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Peer-reviewed veterinary case report

Chronic intestinal blockage from muscle defect in Bengal cat

By Imai, D M et al.·Published in Veterinary pathology·2014·Department of Pathobiological Sciences, United States·View original on PubMed

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Original publication title: Visceral smooth muscle α-actin deficiency associated with chronic intestinal pseudo-obstruction in a Bengal cat (Felis catus x Prionailurus bengalensis).

Species:
cat

Plain-English summary

A Bengal cat with a long history of not eating well, vomiting, and losing weight was found to have serious digestive issues, including a condition called chronic intestinal pseudo-obstruction, which means the intestines weren't moving food properly. During the examination after the cat passed away, the intestines were swollen with gas and fluid, but there were no blockages. The muscle in the intestines showed significant changes, indicating a problem with how the muscles functioned. Unfortunately, the exact cause of these muscle issues couldn't be determined, but it is known that similar problems can occur in humans and can lead to digestive problems.

People also search for: Bengal cat vomiting weight loss · cat intestinal obstruction symptoms · chronic intestinal issues in cats

Abstract

An adult Bengal cat (Felis catus × Prionailurus bengalensis) with a prolonged history of partial anorexia, regurgitation, and weight loss and a clinical, radiographic, and ultrasonographic diagnosis of persistent megaesophagus and gastrointestinal ileus was submitted for necropsy. The intestinal tract was diffusely distended by gas and fluid with appreciable loss of muscle tone and an absence of luminal obstruction, consistent with the clinical history of chronic intestinal pseudo-obstruction. Histologically, the autonomic nervous system was intact, but the smooth muscle within the gastrointestinal wall exhibited a marked basophilia that was most pronounced in the jejunum. Immunohistochemistry for neurofilament, synaptophysin, CD117, and desmin demonstrated that the number of myenteric ganglia, number of interstitial cells, and leiomyocyte desmin content were similar when compared with the unaffected age- and species-matched control. Immunohistochemistry for smooth muscle α-actin demonstrated a striking loss of immunoreactivity, predominantly in the circular layer of the jejunum, that corresponded with the tinctorial change in leiomyocytes. Transmission electron microscopy revealed loss of myofibrils, loss of organelle polarity, and significantly larger central mitochondria (megamitochondria) in affected leiomyocytes, as well as nonspecific degenerative changes. Although the presence of a primary leiomyopathy and a causal relationship could not be confirmed in this case, leiomyopathies are considered a cause of chronic intestinal pseudo-obstruction in human medicine, and loss of smooth muscle α-actin immunoreactivity is one recognized marker for intestinal dysmotility.

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Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/23774747/