A possible case of caprine-associated malignant catarrhal fever in a domestic water buffalo (Bubalus bubalis) in Switzerland

ABSTRACT: BACKGROUND: Malignant catarrhal fever (MCF) is a fatal herpesvirus infection, affecting various wild and domestic ruminants all over the world. Water buffaloes were reported to be particularly susceptible for the ovine herpesvirus-2 (OvHV-2) causing the sheep-associated form of MCF (SA-MCF). This report describes the first case of possibly caprine-associated malignant catarrhal fever symptoms in a domestic water buffalo in Switzerland. CASE PRESENTATION: The buffalo cow presented with persistent fever, dyspnoea, nasal bleeding and haematuria. Despite symptomatic therapy, the buffalo died and was submitted to post mortem examination. Major findings were an abomasal ulceration, a mild haemorrhagic cystitis and multifocal haemorrhages on the epicardium and on serosal and mucosal surfaces. Eyes and oral cavity were not affected. Histopathology revealed a mild to moderate lymphohistiocytic vasculitis limited to the brain and the urinary bladder. Although these findings are typical for MCF, OvHV-2 DNA was not detected in peripheral blood lymphocytes or in paraffin-embedded brain, using an OvHV-2 specific real time PCR. With the aid of a panherpesvirus PCR, a caprine herpesvirus-2 (CpHV-2) sequence could be amplified from both samples. CONCLUSIONS: To our knowledge, this is the first report of malignant catarrhal fever in the subfamily Bovinae, where the presence of CpHV-2 could be demonstrated. The etiological context has yet to be evaluated

Immunohistochemical study of PrPSc distribution in neural and extraneural tissues of two cats with feline spongiform encephalopathy

<p>Abstract</p> <p>Background</p> <p>Two domestic shorthair cats presenting with progressive hind-limb ataxia and increased aggressiveness were necropsied and a post mortem diagnosis of Feline Spongiform Encephalopathy (FSE) was made. A wide spectrum of tissue samples was collected and evaluated histologically and immunohistologically for the presence of PrP^Sc.</p> <p>Results</p> <p>Histopathological examination revealed a diffuse vacuolation of the grey matter neuropil with the following areas being most severely affected: corpus geniculatum medialis, thalamus, gyrus dentatus of the hippocampus, corpus striatum, and deep layers of the cerebral and cerebellar cortex as well as in the brain stem. In addition, a diffuse glial reaction involving astrocytes and microglia and intraneuronal vacuolation in a few neurons in the brain stem was present.</p> <p>Heavy PrP^Scimmunostaining was detected in brain, retina, optic nerve, pars nervosa of the pituitary gland, trigeminal ganglia and small amounts in the myenteric plexus of the small intestine (duodenum, jejunum) and slightly in the medulla of the adrenal gland.</p> <p>Conclusion</p> <p>The PrP^Scdistribution within the brain was consistent with that described in other FSE-affected cats. The pattern of abnormal PrP in the retina corresponded to that found in a captive cheetah with FSE, in sheep with scrapie and was similar to nvCJD in humans.</p

Molecular alterations in dog pheochromocytomas and paragangliomas

Recently, genetic alterations in the genes encoding succinate dehydrogenase subunit B and D (SDHB and SDHD) were identified in pet dogs that presented with spontaneously arising pheochromocytomas (PCC) and paragangliomas (PGL; together PPGL), suggesting dogs might be an interesting comparative model for the study of human PPGL. To study whether canine PPGL resembled human PPGL, we investigated a series of 50 canine PPGLs by immunohistochemistry to determine the expression of synaptophysin (SYP), tyrosine hydroxylase (TH) and succinate dehydrogenase subunit A (SDHA) and B (SDHB). In parallel, 25 canine PPGLs were screened for mutations in SDHB and SDHD by Sanger sequencing. To detect large chromosomal alterations, single nucleotide polymorphism (SNP) arrays were performed for 11 PPGLs, including cases for which fresh frozen tissue was available. The immunohistochemical markers stained positive in the majority of canine PPGLs. Genetic screening of the canine tumors revealed the previously described variants in four cases; SDHB p.Arg38Gln (n = 1) and SDHD p.Lys122Arg (n = 3). Furthermore, the SNP arrays revealed large chromosomal alterations of which the loss of chromosome 5, partly homologous to human chromosome 1p and chromosome 11, was the most frequent finding (100% of the six cases with chromosomal alterations). In conclusion, canine and human PPGLs show similar genomic alterations, suggestive of common interspecies PPGL-related pathways

Ascites secondary to compression of the caudal vena cava by liver abscesses in a cow

Background: Ascites due to thrombosis of the caudal vena cava is relatively seldom in cattle. To our knowledge, there have been no reports of ascites secondary to compression of the caudal vena cava by liver abscesses. This case report describes the findings in a 3.7-year-old Brown Swiss cow with this disease. Case presentation: The cow had a distended, pear-shaped abdomen. Ultrasonography of the abdomen showed a massive accumulation of hypoechoic fluid and dilatation of the caudal vena cava. A tentative diagnosis of thrombosis of the caudal vena cava was made, and because of a poor prognosis, the cow was slaughtered. Incision of the abdominal wall released approximately 100 litres of yellow, clear, non-malodorous fluid from the peritoneal cavity. The liver was markedly enlarged, and two abscesses, approximately 10 cm in diameter, were situated immediately adjacent to the caudal vena cava causing compression of the vein. No microbiology culture was done. The final diagnosis was ascites secondary to compression of the caudal vena cava by two liver abscesses and secondary hepatic fibrosis. Conclusion: This report suggests that compression of the caudal vena cava by liver abscesses should be included in the list of differential diagnosis of conditions associated with ascites and dilatation of the caudal vena in cattle

Intrauterine infection with bovine virus diarrhoea virus on alpine communal pastures in Switzerland

This study involved 13 calves, one to 50 days of age, born to first calf heifers that had been pastured on one of seven alpine communal pastures in the canton of St. Gallen during the summer of 1995. Of a total of 993 cattle pastured, 61 were pregnant heifers that were negative for bovine virus diarrhoea (BVD) antigen and for BVD antibodies at the start of pasturing. Seroconversion occurred in 26 of these pregnant heifers during the pasture period. Blood samples and skin biopsy specimens of calves born to 13 of these were examined for BVD antigen by antigen-ELISA and by an immunohistochemical technique, respectively. Blood samples were positive for BVD antigen in four calves, questionable in one calf, negative in seven and missing in one prematurely born calf. The four calves that were positive for BVD antigen in the blood were also positive in skin biopsies. Of the seven calves with a negative or missing blood test, six had positive and two had negative skin samples. Based on the combined results of blood and skin testing, 11 of 13 calves were positive for BVD antigen. Of the 11 infected calves, six were normal at birth, four were smaller than normal and one was premature and weak and was euthanized on humane grounds. Of the four small calves, two developed diarrhoea and died within the first month of life. The two calves that were negative for BVD antigen were clinically normal. The results of this study not only demonstrate the occurrence of in-utero infection with BVD virus, but also stress the importance of alpine communal pasturing in the spread of BVD virus. Because the prevention of infection with BVD virus on communal pastures does not seem feasible, it is recommended that all calves born to cows from such pastures be tested for BVD antigen