A review of reported cases of inflammatory bowel diseases (IBDs) of horses for which no etiology was identified included cases of granulomatous enteritis (GE), multisystemic eosinophilic epitheliotropic disease (MEED), lymphocytic-plasmacytic enterocolitis (LPE), and idiopathic eosinophilic enterocolitis (EC). The terms EC and MEED were both used to describe a disease in horses characterized by infiltration of intestine and extraintestinal tissues with eosinophils. We use EC to describe IBD characterized by only intestinal infiltration by eosinophils. Horses with GE, MEED, or LPE are usually examined because of weight loss and depression, but horses with EC are usually examined because of signs of abdominal pain. Typically, horses with IBD have low concentrations of serumal proteins, especially albumin, and fail to adequately absorb glucose or xylose. Antemortem diagnosis of IBD can only be made by histologic examination of affected intestine. In some cases, antemortem diagnosis is made from histologic examination of rectal mucosa obtained by biopsy. Suspected causes of IBD in the horse include abnormal immune response to bacterial, viral, parasitic, or dietary antigens. Most horses with IBD do not survive, but horses with EC are more likely than those with LPE, MEED, or GE to respond to treatment. Successful treatments of horses with IBD include resection of grossly affected intestine and administration of corticosteroids.Key words: Eosinophilic enterocolitis; Granulomatous enteritis; Lymphocytic-plasmacytic enterocolitis; Multisystemic eosinophilic epitheliotropic disease.C hronic inflammatory bowel diseases (IBDs) are associated with dysfunction of the gastrointestinal tract due to infiltration of the mucosa and submucosa with populations of eosinophils, plasma cells, lymphocytes, basophils, or macrophages. 1,2 Clinical signs of IBD in the horse include weight loss, dependent edema, and lethargy and are usually associated with protein-losing enteropathy and malabsorption of nutrients, including glucose. Affected horses may have diarrhea or signs of abdominal pain. Signalment, clinical signs, clinicopathologic findings, and postmortem lesions may be highly characteristic of some types of IBD in the horse, but, in general, clinical and gross pathologic features of these diseases are similar, and a final morphologic diagnosis is based on histologic examination. When an etiologic diagnosis of IBD has been reported, mycobacterial 3-12 or parasitic infections, 13,14 or toxins 15 have been identified. The purpose of this report is to describe distinguishing features and discuss possible etiologies of the idiopathic IBDs and to discuss treatment of affected horses. Granulomatous Enteritis (GE)This idiopathic condition was 1st reported in 1974 by Cimprich, 7 who noted the histologic similarity between this disease and Crohn's disease in humans. In our review of the reports of idiopathic GE, we found detailed descriptions of 47 affected horses. 6,7,9,[16][17][18][19][20][21][22][23][24][25] Of these, 32 were Standardbr...

A review of reported cases of inflammatory bowel diseases (IBDs) of horses for which no etiology was identified included cases of granulomatous enteritis (GE), multisystemic eosinophilic epitheliotropic disease (MEED), lymphocytic-plasmacytic enterocolitis (LPE), and idiopathic eosinophilic enterocolitis (EC). The terms EC and MEED were both used to describe a disease in horses characterized by infiltration of intestine and extraintestinal tissues with eosinophils. We use EC to describe IBD characterized by only intestinal infiltration by eosinophils. Horses with GE, MEED, or LPE are usually examined because of weight loss and depression, but horses with EC are usually examined because of signs of abdominal pain. Typically, horses with IBD have low concentrations of serumal proteins, especially albumin, and fail to adequately absorb glucose or xylose. Antemortem diagnosis of IBD can only be made by histologic examination of affected intestine. In some cases, antemortem diagnosis is made from histologic examination of rectal mucosa obtained by biopsy. Suspected causes of IBD in the horse include abnormal immune response to bacterial, viral, parasitic, or dietary antigens. Most horses with IBD do not survive, but horses with EC are more likely than those with LPE, MEED, or GE to respond to treatment. Successful treatments of horses with IBD include resection of grossly affected intestine and administration of corticosteroids.

Pain arising from the sole should not be excluded as a cause of lameness when lameness is attenuated by analgesia of the DIP joint or PD nerves.

Summary The response of horses, with solar pain in the dorsal or palmar aspect of the foot, to 6 or 10 ml local analgesic solution administered into the distal interphalangeal (DIP) joint was examined. Lameness was induced in 7 horses by creating solar pain in the dorsal aspect of one forefoot and, at another time, the palmar aspect of the other forefoot with set‐screws inserted into a custom‐made shoe. Horses were videotaped trotting before and after application of set‐screws and, in separate trials, after 6 or 10 ml local analgesic solution was administered into the DIP joint. Lameness scores were assigned by examining videotaped gaits. Scores were significantly lower (P ± 0.05) for horses with set‐screws applied to the angles of the sole and receiving 10 ml, but not 6 ml, local analgesic solution into the DIP joint. Scores were significantly lower (P<0.05) for all horses with set‐screws in the dorsal margin of the sole receiving either volume of local analgesic solution. Analgesia of the DIP joint was less effective in desensitising the angles of the sole than in desensitising the dorsal margin of the sole, and 10 ml local analgesic solution was more effective than 6 ml in desensitising these regions. The response of horses with solar pain to local analgesic solution in the DIP joint was influenced by the volume administered and the region of sole affected.

We depend upon the olfactory abilities of dogs for critical tasks such as detecting bombs, landmines, other hazardous chemicals and illicit substances. Hence, a mechanistic understanding of the olfactory system in dogs is of great scientific interest. Previous studies explored this aspect at the cellular and behavior levels; however, the cognitive-level neural substrates linking them have never been explored. This is critical given the fact that behavior is driven by filtered sensory representations in higher order cognitive areas rather than the raw odor maps of the olfactory bulb. Since sedated dogs cannot sniff, we investigated this using functional magnetic resonance imaging of conscious dogs. We addressed the technical challenges of head motion using a two pronged strategy of behavioral training to keep dogs' head as still as possible and a single camera optical head motion tracking system to account for residual jerky movements. We built a custom computer-controlled odorant delivery system which was synchronized with image acquisition, allowing the investigation of brain regions activated by odors. The olfactory bulb and piriform lobes were commonly activated in both awake and anesthetized dogs, while the frontal cortex was activated mainly in conscious dogs. Comparison of responses to low and high odor intensity showed differences in either the strength or spatial extent of activation in the olfactory bulb, piriform lobes, cerebellum, and frontal cortex. Our results demonstrate the viability of the proposed method for functional imaging of the olfactory system in conscious dogs. This could potentially open up a new field of research in detector dog technology.

Twenty-four clinically normal horses were castrated by routine methods. Peritoneal fluid was collected prior to castration and at 1, 3, 5, and 7 days postcastration. Peritoneal fluid was collected on days 9 and 11 if nucleated cell (NC) counts were still markedly elevated on day 7. Peritonitis, defined as NC counts greater than 10,000/microliters, was evident in 15 horses following castration. Mean NC counts peaked on day 5 but were less than 10,000/microliters for 74% of the horses by day 7, and 90% of the horses by day 9. One horse had a NC count greater than 60,000/microliters on day 11 when sampling ended. Postcastration peritoneal fluid was obviously blood-tinged in 21 horses. Peak RBC counts occurred on day 3 but markedly decreased by day 5. Elevated peritoneal RBC counts correlated well with elevated NC counts (P less than 0.001). Horses with peritonitis tended to have fever (P less than 0.05). Other clinical signs of peritonitis were not apparent.

No abstract

Summary Lymphocytic‐plasmacytic enteritis (LPE) is a morphological diagnosis given to a type of infiltrative intestinal disease classified within the complex of idiopathic inflammatory bowel disease (IBD). The purpose of this retrospective study was to describe the details of breed, age and sex, clinical and clinicopathological findings and outcome of horses diagnosed with LPE. Data were reported from 14 horses that had a histopathological diagnosis of LPE; the median age was 12 years, and there was no breed or sex predilection. Common clinical signs were weight loss (100%), diarrhoea (50%) and lethargy (50%). Hypoproteinaemia and hypoalbuminaemia were present in 6/13 (46%) and 9/12 (75%) horses, respectively. Results of the oral glucose tolerance tests or D‐xylose absorption tests were abnormal in 9/12 (75%) horses and rectal mucosal biopsies were abnormal in 3/7 (43%) horses. Corticosteroid treatment was used unsuccessfully in 4 horses. All horses were subjected to euthanasia and LPE was diagnosed at necropsy. Diffuse thickening of the small intestine was apparent grossly in 10/13 (77%) horses examined. LPE is an uncommon equine intestinal disease that is difficult to diagnose antemortem and has a poor prognosis.