Death of an African elephant from probable toxemia attributed to chronic pulpitis

A 31-year-old captive male African elephant (Loxodonta africana) of 5,000-kg body weight died suddenly in ventral recumbency. Lesions seen at necropsy were bilateral purulent pulpitis and periodontitis of both tusks, serous atrophy of coronary groove fat, Grammocephalus cholangitis, myocardial and skeletal lipofuscinosis, and scattered segmental necrosis in the pectoral muscles. Nonhemolytic streptococci, Corynebacterium sp, Peptostreptococcus anaerobius, Fusobacterium nucleatum, and Bacteroides sp, were recovered from the exudate around one or both tusks. We postulated that the elephant died of hypoxia from prolonged ventral recumbency because of weakness and inability to rise secondary to toxemia from bilateral pulpitis and periodontitis.     

Nephrotoxicity of sodium arsenate in dogs

Nephrotoxicity of sodium arsenate was evaluated in dogs to determine the pathophysiologic basis for renal lesions caused by this heavy metal. Examination of biopsy specimens indicated that the low dose of the As salt (0.73 mg/kg of body weight) produced histologic changes consisting of mild degeneration and vacuolation of renal tubular epithelium. Vacuolation involved mainly the ascending thick portion of the nephron. Clinical pathologic changes were not demonstrable at this dosage level according to glomerular filtration rate (creatinine clearance), fractional reabsorption of sodium, potassium, and chloride; plasma osmolar and free water clearance; and urinalysis. The medium dose (7.33 mg/kg) resulted in alterations determined by urinalysis, but did not markedly affect other clinical pathologic measurements. Histopathologic changes were equal to or greater than those seen with the low dose. Tubular necrosis was observed in the cortical portion of the nephron and the ascending thick limb. The high dose (14.66 mg/kg) consistently produced marked changes in all parameters evaluated. Clinical pathologic alterations were compatible with acute tubular necrosis involving all segments of the nephron. Histologically, moderate glomerular sclerosis and severe tubular necrosis were observed. During recovery from the high dose of As, a gradual compensatory healing process was observed that was evident in all clinical pathologic parameters and was confirmed from sequential renal biopsy specimens.     

Naturally occurring lethal parvovirus infection of juvenile and young-adult rats

A lethal disease characterized by hemorrhage and necrosis of the brain, testes, and epididymides developed in young adult rats housed in specific pathogen free quarters. Morphological, virological, and serological investigations of the outbreak indicated that the probable causative agent was rat virus (Kilham), a common parvovirus of rats that usually induces persistent, asymptomatic infection in adult rats.     

Traumatic rupture of the bile duct in the dog: a report of seven cases

The paper describes the clinical signs, treatment and post-operative management of seven dogs with bile duct rupture, all of which recovered.     

Radiographic aspects of exercise-induced pulmonary hemorrhage in racing horses

Abnormal pulmonary radiopacities were identified in 13 racing horses in which a diagnosis of exercise-induced pulmonary hemorrhage (EIPH) had been confirmed. The lesions were in the caudal lung lobe in all horses; seven were on the right and three on the left, and the laterality for three could not be determined. In ten horses the opacities, which were large and peripherally located, obliterated the thoracophrenic angle. They merged with the silhouette of the diaphragm and had a circular or ovoid surface directed toward the hilum. The intensity of opacification of the consolidated areas varied, and they often were not sharply marginated. Dorsal displacement of the pulmonary arteries was noted in the region of the radiopacity in seven horses. Varying volumes of pleural effusion were observed in nine horses. Serial radiographic examinations were performed in seven horses. The pulmonary radiopacities cleared within ten days in two horses. In the remaining five horses, gradual resolution, characterized by a reduction in lesion size with improved margination, occurred during several months. The central region of the radiopaque lesion commonly had a patchy appearance, suggesting cavitation. Normal pulmonary vascular and interstitial markings were evident following complete resolution of these lesions. The cause of these abnormal pulmonary opacities has not been determined. Pathologic-radiologic correlations will be required to improve understanding of the pathophysiology of EIPH in the racing horse.