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Pathological and immunohistochemical study of gastrointestinal lesions in dolphins stranded in the Canary Islands
  1. J. R. Jaber, DVM, PhD1,
  2. J. Pérez, DVM, PhD2,
  3. M. Arbelo, DVM1,
  4. R. Zafra, DVM2 and
  5. A. Fernández, DVM, PhD1
  1. 1 Instituto de Sanidad Animal, Facultad de Veterinaria, Universidad de Las Palmas de Gran Canaria, Trasmontaña sn, 35416 Arucas, Las Palmas de Gran Canaria, Spain
  2. 2 Departamento de Anatomía y Anatomía Patológica Comparadas, Facultad de Veterinaria, Universidad de Córdoba, Edificio Sanidad Animal, Campus de Rabanales, Ctra. Madrid-Cádiz km 396, 14014 Córdoba, Spain
  1. Correspondence to Dr Fernández

Abstract

This paper describes the gross, histopathological and immunohistochemical characteristics of gastrointestinal lesions and regional lymph nodes of six common dolphins (Delphinus delphis), 11 striped dolphins (Stenella coeruleoalba) and six Atlantic spotted dolphins (Stenella frontalis) found stranded along the coasts of the Canary Islands. The most common lesion was chronic granulomatous gastritis of the glandular stomach, associated with the parasite Pholeter gastrophilus, and characterised by the parasites, their eggs, or parasite debris in the mucosa, submucosa or tunica muscularis, surrounded by numerous lysozyme-positive macrophages and neutrophils, and more peripherally by abundant fibrous tissue containing variable numbers of immunoglobulin (Ig) G+ plasma cells, and small numbers of cd3+ T lymphocytes and IgM+ and IgA+ plasma cells. Anisakis simplex nematodes were found in two dolphins that were also parasitised by P gastrophilus and had parasitic granulomatous gastritis and multiple small chronic gastric ulcers. Lymphoplasmacytic enteritis was found in eight cases, three of them parasitised by Diphyllobothrium species; the lesion was characterised by moderate to severe infiltrations of cd3+ T lymphocytes and IgG+ plasma cells, with small numbers of IgM+ and IgA+ plasma cells in the lamina propria and submucosa, mainly of the small intestine. One dolphin had severe fibrinopurulent peritonitis, which may have been secondary to gastric perforation caused by the large mural granulomatous gastritis associated with P gastrophilus parasitism.

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