Strongyloidiasis

Introduction

Although not a major cause of morbidity worldwide, the nematode Strongyloides stercoralis is unique in its ability to persist indefinitely within the host through autoinfection, and cause disseminated disease with the prolonged use of cortico-steroids or other causes of immunosuppression.

Life cycle

Adult females are about 2.5 mm in length and are attached to the lamina propria of the duodenum or proximal jejunum (Figure 11.4). Their eggs, which hatch into rhabditiform larvae (250 |im long) and pass via feces into the external environment, where they moult into the infective filariform larvae (550 |im long) which infect by penetrating the skin, like hookworms (see above) or become tissue-penetrating infective larvae by penetrating the colonic wall or perianal skin, becoming reestablished as mature female worms in the small

Disseminated Strongyloidiasis
Figure 11.4 Strongyloides stercoralis lava. Courtesy of UK Tropical International Health.

intestine (autoinfection). Larvae are sensitive to drying, excessive heat (> 40°C) and cold (< 8°C), but may survive for about 2 weeks in soil. Rhabditiform larvae in feces may also moult in moist warm soil to form free-living adult males and females, who mate. The females produce eggs which develop into infective larvae to continue their life cycle in man. The time from skin penetration to mature worms producing eggs is approximately 28 days.

Epidemiology

S. stercoralis is present in virtually all tropical and subtropical regions, but estimates of worldwide prevalence vary widely (3-100 million) with the best estimate probably around 30 million people in 70 countries.113 It is known to be prevalent among children in Cambodia, Laos, India (Bihar), GuineaBissau, Kenya, Sierra Leone, Brazil and the Caribbean. A large study in a Peruvian Amazon community found a 19.5% prevalence of stool larvae, including 25% in preschool children who also had high rates of other parasites.114 Strongyloidiasis accounted for 7.8% of 269 acute diarrheal admissions in Australian Aboriginal children in Darwin, with a mean age of 23.3 (18.1-30.1) months, which was significantly older than the mean age of 12.7 (11.8-13.7) months for other diarrheal admissions.10

Prevalence rates vary with climate, geographical region, environmental conditions, soil characteristics and socioeconomic status, but also with modifiable risk factors such as quality of housing, hygiene standards and high population density. In endemic areas, most affected individuals have a low intensity of infection, but a few are heavily infected. Household aggregation of infection has been documented in Bangladesh, with risk factors being older age (7-10 years), lack of a home latrine and low socioeconomic status.115,116 S. fuelleborni is a more virulent infection affecting young children in Papua New Guinea, which may be transmitted via breast milk.117

Pathophysiology

Malabsorption was recognized as a feature of strongyloidiasis in a 1965 Jamaican study using iron, folate and xylose absorption tests along with jejunal biopsies.118 SBBO and abnormal intestinal permeability to 51Cr-ethylenediaminetetra-acetic acid (EDTA) has also been documented in Brazilian adults with strongyloidiasis and symptoms of abdominal pain, diarrhea and weight loss.119,120 The suggested mechanisms for abnormal permeability were enhanced mucus secretion, increased enterocyte turnover with impaired para-cellular barrier function, and protein-losing enteropathy. The latter was documented by means of increased fecal aj-antitrypsin excretion in 17% (5/29) of Gambian children with persistent diarrhea and malnutrition, including two of six with Strongyloides and two of 17 Giardia cases.121

Small-bowel biopsy studies have reported normal histology in some mild infections, but most show thickening of the bowel wall with edema or fibro-sis in what has been described as catarrhal, edema-tous or ulcerative enteritis.122 In severe cases of autoinfection, larvae hatching from deposited eggs burrow through the lumen causing superficial damage to the mucosa with excess mucus production, larvae in the lymphatics lead to a granuloma-tous lymphangitis, and parasites in the submucosa cause edematous and atrophic changes with fibro-sis. As with other intestinal nematodes, Strongyloides infection elicits Th2-dependent antibodies. Immunoglobulin responses to S. stercoralis indicate that IgA affects larval output, IgE regulates autoinfection and IgG4 blocks IgE responses.123 These immune responses appear to offer little protective immunity, and the relative contributions of genetic versus environmental factors to heavy infections is still unclear. Preexisting malnutrition (wasting) is a risk factor for hospitalization with the acute diarrheal syndrome compared to other causes of diarrhea, increasing the risk 6.5-fold even after adjusting for confounding factors.10

Clinical features

As with hookworm, larval migration may affect the lungs (eosinophilic pneumonitis) or skin ('ground itch' on the foot or 'larva currens' on the buttocks) but these are not usually recognized in children. Larvae from species infecting other mammals may penetrate the skin of humans, causing only local irritation, but cannot complete their life cycle. The most common manifestation of S. stercoralis infec tion in children is an acute diarrheal illness with foul stools with a typical musty odor which can be recognized by experienced staff in high-prevalence areas. Severe dehydration is uncommon, but hypokalemia and malabsorption commonly occur. Eosinophilia (5-15% of total white blood cell (WBC) count) is a common but not universal finding. A syndrome of partial intestinal obstruction with strongyloidiasis has been described in Aboriginal children in the Northern Territory of

Australia.124,125

S. fuelleborni in infants is associated with abdominal swelling, ascites, pleural effusions and a high mortality.126 In contrast to hookworm, with which it is commonly associated in infants in Papua New Guinea, the intensity of infection peaks by about 12 months of age.117,127 A similar S. fuelleborni species affects monkeys and humans in central Africa, causing less virulent disease with fever, lymphadenitis, abdominal pain and eosino-philia.41

Disseminated strongyloidiasis (hyperinfection) occurs with impaired cell-mediated immunity, as in children treated with prolonged courses of steroids (although not from short courses of steroids for asthma) or malignancy (e.g. lymphoma, leukemia) or on immunosuppressive drugs (except cyclosporin, which is antiparasitic). Eradication of Strongyloides is essential before immunosuppressive therapy is commenced. Disseminated infection is always a serious complication with high mortality, usually affecting the bowel, lungs and central nervous system (CNS) and often accompanied by sepsis. Although strongyloidiasis is not a common opportunistic infection in AIDS, there is an increased frequency of larvae with HTLV-I infection, possibly due to suppression of the host IgE response.128

Diagnosis

The diagnosis is established by identification of larvae on stool microscopy, which is very reliable with acute diarrhea, but less reliable with chronic or asymptomatic infection, because rhabditiform larva excretion is irregular and the parasite load is often low. In this situation, a single stool examination may detect larvae in only 30% of cases of latent infections, although this can be increased to

50% with three stool specimens or various concentration techniques. There are a number of culture methods which are particularly useful if no larvae are found on stool microscopy in the face of clinical suspicion. The agar plate technique has a 96% sensitivity, which identifies larval tracks (Strongyloides larvae lash like a whip, whereas hookworm larvae move like a snake).41,129 In an immunocompromised child with suspected overwhelming infection, rapid diagnosis can be made from a duodenal aspirate, although larvae are abundant with hyperinfection so diagnosis is less difficult than with latent infection. S. fuelleborni infection can be diagnosed from abundant eggs shed in the feces.

Owing to the unreliability of stool microscopy and the importance of detecting even low levels of infection, various serological tests are available. An ELISA test for IgG is available, but there is still controversy about its reliability, because of its low specificity and positive predictive value.130,131 The main problems with antibody tests are differentiating current from past infection, cross-reactivity with other helminth infections and false negatives on presentation of acute diarrheal disease in children (when stool is more reliable). Improved diagnostic tests are being developed using more specific antigens and specialized techniques, which have better potential to detect a risk of hyperinfection with immunosuppressive therapy.129

Prevention

Disposal of human excreta, wearing of shoes, treatment of cases and improved hygiene reduce the risk of transmission of strongyloidiasis in communities. Regular mass chemotherapy programs against all geohelminths (e.g. albendazole) may have a modest impact on strongyloidiasis, but less than for the other helminths.

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