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Enteric infections are endemic in many low-income countries but may also be contracted from contaminated food or water in developed countries. Symptoms may range from minimal gastrointestinal distress to life-threatening watery diarrhea or dysentery.
Worldwide, enteric infections are a leading cause of morbidity. In low- and middle-income countries without access to clean water and basic sanitation, young children are disproportionately affected with acute diarrheal illness and suffer sequelae ranging from malnutrition ( Chapter 197 ) and its complications to dehydration and death. Although infrequently fatal in industrialized regions, enteric infections are ubiquitous ailments with pathogens that know no borders because of international travel to and from hyperendemic regions, as well as the globalization of food supplies. Foodborne outbreaks remain common in the United States, where pathogens are distributed widely in produce or other foods. For example, one of the largest outbreaks of Salmonella enteritidis , estimated to involve more than 200,000 people in the United States, resulted from national distribution of contaminated ice cream. For foodborne illnesses traced to retail food establishments, about 40% are due to contamination of food by ill or infectious workers. Fortunately, many outbreaks can be mitigated when pathogens that are isolated from individual patients undergo molecular profiling by public health laboratories linked to the U.S. Centers for Disease Control and Prevention (CDC).
Norovirus is the leading cause of infectious diarrhea in adults worldwide and of enteric infection outbreaks in the United States, but multiple microbial agents can cause enteric infections. Fortunately, the geographic location, exposure history, and clinical presentation often can refine the list of potential causative agents ( Table 262-1 ). For example, a patient who has recently returned from travel to a low-income country with acute watery diarrhea will likely be infected with one of several pathogens associated with traveler’s diarrhea ( Chapter 265 ), particularly enterotoxigenic E. coli , whereas the onset of bloody diarrhea following consumption of poorly cooked ground beef is likely due to Shiga toxin–producing E. coli ( Chapter 280 ). However, it is important to recognize that neither the pathogens nor their epidemiologic associations are static. The dynamic nature of the causes of outbreaks of acute enteric infections is demonstrated by the emergence and international spread of a multidrug-resistant Shigella strain ( Chapter 285 ), as well as by a large European outbreak caused by a novel E. coli strain that had contaminated raw sprouts and acquired the ability to produce Shiga toxin ( Chapter 280 ).
EXPOSURE | LIKELY PATHOGEN(S) |
---|---|
Travel to low- or middle-income countries | Diarrheagenic E. coli (ETEC, EAEC, EPEC; Chapter 280 ), norovirus ( Chapter 350 ), Campylobacter ( Chapter 279 ), Shigella ( Chapter 285 ), nontyphoidal Salmonella ( Chapter 284 ), Giardia ( Chapter 322 ), Cryptosporidia ( Chapter 321 ), Entamoeba histolytica ( Chapter 323 ), Cyclospora spp. ( Chapter 324 ), rarely V. cholerae ( Chapter 278 ), Balantidium coli ( Chapter 324 ). |
Daycare | Low-inocula pathogens: Shiga toxin–producing E. coli (STEC; Chapter 280 ), Shigella ( Chapter 285 ), Giardia ( Chapter 322 ), Cryptosporidia ( Chapter 321 ), norovirus ( Chapter 350 ), rotavirus ( Chapter 350 ) |
Prior antibiotic use | Clostridioides difficile ( Chapter 271 ) |
Immunosuppression, including AIDS | Cytomegalovirus ( Chapter 347 ) , Cryptosporidia ( Chapter 321 ), Cytoisospora belli ( Chapter 324 ), Herpes simplex virus ( Chapter 345 ), Mycobacterium avium complex ( Chapter 300 ), Histoplasma ( Chapter 308 ), microsporidia ( Chapter 324 ) |
Long-term care, prisons | C. difficile ( Chapter 271 ), norovirus ( Chapter 350 ), Shigella ( Chapter 285 ), rotavirus ( Chapter 350 ), STEC ( Chapter 280 ), Giardia ( Chapter 322 ) |
Pet reptiles | Salmonella spp. ( Chapter 284 ) |
Petting farms, pets | STEC , Campylobacter ( Chapter 279 ), Cryptosporidia ( Chapter 321 ), Yersinia ( Chapter 288 ) |
Pigs/pig feces | Yersinia enterocolitica ( Chapter 288 ), Balantidium coli ( Chapter 324 ) |
Hemochromatosis | Yersinia enterocolitica ( Chapter 288 ) |
Raw shellfish | Vibrio spp. ( Chapter 278 ), norovirus ( Chapter 350 ), Plesiomonas shigelloides ( Chapter 126 ) |
Cruise ship travel | Commonly norovirus ( Chapter 350 ), occasionally ETEC ( Chapter 280 ) |
Consumption of untreated fresh water, mountain areas of the United States | Giardia ( Chapter 322 ) |
Imported fresh produce (particularly raspberries), travel to tropical/semitropical regions | Cyclospora spp. ( Chapter 324 ) |
Swimming in public pools, waterparks | Cryptosporidia ( Chapter 321 ) |
Anal contact | Shigella , including MDR spp. ( Chapter 285 ); other pathogens such as E. histolytica ( Chapter 323 ) spread via fecal-oral contact |
Enteric infections ultimately reflect the successful interaction of individual pathogens with their human hosts. Pathogens must overcome innate and acquired host defenses while competing with the normal human microbiota to colonize intestinal epithelia. Once established, pathogens may then elaborate toxins or produce virulence factors that promote adhesion and invasion.
Not all hosts are equally susceptible to enteric infections. The use of acid-blocking agents, such as proton pump inhibitors, impairs an important first line of host defense by decreasing gastric acidity, thereby reducing the effective inocula required for bacterial pathogens. Recent prior or concurrent use of antibiotics can alter the normal intestinal microflora, thereby reducing its ability to impair the growth of newly introduced pathogens. Host genetics can also play critical roles in determining the outcome of infection. For instance, Vibrio cholerae infections ( Chapter 278 ) tend to be most severe in individuals with O blood group, likely due to more efficient intoxication of O enterocytes with cholera toxin. In contrast, enterotoxigenic E. coli infections ( Chapter 280 ) appear to be more severe in individuals who express the A blood group antigen on intestinal epithelia, likely due to an A-specific lectin expressed by these bacteria.
Some pathogens, particularly norovirus ( Chapter 350 ), Shigella ( Chapter 285 ), and Shiga toxin–producing E. coli ( Chapter 280 ), typically require very low inocula to establish infection. This characteristic has contributed to numerous outbreaks of norovirus on cruise ships and a multitude of foodborne outbreaks of Shiga toxin–producing E. coli ( Chapter 280 ).
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