Infiltrative Bowel Diseases

CHAPTER 98 Infiltrative Bowel Diseases



John Schumacher


Infiltration of the horse’s intestinal tract with inflammatory or neoplastic cells may result in clinical and clinicopathologic signs of disease that are similar regardless of the type of cell involved. Infiltration of the mucosa and submucosa of the gastrointestinal tract with large numbers of normal or neoplastic eosinophils, lymphocytes, macrophages, plasma cells, or basophils is termed infiltrative bowel disease. Regardless of the type of cell involved, horses with infiltrative bowel disease often have protein-losing enteropathy and malabsorption of nutrients, which causes clinical signs that often include weight loss, lethargy, diarrhea, and dependent edema. In some cases, the cause of invasion of inflammatory cells is determined to be parasitism or mycobacterial infection, and in other cases, the infiltrating cells may be identified as neoplastic. For many affected horses, the cause is undetermined, and these diseases are collectively referred to as chronic idiopathic inflammatory bowel disease (CIBD). Four types of CIBD in the horse are recognized: granulomatous enteritis (GE); lymphocytic-plasmacytic enterocolitis (LPE); multisystemic, eosinophilic, epitheliotropic disease (MEED); and idiopathic, focal, eosinophilic enterocolitis (IFEE).


Although a horse’s signalment, clinical signs, results of abdominal ultrasound, clinicopathologic findings, and gross lesions often provide clues for diagnosis of infiltrative bowel disease, definitive diagnosis is based on results of histologic examination of an intestinal biopsy specimen. The histologic diagnosis of CIBD is often subjective because it is based on the subjective assessment of severity of inflammatory cell infiltration, which can be difficult to assess because normal populations of intestinal inflammatory cells vary in number between species, individuals, and segment of intestine. The significance of eosinophils or lymphocytes within the intestinal wall is especially difficult to interpret because high numbers of these cells can be found in the intestinal wall of clinically normal horses. Tissue for histologic examination is usually obtained by celiotomy or rectal biopsy. A laparoscopic technique for full-thickness intestinal biopsy in the horse has been described but its use in obtaining tissue from diseased intestine has not been reported. Rectal biopsy was useful in diagnosis in about one-half of reported cases of GE and MEED but is unlikely to be helpful in definitive diagnosis of LPE or IFEE. Gastroduodenoscopy-assisted biopsy of the small intestine might aid in diagnosis of CIBD if inflammatory cells have invaded the duodenum. Data concerning the normal population of inflammatory cells in the region of duodenum have been reported.



GRANULOMATOUS ENTERITIS


Sheets of macrophages or epithelioid cells and circumscribed granulomas in the mucosa or submucosa are seen during histologic examination of diseased intestine of horses with granulomatous enteritis (GE). Granulomatous enteritis has been compared to Johne’s disease in cattle and Crohn’s disease in human beings because the histologic lesions are similar. Granulomatous enteritis has been reported in many different breeds of horses, but many reports involve Standardbreds, some of which were related, indicating a possible genetic predisposition to development of the disease. Affected horses are usually young and are almost invariably examined because of weight loss and poor appetite. The presence of skin disease in horses with MEED is a feature that is often considered to distinguish MEED from GE, but some horses with GE also have skin lesions usually involving the head and limbs, especially the coronet.


The most consistent clinicopathologic finding in horses with GE is hypoalbuminemia. Horses with protein-losing enteropathy have enteric loss of proteins of all molecular weights, but because globulins tend to be produced faster than albumin, the most striking clinicopathologic feature of CIBD in the horse is hypoalbuminemia. Most horses with GE are anemic, but anemia may not be evident because of a diminished plasma volume caused by low plasma albumin concentration. Plasma transfusion may cause a marked drop in the packed cell volume of horses with GE.


Carbohydrate absorption testing of horses with GE usually reveals abnormal absorption of either glucose or xylose. Malabsorption of carbohydrates is attributed to severe villous atrophy throughout the small intestine. Some horses with GE have a normal carbohydrate absorption test, presumably because the disease has not progressed to a point that villous absorptive capacity is exceeded, or because intestinal lesions are focal and do not interfere with absorption.


Horses with GE do not respond to administration of drugs used to treat Crohn’s disease in humans, such as salicylazosulfapyridine and methylsulfapyridine. A few horses with GE were reported to respond favorably to treatment with dexamethasone, but long-term survival with any medical treatment has not been reported. Two horses with GE responded favorably to removal of grossly affected ileum and several meters of distal jejunum. Surgical treatment of most horses with GE is unlikely to be beneficial, however, because gross intestinal lesions are usually diffuse and involve long segments of intestine.


The cause of GE was not determined in most reported cases, despite a detailed history, use of tissue cultures, and histologic examination of affected tissues, including electron microscopy. Aluminum toxicosis coupled with parasitism was diagnosed as the cause of clinical signs and gross and histologic lesions similar to GE in 6 horses on a single farm. Natural or experimental infections of Mycobacterium aviumsubsp. paratuberculosis in horses results in microscopic granulomatous intestinal lesions similar to those found in Crohn’s disease. There is some evidence that Crohn’s disease in humans is caused by Mycobacterium avium subsp. paratuberculosis, but this finding is controversial. The DNA of this organism is commonly found in intestinal mucosal biopsies of patients with Crohn’s disease, leading to speculation that for genetically susceptible individuals, the innate immune response to mycobacterial exposure is inadequate, permitting establishment of a persistent mycobacterial infection. Chronic infection could then activate the inflammatory response, which is characteristic of Crohn’s disease.



LYMPHOCYTIC-PLASMACYTIC ENTEROCOLITIS

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May 28, 2016 | Posted by in EQUINE MEDICINE | Comments Off on Infiltrative Bowel Diseases

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