Introduction

Filarial worms are tissue nematodes that dwell mainly in the subcutaneous

tissue and the lymphatics.

CAUSATIVE AGENTS

Wuchereria bancrofti, Brugia malayi, Loa loa, Onchocerca volvulus,

B. timori, Mansonella perstans, M.ozzardi. Affect 200 million people

world wide.

Lymphatic Filariasis

Lymphatic filariasis is transmitted by mosquitoes and is caused by

Wuchereria bancrofti and Brugia species (B. malayi or B. timori).

Bancroftian filariasis is the most prevalent,Affect 115 million people

throughout Tropical and Subtropical areas. Brugian filariasis affect

only 14 million people and Is restricted to South Asia.

Pathogenesis.

Infective larvae released by mosquitoes into the tissues during a blood

meal develop within lymphatic channels into adult males and females,

which mate and release microfilariae that enter into the bloodstream.

When they bite infected individuals the mosquitoes can take up the

microfilariae and transmit the disease.

Periodicity of Microfilariae

Nocturnal periodic: mf is present in peripheral blood mainly at night

Diurnal subperiodic: mf is present in peripheral blood at all times but

with maximum level in the afternoon

For W. bancrofti

Nocturnal form more prevalent in urban sub urban communities and is

transmitted by night biting species of culex mosquitoes. Diurnal mainly

in rural areas and vector is day biting species of anopheles mosquitoes.

Brugian filariasis

Nocturnal periodic is the transmitted in areas of coastal rice fields by

night biting species of Anopheles mosquito.

Diurnal subperiodic transmitted in forest area by day biting species

of Mansonia mosquito.

Tissue damage occurs in 2 phases: Acute and Chronic

In acute phase, there are transient erytheromatous lymphatic lesions with

lymphadenopathy. Epididiymo-orchitis is another feature in the male.

Chronic lymphangitis results from damage to the lymphatics by the

presence of the adult worms. These elicits TH1 mediated granulomatous

inflammation around the lymphatics. Adult filarial worms—live, dead, or

calcified—are present in the draining lymphatics or nodes, surrounded by

inflammation. The lesions heal by fibrosis and lead to chronic lymphatic

obstruction. Mf virtually absent in the circulation of patients able to mount

this adequate TH1response. Sometimes pts remain asymptomatic even

tough mfs are abundant in the circulation. In such cases, TH2 response
down regulate granuloma formation. This form of response seen more in

patients from endemic zones. Probably due to in-utero exposure to filarial

antigens inducing immune tolerance. Tropical pulmonary eosinophilia is

due to an Ig-E mediated hypersensitivity to mf and may result in

restrictive lung disease.

MORPHOLOGY

Persistent lymphedema of the extremities, scrotum, penis, or vulva

develops. Frequently there is hydrocele and lymph node enlargement. In

severe and long-lasting infections, chylous weeping of the enlarged

scrotum may ensue. A chronically swollen leg may develop tough

subcutaneous fibrosis and epithelial hyperkeratosis, termed

elephantiasis. Elephantoid skin shows dilation of the dermal lymphatics,

widespread lymphocytic infiltrates and focal cholesterol deposits.

LOIASIS

Caused by Loa Loa. Limited to the Western and Central Africa. Affect

1-13 million people. Transmitted by female fly: Chrysops spp.

Transmission greatest in areas where pulling strings and swamps are

located.

PATHOGENESIS

Infection seen mainly in adults probably because of its long incubation

period. Adult lives within the subcutaneous tissues of man & produce mf.

Mf enter the circulation and circulate for most of the daylight hours.
Chrysops pick mf when they bite. Mf undergo cyclical devt within the fly

gut and reach the mouth parts. Injected into another host. Presence of

worms elicits type 1 HSR.

MORPHOLOGY

Characterized by migratory subcutaneous swellings (Calabar swellings)

which are Non pitting, painless and itchy. Swellings are migratory due to

movement of the adult worm. There may be systemic manifestation. May

be associated with Endomyocardial fibrosis.

Onchocerciasis

Onchocerciasis is an infection caused by the nematode Onchocerca

volvulus. Humans acquire onchocerciasis through the bite

of Simulium blackflies. The fly develops and breeds in fast flowing water,

therefore onchocerciasis is commonly found along rivers and is

sometimes referred to as river blindness. Onchocerciasis is endemic to 30

African countries, Yemen, and in parts of Central and South

America. Globally, approximately 18-36 million individuals

have onchocerciasis, 99% of whom reside in Africa. It is the world’s

second leading infectious cause of blindness. Eye impairment takes years

to develop, which is why affected individuals are those over 40 years old.

PATHOGENESIS

In the human host, the adult nematodes live in subcutaneous nodules and

produce microfilariae, which are found throughout the body but

preferentially reside in the skin and eye. Ocular symptoms are caused by

the inflammatory response invoked by the release of Wolbachia antigens

when microfilariae die. Microfilariae and adult worms of O. volvulus

contribute to the pathogenesis of onchocerciasis, both through

consequences of host immune response. Live microfilariae attack several

parts of the eye, but here again may cause small reaction; their deaths

lead to eye lesions. Eosinophils and neutrophils would cover the dead

worms, and then followed by fibroblast proliferation and chronic

inflammatory infiltrates. The most significant cause of blindness

is sclerosing (scarring) keratitis characterized by the hardening

inflammation of the cornea. Adult worms are the least pathogenic, usually

causing no symptoms at all and at worst, stimulate the development of

noticeable subcutaneous nodules called onchocercomas.

MORPHOLOGY

Collagen fibers are the main structural components of a onchocercoma;

these fibers surround one to several adult O. volvulus worms. The worms

rarely calcify or degenerate to form an abscess.. The formation of nodules

is sometimes followed by elephantiasis hanging groin; scrotum and testes

are unaffected, and hydrocoele does not occur. Females are also

affected. Generalized pruritus may occur early in the infection and may

be severe. Chronic cutaneous onchocerciasis(onchodermatitis) causes

a papular rash, scarring, and lichenification. Over time, affected skin

may begin to sag, leading to "hanging groin." Patchy depigmentation on

the legs leads to a condition known as leopard skin. Itchy eyes, redness,

or photophobia may be early symptoms of ocular onchocerciasis. Chronic

ocular onchocerciasis may lead to sclerosing keratitis and iridocyclitis,

and finally to blindness. Weight loss and generalized myalgias may occur.

Lab diagnosis

1. MICROSCOPY (definitive diagnosis)

–THICK/THIN SMEAR

–CONCENTRATION TECHNIQUE

2. ANTIGEN TEST

3. MOLECULAR METHOD

4. ANTIBODY TEST

Treatment

•Use of antibacterial cream on wounds stops bacterial infections and

keeps swelling from worsening.

•Diethylcarbamazine.

•Ivermectin.

•Albendazole.