The effect of intramuscular administration of colistin on the development and course of experimentally induced oedema disease in weaned piglets.

Shiga-toxigenic E. coli (STEC) strains that produce Shiga toxin Stx2e cause oedema disease in weaned piglets. The purpose of the present study was to investigate the impact of Stx2e released in mesenteric lymph nodes on disease pathogenesis. Colistin and ampicillin were intramuscularly administered to piglets of the experimental group simultaneously challenged with STEC strain, type O139:F18ab, Stx2e+. Piglets of the control group were challenged with STEC only. The strain was naturally resistant to ampicillin and susceptible to colistin. After the challenge, colonisation of the intestines was observed in both antibiotic-treated piglets and control piglets without antibiotic treatment. Histochemistry and scanning electron microscopy revealed sporadic colonisation of the small intestine in the piglets. STEC was detected in the mesenteric lymph nodes of untreated piglets. The clinical manifestations of oedema disease were observed in both groups. In the antibiotic-treated group (11 piglets), oedema disease developed in 10 piglets, eight of which died or were euthanized ante finem. In the untreated group (11 piglets), oedema disease developed in five piglets, four of which died or were euthanized ante finem. We therefore propose that the STEC lysed by colistin suddenly released the toxin from bacterial cells immediately after their passage through the intestinal wall. That could explain a more severe course of oedema disease in the treated piglets. Even though high amounts of STEC were present in the lymph nodes of untreated piglets, the toxin was not released abruptly because the bacterial cells were not damaged.