EQUINE VETERINARY EDUCATION / AE / SEPTEMBER 2018


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Eosinophilic intestinal disease MEED EDCI


Likely all the same disease with different manifestations, partly depending on


segment of intestine involved Small intestine Ascending and descending colon SEC IFEE DEE DEE = Diffuse eosinophilic enteritis EDCI = Idiopathic eosinophilic diseases confined to the intestine


IFEE = Focal (or multifocal) eosinophilic enteritis MEED = Multisystemic, eosinophilic, epitheliotropic disease SEC = Segmental eosinophilic colitis


Fig 1: Current terminology and classification of eosinophilic intestinal diseases in the equine is shown. DEE, diffuse eosinophilic enteritis; EDCI, idiopathic eosinophilic diseases confined to the intestine; IFEE, focal (or multifocal) eosinophilic enteritis; MEED, multisystemic, eosinophilic, epitheliotropic disease; SEC, segmental eosinophilic colitis.


et al. (2000) described 22 horses with segmental eosinophilic colitis (SEC) characterised by infiltration of eosinophils into the mucosa, submucosa and muscular layers of a segment of the left dorsal colon slightly aboral to the pelvic flexure. De Bont et al. (2013) described a similar condition occurring in the descending colon of five horses. In many cases, necrosis of the descending colon was grossly evident. These investigators recommended excising oedematous, hyperaemic segments of colon with serosal petechiation because, even if these segments appear viable, they may become necrotic as the disease progresses. Idiopathic focal eosinophilic enteritis, DEE and SEC (in the ascending or descending colon) are probably all manifestations of the same disease (Kerbyson and Knottenbelt 2015). The pathogenesis and aetiology of systemic eosinophilic


disease of horses, as in man, are poorly understood. Authors of some reports speculate that the cause of MEED may be abnormal proliferation of type 2 helper T lymphocytes that overproduce eosinophilopoietic cytokines, such as interleukin 5 (La Perle et al. 1998; Singh et al. 2006). Some human patients affected with systemic hypereosinophilia have populations of phenotypically abnormal, activated T lymphocytes that produce eosinophilopoietic cytokines, particularly interleukin 5, whereas other patients affected with a systemic eosinophilia syndrome have underlying neoplasia (Tefferi et al. 2010). Idiopathic eosinophilic disease confined to the


gastrointestinal tract is also reported in people where the syndrome is often referred to as eosinophilic gastrointestinal disorder (Rothenberg 2004). Diagnostic criteria for this syndrome is based on symptoms of gastrointestinal malfunction and eosinophilic infiltration of the gastrointestinal tract in the absence of known causes for eosinophilia, such as drug reaction, parasitic infections, and malignancy (Rothenberg 2004). Human eosinophilic gastrointestinal disease is thought to be an allergic response with a genetic component, and treatment usually involves administration of a corticosteroid and reduction of exposure to antigens; focal regions of obstructive or ischaemic intestine, however, are often resected to restore function (Yun et al. 2007).


Although the concentration of eosinophils in intestinal


tissues is typically increased in response to infection with helminths, the inflammatory cellular pattern seen in diseased intestine of horses with IFEE makes helminth infection a highly unlikely cause of IFEE (Proudman and Kipar 2006). Results of an epidemiological study demonstrated that the burdens of nematodes and cestodes in horses affected with IFEE were low and not statistically different from those burdens found in randomly selected normal horses (Archer et al. 2008). Definitive ante-mortem diagnosis of MEED is possible


without intestinal biopsy obtained by celiotomy; diagnosis can be made based on clinical signs combined with histological evaluation of tissue obtained by biopsy from affected organs, such as skin, rectal mucosa, liver or lung (Lindberg et al.1985, 1996; McCue et al. 2003). Definitive diagnosis of EDCI is more difficult, because celiotomy is necessary to obtain tissue for histological examination. Provisional diagnosis of EDCI is made while horses are undergoing exploratory celiotomy performed because of abnormalities found during examination of the abdomen per rectum or during ultrasonographic examination, abnormal appearance of peritoneal fluid and/or signs of signs of unremitting abdominal pain (Edwards et al. 2000; Archer et al. 2006; Makinen et al. 2008; De Bont et al. 2013, 2018). Horses with IFEE have been treated by resecting affected


small intestine during exploratory celiotomy (Scott et al. 1999; Archer et al. 2006) but rapid resolution of clinical signs may occur when small intestine is merely decompressed (Perez Olmos et al. 2006). When the ascending colon is observed to be affected with SEC during exploratory celiotomy, resection of the diseased segment may not always be necessary but nevertheless is advised because eventual necrosis of affected colon is likely (Edwards et al. 2000). Resection of affected colon is also likely to be necessary when SEC involves the descending colon (De Bont et al. 2018). Medical treatment of horses for MEED or EDCI generally involves administering a corticosteroid, even though the efficacy of corticosteroids for treatment for EDCI is not proven, and except for rare cases of MEED (Gibson and Alders 1987;


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