Student guest post by D.F. Johnston
As the year marches forward, ever closer to that summer sun we missed so much during dreary winter days, we also get closer to the traditional summer picnics and barbecues. Sometimes, in our hurry to enjoy quality time with friends and family, we get distracted from our usual practices for proper food handling. We might try to get little Billy his hamburger before he has time for a full-fledged temper tantrum, so we hurry it along, figuring a tiny bit of pink in the middle won’t be the end of the world. Or we might realize that we’re short a couple of serving spoons and re-use the meat fork for the raw fruit or veggie tray. After all, even if we’re thinking about foodborne illness, a little diarrhea is our biggest worry, right?
Actually, amongst the wide range of microbes that can cause foodborne illness, one of the more common is a Gram-negative bacterium called Campylobacter jejuni, which lives in the intestines (where the name “jejuni” comes from) and it is most often encountered in undercooked poultry or via cross-contamination. This bacterium does cause the well-known symptom of short-term diarrhea and usually resolves on its own over the course of two to ten days or with antibiotic treatment (1). Many people who worry about foodborne illness worry about the well-known salmonellosis or the dreaded E. coli O157:H7. According to the National Center for Zoonotic, Vector-Borne, and Enteric Diseases estimates for the number of cases of shiga-toxin producing E. coli, enterohemorrhagic E. coli, salmonellosis and an Institute of Medicine estimate for enterotoxigenicE. coli, the combined total number of cases occurring each year in the United States is approximately 880,000 (2-5). Ironically, cases of Campylobacter are over 2.5 times more common, as there are approximately 2.4 million cases in the United States each year (6). Campylobacter probably isn’t as infamous as it tends to occur in small clusters like at family picnics, rather than in high-profile outbreaks and recalls.
Unfortunately, discomfort and dehydration are not the only possible consequences of campylobacteriosis. Lindsay mentions temporary arthritis and hemolytic uremic syndrome, which can result in renal failure, as potential consequences of C. jejuni infection (7). Additional chronic conditions associated with prior infection with C. jejuni are mentioned by the Food Research Institute at the University of Wisconsin-Madison and include appendicitis, carditis, Reiter syndrome, and Miller Fisher syndrome, which is a subtype of Guillain-Barré syndrome (8). There are several forms of Guillain-Barré syndrome (GBS), making the range of symptoms wide as well, but some of the more commonly encountered effects are limb and respiratory weakness, and loss of reflexes (9). Several organisms may precipitate GBS, in addition to C. jejuni, such as cytomegalovirus, Epstein-Barr virus, and Mycoplasma pneumoniae, although Campylobacter-associated forms may be more severe in clinical presentation (10, 11). Typically, GBS associated with C. jejuni follows 1-3 weeks after infection and patients generally recover within weeks to months (11). However, there is a 2-3% mortality rate and 20% of GBS cases may have significant and lasting neurologic effects (12). Between 30-50% of all GBS cases are linked to C. jejuni infection (12).
Since there are several forms of clinical presentation for GBS, the forms also differ in hypothesized mechanisms for how the disease is caused or what part of the nerve cell is directly affected (i.e. the myelin sheath versus the axon or T-cell mediated versus antibody-mediated) (11). Despite this, the current conception for all types is of GBS being caused by the immune system reacting to an external factor (such as C. jejuni) to the degree that human cells become collateral damage in one form or another. One of the more popular theories is that part of a molecule on the surface of the bacterium is very similar to those found on nerve cells in the human body, leading to an antibody attack on nerve cells even after the Campylobacter has been eliminated. This mechanism is further supported by the other agents suspected in causation of GBS since they also have a similarly-shaped molecule on their surface (11). The paralysis or muscle weakness may occur because the immune system breaks open the protective Schwann cells surrounding the nerves, allowing enzymes to begin breaking down the myelin “insulation” of nerve axons that help ensure reception and speed of nerve impulses (11).
The first causal relationship for C. jejuni and GBS was hypothesized in 1982 based on a case report and similar reports continued after this (11). Isolation and growth of Campylobacter from the stool of GBS patients also supported such a relationship, but was assumed to underestimate bacterial presence, as time from initial infection to culture and culture methodology could strongly influence recovery of the bacterium (11). Lab techniques to detect antibodies to C. jejuni have also been used to demonstrate presence of the organism in GBS patients, although this technique is subject to cross-reaction with closely related bacteria (11). That GBS appears 1-3 weeks after bacterial infection (the time it takes to produce an antibody response) also supports an infectious event leading to GBS. Animal models have strengthened support for the association, as rabbits and mice have been injected with molecules similarly shaped to those of C. jejuni and have developed high titers of antibodies that also react against nerve cells (11, 12). The NIH appears to accept the role of Campylobacter in GBS etiology and has moved to outlining steps for improving mechanistic knowledge (11); the published literature also reflects this general acceptance.
This summer, my family reunion is going to use safe food handling techniques in an attempt to lower my family’s risk for the unpleasantness of campylobacteriosis and the subsequent risk for Guillain-Barré syndrome and other Campylobacter-associated chronic conditions. Have a look at the USDA guidelines for proper food handling and enjoy your summer pursuits (13).
1. Ang, J.Y. & Nachman, S. 2009. “Campylobacter Infections.” eMedicine.
2. National Center for Zoonotic, Vector-Borne, and Enteric Diseases. 2009. “Escherichia coli O157:H7.” Centers for Disease Control and Prevention.
3. National Center for Zoonotic, Vector-Borne, and Enteric Diseases. 2009. “Enterohemorrhagic Escherichia coli: Technical Information.” Centers for Disease Control and Prevention.
4. National Center for Zoonotic, Vector-Borne, and Enteric Diseases. 2009. “Salmonellosis.” Centers for Disease Control and Prevention.
5. Stratton, K.R., Durch, J.S., & Lawrence, R.S (Institute of Medicine). 2000. “Vaccines for the 21st Century: A Tool for Decisionmaking–Appendix 5: Enterotoxigenic E. coli.” National Academies Press.
6. National Center for Zoonotic, Vector-Borne, and Enteric Diseases. 2009. “Campylobacter, General Information.” Centers for Disease Control and Prevention.
7. Lindsay, J.A. 1997. “Chronic Sequelae of Foodborne Disease.” Emerg Infect Dis, 3(4): 443-452. http://www.cdc.gov/ncidod/EID/vol3no4/lindsay.htm
8. Doyle, M.E. 1998. “Campylobacter–Chronic Effects.” UW-FRI Briefings.
9. Davids, H.R. & Oleszek, J.L. 2010. “Guillain-Barré Syndrome.” eMedicine.
10. Yu, R.K., Usuki, S., & Ariga, T. 2006. “Ganglioside Molecular Mimicry and Its Pathological Roles in Guillain-Barré Syndrome and Related Diseases.” Infect Immun, 74(12): 6517-6527.
11. Nachamkin, I., Allos, B.M., & Ho, T. 1998. “Campylobacter Species and Guillain-Barré Syndrome.” Clin Microbiol Rev, 11(3): 555-567.
12. Moore, J.E., Corcoran, D., Dooley, J.S.G., Fanning, S., Lucey, B., Matsuda, M., McDowell, D.A., Megraud, F., Millar, B.C., O’Mahony, R., O’Riordan, L., O’Rourke, M., Rao, J.R., Rooney, P.J., Sails, A., & Whyte, P. 2005. Campylobacter.” Vet Res, 36(3): 351-382.
13. USDA: Food Safety and Inspection Service. 2010. “Safe Food Handling Fact Sheets.”
Image from: http://en.wikipedia.org/wiki/Campylobacter