Clinical insights on paratuberculosis in Arabian camels (Camelus dromedarius): A review.

Abstract

Paratuberculosis (PTB) is a long-standing granulomatous infectious disease of both domesticated and wild ruminants. It is caused by Mycobacterium avium subsp. paratuberculosis (MAP). This review emphasizes the clinical, hematobiochemical, sonographic, and pathologic findings as well as therapeutic and control measures in dromedary camels infected with PTB. The clinical signs include intermittent and/or chronic diarrhea, decreased milk yield, emaciation, submandibular edema, dehydration, irregular and weak rumen contractions, and abdominal pain. Hematological changes include leukocytosis, neutrophilia, and decreased erythrocytes, hematocrit percent, and hemoglobin concentration. Biochemical alterations included hypoalbuminemia, hypoproteinemia, hyperglobulinemia, hypomagnesemia, hypoglycemia, increased alanine aminotransferase and aspartate aminotransferase activity, and increased concentration of magnesium and calcium. Sonographically, the intestinal wall is either mildly, moderately, or severely thickened along with mesenteric lymph nodes (LNs) enlargement. The LN capsule is either anechoic or echoic and the contents are either echogenic, anechoic, or heterogenous. Other sonographic findings include bright hepatic parenchyma, aggregation of echogenic materials separated with fluids among the intestines, and pleural and pericardial effusions. The typical pathological lesions are corrugation of the small intestinal mucosa, especially that of the ileum, and the colonic mucosa is folded. Mesenteric and ileocecal LNs are edematous, congested, and granular. Other necropsy findings include fatty liver and peritoneal, pericardial, and pleural effusions. Histologically, proliferative enteritis and lepromatous granulomas are detected. Clusters of acid-fast bacilli are usually found in the intestinal mucosa and lamina propria. Accurate diagnosis of PTB depends on the culture and identification of the causative organism MAP from tissue or feces. Herd screening is also performed through complement fixation, agar gel immunodiffusion, competitive-enzyme linked immunosorbent assay, Ziehl-Neelsen staining of tissue or feces, histologic pattern of a granulomatous reaction, DNA probes, and polymerase chain reaction. A trial for the treatment of PTB in dromedary camels was carried out through IM injection of rifampin and streptomycin for 10 weeks. The diarrhea resolved within 1 week of treatment, and MAP disappeared from rectal scraping 5-9 weeks after treatment. In conclusion, early detection and eradication procedures of PTB should be more implemented for the control and prevention of PTB in dromedary camels. More research should be directed toward vaccination programs in those species.