Epizootiology, pathology, and microbiology of an outbreak of urolithiasis in chickens

An outbreak of urolithiasis that doubled the annual mortality rate of chickens in a large flock of table-egg-layers is described. Despite the presence of a large unilateral urolith and/or severe renal atrophy, the layers often maintained active egg production and apparent homeostasis until a small urolith blocked the ureteral flow from the contralateral kidney. This terminal episode appeared to produce acute obstructive renal failure, rapidly developing visceral gout (visceral urate deposition), uremia, and death. The atrophy observed appeared to be acquired and progressive. Histologic features in the kidneys were acute to chronic glomerulonephritis, interstitial nephritis, and pyelonephritis. Epizootiologic and microbiologic studies indicated that a combination of infectious and noninfectious mechanisms may have been involved. Causative roles for calcium-phosphate imbalance, infectious bronchitis (IB), Newcastle disease (ND), and adenovirus or reovirus infections could be neither excluded nor confirmed. Contributory factors may have been spray ND-IB and other vaccinations of 15-week-old ND-IB-susceptible pullets, water deprivation, shipping stress, Mycoplasma synoviae infection, immune complex disease, and mycotoxins.     

Clostridial myositis in cattle: bacteriology and gross pathology.

In a bacteriological study of 173 cases of clostridial myositis in cattle, Cl chauvoei either alone or with Cl septicum was demonstrated in 97 (56 %)min a further 62 (36%) cases Cl novyi was demonstrated either alone or with Cl septicum. On 11 (6%) occasions Cl septicum only was recovered, and on another three 1-7%) Cl sordelli only. The gross pathology of the lesions was correlated with the bacteriological findings, and prophylaxis in relation to the infections identified is discussed.     

Further studies of the clinical pathology of sweating sickness in cattle

Experimentally-induced cases of sweating sickness in calves were used in an effort to correlate the blood chemistry with some of the known pathological changes. Results showed that the "sweating" associated with necrotic dermatitis did not alter blood electrolyte levels. Laboratory evidence of a disseminated intravascular coagulopathy was found which correlated with the microthrombi described in cases of sweating sickness. A high blood cortisol level was found in one of the animals that died from the disease and could possibly be used as a prognostic indicator in clinical cases. Recommendations are made with regard to the supportive treatment based on the clinical pathological findings.     

The pathology of acute Nolletia gariepina poisoning of cattle

Toxicity in cattle by the shrub Nolletia gariepina was induced experimentally by intraruminal administration of 3 g/kg dried, milled plant material as a single dose. The animals had to be starved for 24 hours before dosing, as dosing on a full rumen did not induce any signs of toxicity during 5 days of observation and clinical pathology monitoring. Clinical signs were not specific and varied according to the duration (acute versus subacute) of the toxicological process. Clinical pathological parameters indicated renal and to a lesser extent hepatic damage, with raised serum concentrations of urea, creatinine, aspartate aminotransferase (AST) and gamma glutamyl transferase (GGT). Increased urinary sodium and potassium concentration and GGT activity, as well as proteinuria, were evident. Histological and electron microscopic examinations revealed acute renal tubular epithelial cell degeneration and necrosis, especially of the proximal convoluted tubules. Mild hepatocellular degeneration was also noticeable.     

The pathology of Cestrum laevigatum (Schlechtd.) poisoning in cattle

The clinical features and pathological findings of 6 steers drenched with dried plant material of Cestrum laevigatum are described. Doses ranging from 0.5 to 10 g/kg/day were given intraruminally for 1 to 38 days. Animals that received 5 to 10 g/kg/day showed nervous signs including ataxia, muscle tremors, hypersensitivity and intermittent chewing. Clinical signs in the steers which received 0,5 to 4 g/kg/day were mild. High doses induced moderate to severe hepatosis characterized by centrilobular to midzonal coagulative necrosis, haemorrhage and congestion. At lower rates only mild hepatic lesions, characterized by disappearance of hepatocytes and collapse of the reticulin stroma in the centrilobular areas were evident. Ultrastructural changes were primarily limited to the hepatocytes and comprised degeneration, necrosis and fatty change. Degeneration and necrosis of endothelial cells and disruption of sinusoidal walls were occasionally observed.     

Early migration of immature Fasciola hepatica and associated liver pathology in cattle

Immature Fasciola hepatica were successfully recovered from the body cavity of cattle from two to 21 days after oral infection. Flukes had penetrated the liver in large numbers by day 7 but there did not appear to be a corresponding reduction in the numbers recovered from the body cavity. Liver pathology showed a typical progressive tissue disruption with a neutrophil and lymphocyte infiltration by day 7 and a marked eosinophil response from day 14. The mesothelium of the liver capsule underwent metaplasia, becoming ultimately highly active and columnar.