release large numbers of minute biflagellate microgametocyte.

• Microgametocyte unite with Macrogametocyte to form Zygot ( immature oocyst ) .

• Immature oocyst rupture, pass out with feces .

• Sporulation of Oocyst occurs after 24 hours in presence of moisture, oxygen, sutible temperature .

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Clinical signs

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Signs include watery and/or bloody droppings. Depression. Mortality (0-50%), and morbidity (0-100%). Culls appear as pale birds with anaemia, depression. Poor weight gain and feed conversion. Drop in egg production

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Emaciation ,pale legs and peak

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Pm lesions

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diagnosis

Case history.

Clinical signs.

Pm lesions.

Microscopic examination.

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Prevention & control

Why Coccidia prevention is better than treatment????

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Prevention based mainly on:

Anticoccidial feed additives.

Vaccination.

Managemental points

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1-Anti coccidial feed additives

A-Chemicals

B-Ionophores

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A-Avialable chemicals

Amprolium 125 p.p.m. Arpinocid 60 p.p.m. Clopidol 125 p.p.m. Decoquinate 30 p.p.m. Dinitolmide 125 p.p.m. Halofuginone 3 p.p.m. Nicarbazine 125 p.p.m. Robendine 33 p.p.m. S.Q+ Ormthoprim 125 p.p.m. S.Quinoxalline 150 p.p.m. Diclazuril 1 p.p.m.

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B-Avialable Ionophore

Lasalocid 75-125 p.p.m. Maduramicin 5 P.p.m. Monensin 80-120 p.p.m. Salinomycin 45- 66 p.p.m. Narasin 70 p.p.m. Semduramycin 25 p.p.m.

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Characters of Ideal anticoccidials :

1-Efficacy : Broad spectrum activity.

2-Safety : Wide margin of safety , at least three-fold difference between registered and toxic level.

3-Cost effectiveness : least effective cost.

4-Residues : Should be metabolized, excreted, without toxic residues.

5-Carcass and meat quality : should not affect organoleptic criteria.

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Characters of Ideal Coccidiostat :

6-Compatibility with feed : electrostatic properties of compound should permit accurate addition, proportioning and distribution, and should be compatible with feed ingredients ( vitamins, minerals and growth enhancers ).

7-Assay techniques : rapid, reliable and inexpensive.

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Programmes of coccidiostate feed additives

• Medication to Market Age( continous program)

• Shuttle Programs

• Rotation program

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Medication to market age( continuous program)

we put broilers on medication until slaughter time, or until laying birds are put into cages. Some governments have regulatory restriction ( Do not feed medicated drugs for 3 – 5 days prior to slaughter ( broilers ) or past 16 wks ( layers ).

This is to allow drug residues to be excreted prior to human consumption of meat or eggs.

Some drugs are considered safe and can be used continuously ( amprolium ).

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Rotation program

Use one Anticoccidial drug every 2 cycles

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Shuttle program

We use anti coccidial drugs till 21 days of age in broiler then change it

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Anticoccidial toxicity

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A- Ionophores toxicity:

1- Monensin 200 p.p.m. to turkeys cause 30% mortality( dose 150-170 p.p.m.).

2-Salinomycin 50 p.p.m. cause paresis to turkeys( dose 60 p.p.m ).

3-Maduramycin 10 p.p.m. for broilers reduce weight by 15%( dose 5p.p.m.).

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B-Chemicals toxicity :

 1-Nicarbazine ( dose 125 p.p.m.)– Higher level in broilers : suppress weight– Broilers under heat stress cause 90%

mortality– Breeders fed 100p.p.m. lead to : low egg, weak

shell– Breeders fed 150p.p.m. for 5-7 days lead to

drop of hatchability by 10%.

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B-Chemicals toxicity :

2-Amprolium ( dose 125 p.p.m. )

–  Three times recommended dose : cause growth depression

– Adding 300p.p.m. in hot climate lead to Thiamine deficiency.

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C-Anticoccidial Interaction :

Tiamulin x Ionophores Sulfa.

Chloramphenicol x ( Monensin )

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Causes of Coccidiostat failure :

Not effective against all species of Eimeria

More than average exposure oocysts Low inclusion level of Coccidiostat Faulty management ( wet litter ) Intercurrent disease Drug resistance after prolonged uses.

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2- vaccination

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immunization

Planned immunity ____(vaccination)

Accidental immunity____ (trickle infection)

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Avialable vaccines

Live virulent vaccine (wild).(coccivac B,D_Immunocox)

Live attenuated vaccine.( livacox , paracox)

Recombinent vaccine.

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• Two- three cycles of infection are usually sufficient to protect chickens.

• more pathogenic ___ less immunogenic

• Keep in mind to make littre moisture from 5 th day after vaccination by sprinkling water to make sporulation easy.

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3-Managemental points.

Keep litter dry.

Prevent fecal contamination of food and water.

Keeping layers in cages.

Slat floor.

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4- disinfection

Ammonia ( for 500 s .meter)– Spread 50 kg. Lime-powder– Add 100 kg. Sulphoric -ammonia– Add 500 liters water– Lit it work for 20 minutes– Left to dry

Results : – Ammonia gas kill oocysts.– Calcium- sulphate close cracks.

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treatment

Amprolium : 30mg./kg./daily/ for 6 days. Ethopabate increase efficacy against

intestinal Coccidiosis.  Sulphadimidine : 200mg./daily/ 2-3 days.  Sulphaquinoxalline : 40mg./kg./daily/ 2-3

days.  Toltrazuril: 25p.p.m., or 7.5mg./kg./daily/

2days.

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treatment

Slpha + diaveridine.

Sulpha + pyrimethamine.

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Thank u very much