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PubMed1981

Diagnosis of human strongyloidiasis by immunofluorescence, using Strongyloides ratti and S. stercoralis larvae.

The sensitivity and specificity of an indirect immunofluorescent antibody assay for the diagnosis of human strongyloidiasis has been investigated. Sera were obtained from 160 Australian ex-servicemen who had been prisoners-of-war in Southeast Asia during World War II, 44 of whom proven parasitologically to have strongyloidiasis; these men did not have concurrent infections with other helminths. In addition, sera were collected from 44 age- and sex-matched Australians who were not thought to have been exposed to S. stercoralis, and from 44 Filipino subjects. Antibodies were measured by using living filariform S. ratti larvae as the source of antigen. The assay was highly sensitive; antibodies were found at a titer of 1:4 or greater in 98% of men with strongyloidiasis and in 2% of Australian control subjects. Fifteen percent of exposed ex-servicemen in whom parasites had not been found had antibody titers of 1:4 or more, and it is thought that they had cryptic infections. Incubation of pooled positive sera with soluble S. ratti antigen produced a marked fall in antibody titer, but no changes were seen after incubation with soluble Ascaris suum or Dirofilaria immitis antigens. It is thought that this indicates that the test is specific and that the 84% of Filipinos with antibody titers of 1:4 or greater had unsuspected strongyloidiasis. When antibody titers against S. ratti were compared with those obtained using living filariform S. stercoralis larvae, a high correlation was found (r = 0.89, P less than 0.001). It is concluded that this assay provides a simple, safe, and specific method for the diagnosis of strongyloidiasis.

Adult↗
PubMed1993

Strongyloides stercoralis: an initial autoinfective burst amplifies primary infection.

Compartmental analysis of Strongloides stercoralis burdens in experimentally infected, serially necropsied dogs was used to test an autoinfective burst hypothesis. The hypothesis states that in well-established, active infections and in chronic infections as well, the rate of larval development is down-regulated so that most larvae do not attain infectivity internally. The majority pass in the feces as preinfective, rhabditiform larvae, but a few (those with the most rapid developmental rate) attain infectivity internally, and therefore are positioned for autoinfectivity. In contrast, in immunologically naive hosts, larval development proceeds without host hindrance and many larvae, proceeding at the most rapid rate of a spectrum of normal intrinsic developmental rates, attain infectivity internally. For a brief period, hyperinfection occurs, during which the adult worm population increases sharply. Gut-level resistance soon occurs, larval development is retarded, and an increasing proportion of larvae are discharged as preinfective rhabditiform larvae. With fewer larvae developing to infectivity internally, recruitment into the adult population decreases, with an attendant increase in the mean age and a gradual decrease in the size of the adult population. The data and the attendant model strongly support this autoinfective burst hypothesis.

Animals↗
PubMed1975

Community control of Strongyloides stercoralis by thiabendazole.

Mass treatment of a community in Costa Rica with thiabendazole in 1965 reduced the prevalence of S. sterocoralis from 19.2% to 0.3%, and the rates remained low 2 years thereafter. Re-examination of the treated population 7 years after initial treatment showed S. stercoralis prevalence still at a 0.5% level.

Animals↗