Onchocerciasis (river blindness) is produced by the filarial bworm Onchocerca volvulus. The gravid female has a life-expectancy of 15 years. The micro filariae are found in the skin and subcutaneous tissue. Humans are the only known definitive host and the day-biting female blackfly of the genus Simulium is the vector. The flies breed in rapidly flowing water both in the rain forest and savannah. The species involved are S. damnosum and S. neavei in Africa and S. metallicum in Venezuela. The disease is confined to West, Central and East Africa, Central and South America, and southern parts of Saudi Arabia.
The incubation period averages 1 year. Initially a papular, reddish, itchy rash develops. With repeated infections, characteristic subcutaneous nodules of various sizes appear. Usually they number fewer than 10 and are unevenly distributed over the body. In chronic disease, lichenification, xeroderma, pseudo ichthyosis and atrophy of the skin occur. The nodules may be associated with the development of genital elephantiasis, hydrocele and the so-called ‘hanging groin’, in which large folds of wrinkled and thickened skin develop in the groin. Ocular lesions represent the most serious manifestation of this disease and in some communities 40% of people are blind by 50 years of age. Eye disease is commoner in the savannah. Initially the patient complains of lacrimation, photophobia and a foreign-body sensation in the eye. Conjunctivitis, iridocyclitis, chorioretinitis, secondary glaucoma and optic atrophy may occur. The eye lesions have been attributed to toxin production by the microfilariae and adult worms, mechanical irritation and hypersensitivity.
This is established by demonstrating micro filariae in snips of bloodless tissue obtained from the nodules and kept in saline for 30 min to 1 hour before microscopic examination. The organism may also be identified in the anterior chamber of the eye by slit-lamp examination. Serological tests are not helpful in the indigenous population as the positivity rate is high. Eosinophilia occurs.
Ivermectin, a broad-spectrum antiparasitic drug, is effective in filariasis and is now the drug of choice. A single dose of 150 J-Lgkg-t orally produces a prolonged reduction in microfilarial levels. Six- to twelve-monthly therapy must be given in endemic areas as ivermectin is not curative and re-infection occurs. DEe is still sometimes used when ivermectin is unavailable but reactions (pruritus and a rash) occur and were used for diagnosis (Mazzotti’s test).
PREVENTION AND CONTROL
Prevention and control depends partly on personal protection to avoid bites and attempts at destroying the vector. Eradication of blackfly is expensive and mass treatment with ivermectin (provided free by the pharmaceutical industry) once a year is being used in endemic areas with good success.
Dracunculiasis (Guinea worm infection) results from infection with Dracunculus medinensis. It is found sporadically throughout the tropics but is common in certain parts of India, Central, East and West Africa, Pakistan, the Middle East, parts of South America and the eastern regions of the former USSR. Humans are the definitive host and are infected by ingestion of water containing infected Cyclops. The larvae are liberated in the human stomach by the action of acid. These penetrate the intestinal wall, where the male dies after fertilizing the female. The gravid female then wanders in connective tissue for several months before emerging through the skin. On reaching the skin, the parasite elicits an allergic reaction with blister formation and later protrusion of the worm associated with the discharge of motile larvae. The larvae are then taken up by Cyclops, which once again are infective to humans.
A generalized reaction can occur that is associated with nausea, vomiting, generalized urticaria and diarrhoea. These symptoms abate with rupture of the blister. Secondary bacterial infection, especially with streptococci, is common and results in cellulitis and abscess formation. In Nigeria, tetanus is a frequent complication. If attempts at extraction of the worm result in damage to it, intense cellulitis may occur. Arthritis, synovitis, ankylosis of joints and epididymitis are rare sequelae.
Keeping the appropriate part of the body immersed in water may induce the worm to wriggle out. Fluorescent antibody tests are useful. Radiography may reveal the presence of the worm.
Gradual physical extraction of the worm by winding it carefully around a stick is the treatment of choice. It may take several days before the entire worm is extruded. Niridazole and thiabendazole are of questionable value in facilitating worm extrusion.
PREVENTION AND CONTROL
Prevention of this parasitosis is easily effected by chemically treating infected sources of water.
Toxocariasis (visceral larva migrans) occurs worldwide and is caused by Toxocara canis or T. cati. The adult worm is found in the intestine of dogs and cats. The infective ova are passed in animal faeces and may be accidentally ingested by humans. The liberated larvae penetrate the intestinal wall and reach the liver and lung via the circulation. Epidemiologically, puppies are the most important natural hosts and the infection is most commonly seen in children between 1 and 4 years of age. Several viscera may be involved and the clinical manifestations are dependent on the organ involved and the intensity of infection. Eosinophilia is common. Urticaria and dermatitis may occur. With pulmonary involvement the presentation is that of bronchial asthma. Chest radiographs may reveal transient pulmonary infiltrates. Splenomegaly and hepatomegaly may occur: Rarely involvement of the myocardium and eNS may result in death. Eye involvement (ocular larva migrans) produces a retinoblastoma-like picture; other organs are usually spared.
The presence of marked eosinophilia, hepatomegaly, and elevated plasma IgG, IgM and IgE is suggestive, as is the identification of foreign-body eosinophilic granulomas in histological sections. Recently detection of specific antibodies by ELISA has been found to be useful.
Treatment is difficult to evaluate in view of the mild nature of the illness and the tendency for spontaneous cure. DEe 2-6 mg kg-t daily in divided doses for 3 weeks or thiabendazole 25 mg kg-t twice daily for 5 days is probably effective. Cutaneous larva migrans Cutaneous larva migrans (creeping eruption) is a disease of the hot, humid areas of tropical and subtropical countries. It is caused by the dog and cat hookworms Ancylostoma braziliense and A. caninum and, occasionally, the human parasites A. duodenale, Necator americanus and Strongyloides stercoralis. The adult forms of these worms are found in the intestine of the host. The filariform larva emerges from the ova passed in the faeces and penetrates intact human skin. An itchy papule develops at the site of larval entry. Two to three days later a markedly itchy, erythematous, serpiginous skin lesion develops. This is due to the larva, which migrates at approximately 1 ern per day. The skin over the lesion may vesiculate. Healing occurs by crusting. Although the lesions are more frequent on the lower limbs, any part of the body may be affected. Secondary bacterial infection may result in a mistaken diagnosis of pyoderma. The only systemic manifestations are transient pulmonary infiltrates and occasional breathlessness. Eosinophilia is seen.
Thiabendazole applied locally as a 10% solution or given -stemically (25 mg kg” for 5 days) is effective.
Anisakiasis (herring worm disease) is caused by the larval stage of several species of Anisakis, and possibly of the related nematode Phocanema, which are found in abuncance in herring, and dolphins, whales and other large sea mammals. The disease is prevalent in Japan and northern Europe, where raw herring and other raw fish are conered a delicacy. In Japan the illness is characterized by acute gastric syndrome that presents as epigastric pain, usea and vomiting. Upper gastrointestinal endoscopy 11 reveal the presence of larvae in the gastric mucosa. In – ntrast, in Europe the small intestine is predominantly ‘oIved and the patient presents with colicky, generalized abdominal pain and fever. Eosinophilia is usual.
is caused by the intestinal nematode Trichinella spirid The larval form is found in rats, hares, pigs, dogs d cats. Although cases of trichinosis have been reported – m all parts of the world, it is found predominantly in the USA and Europe. It is uncommon in India. Transmission to humans occurs when improperly cooked eats, contaminated with infective larvae, are eaten.
“Vomiting, diarrhoea, abdominal pain and headache occur24-72 hours after ingestion of contaminated meat. The erity of the clinical manifestations depends on the aamber of infecting larvae. The larvae mature into the adult form in the intestine, ere they reproduce and discharge larvae into the circuion. When these larvae migrate into the bloodstream and striated muscles (a stage that lasts 10-21 days), periorbital oedema, conjunctivitis, photophobia, fever withchills, and muscle pain and spasm occur. An urticarial rash, diarrhoea, dyspnoea and pleurisy may also occur. Myocardial and CNS involvement is unusual and, if it occurs, may result in death. In the next stage of development, larvae encyst in striated muscle. During encystment symptoms gradually subside, although weakness, muscle pain and cramps may persist for several months.
A firm diagnosis can be made on the clinical presentation, marked eosinophilia, and positive serology using ELISA. If necessary the diagnosis can be established by a biopsy of the deltoid or gastrocnemius muscle 3 weeks after the onset of illness and demonstrating the presence of the larvae.
Analgesics, sedatives and bed rest are the mainstays of treatment. Steroids are indicated only in the presence of myocarditis, CNS involvement or marked allergic phenomena. Thiabendazole 25 mg kg-l body weight twice daily for 7 days is effective against intestinal worms and larvae.