Babesia gibsoni is a tick-transmitted protozoan parasite of wild and domestic canids in Asia, Africa, Europe, the Middle East and North America. The most commonly observed clinical signs in naturally-infected dogs are anemia, pyrexia, anorexia, lethargy and splenomegaly. Experimental infections of B. gibsoni have provided valuable information about the prepatent period following tick-transmitted infection and the role of the spleen in controlling the severity of disease. Diagnosis of B. gibsoni infections is based on the examination of Romanowsky-stained, thin blood smears for intraerythrocytic parasites and/or serodiagnosis, most often using the indirect fluorescent antibody test. Various drugs have been employed to treat B. gibsoni infections, of which diminazene aceturate, phenamidine isethionate, pentamidine isethionate and parvaquone seemed to be most efficacious. Prevention and control of B. gibsoni infection is based on early diagnosis, effective treatment and adequate tick control.
Renal microsomal mixed function oxidase (MFO) system of mice was altered during Plasmodium yoelii nigeriensis infection. Cytochrome P450; cytochrome b5; aniline hydroxylase; aminopyrine-N-demethylase and benzo(a) pyrene hydroxylase were significantly decreased (65-85％) at peak parasitemia (> 60％), on the contrary, microsomal heme content depicted increase with rise in parasitemia (141-383%). Oral administration of pyrimethamine [10mg (kg.b.wt)-1 x 4 days] to infected mice resulted in complete removal of the parasites from the blood within 72 hours. Drug treatment of infected mice restored the altered levels of MFO indices to almost normal. However, elevated levels of heme remained unchanged even after a week of cessation of drug treatment. Pyrimethamine treatment did not affect the renal MFO system of normal mice.
Pyridoxal kinase is an essential enzyme for intracellular protein synthesis. It phosphorylates vitamin B6 to its active coenzyme, pyridoxal-5’-phosphate, which then plays a central role in transamination and other critical biochemical reactions. Since Afro-Americans have a high frequency of the low erythrocyte pyridoxal kinase activity, it has been postulated that this enzyme defect may afford protection against fatal malaria infections. The in vitro growth rates of P. falciparum parasites were measured in erythrocytes with high, low and intermediate PLK enzyme activity and no significant difference in parasite growth rates was observed. Erythrocytes with low PLK activity were capable of supporting normal in vitro growth and development of P. falciparum parasites. Even though, P. falciparum parasites lack PLK activity, their complete dependence on red cell enzyme activity has yet to be established.
Outbreaks of caecal coccidiosis in five batches of 2408 broiler birds in Bangladesh was investigated. An overall 41.4％ morbidity and 6.7％ mortality were recorded within 8 weeks of age. Eimeria tenella was identified as the etiologic agent based on the examination of oocysts morphology and gross lesions in the affected caeca. Clinical signs and necropsy findings encountered in these cases have been described and discussed in the light of available literature. Sulphaclozine sodium (Esb3, Ciba-Geigy) and sulphaquinoxaline (Embazin, Rhone-Poulenc) added to drinking water of broiler chicks during outbreaks of caecal coccidiosis reduced mortality rates, with Embazin being more effective (9.0％ to 0.9％) compared to Esb3 (5.7％ to 2.3％).
Two mouse babesioses, lethal Babesia rodhaini and non-lethal Babesia microti infections, were examined to determine if damage to kidneys and liver is correlated with the prognosis of these infections. All B. rodhaini-infected mice died after a sudden increase of parasitemia, severe hemolysis, and excretion of reddish hemoglobinuria. All B. microti-infected mice survived after a temporary moderate increase of parasitemia, moderate hemolysis, and execretion of greenish urine. B. rodhaini-infected mice showed immune complex-induced mesangiopathic glomerulonephropathy, moderate renal tubular necrosis, and extensive liver necrosis. In the glomerulonephropathy, electron microscopy showed electron-dense deposits in the mesangial matrix and along the glomerular basement membrane. Biochemical analysis of blood and urine from these mice confirmed renal damage in terms of increased BUN and of proteinuria that contained albumin and protein of more than 200kDa molecular weight, and hepatic damage in terms of an increase in serum direct bilirubin. B. macroti-infected mice had relatively mild immune complex-induced mesangiopathic glomerulonephropathy, mild renal tubular necrosis, and focal liver necrosis. BUN and serum direct bilirubin showed no increase, and proteinuria contained no detectable proteins of more than 200kDa. These data suggest that the severity of damage in the kidneys and liver is corrected with the prognosis of the two Babesia infections.