Environmental predictors of bovine Eimeria infection in western Kenya.

Eimeriosis is caused by a protozoan infection affecting most domestic animal species. Outbreaks in cattle are associated with various environmental factors in temperate climates but limited work has been done in tropical settings. The objective of this work was to determine the prevalence and environmental factors associated with bovine Eimeria spp. infection in a mixed farming area of western Kenya. A total of 983 cattle were sampled from 226 cattle-keeping households. Faecal samples were collected directly from the rectum via digital extraction and analysed for the presence of Eimeria spp. infection using the MacMaster technique. Individual and household level predictors of infection were explored using mixed effects logistic regression. The prevalence of individual animal Eimeria infection was 32.8% (95% CI 29.9-35.9). A positive linear relationship was found between risk of Eimeria infection and increasing temperature (OR = 1.4, 95% CI 1.06-1.86) and distance to areas at risk of flooding (OR = 1.49, 95% CI 1.17-1.91). There was weak evidence of non-linear relationship between Eimeria infection and the proportion of the area around a household that was classified as swamp (OR = 1.12, 95% CI 0.87-1.44; OR (quadratic term) = 0.85, 95% CI 0.73-1.00), and the sand content of the soil (OR = 1.18, 95% CI 0.91-1.53; OR (quadratic term) = 1.1, 95% CI 0.99-1.23). The risk of animal Eimeria spp. infection is influenced by a number of climatic and soil-associated conditions.

Attempted infection of calves with Taenia crocutae cysticerci and their subsequent serological response.

The susceptibility of naive cattle to infection with cysticerci of Taenia crocutae was tested using three six- to nine-month-old Ayrshire bull calves, previously unexposed to infection with taeniid eggs. One calf was given 10,000 T crocutae eggs orally, another 5000 hatched unactivated oncospheres orally and the third 5000 hatched and activated oncospheres by intravenous injection. None of the calves contained viable cysticerci at post mortem examination 15 to 17 weeks later. All three calves contained small numbers of lesions in the liver and lesions were also present in the lungs of the calf which received oncospheres intravenously. All the calves developed an antibody response which was most pronounced in the calf given hatched unactivated oncospheres orally.

Peri-portal fibrosis of the liver due to natural or experimental infection with Schistosoma mansoni occurs in the Kenyan baboon.

The chronic granulomatous inflammation that occurs during schistosomiasis mansoni and its reparative healing lead to hepatic fibrosis, with subsequent portal hypertension (a life-threatening sequela). In the murine model, granuloma modulation invariably leads to formation of fibrous tissue and disposition of extracellular matrix. Typically, < 10% of patients infected with Schistosoma mansoni progress to clay-pipe-stem fibrosis. Similar fibrosis occurs in chimpanzees during experimental infections. Although previous studies of schistosomiasis mansoni in Kenyan baboons have failed to demonstrate appreciable liver fibrosis, classical peri-portal fibrosis has now been observed in the livers of three yellow baboons (Papio cynocephalus cynocephalus) with natural S. mansoni infections and three olive baboons (P. c. anubis) with experimental infections after each was challenged with 1000 S mansoni cercariae. The peri-portal fibrosis was indicated by marked fibroblast accumulation, increased collagen deposition, bile-duct hyperplasia and blood-vessel proliferation. The lesions were more severe in the naturally infected baboons than in those experimentally infected. No accompanying portal hypertension, ascites or portocaval anastomosis was noted in any of the animals. The development of the baboon as a model for chronic human schistosomiasis mansoni may be feasible.