Tissue Nematodes Pharmacy

8/6/2019 Tissue Nematodes Pharmacy

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REVISION

Types of Life Cycle in Trematoda

and Cestoda


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Life cycle in human trematodes


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Life cycles in human intestinal cestodes


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Life cycles in human larval cestodiases


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NEMATOD

A

1. Intestinal nematodes

2.

Tissue nematodes


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Classification of nematodes by habitat and

development.

Adult intestinal nematodes with pre adult larval lungmigratory phase:

Ascaris, Hookworms, strongyloides.

Adult Intestinal nematodes without larval migratory phase:

Enterobius, Trichostrongylus, Capillaria and Trichuris.

Intestinal nematodes with post-adult larval tissue invasion:

Trichinella.

Larval tissue nematodes with developmental arrest:

visceral and cutaneous larva migrans.

Adult tissue nematodes:

Dracunculus and filariae.


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Nematodes according to mode of infection

1. Ingestion of eggs:

Ascaris, Enterobius, Trichuris.

2. Ingestion of larva:

Trichostrongylus (on vegetable), Trichinella (in pork),Dracunculus (in cyclops), Capillaria (in fish).

3. Active penetration of skin by larva:

Ancylostoma, Necator, Strongyloides.

4. Entrance of skin by larva transmitted by insect:

Filarial worms : Wucheraria, Onchocerca, Loa,Acanthocheilonema, Mansonella.


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Nematode infection by ingestion


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Nematode infection via skin

By larvae


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Tissue Nematodes

1. Adult tissue nematodes:

Adult tissue nematodiases: filarial wormsand Medina worm

2. Intestinal nematodes with post-adult larvaltissue invasion:

Trichinella. See intestinal nematodes.

3. Larval tissue nematodiases withdevelopmental arrest:

visceral and cutaneous larva migrans.

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Adult Tissue Nematodiases:

Filarial worms

Dr Mohieddin M

Abdul-Fattah

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1. Wucheraria bancrofti and brugia malayi.

A. Biology:

Final host: - Man only in W. bancrofti, - Man, cats andmonkey in B. malayi

Habitat: afferent Lymph vessels and nodes in the lower

half of the body. Exit stage: microfilaria from peripheral blood through

mosquito bite.

Morphology: long and slender worms; (4 cm) & (10 cm) with 100m wide. Brugia is half as long.

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8. L3 migrates to

mosquito proboscis

1. Mosquito takes blood meal

and L3 enters through bit wound

2. Adults in lymphatics

3.Produce sheathed

microfilaria (MF) in

blood & lymph4. Mosquito

takes blood

meal &

ingests MF

5. microfilaria

penetrate the

midgut &

migrate to

thoracic

muscles

6. L1

Wucheraria & Brugia LC


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Wucheraria and Brugia

B. Epidemiology:

1. Distribution: In tropics and subtropics. In Egypt they are present in

Sharqiya, Dakahliya and others.

2. Transmission:

Intermediate host:

Mosquitoes as Culex, Aedes and Anopheles.

Reservoir host:

No. Reser

voir hosts in W.

bancrofti.

Cats and monkeys in B. malayi.

Infective stage: 3rd stage filariform larva.

Mode of infection: Infective larvae enter skin through

the bite wound of the mosquito..14


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Wucheria and Brugia

C.Host parasite relationship:

1. Asymptomatic amicrofilaraemic: Immune persons in endemics , they show specific

antibody seropositivity and antigen negativity).

2. Symptomatic amicrofilaraemic with filarial

antigenemia:

Tropical pulmonary eosinophilia:

hypereosinophilia, cough, wheeze, lung fibrosis, Itresponds to antifilarial therapy.

3. Asymptomatic microfilaraemic:

These are tolerant persons in endemic areas.

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Host-Parasite relationship; continued

C. Host parasite relationship:

4. Early disease: incubation period ~ 1 year followed by

episodes of fever with lymphangitis and epidydmo-orchitis

for years.

5. Late disease:D

amage of lymphvessels due to 2ry

bactaerial infection (the symbionts; Wolbachia)

Obustructive manifestations;

hydrocele, and elephantiasis in the leg, scrotum and breast

(in Wucheraria).

Elehpantiasis is limited below the elbow and knees in

brugian type.

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Acute (early) and chronic (Late)

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Lymphangitis

DermatitisHydrocele Elephantiasis


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D. Lab diagnosis:1. Detect eosinophilia, and sheathed microfilaria in 10

p.m.2 a.m. concentrated blood samples or

2. Detect filarial antigens by immuno-chromatographictest (ICT) or

3. Detect antifilaria antibodies by Elisa.

Characteristics of microfilaria tails

Wucheraria: tapered anucleate tail.

Brugia: with 2 discrete nuclei reaching tip of the tail.

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E. Treatment:

Ivermectin one dose 20g/kg can be repeated every year..

Diethycabamazine (DEC); 2mg/kg tds for 12 days.

For lymphedema Benzopyrone (coumarin) 400 mg/day PO

or using compression garments (hard to use).F. Control:

Mass treatment by:

annual single dose of albendazole (400mg) plus ivermectin

(100-400g) or DEC to stop transmission, and vector

control.

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Loa loa

A. Biology: Final host: - Man only

Habitat: subcutaneous tissue and sub-conjunctival.

Exit stage: 250m tightly sheathed microfilaria from

peripheral blood through mosquito bite.

Morphology: long and slender transparent worms;

(3cm) & (7 cm) with 100m wide.

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Adults in S.C. tissues

3. They produce

sheathed microfilaria

in blood, urine, CSF

and sputum

4. Fly takes blood

meal & ingest

microfilaria (MF)

5. MF

penetrate

midgut to

thoracic

muscles

8. L3 migrateto the fly

mouth parts

1. Fly takes

blood meal &

L3 enter the

bite wound

Human stagesChrysops stages

Loa loa LC

Loa loa LC


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Loa loa

B. Epidemiology:

1. Distribution: Forests of central and West Africa.

2. Transmission:

Intermediate host: Tabanid flies (chrysops).

Reservoir host: No.

Infective stage: 3rd stage filariform larva.

Mode of infection:

I

nfective lar

vae enter the skinthrough the bite of Chrysops

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Loa loaC. Host parasite relationship:

i. Calabar swelling:

non-pitting transient subcutaneous swelling

due to hypersensitivity to worm metabolites.

i. Transient conjunctivitis due to sub-conjunctival

adult migration.

ii. Meningoencephalitis, glomeruolnephritis,and endomyocardial fibrosis in heavy

infections treated by DEC.

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Loa loa

D. Lab diagnosis: detect eosinophilia, tightly sheathed microfilaria in

conc. blood samples,

or Loa antibodies by Elisa.

E. Treatment:

Diethylcarbamazine,

albendazole

F. Control:

clear forest, screen houses

and vector control24


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Onchocerca volvulusA.Biology:

Final host: - Man only

Habitat: subcutaneous tissue,found coiled in nodules.

Exit stage:300-m microfilaria inskin by bite of the black fly(Simulium)

Morphology : long and slenderworms; (3cm) & (50 cm) with100m wide.

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9. L3 moves

to black fly

mouth parts

6. MF migrate

to thoracic

muscles

1. Fly takes blood and L3

enter through bite wound

2. Subcutaneous

tissues (SC)

3. Adults in

SC

4. Adults

shed MF in

skin

Onchocerca Life cycle

Human stagesSimulium

stages

5. Fly takes

microfilaria (MF) in

blood meal


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OnchocercaB. Epidemiology:

1. Distribution: Tropical Africa, Yemen, central and south America

among farmers who get contact with these flies that

concentrate around rivers.

2. Transmission: Intermediate host:

Black fly (Simulium). This breeds in rapidly flowing

freshwater and bite nearby.

Reservoir host: No. Infective stage: 3rd stage filariform larva.

Mode of infection:

Infective larvae enter skin through the wound induce by

bite of Simulium.27


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OnchocercaC. Host parasite relationship:1. Adult enclosed in fibrous tissue over

bony prominences subcutaneous firm

nodules These are seen over the pelvic brim, the

sacrum greater trochanters and head.

2. Immune reactions to dying microfilariain skin and eye lead to:

Dermatitis severe itching thickening, edema, blackening (Sowda),lichenfication, and loss of elastic fibers(hanging groin).

Punctate keratitis and opacities, panus,iritis, and chorioretinitis with opticatrophy.

These lead to blindness called riverblindness.

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Keratitis and liver blindness Chronic microfilaremia in

the eye leads to sclerozingceratitis (a hardeninginflammation of thecornea)

The cornea becomesopaque

Nodules directly on thehead result in more mfburden for the eyes

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D. Lab diagnosis:

Detect unsheathed microfilaria inbloodless skin snips from the vicinity of

nodules or section of adult in excised cutaneous

nodules.

Eosinophilia is moderate.

Detect anti-Filaria IgG4.E. Treatment:

Ivermectin (150g/kg). It should be avoided in patients with

heavy Loa loa infection as this may leadto fatal encephalitis.

F. Control:

Aerial spraying of rivers withinsecticides.30


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Dracunculus medinensisDracontiasis

y Final host: - Man, cattle, horse and dogs.

y Habitat: subcutaneous tissue.

y Exit stage: Adult female gives birth to

rahbditiform larva through ulcer onto water.

y Morphology and life cycle: long and slender

worms; (3cm x 0.5mm) & (100 cmx1.5mm).

I. BIOLOGY


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1. Human drinks water

containing Cyclops

infected with L32. L3 penetrate

the intestine,

migrate to bodycavity and

mature to adults

3.-A year later migrate to

skin, induce blister, emerge

and discharge L1 into water

4. Cyclops ingests

L1 in water

5. L1 molttwice to L3

Dracunculus

LC


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II. Epidemiology

y Distribution: Areas depending on wells waterin Yemen, west and East Africa, India and

Brazil.

y

Transmission:Intermediate host: Cyclops.

Reservoir hosts: cattle, horse and dogs.

Infective stage: Coma shaped larva in theCyclops.

Mode of infection: Drinking water

contaminated by infected Cyclops.


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III. Host-Parasite Relationship

i. When the worm emerges, it cause burningsensation and forms blister..

ii.After discharging larvae,

the worms die in a process that takes manyweeks leading to ulceration and spread of 2rybacteria infection.

causing fever and disability for months especially

in presence of multiple worms.iii.Migrating worms near joints cause arthritis with

effusion.


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IV. Diagnosis, treatment, and control

A. Lab diagnosis: white cloud of larvae,extruded by female worms in water, ischaracteristic.

B. Treatment: Metronidazole, albendazole.Safe extraction of the worm by slow windingon a stick.

C.C

ontrol: 1-Provision of safe drinking water.2-Straining water through to filter out

Cyclops.


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1. Intestinal nematodes with post-

adult larval tissue invasion

Trichinella spiralis

Larval tissue nematodes


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Trichinella spiralisA. Biology:

Final host: Pigs, wild boars, rats, bears, walruses, and manyother carnivores including man.

Habitat: -

i. Adult in Small intestines while females inhabit rows of

epithelial cells of the mucosa of duodenum and jejunum.

ii. Larvae live in Striated muscle fibers (cells).

Exit stage:

i. Males in the faecal streams.

ii. Larvae have no exit as they encyst in muscle fibers.

Morphology: 2.5 mm long with tapering post. end and 1.2mm long with 2 caudal appendages. puts 5000 larvae each

100m long.

1 M i


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Circulation

5. Larva encysts instriated muscles

3. enterintestinalmucosa

copulates

4.Larva deposited in the mucosa

1. Man ingestsencysted larvain undercooked

pork

Rodents

Carnivorism

Pigs

Life cycle of Trichinella

1. Encystedlarva from pigs

2. Larvae releasedin intestine,mature to adults


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B. Epidemiology:

Distribution: Worldwide; prevalent in pork eatingcountries (USA and Europe).

Transmission:

Intermediate host (IH): Pigs.

One host may serve as both final and IH. Humans aredead end IH.

Reservoir host: Pigs, wild boars, rats, bears,

walruses, and many other carnivores. Infective stage: Encysted larvae in muscles.

Mode of infection: Ingestion of pork infected byencysted larvae.


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C. Host-parasite relationship:

1. Intestinal stage (20-24 hours): eneteritis nausea,vomiting, abdominal pain and diarrhea.

2. Migratory stage:

A. Invading skeletal muscles (1-2 weeks): fever, facialedema, conjunctivitis, pain, swelling and weakness ofthe involved muscles.

B. Invading cardiac muscles and CNS (3rd week):Myocarditis and CNS involvement are the mostfrequent two causes of death in trichinosis.

3. Encapsulation (3w 4 w): symptoms subside or decrease. Myocarditis persists

and may precipitate heart failure.

4. If the infective dose 100 larvae morbidity occurs. If it

is 300,000 death occurs

D Di i


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D. Diagnosis:

1. Symptoms.

2. detection of free or encapsulated larvae. From the

7th day onwarda) In compressed (trichinoscopy) or

b) Stained biopsy.

c) Or digested samples from deltoid, biceps,

gastrocnemius or Pectoralis muscles.d) Or by xenodiagnosis in rats.

3. Immune-diagnosis by

a. Bachman intra-dermal skin test (IDT).

b. Serology: from 2 weeks in heav

y infection and3

-4w in lighter ones:

BFT (2w), IFAT (2-3w) and Sandwich Elisa.


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E. Treatment:

Prednisolone 40 mg/day for 5d, with

Mebendazole 50 mg/kg/12h PO for 10 days.

F. Control: Properly cooking pork.

Feeding pigs on cooked garbage.


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2. Larval tissue nematodes withdevelopmental arrest

Dr Mohieddin M Abdul-Fattah

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Visceral larva migrans Cutaneous larva migrans


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Toxocariasis: visceral larva migrans

Final host:1. cats (T.cati, cats Ascaris) and

2. dogs (T. cani; Dogs Ascaris)

Habitat in final host: small intestine.

Man acts only as blind end paratenic IH host

Habitat in man: larvae migrate in visceral tissuewithout further development.

Exit stage from dogs and cats: Ascaris like egg Morphology: beside to 3 characteristic ascarid lips

there are two cervical alae. Length is 4-6 cm in maleand 7-12 cm in females.

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Aetiology: Toxocara cati and T.cani

5 To circulation


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1.Adult in dogIntestine passeseggs in feces

3. Dogs < 5 weekingest the egg

4.Larva releasedin the intestine

5. To circulation,lung alveoli,bronchi.

Then through

swallowed sputumto intestines

4.Larvaereleased inthe intestine

5. Larvae migrate

in various organs

Toxocara LC

Visceral larva

migrans

2

3


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Epidemiology

Distribution: worldwide, young children as they

are likely to ingest soil

Transmission:

1. Intermediate host: man is blind paratenic IH host

2.Reservoir host: old cats, dogs and birds

3. Infective stage: embryonated egg with 2nd stage

larva.

4. Mode of infection: Ingestion of soil, contaminatedwith mature egg.

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Host parasite relationship

Visceral larva migrans (in heavy infection):

due to migration lead to fever pneumonitis,

abdominal pain, myalgia ,.lymphadenopathy,

hepatomegaly and convulsion.

Ocular larva migrans (in lighter infection):

invasion of the eye granuloma in retina and

iridocyclitis with posterior synechiae

diminution ofvision and squint.

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d l


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Diagnosis ,treatment and control

Lab diagnosis: Clinical picture and ELISA to

detect antibodies to (E-S) antigens of laboratorymaintained larvae.

Treatment:

Diethylcarbamazine 2-3 mg/kg PO tds for 3weeks.

Thiabendazole 16 mg/kg tds for 7-28 days,

depending upon tolerance. Prednisolone for ocular disease

Control: Personal hygiene and sanitation of

owned cats and dogs.48

Cutaneous Larva Migrans


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Cutaneous Larva Migrans.

Anckylostoma caninum and A. brasiliense

Final hosts:

1. cats (A. braziliense, cats Ankylostoma) and

2. dogs (A. caninum; Dogs Ankylostoma)

Habitat in final host: small intestine.

1. In man, larvae penetrate the stratum corneum of the

epidermis downwards, only, to the stratum basale.

2. They migrate in the epidermis for weeks or months

and cannot complete its life cycle (i.e. man act as

dead end transport host).

I. Biology


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I. Biology, continued

Exit stage from FH; dogs and cats: Ankylostoma

like egg. No exit stage from man

Life cycle and Morphology: characteristic ant.b

uccal capsule. Post. End of males hascopulatory bursa.

1 Adults in small


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1. Adults in smallintestine of dogs

and cats2. OvipositImmature eggsin intestine

3. Eggspassed in

feces

4. Rhabditiformlarvae hatch

5. Filariformlarvae in soil

6. Penetrateskin of dogsor cats

7. By circulationto lung

Larvae Penetrate

skin of man

Migrate inS.C. tissues

Can notcomplete LC

8. Larvae moltin alveoli

9. Enter bronchi,reach trachea

10. Swallowedinto esophagus,to intestine

11. Larvaemature to adults


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II. Epidemiology

y Distri

bution: worldwide, children andconstruction workers who are exposed to

contaminated soil.

y Transmission:

Intermediate host: man is dead end transport

host. It is not intermediate host.

Reservoir host: birds and other mammals

Infective stage: filariform larvae in soil.

Mode of infection: Larvae in soil penetrate

the skin.

III H i l i hi


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III. Host Parasite Relationship

Migration of the larvae intradermally causes in

inflammatory response. The lesions (creepingeruption) are extremely pruritic.

Other Causes of creeping eruption:

y Strongyloides stercoralis.

y Cutaneous myiasis (Hypoderma and

Gastrophullus).


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IV. Diagnosis, treatment, and control

A. Lab diagnosis: clinically and by serology.

B. Treatment:

Thiabendazole, 25mg/kg PObd for 5 days.It can be repeated after rest of 2 days.

C. Control:

Personal hygiene and sanitation of ownedcats and dogs.

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