Abortion and neonatal mortality in sheep poisoned with Tetrapterys multiglandulosa.

Tetrapterys spp. have been reported as a cause of cardiac fibrosis, status spongiosus of the nervous system, and abortion. To study the intoxication by Tetrapterys multiglandulosa, 24 sheep were divided into 4 experimental groups of 4 sheep each and 1 control group. Groups 1 to 3, respectively, received 1, 1.5, and 3 g/kg body weight of the dry plant daily, starting on the 90th day of pregnancy. Group 4 received 1.5 g/kg from the 120th day of pregnancy to the end of gestation. All sheep from groups 2 and 3, except 1 that was submitted to cesarean delivery, aborted between 110 and 134 days of pregnancy. Seven fetuses had anasarca. Seven lambs from groups 1 and 4 were weak and died or were euthanatized. The other 2 were born weak with mild nervous signs but recovered. Cardiac fibrosis and status spongiosus of the nervous system were observed in newborn lambs and fetuses.

Seasonal allergic dermatitis in sheep in southern Brazil caused by Culicoides insignis (Diptera: Ceratopogonidae).

The incidence of seasonal dermatitis was studied in a Hampshire Down flock on a farm in southern Brazil. Epidemiological data, clinical signs and macroscopic pathology were obtained by visiting the farm. Histological lesions were studied in skin biopsies of affected sheep. Biting insects were collected from January to April 2005 in an attempt to identify the etiological agent of the disease. Disease prevalence was 40%; the age of the affected animals was variable. Disease occurred from December to March, some animals had lesions for the entire year. Clinical signs include pruritus on the ears, around the eyes and ventral abdomen. Initially erythema and small red papules were seen, followed by alopecia and crust formation. Histologically the lesions were characterized by perivascular eosinophilic dermatitis. Hyperkeratosis and acanthosis were observed in the chronic lesions. Both Anopheles albitarsis and Culicoides insignis were captured during the study. C. insignis bites caused pruritus in sheep. Both types of insects were caught when they approached the sheep baits approximately 30min after sunset. Results suggested that the disease occurred as a result of an immediate hypersensitivity reaction to C. insignis.

Ethidium bromide-induced demyelination of the sciatic nerve of adult Wistar rats.

Peripheral nerve ultrastructure was assessed after single or multiple local injections of the intercalating dye ethidium bromide. Thirty-four adult Wistar rats of both sexes were divided into five groups and maintained in a controlled environment with rat chow and water ad libitum throughout the experiment. The experimental animals were injected with 1 microl of 0.1% ethidium bromide in 0.9% saline into the central third of the left sciatic nerve 1 (group 1), 2 (group 2), 4 (group 3), 6 (group 4) or 8 (group 5) times. In groups 2 to 5 the injections were made at 28-day intervals. Control animals received the same amount of 0.9% saline. The animals were killed at different times after injection: group 1 at 7 days (2 rats) and 15 days (2 rats); for groups 2, 3, 4 and 5, all rats were killed 10 days after the last injection and the lesions were investigated by light and transmission electron microscopy. In the acute lesions, intoxicated Schwann cells showed a vacuolated cytoplasm and separation of the sheaths from the axon. Myelin sheaths underwent progressive vesiculation and subsequent segmental demyelination. Myelin debris were withdrawn by macrophages and remyelination by Schwann cells was prominent. With the increase in the number of injections collagen fibers also increased in number and progressively enveloped smaller numbers of remyelinated axons composing new fascicles. Wallerian degeneration of fibers apparently not affected by ethidium bromide was more intense in the nerves from groups 4 and 5. The peripheral nerve repairs itself after demyelinating challenges with a profusion of collagen fibers and new fasciculations. This experimental model is valid to mimic recurrent demyelinating neuropathies.

Periacinar liver fibrosis caused by Tephrosia cinerea in sheep.

Tephrosia cinerea has been associated with ascites and liver fibrosis in sheep in Brazil. The dried plant was fed ad libitum to three sheep for 55-80 days. Three additional sheep were used as controls. All the treated sheep presented with hypoalbuminemia and increased γ-glutamyltransferase and aspartate aminotransferase activities. Anorexia, apathy, rough coat, ascites, and emaciation were observed after 45-60 days of feeding with T. cinerea. At necropsy 55-80 days after feeding of the plant commenced, the treated sheep had ascites, hydrothorax and hydropericardium, and their livers were firm and whitish, with a nodular surface. Histologically, the main hepatic lesions were periacinar fibrosis associated with hemorrhages and necrosis. On electron microscopy, a severe swelling of sinusoidal endothelial cells, frequently obstructing the lumen of the sinusoid was observed. The space of Disse was compressed by the swollen endothelial cells and microvilli usually present on the surface of hepatocytes adjacent to the space of Disse were not apparent. Dense bundles of collagen fibers were present in the spaces of Disse and within the sinusoids between profiles of swollen endothelial cells. It is concluded that T. cinerea causes periacinar fibrosis, similar to poisoning by Galenia africana in sheep and goats and veno-occlusive disease in different species.

Ocorrência de neoplasias em cães e gatos da mesorregião metropolitana de Belém, PA entre 2005 e 2010 / Occurrence of neoplasms in canine and feline from the Metropolitan Mesoregion of Belém, PA from 2005 to 2010

Data on the occurrence of cancers in dogs and cats from the Metropolitan Mesoregion of Belém are not available in the literature. This paper describes the occurrence of neoplasms in these species from 2005 to 2010. The canine cutaneous system was the most affected in this study (47 percent), followed by the mammary gland (39 percent), reproductive system (4 percent), oral cavity (4 percent), bones and joints (2 percent), ocular system (1.5 percent), digestive system (1.5 percent) and urinary tract (1 percent). In feline species, the mammary gland accounted for 87.8 percent, followed by the cutaneous system (6 percent), respiratory system (3 percent) and oral cavity (3 percent).

Ethidium bromide-induced demyelination of the sciatic nerve of adult Wistar rats

Peripheral nerve ultrastructure was assessed after single or multiple local injections of the intercalating dye ethidium bromide. Thirty-four adult Wistar rats of both sexes were divided into five groups and maintained in a controlled environment with rat chow and water ad libitum throughout the experiment. The experimental animals were injected with 1 æl of 0.1 percent ethidium bromide in 0.9 percent saline into the central third of the left sciatic nerve 1 (group 1), 2 (group 2), 4 (group 3), 6 (group 4) or 8 (group 5) times. In groups 2 to 5 the injections were made at 28-day intervals. Control animals received the same amount of 0.9 percent saline. The animals were killed at different times after injection: group 1 at 7 days (2 rats) and 15 days (2 rats); for groups 2, 3, 4 and 5, all rats were killed 10 days after the last injection and the lesions were investigated by light and transmission electron microscopy. In the acute lesions, intoxicated Schwann cells showed a vacuolated cytoplasm and separation of the sheaths from the axon. Myelin sheaths underwent progressive vesiculation and subsequent segmental demyelination. Myelin debris were withdrawn by macrophages and remyelination by Schwann cells was prominent. With the increase in the number of injections collagen fibers also increased in number and progressively enveloped smaller numbers of remyelinated axons composing new fascicles. Wallerian degeneration of fibers apparently not affected by ethidium bromide was more intense in the nerves from groups 4 and 5. The peripheral nerve repairs itself after demyelinating challenges with a profusion of collagen fibers and new fasciculations. This experimental model is valid to mimic recurrent demyelinating neuropathies