Posted by: Chris Maloney | March 21, 2012

Campylobacter: Lyme Disease Lite? UC? And Guillain-Barre?

Campylobacter bacteria

Campylobacter bacteria (Photo credit: Microbe World)

A friend went traveling recently and came back bearing Campylobacter.  Between trips to the bathroom, we discussed this particular little critter and why it continues to be the most common food borne source of diarrhea.

First, Campylobacter loves birds.  There are eight major species, but most the research has been done on C. jejuni, so that’s the one we’ll talk about.  Jejuni loves birds and can’t get enough of chicken.  We also can’t get enough of chicken, so at some point our love of chicken and Campylobacter’s love of chicken are bound to conflict.

When Campylobacter enters our systems, it does what it does in a chicken.  It sets up home and starts to move out the neighbors to make room for relatives.  This spiral bacteria has a range of toxic effects, including being in the guts in a high percentage of Guillain-Barre patients.

If spiral brings to mind Lyme spirochetes, Campylobacter also has an unnerving habit of going into our cells and parking itself there if under stress.  No one has recorded just how far into the body the Campylobacter can burrow itself.

Some people and many animals can have Campylobacter infections and clear them up without intervention.  It’s the host body that can set off problems by overreacting to being invaded.

While wikipedia still lists the newer antibiotics as being treatments to Campylobacter, there is evidence (below) that even the most recent antibiotics, fluoroquinolones, can be resisted.

Bad news for sufferers of Crohns and Ulcerative Colitis, both of which have been associated with Campylobacter.  Maybe Campylobacter just showed up for the inflammation party, but he shows up in twice as many sufferers as controls.

Despair not, there is something so toxic, so nasty, that Campylobacter is not yet resistant.  Even this super-villain cannot face:  garlic.  That’s right, you’ve got to love that unique and stinky sulf-hydryl bonded antibiotic.

Curr Top Microbiol Immunol. 2009;337:197-229.

Molecular mechanisms of campylobacter infection.

van Putten JP, van Alphen LB, Wösten MM, de Zoete MR.


Department of Infectious Diseases & Immunology, Utrecht University, Yalelaan 1, Utrecht, The Netherlands.


Campylobacter jejuni is the principal bacterial foodborne pathogen. A major challenge still is to identify the virulence strategies exploited by C. jejuni. Recent genomics, proteomics, and metabolomics approaches indicate that C. jejuni displays extensive inter- and intrastrain variation. The diverse behavior enables bacterial adaptation to different environmental conditions and directs interactions with the gut mucosa. Here, we report recent progress in understanding the molecular mechanisms and functional consequences of the phenotype diversity. The results suggest that C. jejuni actively penetrates the intestinal mucus layer, secretes proteins mainly via its flagellar apparatus, is engulfed by intestinal cells, and can disrupt the integrity of the epithelial lining. C. jejuni stimulates the proinflammatory pathway and the production of a large repertoire of cytokines, chemokines, and innate effector molecules. Novel experimental infection models suggest that the activation of the innate immune response is important for the development of intestinal pathology.

PMID: 19812984

J Antimicrob Chemother. 2006 Dec;58(6):1154-9. Epub 2006 Oct 5.

Role of the CmeABC efflux pump in the emergence of fluoroquinolone-resistant Campylobacter under selection pressure.

Yan M, Sahin O, Lin J, Zhang Q.


Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, USA.



The objective of this study was to determine the contribution of the CmeABC efflux pump to the emergence of fluoroquinolone (FQ)-resistant mutants in Campylobacter jejuni under various levels of selection pressure.


The frequency of emergence of ciprofloxacin-resistant mutants was measured in wild-type C. jejuni NCTC 11168 and its isogenic cmeB mutant and cmeR mutant (overexpressing cmeABC) using plates containing various concentrations of ciprofloxacin. Representative ciprofloxacin-resistant mutants were selected for gyrA sequence analysis and MIC determination. Accumulation of ciprofloxacin in Campylobacter cells was measured using spectrofluorometry.


Mutation of cmeB drastically reduced the frequency of emergence of FQ-resistant mutants at 10x and 32x the MIC of ciprofloxacin, while the cmeR mutant displayed an approximately 17-fold increase in the frequency of emergence of the mutants at 32x the MIC when compared with the wild-type strain. Various point mutations occurred in gyrA in the FQ-resistant mutants selected at 5x and 10x the MIC, while the Thr-86–>Ile mutation was predominant in the mutants selected at 32x the MIC. The Thr-86–>Ile change conferred a high-level resistance to FQs, but other mutations only conferred an intermediate-level FQ resistance. In contrast, all types of gyrA mutations in the CmeABC-overexpressed background conferred high-level resistance to ciprofloxacin. Overexpression of cmeABC significantly reduced the amount of ciprofloxacin accumulated within bacterial cells.


CmeABC is not only important for maintaining high-level resistance to FQs but also contributes significantly to the emergence of FQ-resistant mutants. Inhibition of this efflux pump may prevent the emergence of clinically relevant FQ-resistant Campylobacter mutants.

PMID: 17023497

Appl Environ Microbiol. 2011 Aug;77(15):5257-69. Epub 2011 Jun 3.

Investigating antibacterial effects of garlic (Allium sativum) concentrate and garlic-derived organosulfur compounds on Campylobacter jejuni by using Fourier transform infrared spectroscopy, Raman spectroscopy, and electron microscopy.

Lu X, Rasco BA, Jabal JM, Aston DE, Lin M, Konkel ME.


School of Food Science, Washington State University, Pullman, WA 99163, USA.


Fourier transform infrared (FT-IR) spectroscopy and Raman spectroscopy were used to study the cell injury and inactivation of Campylobacter jejuni from exposure to antioxidants from garlic. C. jejuni was treated with various concentrations of garlic concentrate and garlic-derived organosulfur compounds in growth media and saline at 4, 22, and 35°C. The antimicrobial activities of the diallyl sulfides increased with the number of sulfur atoms (diallyl sulfide < diallyl disulfide < diallyl trisulfide). FT-IR spectroscopy confirmed that organosulfur compounds are responsible for the substantial antimicrobial activity of garlic, much greater than those of garlic phenolic compounds, as indicated by changes in the spectral features of proteins, lipids, and polysaccharides in the bacterial cell membranes. Confocal Raman microscopy (532-nm-gold-particle substrate) and Raman mapping of a single bacterium confirmed the intracellular uptake of sulfur and phenolic components. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) were employed to verify cell damage. Principal-component analysis (PCA), discriminant function analysis (DFA), and soft independent modeling of class analogs (SIMCA) were performed, and results were cross validated to differentiate bacteria based upon the degree of cell injury. Partial least-squares regression (PLSR) was employed to quantify and predict actual numbers of healthy and injured bacterial cells remaining following treatment. PLSR-based loading plots were investigated to further verify the changes in the cell membrane of C. jejuni treated with organosulfur compounds. We demonstrated that bacterial injury and inactivation could be accurately investigated by complementary infrared and Raman spectroscopies using a chemical-based, “whole-organism fingerprint” with the aid of chemometrics and electron microscopy.

PMID: 21642409



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