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Epiploic foramen entrapment (EFE) is a common cause of small intestinal colic in horses and may lead to intestinal strangulation. Strangulating intestinal obstruction impairs the gastrointestinal outflow and can lead to secondary gastric rupture and endotoxemia. Clostridioides difficile can cause enterotyphlocolitis with colic in horses of all ages, and the process is commonly referred to as C. difficile-associated disease (CDAD). Here we report the results of the postmortem examination of a 7-y-old Thoroughbred racehorse with concurrent CDAD, EFE, and gastric rupture that was euthanized following a history of colic over several days. A segment of distal jejunum and proximal ileum had passed through the epiploic foramen, and the intestinal wall was thickened and dark-red. The remaining small intestinal loops were distended and filled with blood-tinged contents. Peritonitis had resulted from escape of gastric contents into the abdominal cavity through a tear in the major curvature of the stomach. Histologically, the incarcerated segment had acute transmural hemorrhage with congestion and mucosal necrosis; neutrophilic infiltrates with fibrin thrombi were in the mucosa of the non-incarcerated small intestinal segments. C. difficile toxins were detected in the small intestinal contents, and C. difficile was isolated from the small intestine, colon, and cecum.

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.

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.

An outbreak of rabbit hemorrhagic disease virus 2 (RHDV2)-associated disease occurred in the southwestern United States following its first detection in New Mexico in March 2020. The disease spread throughout several states and was diagnosed for the first time in California on May 11, 2020, in a black-tailed jackrabbit (Lepus californicus). The following day, the California Department of Food and Agriculture (CDFA) issued an order banning the entrance into California of several lagomorph species and their products from any state in which the disease had been detected in the last 12 mo. RHDV2 is a threat to wild lagomorph species in California, including the endangered riparian brush rabbit (Sylvilagus bachmani riparius). Therefore, the California Department of Fish and Wildlife (CDFW) started tracking any mortality event in wild lagomorph populations. As of August 9, 2020, RHDV2 had been detected in wild and domestic lagomorphs of several counties in southern California that were submitted to the California Animal Health and Food Safety laboratory system by the CDFA or the CDFW. These positive cases included 2 additional black-tailed jackrabbits and 3 desert cottontail rabbits (Sylvilagus audubonii). In addition, the infection spilled over to domestic populations, whereby it was confirmed on July 10, 2020, in a domestic rabbit (Oryctolagus cuniculus).

The different ovine production and breeding systems share the cornerstone of keeping a good body condition to ensure adequate productivity. Several infectious and parasitic disorders have detrimental effects on weight gains and may lead to emaciation. Flock health management procedures are aimed to prevent such conditions. Nutritional management is equally important to guarantee adequate body condition. Persistent bouts of low ruminal pH due to excess concentrate in the diet may lead to subacute ruminal acidosis. Pre-stomach motility disorders may also lead to ill-thrift and emaciation. An adequate mineral supplementation is key to prevent the effects of copper, selenium, and other micronutrients deprivation, which may include, among others, loss of condition. This review elaborates on the clinico-pathologic, diagnostic, and therapeutic aspects of some of these conditions, and highlights the necessity of considering them as contributors to states of wasting in sheep flocks.

Infectious and parasitic agents have been frequently associated with debilitating and wasting conditions in sheep. The prevalence of these agents has probably undermined the role of toxic causes as contributors to such disorders. In addition, many of these intoxications frequently produce acute clinical disease with specific and characteristic lesions, thus a causal relationship with the toxic substance may be relatively easy to establish. However, persistent exposure to some of these organic or inorganic toxic substances may lead to emaciation, ill-thrift, and poor external aspect. The anti-nutritional factors and alkaloids of several plants, including pyrrolizidine alkaloids, among others, have also been associated with emaciation and/or poor general performance in sheep flocks. In this review, some of these disorders are discussed with an emphasis on clinical signs and lesions, relevant diagnostic aspects, and available therapeutic approaches. In most cases, demonstrating a history of exposure should be one of the most relevant aspects of the diagnostic approach, and removing the animals from the toxic source is the cornerstone of the majority of the treatment strategies.

Enteric disease in horses may be caused by a variety of microorganisms, including several clostridial species. Paeniclostridium sordellii (previously Clostridium sordellii) has been frequently associated with gas gangrene in humans and several animal species, including horses. However, its role in enteric diseases of animals has not been fully determined. We describe herein 7 cases of enteric disease in horses associated with P. sordellii infection. Grossly, the small and/or large intestines were necrotic, hemorrhagic, and edematous. Microscopically, there was severe mucosal necrosis and hemorrhage of the small and/or large intestine of all horses. P. sordellii was isolated and/or demonstrated by immunohistochemistry and/or PCR in the intestine of all horses. All other known causes of enteric disease in horses were ruled out in these 7 cases. P. sordellii should be considered among the differential diagnoses in cases of enteric disease in horses.

Streptococcus equi subspecies zooepidemicus septicemia of alpacas and llamas, also called alpaca fever, is characterized clinically by fever, depression, recumbency, and death, and pathologically by polyserositis. Although a few natural and experimental cases of the disease have been reported, very little information about the pathology of spontaneous cases has been published. We present a detailed gross and microscopic description of 3 spontaneous cases of alpaca fever and review the literature on this condition. Typical of spontaneous and experimental infections with S. equi ssp. zooepidemicus, the 3 animals had disseminated fibrinosuppurative polyserositis with vascular thrombosis and intralesional gram-positive cocci. In addition, 2 of the animals had severe fibrinosuppurative pneumonia, endocarditis, and myocardial necrosis; the third animal had transmural pleocellular enteritis with prominent lymphangitis. The enteric lymphangitis observed in the latter suggests that dissemination of S. equi ssp. zooepidemicus occurred through lymphatic circulation and that, at least in this animal, the portal of entry of infection was the alimentary system.

A 14-y-old bay Quarter Horse gelding was presented with progressive neurologic signs, elevated rectal temperature, and icterus for 3 d prior to death. Postmortem examination revealed icterus, large amounts of serosanguineous fluid in the abdominal cavity, widespread petechiae and ecchymoses in several organs, and a large, pale, and well-demarcated focus of necrosis in the liver. Histologically, there was coagulative necrosis surrounded by a rim of inflammatory cells and large numbers of gram-positive rods, which were identified as Clostridium novyi by immunohistochemistry. Liver samples tested by PCR were positive for C. novyi type B flagellin and alpha toxin genes, but negative for Clostridium haemolyticum and other clostridia. Based on postmortem findings and ancillary tests, a definitive diagnosis of infectious necrotic hepatitis (INH) was made. Mostly a disease of ruminants, also known as black disease, INH has rarely been reported in horses, and a definitive etiologic diagnosis has not been achieved previously; the etiology of all cases reported to date was identified as C. novyi but the type was not determined. Animals are predisposed to clostridial hepatitis when hepatic anaerobiosis is established. Such conditions allow germination and proliferation of bacterial spores, resulting in production and release of toxins. INH, caused by C. novyi type B, and bacillary hemoglobinuria, caused by C. haemolyticum, are mechanistically and pathologically almost indistinguishable. Because these 2 microorganisms are closely related, differentiation requires molecular tools.

Five horses originating from 4 different California race tracks were submitted to the California Animal Health and Food Safety Laboratory for necropsy and diagnostic workup. The 5 horses had a history of sudden collapse and death during exercise. In all of them, massive hemoperitoneum and hemorrhages in other cavities or organs were observed. The liver from these 5 animals and from 27 horses that had been euthanized due to catastrophic leg injuries (controls) were subjected to a rodenticide anticoagulant screen. Traces of brodifacoum, diphacinone, or bromadiolone were detected in the 5 horses with massive bleeding (5/5), and no traces of rodenticides were detected in control horses (0/27). Other frequent causes of massive hemorrhages in horses were ruled out in 4 of the cases; one of the horses had a pelvic fracture. Although only traces of anticoagulants were found in the livers of these horses and the role of these substances in the massive bleeding remains uncertain, it is speculated that exercise-related increases in blood pressure may have reduced the threshold for toxicity of these anticoagulants.

Notoedric mange, caused by the contagious, burrowing mite Notoedres centrifera, has been associated with several large-scale population declines of western gray squirrels (Sciurus griseus) and has been a significant obstacle to population recovery in Washington State where the species is listed as threatened. In 2009, residents and wildlife rehabilitators in the isolated San Bernardino Mountains of southern California reported a dramatic die-off of western gray squirrels, in what had been a previously dense and robust population. Individuals were observed suffering from abnormal neurologic behaviors (ataxia and obtundation) and severe skin disease. Full necropsy of five squirrels from the epidemic showed that all had moderate to severe infestation with mange mites and severe dermatitis characterized by hyperkeratosis, acanthosis, intralesional mites, intracorneal pustules and superficial bacteria. Mites from affected squirrels were evaluated by light and electron microscopy and identified as N. centrifera based on morphologic criteria. Additionally, the internal transcribed spacer-2 region of the mite was cloned, sequenced and accessioned in GenBank. The cause for the abnormal neurologic behavior was not confirmed on post-mortem examination. However, we hypothesize that mange can cause incoordination and obtundation as a result of malnutrition and dehydration, and intense pruritis may induce abnormal or erratic behavior that could be mistaken for neurologic signs. While we have characterized the severe impact this disease can have on individual animals, more work is needed to understand the impact on squirrel populations, particularly in view of the anecdotal reports of dramatic population declines that may take decades to recover.