The effect of intramuscular administration of colistin on the development and course of experimentally induced oedema disease in weaned piglets
Language English Country Netherlands Media print-electronic
Document type Comparative Study, Journal Article, Research Support, Non-U.S. Gov't
PubMed
17977672
DOI
10.1016/j.vetmic.2007.09.021
PII: S0378-1135(07)00481-6
Knihovny.cz E-resources
- MeSH
- Ampicillin administration & dosage pharmacology MeSH
- Anti-Bacterial Agents administration & dosage pharmacology MeSH
- Time Factors MeSH
- Edema Disease of Swine drug therapy microbiology mortality MeSH
- Feces microbiology MeSH
- Escherichia coli Infections drug therapy microbiology mortality veterinary MeSH
- Injections, Intramuscular veterinary MeSH
- Colistin administration & dosage pharmacology MeSH
- Lymph Nodes microbiology MeSH
- Weaning MeSH
- Swine MeSH
- Ampicillin Resistance MeSH
- Shiga-Toxigenic Escherichia coli drug effects growth & development pathogenicity MeSH
- Intestines microbiology MeSH
- Case-Control Studies MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Comparative Study MeSH
- Names of Substances
- Ampicillin MeSH
- Anti-Bacterial Agents MeSH
- Colistin MeSH
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.
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