Abstract
Obviously, one of the most important causes of Enterotoxaemia in domestic animals is Clostridium perfringens. In present study, C. perfringens type A (56.66%), type D (26.66%) and type B (16.66%) were respectively the most abundant bacteria in intestinal samples of 30 cattle and calves with enterotoxaemia. The incidence of α, β and e toxins in extracted intestinal contents, by Sandwich ELISA method, were determined 89/98%, 99/19% and 33.33% respectively. Histopathologic examination of different organs from 12 cattle and calves with enterotoxaemia and C.perfringens affection indicated following lesions; Heart: congestion (40%), hemorrhage (30%), mild myolysis (10%), sarcocystosis (30%), lymphocytic endocarditis (10%), pericarditis (10%) and myocardiocyte hypertrophy (20%). Liver: hepatitis (27%), coagulative necrosis (36%), hemorrhage (19%), severe hepatic fibrosis (9%) and hepatic abscess (9%). Spleen: congestion (33%), hemorrhage (33%), lymphoid tissue depletion (16%), capsular fibrinohemorrahgic Inflammation (16%) and hemosidrosis (33%). Intestine: necrohemorrahgic enteritis (40%), lymphoplasmocytic enteritis (50%), necrotic and suppurative subserosal Inflammation (10%), congestion (10%), edema (10%) and shortening and fusion of Villi (10%). Lymph nodes: congestion (25%), thrombosis and hemorrhage (25%), edema (25%), lymphocytolysis (25%) and fibrinous lymphadenitis (25%). Lung: congestion (36%), hemorrhage (9%), edema (27%), atelectasis (9%), emphysema (9%), embolic pneumonia (9%), purulent bronchopneumonia (18%), fibrinous pneumonia (45%), cuffing pneumonia (18%), Interlobular fibrosis (9%) and pulmonary abscess (9%). Kidney: congestion (12.5%), acute tubular necrosis (25%), glomerular atrophy (12.5%), interstitial nephritis (50%) and hyaline droplets (12.5%). The present data demonstrate that in the laboratory setting the reproducibility, sensitivity and linear dose response of ELISA allows quantitative estimation of different types of bacteria and respective toxins activity. This could be useful for monitoring toxin production. Our study suggested that although some of the lesions were triggered by C. perfringens, some may be caused by other pathogens which were not investigated in this research.
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