The species Escherichia coli consists of a diverse group of bacteria. Most E. coli strains do not cause illness; many are present as commensals in healthy human gut flora. However, some E. coli strains have acquired virulence genes and can cause disease in the intestinal tract or extraintestinally. Pathogenic E. coli strains are categorized into pathotypes on the basis of their virulence genes. Six pathotypes are associated with diarrhea (diarrheogenic): enterotoxigenic E. coli (ETEC), Shiga toxin–producing E. coli (STEC), enteropathogenic E. coli (EPEC), enteroaggregative E. coli (EAEC), enteroinvasive E. coli (EIEC), and possibly diffusely adherent E. coli (DAEC). Other pathotypes are common causes of urinary tract infections, bloodstream infections, and meningitis but will not be covered here. Many serotypes of E. coli are determined by surface antigens (H and O), and specific serotypes tend to cluster within a specific pathotype.
STEC are also called verotoxigenic E. coli (VTEC), and the term enterohemorrhagic E. coli (EHEC) is commonly used to specify STEC strains capable of causing human illness, especially bloody diarrhea and hemolytic uremic syndrome (HUS).
Diarrheogenic pathotypes can be passed in the feces of humans and other animals. Transmission of E. coli occurs through the fecal-oral route, primarily via contaminated food or water. Transmission also occurs through person-to-person contact, as well as contact with animals or their environment. The intestinal tracts of animals, especially cattle and other ruminants, are the primary reservoirs of STEC.
Travel to less-developed countries is associated with higher risk for travelers’ diarrhea, including E. coli infection. ETEC is the most common cause of diarrhea among travelers returning from most regions, and other pathotypes can also cause travelers’ diarrhea. ETEC was first recognized as a cause of human diarrheal illness in the 1960s. It has since emerged as a major bacterial cause of diarrhea among children in the developing world. Additionally, ETEC is a major bacterial cause of diarrhea in travelers to the developing world. ETEC produces 2 toxins, a heat-stable toxin (known as ST) and a heat-labile toxin (LT). Although different strains of ETEC can secrete either or both of these toxins, the illness caused by each toxin is similar. Both toxins stimulate the lining of the intestines to secrete excessive fluid, thus producing diarrhea. Due to limitations in detection, the relative contribution of pathotypes other than STEC to the prevalence of travelers’ diarrhea is unclear and likely underrecognized. Additional information about travelers’ diarrhea is available in Chapter 2, Travelers’ Diarrhea.
STEC infections are mainly observed in industrialized countries, and most STEC infections do not occur as part of an outbreak. The serogroup most frequently isolated from patients in the United States is O157, but collectively, non-O157 serogroups are estimated to cause more infections. Compared with patients with STEC O157 infection, patients diagnosed with non-O157 STEC infections may be more likely to have recently traveled outside the United States. In 2011, a Shiga toxin–producing EAEC O104:H4 strain caused a large outbreak in Europe; several cases were identified among returning US travelers.
Where information is available, non-STEC diarrheogenic E. coli infections have an incubation period ranging from 9 hours to 3 days. The median incubation period of STEC infections is 3–4 days, with a range of 1–10 days. The clinical manifestations of diarrheogenic E. coli vary by pathotype (Table 3-01).
Table 3-01. Mechanism of pathogenesis and typical clinical syndrome of Escherichia coli pathotypes
MECHANISM OF PATHOGENESIS
TYPICAL CLINICAL SYNDROME
Heat stable/heat labile enterotoxin production
Acute watery diarrhea, afebrile, occasionally severe
Small and large bowel adherence; enterotoxin and cytotoxin production
Watery diarrhea, bloody diarrhea; can cause prolonged or persistent diarrhea in children
Small bowel adherence and epithelial cell effacement mediated by intimin
Severe acute watery diarrhea, bloody diarrhea; may be persistent; common cause of infant diarrhea in developing countries
Adherence, mucosal invasion and inflammation of large bowel
Watery diarrhea, dysenterylike diarrhea, fever
Diffuse adherence to epithelial cells
Pathogenicity not conclusively demonstrated but may be associated with watery diarrhea
Large bowel adherence (frequently mediated via intimin); Shiga toxin 1, Shiga toxin 2 production
Watery diarrhea that may progress to bloody diarrhea in 1–3 days; pain with defecation; abdominal tenderness; patients may report a history of fever but be afebrile on presentation, often >5 stools in 24 hours
Abbreviations: ETEC, enterotoxigenic E. coli; EAEC, enteroaggregative E. coli; EPEC, enteropathogenic E. coli; EIEC, enteroinvasive E. coli; DAEC, diffusely adherent E. coli; STEC, Shiga toxin–producing E. coli.
Many patients with travel-associated E. coli infections, especially those with nonbloody diarrhea, as commonly occurs with ETEC infection, are likely to be managed symptomatically and are unlikely to have the diagnosis confirmed by a laboratory. Most clinical laboratories in the United States do not use tests that can detect diarrheogenic E. coli other than STEC. Testing for non-STEC pathotypes is typically done at public health laboratories and only when an outbreak of diarrheal illness of unknown origin is being investigated. In this situation, isolates for testing may be submitted to CDC via state health departments. These tests typically involve PCR testing for the specific virulence genes of ETEC, EPEC, EAEC, EIEC, and DAEC.
When a decision is made to identify a cause of an acute diarrheal illness, in addition to routine culture for Salmonella, Shigella, and Campylobacter, the stool sample should be cultured for E. coli O157:H7 and simultaneously assayed for non-O157 STEC with a test that detects Shiga toxin. For more information, see www.cdc.gov/mmwr/preview/mmwrhtml/rr5812a1.htm.
All presumptive E. coli O157 isolates and Shiga toxin–positive specimens should be sent to a public health laboratory for further characterization. Rapid, accurate diagnosis of STEC infection is important, because treatment with parenteral volume expansion may decrease renal damage and improve patient outcome.
Patients with profuse diarrhea or vomiting should be rehydrated. Evidence from pediatric studies indicates that early use of intravenous fluids (within the first 4 days of diarrhea onset) may decrease the risk of HUS in patients with STEC O157 infections. Some people choose to travel with an antibiotic (usually ciprofloxacin, rifaximin, or azithromycin) and take it if they develop loose stools. CDC does not recommend chemoprophylaxis with antibiotics to prevent travelers’ diarrhea. (See Chapter 7, Traveling Safely with Infants & Children, for information about managing travelers’ diarrhea in children.)
Non-STEC diarrheogenic E. coli are often resistant to traditional antimicrobial agents, including ampicillin and trimethoprim-sulfamethoxazole.
Clinicians treating a patient whose clinical syndrome suggests STEC infection (Table 3-01) should be aware that administering antimicrobial agents may increase the risk of HUS. Additionally, antimotility agents should be avoided in patients with bloody diarrhea or patients with confirmed STEC infections, because some studies have found that these agents may increase the risk of HUS or neurologic complications.
There is no vaccine for E. coli infection, nor is chemoprophylaxis recommended. Food and water are primary sources of E. coli infection, so travelers should be reminded of the importance of adhering to food and water precautions (see Chapter 2, Food & Water Precautions). People who may be exposed to livestock, especially ruminants, should be instructed on the importance of handwashing in preventing E. coli infection. During E. coli outbreaks, clinicians should alert people traveling to affected areas and be cognizant of possible infections among returning travelers.
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