Natural Outbreak of BVDV-1d-Induced Mucosal Disease Lacking Intestinal Lesions.

Bovine viral diarrhea virus (BVDV) belongs to the Pestivirus genus, which is further divided into subgenotypes (1a-1u and 2a-c). When persistent infection occurs, the calf will be immunotolerant to BVDV and possibly develop mucosal disease. This study describes an outbreak of BVDV-1d-induced mucosal disease lacking intestinal lesions. Eleven calves presented with anorexia, sialorrhea, lameness, recumbency, and death. Three calves were necropsied, showing ulceration of the interdigital skin and the oral and nasal mucosa; linear ulcers in the tongue, esophagus, and rumen; and rounded ulcers in the abomasum. Microscopically, mucosa and skin had superficial necrosis, with single-cell necrosis and vacuolation in epithelial cells, and severe parakeratosis. Immunohistochemistry (IHC) showed BVDV antigen in the cytoplasm of epithelial cells in skin and mucosa. All 11 dead calves were positive upon reverse transcription-polymerase chain reaction (RT-PCR) for the detection of Pestivirus along with another 11 live calves from the herd, which were positive again by RT-PCR and IHC after a 4-week interval. Sequencing of the 5' untranslated region and N-terminal protease showed that viruses from these 22 calves were homologous and of subgenotype BVDV-1d. Cytopathic BVDV was isolated from 8 of 11 dead calves, but only noncytopathic BVDV was isolated from the 11 live animals. The findings indicate that this was an outbreak of mucosal disease caused by BVDV-1d, with high morbidity, and lesions restricted to the upper alimentary system and skin and absent from intestine. Thus, the epidemiological and pathological features in this form of mucosal disease may be similar to vesicular diseases, including foot and mouth disease.

Aging affects the response of female rats to a hypercaloric diet.

Metabolic syndrome is a major risk factor for the development of cardiovascular diseases and diabetes, among other conditions. Studies have shown that aging and metabolic syndrome share several metabolic alterations, and that aged individuals, in particular females, are at an increased risk of developing metabolic disorders. Although several studies have investigated the effects of hypercaloric diets in the development of obesity and metabolic syndrome in young animals, few studies have investigated these parameters in aged animals, especially in females. Therefore, the aim of this study was to investigate the effects of a hypercaloric diet in metabolic parameters of young and aged female rats, including its effects on lipid and glycemic profile and on liver lipid content. When compared to young animals, the aged rats presented increased serum levels of triglycerides and decreased serum levels of HDL cholesterol and glycemia, as well as increased hepatic levels of triglycerides and total cholesterol. The hypercaloric diet increased food intake, body weight gain and adiposity index, leading both young and aged animals to a dyslipidemia, represented by increased serum levels of triglycerides. The hypercaloric diet increased the glycemia and the HOMA index only in the young animals. On the other hand, the diet increased the frequency of hepatocellular microvacuolar degeneration only in the aged animals. In summary, it was observed that the females from different ages respond differently to hypercaloric diet intake: while the aged animals were more resistant to the changes in the glycemic profile, they were more susceptible to the hepatic damage caused by this diet.

Neurotoxicosis in horses associated with consumption of Trema micrantha.

BACKGROUND: Trema micrantha is a tree widely distributed throughout the Americas. The tree produces highly palatable leaves that have been associated with natural poisoning in goats, sheep and horses, in which hepatic necrosis and hepatic encephalopathy have been observed. OBJECTIVES: This study describes malacia and haemorrhage in the central nervous system (CNS) due to T. micrantha consumption, with minimal to absent hepatic lesions. STUDY DESIGN: Retrospective case series. METHODS: A total of 14 horses with a history of neurological signs and spontaneous consumption of T. micrantha leaves were submitted to necropsy and multiple samples were collected for histopathology. Details of clinical history and signs of the horses were obtained through inquiries to the owners and attending veterinarians. RESULTS: All the 14 horses had neurological signs of ataxia, severe sialorrhoea, involuntary running movements, sternal and lateral recumbency, and death after a clinical course that lasted from 24 h to 9 days. For a few days prior to onset of clinical signs, all horses had spontaneously consumed, potentially toxic doses of T. micrantha leaves. All 14 brains had diffuse yellowish discoloration affecting the rhombencephalon, mesencephalon, diencephalon, telencephalon and corpus striatum. In all cases, the most severe lesions were observed in the pons. Spinal cord lesions were observed affecting the lumbar intumescence, which was swollen with darken and depressed areas at the dorsal and ventral horns, and at the sacral level, which on cut surface displayed a friable and yellowish grey matter. The lesions observed grossly in brain and spinal cord consisted microscopically of severe vasculitis and liquefactive necrosis of white and grey matter of the brainstem, cerebellum and spinal cord. MAIN LIMITATIONS: This is a small retrospective series relying on clinical observations reported by owners and attending veterinarians. The mechanism of action of the plant toxin in the CNS is still unidentified. CONCLUSION: T. micrantha poisoning in horses causes predominantly a neurological disease, with minimal to absent hepatic lesions.

Cutaneous leishmaniasis in Cavia porcellus (guinea pig): case report / Leishmaniose cutânea em Cavia porcellus (cobaia): relato de caso

Leishmaniasis is a parasitic disease of worldwide spread. It is caused by protozoa of the genus Leishmania and is transmitted to animals and humans through the bite of sand flies. In Brazil, leishmaniasis is one of the zoonoses of major importance and expansion. The objective of this work is to describe the clinical, pathological, immunohistochemical and molecular findings of cutaneous leishmaniasis by Leishmania enriettii in guinea pig (Cavia porcellus). Three animals had nodular and alopecia lesions on the muzzle, ears and ulcerated lesions on the distal extremities of the pelvic limbs. The males (2) also had diffuse thickening of the scrotal skin. Samples of the ulcerated cutaneous lesions were evaluated by cytology which were observed as amastigote forms of Leishmania. One of the animals was euthanized and necropsied. Histopathology showed abundant dermal infiltrate of macrophages, plasma cells, lymphocytes and multinucleated giant cells. Numerous macrophages contained parasitoid vacuoles with amastigote forms, evidenced by immunohistochemical examination. The molecular characterization based on the SSUrDNA gene identified the species as L. enrietti. The diagnosis of cutaneous leishmaniasis in these cases was based on pathological findings and confirmed by immunohistochemistry, PCR and sequencing.(AU)

A leishmaniose é uma doença parasitária de distribuição mundial. É causada por protozoários do gênero Leishmania e é transmitida para animais e seres humanos por meio da picada de flebotomíneos. No Brasil, a leishmaniose é uma das zoonoses de maior importância e expansão. O objetivo deste trabalho é descrever os achados clínicos, patológicos, imuno-histoquímicos e moleculares de leishmaniose cutânea por Leishmania enriettii em cobaia (Cavia porcellus). Três animais apresentavam lesões nodulares e alopécicas no focinho e orelhas, além de lesões ulceradas nas extremidades distais dos membros pélvicos. Nos machos (2), foi observado espessamento difuso da pele escrotal. Amostras das lesões cutâneas ulceradas foram avaliadas por citologia, nas quais foram observadas formas amastigotas de Leishmania. Um dos animais foi submetido à eutanásia e necropsiado. Na histopatologia, foi observado infiltrado dérmico abundante de macrófagos, plasmócitos, linfócitos e com células gigantes multinucleadas. Numerosos macrófagos continham vacúolos parasitóforos com formas amastigotas, evidenciados por meio do exame de imuno-histoquímica. A caracterização molecular baseada no gene de SSUrDNA identificou a espécie como L. enrietti. O diagnóstico de leishmaniose cutânea nesses casos foi baseado nos achados patológicos e confirmado pelas técnicas de imuno-histoquímica, PCR e sequenciamento.(AU)