Blood Tissue Nematodes

8/10/2019 Blood Tissue Nematodes

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Blood and Tissue Nematodes

General Characters1-Adult worms live in the lymphatic, subcutaneous

connective tissue or body cavities.

2- Female worms are viviparous.

3- The early first-stage larvae, known as microfilariae

that have no differentiated organs inside, instead

there are columns of cells with prominent nuclei.

4- Filarial worms are transmitted through the bite of aninsect vector.


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Filarial worms

They include the following species:

1- Wuchereria bancrofti.

2- Brugia malayi.

3- Onchocerca volvulus.

4- Loa loa.

5- Mansonella perstans.

6- Mansonella ozzardi.


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Infective stage:

Filariform larva [3rd stage larva]:

It is about 1.5-2 mm x 20 um, with

cylindrical oesophagus and lies in

the labium of mosquito vector.

Mode of infection:

During bite by mosquito I.H,

filariform larva pierces human skin

through the puncture wound.


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Wuchereria bancrofti

Disease: Bancroftian filariasis, wuchereriasis,elephantiasis.

D. H.: Man.

I.H. (vector): Female CulexMosquitoes.

Habitat: Lymphatic tissues of lower limbs &

external genitalia.

Microfilariae appear in the peripheral blood

by night [nocturnal periodicity] & disappearby day time.


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Geographical distribution

Tropical & subtropical countries.


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Morphology

Microfilaria:250-300x8 m in length & surrounded by a loose

sheath.

Body forms smooth (graceful) curves, has rounded anterior end

and tapering tail. Both ends are free of nuclei. It has a nocturnal

periodicity.


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Nocturnal [microfilarial]periodicity theories

1- Biological adaptation between M.F. & night biting activity ofmosquito.

2- Chemical attraction between M.F. & saliva of mosquito.

3- During sleep, decrease oxygen content & increase carbon dioxide

content stimulate M.F. to migrate from blood vessels of lung toperipheral blood.

4- Khalils theory: Blockage of lymphatics; during day on upright

position of the patient; prevents M.F. to find their way to the

circulation.By night time & during sleep, relaxation of the patients body will

open the lymphatics allowing M.F. to reach the peripheral blood.


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Life cycle of Wuchereria bancrofti


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Life cycle

A- Development in man:

1- When an infected mosquito bites man to take a

blood meal, infective larvae are deposited on human

skin usually in pairs, penetrate the skin through the

bite wound or by its own activity.

2- Larvae pass to lymphatic vessels & nodes where

they mature in about one year & mate. The adult

worms are found in lymphatic of lower limbs, groin &

epididymis in males and labial glands in females.

3- Female mosquitoes produce many sheathedmicrofilariae which appear in peripheral blood at night

between 10 PM- 2 AM reaching a peak about

midnight [nocturnal periodicity].


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Life cycle

B- Development in mosquito:

4- Microfilariae are taken up by a female mosquito

when it sucks a blood meal.

5- In the stomach of mosquito, microfilariae loose their

sheath, penetrate the wall of mid gut & migrate to the

thoracic muscles where they develop into infective

larvae.

6- Development in the mosquito takes 2-3 weeks.

Each ingested microfilaria develops into one filariform

larva [cyclo-developmental transmission].

7- Infective larvae migrate to the head region within

the labium ready to be transmitted when mosquito

takes another blood meal.


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Pathogenesis & Clinical picture

1- Many infections are asymptomatic & are

detected only by blood examination.

2- The main pathology of filariasis is caused

mainly by living or dead adult worms.

3- Incubation period: one year or more.

The disease passes in 2 stages:

I-Acute (inflammatory) stage.

II- Chronic (obstructive) stage.


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I- Acute (inflammatory) stage

Due to immune response to toxic products of living or dead

adult worms with superimposed 2nd infection.

There is infiltration with plasma cells, eosinophils &

macrophages in & around affected area.

Microfilariae cause less pathology.

Acute stage is characterized by

recurrent attacks of fever, lymphangitis & lymphadenitis.


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II- Chronic (obstructive) stage

Fibrosis following the inflammatory process around worms & presence

of coiled worms inside lymphatics result in:

a- Dilatation of lymphatics leading to varicosity as hydrocele,

scrotal lymphoedema and lymphatic varices.

Hydrocele is the most common chronic manifestation & results from

accumulation of straw lymphatic fluid in sacs around testes.

b- Rupture of distended lymphatics proximal to the obstruction e.g. in

the pleural sac (chylothorax), peritoneal cavity (chylous ascitis), tunica

vaginalis of testis (chylocele), intestine (chylous diarrhea) or in urinary

passages (chyluria) with passage of microfilariae with urine.

c- Elephantiasis: Thickening & hypertrophy of the skin & subcutaneous

connective tissue of legs and genitalia [scrotum, penis& vulva] due to

disturbance of lymph drainage.


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Mechanism of Elephantiasis

Increased permeability of obstructed lymphatic walls, leading to

leakage of lymph rich in protein under the skin causing cellular

proliferation of connective tissue & deposition of fibrous tissue.

Clinically: At first, the swelling is pitting but later becomes non-

pitting then the skin becomes thickened, rough, fissured and

susceptible to ulceration and 2nd infections with bacteria or

fungi.

Elephantiasis occurs after persistent high infection

for 5-10 years.


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Bancroftian filariasis & Elephantiasis


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II- Laboratory diagnosis

a- Detection of M.F. in peripheral blood at night [between 10 pm

& 2 am] by

1- Wet drop: for living moving microfilariae.

2- Giemsa stained thin & thick smears: show the

morphological characters of microfilariae .

3- Concentration method: if M.F. are scanty;

* Knott's technique: In a centrifuge tube, mix 5-10 ml of blood withequal volume of 2% formaline. Allow the mixture to stand for 10

minutes then centrifuge. Decant the supernatant and examine

the sediment for microfilariae.

* Nucleopore filter technique: Filtration of 1-5 ml of heparinized

blood through 5 m Nucleopore filter then stain & examine thefilter on a slide.

Provocative testTo obtain blood at day time, give the patient 50-100 mg DEC orally &

examine the blood within 30- 60 min.


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Laboratory diagnosis (Cont.)

b- Detection of M.F. in chylous urine or in fluid aspirated from

hydrocele or peritoneal cavities.c- Demonstration of the adults worms in lymph node biopsy.

d- Immunodiagnosis

1- Skin test with antigenic extract of the dog filaria Dirofilaria

immitis.2- IHAT, IFAT and ELISA: for detection of filarial antibodies.

3- Detection of filarial antigens is specific & sensitive and can

detect early infection saving patients from complications of the

disease.

e- Molecular techniques: PCR.

f- High eosinophilia.

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III- Imaging techniques

a- Ultrasonography: Viable adults may be seen

moving in lymphatics (filarial dance sign).

b- X-ray: shows calcified worms.

c- Lymphangiography: Shows lymphatic changes

e.g. dilatation of vessels.


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Treatment

1- Antifilarial drugs:

a- Diethylcarbamazine [DEC]: 6mg/Kg/day for 12days, repeated every 6 months as long as the patient

remains microfilaraemic or has symptoms.

b- Ivermectin: Single oral dose of 150 ug/Kg body weight.

c- Combination of DEC & ivermectin: gives better results.

2- General measures:

Rest, antibiotics, antifungal, physiotherapy & bandaging.

3- Elephantoid tissues: Corrected surgically.

Prevention & control1- Mosquito control.

2- Treatment of patients.


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Occult Filariasis

* Clinical conditions of hyper-sensitivity reactions tomicrofilarial antigens.

* The classical features of lymphatic filariasis are absent.

* Microfilariae are not seen in peripheral blood (due to its

destruction in the lung by the immune response) but

adult worms and microfilariae may be seen in the tissues.

* The condition may be caused by Wuchereria bancrofti,

Brugia malayi or by some animal filarial worms.


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Tropical pulmonary eosinophilia (TPE)

TPE is the most important manifestation of occult filariasis.

There are low-grade fever, loss of weight, anorexia & pulmonary

symptoms (as dry nocturnal cough, asthmatic attacks), persistent

hyper-eosinophilia & glandular enlargement.

The condition is associated with a high level of filarial antibodies and

elevated IgE level.

These symptoms are relieved by ant-filarial therapy

[diethylcarbamazine (DEC)].


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Brugia malayi

Similar to W. bancrofti in life cycle, diagnosis, treatment& control and differs as regards:

1- Disease: Malayan filariasis.

2- Distribution: Far East.3- I.H. (Vector):

Female Mansoniamosquito.

4- Reservoir hosts: Cats & monkeys.

5- Habitat: Lymphatic of upper limbs.


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Microfilaria of Brugia malayi

Has loose sheath, with kinky curves & tail end

with 2 deeply stained nuclei; one in front of the other.

Microfilaria shows non periodicity or nocturnal periodicity


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Pathogenesis & clinical features are also similar to bancroftian

filariasis, but hydrocele is rare.

Brugian filariasis: Elephantiasis affects legs below the knees

and arms below elbows.

Blood Tissue Nematodes

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