The effect of intramuscular administration of colistin on the development and course of experimentally induced oedema disease in weaned piglets
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu srovnávací studie, časopisecké články, práce podpořená grantem
PubMed
17977672
DOI
10.1016/j.vetmic.2007.09.021
PII: S0378-1135(07)00481-6
Knihovny.cz E-zdroje
- MeSH
- ampicilin aplikace a dávkování farmakologie MeSH
- antibakteriální látky aplikace a dávkování farmakologie MeSH
- časové faktory MeSH
- edémová nemoc u prasat farmakoterapie mikrobiologie mortalita MeSH
- feces mikrobiologie MeSH
- infekce vyvolané Escherichia coli farmakoterapie mikrobiologie mortalita veterinární MeSH
- injekce intramuskulární veterinární MeSH
- kolistin aplikace a dávkování farmakologie MeSH
- lymfatické uzliny mikrobiologie MeSH
- odstavení MeSH
- prasata MeSH
- rezistence na ampicilin MeSH
- shiga-toxigenní Escherichia coli účinky léků růst a vývoj patogenita MeSH
- střeva mikrobiologie MeSH
- studie případů a kontrol MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
- Názvy látek
- ampicilin MeSH
- antibakteriální látky MeSH
- kolistin 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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