Antimicrobial Resistance Mechanisms amongCampylobacter

Abstract

Campylobacter jejuni and Campylobacter coli are recognized as the most common causative agents of bacterial gastroenteritis in the world. Humans most often become infected by ingesting contaminated food, especially undercooked chicken, but also other sources of bacteria have been described. Campylobacteriosis is normally a self-limiting disease. Antimicrobial treatment is needed only in patients with more severe disease and in those who are immunologically compromised. The most common antimicrobial agents used in the treatment of Campylobacter infections are macrolides, such as erythromycin, and fluoroquinolones, such as ciprofloxacin. Tetracyclines have been suggested as an alternative choice in the treatment of clinical campylobacteriosis but in practice are not often used. However, during the past few decades an increasing number of resistant Campylobacter isolates have developed resistance to fluoroquinolones and other antimicrobials such as macrolides, aminoglycosides, and beta-lactams. Trends in antimicrobial resistance have shown a clear correlation between use of antibiotics in the veterinary medicine and animal production and resistant isolates of Campylobacter in humans. In this review, the patterns of emerging resistance to the antimicrobial agents useful in treatment of the disease are presented and the mechanisms of resistance to these drugs in Campylobacter are discussed.

Detection of fluoroquinolone resistance by mutation in gyrA gene of Campylobacter spp. isolates from broiler and laying (Gallus gallus domesticus) hens,from Rio de Janeiro State, Brazil

“…Usually Campylobacter infections are self-limiting, but in some cases, as in persistent and severe infections or pregnant women, children and elderly and immunosuppressed the use of antimicrobials is necessary (WIECZOREK & OSEK, 2013). In some cases, after infection, in long term, there may be serious consequences as Miller Fisher syndrome, irritable bowel syndrome and GuillainBarre Syndrome, one of the most common sequela in Campylobacter spp.…”

“…Most of the highly resistant C. jejuni strains have the Thr-86-Ile mutation, resulting in the replacement of the amino acid threonine by isoleucine (WILSON et al, 2000). Other substitutions were reported, such as Asp-90-Asn, Ala-70-Thr, Asp-85-Tyr, Pro-104-Ser (IOVINE, 2013;QIN et al, 2011;WIECZOREK & OSEK, 2013), but a role in the resistance to fluoroquinolones has not been established for these mutations. Other mutations seen as changes in the gyrB gene have not been documented in Campylobacter and few studies show mutations in the parC gene associated with resistance to fluoroquinolones (PIDDOCK et al, 2003).…”

Molecular mechanisms of quinolone, macrolide, and tetracycline resistance amongCampylobacterisolates from initial stages of broiler production

“…This protein is coded by the tetO gene and can be located on the chromosome and plasmids (Avrain et al, 2004). The presence of conjugative plasmids containing tetO gene is likely to play a substantial role in dissemination of the resistance (Wieczorek & Osek, 2013).…”

Detecção de resistência às fluoroquinolonas em Campylobacter isolados de frangos de criação orgânica

“…às fluoroquinolonas (Wang et al 1993, Wilson et al 2000, Bachoual eu al. 2001, Hakanen et al 2002, Qin et al 2011, Iovine 2013, Wieczorek & Osek 2013, Hungaro et al 2015. A mutação por deleção no códon 73 (GTG→G_G) observada em duas cepas de C. jejuni não foi aparentemente descrita anteriormente em cepas de Campylobacter resistentes à fluoroquinolonas.…”

“…está relacionada principalmente à mutação Tre-86-Ile na RDRQ do gene gyrA da DNA girase, de acordo com vários autores (Yang et al 2006, Qin et al 2011, Iovine 2013, Frasao & Aquino 2014. Entretanto, outras mutações (Tre-86-Ile, Asp-90-Asn, Ala-70-Tre, Asp-85-Tir, Pro-104-Ser) nessa região já foram descritas como relacionadas à resistência em Campylobacter, além de mutações no gene parC, da topisomerase IV e da ação exacerbada da bomba de efluxo CmeABC devido à mutação no gene cmeR (Bachoual et al 2001, Piddock et al 2003, Yang et al 2006, Qin et al 2011, Wieczorek & Osek 2013, Iovine 2013, Hungaro et al 2015.…”