Response of Campylobacter jejuni to Erythromycin Exposure

Campylobacter jejuni. Photo courtesy of Dr. Patricia Fields
and Dr. Collette Fitzgerald.

Cara N. Wilder, Ph.D.

Campylobacter jejuni is a Gram-negative, motile bacterium that is commonly present in the intestinal tract of both domestic and wild animals. In humans, C. jejuni causes a foodborne infection termed campylobacteriosis, which results in symptoms that range from mild enteritis to fever, headache, and bloody diarrhea. In some cases, Campylobacter infection has been associated with Guillain-Barré syndrome, which is a post-infection autoimmune disorder that damages nerve tissue.

Although most cases of campylobacteriosis are self-limiting, antibiotic treatment may be necessary for patients that are either immunologically compromised, or exhibit severe or persistent infection. The most common antimicrobial therapy used to treat campylobacteriosis is erythromycin, which is a macrolide antibiotic that inhibits bacterial protein translation. However, due the regular use of this antibiotic in animal production and veterinary medicine, an increasing number of C. jejuni isolates have become drug-resistant. In many of these strains, the mechanism of resistance is frequently conferred by target modification or through the expression of antibiotic efflux pumps.

Though the genetic basis of erythromycin resistance has been well-studied, the initial response and adaptive mechanisms directly following erythromycin exposure is not well understood. To analyze this, Xia et al. performed a competitive microarray hybridization study that examined the genome-wide transcriptional response of a sensitive and resistant strain of C. jejuni upon exposure to inhibitory and sub-inhibitory doses of erythromycin. Following treatment with erythromycin, the resistant strain of C. jejuni exhibited little to no differential gene expression. In contrast, a number of genes were differentially regulated in the sensitive strain, including the up-regulation of genes associated with motility, and the down-regulation of genes associated with energy production and conversion. Moreover, the inactivation of several differentially expressed genes appeared to negatively affect host colonization and the ability to tolerate high levels of oxygen. Overall, these results provide new insight into the adaptive response of C. jejuni to antibiotic treatment, and my help provide further understanding into the mechanisms underlying the emergence of antibiotic resistance.



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