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From 2014–2019, 8 juvenile black bears ( Ursus americanus) from different geographic regions were presented to the California Department of Fish and Wildlife because of emaciation, alopecia, and exfoliative dermatitis that resulted in death or euthanasia. Autopsy and histopathology revealed that all 8 bears had generalized hyperkeratotic dermatitis, folliculitis, and furunculosis. Skin structures were heavily colonized by fungal hyphae and arthrospores; fungal cultures of skin from 7 bears yielded Trichophyton equinum, a zoophilic dermatophyte reported only rarely in non-equid species. Additional skin conditions included mites (5), ticks (2), and coagulase-negative Staphylococcus sp. infections (2). No other causes of morbidity or mortality were identified. Molecular comparisons performed at the University of Texas Fungal Reference Laboratory determined that all isolates produced identical banding patterns, potentially representing a clonal population. Dermatophytosis is commonly localized and limited to the stratum corneum of the epidermis and hair follicles. Generalized disease with dermal involvement is rare in immunocompetent individuals; illness, malnutrition, age, or immunosuppression may increase susceptibility. Underlying causes for the severe disease impact in these bears were not evident after physical or postmortem examination. The mechanism by which bears from different geographic locations had severe, T. equinum–associated dermatophytosis from a potentially clonal dermatophyte could not be explained and warrants further investigation.

Rabbit haemorrhagic disease virus type 2 (RHDV2) causes a severe systemic disease with hepatic necrosis. Differently from classic RHDV, which affects only European rabbits (Oryctolagus cuniculus), RHDV2 can affect many leporid species, including hares (Lepus spp.) and cottontail rabbits (Sylvilagus spp.). RHDV2 emerged in Europe in 2010 and spread worldwide. During the last 5 years, there have been multiple outbreaks in North America since the first known event in 2016 in Quebec, Canada, including several detections in British Columbia, Canada, between 2018 and 2019, Washington State and Ohio, USA, in 2018 and 2019, and New York, USA, in 2020. However, the most widespread outbreak commenced in March 2020 in the southwestern USA and Mexico. In California, RHDV2 spread widely across several southern counties between 2020 and 2021, and the aim of this study was to report and characterize these early events of viral incursion and circulation within the state. Domestic and wild lagomorphs (n = 81) collected between August 2020 and February 2021 in California with a suspicion of RHDV2 infection were tested by reverse transcription quantitative real-time PCR on the liver, and histology and immunohistochemistry for pan-lagovirus were performed on liver sections. In addition, whole genome sequencing from 12 cases was performed. During this period, 33/81 lagomorphs including 24/59 domestic rabbits (O. cuniculus), 3/16 desert cottontail rabbits (Sylvilagus audubonii), and 6/6 black-tailed jackrabbits (Lepus californicus) tested positive. All RHDV2-positive animals had hepatic necrosis typical of pathogenic lagovirus infection, and the antigen was detected in sections from individuals of the three species. The 12 California sequences were closely related (98.9%-99.95%) to each other, and also very similar (99.0%-99.4%) to sequences obtained in other southwestern states during the 2020-2021 outbreak; however, they were less similar to strains obtained in New York in 2020 (96.7%-96.9%) and Quebec in 2016 (92.4%-92.6%), suggesting that those events could be related to different viral incursions. The California sequences were more similar (98.6%-98.7%) to a strain collected in British Columbia in 2018, which suggests that that event could have been related to the 2020 outbreak in the southwestern USA.

A 22-y-old American Quarter Horse gelding was presented with a history of chronic progressive respiratory problems and a diffuse pulmonary nodular pattern in thoracic radiographs. The horse was euthanized, and 4 formalin-fixed samples of lung were submitted for histopathology. There were multifocal areas of marked thickening of alveolar septa as a result of proliferation of myofibroblasts embedded in fibromyxoid matrix (interpreted as “Masson bodies”), focal areas of fibrosis, and numerous papillary projections of connective tissue into bronchioles. A diagnosis of organizing pneumonia was reached. No etiology was found for this lesion. It is important to consider causes of chronic interstitial pneumonia with fibrosis in horses other than equid herpesvirus 5, such as complicated viral or bacterial pneumonia or chronic toxicoses.

Leptospirosis is reported infrequently in wild and domestic felids. We estimated the prevalence of Leptospira spp. infection and exposure using real-time PCR and serology, respectively, in 136 mountain lions (Puma concolor) and 39 bobcats (Lynx rufus) that died or were euthanized between 2009 and 2017 from several regions of California, US. Felids were classified as Leptospira-positive if they were test-positive using real-time PCR targeting the LipL32 gene of pathogenic Leptospira spp. or microscopic agglutination test for six serovars of Leptospira spp. The overall Leptospira spp. prevalence was 46% (63/136) for mountain lions and 28% (11/39) for bobcats. The most common serovar detected in both felid species was Leptospira interrogans serovar Pomona. Age class and geographic location were significantly associated with Leptospira spp. in mountain lions, but not in bobcats. Interstitial nephritis, predominately lymphocytic, was diagnosed in 39% (41/106) of mountain lions and 16% (4/25) of bobcats evaluated histologically and was significantly associated with being Leptospira spp.-positive in both species. Our findings suggest that Leptospira spp. infection is common and widespread in California's wild felids and may have clinical impacts on renal and overall health of individuals. Key words: Bobcat, Leptospira spp., leptospirosis, Lynx rufus, mountain lion, nephritis, pathology, Puma concolor.

Lysosomal storage diseases are inherited and acquired disorders characterized by dysfunctional lysosomes. Intracytoplasmic accumulation of undegraded substrates leads to impaired cellular function and death. Several plant species are toxic to livestock because of the presence of indolizidine alkaloids, including swainsonine, which cause a storage disease. Swainsonine-induced nervous disease (i.e., locoism) of sheep and cattle is well recognized in several parts of the world, particularly in the western United States and in parts of Australia. Spontaneous intoxication by Astragalus garbancillo var. garbancillo was suspected in a group of 70 llamas (Lama glama) in Jujuy Province, northwestern Argentina. The animals grazed an area dominated by stands of A. garbancillo var. garbancillo. Clinical signs were staggering, ataxia, hypermetria, and progressive weight loss. The clinical course in individual animals was ~50 d. The main microscopic changes were Purkinje cell degeneration, necrosis, and loss, associated with intracytoplasmic vacuolation, meganeurite formation, and Wallerian degeneration. Specific positive labeling for ubiquitin was observed in axonal spheroids. Composite leaf and stem samples of A. garbancillo var. garbancillo analyzed by high-performance liquid chromatography contained 0.03% swainsonine. Based on the microscopic lesions, clinical history, and plant analysis, a diagnosis was made of storage disease caused by consumption of swainsonine-containing A. garbancillo var. garbancillo. EEA Salta Fil: Marín, Raúl E. Universidad Nacional de Jujuy. Facultad de Ciencia Agrarias; Argentina. Fil: Micheloud, Juan Francisco. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Salta. Área de Sanidad Animal; Argentina. Fil: Vignale, Nilda D. Universidad Nacional de Jujuy. Facultad de Ciencias Agrarias; Argentina. Fil: Gimeno, Eduardo Juan. Universidad Nacional de la Plata. Facultad de Ciencias Veterinarias. Cátedra de Patología General;Argentina. Fil: O'Toole, Donal. Wyoming State Veterinary Laboratory ; Estados Unidos Fil: Gardner, Dale R. USDA-ARS Poisonous Plant Research Laboratory; Estados Unidos Fil: Woods, Leslies. University of California–Davis. California Animal Health and Food Safety Laboratory System; Estados Unidos Fil: Uzal, Francisco A. University of California–Davis. California Animal Health and Food Safety Laboratory System, San Bernardino; Estados Unidos

Viral infections were investigated in American black bears (Ursus americanus) from Nevada and northern California with and without idiopathic encephalitis. Metagenomics analyses of tissue pools revealed novel viruses in the generaCircoviridae,Parvoviridae,Anelloviridae,Polyomaviridae, andPapillomaviridae. The circovirus and parvovirus were of particular interest due to their potential importance as pathogens. We characterized the genomes of these viruses and subsequently screened bears by PCR to determine their prevalence. The circovirus(Ursus americanuscircovirus, UaCV) was detected at a high prevalence (10/16, 67%), and the chaphamaparvovirus (Ursus americanusparvovirus, UaPV) was found in a single bear. We showed that UaCV is present in liver, spleen/lymph node, and brain tissue of selected cases byin situhybridization (ISH) and PCR. Infections were detected in cases of idiopathic encephalitis and in cases without inflammatory brain lesions. Infection status was not clearly correlated with disease, and the significance of these infections remains unclear. Given the known pathogenicity of a closely related mammalian circovirus, and the complex manifestations of circovirus-associated diseases, we suggest that UaCV warrants further study as a possible cause or contributor to disease in American black bears.

Este artículo se encuentra disponible en la siguiente URL: https://journals.sagepub.com/doi/pdf/10.1177/1040638719877844 This is the pre-peer reviewed version of the following article: Sacco, S. C., Ortega, J., Navarro, M. A., Fresneda, K. C., Anderson, M., Woods, L. W., Moore, J., & Uzal, F. A. (2020). Clostridium sordellii-associated gas gangrene in 8 horses, 1998-2019. Journal of Veterinary Diagnostic Investigation, vol. 32, i. 2 (01 mar.), pp. 246?251, which has been published in final form at https://doi.org/10.1177/1040638719877844 Este es el pre-print del siguiente artículo: Sacco, S. C., Ortega, J., Navarro, M. A., Fresneda, K. C., Anderson, M., Woods, L. W., Moore, J., & Uzal, F. A. (2020). Clostridium sordellii-associated gas gangrene in 8 horses, 1998-2019. Journal of Veterinary Diagnostic Investigation, vol. 32, i. 2 (01 mar.), pp. 246?251, que se ha publicado de forma definitiva en https://doi.org/10.1177/1040638719877844 En este artículo de investigación también participan: Joaquín Ortega, Mauricio A. Navarro, Karina C. Fresneda, Mark Anderson, Leslie W. Woods, Janet Moore y Francisco A. Uzal. Gas gangrene occurs in several animal species, and it is caused by one or more clostridial species. In horses, the disease is most often caused by Clostidium perfringens type A. Although Clostridium sordellii has been associated with gas gangrene in ruminants and humans, cases of the disease associated with this microorganism have not been described in horses. We report 8 cases of gas gangrene by C. sordellii in horses. These cases were characterized by myonecrosis and cellulitis, associated with systemic changes suggestive of toxic shock. The diagnosis was confirmed by gross and microscopic changes combined with anaerobic culture, fluorescent antibody test, immunohistochemistry and/or PCR. The predisposing factor in these cases was an injection or a traumatic skin injury. C. sordellii should be considered as a possible etiologic agent in cases of gas gangrene in horses.

The San Joaquin kit fox ( Vulpes macrotis mutica) is a federally endangered small carnivore whose distribution is limited to the San Joaquin Valley in central California. Population decline is due to profound habitat loss, and conservation of all remaining populations is critical. A robust urban population occurs in the city of Bakersfield. In spring of 2013, putative cases of mange were reported in this population. Mites from affected animals were confirmed to be Sarcoptes scabiei morphologically and by DNA sequencing. By the end of 2014, 15 cases of kit foxes with mange had been confirmed. As with other species, sarcoptic mange in kit foxes is characterized by intense pruritus and dermatitis, caused by mites burrowing into the epidermal layers, as well as alopecia, hyperkeratosis, and encrustations, secondary bacterial infections, and finally extreme morbidity and death. Of the 15 cases, six foxes were found dead, six were captured but died during attempted rehabilitation, and three were successfully treated. We have no evidence that untreated kit foxes can recover from mange. Sarcoptic mange constitutes a significant threat to the Bakersfield kit fox population and could pose an even greater threat to this imperiled species if it spreads to populations in nearby natural lands.

Avian trichomonosis, caused by the flagellated protozoan parasite Trichomonas gallinae, has variable pathogenicity among bird species ranging from asymptomatic infections to severe disease periodically manifesting in epidemic mortality. Traditionally, columbids are identified as highly susceptible to infection with occasional spillover into raptors that prey on infected birds. We identified avian trichomonosis in two dead California spotted owls (Strix occidentalis occidentalis) and three dead northern spotted owls (S. o. caurina) in California during 2011–2015; infection was confirmed in four owls by PCR. Pathologic lesions associated with trichomonosis in the owls included caseonecrotic lesions of the upper palate accompanied by oropharyngitis, cellulitis, myositis, and/or sinusitis. Spotted owls are known to mainly feed on small mammals; therefore, the source of infection as well as the significance of the disease in spotted owls is unclear. These owl trichomonosis cases coincided temporally and spatially with three trichomonosis epidemics in band-tailed pigeons (Patagioenas fasciata monilis). The same parasite, T. gallinae subtype A2, was isolated from the spotted owls and band-tailed pigeons, suggesting the owls became infected when opportunistically feeding on pigeons during mortality events. Avian trichomonosis is an important factor in the decline of the Pacific Coast band-tailed pigeon population with near-annual mortality events during the last 10 years and could have conservation implications for raptor species at risk, particularly those that are facing multiple threats., Graphical abstract Image 1, Highlights • Band-tailed pigeons evaluated for trichomonad infections during mortality events. • Spotted owls evaluated for trichomonad infections coinciding with mortality events. • Trichomonads characterized using ITS1/5.8S rRNA/ITS2 and Fe-hydrogenase loci. • Trichomonas gallinae subtype A2 was predominant parasite in both pigeons and owls.

© 2016, © 2016 The Author(s). Infestation with nonnative, “exotic” lice was first noted in Washington black-tailed deer (Odocoileus hemionus columbianus) in 1994 and has since then spread throughout the western United States. In California, infestation with the exotic louse Damalinia (Cervicola) sp. was first detected in black-tailed deer from northern California in 2004, and, in 2009, the exotic louse species Bovicola tibialis and Linognathus africanus were identified on mule deer (Odocoileus hemionus californicus) in central Sierra Nevada in association with a mortality event. Exotic lice have since been detected in various locations throughout the state. We describe the geographic distribution of these exotic lice within California, using data from 520 live-captured and 9 postmortem-sampled, free-ranging mule deer examined between 2009 and 2014. Data from live-captured deer were used to assess possible associations between louse infestation and host age, host sex, migratory behavior, season, and blood selenium and serum copper concentrations. Damalinia (Cervicola) sp. and B. tibialis lice were distinctively distributed geographically, with D. (Cervicola) sp. infesting herds in northern and central coastal California, B. tibialis occurring in the central coastal mountains and the Sierra Nevada, and L. africanus occurring only sporadically. Younger age classes and low selenium concentrations were significantly associated with exotic louse infestation, whereas no significant relationship was detected with serum copper levels. Our results show that exotic lice are widespread in California, and younger age classes with low blood selenium concentrations are more likely to be infested with lice than older deer.

Aspergillosis continues to be a significant infection resulting in morbidity and mortality in a variety of animal hosts, ranging from sea fans to elephants. Infections with this ubiquitous saprophytic mold have a significant impact on our domestic pets, livestock, commercial poultry, captive birds, as well as a variety of wildlife species. In mammals and birds, infection is usually acquired after inhalation of conidia (spores). Infection often results from invasion by the opportunistic Aspergillus spp., as a secondary invader or when immune defenses wane. However, Aspergillus spp. can also act as primary pathogens in some animals, such as birds, dogs, or horses. Clinical presentation and site of infection in the various animal species are varied due to unique anatomopathological characteristics (e.g., air sac in birds, guttural pouch in horses, sinus cavity in dogs, etc.) which also require varied methods of diagnosis and treatment (e.g., lavage treatment of dogs with sinus cavity disease versus oral or parenteral therapy of pulmonary infections). Aspergillus fumigatus is the most common pathogenic species identified in the animal kingdom; however, other Aspergillus spp. have also been implicated in disease. Early antemortem diagnosis remains challenging even with the variety of test modalities. Evaluation of environmental fungal loads and newer molecular tools such as microsatellites have helped identify risks and origin of infection. Animals also serve as useful models for human infection and treatment, so understanding the pathogenesis in these models may provide insight into human prevention, diagnosis, and treatment. The broad health and economic impacts of aspergillosis to veterinary medicine across so many animal species makes additional studies crucial.

Seven colostrum-deprived, 3–4-wk-old Rambouillet–Hampshire lambs were inoculated via the mucous membranes with deer adenovirus (DAdV) and monitored for clinical signs for 21 d post-inoculation at which time animals were euthanized and postmortem examinations were performed. Pre-inoculation and post-inoculation serum samples were tested for antibodies to DAdV, ovine adenovirus 7, bovine adenovirus 7, and goat adenovirus 1. Evidence for DAdV infection was determined by virus isolation, PCR tests, and histopathology with immunohistochemistry tests for DAdV. No clinical signs or lesions consistent with adenoviral hemorrhagic disease (AHD) in deer were seen in the lambs, and the lambs did not seroconvert to DAdV. DAdV was not detected by PCR, virus isolation, or immunohistochemistry in any of the samples tested from the lambs. A positive control deer similarly inoculated with DAdV developed fatal AHD 1 wk post-inoculation. Our colostrum-deprived lambs did not become infected when inoculated with DAdV.

Avian trichomonosis is an upper digestive tract disease of birds typically caused by the protozoan parasite Trichomonas gallinae. In California (U.S.A), trichomonosis is known to cause periodic epidemics in the Pacific Coast band-tailed pigeon (Patagioenas fasciata monolis), a migratory upland game bird. We summarize the mortality events that occurred during winter 2014–2015 including the duration, estimated mortality, pathology, and genetic identity of infecting parasites. Increased mortality was reported from locations in 25 counties between November 2014 and June 2015. Based on reports, carcasses received, wildlife rehabilitation center admissions, site visits, and regular monitoring by local personnel, total mortality was estimated at 18,440. At necropsy, birds had multiple coalescing lesions in the oral cavity involving the upper palate and/or around the tongue and glottis, esophagus, crop, and/or proventriculus. Birds collected from Contra Costa (63.9%; 30/47); Marin (75.0%; 6/8), San Mateo (46.7%; 14/30), and Santa Clara (35.0%; 37/106) counties were more likely to have lesions extending into their head involving muscle, sinuses, ear canals, eye sockets, and bone (χ2 = 62.9; df = 11; P < 0.001). Histopathologic findings included pharyngitis, esophagitis, myositis, and air sacculitis of the pneumatic bone of the skull. Mixed bacterial colonies were found multifocally at the fronts of the necrosis in six of the eleven birds examined histologically. Infecting trichomonads included T. gallinae subtype A2 (n = 5), un-typed T. gallinae (n = 4), mixed infection with T. gallinae subtype A2 and T. stableri (n = 1), and mixed infection with un-typed T. gallinae and T. stableri (n = 1). The winter 2014–2015 epidemic was the largest on record in terms of duration, locations, and birds affected. Infection dynamics may have been exacerbated by the drought in California. Increased monitoring of band-tailed pigeons is needed to understand the long-term impacts of large-scale mortality events on their population. Keywords: Avian trichomonosis, Band-tailed pigeon, Epidemic, Trichomonas gallinae, ITS1/5.8S rRNA/ITS2, Fe-hydrogenase

We reviewed case records from the California Animal Health and Food Safety (CAHFS) laboratory and the California Department of Fish and Wildlife (CDFW) spanning 25 years (1990–2014) for all deer accessions submitted to CAHFS for pathology and/or histopathology, with and without a diagnosis of adenoviral hemorrhagic disease (AHD), in order to determine the prevalence of AHD in California. We also examined spatial and temporal distribution, age, and mule deer subspecies in deer that died from AHD. Of 483 deer submitted to CAHFS for diagnostic testing in 1990–2014, 17.2% were diagnosed with confirmed AHD, and 26.5% were confirmed plus suspected cases of AHD. Columbian black-tailed deer ( Odocoileus hemionus columbianus), particularly fawns and juveniles, were most frequently affected. Deer adenovirus ( Odocoileus adenovirus 1; OdAdV-1) was detected by immunohistochemistry in archived CDFW formalin-fixed, paraffin-embedded tissues from deer that died in mortality events in 1981, 1983, and 1986–1987. OdAdV-1 is a common cause of hemorrhagic disease mortality events in California deer, and mortality as a result of AHD is documented as early as 1981.

Used in both beef cattle and dairy cows, monensin can provide many health benefits but can, when unintended overexposures occur, result in adverse effects. Information on serum and tissue concentrations following overexposure and/or overt toxicosis which may aid in diagnostics and clinical outcome is lacking. The aim of this study was to determine concentrations of monensin in biological specimens following oral exposure for 10 days to an approved dose (1 mg/kg) and a higher dose (5 mg/kg) of monensin given daily on a body weight basis to 10 dairy cows. No deaths were reported; cows receiving 5 mg/kg showed early signs of toxicosis including depression, decreased feed intake, and diarrhea after 4 days of exposure. Histopathological findings were minimal in most cows. Pharmacokinetic modeling of the detected serum concentrations for the 1 and 5 mg/kg dose groups determined the Cmax , Tmax, and t1/2λ to be 0.87 and 1.68 ng/mL, 2.0 and 1.0 h, and 1.76 and 2.32 days, respectively. Mixed regression models showed that the dose level and days since last dose were significantly associated with monensin concentrations in all four tissues, and with cardiac troponin levels. The high dose resulted in a significant elevation of monensin in tissues at approximately 4.7 times compared to the monensin concentrations in the tissues of animals from the low-dose group. The cTnI concentrations in the high-dose group were 2.1 times that of cTnI in the low-dose group. Thus, the ability to diagnose monensin overexposure and/or toxicosis will improve from knowledge of biological monensin concentrations from this study.

Fishers (Pekania pennanti) in the west coast states of Washington, Oregon, and California, USA have not recovered from population declines and the United States Fish and Wildlife Service has proposed options for listing them as threatened. Our objectives were to evaluate differences in survival and mortality risk from natural (e.g., predation, disease, injuries, starvation) and human-linked causes (e.g., rodenticide exposure [toxicants], vehicle strikes). We monitored survival of 232 radio-collared fishers at a northern and southern study site in the Sierra National Forest, California. We retrieved fisher carcasses, and used necropsy examinations to determine causes of death. We estimated survival and mortality rates using the Kaplan–Meier estimator and nonparametric cumulative incidence functions, respectively, and integrated risk-specific survival rates into a Leslie matrix to evaluate how population growth (λ) might improve if management can reduce mortality from any of the risks. We determined cause of death for 93 of 121 fishers, and annual survival was 0.69 for all fishers, and 0.72 for female fishers. Mortality rates were 19.5% for predation; 2.5% for disease, injury, and starvation; and 1.9% for toxicant exposure and vehicle strikes. Predation rates were similar between sexes, and relative risk was 51% lower in fall and winter compared to spring and summer. Combined mortality from disease, injuries, starvation, vehicle strikes, and toxicants was 4.4%, and 11 times higher for males than females. We estimated a base λ at the northern site of 0.96, which had the potential to increase to 1.03 or 1.11 if predation were reduced by 25% or 50%, respectively, whereas λ could increase to 0.97 in the absence of deaths from all other risks except predation. Predation was the dominant limiting factor in our study population, and was also the most common mortality risk for fishers in the 3 West Coast states (67%), followed by disease, injury, and starvation (12%) and vehicle strikes (8%). Direct mortality from toxicants appeared limited to fishers in California. Our results identified the need for continued and potential expanded restrictions on habitat disturbance in fisher denning habitats. Research is needed on contact rates between larger predators and fishers, including whether fishers are more vulnerable to attack in open forests or along roads used by coursing predators. © 2015 The Wildlife Society.

Measuring trace mineral concentrations can be an important component of assessing the health of free-ranging deer. Trace mineral concentrations in liver most accurately reflect the trace mineral status of an individual, but, in live animals, whole blood or serum are the most commonly used sample types. Trace minerals measured in serum, such as copper, zinc, and iron, do not always accurately correlate to liver concentrations, and supplementary samples for evaluating the trace mineral status in live deer would be useful. We evaluated the utility of body and tail hair for measuring selenium, copper, zinc, iron, and manganese in free-ranging mule deer ( Odocoileus hemionus) by using Spearman rank correlations and linear regression. Correlations were strongest at the time of or shortly after growth of the winter coat and in resident deer. In live deer, strong correlations and moderate linear associations ( R2 = 0.57) were detected between body and tail hair and whole blood selenium in December. In postmortem-sampled deer, a strong correlation and linear association ( R2 = 0.80) were found between liver and body hair selenium in August–November. Results indicate that body hair, if collected during or shortly after growth of the winter coat, can be used as a supplementary sample for measuring selenium concentrations in deer. None of the other correlations and linear associations were found to be sufficiently strong to conclude that hair can reliably be utilized as a complementary sample for measuring these trace mineral concentrations.

We characterize the genome of the first reported deer parvovirus, Ungulate tetraparvovirus 5, which we detected by PCR in multiple tissues from 2/9 California mule deer (Odocoileus hemionus californicus) with hair loss syndrome (HLS) and in 4/12 deer without HLS, suggesting this common infection does not cause HLS.

We present the first complete genome sequence of Odocoileus hemionus deer adenovirus 1 (OdAdV-1). This virus can cause sporadic haemorrhagic disease in cervids, although epizootics with high mortality have occurred in California. OdAdV-1 has been placed in the genus Atadenovirus, based on partial hexon, pVIII and fibre genes. Ten field isolates recovered from naturally infected mule deer (Odocoileus hemionus), white-tailed deer (Odocoileus virginiana) and moose (Alces alces) from Wyoming, black-tailed deer (Odocoileus hemionus columbianus) from California, and Rocky Mountain elk (Cervus elaphus nelsoni) from Colorado and Washington state were sequenced. The genome lengths ranged from 30 620 to 30 699 bp, contained the predicted proteins and gene organization typical of members of genus Atadenovirus, and had a high percentage of A/T nucleotides (66.7 %). Phylogenic analysis found that the closest ancestry was with ruminant atadenoviruses, while a divergence of the hexon, polymerase and penton base proteins of more than 15 % supports classification as a new species. Genetic global comparison between the 10 isolates found an overall 99 % identity, but greater divergence was found between those recovered from moose and elk as compared to deer, and a single variable region contained most of these differences. Our findings demonstrate that OdAdV-1 is highly conserved between 10 isolates recovered from multiple related cervid species, but genotypic differences, largely localized to a variable region, define two strains. We propose that the virus type name be changed to cervid adenovirus 1, with the species name Cervid atadenovirus A. Sequence data were used to develop molecular assays for improved detection and genotyping.

Tyzzer's disease was diagnosed as the cause of mortality in free-ranging hatch-year passerine birds in Southern California, US. Birds presented with ataxia, tremors, and opisthotonos and died or were euthanized. Postmortem examination of four birds identified encephalitis on microscopy with characteristic stacked, slender bacterial rods visible with special stains. Infection with Clostridium piliforme was confirmed by real-time PCR.

Causes of morbidity and mortality and a survey of infectious disease agents were collated from wild and colony-raised endangered Amargosa voles (Microtus californicus scirpensis). Six voles from the wild and 295 voles in the captive-breeding colony were included in the study upon identification of an infectious agent during screening, identification of clinical signs of disease, or finding a pathological condition or infectious agent on necropsy. Findings included 28 significant or incidental pathological conditions of seven organ systems and 19 parasitic, viral, bacterial, or fungal agents. Several voles captured in the wild had fungal osteomyelitis of the tail that disseminated systemically in a vole brought from the wild to the colony and may have been caused by a Penicillium sp. Three voles reintroduced from the colony to the wild experienced inanition and subsequent severe hepatic and moderate renal tubular lipidosis. The most common significant pathological conditions in colony-reared voles were chronic interstitial nephritis with proteinosis; cardiomyopathy; trichobezoars that, in intestines or cecocolic junctions, sometimes induced local rupture or infarction with peritonitis; multifocal gastrointestinal ulceration and colibacillosis; acute renal tubular necrosis or nephritis; sepsis; hepatic and renal lipidosis; molar apical elongation sometimes progressing to invasion of the calvarium; and mammary tumors. Uncommon diagnoses included intervertebral disc disease; microvascular dysplasia; and multifocal bacterial abscessation. Common or clinically important infectious agents included Demodex sp. mites in hair follicles, Demodex sp. in esophageal mucosa, and an outbreak of tropical rat mites thought to have been introduced via the straw bedding; gastrointestinal Helicobacter sp.; attaching and effacing Escherichia coli; and Citrobacter braakii, a possible zoonotic bacterium. This survey of species-specific diseases and pathogens was possible because the established health surveillance program that is part of the species recovery plan allowed for monitoring of voles throughout the duration of their natural life spans in captivity.

Two horses were referred for methemoglobinemia and hemolytic anemia following 5 acute deaths in their herd from an unidentified toxin source. Horses have a greater risk than other mammalian species of developing methemoglobinemia and hemolytic anemia following ingestion of oxidizing toxins, due to deficiencies in the mechanisms that protect against oxidative damage in erythrocytes. Their susceptibility to oxidative erythrocyte damage is evident in the numerous cases of red maple ( Acer rubrum) toxicosis. The suspected toxins causing A. rubrum toxicosis are tannic acid, gallic acid, and a metabolite of gallic acid, pyrogallol. These compounds can be found in a variety of plants, posing a risk to equine health. In order to quickly identify toxin sources, 2 rapid in vitro assays were developed to screen plant extracts for the ability to induce methemoglobin formation or cause hemolysis in healthy equine donor erythrocytes. The plant extract screening focused on 3 species of the genus Pistacia: P. atlantica, P. terebinthus, and P. chinensis, which were located in the horse pasture. Extracts of the seeds and leaves of each species induced methemoglobin formation and resulted in hemolysis, with seed extracts having greater potency. The in vitro assays used in the current study provide a useful diagnostic method for the rapid identification of oxidizing agents from unidentified sources. There is no effective treatment for oxidative erythrocyte damage in horses, making rapid identification and removal of the source essential for the prevention of poisoning.

American crows are acutely sensitive to West Nile virus (WNV) infection, and crow mortality has been used in WNV surveillance to monitor enzootic transmission. However, non-WNV sources of mortality could reduce the reliability of crow death as a surveillance tool. Here, using a combination of histopathologic, toxicologic, virologic, and molecular techniques we describe causes of mortality in 67 American crows (Corvus brachyrhynchos) that were collected from a population in the Sacramento Valley of California in 2012 and 2013. Evidence of infectious disease was detected in 70% (47/67) of carcasses. The majority of deaths were linked to a suite of non-WNV viral, bacterial, and fungal infections (39%; 23/59 cases), WNV (36%; 24/67 cases), and an acute toxic event (25%; 15/59 cases). Coinfections were detected in 20% (12/59) of birds and frequently were associated with WNV and poxviral dermatitis. Inferences about WNV activity based on crow mortality should be supported by laboratory confirmation because crow mortality frequently can be caused by other infectious diseases or toxic events.

Interspecific killing is common among carnivores and can have population-level effects on imperiled species. The fisher (Pekania [Martes] pennanti) is a rare forest carnivore in western North America and a candidate for listing under the United States Endangered Species Act. Interspecific killing and intraguild predation are poorly understood in fishers and potential threats to existing western populations. We studied the prevalence and patterns of interspecific killing of fishers in the southern Sierra Nevada and Coastal Range of California. We collected forensic evidence and samples from the carcasses and predation sites, conducted full necropsies when possible, and used molecular methods to determine species of predators responsible for killing fishers. We recovered 101 (59 female, 42 male) fisher carcasses; for 62 (61%) carcasses, we attributed cause of death to interspecific killing. We found that bobcats (Lynx rufus, n = 25 fisher mortalities), mountain lions (Puma concolor, n = 20), and coyotes (Canis latrans, n = 4) were predators of fishers in our study areas. Bobcats killed only female fishers, whereas mountain lions more frequently killed male than female fishers, confirming our hypothesis that female fishers would suffer lethal attacks by smaller predators than would male fishers. Coyotes rarely killed fishers. We found differences in pathologic characteristics of the predation events among the 3 predator species, which may be helpful in identifying predator species. © 2014 The Wildlife Society.

Graphical abstract, Highlights • Trichomonad protozoa infecting free-ranging band-tailed pigeons were characterized. • Trichomonas gallinae and novel species T. stableri were isolated in sick birds. • T. stableri is significantly smaller in length and width than T. gallinae. • T. stableri is genetically more similar to T. vaginalis than to T. gallinae. • T. stableri is a secondary agent of trichomonosis in band-tailed pigeons., Trichomonas gallinae is a ubiquitous flagellated protozoan parasite, and the most common etiologic agent of epidemic trichomonosis in columbid and passerine species. In this study, free-ranging Pacific Coast band-tailed pigeons (Patagioenas fasciata monilis) in California (USA) were found to be infected with trichomonad protozoa that were genetically and morphologically distinct from T. gallinae. In microscopic analysis, protozoa were significantly smaller in length and width than T. gallinae and were bimodal in morphology. Phylogenetic analysis of the ITS1/5.8S/ITS2, rpb1, and hydrogenosomal Fe-hydrogenase regions revealed that the protozoan shares an ancestor with Trichomonas vaginalis, the sexually-transmitted agent of trichomoniasis in humans. Clinical and pathologic features of infected birds were similar to infections with T. gallinae. Evidence presented here strongly support taxonomical distinction of this parasite, which we hereby name Trichomonas stableri n. sp. This work contributes to a growing body of evidence that T. gallinae is not the sole etiologic agent of avian trichomonosis, and that the incorporation of molecular tools is critical in the investigation of infectious causes of mortality in birds.

Mortality of 20% of a flock of 1000 chukar partridge chicks occurred over a 6-week period in Northern California from August to September 2012. Affected birds were 2 to 42 days old and died without premonitory clinical signs or after showing ruffled feathers and anorexia for 24 to 72 hours. Three carcasses were submitted for necropsy, 2 birds had hemorrhagic tracheitis grossly, and all 3 had lymphoplasmacytic and histiocytic myocarditis with myocardial necrosis microscopically. The differential diagnoses and the diagnostic workup to achieve a final diagnosis are discussed. The detection of 2 zoonotic agents in these birds makes this an interesting case from a public health perspective.

Retrospective analysis of pigeon necropsy submissions to the California Animal Health and Food Safety Laboratory System from 2000 to 2018 revealed 14 submissions diagnosed with rotavirus A hepatic necrosis or “reoviruslike” viral hepatitis. Nine of the 14 submissions (64%) occurred in 2018. Submissions were racing pigeons and squab breeders from flocks with increased mortality. Juvenile and adult pigeons were submitted with a history of depression, diarrhea, regurgitation, labored breathing, and weakness. Flock morbidity peaked at 80% and mortality at 28%. The most consistent findings on postmortem examination were variably congested, mottled, and enlarged livers and spleens. Microscopically, mild to severe hepatic necrosis was observed with variable bile duct hyperplasia, sinusoidal congestion, hemosiderosis, and portal lymphoplasmacytic inflammation. Rotavirus A was detected in hepatocytes and inflammatory cells by immunohistochemistry. Negative-stain electron microscopy identified viral particles consistent with a member of Reoviridae in all negatively stained liver homogenates. Eleven cases were analyzed by reverse transcriptase-PCR targeting rotavirus A viral protein (VP) 6 and VP7 genes. Subsequent phylogenetic analysis of the VP6 and VP7 sequences compared to published Chinese, Nigerian, and German rotavirus A VP6 and VP7 sequences demonstrated the formation of two and three distinct clades, respectively. To the authors’ knowledge, rotavirus A hepatic necrosis in pigeons has not been previously reported in the United States and represents a significant emerging disease for the pigeon industry due to the potential for high flock mortality and lost production.

We describe an investigation of an outbreak of conjunctivitis in juvenile House Finches (Haemorhous mexicanus) and California Scrub-jays (Aphelocoma californica) at a central California wildlife rehabilitation facility. In late May 2015, the facility began admitting juvenile finches, the majority with normal eyes at intake. In June, with juvenile finches already present, the facility admitted additional juvenile scrub-jays, again all with normal eyes at intake. In July, after conjunctivitis was observed in increasing numbers of juvenile finches and scrub-jays, carcasses were submitted for postmortem examination. Histopathology of five finches and three scrub-jays identified lymphocytic infiltrates in the ocular tissues. Conjunctival swabs from 87% (13/15) finches and 33% (4/12) scrub-jays were PCR-positive for Mycoplasma gallisepticum. One finch and two scrub-jays were PCR-positive for Mycoplasma synoviae. Additionally, gene sequencing (16S rRNA and 16S-23S intergenic spacer region) identified Mycoplasma sturni from 33% (3/9) scrub-jays. This outbreak of conjunctivitis suggested that M. gallisepticum-infected juvenile finches admitted to and maintained in a multispecies nursery likely resulted in transmission within the facility to healthy juvenile finches and scrub-jays. Evidence of other Mycoplasma spp. in finches and scrub-jays indicates that these species are susceptible to infection and may act as carriers. This outbreak highlighted the need for effective triage and biosecurity measures within wildlife rehabilitation facilities.

Diisocyanates, commonly used in the production of polyurethane foams, paints, elastomers, varnishes, and coatings, are considered among the most hazardous inhalation toxicants. The present report describes 2 unusual cases of mortality in pigeon chicks associated with nesting material contaminated by diisocyanates. Case 1 was submitted by a racing pigeon breeder who had lost all the hatchlings ( n = 125) following replacement of the nesting material with a different lot. All adult birds appeared healthy, and hatchability was not significantly affected, but hatchlings became lethargic and dyspneic after a day of hatch. At necropsy, dark wet lungs were found in the hatchlings. Case 2 was submitted by a show-roller pigeon breeder. In this case, the owner reported lower hatchability, and all hatchlings (approximately 100) died within 2 days of hatching with clinical signs similar to the first case. Necropsy did not reveal any significant findings. For both cases, nesting materials were screened for toxic compounds using gas chromatography–mass spectrometry. Toluene-2,4-diisocyanate (approximately 190–290 ppm) and 4,4′-methylene diphenyl diisocyanate (unquantified) were detected in the nesting pads. While there is very limited information on toxicosis in birds, there are reports of inhalant exposure of diisocyanates causing pulmonary edema and death in various mammalian species. Although cause–effect relationship of mortality and the nesting material was not established in the present cases, the presence of toxic compounds in the nesting materials is a cause for concern. Further investigation is needed to determine the prevalence and toxicity of diisocyanates-contaminated nesting material in avian species.

Notoedric mange was responsible for a population decline of bobcats ( Lynx rufus ) in 2 Southern California counties from 2002-2006 and is now reported to affect bobcats in Northern and Southern California. With this study we document clinical laboratory and necropsy findings for bobcats with mange. Bobcats in this study included free-ranging bobcats with mange (n = 34), a control group of free-ranging bobcats without mange (n = 11), and a captive control group of bobcats without mange (n = 19). We used 2 control groups to evaluate potential anomalies due to capture stress or diet. Free-ranging healthy and mange-infected bobcats were trapped or salvaged. Animals were tested by serum biochemistry, complete blood count, urine protein and creatinine, body weight, necropsy, and assessment for anticoagulant rodenticide residues in liver tissue. Bobcats with severe mange were emaciated, dehydrated, and anemic with low serum creatinine, hyperphosphatemia, hypoglycemia, hypernatremia, and hyperchloremia, and sometimes septicemic when compared to control groups. Liver enzymes and leukocyte counts were elevated in free-ranging, recently captured bobcats whether or not they were infested with mange, suggesting capture stress. Bobcats with mange had lower levels of serum cholesterol, albumin, globulin, and total protein due to protein loss likely secondary to severe dermatopathy. Renal insufficiency was unlikely in most cases, as urine protein:creatinine ratios were within normal limits. A primary gastrointestinal loss of protein or blood was possible in a few cases, as evidenced by elevated blood urea nitrogen, anemia, intestinal parasitism, colitis, gastric hemorrhage, and melena. The prevalence of exposure to anticoagulant rodenticides was 100% (n = 15) in bobcats with mange. These findings paint a picture of debilitating, multisystemic disease with infectious and toxic contributing factors that can progress to death in individuals and potential decline in populations.

Fatty liver hemorrhagic syndrome, characterized by sudden death in overconditioned hens due to hepatic rupture and hemorrhage, is one of the leading noninfectious idiopathic causes of mortality in backyard chickens. Nutritional, genetic, environmental, and hormonal factors, or combinations of these, have been proposed yet not proven as the underlying cause. In an attempt to characterize the hepatic changes leading to the syndrome, this retrospective case study examined 76 backyard chickens that were diagnosed with fatty liver hemorrhagic syndrome between January 2007 and September 2012 and presented for necropsy to the diagnostic laboratory of the California Animal Health and Food Safety Laboratory System. A majority of the birds were female (99%), obese (97.5%), and in active lay (69.7%). Livers were examined histologically, and the degree of hepatocellular vacuolation (lipidosis), the reticular stromal architecture, the presence of collagenous connective tissue, and vascular wall changes were evaluated and graded using hematoxylin and eosin, Gomori’s reticulin, oil red O, Masson’s trichrome, and Verhoeff-Van Gieson stains. Interestingly, there was no correlation between lipidosis and reticulin grades; hepatocellular lipidosis was absent in 22% of the cases and mild in 26% of the cases. Additionally, there was evidence of repeated bouts of intraparenchymal hemorrhage before the acute “bleed-out” in 35.5% of the cases. These data are not supportive of the previously proposed causes and provide a framework for future studies to elucidate the pathogenesis of this condition. Furthermore, the data shown in this study support hemorrhagic liver syndrome as a more accurate name, as hepatic lipidosis is absent in a significant proportion of ruptured livers.

Avian poxvirus (genus Avipoxvirus, family Poxviridae) is an enveloped double-stranded DNA virus that may be transmitted to birds by arthropod vectors or mucosal membrane contact with infectious particles. We characterized the infection in Anna's Hummingbird (Calypte anna; n = 5 birds, n = 9 lesions) by conducting diagnostic tests on skin lesions that were visually similar to avian poxvirus lesions in other bird species. Skin lesions were single or multiple, dry and firm, pink to yellow, with scabs on the surface, and located at the base of the bill, wings, or legs. Microscopically, the lesions were characterized by epidermal hyperplasia and necrosis with ballooning degeneration, and intracytoplasmic inclusions (Bollinger bodies) in keratinocytes. The 4b core gene sequence of avian poxvirus was detected by PCR in samples prepared from lesions. Nucleotide sequences were 75-94% similar to the sequences of other published avian poxvirus sequences. Phylogenetic analyses showed that the Anna's Hummingbird poxvirus sequence was distinguished as a unique subclade showing similarities with sequences isolated from Ostrich (Struthio camelus), Wild Turkey (Meleagris gallopavo), falcons (Falco spp.), Black-browed Albatross (Diomedea melanophris), Mourning Dove (Zenaida macroura) and White-tailed Eagle (Haliaeetus albicilla). To our knowledge this is the first published report of definitive laboratory diagnosis of avian poxvirus in a hummingbird. Our results advance the science of disease ecology in hummingbirds, providing management information for banders, wildlife rehabilitators, and avian biologists.

Reports of primary nervous system tumors in wild raccoons are extremely rare. Olfactory tumors were diagnosed postmortem in 9 free-ranging raccoons from 4 contiguous counties in California and 1 raccoon from Oregon within a 26-month period between 2010 and 2012. We describe the geographic and temporal features of these 10 cases, including the laboratory diagnostic investigations and the neuropathologic, immunohistochemical, and ultrastructural characteristics of these tumors in the affected animals. All 9 raccoons from California were found within a localized geographic region of the San Francisco Bay Area (within a 44.13-km radius). The tight temporal and geographic clustering and consistent anatomic location in the olfactory system of tumor types not previously described in raccoons (malignant peripheral nerve sheath tumors and undifferentiated sarcomas) strongly suggest either a common cause or a precipitating factor leading to induction or potentiation of neuro-oncogenesis and so prompted an extensive diagnostic investigation to explore possible oncogenic infectious and/or toxic causes. By a consensus polymerase chain reaction strategy, a novel, recently reported polyomavirus called raccoon polyomavirus was identified in all 10 tumors but not in the normal brain tissue from the affected animals, suggesting that the virus might play a role in neuro-oncogenesis. In addition, expression of the viral protein T antigen was detected in all tumors containing the viral sequences. We discuss the potential role of raccoon polyomavirus as an oncogenic virus.

Within a 24-hour period, 7 out of 200 three- to four-week-old pastured Katahdin lambs died after showing clinical signs of hemoglobinuria, red-tinged feces, weakness, and recumbency. One of the lambs that was examined clinically before natural death also had abdominal pain, trembling, tachycardia, and severe anemia with a packed cell volume of 4%. Pathologic findings included icterus, hemoglobinuric nephrosis, dark red urine, pulmonary edema, hydrothorax, splenomegaly, and acute centrilobular to midzonal hepatocellular degeneration and necrosis with cholestasis. The differential diagnoses and diagnostic workup to achieve the diagnosis are briefly discussed.

The entire range of the critically endangered Amargosa vole (Microtus californicus scirpensis) consists of less than 20 km(2) of riparian habitat in the Amargosa River drainage of the Mojave Desert in southern California. In September 2010, deformities on ears and chiggers on the ears and genitalia were detected, with some individuals so severely affected that they were missing ear pinnae altogether. Follow-up trapping was performed to document the presence of mites and mite-associated disease, and molecular characterization was performed on the mites. Of 151 Amargosa voles sampled from February to April of 2011, 60 (39.7%) voles had hard orange mites adhered to some part of their bodies, on ears of 46 (76.7%), on genitalia of 11 (18.3%), and near mammary tissue of 13 (21.7%) voles. Gross lesions were not detected on genitalia, but 47% of all individuals examined showed pinnal lesions and deformities, which included alopecia, swelling, marginal necrosis, and ulceration, as well as scarring, scabbing, and loss of pinna mass covering 25-100% of the pinnae. Biopsies revealed parakeratotic hyperkeratosis and acanthosis with diffuse neutrophilic exocytosis and dense necrotic granulocytes in the epidermis and superficial dermis associated with focal erosion and ulceration. In the underlying dermis, there were dense pleocellular inflammatory cell infiltrates composed primarily of necrotic granulocytes and multifocal hemorrhage. In some samples, mite mouthparts could be seen penetrating the superficial epidermis associated with focal necrosis, and mite fragments were found on the surface epidermis and within hair follicles. Microscopic examination of the mites documented that they were a larval trombiculid in the genus Neotrombicula with anatomical features that most closely resemble Neotrombicula microti, based on scutal shape, setation, and texture. PCR of 2 mite pools (each consisting of 3 mites from an individual animal) amplified 331 bp amplicons, which had 92-97% homology with the 18S rRNA gene of Leptotrombidium deliense, although coverage of Trombiculidae in GenBank is sparse. The severity and prevalence of lesions due to this chigger were atypical and distinct. Severe clinical trombiculiasis in this endangered species could negatively impact individual health and fitness.

During 2010 and 2011, 933 recently deceased birds, submitted as part of the dead bird surveillance program, tested positive for West Nile virus RNA at necropsy. The relative amount of RNA measured by qRT-PCR cycles ranged from 8.2 to 37.0 cycle threshold (Ct) and formed a bimodal frequency distribution, with maxima at 20 and 36 Ct and minima at 28–30 Ct. On the basis of frequency distributions among different avian species with different responses to infection following experimental inoculation, field serological data indicating survival of infection, and the discovery of persistent RNA in experimentally infected birds, dead birds collected in nature were scored as “recent” or “chronic” infections on the basis of Ct scores. The percentage of birds scored as having chronic infections was highest during late winter/spring, when all birds were after hatching year, and lowest during late summer, when enzootic transmission was typically highest as indicated by mosquito infections. Our data indicated that intervention efforts should not be based on dead birds with chronic infections unless supported by additional surveillance metrics.

An orphaned 4-mo-old female mountain lion cub (Puma concolor) was captured along the coastline in Montana de Oro State Park in Los Osos, California, USA. Following suspicion that the cub was visually impaired, ophthalmic examination revealed diffuse bilateral retinal atrophy. Due to a poor prognosis, humane euthanasia was elected. Necropsy and histopathological findings were consistent with photoreceptor degeneration. Based on the cub's signalment, history, and histopathology, a genetic or nutritional etiology was suspected, with the former etiology more strongly supported. To the authors' knowledge, this is the first report of photoreceptor degeneration in a wild felid and should be considered in cases of blindness.

Summary Between 2008 and 2009, three pet ferrets from different sources presented with acute episode of dyspnoea. Cytological examination of pleural exudates revealed severe purulent inflammation with abundant clusters of rod-shaped microorganisms with a clear surrounding halo. Treatment was ineffective and the ferrets died 2–5 days later. Two ferrets were subjected to necropsy examination, which revealed pyothorax, mediastinal lymphadenopathy and multiple white nodules (1–2 mm) in the lungs. Microscopical examination showed multifocal necrotizing-pyogranulomatous pleuropneumonia and lymphadenitis with aggregates of encapsulated microorganisms, some of which were positively stained by periodic acid–Schiff and alcian blue. In-situ hybridization for Pneumocystis spp., Ziehl–Neelsen staining and immunohistochemistry for distemper, coronavirus and influenza antigen were negative in all cases. Electron microscopically, the bacteria were 2–3 μm long with a thick electron-lucent capsule. Microbiology from one ferret yielded a pure culture of gram-negative bacteria identified phenotypically as Pseudomonas luteola. This speciation was later confirmed by 16S RNA gene amplification.

Two 2- and 3-month-old beef calves from 2 separate herds, locations, and times were found dead and were submitted to the veterinary diagnostic laboratory for diagnostic work-up. In both cases, no premonitory signs were seen by the owners. Histopathology revealed acute panlobular hepatic necrosis in both calves. In addition, calf A had copper and selenium deficiency, and calf B had oxalate nephrosis, and selenium and zinc deficiencies. Alpha-amanitin was detected in the urine from calf A, and in the liver and rumen contents from calf B using liquid chromatography–mass spectrometry. The cause of panlobular hepatic necrosis and death of both calves was determined to be amanitin toxicosis from ingestion of amanitin-containing mushrooms based on microscopic changes and toxicological analysis of tissues. In cases of sudden death in cows with histopathological findings of panlobular hepatic necrosis, toxicological analysis for amanitin is needed for a definitive diagnosis of poisoning by amanitin-containing mushrooms.

The devastating effect of West Nile virus (WNV) on the avifauna of North America has led zoo managers and conservationists to attempt to protect vulnerable species through vaccination. The Island Scrub-Jay (Aphelocoma insularis) is one such species, being a corvid with a highly restricted insular range. Herein, we used congeneric Western Scrub-Jays (Aphelocoma californica) to test the efficacy of three WNV vaccines in protecting jays from an experimental challenge with WNV: (1) the Fort Dodge West Nile-Innovator(®) DNA equine vaccine, (2) an experimental DNA plasmid vaccine, pCBWN, and (3) the Merial Recombitek(®) equine vaccine. Vaccine efficacy after challenge was compared with naïve and nonvaccinated positive controls and a group of naturally immune jays. Overall, vaccination lowered peak viremia compared with nonvaccinated positive controls, but some WNV-related pathology persisted and the viremia was sufficient to possibly infect susceptible vector mosquitoes. The Fort Dodge West Nile-Innovator DNA equine vaccine and the pCBWN vaccine provided humoral immune priming and limited side effects. Five of the six birds vaccinated with the Merial Recombitek vaccine, including a vaccinated, non-WNV challenged control, developed extensive necrotic lesions in the pectoral muscle at the vaccine inoculation sites, which were attributed to the Merial vaccine. In light of the well-documented devastating effects of high morbidity and mortality associated with WNV infection in corvids, vaccination of Island Scrub-Jays with either the Fort Dodge West Nile-Innovator DNA vaccine or the pCBWN vaccine may increase the numbers of birds that would survive an epizootic should WNV become established on Santa Cruz Island.

West Nile virus (WNV) infection was diagnosed in 38 psittacine birds based on histology, immunohistochemistry, and reverse transcriptase polymerase chain reaction (RT-PCR). Rosellas ( Platycercus spp, n = 13), conures ( Enicognathus, Aratinga, and Nandayus spp, n = 6), and lorikeets ( Trichoglossus spp, n = 6) represented the most commonly affected species. Clinical signs ranged from lethargy, ruffled feathers, anorexia, and weight loss in most birds to sudden death in others. Except for mild to moderate enlargement of liver and spleen, there were no significant gross lesions at necropsy. Histopathologic findings included lymphoplasmacytic and histiocytic hepatitis, interstitial nephritis, myocarditis, splenitis, enteritis, pancreatitis, and occasionally, encephalitis. Viral antigen was detected by immunohistochemistry in 34 of 35 hearts (97.1%), 29 of 32 pancreata (90.6%), 33 of 37 kidneys (89.2%), 31 of 35 intestines (88.6%), 27 of 33 gizzards (81.8%), 8 of 10 ovaries (80%), 27 of 34 spleens (79.4%), 30 of 38 livers (78.9%), 23 of 32 lungs (71.9%), 21 of 31 proventriculi (67.7%), 14 of 21 adrenals (66.7%), 10 of 16 testes (62.5%), 17 of 30 brains (56.7%), 15 of 27 skins (55.5%), 3 of 6 oviducts (50%), 15 of 34 skeletal muscles (44.1%), 11 of 27 crop or esophagus (40.7%), and 1 of 6 thymuses (16.7%). Kidney was positive for WNV by RT-PCR in all the cases tested. In conclusion, Psittaciformes are susceptible to West Nile virus infection, and WNV infections are often associated with nonspecific clinical signs and widespread viral distribution in this order of birds.

Aspergillus fumigatus causes disease in birds. Our objectives were to determine pharmacokinetic parameters and evaluate efficacy of voriconazole (VCZ) in a novel experimental quail model. After a single oral VCZ dose of 20 or 40 mg/kg, plasma concentrations peaked 2 h postdose (5.8 and 6.9 μg/ml) and remained above 0.5 μg/ml for 4 and 12 h postdose, respectively. For the efficacy study, ten-day-old Japanese quail (n = 60) were infected intratracheally with A. fumigatus conidia. Daily oral VCZ at 20 or 40 mg/kg was initiated 24 h postinfection (PI); infected diluent-treated birds were given de-ionized water orally. Preassigned birds were euthanized on days 5 or 10 PI. VCZ at 40 mg/kg prolonged survival compared to 20 mg/kg or diluent-treatment (P < 0.05) and lungs from birds given VCZ at 40 mg/kg had fewer colony forming units (CFU) than diluent-treated (P = 0.03). At day 10 PI, birds treated with VCZ at 20 mg/kg had significantly fewer fungi in the lungs as demonstrated by methenamine silver stain (P = 0....

A group of finches were accidentally overdosed with ronidazole, a 5-nitroimidazole used for treatment of trichomoniasis. Finches developed neurologic signs on the third day of treatment and were euthanized (or died). Three finches were submitted for necropsy. Focal necrosis of the cerebellar nucleus was seen in all 3 birds, as characterized by neuronal necrosis, vacuolation of the neuropil, gemistocytic astrocytosis, hemorrhage, and axonal swelling (spheroids) with demyelination. The liver from 1 finch was analyzed for ronidazole and its metabolite, 2-hydroxymethyl-1-methyl-5-nitroimidazole, by high-performance liquid chromatography–mass spectrometry. Ronidazole was detected in the liver tissue at 2,700 ng/g (wet weight), and 2-hydroxymethyl-1-methyl-5-nitroimidazole was detected at 140 ng/g (wet weight).

Abortion and death caused by Francisella tularensis were well recognized in range flocks of domestic sheep in Idaho, Montana, and Wyoming in the first 6 decades of the 20th century. The current report describes 4 episodes of tularemia in 3 range flocks in Wyoming and South Dakota in 1997 and 2007 (1 flock was affected twice). Flock owners reported that ticks were unusually numerous and commonly present on sheep during outbreaks. Tularemia presented as late-term abortions (3 episodes) or listlessness and death in lambs and, to a lesser extent, ewes (1 episode). Lesions were multifocal pinpoint necrotic foci in tissues, particularly spleen, liver, and lung. An immunohistochemical procedure demonstrated F. tularensis, particularly in necrotic foci. The diagnosis was corroborated by bacterial isolation and, in individual cases, by serology, fluorescent antibody assay, and/or polymerase chain reaction detection of F. tularensis. Diagnosticians in endemic areas should include tularemia as a differential diagnosis when investigating late-term abortions or outbreaks of fatal illness in young lambs, particularly in years of high tick activity and when characteristic necrotic foci occur in spleen, liver, and lung.