Purpose of review
Travelers' diarrhea affects 20–60% of travelers to low-income regions of the world. Much of the evidence for the clinical description and management of travelers' diarrhea was generated years ago, however, there is new information on geographic and host risk, etiology, and prevention strategies.
Travel to South Asia, followed by sub-Saharan Africa and South America, carries the highest risk for diarrheal syndromes in returned travelers. Women are more susceptible to travel-related diarrhea than men. Host genetic studies have demonstrated that single nucleotide polymorphisms in the lactoferrin, osteoprotegerin, and IL-10 genes are associated with small but increased risks for diarrhea and enteric pathogens. Enterotoxigenic Bacteroides fragilis is likely to be a new agent identified as causing travelers' diarrhea, and heat-stable toxin-producing Escherichia coli appears to be more common than heat-labile toxin E. coli. Overall levels of sanitation at the travel destination, including individual eating establishments, are strong predictors for acquisition of travelers' diarrhea. A new transdermal LT vaccine shows promise in modifying the severity of travelers' diarrhea. It remains uncertain whether prophylaxis or prompt self-treatment of travelers' diarrhea will prevent late-onset irritable bowel syndrome. For self-treatment, azithromycin is the drug of choice in travelers to areas where there is a high risk of fluoroquinolone-resistant Campylobacter spp., such as South and Southeast Asia and possibly North Africa, Central and South America.
There is increased understanding of the determinants of travelers' diarrhea. Despite this travelers' diarrhea remains one of the most common illnesses in travelers. Continued focus on intervention strategies may ultimately lead to decreased incidence.