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EQUINE VETERINARY EDUCATION / AE / NOVEMBER 2020


Fig 1: Case 3. Post-mortem photograph of infarction of the jejunum. There is also fibrin on serosal surfaces of multiple areas of jejunum and the mesentery. [Colour figure can be viewed at wileyonlinelibrary.com]


Fig 3: Case 2. Large colon. Photomicrograph showing thrombosis of sub mucosal and mucosal vessels. Haemorrhage, oedema, necrosis of mucosa. H&E x4. [Colour figure can be viewed at wile yonlinelibrary.com]


Fig 2: Case 9. Post-mortem photograph of a focal infarction of the left dorsal colon and adjacent pelvic flexure. [Colour figure can be viewed at wileyonlinelibrary.com]


intestinal segments supplied by the cranial mesenteric artery, including the small intestine (jejunum and ileum) and large intestines (caecum and ascending colon). No lesions were seen in the duodenum (which receives its arterial supply from the coeliac artery) or the descending colon (caudal mesenteric artery). In addition, no renal infarcts were identified in our cases, unlike the horses described by Pihl et al. (2018). In the absence of any evidence of S. vulgaris associated arteritis in our cases, the reason for the limited distribution of lesions to areas of intestine supplied by the cranial mesenteric artery are unclear. Exclusion of S. vulgaris larval migration as the cause of NSII in our horses was based on the absence of any gross or histopathological evidence of verminous arteritis at post-mortem examination. However, since the S. vulgaris antibody ELISA (Nielsen et al. 2016) was not available at the time that these horses were examined, we cannot completely exclude verminous arteritis that may have been missed during the post-mortem examinations.


© 2019 EVJ Ltd


Fig 4: Case 1. Jejunum. Photomicrograph showing coagulative necrosis of the intestinal wall. [Colour figure can be viewed at wileyonlinelibrary.com]


Future studies should use this ELISA test in horses affected by NSII in the UK. The underlying aetiopathogenesis of the NSII in these


horses appeared to fall into one of three groups. Five horses (33%) had pre-existing colitis or typhlocolitis; all of these horses presented with diarrhoea (one also showed acute colic signs). In three horses (20%) there was an initial strangulating small intestinal obstruction that required surgical treatment; these horses subsequently developed NSII post-operatively. In seven horses (47%), no underlying or predisposing disease was identified; all of these horses presented with a history of acute or chronic/recurrent colic, and the diagnosis of NSII was made at exploratory celiotomy. In the cases of the horses with colitis/typhlocolitis and those with strangulating small intestinal lesions, it seems likely that the NSII occurred as a result of endotoxaemia, systemic inflammatory response syndrome, and disseminated intravascular coagulation/ hypercoagulability. Intestinal infarction following colic surgery


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