Acute hepatotoxicity with resultant pulmonary and cerebral embolism in guinea pigs given tunicamycin.

The hepatotoxicity of tunicamycin was studied in 8 to 10-week-old guinea pigs. Acute hepatic damage was produced consistently in guinea pigs given a single dose of 400 micrograms/kg of tunicamycin and observed at intervals up to 72 h post-injection. Significant elevations occurred in serum levels of liver enzymes and ammonia, while concentrations of serum proteins were lowered.

Pathological and pathogenetic changes in the central nervous system of guinea pigs given tunicamycin.

Guinea pigs were injected with tunicamycin and the sequential morphological alterations in the brain examined to investigate further the pathogenesis of cerebral lesions in this experimental model of annual ryegrass toxicity, a central nervous system disease of livestock caused by members of the tunicamycin group of antibiotics. Brain damage was most commonly observed in the cerebellum, and the important alterations in the development of degenerative parenchymal lesions appeared to be largely referrable to changes in small blood vessels. Endothelial damage, with increased vascular permeability, resulted in capillary obstruction leading to localised ischaemia and hypoxic neuronal damage.

Focal spongy changes in the central nervous system of sheep and cattle.

A focal form of vacuolation in the white matter of the thalamus of 13 sheep and 2 cattle is described. The individual vacuoles were similar in appearance to those reported in other forms of spongy degeneration, but they were differentiated by their consistent neuroanatomical localization in the thalamic radiation of all 15 animals. Thirteen of these were sheep used in toxicity experiments and 11 had shown signs of convulsive activity.

Ultrastructural changes in cerebral blood vessels of sheep injected with tunicamycin.

Changes resembling those of annual ryegrass toxicity were produced in sheep by the subcutaneous injection of tunicamycin and the cerebellum was examined by electron microscopy. The results suggested vascular endothelial damage as the basis for the cerebral lesions in this condition.

Ultrastructural changes in the cerebellum of nursling rats given corynetoxin, the aetiological agent of annual ryegrass toxicity.

Nursling rats were given a lethal dose of corynetoxin and the sequential morphological alterations in the cerebellum were examined at daily intervals up to 3 days post-inoculation. Ultrastructural changes were those of cerebral vascular damage, which was usually focal in affected endothelial cells, and resulted in vascular stasis or thrombosis. These changes ultimately constituted a failure of perfusion in focal areas of brain parenchyma supplied by these vessels, resulting in necrosis.

Ultrastructural changes in the brain of mice given Clostridium perfringens type D epsilon toxin.

Mice were given lethal and sublethal doses of Clostridium perfringens Type D epsilon toxin and the early morphological changes in perfusion-fixed intoxicated brains were examined from 30 min to 6 h post-inoculation. The initial ultrastructural finding was swelling of astrocytes, especially the perivascular extensions of these cells. Astrocytes in the cerebellum appeared to be particularly sensitive to this toxin.

Histopathological changes in the brain of mice given Clostridium perfringens type D epsilon toxin.

The distribution, severity and frequency of brain lesions produced in mice by the administration of Clostridium perfringens Type D epsilon toxin were examined by light microscopy. The granular layer of the cerebellum was the area most frequently affected in mice given single doses of toxin. Sequential changes in brain morphology were examined from 1 h to 7 days after injection of toxin.

The effect of decomplementation on the infectious course of Sendai virus in mice.

The course of intranasal infection of Sendai virus in CBA and DBA mice was investigated in animals decomplemented with purified cobra venom factor. The mice were decomplemented either immediately before inoculation or at 4 days postinfection. Depletion of complement after the infection had been established had no apparent effect on the course of the viral infection in the two strains of mice.

Acute and chronic canine parvovirus myocarditis following intrauterine inoculation.

Canine myocarditis virus was inoculated into puppies in utero 8 days before parturition. Puppies were clinically normal at birth. One puppy died 23 days after inoculation and a second puppy was comatose before euthanasia on day 27 post inoculation.

Oil folliculitis. A study of 200 men employed in an engineering factory.

Occupational skin disease is a problem of major importance in the engineering industry. Little is known about the occupational distribution of oil folliculitis and its varying degrees of severity. This investigation was undertaken in an attempt to discover which occupations are at risk and why.