Clinicopathological Indications of Resilience of Swamp Buffaloes to Infection with Fasciola gigantica
Fasciolosis caused by Fasciola gigantica is a common disease among livestock such as swamp buffaloes (Bubalus bubalis) in rice-producing areas in humid tropical regions. It causes a significant reduction in meat and milk production, growth rate, fertility and draught power in infected animals (Dargie, 1987). However, the extent to which infection adversely affects the production of infected animals depends on several factors, among which is the breed of susceptible animals. Different breeds of animals and individuals within the same breed manifest varying responses and resilience to infection (Spithill et at., 1999). For instance, differences in response to infection with F. gigantica were seen in Bali, Ongole and buffalo calves in terms of weight gain (E. Wiedosari, personal communication, 1997). This information demonstrates breed differences in response to F. gigantica infection and shows that swamp buffaloes are more resilient than cattle to F. gigantica. The clinicopathological responses of swamp buffaloes naturally infected with F. gigantica were evaluated in this study to determine whether these parameters would indicate resilience to natural infection with parasites.
The impact on production and mechanisms of pathogenesis of trematode infections in cattle and sheep.
Abstract Trematodes can have marked effects on several components of individual animal productivity—particularly growth and wool production, but there is a need for better definition of their effects upon overall flock and herd productivity and of the economic benefits to be derived from their control by chemical, immunological and/or genetic approaches. The reasons for reduced productivity are complex and include reduced appetite coupled with a protein/energy drain arising from increased protein turnover, and in some cases derangements in gastrointestinal function and mineral metabolism are to be anticipated. Knowledge of the effects of trematodes on animal productivity and metabolism lags far behind that of gastrointestinal nematodes and while there is certainly a need for more study of the effects of trematodes per se , there is perhaps an even more pressing need for experimental and field work on mixed infections.
Erythrokinetics and albumin metabolism in primary experimental Schistosoma bovis infections in Zebu calves.
Red cell kinetics and albumin metabolism were studied in calves infected with either 100 or 200 Schistosoma bovis cercariae per kg body weight, by the use of 59Fe-labelled transferrin, 51Cr-labelled erythrocytes and 125I-labelled albumin; a third group of worm-free animals acted as controls. The anaemia which developed in the infected calves was shown to be due basically to an accelerated rate of red cell loss from the circulation, and became evident around the seventh week of infection, increased in severity during the following two months, and subsequently subsided. In view of its close similarity to the pattern of faecal egg excretion, it was concluded that haemorrhage into the intestine caused by the exit of eggs was the principal aetiological factor: haemolysis was excluded by the absence of both splenomegaly and hyperferraemia . Erythropoiesis was also accelerated in infected animals, but could not keep pace with the rate of red cell breakdown to which the animals were concurrently subjected. Haemodilution was involved, but not to a significant extent. The hypoalbuminaemia associated with infection was caused by an increased rate of albumin catabolism, and a plasma volume expansion, and was accompanied by marked depletion of all albumin pools, but particularly the extravascular pool. The pattern of albumin catabolism closely followed that of red cell loss, suggesting that passage of plasma as whole blood into the intestine was the basic cause of hypoalbuminaemia. Red cell losses and albumin hypercatabolism were more severe in the more heavily infected group, and although both subsided as egg counts fell, they remained evident even 1 year after infection. This may partly explain the failure of infected animals to regain the weight lost during earlier stages of disease.