Yersinia pseudotuberculosis serotype O:1 infection in a captive Seba's short tailed-fruit bat (Carollia perspicillata) colony in Switzerland.

BACKGROUND: Between February and April 2016, a slight increase in mortality was observed in a colony consisting of 400 captive Seba's short-tailed bats (Carollia perspicillata). These animals cohabited with other nocturnal animal species in a dome of a private zoo in Switzerland. RESULTS: Gross and histological analysis of two (14.3%) out of the 13 animals submitted for necropsy within this period revealed a necrosuppurative pneumonia, hepatitis, splenitis, enterocolitis, and endometritis, with abundant intralesional colonies of Gram-negative rods. Yersinia (Y.) pseudotuberculosis serotype O:1 and biotype 1 belonging to the sequence type ST90 was isolated from the affected organs in both animals. Following this diagnosis, » of the colony (99 animals) was culled and submitted for gross and histopathological analysis, and a bacterial culture selective for Yersinia spp. of lung, liver, and spleen was performed. From these 99 animals, one gravid female was tested and found to be positive for Y. pseudotuberculosis in the absence of clinical symptoms and histopathological lesions. PCR analysis of altogether three bacterial isolates for virulence factors revealed the presence of the ail gene, and one isolate was also positive for the virF and yadA plasmid genes. CONCLUSIONS: These findings suggest that Carollia perspicillata are susceptible to lethal yersiniosis but do not represent a regular reservoir for Y. pseudotuberculosis. Culling of » of the population was sufficient to limit the spread of this infection among the colony. Moreover, no infections were detected in cohabitant nocturnal animals and caretakers, indicating that the zoonotic risk in this case was low.

Lethal Gastric Mucosal Necrosis due to Administration of Oral Ferrous Bisglycinate Chelate to Suckling Piglets.

The oral application of a newly developed ferrous bisglycinate paste for suckling piglets at a dose of 180 mg/kg body weight led to increased death rates in 10% (n = 10) of Swiss test pig breeding farms (n = 100). Necropsy examination of suckling piglets (n = 12), selected randomly from the test farms with increased death rates, demonstrated severe gastric mucosal ulceration and necrosis. Due to the presence of crystalline iron surface coating within the gastric lesions, the iron was considered as the toxic principle and cause of death. To demonstrate the direct toxicity of ferrous bisglycinate, the paste was administered experimentally to a litter of suckling piglets (n = 11). Different time points (24, 48 and 72 h post partum) and doses (180 mg/kg and 360 mg/kg) were investigated. The manufacturer's recommended dose of 180 mg/kg corresponded to approximately 36 mg Fe/kg and to 6.4 % of the acute lethal dose50 of oral iron in rats. In all piglets the lesions were reproduced and most severe at the earliest time point (24 h post partum) and with the highest applied dose (360 mg/kg). The lesions were in accordance with those described from oral iron intoxication in man, suggesting pigs as an ideal animal model for oral iron toxicity studies.

Clinicopathological Phenotype of Autosomal Recessive Cholesterol Deficiency in Holstein Cattle.

BACKGROUND: Cholesterol deficiency (CD), a newly identified autosomal recessive genetic defect in Holstein cattle, is associated with clinical signs of diarrhea, failure to thrive, and hypocholesterolemia. HYPOTHESIS/OBJECTIVES: The objective is to describe the clinicopathological phenotype of affected Holstein cattle homozygous for the causative apolipoprotein B gene (APOB) mutation. ANIMALS: Six Holstein cattle, 5 calves with a clinical history of chronic diarrhea, and 1 heifer with erosions in the buccal cavity and neurologic symptoms were admitted to the Clinic for Ruminants. METHODS: This case review included a full clinical examination, a complete blood count, blood chemistry, and measurements of cholesterol and triglycerides. The animals were euthanized and necropsied. A PCR-based direct gene test was applied to determine the APOB genotype. RESULTS: All 6 animals were inbred, could be traced back to the sire Maughlin Storm, and were confirmed homozygous for the APOB mutation. The clinical phenotype included poor development, underweight, and intermittent diarrhea in the calves, and neurologic signs in the heifer included hypermetria and pacing. Hypocholesterolemia and low triglycerides concentrations were present in all animals. The pathological phenotype of all animals was steatorrhea with enterocytes of the small intestine containing intracytoplasmic lipid vacuoles. The peripheral nervous system of the heifer displayed degenerative changes. CONCLUSIONS AND CLINICAL IMPORTANCE: Suspicion of CD in Holstein cattle is based on the presence of chronic diarrhea with no evidence of primary infections. Confirmation of the associated APOB gene mutation is needed. Additionally, the heifer demonstrated primarily signs of neurologic disease providing an unexpected phenotype of CD.

A transposable element insertion in APOB causes cholesterol deficiency in Holstein cattle.

Cholesterol deficiency, a new autosomal recessive inherited genetic defect in Holstein cattle, has been recently reported to have an influence on the rearing success of calves. The affected animals show unresponsive diarrhea accompanied by hypocholesterolemia and usually die within the first weeks or months of life. Here, we show that whole genome sequencing combined with the knowledge about the pedigree and inbreeding status of a livestock population facilitates the identification of the causative mutation. We resequenced the entire genomes of an affected calf and a healthy partially inbred male carrying one copy of the critical 2.24-Mb chromosome 11 segment in its ancestral state and one copy of the same segment with the cholesterol deficiency mutation. We detected a single structural variant, homozygous in the affected case and heterozygous in the non-affected carrier male. The genetic makeup of this key animal provides extremely strong support for the causality of this mutation. The mutation represents a 1.3kb insertion of a transposable LTR element (ERV2-1) in the coding sequence of the APOB gene, which leads to truncated transcripts and aberrant splicing. This finding was further supported by RNA sequencing of the liver transcriptome of an affected calf. The encoded apolipoprotein B is an essential apolipoprotein on chylomicrons and low-density lipoproteins, and therefore, the mutation represents a loss of function mutation similar to autosomal recessive inherited familial hypobetalipoproteinemia-1 (FHBL1) in humans. Our findings provide a direct gene test to improve selection against this deleterious mutation in Holstein cattle.

Detection of Chlamydia pneumoniae in a collection of captive snakes and response to treatment with marbofloxacin.

In a collection of 58 snakes comprising predominantly Eurasian vipers in Switzerland, five snakes died unexpectedly during hibernation from 2009 to 2012. In one snake, organisms resembling chlamydiae were detected by immunohistochemistry in multiple histiocytic granulomas. Real-time quantitative PCR and microarray analysis were used to determine the presence of Chlamydia pneumoniae in tissue samples and cloacal/choanal swabs from snakes in the collection; 8/53 (15.1%) of the remaining snakes were positive. Although one infected snake had suppurative periglossitis, infection with C. pneumoniae did not appear to be associated with specific clinical signs in snakes. Of seven snakes treated with 5 mg/kg marbofloxacin IM once daily, five became PCR negative for C. pneumoniae following treatment, whereas one animal remained positive and one snake was lost to follow-up.