Rio-Grandense (1965-2004. Other disorders, including multifactorial or idiopathic diseases contributed 80 (1.6%) cases. In 1,548 (32.0%) out of the 4,844 cases it was not possible to establish either cause of death or reason for euthanasia. Infectious and parasitic diseases (mainly canine distemper, parvoviral enteritis and intestinal parasitism), neoplasia (mainly mammary neoplasms and lymphoma), disorders caused by physical agents (mainly accidents caused by automotive vehicles) and degenerative diseases (mainly chronic renal failure, cirrhosis, and congestive heart failure) were the main disease categories causing death or motivating euthanasia in dogs of this midland region. However, when cases were evaluated in relation with the age of the dog, the disease prevalence differed. The main causes of death in puppies were infectious and parasitic disease (mainly parvoviral enteritis, canine distemper, and intestinal parasitism). In adult dogs the most important causes of death were canine distemper, neoplasia and trauma. In age dogs, approximately half of the deaths could be attributed to neoplasia and degenerative disease.INDEX TERMS: Diseases of dogs, causes of death, reasons for euthanasia.

Areas of demyelination were produced by injecting ethidium bromide into the white matter of the lumbar spinal cord of rats. There was variation in the nature of the process of demyelination and a difference in the speed with which Schwann cells remyelinated the demyelinated axons. In some lesions, or areas within lesions, myelin debris was rapidly processed by macrophages and axons were rapidly remyelinated by Schwann cells, while in other lesions of similar duration, or in areas within the same lesion, the myelin was transformed into lattices of membranous profiles which persisted around axons for long periods of time. In the lesions containing such myelin derived membranes, there were few macrophages and remyelination by Schwann cells was delayed compared to that seen in the more rapidly resolving lesions. It was concluded that the slow resolution of some lesions resulted from the delay between intoxication and cell disintegration (7-10 days) which meant that the cell responses to demyelination took place in a glial free area which could not support cell movement needed for removal of myelin debris and remyelination. This study indicates that the tempo and results of demyelination can be altered by the cellular events which accompany degeneration of oligodendrocytes.

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Oxidative stress is an important molecular mechanism for kidney injury in mercury poisoning. We studied lycopene, a potent carotenoid found in tomatoes due to its large antioxidant properties, and also evaluated the ability of lycopene to prevent HgCl 2 nephrotoxicity. Rats were injected with HgCl 2 (0 or 5 mg/kg body weight, subcutaneously) 6 hr after lycopene administration (0, 10, 25 or 50 mg/kg by gavage) and were killed 12 hr after HgCl 2 exposure. HgCl 2 -induced inhibition of δ -aminolevulinate dehydratase activity ( ∼ 35%) and increase of lipid peroxidation in kidney ( ∼ 37%) were prevented by lycopene. However, lycopene did not prevent the increase of plasma creatinine levels ( ∼ 123%) and renal tubular necrosis induced by HgCl 2 . Glutathione peroxidase and catalase activities were enhanced ( ∼ 71% and ∼ 41%), while superoxide dismutase activity was depressed ( ∼ 44%) in HgCl 2 -treated rats when compared to control and these effects were prevented by lycopene. Our results indicate that although lycopene did not prevent HgCl 2 -induced renal failure, it could play a beneficial role against HgCl 2 toxicity by preventing lipid peroxidation and changes in the activity of δ -aminolevulinate dehydratase and antioxidant enzymes.

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 µl 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.

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FIG 2: Clinical and microscopic findings in the liver of a sevenmonth-old cross Saanen goat with accidental acute closantel toxicosis, five days after closantel administration. (a) The left middle liver lobe shows an area of yellow discoloration (arrow) interposed by thin stripes of normal colour. (b) Massive hepatocellular centrolobular coagulative necrosis (arrow). Haematoxylin and eosin. x 200 (a) (b)