Erosive Colitis in Experimental Canine Leishmaniasis

Abstract

Summary Six 4 month‐old beagles were inoculated with Leishmania infantum, three of them intraperitoneally (Group A) and the other three intravenously (Group B). The animals from Group A were killed at 109, 433 and 592 days after inoculation and animals from Group B 109, 171 and 334 days after inoculation. At 350 days (Group A) and 275 days (Group B) after inoculation, dogs started to develop a chronic large bowel diarrhoea. At necropsy a diffuse colonic and rectal wall thickening of gradually increasing severity was observed. Histological examination of the colon showed a diffuse inflammatory infiltration of the mucosa and submucosa by macrophages with amastigotes, lymphocytes, plasma cells and some neutrophils and eosinophils. The surface epithelium developed increasingly extensive degeneration, which caused the development of erosions on the mucosal surface. The crypts of Lieberkühn decreased in number and showed degeneration of the crypt epithelium.

Expression of Regulatory T Cells in Jejunum, Colon, and Cervical and Mesenteric Lymph Nodes of Dogs Naturally Infected with Leishmania infantum

“…We observed parasites associated with the inflammatory response throughout the mucosa, but without inducing severe pathologies, such as ulcers or necrosis. The immunohistochemical morphometric analysis revealed higher parasite loads in the colon than in the jejunum, as previ-ously reported by our group (25) and in accordance with other reports (31)(32)(33)(34)(35)(36).…”

Correlation study and histopathological description of intestinal alterations in dogs infected with Leishmania infantum

“…In the previous works, the presence of amastigotes of L. infantum has been described in gastrointestinal tissues of dogs infected with CVL, particularly in the mucosa of cecum and colon where the parasites were detected in higher burden (KEENAN et al, 1984 a, b;GONZÁLEZ et al, 1990;ADAMAMA-MORAITOU et al, 2007;PINTO et al, 2011;FIGUEIREDO et al, 2013). In the present work, macrophages containing L. infantum amastigotes were also found in the large (colon) and in the small intestines (duodenum, jejunum and ileum) with a mononuclear inflammatory infiltration, represented mainly by macrophages, lymphocytes and plasma cells in the majority of the cases of infected dogs from G1 group.…”

“…In cases of experimental infection, González et al (1990) observed a severe chronic inflammatory process in the mucosa and submucosa of the colon and rectum of dogs. As a result, focal micro-erosions developed in the mucosal surface, thereby reducing the area of the large bowel available for water absorption and causing diarrhea.…”

“…Diarrhea had already been reported in dogs affected with leishmaniasis, but in these cases the animals showed other systemic signs, including anorexia, emaciation, anemia, lymphadenopathy and skin lesions (CHAPMAN & HANSON, 1984). Furthermore, González et al (1990) and Ferrer et al (1991) reported cases of chronic colitis and diarrhea in dogs that were naturally infected with L. infantum. However, Ferrer et al (1991) questioned whether Leishmania spp caused these conditions or whether they were incidental findings, which would be particularly relevant if the parasite load was low.…”

“…In experimental studies using hamsters as models for this infection, González et al (1986) described the pathological alterations occurred in the intestinal lamina propria and submucosa of the colon, caused by the parasites associated with inflammatory cell infiltration of lymphocytes, plasma cells and macrophages. Although uncommon, occurrences of erosive and ulcerative colitis and hemorrhagic diarrhea have sometimes been described in dogs in association with severe clinical signs of this disease (GONZÁLEZ et al, 1990;FERRER et al, 1991). However, the prevalence of Leishmania parasitism detected in the colonic mucosa through colonoscopy, but without overt colitis, was surprisingly high in dogs with symptomatic leishmaniasis (ADAMAMA-MORAITOU et al, 2007).…”