Studies on the effect of variations in ambient temperature on pathogenicity and on host immune response in trypanosome infections

LeonardOtieno; (1972) Studies on the effect of variations in ambient temperature on pathogenicity and on host immune response in trypanosome infections. PhD thesis, London School of Hygiene & Tropical Medicine. DOI: 10.17037/PUBS.00682435
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Studies on the effects of ambient temperature on the course of salivarian trypanosome infections in mice showed that the mortality of infected animals was influenced by the environments in which they were maintained. Virulent strains of T. (N. ) congolense and T. (T .) brucei caused mild and chronic infections when infected animals were maintained at high (35°C) ambient temperature; T. (D. ) vivax and T. (T. ) evansi inoculated mice either failed to become parasitaemic or developed transient infections at this temperature. Infections became rapidly fatal when T. (T.) brucei infected mice were transferred from 35°C to normal room temperature (22-27°C). Mice kept at the high ambient temperature had significantly higher (39.3°C) mean body temperature than (37.5°C) mice kept at room temperature. They suffered a big weight loss and their spleen weights were comparatively much smaller than mice kept at 22-27°C. Monomorphic strains of T. (N. ) congolense and T. (T ) brucei became pleomorphic when inoculated mice were maintained at 35°C. At this temperature, the infectivity of T. (T. ) brucei was not altered, it reacquired its capability to produce variants and was able to develop in salivary glands of Glossina. It became highly pleomorphic when inoculated into chick embryos incubated at 39 °C but not at 37°C. The morphological changes were thought to be a direct heat effect on the trypanosome organisms. Attempts to find tissue phase of T. (T. ) brucei and T.(T. ) evansi during chronic infections in mice kept at high ambient temperature was unsuccessful, neither was there any evidence that these species could develop in mouse peritoneal macrophages. The presence of released antigens in T. (T. ) brucei infected mouse serum was demonstrated only at certain parasitaemic level Anti log 8 trypanosomes/ml). Infected serum obtained from mice ( kept at 35°C was less immunogenic than that obtained from parasitaemic mice kept at room temperature. Many bizarre forms of T. (T. ) brucei appeared when infected mice kept at 35°C had previously been immunosuppressed (x-irradiated or cyclophosphamide treated). These mice had very high parasitaemias. However, treatment with Betamethasone or anti-lymphocyte serum failed to produce the same effect. Fewer antibody producing cells was observed in mice kept at 35 °C than in those kept at control conditions. It is suggested that the enhanced resistance to trypanosome infections observed in mice kept at 35°C is due to direct effect of temperature on trypanosomes.



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