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This study presents the gross and histopathological findings of adenoviral hemorrhagic disease (AHD) in two yearling and one adult mule deer (Odocoileus hemionus). These cases represent the first known outbreak of deer adenovirus (Odocoileus adenovirus 1) in Arizona. Over the span of a month, three female captive mule deer were submitted to Midwestern University's Animal Health Institute for postmortem examination. All of these deer were from the same deer farm and historical findings were similar, consisting of acute presentation of hemorrhagic diarrhea and sudden death. Grossly and histopathologically, all cases had severe pulmonary edema and hemorrhagic enteritis. Additionally, two of the three cases had low numbers of large amphophilic intranuclear inclusions expanding endothelial cells within the small intestine and lungs. Viral PCR of pooled small intestine, lung, and spleen from each of the three cases were positive for deer adenovirus and negative for blue tongue and epizootic hemorrhagic disease.Baseline health parameters are limited in the primary literature for gray seals (Halichoerus grypus) in the northwest Atlantic. Accurate normal physiologic reference ranges for both species and specific geographic populations are vital tools for assessing the health of individuals and understanding the health of the entire population. This study developed comprehensive reference intervals for biochemical and hematologic parameters of recently weaned gray seal pups on Cape Cod, Massachusetts from samples collected in 2013, 2016, and 2017. Reference ranges were developed using methodology outlined by the American Society of Clinical Veterinary Pathology. By establishing more comprehensive biochemical and hematologic reference ranges for this population based on a robust sample size, this study provides a new tool for clinicians, researchers, and rehabilitation organizations to improve individual patient care and population research.Leptospirosis is the most common zoonotic disease worldwide and is considered endemic in countries with tropical climates. It is caused by 10 species of the Leptospira genus and by more than 275 serovars which can affect a wide range of vertebrates. In the Americas, 122 species of four classes of vertebrates have been reported to be infected or exposed to many Leptospira species. Many of these reports are from zoos and rehabilitation centers. Mexico has one single study that reported antibody titers against Leptospira in zoo animals. The purpose of this research was to identify the degree of exposure of some captive mammals and reptiles in Veracruz, a Mexican state with endemic leptospirosis, through microagglutination using 14 live strains of five Leptospira species. Sera samples were collected from 55 animals of 11 species from two classes (Mammalia and Reptilia), four orders (Primates, Artiodactyla, Carnivora, Crocodilia), and nine genera. The more prevalent serovars were Icterohaemorrhagiae and Tarassovi and the highest titers were reactive to the serovar Icterohaemorrhagiae with a value of 1 51,200.An anorexic 5-yr-old female giant anteater (Myrmecophaga tridactyla) developed multifocal ulcerative and vesicular lesions affecting the rostrum, oral cavity, and tongue. Disseminated skin lesions were also found on the body, affecting the feet, flanks, and genital area. Polymerase chain reaction confirmed a systemic viremic orthopoxvirus infection. Cowpox virus was considered to be the only likely etiological agent. Intensive supportive treatment, including daily fluid therapy, force-feeding, and anti-inflammatory administration achieved a successful outcome after 3 wk. To the authors' knowledge, this is the first time a giant anteater with severe orthopoxvirus lesions has survived the disease. This unique case discusses current and possible future therapeutic and prophylactic options for the treatment of orthopoxvirus infections in giant anteaters and other nondomestic animal species.Cheetahs (Acinonyx jubatus) are particularly susceptible to feline herpesvirus-1 (FHV-1). Recommendations for preventive health care in cheetahs include vaccination against FHV-1 using killed and modified live virus (MLV) vaccines. Although MLV vaccines tend to induce a more robust immune response than killed vaccines, they can induce disease. This case series details an FHV-1 outbreak in four adult cheetahs following the use of MLV vaccine in one of them. All four cheetahs developed severe FHV-1 clinical signs and were euthanized. Clinical signs included depression, anorexia, nasal discharge, ocular discharge, sneezing, and ulcerative dermatitis. Herpesvirus infection was diagnosed using history, clinical signs, polymerase chain reaction, and histologic evaluation. The timeline of events suggests the MLV vaccine was the inciting cause, although this was not conclusively proven. Outcome of this case suggests that when considering MLV vaccines for cheetahs, careful risk and benefit discussions are merited.Nine cases of amyloidosis in caracals (Caracal caracal) from three different institutions in Europe were reviewed and evaluated histopathologically. find more The six males and three females died between 2008 and 2018 at an age of 6 yr ± 2.5 mo (median ± interquartile range). In two out of nine (2/9) animals, amyloidosis was an incidental postmortem finding; the animals died of bronchopneumonia and gastric ulceration due to Helicobacter spp., respectively. Seven (7/9) animals suffered from acute renal failure due to amyloidosis, one of them additionally of cardiac decompensation. The predominant clinical signs were weight loss, lethargy, dys- or anorexia, dehydration, increased BUN and creatinine, and azotemia. The main gross lesion was a pale renal cortex on cut surface; in two animals, the kidneys appeared enlarged. Histologically, glomerular amyloid was present in every animal (9/9), and was the predominant renal manifestation of amyloidosis. Additional findings included splenic amyloid (8/8), amyloid in the lamina propria of the intestine (5/5), and amyloid in the lingual submucosa (4/4). Gastric mineralization was present in four animals suffering from renal failure. In the animal dying from bronchopneumonia, severe pancreatic amyloid deposits mainly affecting the exocrine pancreas (1/5) were identified. Immunohistochemistry was employed to identify amyloid AA in eight cases; only in the caracal dying from bronchopneumonia AA was amyloid confirmed. In several organs, especially in those where only small amyloid deposits were detected, a Congo red stain was often necessary to confirm the deposition. The etiology of the amyloidosis remains unknown. Three caracals were related within two generations, another three within four generations, so one might hypothesize a familial trait. In conclusion, amyloidosis should be considered as a significant disease in the caracal. Particularly in cases with renal disease, it should be included as a major differential diagnosis.