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Parasitology,
1981]
The effects of prednisolone were investigated in C57Bl/6 mice infected with Strongyloides ratti. In primary infections, the numbers of adult worms in the small intestine and larvae in the stools were increased and there was a slight delay in the spontaneous expulsion of worms. In secondary infections, there was an initial suppression of acquired resistance, with larvae appearing normally in the stools on the 5th day after infection. This was followed, however, by a rapid development of resistance and expulsion of worms over the next few days. Prednisolone treatment did not alter fecundity in primary or secondary infections. There was no evidence of autoinfection in control or corticosteroid-treated animals. Prednisolone abrogated innate resistance to infection in C3H mice. It is concluded that prednisolone probably facilitated infection by non-specific mechanisms as well as by suppressing specific acquired immunity.
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[
Am J Trop Med Hyg,
1978]
A study was undertaken to define the sensitivity and specificity of serological tests in bancroftian and malayan filariasis and correlate the findings with clinical disease. Sera were collected from subjects on three different islands in the Philippines: one endemic for bancroftian filariasis, another endemic for malayan filariasis and the third without endemic filariasis. Antibodies were measured, using rugia malayi as the source of antigen. Antibodies against adult worms measured by indirect immunofluorescence were found at a titer of 1:8 or greater in all patients with bancroftian or malayan filariasis but not in the control subjects. There was no relationship of antibody titer to clinical status. Antibodies against microfilariae were measured by indirect immunofluorescence and microfilarial agglutination. A high correlation was observed between the two methods. These antibodies were found in only one quarter, approximately, of patients with filariasis. Microfilarial antibodies were found more commonly in those patients with chronic lymphatic obstruction. It is concluded that measurement of antibodies to adult worms is a useful indicator of infection while microfilarial antibodies are correlated with disease.
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Rev Infect Dis
]
At least 250 million people throughout the world are infected with filariae, and the number of such persons is increasing. Three species infect humans: Wuchereria bancrofti, Brugia malayi, and Brugia timori. The peak of microfilarial density in the blood usually occurs nocturnally. Transmission of filariasis is remarkably inefficient. In an endemic area, approximately 100,000 mosquito bites yearly are required for production of each new case of microfilaremia. Only a small proportion of those infected suffer any ill effects from these worms. Clinical filariasis can present with acute inflammation such as lymphangitis and lymphadenitis and with chronic lymphatic obstruction such as hydrocele and lymphedema of the limbs. Measures available for potential control include the widespread usage of mosquito nets, vector control, and chemotherapy with diethylcarbamazine. Unfortunately, the efficacy of the first of these is untested and the latter two are inadequate. More research is required on vector control, assessment of new drugs, and the development of vaccines.
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Ann Trop Med Parasitol,
1983]
The efficacy of the avermectin compound 22, 23-dihydroavermectin B1 against murine strongyloidiasis has been examined. A daily dose of 4 micrograms (200 micrograms kg-1) totally suppressed excretion of Strongyloides ratti larvae in the faeces. A similar marked suppression was seen when 10 micrograms (500 micrograms kg-1) of the drug was given on two days during the phase of larval migration or during the intestinal phase. Avermectin did not affect larval numbers in the skin but reduced larval numbers in the lungs by 91%. Administration of avermectin during the phase of larval migration completely prevented the subsequent appearance of adult worms in the gut. A single dose of 50 micrograms (2.5 mg kg-1) eradicated intestinal adult worms. Some variability was noted in dose-response studies, but the drug was very potent and a dose of 50 micrograms (2.5 mg kg-1) always eradicated the worms. Avermectin greatly reduced the numbers of S. stercoralis larvae in the muscles, whether it was given early or late in the infection. Eradication of S. stercoralis larvae from muscle followed a single dose of 100 micrograms (5 mg kg-1). It is concluded that this avermectin could be valuable in the treatment of human strongyloidiasis.
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Am J Trop Med Hyg,
1982]
The effects of benzimidazole anthelmintics in murine strongyloidiasis were examined. Thiabendazole 50 mg/kg daily produced a 91% reduction in the numbers of Strongyloides ratti larvae in the feces. A similar suppression was seen when thiabendazole was given during the intestinal phase, but no effect was noted when the drug was administered during the phase of larval migration. Thiabendazole had no effect on larvae in the skin or lungs, did not inhibit maturation of worms, and did not expel adult worms from the gut, but did reduce fecundity of adult worms in the intestines by 84%. Mebendazole and cambendazole 50 mg/kg daily totally suppressed excretion of S. ratti in the feces. A similar suppression was seen when the two drugs were given during the phase of larval migration or during the intestinal phase. They had no effect on larvae in the skin, and the reduction in larval numbers in the lungs was not statistically significant. When given during the migratory phase and early intestinal phase, they reduced the numbers of fourth stage larvae recovered from the gut by 95%. Mebendazole and cambendazole totally eliminated intestinal adult worms. Dose response studies indicated that in terms of orally administered dose, cambendazole was 100-1,000 times more active than mebendazole. Thiabendazole and mebendazole had no significant effect on S. stercoralis larvae in the muscles. In contrast, cambendazole 50 mg/kg daily for 4 days eradicated S. stercoralis larvae from the muscles. It is concluded that cambendazole may have significant advantages over both thiabendazole and mebendazole in the treatment of strongyloidiasis.
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J Parasitol,
1987]
Previous indications using radiolabelled larvae that Strongyloides ratti free-living infective larvae lose a surface coat during penetration of the skin were further investigated by transmission electron microscopy of the cuticle of S. ratti infective larvae in the free-living stage, after penetration of mouse skin, and after migration to the lungs. These studies demonstrated the presence of a faint electron-dense surface coat external to the epicuticle on free-living worms which was absent from larvae recovered from the skin and lungs. When free-living infective larvae were incubated in 10% CO2 at 37 C and then examined with phase-contrast microscopy, worms were observed in the process of losing this coat. These observations confirm the hypothesis that S. ratti infective larvae lose a surface coat during penetration of the skin.
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Am J Trop Med Hyg,
1977]
Saline antigen extracts of microfilariae, adult worms and third-stage larvae of subperiodic Brugia malayi maintained in gerbils were prepared for use as skin test reagents. Patients were studied on three different islands in the Philippines, one endemic for Bancroftian filariasis (Sorsogon, Luzon), another endemic for Malayan filariasis (Palawan) and the third without endemic filariasis (Cebu). A dose-response curve was established initially in patients with Bancroftian filariasis: thereafter 1.0 microng of the B. malayi antigens and 0.05 microng of Dirofilaria immitis FST antigen (obtained from Dr. T. Sawada) were used. Sizes of reactions were measured by recording the diameters of wheals at 20 minutes, 24 and 48 hours. There was a very high correlation in immediate hypersensitivity reactions among the three B. malayi antigens. Reaction sizes followed a normal distribution. When an area of an antigen-induced wheal 3 X that of the saline control was considered a positive reaction, 99% of 150 patients with Bancroftian filariasis and 96% of 45 subjects with Malayan filariasis reacted to B. malayi larval antigen. Only 68% of patients with Bancroftian filariasis but 90% of those with Malayan filariasis reacted to D. immitis FST antigen. There was no relationship between skin reactivity and age, sex, microfilaremia or severity of clinical disease. Approximately half of 50 patients who lived in an endemic area for W. bancrofti but had neither patent infection nor clinical disease reacted to B. malayi antigens. A maximum of 7% of 120 age- and sex-matched controls from Cebu gave false positive reactions with any of the antigens. Only a small proportion of patients gave 24- and 48-hour reactions. It is concluded that the use of antigens prepared from a human parasite, subperiodic B. malayi, which is easily maintained in a laboratory animal host, improves the ability to diagnose filarial infections by immunological means.
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Aust J Exp Biol Med Sci,
1985]
When Strongyloides ratti free-living infective larvae were incubated with peritoneal exudate cells from normal or previously infected mice, cell attachment occurred only in the presence of normal (NMS) or immune mouse serum (IMS). This non-specific effect was transitory with larvae being alive and free of cells 24 h after incubation. Cell attachment was mediated by complement. When incubated with infective larvae which had penetrated mouse skin, both normal and immune cells attached to larvae in the absence of serum. This effect was again transitory except when immune cells or immune serum were present, indicating a specific immunological mechanism. Again, larvae remained viable. When incubated with isolated parasitic adult worms, persistent cell attachment occurred in the presence of immune serum, immune cells or both, but all worms remained viable. This system provides a means for investigating the mechanisms of resistance to reinfection in strongyloidiasis.
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Parasite Immunol,
1988]
Mice were infected once, twice or many times with Strongyloides ratti infective larvae, and the parasite was allowed to complete its development. Other mice were infected many times with either infective larvae only, by aborting the infection with cambendazole, or with adult worms transferred by intra-oesophageal intubation. Sera from these animals were analysed by immunoblotting against SDS-PAGE separations of larval and adult worm water-soluble, deoxycholate-soluble, sodium dodecyl sulphate-soluble and excretory/secretory antigens. Minimal antibody responses were observed after primary and secondary infections. Mice exposed to multiple complete infections reacted strongly to both larval and adult antigens but greater responses were observed against the larval preparations. Stage-specific effects were noted in mice infected with larvae only or adult worms only. Mice exposed only to larvae reacted with larval antigens and to a minor degree to somatic adult worm antigens while those mice which were exposed only to adult worms failed to react with any of the antigen preparations. Some cross-reactions were found, however, as mice infected only with larvae displayed strong reactions against both larval and adult excretory/secretory products. These data demonstrate differences in sero-reactivity to infective larvae and adult worms and suggest that humoral immunity is induced by larvae migrating through the tissues and not by adult worms in the gut.