Mechanisms of resistance of Campylobacter spp. to antimicrobial agents

Campylobacter is recognized as the major cause of acute bacterial gastroenteritis in the world. Two species of the genus Campylobacter, C. jejuni and C. coli, are most frequently isolated from cases of human infection. Patients usually recover without any antimicrobial therapy, but treatment with erythromycin or fluoroquinolones may be needed in some cases of prolonged illness. Increasing antimicrobial resistance of Campylobacter strains in both medicine and agriculture has been recognized. Some reports have suggested that the use of fluoroquinolones for veterinary medicine results in the establishment of fluoroquinolone-resistant Campylobacter strains. Moreover it has been found that C. jejuni is able to acquire resistance determinants from outside of the genus (from Gram-positive organisms) by horizontal transfer and genes can be incorporated into plasmids or the chromosome. High-level resistance to erythromycin is mediated by mutation in the domain V of the 23S rRNA gene. Fluoroquinolone resistance appears to be mainly due to mutations in the gyrA gene encoding part of the GyrA subunit of DNA gyrase. In this article, the mechanisms of antimicrobial resistance in Campylobacter spp. are presented.