Natural Infection with H5N1 Highly Pathogenic Influenza (HPAI) Virus in 5- and 10-Day-Old Commercial Pekin Ducklings (Anas platyrhynchos domesticus).

Highly pathogenic avian influenza (HPAI) has resulted in catastrophic economic losses globally in poultry. This case report describes the diagnostic detection and pathology of HPAI H5N1 in 5-day-old commercial ducklings, which is an atypical age for detection of natural infection of HPAI in poultry. The pathology observed at 5 days of age was also compared to lesions observed in ducklings from the same flock evaluated at 10 days of age before depopulation. The California Animal Health and Food Safety (CAHFS) Laboratory, Tulare, received ten 5-day-old Pekin duckling (Anas platyrhynchos domesticus) carcasses for diagnostic evaluation due to mortality that started increasing at 3 days of age. The most common gross findings included bilateral pulmonary edema with congestion and enlarged, mottled livers and spleens. Microscopically, cerebral neuronophagia, pancreatic necrosis, and interstitial pneumonia with pulmonary edema were observed in the 5-day-old ducklings. Oropharyngeal and cloacal swabs were positive for avian influenza virus (AIV) by real-time reverse transcriptase PCR. The AIV was typed as HPAI, EA/AM 2.3.4.4b H5N1 goose/Guangdong clade lineage by the National Veterinary Services Laboratory. Ducks at the affected premises were depopulated 4 days after the 5-day-old ducklings were submitted to the CAHFS lab, at which time additional tissue samples were collected for comparison to 10-day-old ducklings on the same premises. Differences in microscopic lesions and AIV tissue distribution were observed between the 5-day and 10-day tissues collected. Notably, microscopic lesions were more severe in the brain and pancreas at 10 days of age. Findings in 10-day-old ducklings included cerebral lymphoplasmacytic perivascular cuffing, gliosis, neuronal degeneration, and pancreatic necrosis. AIV antigen distribution and intensity was greatest in the cerebral tissue of the brains at 10 days and in the lungs at 5 days of age. To the authors' knowledge, published studies are limited on AIV natural infection in domestic ducks less than 9 days of age.

Infección natural con el virus de la influenza altamente patógena (HPAI) H5N1 en patitos Pekín comerciales (Anas platyrhynchos domesticus) de 5 y 10 días de edad. La influenza aviar altamente patógena (HPAI) ha provocado pérdidas económicas catastróficas en todo el mundo entre las aves de corral. Este reporte de caso describe la detección diagnóstica y la patología de la infección por un virus de influenza aviar de alta patogenicidad H5N1 en patitos comerciales de 5 días de edad, que es una edad atípica para la detección de la infección natural del virus de la influenza aviar de alta patogenicidad en avicultura. La patología observada a los 5 días de edad también se comparó con las lesiones observadas en patitos de la misma parvada evaluados a los 10 días de edad, antes de la despoblación. El Laboratorio de Salud Animal y Seguridad Alimentaria de California (CAHFS), con sede Tulare, recibió 10 cadáveres de patito Pekín (Anas platyrhynchos domesticus) de 5 días de edad para su evaluación diagnóstica debido a que la mortalidad comenzó a aumentar a los 3 días de edad. Los hallazgos macroscópicos más comunes incluyeron edema pulmonar bilateral con congestión en hígado y bazos agrandados y moteados. Microscópicamente se observó neuronofagia cerebral, necrosis pancreática y neumonía intersticial con edema pulmonar en los patitos de 5 días de edad. Los hisopos orofaríngeos y cloacales fueron positivos para el virus de la influenza aviar (AIV) mediante transcripción reversa y PCR en tiempo real. El Laboratorio Nacional de Servicios Veterinarios clasificó al virus como de alta patogenicidad EA/AM 2.3.4.4b H5N1 clado de linaje de ganso/clado Guangdong. Los patos en las instalaciones afectadas fueron despoblados 4 días después de que los patitos de 5 días fueran enviados al laboratorio de CAHFS, momento en el cual se recolectaron muestras de tejido adicionales para compararlas con patitos de 10 días de las mismas instalaciones. Se observaron diferencias en las lesiones microscópicas y la distribución del tejido del AIV entre los tejidos recolectados de 5 y 10 días. En particular, las lesiones microscópicas fueron más severas en el cerebro y en el páncreas a los 10 días de edad. Los hallazgos en patitos de 10 días incluyeron infiltraciones linfoplasmocitarias perivasculares en el cerebro, gliosis, degeneración neuronal y necrosis pancreática. La distribución e intensidad del antígeno de influenza aviar fue mayor en el tejido cerebral de los cerebros a los 10 días y en los pulmones a los 5 días de edad. De acuerdo al conocimiento de los autores, los estudios publicados sobre la infección natural por el virus de la influenza aviar en patos domésticos de menos de 9 días de edad son limitados.

Salmonellosis in elephants in managed care: report of 2 cases and literature review.

In animals, salmonellosis is seen typically as enteritis and/or septicemia. Subclinical infection also occurs, and outwardly healthy animals can serve as reservoirs of infection. Reports of salmonellosis in elephants are rare, limited to a few serovars, and the gross and microscopic lesions of enteric salmonellosis in this species have not been described in detail. We present here, in 2 elephants in managed care settings, cases of salmonellosis that resulted from infection by Salmonella enterica serovar Muenchen and S. enterica serovar Montevideo, serovars that have not been described previously as the cause of salmonellosis in elephants, to our knowledge. We also review the literature on salmonellosis in elephants. Animal A, an adult Asian elephant that was euthanized because of gastrointestinal hemorrhage, had multifocal, necrotizing, suppurative enterocolitis, and necrotizing gastritis. Animal B, an adult African elephant with chronic, recurrent colic, followed by death, had necrotizing typhlocolitis. The origin of infection was not determined in either case. The animals came from different facilities and did not have a common feed source. Previously reported cases of salmonellosis in elephants were caused by Salmonella Dublin, Salmonella Typhimurium, or Salmonella Enteritidis. The definitive diagnosis of salmonellosis is made based on compatible gross and microscopic lesions, coupled with the detection of Salmonella spp. in the affected tissues. Effective biosecurity should be adopted to minimize the risk of salmonellosis in elephants in managed care.

Coccidioidomycosis in 26 horses in California, USA: case series and review of the literature.

Coccidioidomycosis is a fungal disease caused by Coccidioides immitis or Coccidioides posadasii. We searched the records of the California Animal Health and Food Safety Laboratory from 1990 through 2020 for cases of coccidioidomycosis in horses. The selection criteria for these cases were: 1) live-born horses submitted for autopsy, and 2) a diagnosis of coccidioidomycosis was established, regardless of cause of death. During that time, 19,054 horses were received, and 26 cases (0.14%) of coccidioidomycosis were diagnosed in horses, of which 19 (73%) cases had pneumonia and/or pleuritis with or without lesions in other organs, and 7 (27%) cases had lesions only in organs other than the lungs (nasal mucosa, spleen, thoracic lymph nodes, heart, pericardial sac, liver, kidney, mediastinum, and/or mesentery). Pneumonia was diagnosed as the cause of death in 1,838 (9.64%) of the horses received; Coccidioides spp. was the cause of pneumonia in 19 (1.0%) of these animals. Horses have been reported to have low susceptibility to coccidioidomycosis, and the severity and chronicity of the disease can be variable. Lesions in our cases consisted of multifocal-to-coalescing pyogranulomas with intralesional fungal spherules. Coccidioidomycosis must be considered a differential diagnosis in cases of persistent cough, chronic weight loss, fever, and cases with a travel history to, or living in, a region considered endemic for coccidioidomycosis. Coccidioides spp. infection should also be considered when pyogranulomatous inflammation is found within lung, spleen, nasal mucosa, and lymph nodes of horses.

Renal Lesions in Horses with Oleander (Nerium oleander) Poisoning.

A presumptive postmortem diagnosis of oleander (Nerium oleander) poisoning is made based on the histological observation of cardiomyocyte degeneration and necrosis, which is considered to be a reliable diagnostic marker, and can be confirmed via the detection of oleandrin in tissues or fluids. However, cardiac lesions may not be present in every case, and autolysis can often preclude the identification of subtle changes in the cardiomyocytes. Several studies of experimental oleander poisoning have noted the presence of renal lesions in multiple mammalian species, and case studies of accidental exposure have found similar, although more variably severe, renal abnormalities. Kidney pathology in horses with oleander poisoning has been only briefly mentioned. In this study, we reviewed 21 cases of spontaneous oleander poisoning in horses, evaluated the kidneys microscopically, and compared the renal microscopic lesions with those detected in 10 horses that died or were euthanized due to other causes to assess if histological renal changes could serve as an additional diagnostic marker for oleander poisoning in horses. We found that microscopic renal lesions, principally mild to moderate tubular changes such as hyaline cast formation, neutrophilic casts, epithelial attenuation and necrosis, as well as mineralization and congestion, occur in horses with oleander poisoning. Most of these changes match the descriptions of lesions previously noted in other species, although with less frequency and severity. Similar lesions were found in horses that died spontaneously due to different causes or were euthanized. We concluded that microscopic renal lesions may be detected in horses with oleander poisoning but they cannot be used as a diagnostic marker that allows differentiation from other disease processes or causes of death.

Endemic Skunk amdoparvovirus in free-ranging striped skunks (Mephitis mephitis) in California.

The genus Amdoparvovirus includes the newly discovered skunk amdoparvovirus and the well-characterized Aleutian disease virus which causes significant health impacts in farmed mink worldwide. In 2010-2013, an outbreak of fatal amdoparvovirus-associated disease was documented in free-ranging striped skunks (Mephitis mephitis) from the San Francisco Bay Area of California. To characterize the geographic distribution, earliest occurrence and abundance of this virus, as well as possible impacts on sympatric mustelids of conservation concern, we tested blood samples from skunks throughout California and fishers (Pekania pennanti) from northern California for amdoparvovirus DNA. Amdoparvovirus DNA was detected in 64.8% of sampled skunks (140/216), and test-positive skunks were distributed widely throughout the state, from as far north as Humboldt County and south to San Diego County. The first test-positive skunks were detected from 2004, prior to the 2010-2013 outbreak. No significant spatial or temporal clustering of infection was detected. Although healthy and clinically ill animals tested positive for amdoparvovirus DNA, histopathologic evaluation of a subset from clinically ill skunks indicated that positive PCR results were associated with pneumonia as well as there being more than one inflammatory type lesion. None of 38 fishers were PCR-positive. Given the widespread geographic distribution and lack of a clear epizootic centre, our results suggest the presence of an endemic skunk-associated amdoparvovirus strain or species. However, if the virus is not host-specific, skunks' ubiquitous presence across rural and urban habitats may pose a risk to susceptible domestic and wild species including mustelids of conservation concern such as fishers and Pacific martens (Martes caurina).

Retrospective Study of Pasteurella multocida Diagnosed in Commercial Turkeys Submitted to California Animal Health and Food Safety Laboratory System; 1991-2017.

Fowl cholera is caused by the bacterium Pasteurella multocida and is known to cause significant economic losses in the commercial turkey industry. Four hundred and thirty cases of P. multocida in commercial turkeys, submitted to the California Animal Health and Food Safety Laboratory System (CAHFS) from January 1, 1991, to December 31, 2017, were analyzed. Records examined included CAHFS branch location, date of submission, clinical signs, company and premise of origin, age and sex of submitted turkeys, macroscopic findings, organs in which P. multocida was isolated, and serotype and fingerprint information. Increased mortality as high as 1200 birds per day was the most common complaint at submission, with acute septicemic lesions observed in the majority of cases. The mean age of turkeys diagnosed with fowl cholera was 14 wk, with a median age of 17 wk. Cases most frequently occurred from September to November, with 36% of cases occurring during this time period. Serotyping was performed in 350 cases, while fingerprinting was performed in 171 cases. Serotypes 3 and 3,4 were frequently identified in the 26-yr time period, while the fingerprints identified varied over time. Despite the decreasing population of commercial turkeys in California since the 1990s, fowl cholera continues to be an economically significant disease in this sector.

Estudio retrospectivo de Pasteurella multocida diagnosticado en pavos comerciales remitidos al Sistema de Laboratorios de Salud Animal y Seguridad Alimentaria del Estado de California; 1991­2017. La enfermedad de cólera aviar es causada por la bacteria Pasteurella multocida y se sabe que causa importantes pérdidas económicas en la industria comercial de pavos. Se analizaron cuatrocientos treinta casos de P. multocida en pavos comerciales, presentados al Sistema de Laboratorios de Salud Animal y Seguridad Alimentaria del Estado de California (CAHFS) desde el primero de enero del 1991 hasta el 31 de diciembre del 2017. Los registros examinados incluyeron la ubicación de la sede de CAHFS, la fecha de presentación, los signos clínicos, la compañía avícola y la granja de origen, la edad y el sexo de los pavos presentados, los hallazgos macroscópicos, los órganos en los que se aisló P. multocida y la información sobre serotipos y de genotipificación. El aumento de la mortalidad hasta 1200 aves por día fue la reclamación más común en el momento de la presentación, con lesiones septicémicas agudas observadas en la mayoría de los casos. La edad media de los pavos diagnosticados con cólera aviar fue de 14 semanas, con una edad media de 17 semanas. Los casos ocurrieron con mayor frecuencia de septiembre a noviembre, con el 36% de los casos ocurridos durante este período. La serotipificación se realizó en 350 casos, mientras que la genotificación se realizó en 171 casos. Los serotipos 3 y 3,4 se identificaron con frecuencia en el período de 26 años, mientras que los genotipos identificados variaron con el tiempo. A pesar de la disminución de la población de pavos comerciales en California desde la década de los 1990s, cólera aviar sigue siendo una enfermedad económicamente significativa en este sector.

Transcriptional Profiling of a Cross-Protective Salmonella enterica serovar Typhimurium UK-1 dam Mutant Identifies a Set of Genes More Transcriptionally Active Compared to Wild-Type, and Stably Transcribed across Biologically Relevant Microenvironments.

Vaccination with Salmonella enterica serovar Typhimurium lacking DNA adenine methyltransferase confers cross-protective immunity against multiple Salmonella serotypes. The mechanistic basis is thought to be associated with the de-repression of genes that are tightly regulated when transiting from one microenvironment to another. This de-repression provides a potential means for the production of a more highly expressed and stable antigenic repertoire capable of inducing cross-protective immune responses. To identify genes encoding proteins that may contribute to cross-protective immunity, we used a Salmonella Typhimurium DNA adenine methyltransferase mutant strain (UK-1 dam mutant) derived from the parental UK-1 strain, and assessed the transcriptional profile of the UK-1 dam mutant and UK-1 strain grown under conditions that simulate the intestinal or endosomal microenvironments encountered during the infective process. As expected, the transcriptional profile of the UK-1 dam mutant identified a set of genes more transcriptionally active when compared directly to UK-1, and stably transcribed in biologically relevant culture conditions. Further, 22% of these genes were more highly transcribed in comparison to two other clinically-relevant Salmonella serovars. The strategy employed here helps to identify potentially conserved proteins produced by the UK-1 dam mutant that stimulate and/or modulate the development of cross-protective immune responses toward multiple Salmonella serotypes.

MyD88- and TRIF-independent induction of type I interferon drives naive B cell accumulation but not loss of lymph node architecture in Lyme disease.

Rapidly after infection, live Borrelia burgdorferi, the causative agent of Lyme disease, is found within lymph nodes, causing rapid and strong tissue enlargement, a loss of demarcation between B cell follicles and T cell zones, and an unusually large accumulation of B cells. We sought to explore the mechanisms underlying these changes, as lymph tissue disruption could be detrimental for the development of robust Borrelia-specific immunity. A time course study demonstrated that the loss of the normal lymph node structure was a distinct process that preceded the strong increases in B cells at the site. The selective increases in B cell frequencies were due not to proliferation but rather to cytokine-mediated repositioning of B cells to the lymph nodes, as shown with various gene-targeted and bone marrow irradiation chimeras. These studies demonstrated that B. burgdorferi infection induced type I interferon receptor (IFNR) signaling in lymph nodes in a MyD88- and TRIF-independent manner and that type I IFNR indirect signaling was required for the excessive increases of naive B cells at those sites. It did not, however, drive the observed histopathological changes, which occurred independently also from major shifts in the lymphocyte-homing chemokines, CXCL12, CXCL13, and CCL19/21, as shown by quantitative reverse transcription-PCR (qRT-PCR), flow cytometry, and transwell migration experiments. Thus, B. burgdorferi infection drives the production of type I IFN in lymph nodes and in so doing strongly alters the cellular composition of the lymph nodes, with potential detrimental effects for the development of robust Borrelia-specific immunity.

Computed tomography findings in a 5-year-old Australian Cashmere goat (Capra hircus) suffering leukoencephalomyelitis due to caprine arthritis encephalitis virus.

Computed tomography was used to aid in the antemortem diagnosis of leukoencephalomyelitis in a goat infected by caprine arthritis encephalitis virus (CAEV). Imaging results were corroborated by histologic examination. This report discusses various methods of imaging the nervous system and their potential for use in the antemortem diagnosis of CAEV neurologic changes.

Résultats d'une tomodensitométrie chez une chèvre cachemire de l'Australie(Capra hircus)âgée de 5 ans souffrant d'une lymphoencéphalomyélite en raison du virus de l'arthrite caprine. La tomodensitométrie a été utilisée pour faciliter le diagnostic antemortem de la lymphoencéphalomyélite chez une chèvre infectée par le virus de l'arthrite-encéphalite caprine (VAE). Les résultats de l'imagerie ont été corroborés par l'examen histologique. Ce rapport discute les diverses méthodes d'imagerie du système nerveux et leur utilisation potentielle pour le diagnostic antemortem des changements neurologiques du VAE.(Traduit par Isabelle Vallières).