By Kelly A. Reynolds, MSPH, Ph.D.

Recently, a colleague posed the question of why travelers to other countries become sick from drinking the water whereas local residents do not. Given that immunity to most common waterborne pathogens is typically ineffective or at least short-term, the cause of this innate ‘immunity’ was a mystery. After perusing the scientific literature and chatting with other experts in the field, my conclusion is that the answer lies somewhere between fact and myth.

Traveler’s diarrhea
According to the US Centers for Disease Control and Prevention, an estimated 20 to 50 percent of international travels (approximately 10 million people per year) will develop traveler’s diarrhea. Diarrhea is defined as three or more unformed stools in a 24-hour period. Symptoms may include abdominal cramps, nausea, vomiting, fever and bloating but are normally self-limiting within a few days. For some, illness can be more serious, lasting for weeks and potentially resulting in hospitalization or even death. International travel, particularly to developing countries where food and water sanitation are sub-optimal, is the primary risk factor of traveler’s diarrhea. High-risk destinations include Latin America, Africa, Asia and the Middle East. Similarly, hikers and backpackers in developed nations are at risk due to the transmission of pathogens from wild animal contamination of perceived pristine, untreated drinking water sources (hence the term ’beaver fever‘). As with most waterborne outbreak risks, sensitive populations (i.e., the young, elderly, immunocompromised) are more likely to become infected and experience illness when exposed to a waterborne pathogens.

Although traveler’s diarrhea is most commonly associated with an enterotoxigenic strain of Escherichia coli (E. coli), many other organisms also cause the disease, including viruses (i.e., rotavirus, norovirus, hepatitis A virus); protozoa (i.e., Cryptosporidium, Giardia, Entamoeba histolytica) and other bacteria (i.e., Shigella, Campylobacter, Vibrio parahemolyticus). Treatment options vary, depending on the infectious agent, which may be difficult to definitively characterize. Some pathogens produce toxins and thus, it is advantageous for them to be purged from the gut. Some infections are best left untreated, but the risk of complications due to dehydration must be managed.

Gut flora
Conditions of altered intestinal integrity also mimic symptoms of infectious diarrhea. An imbalance in the normal gut flora, food allergies and other immune reactions, bowel syndromes, cancer and the ingestion of toxins can also cause stomach upset and diarrhea. The gut consists of a complicated mixture of microbes that is thought to be patterned spatially and temporally. For example, genetically related individuals are thought to have similar patterns of gut flora. Over time, the flora changes relative to variations in food and water microbes.1 Gut flora refers to the microbiota in the intestines. Human guts are rich with diverse microbial populations, with estimates of between 300 and 1,000 different bacterial species and concentrations above 100 billion per gram of bowel content. Many species have not been identified, but more than half the mass of dry feces is comprised of bacteria.2 The gastrointestinal tract of a healthy newborn is sterile; however, during birth and exposure to the post-natal environment, their guts are rapidly colonized, reaching the billions of bacteria per gram of feces within a few days. Gut flora varies in babies, relative to the composition of their early diets.3

Much research around pathogens and gut flora is focused on the bacteria Clostridium difficile. C. difficile is the cause of up to 35 percent of antibiotic-associated diarrhea and the main infectious cause of diarrhea in hospitals and long-term care facilities. Virulent strains of the bacteria have been found in food supplies in developed countries. Disruption of gut flora is a major risk factor of the disease. Fecal transplants, from genetically related donors, provide a greater chance for successful treatment of chronic infections.4 A recent article published in PLoS One (2010) discusses how very little is known about flora in the human gastrointestinal tract.5 Interestingly, researchers have found that the stool of healthy persons is teeming with viruses. The most common was the pepper mild mottle virus. Billions of this plant pathogen were isolated from a single gram of feces in study participants. Prevalence ranged from 7 to 67 percent of volunteers in developed regions testing positive. This common gut microbe has been linked to immune reactions and clinical symptoms as well.

Innate immunity
Very little scientific research is available on the possibility of innate immunity to waterborne pathogens. Most of my colleagues in the field of environmental microbiology believe it is just a myth. While people have theorized that different bacteria or chemicals in foods and water in various geographical areas cause disease in visitors but not the indigenous population, there simply is not clear evidence to support the hypothesis. There is, however, evidence of mild- or short-term immunity and possibly some cultural influences contributing to the story.

In risk analysis, consideration of host state in the manifestation of waterborne disease is necessary for accuracy in the estimate.6 A host may indeed acquire immunity to a pathogen. Hepatitis A, for example, is one organism that confers lifelong immunity to the infected. For most waterborne pathogens, however, protection is not lifelong or complete. This partial protection may last for months or years, or exposed individuals may become sickened repeatedly over their lifetime. Herein lies the innate immunity

myth. The fact is, indigenous populations in developing countries with poor sanitation and water treatment regularly experience diarrhea and complications from waterborne pathogens. The perception that they are innately immune to pathogens in their water is likely due to their condition of being between some stage of temporary or partial immunity and/or a lack of recognition and reporting of disease.

That being said, there are small segments of populations with the ability to ward off infection more effectively than others. These defenses may be due in part to genetically evolved traits leading to protection or to undefined exposure factors. Certain individuals, for example, have a genetic mutation that protects them from symptomatic norovirus infections.7 Farmers in Scotland also appear to be immune to certain E. coli strains, suggesting that repeated exposure may be beneficial.8 An understanding of how much/how often one should be exposed is a major data gap. Nonetheless, these discoveries suggest approaches for future prevention and control options.

Persistent hazards
The CDC has published a list of precautions aimed at preventing traveler’s diarrhea. Ingesting only treated, purified bottled or boiled water; avoiding uncooked or already peeled fruits and vegetables and avoiding street food-vendors are a few of the suggestions to minimize transmission of disease via food and waterborne routes. Other researchers have found that following these recommendations had little effect on the traveler’s risk of illness, suggesting broader transmission routes of pathogens in the environment.9

Vaccines, and prophylactic medications, including antibody cocktails or broad-spectrum antibiotics, and/or probiotics, are available and have been used with some success but are not without their own risks, ranging from a false sense of security to concerns of antibiotic resistance and harmful alterations in normal flora.

According to an article published in the scientific journal Gut (1998), modern changes in the Western diet, including higher rates of sugar and salt consumption leading to increased diabetes and heart disease, also includes changes in the consumption of probiotic bacteria, prehistorically found in dried and naturally fermented foods.10

In conclusion, persistent diarrhea is very common in developing countries due to chronic exposure to microbial pathogens causing serial infections. The disease occurs in both travelers and indigenous populations. There are many data gaps in the research of gastrointestinal disease risks in various populations. An understanding of gut flora, sources of natural and pathogenic microbes, and immune responses to both, is vital to evaluating the true risk of waterborne illness.

Acknowledgement
Thank you to Peter Cartwright, P.E., CWS-VI, President of Cartwright Consulting Co. and Charles Gerba, Ph.D., Professor, University of Arizona for initiating and participating in conversations related to this topic.

References

  1. Bengmark, S. 1998. Ecological control of the gastrointestinal tract. The role of probiotic flora. Gut. 42: 2-7.
  2. Guarner, F. 2003. Gut flora in health and disease. Lancet. 361:512-519.
  3. Harmsen H.J. et al., 2000. Analysis of intestinal flora development in breast-fed and formula-fed infants by using molecular identification and detection methods. Journal of Pediatric Gastroenterology and Nutrition. 30:61-67.
  4. Tucker, M.E, 2009. Fecal transfer cures relapsing C. diff infection. Internal Medicine News. http://imn.gcnpublishing.com/fileadmin/con- tent_pdf/imn/archive_pdf/vol42iss1/70028_main.pdf
  5. Colsen P. et al., 2010. Pepper mild mottle virus, a plant virus associated with specific immune responses, fever, abdominal pains, and pruritus in humans. PLoS One. 5:e10041.
  6. Eisenberg, J.N.S. et al., Disease transmission models for public health decision making: analysis of epidemic and endemic conditions caused by waterborne pathogens. Environmental Health Perspectives. 110: 783-790.
  7. Kindberg, E. 2007. Host genetic resistance to symptomatic norovirus (GGII.4) infections in Denmark. Journal of Clinical Microbiology. 45:2720- 2722.
  8. Moss, L. 2010. Farmers hold clue to vaccine against E. coli. Scotsman. com News. http://news.scotsman.com/health/Farmers-hold-clue-to- vaccine.6463083.jp
  9. Yates, J. 2005. Traveler’s diarrhea. American Family Physician. 71: 2095-2100.

About the author

Dr. Kelly A. Reynolds is an Associate Professor at the University of Arizona College of Public Health. She holds a Master of Science Degree in public health (MSPH) from the University of South Florida and a doctorate in microbiology from the University of Arizona. Reynolds has been a member of the WC&P Technical Review Committee since 1997. She can be reached via email at reynolds@u.arizona.edu

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