We reviewed the records of 5,083 cattle necropsies performed from January 1995 to December 2018 and filed at the Laboratory of Anatomic Pathology (LAP) of the “Universidade Federal de Mato Grosso do Sul” (UFMS). These necropsies were performed either by LAP-UFMS faculty (22.33%) or by field veterinary practitioners (77.67%) who subsequently submitted material for histological evaluation at the LAP-UFMS. Conclusive diagnoses were reached in 46.21% of the protocols (2,349 cases), and approximately 65% of the cases were classified as inflammatory or parasitic diseases, with rabies being the most diagnosed disease (20.82% of total conclusive diagnosis). There were a large number of protocols in which the diagnosis was of nonsuppurative meningoencephalitis of unknown cause (NSMUC). Those were the main differentials for rabies and bovine herpesvirus-5 necrotizing meningoencephalitis (NME); that is, the number of rabies cases may be even higher if one considers that many cases of NSMUC might be undiagnosed rabies cases. Toxic and toxic-infectious diseases were the second most prevalent category, and botulism cases represented 41% of this category. The other categories corresponded to less than 20% of the total diagnoses and were distributed in decreasing order of frequency as degenerative diseases (9.79%), diseases caused by physical agents (3.87%), other diseases (2.13%), neoplasms and tumor-like lesions (1.79%), metabolic or nutritional disorders (1.75%) and congenital malformations (0.64%). The large number of inconclusive diagnoses was mainly due to improper conditions of mailed-in material for histopathological evaluation, namely, nonrepresentative samples of all organs, autolysis, and the absence of epidemiological and clinical-pathological information.

Background: Stryphnodendron fissuratum is a tree from the Brazilian Cerrado. Its fruit is toxic to cattle and can cause clinical digestive signs, hepatogenous photosensitization, and abortion. Cases of poisoning in cattle, goats and guinea pigs have been experimentally reproduced; however, photosensitization could not be reproduced. The aim of this work was to describe an outbreak of natural poisoning and experimental reproduction in cattle, both with hepatogenous photosensitization.Materials, Methods & Results: Its described and natural outbreak and an experimental poisoning. In the outbreak, three bovines in the acute phase and three in the chronic phase were examined. Blood samples were collected from all of these animals in order to measure serum levels of aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), urea, and creatinine. The first three animals underwent necropsy and histopathological evaluation. The experiment was conducted with two nine-month-old calves that received an oral paste made with crushed S. fissuratum fruits mixed with water. These fruits were collected at a farm at which cattle poisoning cases had occurred. Blood samples were collected in order to measure serum levels of AST, GGT, urea, and creatinine, before plant administration and then daily during the experimental period. Skin biopsies were taken before plant administration and new one after the first signs of skin lesions. The natural outbreak affected 52 of 160 bovine (31 calves and 21 cows) in the lot. Two calves and 14 cows died. Clinical signs consisted of depression, ataxia, incoordination, behavioral changes, decubitus, and death. One animal that died and 36 others that recovered had photodermatitis. Necropsy findings in the animals consisted of bad corporal condition, pale kidneys, evidence of liver lobular pattern, dry rumen contents, and full bladder. In two animals, fruit seeds were found in the rumen, and one animal had ulcers and transmural edema in the abomasum. Microscopically, mild to moderate renal tubular distension, accumulation of proteinaceous material in lumen with mild to moderate swelling, and epithelial necrosis. In the liver, swelling of hepatocytes and moderate bile stasis was detected. Enzymes values in all evaluated bovines were higher than those considered normal for the species. Experimentally, both calves became ill and one died. The clinical signs were apathy, inappetence, wobbling, weight loss, and goosebumps. One of them had jaundice, tearing, photophobia, ear skin detachment, and ulcers at the muzzle, nostrils and ventral face of the tongue. This animal was euthanized in extremis, and the necropsy findings showed generalized jaundice, evidence of increased liver lobular pattern, thick bile, pale kidneys, and esophageal, tongue, and epiglottal ulcers. Microscopically, the lesions were similar to those described during the natural outbreak. The skin biopsy from the calf that recovered showed perivascular edema and mild eosinophilia.Discussion: The diagnosis was made based on clinical signs, necropsy findings, histopathological lesions, and epidemiological analysis. Experimentally, the plant was toxic at the administered doses. Photosensitization was the most common clinical sign during the natural outbreak and until now, has never been experimentally reproduced. Based on histopathological lesions observed in this study, we can consider that is from hepatogenous origin. The results showed that the kidney lesions have an important role during the pathogenesis caused by this poisoning and during disease evolution.

To evaluate the outcome of acute lesions in the brains of sheep that completely clinically recover from acute polioencephalomalacia (PEM), ten sheep were used in this experiment. Eight of those sheep received varying doses of amprolium to induce PEM. Four sheep were treated intramuscularly with 40mg/kg/body weight with thiamine to allow recovery and four sheep were left untreated. Two control sheep did not receive either amprolium or thiamine and were kept along with the other eight sheep for the duration of the experiment. Except for the two drugs, the diet and water source were the same for the ten sheep. Two sheep receiving high daily doses of amprolium and one sheep receiving a lower dose had acute deaths and developed acute brain lesions consisting of neuronal laminar cortical necrosis (red neurons), edema, reactive astrocytes, swollen endothelial cells and gitter cells infiltration. Four sheep that recovered from lower doses of amprolium-induced PEM after being treated with thiamine and another one that recovered spontaneously were euthanatized six months after clinical recovery and had gross changes consisting of segmental absence of cortical tissue. Histologically these segmental cortex-deprived areas corresponded to quasi-empty spaces where only vessels and gitter cells existed. No changes were seen in the brains of the two control sheep.

The aim of this study was to describe the epidemiological, clinical, and pathological findings of two outbreaks of gastrointestinal nematode infections in beef cattle kept under an inadequate sanitary protocol. An outbreak of trichostrongylosis occurred in Amambai, Mato Grosso do Sul (MS), from May to July 2016. The herd consisted of 3,000 Nellore cows, and of these, fifteen died after showing emaciation and diarrhea and remaining in recumbency. At necropsy, the abomasum showed edema in the folds, white, raised areas, multifocal to coalescent, and small ulcers. Histopathology showed larvae compatible with trichostrongylid nematodes were present inside the abomasum glands. Trichostrongylus axei was identify in the abomasum. The hemonchosis outbreak began in October 2018, in a breeding and finishing property in Santa Rita do Pardo, MS. Of 4,000 cattle aged 8 to 18 months, 673 became ill and 117 died. Clinical signs were emaciation, weakness, dehydration, submandibular edema, and soft stools. At necropsy, large numbers of nematodes were found in the abomasum; they were morphologically classified as Haemonchus placei. Both outbreaks were caused by failures in the parasite control protocol. However, in Outbreak I, frost and immune stress caused by lack of food may have contributed to the deaths. In Outbreak I, the main failure in the devermination protocol was the use of anthelmintics without carrying out an efficacy test. In Outbreak II, there was no parasite control protocol in the rearing and finishing property, and in the breeding property, there was resistance to the anthelmintic used (ivermectin). The two outbreaks highlight the importance of gastrointestinal nematode control protocols in cattle and demonstrate that infections by T. axei and H. placei can be lethal for this species.

Background:Copper is an essential micronutrient for the body to function properly. However, although it is a vital element, an excess of copper in the body is extremely toxic. Copper toxicity has been reported mainly in sheep. In dogs, clinicopathological signs of toxicity are characterized by chronic liver failure. This means that the hemolytic crisis so common in sheep is a condition rarely associated with toxicity in dogs, so there are very few descriptions of this condition in the veterinary literature. The purpose of this report is to describe a case of hemolytic crisis in a dog with copper-associated chronic hepatitis. Case: A medium-sized 6-year-old bitch was brought to the Veterinary Hospital of the Federal University of Santa Maria, with clinical presentation of apathy, anorexia and red urine. A physical examination revealed mildly jaundiced mucosa and dark brown urine. A urinalysis indicated the presence of protein, bilirubin and occult blood. The blood count revealed hypochromic macrocytic anemia, leukocytosis due to left shift neutrophilia and thrombocytopenia. Serum biochemistry showed elevated levels of alanine aminotransferase and alkaline phosphatase. The animal was given a blood transfusion due to the severity of her anemia, but her clinical condition worsened and she died, whereupon her body was sent for necropsy. This necropsy revealed conspicuous signs of jaundice, splenomegaly and altered liver and kidney color. The liver was brownish, with its natural surface firm and slightly irregular. The kidneys were diffusely blackened. The urine was dark brown. Fragments of different organs were collected, fixed in 10% buffered formalin solution, routinely processed for histopathology and stained with hematoxylin and eosin. A histological dissection of the liver showed the hepatic lobes dissected by fibrosis, forming islands of hepatocytes and numerous lymphocytes and plasmocytes. Brown granular pigment was observed in periportal hepatocytes. Perls Prussian blue and rubeanic acid staining techniques were performed to characterize this pigment.