Yellow lamb disease is an infrequent disease in sheep for which there is scant literature, and that has been reported in the US, Australia, New Zealand, South Africa and Europe, although anecdotal evidence indicates that it may have also been diagnosed in South America. The disease is produced by some strains of Clostridium perfringens type A that produce unusually high levels of alpha- toxin. Because C. perfringens type A is ubiquitous and is found in the intestine of most clinically healthy sheep, diagnosis of yellow lamb disease is challenging and requires quantitating the amount of this microorganism present in feces and/or intestinal content. Clinically, yellow lamb disease is characterized by depression, anemia, icterus and hemoglobinuria. Occasionally, sudden death may occur. Gross findings include generalized icterus, red urine in the bladder, enlarged, pale, and friable spleen, enlarged liver with an acinar pattern, and dark, swollen kidneys. Microscopically, yellow lamb disease is characterized by centrilobular necrosis of the liver, hemoglobinuria-associated acute tubular injury, splenic congestion, pulmonary congestion and edema. Although there are no vaccines specifically designed to prevent yellow lamb disease, several vaccines against the different types of C. perfringens may afford at least some level of protection against yellow lamb disease.

The clostridial diseases of horses can be divided into three major groups: enteric/enterotoxic, histotoxic, and neurotoxic. The main enteric/enterotoxic diseases include those produced by Clostridium perfringens type C and Clostridioides difficile, both of which are characterized by enterocolitis. The main histotoxic diseases are gas gangrene, Tyzzer disease, and infectious necrotic hepatitis. Gas gangrene is produced by one or more of the following microorganisms: C. perfringens type A, Clostridium septicum, Paeniclostridium sordellii, and Clostridium novyi type A, and it is characterized by necrotizing cellulitis and/or myositis. Tyzzer disease is produced by Clostridium piliforme and is mainly characterized by multifocal necrotizing hepatitis. Infectious necrotic hepatitis is produced by Clostridium novyi type B and is characterized by focal necrotizing hepatitis. The main neurotoxic clostridial diseases are tetanus and botulism, which are produced by Clostridium tetani and Clostridium botulinum, respectively. Tetanus is characterized by spastic paralysis and botulism by flaccid paralysis. Neither disease present with specific gross or microscopic lesions. The pathogenesis of clostridial diseases involves the production of toxins. Confirming a diagnosis of some of the clostridial diseases of horses is sometimes difficult, mainly because some agents can be present in tissues of normal animals. This paper reviews the main clostridial diseases of horses.

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.

Gastrointestinal disorders are among the most common disease processes in captive elephants. Colic is a frequent clinical presentation and may have several infectious and noninfectious causes. Ingestion of sand has been reported in elephants living in enclosures with loose sandy soils. Similar to the situation in horses, sand ingestion can cause intestinal impaction and colic in elephants. Here we describe a case of colonic sand impaction with cecal rupture and peritonitis in an African savanna elephant from a zoologic collection that died after several days of colic. On autopsy, abundant, gritty, sandy material was found within a segment of colon immediately aboral to the cecum. There was a full-thickness tear in the cecal wall, free intestinal contents within the abdominal cavity, and peritonitis. To our knowledge, the postmortem examination of an elephant with sand impaction and cecal rupture has not been reported previously; this condition should be included among the differential diagnoses in elephants with colic. We review the reports of noninfectious causes of gastrointestinal disease in elephants, which include cases of small intestinal and colonic torsion and of intestinal obstruction by fecal boluses.

Squamous cell carcinoma (SCC), which is a neoplasm that usually arises from the integument, is reported uncommonly in pet birds. Only a few reports of SCCs in the alimentary tract of birds, including psittacines, have been published, and a detailed description of the pathology is not available in the literature. We present here 12 cases of alimentary SCC in psittacines. The average age of the birds was 22.2 y (range: 15-29 y), and affected species included 4 Amazon parrots (Amazona sp.), 3 cockatiels (Nymphicus hollandicus), 3 macaws (Ara sp.), 1 conure (Eupsittula sp.), and 1 Senegal parrot (Poicephalus sp.). Frequent clinical complaints included regurgitation, dysphagia, dyspnea, lethargy, and/or weight loss. SCC primarily affected the oral cavity in 6 of 12 cases, the crop alone in 2 of 12 cases, the crop and esophagus in 1 of 12 cases, the proventriculus alone in 1 of 12 cases, and the crop, esophagus, and proventriculus in 2 of 12 cases. Histologically, alimentary SCCs were locally invasive and often resulted in mucosal ulceration. Although there were no metastases in any of our cases, poor clinical outcomes were frequent and associated most commonly with complete effacement of the alimentary segment and severe inflammation with opportunistic bacterial infection. Our review of the literature records commonly affected species, variability of gross presentations and clinical signs, plausible etiologies, and current diagnostic developments.

Rickets is a metabolic bone disease associated with failure of endochondral ossification and impaired osteoid mineralization in growing animals. As a consequence, affected individuals can develop gross and microscopic bone malformations. The most common causes of rickets in domestic species include vitamin D and phosphorus deficiency. Rickets has been described in multiple species; however, comprehensive postmortem characterizations with confirmatory histopathology in equids have not been published. A 6-mo-old, Thoroughbred-cross foal was diagnosed with rickets based on gross autopsy findings and microscopic examination of the ribs and long bones. Grossly, all costochondral junctions of the ribs were enlarged with a "rachitic rosary" appearance, and there were multiple fracture calluses in the rib bodies. Epiphyses and metaphyses of the long bones appeared widened on sagittal section, and their physes were irregularly thickened. Histologically, there were poorly organized columns of hypertrophic chondrocytes within the physes of affected bones, islands of chondrocytes embedded within the primary and secondary spongiosa, and faintly eosinophilic seams of poorly mineralized osteoid within the bone trabeculae. Areas of focally increased osteoclastic activity were observed in some of the sections, perhaps pointing to a more complex metabolic bone disease in a growing animal. Low serum concentrations of calcium and 25-hydroxyvitamin D were detected in an antemortem sample. The pathogenesis of these imbalances was not definitively established, but lack of sunlight exposure, low concentration of vitamin D precursors in the diet (perhaps secondary to malnutrition), or both, were suspected; a genetic basis cannot be ruled out.

Enteritis, colitis, and enterocolitis are considered some of the most common causes of disease and death in horses. Determining the etiology of these conditions is challenging, among other reasons because different causes produce similar clinical signs and lesions, and also because some agents of colitis can be present in the intestine of normal animals. We review here the main bacterial and viral causes of enterocolitis of horses, including Salmonella spp., Clostridium perfringens type A NetF-positive, C. perfringens type C, Clostridioides difficile, Clostridium piliforme, Paeniclostridium sordellii, other clostridia, Rhodococcus equi, Neorickettsia risticii, Lawsonia intracellularis, equine rotavirus, and equine coronavirus. Diarrhea and colic are the hallmark clinical signs of colitis and enterocolitis, and the majority of these conditions are characterized by necrotizing changes in the mucosa of the small intestine, colon, cecum, or in a combination of these organs. The presumptive diagnosis is based on clinical, gross, and microscopic findings, and confirmed by detection of some of the agents and/or their toxins in the intestinal content or feces.

Reproductive failure represents an important cause of economic loss for the equine industry. We reviewed the cases of equine abortion and stillbirth submitted to the California Animal Health and Food Safety Laboratory System, University of California-Davis from 1990 to 2022. A total of 1,774 cases were reviewed. A confirmed cause of abortion was determined in 29.2% of the cases. Abortion or stillbirth was attributed to infectious agents in 18.7% of the cases, with Streptococcus spp., equine herpesvirus 1, and Leptospira spp. being the most prevalent. Noninfectious causes of abortion were established in 10.5% of the cases, with umbilical cord torsion being the most common. In 70.8% of the cases, a definitive cause of abortion could not be established. Our study demonstrated the difficulties in establishing an etiologic diagnosis, even when following a standard diagnostic work-up. New diagnostic approaches are needed to improve the likelihood of reaching a final diagnosis in cases of equine abortion and stillbirth.

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.

Enterotoxemia caused by Clostridium perfringens type D usually affects sheep and goats ≥ 2-wk-old. The main clinical signs and lesions of the disease are produced by the epsilon toxin (ETX) elaborated by this microorganism. However, ETX is produced in the form of a mostly inactive prototoxin that requires protease cleavage for activation. It has traditionally been believed that younger animals are not affected by type D enterotoxemia given the low trypsin activity in the intestinal content associated with the trypsin-inhibitory action of colostrum. Two Nigerian dwarf goat kids, 2- and 3-d-old, with a history of acute diarrhea followed by death, were submitted for postmortem examination and diagnostic workup. Autopsy and histopathology revealed mesocolonic edema, necrosuppurative colitis, and protein-rich pulmonary edema. Alpha toxin and ETX were detected in intestinal content, and C. perfringens type D was isolated from the colon of both animals. The isolates encoded the gene for lambda toxin, a protease that has been shown previously to activate ETX in vitro. Type D enterotoxemia has not been reported previously in neonatal kids, to our knowledge, and we suggest that lambda toxin activated the ETX.