Genetic basis of quinolone resistance and epidemiology of resistant and susceptible isolates of porcine Campylobacter coli strains.
OBJECTIVE
The aims of this study were to investigate the epidemiology of quinolone-resistant and -susceptible porcine isolates of Campylobacter coli and to characterize the genetic basis of quinolone resistance.


RESULTS
Penner serotyping and flagellin gene sequence polymorphisms were used to investigate the epidemiology of the C. coli isolates. A total of 55 isolates were included, of which 30 were paired resistant and susceptible isolates from 15 pigs. Amplification of gyrA, gyrB and parC, followed by direct sequencing of amplicons was used to identify mutations in the targets of quinolones. Overall, 31 of the isolates were resistant to ciprofloxacin (minimum inhibitory concentrations (MIC), 2- >or = 32 microg x ml(-1)). Thirteen DdeI-flaA profiles were observed and resistant and susceptible strains were identified for nine profiles. The majority of resistant strains exhibited either profile 1 or 6. While profile 1 comprised susceptible and resistant strains, all of the strains with profile 6 were resistant to ciprofloxacin. The serogroup (O:24) of the profile 6 strains was identical. The only other serogroup to be uniformly associated with quinolone resistance was O:5. Strains with this phenotype comprised a number of genotypes, including profile 1. Only four of the paired isolates from individual pigs had the same profile. The genetic basis of quinolone resistance was investigated in two strains with ciprofloxacin MICs of 2 and > or = 32 miccrog x ml(-1), respectively. The amino acid substitution of isoleucine for threonine at position 86 was identified in the GyrA proteins from both strains. No mutations were identified in the GyrB proteins.


CONCLUSIONS
There was an association between two of the genotypes, serotypes 5 and 24, and quinolone resistance. The association between genotype, serotype and resistance in C. coli isolates has not been reported previously. Only the mutation in GyrA associated with quinolone resistance was identified. No mutations in GyrB were identified. Amplification products of parC were not obtained and it may be that this gene is not present in some Campylobacter spp.


CONCLUSIONS
This study provides data on the distribution of ciprofloxacin resistance between subtypes of C. coli.
Cooper
R
R
Division of Medical Microbiology, University of Cape Town, South Africa, Groote Schuur Hospital, Cape Town, South Africa.
Segal
H
H
Lastovica
A J
AJ
Elisha
B G
BG
D000818:Animals; D000890:Anti-Infective Agents / Q000494:pharmacology; D002169:Campylobacter Infections / Q000188:drug therapy / Q000453:epidemiology* / Q000662:veterinary*; D017000:Campylobacter coli / Q000145:classification / Q000187:drug effects / Q000235:genetics*; D002939:Ciprofloxacin / Q000494:pharmacology; D027081:DNA Gyrase / Q000235:genetics; D027101:DNA Topoisomerase IV / Q000235:genetics; D024881:Drug Resistance, Bacterial / Q000235:genetics*; D005408:Flagellin / Q000235:genetics; D012150:Polymorphism, Restriction Fragment Length; D012703:Serotyping; D013552:Swine / Q000382:microbiology*
D000890:Anti-Infective Agents; D005408:Flagellin; C067138:flaA protein, bacteria; D002939:Ciprofloxacin; D027101:DNA Topoisomerase IV; D027081:DNA Gyrase