More than 4 000 E. coli strains isolated from diarrhoeic piglets in 111 pig herds in the Czech Republic during the period 19952000 were examined for serogroup and virulence factors. Gene typing of the K88 marker by polymerase chain reaction (PCR) was used for the examination of 283 enterotoxigenic strains (ETEC) which agglutinated with antisera against K88 or adhered to intestinal brush borders. The K88 gene was detected in 237 strains; among them 232 strains possesed the K88 variant. Genotype K88ab was found in two strains of the serogroup O8 from one herd and the gene K88ad was detected in three strains of the serogroup O8 originating from another herd. The results show that the type K88ac is predominant in ETEC strains with colonisation factors K88 in pig herds in the Czech Republic.
Experiments were focused on the prevention of diarrhoea in weaned piglets by means of enterotoxigenic strains of Escherichia coli (ETEC) with colonizing factors K88 (F4). The process of immunization consisted of intramuscular administration of ETEC strain bacterin one day prior to weaning and oral administration of a live culture of non-pathogenic E. coli strain containing colonizing factors (O149:K88; STa-, LT-) in 3 hours after weaning. The shedding of the K88 positive E. coli strains was monitored for 3 weeks after weaning by the culture of rectal swabs. The efficacy of such immunization protocol was tested by challenge exposure to enterotoxigenic E. coli O149:K88, LT+ strain on the third or the tenth day after weaning. Following the oral administration of non-pathogenic E. coli strain containing colonizing factors K88 to piglets, the shedding of the administered strain continued for 9 days. No or very small protection against diarrhoea following the challenge exposure to enterotoxigenic E. coli was found in immunized piglets.
Hyperimmune sera against Shiga toxin Stx2e with antibody titres 8 000-32 000, prepared by immunization of slaughter pigs, were administered subcutaneously to piglets (n = 73) 3 days a�er weaning. The titres of Stx2e neutralizing antibodies in sera of piglets ranged from 16 to 512 following application of the immune serum. In most of the piglets, passively acquired antibodies disappeared during 4 to 8 weeks a�er application. The recorded serum titres were in all of the piglets 8 or higher fourteen days following administration. In another experiment, an immune porcine serum with antibody titre against Stx2e of 130 000 was applied subcutaneously into a knee fold to 30 piglets. The serum was applied at the dose 3 ml, 1.5 ml, 0.75 ml, 0.4 ml, 0.2 ml, 0.1 ml, and 0.05 ml based on the group of piglets. Antibody-free serum was applied to pigs of the control group (n = 5). The following day, supernatant of STEC culture with Stx2e titre of 150 000 was applied to piglets of both experimental and control groups into the opposite knee fold that the above serum. Piglets that received 0.2 to 3 ml of serum remained unaffected throughout the experiment following application of supernatant containing Stx2e. Piglets that received 0.05 ml of serum and those of the control group showed severe clinical manifestations of edema disease following Stx2e application and were sacrificed ante finem. Marked signs of the disease could already be observed 18 hrs following Stx2e application. In a group of 3 piglets that received 0.1 ml of serum, mild paralysis was observed in 1 piglet 18 hrs following Stx2e application.
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