Beyond Campylobacter jejuni: understanding Campylobacter coli infections in a systemic model of disease.

In this issue of Virulence, the authors of the article entitled “Virulence genes and cytokine profile in systemic murine Campylobacter coli infection” utilized a mouse model in order to explore the pathogenic mechanisms and cytokine responses involved in Campylobacter coli (C. coli) systemic infections. The clinical isolate C. coli 26536 was first analyzed for the presence of known virulence genes by polymerase chain reaction, and then these genes were sequenced before and after C. coli 26536 infection of Balb/c mice to ensure that these genes were stable. C. coli 26536 were found to persist in the liver and the spleen of the Balb/c mice for at least 8 days, with greater persistence in the liver. The observed cytokine profiles in the plasma and liver of infected mice were clearly different, demonstrating differences between the systemic and local inflammatory responses. This study is the first to focus on clarifying some of the mechanisms involved in the pathogenesis of systemic. C. coli infections that can occur in immunocompromised individuals. Campylobacter continues to cause the greatest number of confirmed foodborne bacterial infections in developed countries, and the incidence of infections caused by Campylobacter has increased from 2008 to 2012. Campylobacter are gram negative, curved, microaerophilic bacteria that can be transmitted to humans through consumption or handling of contaminated poultry, which are the reservoir for most human campylobacteriosis cases. Infection with Campylobacter usually results in gastroenteritis, including watery or bloody diarrhea, cramps, and fever, depending on the virulence of the bacterial strain and host susceptibility. Campylobacter infections can also result in extra-intestinal manifestations including, but not limited to bacteremia, GuillainBarre syndrome, reactive arthritis, sepsis, or meningitis in immunocompromised individuals. According to the Centers for Disease Control and Prevention, the most commonly identified causes of campylobacteriosis are C. jejuni and C. coli. The most common causes of bacteremia are C. jejuni, C. coli, and C. fetus, however other emerging Campylobacter spp. have also been identified as causes of both gastrointestinal and extra-intestinal diseases. As most studies involving Campylobacter pathogenesis have focused on C. jejuni, there is little known about the pathogenic mechanisms of less prevalent Campylobacter spp, such as C. coli. It has been reported that C. coli are able to invade the human intestinal epithelial cell lines T84 and Caco-2, as well as transcytose a polarized T84 monolayer, suggesting that they can cross the gut epithelium to cause systemic disease in susceptible individuals. Klancnik et al. have begun to try to understand the mechanisms by which C. coli affect the host during a systemic infection, which is not common, but can result in a 10–15% mortality rate in immunocompromised individuals. Ongoing research continues to add to our knowledge base of Campylobacter, and different strains can be categorized based on the presence or absence of specific genes, allowing us to determine how these pathogens might cause illnesses and how we can prevent them from causing disease. Since Campylobacter are genetically diverse, it is important to confirm the presence of known virulence factors in different strains as they are introduced to various experimental conditions. Klancnik et al. demonstrated that C. coli 26536 stably expressed the known virulence factors cadF, virB11, cdtB, and ceuE, whether they were detected after being grown from ¡80 C frozen stocks or isolated from livers of intravenously infected mice. In addition to confirming which virulence genes were present in C. coli 26536, the authors took advantage of a mouse model of systemic infection to observe the spread and persistence of this clinical isolate in the liver and spleen. C. coli 26536 CFU in the liver peaked on day 1 post-infection, and gradually decreased over 8 days, which is similar to what the authors reported previously in mice infected with C. jejuni. In contrast, bacterial numbers in the spleen gradually increased from day 1 to day 8 post infection, but not to the levels present in the liver. The authors mention a possible role for macrophages in acting as a reservoir for Campylobacter survival. Although the authors report that hematoxylin/eosin staining in the liver and spleen reveals inflammatory infiltrate,