Strongyloidiasis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Synonyms and keywords: Strongyloides Infection
Overview
Epidemiology and Demographics
Tropical and subtropical areas, but cases also occur in temperate areas (including the South of the United States). More frequently found in rural areas, institutional settings, and lower socioeconomic groups. [1]
Pathophysiology & Etiology
The nematode (roundworm) Strongyloides stercoralis. Other Strongyloides include S. fülleborni, which infects chimpanzees and baboons and may produce limited infections in humans.
Life Cycle
The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist:
Free-living cycle: The rhabditiform larvae passed in the stool 1 can either molt twice and become infective filariform larvae (direct development) 6 or molt four times and become free living adult males and females 2 that mate and produce eggs 3 from which rhabditiform larvae hatch 4 . The latter in turn can either develop 5 into a new generation of free-living adults (as represented in 2), or into infective filariform larvae 6 . The filariform larvae penetrate the human host skin to initiate the parasitic cycle 6.
Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin 6 , and are transported to the lungs where they penetrate the alveolar spaces; they are carried through the bronchial tree to the pharynx, are swallowed and then reach the small intestine 7 . In the small intestine they molt twice and become adult female worms 8 The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs 9 , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool 1 (see "Free-living cycle" above), or can cause autoinfection 10 . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may follow the previously described route, being carried successively to the lungs, the bronchial tree, the pharynx, and the small intestine where they mature into adults; or they may disseminate widely in the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in Strongyloides stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals.[2]
Diagnosis
Symptoms
Pulmonary symptoms (including Loeffler’s syndrome) can occur during pulmonary migration of the filariform larvae. Dermatologic manifestations include urticarial rashes in the buttocks and waist areas. Disseminated strongyloidiasis occurs in immunosuppressed patients, can present with Abdominal Pain, Distension, shock, pulmonary and neurologic complications and septicemia, and is potentially fatal.
Laboratory Findings
Eosinophilia
Blood eosinophilia is generally present during the acute and chronic stages, but may be absent with dissemination.[3]
Stool Smaples
Diagnosis
Diagnosis rests on the microscopic identification of larvae (rhabditiform and occasionally filariform) in the stool or duodenal fluid. Examination of serial samples may be necessary, and not always sufficient, because stool examination is relatively insensitive.
The stool can be examined in wet mounts:
- directly
- after concentration (formalin-ethyl acetate)
- after recovery of the larvae by the Baermann funnel technique
- after culture by the Harada-Mori filter paper technique
- after culture in agar plates
The duodenal fluid can be examined using techniques such as the Enterotest string or duodenal aspiration. Larvae may be detected in sputum from patients with disseminated strongyloidiasis.
Rhabditiform larvae of Strongyloides stercoralis in wet mounts after fixation in formalin 10%. Diagnostic characteristics: length 200 to 250 µm (up to 380 µm); buccal cavity short, and prominent genital primordium.
A: The prominent genital primordium in the mid-section of the larva (black arrow) is readily evident. Note also the Entamoeba coli cyst (white arrow) near the posterior end of the larva.
Antibody Detection
Immunodiagnostic tests for strongyloidiasis are indicated when the infection is suspected and the organism cannot be demonstrated by duodenal aspiration, string tests, or by repeated examinations of stool. Antibody detection tests should use antigens derived from Strongyloides stercoralis filariform larvae for the highest sensitivity and specificity. Although indirect fluorescent antibody (IFA) and indirect hemagglutination (IHA) tests have been used, enzyme immunoassay (EIA) is currently recommended because of its greater sensitivity (90%). Immunocompromised persons with disseminated strongyloidiasis usually have detectable IgG antibodies despite their immunodepression. Cross-reactions in patients with filariasis and some other nematode infections may occur. Antibody test results cannot be used to differentiate between past and current infection. A positive test warrants continuing efforts to establish a parasitological diagnosis followed by antihelminthic treatment. Serologic monitoring may be useful in the follow-up of immunocompetent treated patients: antibody levels decrease markedly within 6 months after successful chemotherapy. [4]
Treatment
Pharmacotherapy
The drug of choice for the treatment of uncomplicated strongyloidiasis is ivermectin with albendazole as the alternative. All patients who are at risk of disseminated strongyloidiasis should be treated. (Albendazole is approved by the FDA, but considered investigational for this purpose).[5]