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Campylobacter jejuni is among the most common causes of enteric infection worldwide, and its complex relationship with the human host is just starting to be understood. C. jejuni causes inflammatory enteritis manifested by diarrhea or dysentery, fever, and abdominal cramping. Asymptomatic infection/colonization is also common, as described in children after repeated exposure to C. jejuni in resource-poor countries [1, 2]. Recently, incidence estimates of 1 symptomatic or asymptomatic C. jejuni infection every 2 years have also been reported in adults in developed countries [2]. C. jejuni infections have strong associations with postinfectious sequelae, strain variability, and increasing resistance to antibiotics. These include the demyelinating neurologic syndrome Guillain-Barre, chronic gastrointestinal symptoms, and postinfectious arthritis [3–6]. The kinetics and composition of the human immune response to C. jejuni are poorly understood and difficult to evaluate in field settings because of the inability to know onset of infection, strain differences, and previous exposures. Human challenge models, in contrast, provide a controlled method to understand and define immunologic responses to infection and/or correlates of protection [7–9]. We and others have described the human challenge model development of C. jejuni, most recently using strain CG8421 [9]. This strain, which lacks ganglioside mimicry in its lipo-oligosaccaharide, replaced strain 81-176, which expresses ganglioside 2 and ganglioside 3 and was epidemiologically linked to Guillain-Barre [7, 10]. Previous human challenge studies with 81-176 and A3249 demonstrated that Campylobacter-specific immunoglobulin A (IgA) and interferon γ (IFN-γ) are associated with resistance to clinical disease, suggesting these components might be important markers of protective immunity [7, 8]. To better define protective immunity to C. jejuni and to further develop the model, we challenged healthy, immunologically naive adults with C. jejuni CG8421 and then rechallenged subjects 3 months later with the same strain. As with previous challenge trials, this study was performed with the expectation that a primary infection would afford significant, if not complete, clinical protection after rechallenge [7, 8].

We conducted clinic-based, influenza-like illness and diarrheal disease surveillance among U.S. service members participating in Operation Bright Star 2009. Epidemiologic data and samples were collected. Nasopharyngeal swab specimens were tested for viruses, and feces was tested for microbiologic, immunologic, and molecular diagnostics. A survey was used to collect self-reported data. From 1,529 surveys, 41% reported diarrheal disease and 25% reported respiratory illness (incidence rate = 62 of 100 versus 37 of 100 person-months; incidence rate ratio = 1.7, 95% confidence interval = 1.5–1.9). Enterotoxigenic Escherichia coli was identified in 74% (69 of 93) of fecal samples. In the influenza-like illness case series, 17% (9 of 52) were positive for influenza A; all were positive for pandemic (pH1N1) 2009 virus. Rates of decreased work performance reported by patients with diarrhea and influenza-like illness were similar (46% versus 48%; P = 0.8). Diarrheal diseases and respiratory illness remain common among deployed military personnel, with important operational impact. Despite an ongoing influenza pandemic, diarrheal disease incidence was higher than that of respiratory illness.

Learning Objective - Readers will be able to answer the following question in such a manner as to be of significant use in their official duties: Question: When do I give antibiotics in the setting of traveler's diarrhea while deployed?