Postmortem bacterial culture is controversial in human medicine, and veterinary-specific research in this area is lacking. To address this knowledge gap, we cultured liver, kidney, and spleen individually from on-farm calf mortalities to determine the number of bacterial species present, concordance between organ cultures, and agreement with gross and histologic findings. We hypothesized that the spleen, a filtering organ, would be the most useful organ with the least amount of postmortem contamination given that it does not have a direct conduit to a bacterial population. Fresh liver, kidney, and spleen were collected for culture from 30 calves 5–28-d-old with various causes of mortality. Bacterial growth of ≥2 species was observed in ~48% of cultures, with Escherichia coli and Streptococcus spp. being most frequent. One bacterial species was present in 20% of cultures, with E. coli predominating. No growth was observed in ~32% of cultures. In 43% of cases, there was agreement in the culture results for all 3 organs; however, the majority were mixed bacterial growth. The best agreement was observed when there were no gross and/or histologic septic lesions in target organs and no bacterial growth on culture. The spleen was not helpful in determining bacterial significance in comparison to kidney or liver.

Abstract A respiratory disease epizootic at the National Bison Range (NBR) in Montana in 2016–2017 caused an 85% decline in the bighorn sheep population, documented by observations of its unmarked but individually identifiable members, the subjects of an ongoing long‐term study. The index case was likely one of a small group of young bighorn sheep on a short‐term exploratory foray in early summer of 2016. Disease subsequently spread through the population, with peak mortality in September and October and continuing signs of respiratory disease and sporadic mortality of all age classes through early July 2017. Body condition scores and clinical signs suggested that the disease affected ewe groups before rams, although by the end of the epizootic, ram mortality (90% of 71) exceeded ewe mortality (79% of 84). Microbiological sampling 10 years to 3 months prior to the epizootic had documented no evidence of infection or exposure to Mycoplasma ovipneumoniae at NBR, but during the epizootic, a single genetic strain of M. ovipneumoniae was detected in affected animals. Retrospective screening of domestic sheep flocks near the NBR identified the same genetic strain in one flock, presumptively the source of the epizootic infection. Evidence of fatal lamb pneumonia was observed during the first two lambing seasons following the epizootic but was absent during the third season following the death of the last identified M. ovipneumoniae carrier ewe. Monitoring of life‐history traits prior to the epizootic provided no evidence that environmentally and/or demographically induced nutritional or other stress contributed to the epizootic. Furthermore, the epizootic occurred despite proactive management actions undertaken to reduce risk of disease and increase resilience in this population. This closely observed bighorn sheep epizootic uniquely illustrates the natural history of the disease including the (presumptive) source of spillover, course, severity, and eventual pathogen clearance.

Mycoplasma ovipneumoniae is a globally distributed pathogen that has been associated with pneumonia in both domestic and wild Caprinae. It is closely related to M. hyopneumoniae, a respiratory pathogen of swine that is associated with decreased growth rates of pigs as well as clinical respiratory disease. In order to assess the effects of M. ovipneumoniae on lamb performance, we generated a cohort of lambs free of M. ovipneumoniae by segregation of test negative ewes after lambing, then compared the growth and carcass quality traits of M. ovipneumoniae-free and -colonized lambs from weaning to harvest. Some signs of respiratory disease were observed during the feeding trial in both lamb groups, but the M. ovipneumoniae-exposed group included more affected lambs and higher average disease scores. At harvest, lungs of lambs in both groups showed few grossly visible lesions, although the M. ovipneumoniae-exposed group did exhibit increased microscopic lung lesions (P<0.05). In addition, M. ovipneumoniae exposed lambs produced lower average daily gains (P<0.05), and lower yield grade carcasses (P<0.05) compared to those of non-exposed lambs. The results demonstrated the feasibility of test and segregation for elimination of M. ovipneumoniae from groups of sheep and suggested that this pathogen may impair lamb growth and productivity even in the absence of overt respiratory disease.

We documented bronchopneumonia in seven mountain goat ( Oreamnos americanus) kid mortalities between 2011 and 2015 following a pneumonia epizootic in bighorn sheep ( Ovis canadensis) and sympatric mountain goats in the adjacent East Humboldt Range and Ruby Mountains in Elko County, Nevada, US. Gross and histologic lesions resembled those described in bighorn lambs following all-age epizootics, and Mycoplasma ovipneumoniae was detected with real-time PCR in the lower and upper respiratory tracts of all kids. Mannheimia haemolytica, with one isolate being leukotoxigenic, was cultured from the upper respiratory tract of five kids, and in one kid, a leukotoxigenic strain of Mannheimia glucosida was isolated from both upper and lower respiratory tracts. During this same period, 75 mountain goats within the two populations were marked and sampled for respiratory pathogens, and M. ovipneumoniae, leukotoxigenic Bibersteinia trehalosi, and Mannheimia haemolytica were identified. The M. ovipneumoniae recovered from the kid mortalities shared the same DNA sequence-based strain type detected in the adult goats and sympatric bighorn sheep during and after the 2009-10 pneumonia outbreak. Clinical signs in affected kids, as well as decreased annual kid recruitment, also resembled reports in bighorn lambs from some herds following all-age pneumonia-associated die-offs. Mycoplasma ovipneumoniae, Pasteurellaceae spp., and other respiratory bacterial pathogens should be considered as a cause of pneumonia with potential population-limiting effects in mountain goats.

The primary lipid source in feeds used at Pacific salmon (Oncorhynchus spp.) and steelhead (anadromous O. mykiss) conservation hatcheries in California and the Pacific Northwest United States is marine fish oil which is characterized by high levels of long-chain polyunsaturated fatty acids (LC-PUFAs). As these fatty acids are prone to peroxidation, the high marine fish oil content of salmonid feeds is likely a contributing factor in a disease called steatitis which is an ongoing issue at some hatcheries. Dermal lesions associated with steatitis have been observed when affected fish were transferred from enclosed hatchery buildings to outdoor rearing units exposed to sunlight. Therefore, a two-factor study examining possible interactive effects of dietary lipid source and ultraviolet (UV) radiation on growth responses, histology and tissue fatty acid profiles of juvenile steelhead was conducted. For 10weeks, fish were fed diets containing canola oil (CO), fish oil (FO) or oxidized fish oil (OFO) while exposed to fluorescent or UV light. Each treatment was randomly assigned to triplicate groups of 50 fish initially weighing 1.6g/fish. The main effects of lipid and light source on growth responses and survival were not statistically significant, but percent weight gain was significantly affected by interaction of the main effects. Whole body histopathology revealed significantly higher (more severe) steatitis scores in fish fed FO or OFO compared with fish fed CO and in fish exposed to UV light compared with fish exposed to fluorescent light. Whole body lipid concentration and tissue fatty acid profile were significantly affected by lipid and light source but not their interaction. These results suggest reducing dietary LC-PUFAs and minimizing UV light exposure may reduce steatitis in steelhead.

Respiratory failure and death in East Coast Fever (ECF), a clinical syndrome of African cattle caused by the apicomplexan parasite Theileria parva, has historically been attributed to pulmonary infiltration by infected lymphocytes. However, immunohistochemical staining of tissue from T. parva infected cattle revealed large numbers of CD3- and CD20-negative intralesional mononuclear cells. Due to this finding, we hypothesized that macrophages play an important role in Theileria parva disease pathogenesis. Data presented here demonstrates that terminal ECF in both Holstein and Boran cattle is largely due to multisystemic histiocytic responses and resultant tissue damage. Furthermore, the combination of these histologic changes with the clinical findings, including lymphadenopathy, prolonged pyrexia, multi-lineage leukopenia, and thrombocytopenia is consistent with macrophage activation syndrome. All animals that succumbed to infection exhibited lymphohistiocytic vasculitis of small to medium caliber blood and lymphatic vessels. In pulmonary, lymphoid, splenic and hepatic tissues from Holstein cattle, the majority of intralesional macrophages were positive for CD163, and often expressed large amounts of IL-17. These data define a terminal ECF pathogenesis in which parasite-driven lymphoproliferation leads to secondary systemic macrophage activation syndrome, mononuclear vasculitis, pulmonary edema, respiratory failure and death. The accompanying macrophage phenotype defined by CD163 and IL-17 is presented in the context of this pathogenesis.

Bovine viral diarrhea virus (BVDV) is a pestivirus best known for causing a variety of disease syndromes in cattle, including gastrointestinal disease, reproductive insufficiency, immunosuppression, mucosal disease, and hemorrhagic syndrome. The virus can be spread by transiently infected individuals and by persistently infected animals that may be asymptomatic while shedding large amounts of virus throughout their lifetime. BVDV has been reported in over 40 domestic and free-ranging species, and persistent infection has been described in eight of those species: white-tailed deer, mule deer, eland, mousedeer, mountain goats, alpacas, sheep, and domestic swine. This paper reviews the various aspects of BVDV transmission, disease syndromes, diagnosis, control, and prevention, as well as examines BVDV infection in domestic and wild small ruminants and camelids including mountain goats (Oreamnos americanus).

Evidence for bovine viral diarrhea virus (BVDV) infection was detected in 2009-2010 while investigating a pneumonia die-off in Rocky Mountain bighorn sheep (Ovis canadensis, canadensis), and sympatric mountain goats (Oreamnos americanum) in adjacent mountain ranges in Elko County, Nevada. Seroprevalence to BVDV-1 was 81% (N = 32) in the bighorns and 100% (N = 3) in the mountain goats. Serosurveillance from 2011 to 2015 of surviving bighorns and mountain goats as well as sympatric mule deer (Odocoileus hemionus), indicated a prevalence of 72% (N = 45), 45% (N = 51), and 51% (N = 342) respectively. All species had antibody titers to BVDV1 and BVDV2. BVDV1 was isolated in cell culture from three bighorn sheep and a mountain goat kid. BVDV2 was isolated from two mule deer. Six deer (N = 96) sampled in 2013 were positive for BVDV by antigen-capture ELISA on a single ear notch. Wild ungulates and cattle concurrently graze public and private lands in these two mountain ranges, thus providing potential for interspecies viral transmission. Like cattle, mule deer, mountain goats, and bighorn sheep can be infected with BVDV and can develop clinical disease including immunosuppression. Winter migration patterns that increase densities and species interaction during the first and second trimester of gestation may contribute to the long term maintenance of the virus in these wild ungulates. More studies are needed to determine the population level impacts of BVDV infection on these three species.

Veterinary Clinical PathologyVolume 44, Issue 2 p. 327-328 What Is Your Diagnosis? What is your diagnosis? Oral soft tissue and cystic lesion in a dog Meredeth C. McEntire, Corresponding Author Meredeth C. McEntire Washington State University College of Veterinary Medicine, Pullman, WA, USA Correspondence M.C. McEntire, PO Box 647010, Washington State University, Pullman, WA 99164-7010, USA E-mail: [email protected]Search for more papers by this authorJohanna D. Rigas, Johanna D. Rigas Utah State University School of Veterinary Medicine, Logan, UT, USASearch for more papers by this authorRaelynn K. Farnsworth, Raelynn K. Farnsworth Washington State University College of Veterinary Medicine, Pullman, WA, USASearch for more papers by this authorDanielle D. Nelson, Danielle D. Nelson Washington State University College of Veterinary Medicine, Pullman, WA, USA Washington Animal Disease Diagnostic Laboratory, Pullman, WA, USASearch for more papers by this authorKevin Choy, Kevin Choy Oncology, Seattle Veterinary Specialists, Seattle, WA, USASearch for more papers by this author Meredeth C. McEntire, Corresponding Author Meredeth C. McEntire Washington State University College of Veterinary Medicine, Pullman, WA, USA Correspondence M.C. McEntire, PO Box 647010, Washington State University, Pullman, WA 99164-7010, USA E-mail: [email protected]Search for more papers by this authorJohanna D. Rigas, Johanna D. Rigas Utah State University School of Veterinary Medicine, Logan, UT, USASearch for more papers by this authorRaelynn K. Farnsworth, Raelynn K. Farnsworth Washington State University College of Veterinary Medicine, Pullman, WA, USASearch for more papers by this authorDanielle D. Nelson, Danielle D. Nelson Washington State University College of Veterinary Medicine, Pullman, WA, USA Washington Animal Disease Diagnostic Laboratory, Pullman, WA, USASearch for more papers by this authorKevin Choy, Kevin Choy Oncology, Seattle Veterinary Specialists, Seattle, WA, USASearch for more papers by this author First published: 12 February 2015 https://doi.org/10.1111/vcp.12231Citations: 2Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article.Citing Literature Volume44, Issue2June 2015Pages 327-328 RelatedInformation

An 11 yr old castrated male greyhound presented to the Washington State University's Veterinary Teaching Hospital (WSU VTH) for evaluation of a 4 day history of pleural effusion. The pleural effusion had a gelatinous appearance, suggestive of mucus, and was characterized cytologically as a pyogranulomatous exudate with some features suggestive of a carcinoma. Postmortem examination identified a pulmonary mass with evidence of carcinomatosis. Pulmonary papillary adenocarcinoma with carcinomatosis was the histologic diagnosis. Abundant mucin production was present, consistent with a mucinous pulmonary adenocarcinoma. To the authors' knowledge, this is the first report of a mucinous pulmonary adenocarcinoma with mucus pleural effusion in a dog.

Fifteen cases of Francisella tularensis infection (tularemia) were identified in western gray ( Sciurus griseus) and eastern gray ( Sciurus carolinensis) squirrels submitted to the Washington Animal Disease Diagnostic Laboratory between 2008 and 2011. All of the squirrels originated in Washington State, a geographical area with endemic tularemia in wildlife. Nine of the 15 squirrels with F. tularensis infection had gross (2/15) or microscopic (9/15) multifocal necrotizing lesions in the spleen, liver, or lymph nodes, typical of tularemia. Special stains did not reliably identify intralesional bacteria microscopically. Six of the 15 squirrels infected with F. tularensis lacked gross and microscopic lesions typical of tularemia. All 15 squirrels with F. tularensis infection were identified by polymerase chain reaction tests on the spleen, liver, or lymph node (including all 6 squirrels without typical tularemia lesions); 8 out of 9 squirrels were positive by direct fluorescent antibody test of tissues, and 5 out of 15 squirrels were positive by culture of tissues. The findings underscore the importance of considering tularemia as a possible cause of death when no lesions of tularemia can be identified at necropsy. Furthermore, the findings suggest the possibility of subclinical infections in gray squirrels, and the importance of molecular diagnostics for definitive diagnosis of F. tularensis infection in wild squirrels.

American bison (Bison bison) are particularly susceptible to developing fatal sheep-associated malignant catarrhal fever (SA-MCF) caused by ovine herpesvirus-2 (OvHV-2), a γ-herpesvirus in the Macavirus genus. This generally fatal disease is characterized by lymphoproliferation, vasculitis, and mucosal ulceration in American bison, domestic cattle (Bos taurus), and other clinically susceptible species which are considered non-adapted, dead-end hosts. The pathogenesis and cellular tropism of OvHV-2 infection have not been fully defined. An earlier study detected OvHV-2 open reading frame 25 (ORF25) transcripts encoding the viral major capsid protein in tissues of bison with SA-MCF, and levels of viral transcript expression positively correlated with lesion severity. To further define the cellular tropism and replication of OvHV-2 infection in vascular lesions of bison, immunofluorescence studies were performed to identify cell type(s) expressing ORF25 protein within tissues. Cytoplasmic and not nuclear ORF25 protein was demonstrated in predominantly perivascular fibroblasts in six bison with experimentally-induced SA-MCF, and there was no evidence of immunoreactivity in vascular endothelium, smooth muscle, or infiltrating leukocytes. The cytoplasmic distribution of viral major capsid protein suggests that viral replication in perivascular fibroblasts may be abortive in this dead-end host. These findings provide a novel foundation for defining the pathogenesis of vasculitis in non-adapted hosts with SA-MCF.

Sheep-associated malignant catarrhal fever (SA-MCF) caused by ovine herpesvirus-2 (OvHV-2), a γ-herpesvirus in the Macavirus genus, is a fatal disease associated with lymphoproliferation, lymphocytic vasculitis, and mucosal ulceration in clinically susceptible species. SA-MCF is an important threat to American bison (Bison bison) due to their high susceptibility to this disease. Currently, the pathogenesis of disease in SA-MCF is poorly understood, and the immunophenotype of lymphocytes that infiltrate the vascular lesions of bison and cattle with SA-MCF has been only partially defined. Previous single-color immunohistochemistry studies have demonstrated that CD8+ cells and CD4+ cells predominate within vascular infiltrates in cattle and bison. The CD8+ cells detected in the vascular lesions of cattle and bison were assumed to be cytotoxic αβ T lymphocytes. However, polychromatic immunophenotyping analyses in this study showed that CD8+/perforin+ γδ T cells, CD4+/perforin− αβ T cells, and B cells infiltrate vascular lesions in the urinary bladder, kidney, and liver of six bison with experimentally-induced SA-MCF. CD8+ αβ T cells and WC1+ γδ T cell cells were only infrequently and inconsistently identified. This study confirmed our hypothesis that the predominant CD8+ lymphocytes infiltrating the vascular lesions of bison with SA-MCF are cytotoxic lymphocytes of the innate immune system, not CD8+ αβ T cells. Results of the present study support the previous suggestions that MCF is fundamentally a disease of immune dysregulation.

Bovine viral diarrhea (BVD) viruses are pestiviruses that have been isolated from domestic and wild ruminants. There is serologic evidence of pestiviral infection in more than 40 species of free-range and captive mammals. Vertical transmission can produce persistently infected animals that are immunotolerant to the infecting strain of Bovine viral diarrhea virus (BVDV) and shed virus throughout their lives. Seven species (white-tailed deer, mouse deer, eland, domestic cattle, alpaca, sheep, and pigs) have been definitively identified as persistently infected with BVDV. This study provides serological, molecular, immunohistochemical, and histological evidence for BVDV infection in 2 captive mountain goats from a zoological park in Idaho. The study was triggered by isolation of BVDV from tissues and immunohistochemical identification of viral antigen within lesions of a 7-month-old male mountain goat (goat 1). Blood was collected from other mountain goats and white-tailed and mule deer on the premises for BVDV serum neutralization, viral isolation, and reverse transcription polymerase chain reaction. One 3-month-old mountain goat (goat 2) was antibody negative and BVDV positive in serum samples collected 3 months apart. This goat subsequently died, and though still antibody negative, BVDV was isolated from tissues and identified by immunohistochemistry within lesions. Sequencing and phylogenetic analysis identified the isolates as BVDV-2. These findings provide evidence of persistent infection in a mountain goat, underscoring the need for pestivirus control strategies for wild ruminants in zoological collections.