Leukocyte numbers and intestinal mucosal morphometrics in horses with no clinical intestinal disease

Healthy horses and other animals have large numbers of resident leukocytes in the intestinal wall, but there is scant information regarding which and how many leukocytes are normally present in the equine intestinal wall. Our aim was to provide a reference range of leukocytes in the intestinal mucosal and submucosal propria of normal horses. We included in our study intestinal tissues from 22 Thoroughbred racehorses with no clinical intestinal disease, which had been euthanized because of catastrophic musculoskeletal injuries. Neutrophils, lymphocytes, eosinophils, macrophages, and plasma cells were counted in 5 random 17,600-µm(2) areas of villus lamina propria of the duodenum, jejunum, and ileum, and deep lamina propria of the duodenum, jejunum, ileum, right ventral colon, left ventral colon, left dorsal colon, right dorsal colon, and small colon. Other features investigated in the same intestinal segments included villus height and width (small intestine), presence of ciliated protozoa, Paneth cells number, subcryptal leukocyte layers (number of leukocyte layers between the bottom of the crypts and the muscularis mucosae), and submucosal leukocytes. Lymphocytes were the most numerous cells in all segments analyzed, followed by plasma cells, eosinophils, macrophages, and neutrophils. Eosinophil numbers were significantly higher in both lamina propria and submucosa of the large intestine than in the small intestine. The duodenum had shorter and thinner villi than either jejunum or ileum. The data provided from our study will be useful for diagnosticians examining inflammatory processes in the intestinal tract of horses

Sudden death caused by spinal cord injury associated with vertebral fractures and fetlock failure in a Thoroughbred racehorse.

The most prevalent causes of death in racehorses are musculoskeletal injuries, causing ~83% of deaths within the racing industry in California and elsewhere. The vast majority of these injuries have preexisting lesions that predispose to fatal injury. A 4-y-old Thoroughbred colt suffered an acute suspensory apparatus failure, including biaxial proximal sesamoid bone fractures of the right front fetlock, causing loss of support of the fetlock joint and consequent fall with fractures of the cervical and sacral spine. Cervical fracture caused spinal cord damage that resulted in sudden death. A preexisting lesion in the medial proximal sesamoid bone likely predisposed to complete fracture of this bone and fetlock breakdown. Interestingly, a comparable osteopenic lesion was present in the intact medial proximal sesamoid bone of the left forelimb, which is consistent with bilateral repetitive overuse injury in racehorses. The morphologic features of the cervical and sacral spine fractures were compatible with acute injury; no evidence of preexisting lesions was seen. Most likely, these acute vertebral fractures occurred as a result of the horse falling. This case emphasizes the importance of performing a detailed autopsy in horses that suffer an appendicular musculoskeletal injury, particularly in fatal cases when the horse dies following a leg injury

Rickets in a Thoroughbred-cross foal: case report and review of the literature.

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

Colonic sand impaction with cecal rupture and peritonitis in an adult African savanna elephant, and review of noninfectious causes of gastrointestinal disease in elephants.

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

Detection and residence time of bisphosphonates in bone of horses.

Bisphosphonates are potent anti-resorptive agents that have the potential to adversely affect bone healing in equine athletes, and normal bone adaption in young racehorses. A concern exists that bisphosphonate inhibition of normal bone metabolism could lead to increased bone fractures during high-intensity exercise. We found only a single report describing concentrations of tiludronate in the bone of horses, and no studies describing clodronate. Knowledge of the residence time in bone could allow for a better understanding of the long-term effects of these compounds. Our objectives were to develop a method for detection of bisphosphonates in bone and add to the limited information available regarding the disposition of these drugs in the bone of horses. Two horses received clodronate and 2 tiludronate disodium. Postmortem collection of bones and teeth occurred either 4 or 30 d post drug administration. Additionally, postmortem blood, synovial fluid, aqueous humor, and bone samples from racehorses with various histories of bisphosphonate administration were collected, and concentrations determined using the developed LC-MS/MS method. Bisphosphonates were detected in bones and teeth tested at 4 and 30 d. In a postmortem sample, clodronate was detected in bone from a horse with reported administration 18 mo prior; clodronate was not detected in other sample types collected from this horse. Bisphosphonates reside in bone for extended periods of time, which could lead to potential long-term effects, increasing the potential for bone fractures in young and/or athletic horses