Bovine tuberculosis is a chronic disease of a zoonotic character that occurs in cattle and a wide range of domestic and wild animals. In this paper, bovine tuberculosis caused by M. caprae in six small household herds in Bosnia and Herzegovina was described. For the identifi cation of the disease and determination of the causative agent comparative tuberculin skin test (TST), pathomorphology, microbiology and molecular methods were applied. Twenty-eight cows from fi ve households from the Livno region (25/28 animals) and one household from the Vitez region (3/28 animals) were euthanized after being found positive by the comparative TST test. Eleven animals from fi ve households from the Livno region (9/11 animals) and one household from the Vitez region (2/11 animals) were subject to fi eld necropsy, and lesions consistent with tuberculosis were observed on the lymph nodes of the thoracic cavity and lungs in all carcasses. Histopathologic examination by hematoxylin and eosin staining confi rmed the presence of specifi c granulomatous lesions, while Ziehl- Neelsen staining demonstrated the presence of very few acid fast bacteria. Mediastinal lymph nodes from seven necropsied animals (two animals from the Vitez region and fi ve animals from fi ve fl ocks from the Livno region) were submitted for bacteriology. Acid fast bacteria from fi ve out of the seven submitted samples from one animal from the Vitez region and four animals from four households from the Livno region were isolated. All isolates were identifi ed as M. caprae. By MIRU typing we found two different M. caprae genotypes, unique to Bosnia and Herzegovina. Our fi ndings represent the fi rst evidence of bovine tuberculosis caused by M. caprae in Bosnia and Herzegovina.

The aim of the present study was to investigate the histopathological changes on the kidneys of the brown trout (Salmo trutta m. Fario) inflicted by per os lead poisoning in the 46-week experimental period. The fish were kept in well-oxygenated freshwater basins. Approximately calculated toxic doses of lead-acetate for fish were 550 mg/kg. Following the experimental period, fish organs, in particular kidneys, were examined by light microscopy. Only fish with lesions observed in kidneys were further examined by electron microscopy. An accumulation of proteinaceous material in the glomeruli of the kidneys, and thickening of the basal membrane were observed histopathologically. This proteinaceous material was also observed in the lumina of the kidney tubules. Electron microscopic examination completely supported this finding. Furthermore, to the authors' previous knowledge, undocumented damage of the brush borders of the proximal kidney tubules was also observed.

The aim of the study was to explore the effect of lactate on insulin-stimulated glucose uptake in rats. Thirty Wistar rats, weighing 250 - 300 g. were arbitrarily divided into one of three groups (n =10): insulin (1 IU/kg) treated group, lactate (80 mg/kg), and insulin plus lactate treated groups. Blood glucose levels were measured in venous samples collected from the tail vein over 3 hour period after insulin or/and lactate administration in 30-minute intervals. To estimate the influence of lactate on insulin blood level, a total of 20 rats were divided into 4 groups (n = 5): saline, insulin, lactate, and insulin plus lactate treated group, respectively. Sixty minutes after the appropriate application of the same doses of insulin, lactate, and lactate plus insulin, as in the previous part of the experiment, plasma insulin and blood glucose levels were determined in blood samples drawn from the abdominal aorta. Lactate in combination with insulin, in comparison to insulin application alone, caused a dramatic increase in plasma insulin level (p<0,001) and more profound hypoglicaemia (p<0,001). The results of this investigation indicate that lactate application significantly increases the rate of glucose uptake from peripheral blood caused by exogenous insulin action. The possible involvement of lactate in the mechanism of enhanced glucose uptake due to insulin action after physical exercise is discussed.