GEOGRAPHICAL DISTRIBUTION
The parasite has a world wide distribution but more common in tropical and subtropical regions.
LOCATION IN THE HOST
It is found embedded on the mucosa of the small intestine
MORPHOLOGY
Only females are seen in the parasitic cycle (in the intestine of infected persons). These parasites measures 2-2.5 mm in length. In free-living cycle (outside the human body) both males and females are found. Free-living females are smaller and measure 0.95-1.5 mm in length. Males are smaller.
PARASITE
Strongyloides stercoralis is a unique parasite. It is the only nematode or helminth parasite that multiplies in the human body. A process known as ‘internal autoinfection’ accomplishes this. It differs from hookworms in that; no males in the parasitic cycle: no eggs are passed in the faeces but L1 rhabditiform larvae: internal and external autoinfection occurs when L1 larvae undergo accelerated development into rhabditiform L2 and then into L3 which is the filariform/infective larvae while moving down the intestinal tract: has a free-living cycle in the soil: may cause severe disseminated disease with larvae in vital organs in immunocompromised patients.
LIFE CYCLE

The parthenogenetic females lay eggs in the mucosa of the small intestine. Generally they have a low egg output per day. The eggs hatch in the mucosa itself and the L1 rhabditiform larvae enter the lumen and are excreted in the faeces.
The subsequent development and the rate depend on the internal and the external conditions. When external conditions are unfavorable L1 larvae rapidly develop into L2 and to the infective L3 larvae stage. The infective larvae develop into free-living males and females. The larvae produced by the free-living adults mature into free-living L3 stages. These larvae penetrate the skin of humans and once again start a parasitic cycle. The L3 larva of S.stercoralis differs from that of hookworms in; not having a sheath: having tri-radiate tip of tail.
PATHOGENESIS AND CLINICAL FEATURES
At the site of penetration of the skin, L3 larvae may cause ‘ground itch ( see hookworms). Pulmonary migration of larvae can cause lung symptoms and pneumonitis. But severe symptoms (as in ascariasis) are rare.
In mild infections, catarrhal enteritis is seen with increased amount of mucous secreted into the lumen. The mucosa is congested with hyperplasia of goblet cells with normal looking villi.
In heavy infections the villi become flattened and atrophied. Epigastric pain, nausea, anorexia and finally incessant diarrhea result.
In the hyperinfection syndrome seen in immunocompromised patients L1 develop rapidly to infective L3 stage, which penetrate the gut wall and enter the blood stream (internal autoinfection). Larvae in large numbers are carried into various organs resulting in serious damage to respective tissues. Organs and systems that can be damaged by larvae include brain, heart, pancreas, hepatobilliary system, lungs, genitourinary system and the skin.
In external autoinfection where L1 larvae develop into infective stage in soiled clothes, bed linen or around the anal verge the migrating larvae produce a characteristic epigenous dermatitis starting in the per anal region extending rapidly to the buttocks and lower abdomen. This condition is called ‘larva currens’.
DIAGNOSIS
Diagnosis is difficult. Because of low fecundity female worms produce only small numbers of larvae and it is also not regular. In cases suspected of having strongyloidiasis, negative report on a single wet smear of faeces does not exclude the infection. Several samples over period of 3-7 days may be necessary to exclude the infection. In the faeces rhabditiform larvae are looked for. In old samples sometimes hookworm larvae may be found. Then, the larvae have to be distinguished from those of Strongyloides. Duodenal intubation or ‘entero test’ may be used to obtain larvae directly from the small intestine.
PREVENTION AND CONTROL
Avoidance of indiscriminate defaecation and use of footwear help in prevention. Provision of hygienic latrines, chemotherapy of infected people and health education are important in control of the infection.
TREATMENT
Even in the asymptomatic state, strongyloidiasis must be treated because of the potential for fatal hyperinfection. Ivermectin (200 µg/kg daily for 1 or 2 days) is more effective than albendazole (400 mg daily for 3 days, repeated at 2 weeks) and is better tolerated than thiabendazole (25 mg/kg twice daily for 2 days), whose common adverse effects include nausea, vomiting, diarrhea, dizziness, and neuropsychiatric disturbances. Because thiabendazole is not uniformly effective, stool examinations, eosinophil counts, and monitoring of clinical symptoms should be continued after treatment. For disseminated strongyloidiasis, treatment with Ivermectin should be extended for at least 5 to 7 days or until the parasites are eradicated.

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