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Escherichia coli (E coli) is a gram-negative bacillus that normally inhabits the human intestinal tract but can also act as a pathogen, causing a wide spectrum of disease. While many strains remain harmless, pathogenic variants cause intestinal illnesses—such as enterotoxigenic, enterohemorrhagic, and enteropathogenic infections—and extraintestinal conditions including urinary tract infections, pneumonia, bacteremia, and peritonitis. The activity explores the organism’s adaptability, virulence, and growing antibiotic resistance that make it a significant cause of both community-acquired and healthcare-associated infections, as well as the accurate identification of E coli subtypes. This course reviews E coli pathophysiology, diagnostic strategies utilizing culture and molecular methods, coupled with awareness of resistance mechanisms, and evidence-based management of both intestinal and extraintestinal infections essential for effective diagnosis, treatment, and infection control. Participants will gain practical knowledge for differentiating pathogenic strains, interpreting laboratory findings, and implementing appropriate therapeutic interventions based on resistance patterns. This activity for healthcare professionals is designed to enhance the learner's competence in identifying E coli–related diseases across a wide spectrum, performing the recommended evaluation, and implementing an appropriate interprofessional approach when managing E coli infections to improve patient safety, reduce complications, and optimize outcomes. Objectives: Identify the characteristic clinical features of Escherichia coli infections. Differentiate between pathogenic E coli subtypes using diagnostic criteria from various evaluation studies. Apply evidence-based strategies to manage diarrheal illnesses while minimizing unnecessary antibiotic use. Collaborate with the interprofessional team to optimize outcomes in patients with severe or complicated E coli infections. Access free multiple choice questions on this topic.

Escherichia coli, a gram-negative bacillus that normally inhabits the intestinal flora, is also widely present in the environment.[1] With hundreds of identified strains, E coli produces a broad spectrum of disease, ranging from mild, self-limited gastroenteritis to severe complications, eg, renal failure and septic shock. Its virulence is marked by the ability to evade host defenses and develop resistance to commonly used antibiotics, making E coli a significant cause of both community-acquired and healthcare-associated infections. Additionally, E coli infections can be divided into intestinal and extraintestinal categories. Intestinal illnesses are further subtyped into enterotoxigenic (ETEC), enterohemorrhagic/Shiga toxin-producing (EHEC/STEC), enteroinvasive (EIEC), enteropathogenic (EPEC), and enteroaggregative E coli (EAEC).[2] Extraintestinal illnesses are discussed based on clinical disease manifestations, eg, urinary tract infections, bacteremia, pneumonia, and peritonitis. Understanding these distinctions is essential for accurate diagnosis, evidence-based management, and the prevention of complications associated with E coli infections.

E coli is part of commensal intestinal flora and is also found on the floors of hospitals and long-term care facilities. E coli is the most common gram-negative bacterium in the human gastrointestinal tract and lacks virulence in this setting. However, when found outside of the intestinal tract, E coli can cause urinary tract infections (UTI), pneumonia, bacteremia, and peritonitis, among others.[3][4][5] E coli is also a significant cause of nosocomial infections, including catheter-associated UTIs and ventilator-associated pneumonia.[6] E coli can also be found in soil, on vegetables, and in water, as well as in undercooked meats. Pathogenic strains cause intestinal illness in humans when ingested.

Escherichia coli can cause intestinal illness as well as infections outside of the intestine. Intestinal illness caused by E coli is caused by 1 of 5 subtypes, identified according to their O and H antigens. The O antigen is determined by a repeating polysaccharide chain present in the lipopolysaccharide outer membrane, and the flagellum determines the H antigen.[2] Intestinal Infections Enterotoxigenic E coli ETEC causes watery diarrhea in resource-limited settings and is commonly found in food and water in areas without adequate sanitation. Approximately 100,000,000 organisms must be ingested to cause illness in a healthy person. ETEC is the single most important organism causing traveler’s diarrhea and is also a significant contributor to dehydrating diarrheal illness in infants and children in resource-limited settings.[7] Enteropathogenic E coli EPEC was the first E coli pathotype identified as a causative agent of watery diarrhea primarily in infants and young children in resource-limited settings and is responsible for sporadic and epidemic outbreaks.[8] Diarrheal illness caused by EPEC is most commonly contracted through ingestion but can also be spread person-to-person.[9] Enteroaggregative E coli EAEC is a causative organism of acute and chronic watery diarrhea in both resource-limited and resource-rich regions. This E coli subtype has recently been increasingly identified as a cause of traveler’s diarrhea.[10][11] Enterohemorrhagic/Shiga toxin-producing E coli EHEC/STEC produces Shiga toxin and has a variety of serotypes, including serotype O157:H7.[12][13][14] EHEC/STEC has been responsible for large diarrheal outbreaks after ingesting contaminated produce (eg, spinach, sprouts, lettuce, fruit), raw dairy products, and undercooked beef. Relatively low inocula (102 CFU) result in illness, facilitating the ease of transmission from the environment to humans and then from humans to humans.[15][16] EHEC/STEC infections are common across all age groups, but hemolytic uremic syndrome (HUS) resulting from EHEC/STEC infections is most common in children less than 5 years old.[17] Please see StatPearls' companion resource, "Enterohemorrhagic Escherichia coli," for further information on the epidemiology of EHEC/STEC. Enteroinvasive E coli

EHEC/STEC produces Shiga toxin and has a variety of serotypes, including serotype O157:H7.[12][13][14] EHEC/STEC has been responsible for large diarrheal outbreaks after ingesting contaminated produce (eg, spinach, sprouts, lettuce, fruit), raw dairy products, and undercooked beef. Relatively low inocula (102 CFU) result in illness, facilitating the ease of transmission from the environment to humans and then from humans to humans.[15][16] EHEC/STEC infections are common across all age groups, but hemolytic uremic syndrome (HUS) resulting from EHEC/STEC infections is most common in children less than 5 years old.[17] Please see StatPearls' companion resource, "Enterohemorrhagic Escherichia coli," for further information on the epidemiology of EHEC/STEC. Enteroinvasive E coli EIEC-induced diarrheal illness is uncommon due in part to the relatively large inoculum required, although recent studies suggest EIEC-induced diarrhea may be underdiagnosed. EIEC is closely related to Shigella and is contracted through ingesting undercooked meats and contaminated vegetables.[18] Extraintestinal Infections Extraintestinal illness caused by E coli results from a translocation of gut bacteria into other parts of the body or from environmental spread in hospitals and long-term care facilities. E coli is the predominant gram-negative bacterium to cause extraintestinal illness in humans and can cause urinary tract infection, abdominal and pelvic infection, pneumonia, bacteremia, and meningitis, among others. Between 2009 and 2016, 71,909 extraintestinal E coli infections were identified in patients in United States hospitals; of these, urinary tract infections were found to be the most common (66%). Not surprisingly, approximately half of all E coli bacteremia is thought to be the result of a genitourinary source.[19][20]

Intestinal illness caused by E coli results from the ingestion of bacteria and the innate ability of E coli to overcome host defenses. Gram-negative bacteria are characterized by their cell envelope, which comprises an inner cytoplasmic cell membrane, peptidoglycan cell wall, and outer membrane. The outer membrane is composed of a lipid bilayer, associated proteins, and lipopolysaccharide, and causes a toxic reaction if lysed. Pathogenic E coli strains each have distinctive virulence factors encoded on plasmids, transposons, and bacteriophages.[21] Intestinal Infections Enterotoxigenic E coli pathophysiology Colonizing fimbriae expressed by ETEC enable the bacteria to attach to the intestinal wall. Once connected, ETEC expresses either a heat-labile toxin or a heat-stable toxin, both of which are secretory toxins encoded on plasmids.[22] Heat-labile toxin stimulates adenylate cyclase, leading to increased intracellular cyclic adenosine monophosphate (cAMP) and subsequent chloride secretion from intestinal crypt cells. This mechanism also inhibits intestinal villi from absorbing sodium chloride. The resulting increase in electrolytes leads to the secretion of free water into the intestinal lumen, thus producing watery diarrhea. The heat-stable toxin stimulates guanylate cyclase, leading to increased intracellular cyclic guanosine monophosphate. This results in subsequent chloride secretion and inhibition of sodium chloride absorption in the intestinal lumen, thereby producing watery diarrhea.[23] Enteropathogenic E coli pathophysiology A bundle-forming pilus is encoded by the plasmid (pEAF), enabling EPEC to form a localized attachment to enterocytes in the small intestine. Once bound, the outer membrane protein colonization factor, intimin, facilitates enhanced adherence. Intimin is an outer membrane protein colonization factor encoded on the eae gene within the locus of enterocyte effacement (LEE) chromosomal island.[24] The LEE chromosomal island elaborates approximately 20 secretory toxins that are injected into the enterocyte by a type III injectisome.[25][26] These toxins trigger a series of events that ultimately lead to the characteristic effacement of microvilli, increased permeability of tight junctions, and alterations in water and electrolyte secretion and absorption.

A bundle-forming pilus is encoded by the plasmid (pEAF), enabling EPEC to form a localized attachment to enterocytes in the small intestine. Once bound, the outer membrane protein colonization factor, intimin, facilitates enhanced adherence. Intimin is an outer membrane protein colonization factor encoded on the eae gene within the locus of enterocyte effacement (LEE) chromosomal island.[24] The LEE chromosomal island elaborates approximately 20 secretory toxins that are injected into the enterocyte by a type III injectisome.[25][26] These toxins trigger a series of events that ultimately lead to the characteristic effacement of microvilli, increased permeability of tight junctions, and alterations in water and electrolyte secretion and absorption. EspF is a LEE-secreted protein that is not involved with attaching and effacing. EspF appears to disrupt the intestinal barrier function by altering electrical resistance, thereby increasing monolayer permeability.[27] This LEE-secreted protein has several protein-protein interaction domains that may function by interacting with endocytic regulation. EspG and EspG2 are 2 other secreted proteins that inhibit luminal membrane chloride absorption by decreasing surface expression of the Cl-/OH-exchanger via disruption of microtubules.[27] Enteroaggregative E coli pathophysiology EAEC exhibits a stacked brick pattern of adherence to epithelial cells.[28] The virulence plasmid encodes the transcriptional activator AggR, which activates several virulence factors, although the scientific understanding of this process is incomplete.[29] AggR likely induces aggregative adherence fimbriae, adhesin, surface protein dispersin, and the enterotoxins Pet, EAST-1, ShET1, and ShET2. Dispersin likely promotes aggregative adherence fimbriae-mediated colonization.[30] Enterohemorrhagic/Shiga toxin-producing E coli pathophysiology EHEC/STEC produces bloody diarrhea due to its ability to express Shiga toxin 1 (Stx1) and Shiga toxin 2 (Stx2).[31][32] Stx1 and Stx2 are closely related to Shiga toxin (Stx) produced by Shigella dysenteriae. EHEC/STEC, which expresses Stx2, results in bloody diarrhea and may also express Stx1, while bacteria that do not express Stx2 do not induce bloody diarrhea. These toxins inhibit protein synthesis, leading to enterocyte cell death and inflammatory colitis.[33][34]

EHEC/STEC produces bloody diarrhea due to its ability to express Shiga toxin 1 (Stx1) and Shiga toxin 2 (Stx2).[31][32] Stx1 and Stx2 are closely related to Shiga toxin (Stx) produced by Shigella dysenteriae. EHEC/STEC, which expresses Stx2, results in bloody diarrhea and may also express Stx1, while bacteria that do not express Stx2 do not induce bloody diarrhea. These toxins inhibit protein synthesis, leading to enterocyte cell death and inflammatory colitis.[33][34] EHEC/STEC is also known for its ability to induce hemolytic uremic syndrome (HUS). The classic triad of microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency characterizes HUS.[35] Please see StatPearls' companion resource, "Enterohemorrhagic Escherichia coli," for further information on the pathophysiology and toxicokinetics of EHEC/STEC. Enteroinvasive E coli Like EHEC, enterotoxins induce secretory diarrhea. Subsequent colonization and invasion of the colonic mucosa, along with replication and cell-to-cell spread, result in inflammatory colitis.[18][28] Extraintestinal Infections Extraintestinal infections caused by E coli are generally the result of the translocation of commensal E coli outside of the intestine.[36] The urinary tract is the most common extraintestinal site of infection caused by E coli.[37] UTIs are a significant reason for ambulatory care visits in the United States and are the second most common cause of hospitalization after pneumonia.[38][39] UTIs from E coli result from bacteria ascending the urethra and are more common in women than men, given the proximity of the urethra. E coli is also a frequent cause of ventilator-associated pneumonia, a major life-threatening hospital-acquired infection with a suspected pathogenesis as a result of aspiration of gastric contents.[40][41] In contrast, E coli rarely causes community-acquired pneumonia, but is associated with severe outcomes when it does cause this infection.[42] E coli bacteremia is typically the result of spread from a primary E coli infection at another site.[37]

Clinical History An in-depth clinical assessment is important in establishing the diagnosis of E coli infection. Symptom onset, duration, and severity, as well as any alleviating and aggravating factors, including any over-the-counter medications trialed, may help distinguish it from other intestinal illnesses. Distinguishing between watery and bloody diarrhea and asking about recent travel and diet history, which may provide clues to suggest E coli as the etiology of illness, is also essential. ETEC is the most common bacterial cause of traveler's diarrhea, and management relies on high clinical suspicion. Symptoms of E coli infection usually start more than 16 hours after the ingestion of contaminated food, whereas diarrheal illnesses caused by organisms other than E coli may have much more rapid onsets. If a patient presents with an extraintestinal manifestation of E coli, clinicians should ask about prior infections and assess for the risk of drug-resistant organisms. Furthermore, when a patient presents with symptoms consistent with cystitis, clinicians should inquire about the presence of indwelling instrumentation, eg, ureteral stents or Foley catheters. Physical Examination The physical examination allows health practitioners to assess the severity of illness. Patients presenting with vital signs suggestive of systemic disease should be cared for in an appropriate setting, eg, a hospital-based emergency department or inpatient ward, where comprehensive care can be provided. All patients should be assessed for clinical signs of dehydration by evaluating mucous membranes and skin turgor. Clinicians should auscultate the heart and lungs in all patients suspected of disease caused by E coli. Furthermore, a focused exam should support the patient-provided history that may yield additional findings to guide patient care. Patients presenting with intestinal and genitourinary symptoms should receive a thorough abdominal exam, whereas patients suspected of having sepsis should undergo a comprehensive physical examination.

Routine laboratory evaluation is not generally required in well-appearing patients with diarrheal illness, as the disease is often self-limiting. However, laboratory testing may support clinical suspicion and guide treatment in patients with concerning signs or symptoms suggestive of systemic illness (see Table 1).[43] Patients with suspected EHEC/STEC infection should have a baseline complete blood count and a basic metabolic panel obtained. Additionally, stool cultures should be obtained in patients with prolonged diarrheal illness, systemic signs or symptoms, or dysentery.[44] Pathogenic E coli subtypes are not distinguishable from one another based solely on appearance; therefore, further biochemical tests are necessary. E coli are non-spore-forming, flagellated, and facultatively anaerobic. They have the inherent ability to ferment lactose and produce indole. Before polymerase chain reaction (PCR)-based assays, E coli were identified via selective culture media. E coli are classically grown on MacConkey agar, a culture medium containing lactose. E coli also produces indole during metabolism, and bacterial growth on MacConkey agar with indole production is diagnostic for E coli. EHEC/STEC can also ferment sorbitol. Therefore, to further distinguish EHEC/STEC from other E coli strains, bacteria are grown on sorbitol-containing media.[2] However, non-O157:H7 EHEC strains that do not ferment sorbitol have been identified.[45] As PCR-based assays become more readily available, these strains will continue to be identified more frequently. All patients with inflammatory diarrhea acquired outside of the United States should have stool cultured for E coli, as well as Salmonella, Shigella, and Campylobacter.[44] While molecular diagnosis is not required in mild illness, specific pathogens can be identified via PCR-based assays. The identification of heat-labile or heat-stable genes distinguishes ETEC. EPEC is identified by the detection of the pEAF plasmid or its encoded bundle-forming pilus factor. EAEC is identified through the detection of the AggR regulon. EHEC/STEC is identified through the nucleic acid amplification test (NAAT) of Shiga toxin 1 (Stx1) and Shiga toxin 2 (Stx2).[46] EIEC can be detected via NAAT. Many EIEC strains are identified by the presence of the lacY gene, which encodes lactose permease. Table Table 1. Laboratory Evaluation of Escherichia coli.

While molecular diagnosis is not required in mild illness, specific pathogens can be identified via PCR-based assays. The identification of heat-labile or heat-stable genes distinguishes ETEC. EPEC is identified by the detection of the pEAF plasmid or its encoded bundle-forming pilus factor. EAEC is identified through the detection of the AggR regulon. EHEC/STEC is identified through the nucleic acid amplification test (NAAT) of Shiga toxin 1 (Stx1) and Shiga toxin 2 (Stx2).[46] EIEC can be detected via NAAT. Many EIEC strains are identified by the presence of the lacY gene, which encodes lactose permease. Table Table 1. Laboratory Evaluation of Escherichia coli. For patients with extraintestinal illness, culturing blood, urine, or sputum will often identify E coli.[47][48][49] Testing for antimicrobial susceptibility is important as E coli, like many bacterial organisms, may possess antibiotic resistance genes that confer resistance to many commonly prescribed antibiotics. Extended-spectrum beta-lactamase (ESBL)-producing E coli confer resistance to most beta-lactamase antibiotics (eg, cephalosporins, monobactams). In contrast, carbapenemase-producing E coli strains possess genes conferring resistance to carbapenems (eg, imipenem, ertapenem, and meropenem). E coli may also develop resistance to most other classes of antibiotics.[50]

Treatment is dependent on the strain, as well as the illness (see Table 2). Care of the patient with an intestinal disease caused by E coli begins with symptomatic management.[44][51] Diarrheal illness can be extremely distressing for patients. Experts recommend rehydration and antidiarrheals as the mainstays of treatment for mild disease. Oral rehydration is recommended as first-line therapy for all patients with diarrheal illness when tolerated and is equally efficacious as compared to intravenous (IV) hydration. However, IV hydration is recommended when patients cannot tolerate oral intake. Distressing symptoms should be treated with antimotility agents, eg, bismuth subsalicylate and loperamide. Antibiotics are not recommended as first-line treatment for diarrheal illness caused by E coli for most patients due to the harmful adverse effects and association with antibiotic resistance. For patients with severe disease (eg, more than 6 stools per day, fever, dehydration necessitating hospitalization, diarrhea lasting more than 7 days, or bloody diarrhea), antibiotics may be reasonable. Rifaximin, azithromycin, and ciprofloxacin are currently recommended by the Infectious Diseases Society of America (IDSA) and the International Society of Travel Medicine (ISTM) for the treatment of E coli diarrheal illness. For patients suspected of having EHEC/STEC, antibiotics are not recommended, especially in children and older adults, due to the increased risk of hemolytic uremic syndrome. Table Table 2. Management of Escherichia coli Symptoms. Enterohemorrhagic/Shiga toxin-producing E coli Patients identified as having EHEC/STEC, particularly children younger than 12 years of age, should be hospitalized. Hospitalization reduces the risk of community spread and allows for aggressive therapy and close monitoring.[52] In patients requiring hospitalization, intravenous hydration with isotonic fluids (0.9% NaCl or Lactated Ringer's) is recommended.[53] Antibiotics, as previously mentioned, are not routinely recommended for patients with confirmed EHEC/STEC infections due to the increased risk of HUS.[54] Unlike other diarrheal illnesses, antimotility agents may increase the risk of HUS in patients with EHEC/STEC infections and should not be recommended.

Patients identified as having EHEC/STEC, particularly children younger than 12 years of age, should be hospitalized. Hospitalization reduces the risk of community spread and allows for aggressive therapy and close monitoring.[52] In patients requiring hospitalization, intravenous hydration with isotonic fluids (0.9% NaCl or Lactated Ringer's) is recommended.[53] Antibiotics, as previously mentioned, are not routinely recommended for patients with confirmed EHEC/STEC infections due to the increased risk of HUS.[54] Unlike other diarrheal illnesses, antimotility agents may increase the risk of HUS in patients with EHEC/STEC infections and should not be recommended. Additionally, avoidance of other medications that could worsen renal function is essential, including nonsteroidal anti-inflammatory drugs (NSAIDs). Patients with EHEC/STEC-induced HUS commonly develop hemolytic anemia and thrombocytopenia and may require transfusion. These patients experience ongoing hemolysis and should not receive blood transfusions early in illness unless they are hemodynamically unstable. Platelet transfusion should also be avoided unless severe thrombocytopenia or bleeding occurs due to the increased risk of thrombosis associated with HUS. Extraintestinal Illness Antimicrobial therapy directed against E coli should be based on local antibiograms demonstrating susceptibility and resistance patterns. Choosing between oral and intravenous formulations is disease-specific and should be guided by clinical presentation. In general, extraintestinal infections caused by E coli are susceptible to a variety of antibiotics, as listed below. E coli can harbor genes for antibiotic resistance; therefore, antibiotic therapy should be tailored to target these organisms, including: Antibiotics suitable for E coli infections Beta-lactam antibiotics Cephalosporins Carbapenems Monobactams Nitrofurantoin Trimethoprim-sulfamethoxazole Fosfomycin Fluoroquinolones ESBL-producing E coli (antibiotic choice is dependent on local resistance patterns) Cefepime Ceftazidime Imipenem Ertapenem Meropenem Carbapenemase-producing E coli Ceftazidime-avibactam Colistin Polymyxin B [55][56]

A variety of organisms can cause intestinal illness. Watery diarrheal illness is most commonly caused by viruses, including norovirus and rotavirus, but can also be caused by bacteria, eg, Staphylococcus aureus, Bacillus cereus, and Vibrio cholerae. For patients presenting with inflammatory or bloody diarrhea, etiologies including Shigella spp, Salmonella spp, Campylobacter jejuni, and Yersinia enterocolitica should be considered. A variety of viruses and bacteria can cause extraintestinal infections, and their effects depend on the specific illness.

Most diarrheal illnesses have a favorable prognosis, and those caused by E coli are no different. E coli infections resulting in watery diarrhea are generally self-limited, but even when antibiotics are required, the illness is treatable, and patients make a full recovery. Children who develop HUS due to EHEC/STEC are at the most significant risk for morbidity and mortality. Approximately 4% of children who develop EHEC/STEC-induced HUS will die, and another 5% will develop significant long-term sequelae, including end-stage renal disease and stroke.[57][58] Another 20% to 30% will develop other sequelae; those who do not suffer the harmful effects often make a full recovery within 2 weeks.[59][60][61] The prognosis of patients who develop extraintestinal infections caused by E coli is dependent on comorbid conditions. E coli itself is not an indicator of poor prognosis. However, patients with extraintestinal infections caused by E coli (except cystitis) are generally sicker at baseline. For example, E coli is a common cause of spontaneous bacterial peritonitis in patients with ascites, and even when treated, spontaneous bacterial peritonitis is associated with up to a 4% mortality risk.[62]

Patients who develop diarrheal illness are at an increased risk for dehydration, but this can often be prevented through adequate hydration and early symptomatic intervention. Long-term complications include chronic diarrhea and irritable bowel syndrome, but these occur in a small number of patients. Patients with EHEC/STEC diarrheal illness are at risk for developing hemolytic uremic syndrome, which is more common in children younger than 5 years old and adults older than 60. The risk of developing HUS depends on several factors, including Stx gene expression. In infections caused by Stx2-expressing EHEC/STEC, the risk of HUS may be as high as 24%. Children who develop EHEC/STEC-induced HUS are at the most significant risk for long-term sequelae. As previously mentioned, approximately 5% will develop end-stage renal disease or stroke, and another 20% to 30% will develop sequelae, including hypertension, proteinuria, and subclinical decline in glomerular filtration rate. Complications associated with extraintestinal E coli infections are disease-specific and out of the scope of this review.

Effective coordination among consultants ensures timely diagnosis, optimized treatment, and prevention of complications associated with E coli infections. Consultations play an essential role in the comprehensive management of E coli infections, particularly when patients present with severe disease, systemic involvement, or suspected antimicrobial resistance, including: Infectious disease specialists provide guidance on diagnostic interpretation, resistance mechanisms, and tailored antimicrobial therapy, especially in cases involving ESBL- or carbapenemase-producing strains. Nephrology consultation may be necessary for patients with EHEC/STEC-associated hemolytic uremic syndrome who require close renal monitoring or potential renal replacement therapy. Critical care specialists support the management of patients with sepsis or hemodynamic instability. Gastroenterology input may be helpful for severe or persistent diarrheal illness requiring endoscopic evaluation.

Illnesses caused by E coli can be prevented by regular hand washing, washing fruits and vegetables, and thoroughly cooking meat. When traveling to areas with inadequate sanitation practices, eg, in many developing regions, illness can be avoided by consuming purified water, thoroughly cooking food, or rinsing raw fruits and vegetables in purified water. When infection cannot be avoided, or patients are at high risk for complications of diarrheal illness (eg, immunosuppressed), prophylactic antibiotics can significantly reduce disease. The ISTM recommends that travelers at risk for contracting diarrheal illnesses who require antibiotic prophylaxis should take the following rifaximin or bismuth-subsalicylate regimens for chemoprophylaxis:[51] Rifaximin: 200 mg 1 to 3 times daily for the duration of travel; not to exceed 2 weeks (first line) Bismuth-subsalicylate: 524 mg every 30 to 60 minutes as needed up to 8 doses in 24 hours (second line) [51] Reducing the risk of extraintestinal infections is disease-specific but includes interventions such as reducing the use of indwelling medical devices to prevent catheter-associated urinary tract infections. Developing ICU protocols to reduce aspiration risks, including elevating the patient’s head of the bed to 30 degrees, leads to lower rates of ventilator-associated pneumonia.[63] Chemoprophylaxis minimizes the risk of spontaneous bacterial peritonitis in high-risk groups.[64]

Escherichia coli is a gram-negative bacillus that exists as part of the normal intestinal flora but can also cause a wide range of illnesses when pathogenic strains are acquired, including intestinal infections such as those caused by enterotoxigenic, enterohemorrhagic/Shiga toxin-producing, enteroinvasive, enteropathogenic, and enteroaggregative subtypes, as well as extraintestinal infections like urinary tract infections, bacteremia, pneumonia, and peritonitis. The clinical impact of E coli is amplified by its virulence factors and its increasing resistance to commonly prescribed antibiotics, making accurate diagnosis and evidence-based management essential for patient safety and improved outcomes. Clinicians trained in travel medicine can identify candidates for chemoprophylaxis against traveler’s diarrhea and help initiate appropriate therapy.[65] Travel clinics are readily available in many urban areas and are staffed with clinicians and nursing staff who can discuss and prescribe chemoprophylaxis based on the most recent recommendations. These clinicians can also take time with patients to discuss how to avoid contracting an illness while traveling. Managing E coli infections effectively requires a coordinated, interprofessional approach. Physicians, general practitioners, and advanced practitioners must identify high-risk patients, apply updated diagnostic strategies, and select appropriate therapies. Nurses play a key role in monitoring patient status, preventing dehydration, and facilitating patient education. Pharmacists ensure proper antimicrobial use, address resistance concerns, and support stewardship efforts. Effective interprofessional communication and care coordination strengthen team performance, improve patient-centered care, and help reduce complications such as hemolytic uremic syndrome and healthcare-associated infections. This collaborative strategy enhances both individual outcomes and broader public health goals.[66]