Quinolone resistance and Campylobacter

Piddock, Laura J. V.

doi:10.1111/j.1469-0691.1999.tb00135.x

Cited by 15 publications

(13 citation statements)

References 48 publications

(57 reference statements)

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“…The similar proportions of resistance to nonfluorinated and fluorinated quinolones (82 versus 81%) and the speed at which this level of resistance has been reached (23) are probably related and are due to the fact that a single mutation in either topoisomerase can confer resistance to both nonfluorinated and fluorinated quinolones (11,13,37,50). Similar data have been reported from other locations in Spain (36,39) and elsewhere (1,10,32,40).…”

Section: Discussionsupporting

confidence: 71%

Antibiotic Resistance Trends in Enteropathogenic Bacteria Isolated in 1985–1987 and 1995–1998 in Barcelona

Prats

Mirelis

Llovet

et al. 2000

Antimicrob Agents Chemother

131

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Trends in resistance to antimicrobial agents used for therapy have been evaluated with 3,797 enteropathogenic bacteria, Campylobacter, Salmonella, Shigella, and Yersinia, between 1985-1987 and 1995-1998. The greater increase in the rate of resistance was observed in Campylobacter jejuni for quinolones (from 1 to 82%) and tetracycline (from 23 to 72%) and in gastroenteric salmonellae for ampicillin (from 8 to 44%), chloramphenicol (from 1.7 to 26%), and trimethoprim-sulfamethoxazole and nalidixic acid (from less than 0.5 to 11%). Multidrug resistance was detected in several Salmonella serotypes. In the 1995-1998 period, 76% of Shigella strains were resistant to trimethoprim-sulfamethoxazole, 43% were resistant to ampicillin, and 39% were resistant to chloramphenicol. Seventy-two percent of Yersinia enterocolitica O3 strains were resistant to streptomycin, 45% were resistant to sulfonamides, 28% were resistant to trimethoprim-sulfamethoxazole, and 20% were resistant to chloramphenicol.

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Section: Discussionsupporting

confidence: 71%

Antibiotic Resistance Trends in Enteropathogenic Bacteria Isolated in 1985–1987 and 1995–1998 in Barcelona

Prats

Mirelis

Llovet

et al. 2000

Antimicrob Agents Chemother

131

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“…Resistance to fluoroquinolone antibiotics has been recognized in Campylobacter strains for many years (Gaunt and Piddock 1996; Piddock 1999; Engberg et al . 2001).…”

Section: Introductionmentioning

confidence: 99%

Genetic basis of quinolone resistance and epidemiology of resistant and susceptible isolates of porcine Campylobacter coli strains

et al. 2002

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Aims: 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. Methods and 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- ‡ 32 lg 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 ‡ 32 lg 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.

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“…are a common cause of gastroenteritis in humans, and while most cases of campylobacteriosis do not require antimicrobial therapy, treatment may be essential for vulnerable patients and for the management of invasive disease. Fluoroquinolones have been widely used for the treatment of Campylobacter infections, but the incidence of resistance among Campylobacter jejuni and C. coli strains isolated from humans increased significantly throughout the world during the 1990s (10,29).…”

mentioning

confidence: 99%

Incidence and Mechanism of Ciprofloxacin Resistance in Campylobacter spp. Isolated from Commercial Poultry Flocks in the United Kingdom before, during, and after Fluoroquinolone Treatment

Griggs

Johnson

Frost

et al. 2005

Antimicrob Agents Chemother

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Five commercial broiler flocks were treated with a fluoroquinolone for a clinically relevant infection. Fresh feces from individual chickens and environmental samples were cultured for campylobacters before, during, and weekly posttreatment until slaughter. Both Campylobacter jejuni and C. coli were isolated during all treatment phases. An increased proportion of quinolone-resistant strains was seen during treatment, and these strains persisted posttreatment. One quinolone-resistant isolate of each species, each serotype, and each phage type from each sample at all treatment phases was examined for its phenotype and mechanism of resistance. Two resistant phenotypes were isolated: Nal r Cip r and Nal r Cip s . The majority (269 of 290) of fluoroquinoloneresistant isolates, whether they were C. jejuni or C. coli, had a mutation in gyrA that resulted in the substitution Thr-863Ile. The other gyrA mutations detected were Thr-863Ala (n ‫؍‬ 17) and Asp-903Asn (n ‫؍‬ 10). The genotypic variation, based on the silent mutations in gyrA identified by the denaturing high-performance liquid chromatography pattern and DNA sequencing, was used to supplement typing data and provided evidence for both the spread of preexisting resistant strains and the selection of spontaneous resistant mutants in treated flocks. Multidrug resistance was significantly (P < 0.01) associated with resistance to ciprofloxacin. Twentyfive percent (73 of 290) of ciprofloxacin-resistant isolates but only 13% (24 of 179) of susceptible isolates were resistant to three or more unrelated antimicrobial agents. In conclusion, quinolone-resistant campylobacters were isolated from commercial chicken flocks in high numbers following therapy with a veterinary fluoroquinolone. Most ciprofloxacin-resistant isolates had the GyrA substitution Thr-863Ile. Resistant isolates were isolated from the feces of some flocks up to the point of slaughter, which may have consequences for public health.

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Quinolone resistance and Campylobacter

Cited by 15 publications

References 48 publications

Antibiotic Resistance Trends in Enteropathogenic Bacteria Isolated in 1985–1987 and 1995–1998 in Barcelona

Antibiotic Resistance Trends in Enteropathogenic Bacteria Isolated in 1985–1987 and 1995–1998 in Barcelona

Genetic basis of quinolone resistance and epidemiology of resistant and susceptible isolates of porcine Campylobacter coli strains

Incidence and Mechanism of Ciprofloxacin Resistance in Campylobacter spp. Isolated from Commercial Poultry Flocks in the United Kingdom before, during, and after Fluoroquinolone Treatment

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