Pediatric Escherichia Coli Infections

Updated: Mar 19, 2019
Author: Archana Chatterjee, MD, PhD; Chief Editor: Russell W Steele, MD 



Escherichia coli, a facultatively anaerobic gram-negative bacillus, is a major component of the normal intestinal flora and is ubiquitous in the human environment. First described in 1885, E coli has become recognized as both a harmless commensal and a versatile pathogen.


In contrast to the essential and beneficial role of most E coli isolates in the human intestine, pathogenic E coli are responsible for a broad spectrum of human disease. E coli has emerged as an important cause of diarrheal illness, with diverse phenotypes and pathogenic mechanisms. Hemolytic-uremic syndrome (HUS) is a potentially devastating consequence of enteric infection with specific E coli strains. E coli is also a commonly identified cause of urinary tract infections (UTIs), as well as neonatal sepsis and meningitis.

Uropathogenic E coli (UPEC) has the ability to colonize the uroepithelium by means of surface fimbriae. Although only partially understood, UPEC has been suggested to cause either direct cellular damage or direct invasion of the renal epithelial cells.[1]

Five pathotypes have of diarrheagenic E coli have been recognized; each pathotype has a distinct pathogenesis. The pathotypes are as follows:

  • Enterotoxigenic E coli (ETEC)

  • Enterohemorrhagic E coli (EHEC)

  • Enteropathogenic E coli (EPEC)

  • Enteroinvasive E coli (EIEC)

  • Enteroaggregative E coli (EAEC)

ETEC adheres to the small bowel mucosa by means of several different fimbrial colonization factor antigens (CFAs). Once colonization is achieved, one or both of the enterotoxins are released (ie, heat labile toxin [LT] and heat stable toxin [ST]). These toxins draw fluid and electrolytes from the small bowel mucosa. ST is reportedly the more virulent of the toxins.[1] LTs are closely related in structure and function to the enterotoxin expressed by Vibrio cholerae. Immunity develops to ETEC surface antigens, confining most disease to immunologically naïve travelers and weaning infants.

EHEC, also known as Shiga-toxin producing E coli (STEC), induces an attaching and effacing (AE) lesion in the large bowel. Once established in the colon, EHEC releases one or more toxins known as Shiga-like toxin (Stx). Stx is related to the Shiga toxin of Shigella dysenteriae and is cytotoxic to the vascular endothelium. The systemic circulation of Stx accounts for the potential development of HUS but is not required for EHEC hemorrhagic colitis to occur. E coli O157:H7 is the most virulent of the EHEC.[2, 1]

HUS consists of the triad of microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency. HUS typically develops in the second week of illness (range, 2-14 d), often after the diarrhea has resolved. Patients present with pallor, weakness, irritability, and oliguria or anuria.

EPEC also produce AE lesions; however, it does so in the absence of Shiga toxin production. The pathogenesis includes colonization of the small intestine, followed by the formation of AE lesions and a subsequent net secretory state.[2, 1]

The pathogenesis of EIEC mimics that of the Shigella species. The EIEC invades the large bowel epithelial cells, producing secretogenic enterotoxins and subsequent colonic epithelial cell death. These enterotoxins are typically lactose nonfermenting and are responsible for the local colonic inflammatory response.[2, 1] Invasiveness derives from a virulence plasmid closely related to that possessed by Shigella species.

EAEC adheres to the small and large bowel by means of aggregative adherence fimbriae (AAFs), and colonization ensues. This colonization produces enterotoxins and cytotoxins, which, in turn, damages the intestinal mucosa.[2, 1]

Systemic infections caused by E coli are frequently seen in neonates either by means of vertical or horizontal transmission. The characteristic serotype of this pathogenic E coli displays the K1 antigen, which is responsible for 40% of the cases of bacteremia and 80% of the cases of meningitis caused by E coli.[2] The virulent activity of the K1 antigen reduces the ability of the host to develop an antibody specific response and to activate the alternative complement system. In addition, S fimbriae have been associated with many of the E coli of patients with CNS infections. S fimbriae enhance the ability of E coli to adhere to vascular epithelium as well as the spread of the bacterium within the CNS.[1]



United States

Statistics on pathogenic E coli strains reflect increasing recognition and surveillance over the past 2 decades. According to the Foodborne Diseases Active Surveillance Network (FoodNet) of the Centers for Disease Control and Prevention (CDC) Emerging Infections Program, in 2007, the incidence of Shiga-toxin–producing Ecoli (O157) was 1.20 cases per 100,000 population, and the incidence of Shiga-toxin–producing E coli (non-O157) was 0.57 cases per 100,000 population). Since the beginning of surveillance in 1996, the incidence of Shiga-toxin–producing E coli (O157) has decreased 25%.[3]


Many strains of diarrheagenic E coli primarily affect developing nations due to inadequate sanitary conditions. Statistics on the prevalence of the strains vary by location and surveillance activity. Worldwide, enterotoxigenic E coli are estimated to cause more than 600 million cases of diarrhea annually and 700,000 deaths in children younger than 5 years.

ETEC is the most common enteropathogen in developing countries, accounting for approximately 210 million diarrhea episodes and approximately 380,000 deaths.[4, 5] Traveler’s diarrhea is primarily caused by ETEC; thus, persons traveling to endemic areas regularly import the pathogen to the developed world.[6, 7, 8, 9, 10]

The outbreak of gastroenteritis and hemolytic uremic syndrome caused by Shiga-toxin–producing E coli in Germany in May, June, and July, 2011 was linked to the consumption of sprouts.[11] Reported were 3816 cases, which included 54 deaths; 22% involved hemolytic uremic syndrome, which occurred predominantly in female adults.[12]


Several E coli pathotypes have been implicated in chronic diarrhea among severely immunocompromised patients (eg, patients with human immunodeficiency virus [HIV]).[13, 14, 15] ETEC causes more dehydrating diarrhea cases among infants in developing countries than any other pathotype.[16, 17]


People of any age can become infected. Very young individuals and the elderly are the most likely groups to become seriously ill and to develop HUS.




Symptoms of Escherichia coli infection may be subtle and nonspecific in infants and young children. Even in older children, symptoms may resemble those of common viral illnesses, leading to missed or delayed diagnosis. A thorough history, including any history of a prior urinary tract infection (UTI), and thoughtful analysis of the information provided is essential. Pertinent details can guide further diagnostic investigation.

  • Neonates and infants with UTIs, bacteremia, or sepsis may present with the following symptoms:

    • Fever

    • Hypothermia

    • Jaundice

    • Respiratory distress

    • Apnea

    • Poor feeding

    • Vomiting

    • Diarrhea

    • Fussiness

    • Irritability

    • Lethargy

  • Particularly in young infants, meningitis may be present without overt signs attributable to the CNS.

  • Infants with histories of prematurity, low birth weight, difficult or prolonged labor, intrapartum maternal fever, or antibiotic administration may have higher risk for serious bacterial infection.

  • Older children with bacterial enteritis or UTI may have fever, vomiting, abdominal pain, or diarrhea with or without blood or mucus. In young children with UTI, urinary symptoms (eg, frequency, urgency, dysuria) vary and are often not present; daytime urinary incontinence or new onset of bedwetting may be more suggestive of UTI. Always consider UTI in the differential diagnosis of fever without apparent source. Constipation is not a symptom of UTI but is instead associated with incomplete voiding and urinary stasis. Constipation may predispose a child to UTI and may complicate treatment. In children with recurrent UTI, aggressive treatment of constipation may reduce subsequent UTIs.

  • In cases of diarrheal illness, determine stool frequency (ie, number of stools or diaper changes in past 12-24 h), appearance (eg, loose, watery), and presence of blood or mucus. Inquire about a history of exposure to a child with bloody diarrhea or a known local outbreak of hemorrhagic colitis. Specific quantification of stool number and character is important because parents often describe a single loose stool as diarrhea. Also, remember various substances (eg, Kool-Aid, other foods containing red dyes) may tint stools red. Guaiac testing confirms the presence of blood.

    • Enterotoxigenic E coli (ETEC) diarrhea is watery without blood, mucous, or fecal leukocytes and ranges from mild to severe.

    • Enterohemorrhagic E coli (EHEC) disease ranges from mild watery diarrhea to severe hemorrhagic colitis, often accompanied by abdominal cramping and vomiting. Diarrhea becomes bloody in 1-2 days in most patients but is usually not associated with fecal leukocytes. Fever is present in about a third of cases.

    • Enteroinvasive E coli (EIEC) causes watery diarrhea, dysentery, fever, vomiting, painful abdominal cramps, and tenesmus. Stools often contain blood and leukocytes.

    • Enteropathogenic E coli (EPEC) and Enteroaggregative E coli (EAEC) cause watery diarrhea and dysentery. The resultant acute watery diarrhea may cause dehydration or become chronic and lead to failure to thrive.

  • Evaluate the ability of patients who are vomiting or at risk of dehydration to take and tolerate fluids orally. Assess frequency of urination (ie, last void or wet diaper, number of voids in past 8-24 h). Vomiting may occur with ETEC.

  • If the patient is experiencing abdominal pain, assess pain for the following features:

    • Severity and character (eg, sharp, dull, cramplike)

    • Location

    • Radiation

    • Duration

    • Nature (eg, constant, intermittent)

    • Aggravating and relieving factors


The child's overall appearance and behaviors (eg, alert, playful, fussy but consolable, lethargic, irritable, toxic) are valuable because these factors may direct diagnostic and therapeutic choices and influence decisions regarding outpatient management or admission.

  • Among the aspects of general appearance to consider are alertness, activity, tone, age-appropriate interaction, and whether the child can be consoled. Observe, for example, whether the child explores the room, clings to the parent, or lies still on the table.

  • Evidence of dehydration may be present in patients with bacterial enteritis. Ill appearance, tachycardia, and dry mucous membranes suggest significant volume depletion. Fontanelle and/or eyes may be sunken, but skin turgor change is a late finding and is often not present. If previous weight is known, documented weight loss can help approximate the degree of dehydration.

  • Assess peripheral perfusion by observing for extremity mottling, coolness, or delayed capillary refill. Evaluate the quality of central and peripheral pulses.

  • Patients may have abdominal pain from either bacterial enteritis or a UTI. Flank pain or costovertebral angle tenderness suggests pyelonephritis. Abdominal pain sometimes is sufficiently severe to mimic appendicitis. Examine the abdomen for distention, increased or decreased bowel sounds, diffuse or localized tenderness, and signs of acute abdomen (eg, rigidity, rebound, guarding).

  • Examine anogenital region in children who have urinary or abdominal symptoms or a history of bloody stools. Examination may reveal vulvovaginitis, perianal excoriation, or anal fissures.

  • Complete examination should include adequate visualization of all skin surfaces. Subtle findings, such as petechiae or bruising, may be overlooked if the examination is rushed or limited.


See the list below:

  • ETEC infection: ETEC is the primary cause of traveler's diarrhea and the major cause of infantile diarrhea in less affluent countries. ETEC is widespread in areas with poor sanitation and is a ubiquitous contaminant of food and water sources. ETEC's incubation period is 1-3 days. Infection usually is self-limited and persists less than 5 days.[9, 10]

  • EHEC infection

    • EHEC is an emerging cause of food-borne illness, particularly in the northern United States and Canada.[18]

    • Recent highly publicized outbreaks of hemolytic-uremic syndrome (HUS) that caused fatalities have focused public attention on food safety.

    • Cattle are the primary reservoir of the EHEC strains that produce diarrhea in humans. Because EHEC is a common inhabitant of the bovine intestine, it may contaminate beef products or foods that contact bovine-exposed soil.

    • Sources identified in outbreaks include ground beef, apple juice, and alfalfa sprouts,[11, 12] as well as fecally contaminated drinking water and swimming pools.

    • Most outbreaks have been linked to 0157:H7 strains, although other serotypes have been implicated.[19, 13, 20, 21]

    • Of particular concern in pediatric populations, E coli 0157:H7 requires a relatively small inoculum for infection and spreads easily from child to child by the fecal-oral route. The incubation period of EHEC is 1-5 days, with illness duration typically 4-10 days.

    • HUS develops in 10-15% of pediatric patients. Chronic renal failure develops in as many as 10% of patients with HUS, and HUS kills 3-5% of affected patients.[22]

  • EPEC infection: EPEC is most often found in developing countries, primarily affecting infants and children. EPEC has been associated with outbreaks of diarrhea in newborn nurseries in the United States, primarily in the 1950s and 1960s.

  • EAEC infection: EAEC is similar in geographic distribution, mechanism, and effect to EPEC. The CDC's Traveler's Health Web site provides additional information to physicians and the public.

  • UTIs

    • E coli is the most commonly isolated pathogen in pediatric UTIs. Virulence factors, such as pili, contribute to the pathogenicity of UTIs.

    • HUS has been reported following UTIs with enterohemorrhagic serotypes of E coli in patients who did not have a diarrheal illness.

  • Neonatal infections

    • E coli infection in neonates may manifest as bacteremia, sepsis, UTI, or meningitis; it rarely manifests as pneumonia, soft tissue, or bone infection.

    • E coli strains with the K1 capsular polysaccharide antigen cause approximately 40% of the septicemia cases and 80% of the meningitis cases attributed to E coli.

    • The usual source of E coli in neonatal infections is the maternal GI tract. The organism also may be acquired nosocomially, particularly in infants who are premature or who require mechanical ventilation.

    • Predisposing factors include maternal perinatal infection, low birth weight, prolonged rupture of membranes, and traumatic delivery. Fetal hypoxia and skin or mucosal defects also increase the risk of gram-negative infection. Infants with galactosemia appear to have an increased susceptibility to serious bacterial infection, particularly E coli sepsis.

    • In intensive care nurseries, mechanical ventilation, invasive procedures, indwelling catheters, and the frequent use of antimicrobial agents allow selection and proliferation of resistant strains of pathogenic gram-negative bacilli.





Laboratory Studies

See the list below:

  • Culture stools in all patients with bloody diarrhea for pathogenic Escherichia coli, primarily the 0157:H7 serotype. If exposure is suspected (ie, as in the case of a known outbreak), assay even watery stools without blood for these pathogens. Enterohemorrhagic E coli (EHEC) isolation from stool may be impossible by the time hemolytic-uremic syndrome (HUS) has developed; thus, when EHEC is suspected, a stool culture should be obtained as early in the illness as possible (eg, within the first week).

  • Routine stool cultures generally screen for Salmonella, Shigella and Campylobacter species. Because E coli organisms are normal fecal flora, laboratories must be advised specifically to assay for pathogenic E coli when a sample is submitted. Most 0157:H7 isolates do not ferment sorbitol; therefore, cultivation of specimens on sorbitol MacConkey medium is a convenient method for detection. Confirmation requires identification of presumptive isolates with O and H antiserum.

  • Detection of Shiga-toxin–producing E coli in contaminated food or a patient's stool specimens may present a diagnostic challenge because of low copy numbers in the sample. Recently, more sensitive nucleic acid amplification methods, such as polymerase chain reaction (PCR) assays, have been developed for rapid identification of this organism directly from clinical specimens. Multiplex PCR assays for detection of all categories of diarrheagenic E coli are also available.[2, 23]

  • Rapid enzyme immunoassays (nonculture tests) for E coli 0157:H7 have been developed.[24] Such tests may be available at large university hospitals or through reference laboratories. Stool culture remains the diagnostic criterion standard.

  • Enterotoxigenic E coli (ETEC) diarrhea (traveler's diarrhea) is primarily diagnosed by clinical history, and treatment is empirically initiated. Laboratory assays involve detection of the associated enterotoxin, usually by enzyme immunoassay, and are not widely available.[25]

  • Fecal leukocyte presence varies but is more likely with enteroinvasive E coli (EIEC). Stool guaiac testing may reveal occult blood. Test the stools of infants and toddlers with profuse watery diarrhea for rotavirus antigen, especially during fall and winter.

  • Other laboratory findings associated with bacterial enteritis are nonspecific. Electrolyte changes may reflect fluid loss, and CBC counts generally reveal an elevated leukocyte count with left shift.

    • Accurate urinary tract infection (UTI) diagnosis requires an appropriately collected urine specimen. A clean-catch specimen is acceptable if the child is able to provide it. If not, urethral catheterization or suprapubic bladder aspiration is necessary.

    • Externally collected bag urine specimens are unsuitable for accurate diagnosis of pediatric UTI, and use of this collection technique is strongly discouraged.

  • Externally collected urine samples are likely to be contaminated with skin or rectal flora, rendering them unreliable and their cultures uninterpretable.

    • Urinalysis results help make the decision whether to begin antibiotic treatment.

    • Urinary nitrite and leukocyte esterase are specific but poorly sensitive assays for UTI.

    • Pyuria strongly suggests a UTI, but may be absent even when infection is present.

  • Perform a urine culture despite negative urinalysis results, particularly in infants and children younger than 3 years.

  • All neonates with suspected sepsis should have specimens of blood, urine, and cerebrospinal fluid sent for culture and Gram stain prior to initiating antimicrobial therapy.

Imaging Studies

See the list below:

  • Abdominal radiography is not necessarily indicated. Consider flat and upright views when the differential diagnosis includes appendicitis or obstruction, including constipation. A CT scan of the abdomen with contrast is more sensitive than plain radiography for detection of E coli– induced colitis.[26]

  • An air-contrast enema is both diagnostic and therapeutic for patients with a suspected intussusception.

  • All children with a documented UTI should have imaging studies of the urinary tract to exclude an anatomic abnormality or vesicoureteral reflux. Renal ultrasonography and voiding cystourethrography are the currently recommended tests. Schedule both tests promptly. Girls older than 10 years with their first UTI may not require such extensive evaluation.



Medical Care

Treatment of bacterial gastroenteritis is primarily supportive and directed toward maintaining hydration and electrolyte balance. Antibiotic therapy is rarely indicated and should be deferred until culture results are available.

Oral rehydration therapy (ORT) is the preferred treatment for fluid and electrolyte losses caused by diarrhea in children with mild-to-moderate dehydration. Intravenous hydration is often administered for severe dehydration or when vomiting prevents ORT. In most cases, even children who are vomiting can tolerate oral fluids if administered frequently in small amounts.[27, 28]

  • Do not use antimotility agents to treat acute diarrhea in pediatric patients. Antimotility agents may prolong the clinical and bacteriologic course of the disease and may be associated with other unacceptable morbidities such as excessive sedation. A retrospective study reported hemolytic-uremic syndrome (HUS) was more likely to develop in patients with E coli 0157:H7 infection who received antimotility agents.[29]

  • Antibiotic treatment of E coli 0157:H7 colitis is controversial. Early data indicated antimicrobials offer no substantial benefit and may increase the risk of developing HUS.[29] In vitro studies have shown subinhibitory antibiotic concentrations can increase toxin production.[30] However, a subsequent meta-analysis reported no association between the use of antimicrobials and higher risk of HUS.[31] In the absence of conclusive evidence, empiric antibiotics should not be administered due to the potential risk of HUS.[2]

  • Administer intravenous antibiotics to children who have evidence of systemic infection (eg, bacteremia, sepsis). Include a combination of ampicillin and an aminoglycoside in the initial empiric treatment of a neonate with suspected sepsis. Alternative regimens of ampicillin and a cephalosporin, such as cefotaxime, are also acceptable. Coverage may be narrowed when the etiologic agent and its antimicrobial susceptibilities have been determined. Base therapy duration on the patient's response and established treatment guidelines (usually 10-14 d for uncomplicated sepsis, >21 d for meningitis).[2]

  • Urinary tract infections (UTIs) may be treated with oral antibiotics if the child can tolerate oral medication without vomiting. Antibiotic regimens of 3 days are inadequate; continue treatment for 10 days.

  • Treatment of HUS is supportive and includes management of fluid and electrolyte status and dialysis, if necessary. Ake et al (2005) propose that early volume expansion with parenteral isotonic fluids during the pre-HUS interval is essential to attenuate renal injury associated with HUS.[32] Leukocytosis has been identified as an early predictor of the development of HUS following an E coli O157:H7 infection.[33, 34]

  • A systematic review and meta-analysis by Grisaru et al that included 1,511 children reported that the lack of intravenous fluid administration prior to establishment of HUS and a higher hematocrit value at presentation were predictors of poor outcomes for shiga toxin-producing Escherichia coli infected children.[35]


See the list below:

  • In cases of hemorrhagic colitis, consultation with a pediatric infectious disease specialist is recommended, especially if considering antibiotic therapy.

  • When HUS is suspected or confirmed, a pediatric nephrologist should assist with patient management because dialysis may be necessary. Early dialysis is associated with improved outcome.

  • Ongoing research protocols investigating the benefit of a toxin-adsorbing preparation appear promising.[30] Enrollment in such a treatment study may be an option at selected tertiary care settings.


See the list below:

  • Children who have diarrhea should continue to receive age-appropriate diets.

  • Feed dehydrated children as soon as they have been rehydrated.

  • Feeding may be withheld briefly for children who are vomiting, but prolonged periods of fasting or specialized diets are unnecessary once vomiting ceases.


See the list below:

  • Increase allowable activities, as tolerated, for all affected children. In general, children eagerly resume vigorous activity as their illness resolves and restrictions are unnecessary.

  • Children with E coli 0157:H7 infection should not return to group childcare settings until the diarrhea has resolved and 2 stool culture results are negative.



Medication Summary

Antibiotic therapy is not indicated in most cases of Escherichia coli enteritis; guidelines for specific circumstances are outlined below.

Antimotility agents are contraindicated for all cases of pediatric gastroenteritis.

Urinary tract infections (UTIs) may be treated with various oral antibiotics, most commonly trimethoprim and sulfamethoxazole, amoxicillin, or cefixime. Duration of therapy is 10 days.

Neonatal sepsis and meningitis are treated based on identified organism susceptibility and clinical response.


Class Summary

Treatment of traveler's diarrhea is rarely necessary. Prophylaxis for traveler's diarrhea with medications (eg, bismuth subsalicylate, trimethoprim and sulfamethoxazole) is not recommended for children because of potential salicylate accumulation and allergic reactions. Efficacy of antibiotic treatment of enteroinvasive E coli (EIEC) and enterohemorrhagic E coli (EHEC) is not established. Data suggest treating EHEC does not alter the course of infection and increases risk of subsequent hemolytic-uremic syndrome (HUS). UTI in infants and children is treated for 10 days because of the difficulty distinguishing between uncomplicated cystitis and pyelonephritis.

Sulfamethoxazole and Trimethoprim (Bactrim, Cotrim, Septra)

First-line therapy for UTI and most E coli diarrheal illness; resistant organisms are fairly common.

Amoxicillin (Amoxil, Biomox, Trimox)

Reasonable choice to treat pediatric UTI. Liquid preparation is palatable and well tolerated. It is concentrated in the urine and active against most gram-positive and some gram-negative organisms.

Cefixime (Suprax)

Third-generation cephalosporin is a second-line choice to treat UTI or traveler's diarrhea; liquid preparation is pleasant tasting.

Ampicillin (Marcillin, Omnipen, Polycillin, Principen, Totacillin)

Administer parenterally in combination with an aminoglycoside or cephalosporin in cases of neonatal sepsis or meningitis; PO preparation is a second-line therapy for traveler's diarrhea and dysentery.


Aminoglycoside antibiotic used in combination with ampicillin to treat neonatal sepsis and meningitis; provides gram-negative coverage and works synergistically against gram-positives.

Cefotaxime (Claforan)

Third-generation cephalosporin administered parenterally in combination with ampicillin to treat neonatal sepsis or meningitis.

Ciprofloxacin (Cipro, Ciloxan)

Quinolone antibiotics are an alternative therapy for adult UTI or bacterial enteritis. Use is contraindicated in pediatric patients when an acceptable alternative is available.

Rifaximin (Xifaxan, RedActiv, Flonorm)

Nonabsorbed (< 0.4%), broad-spectrum antibiotic specific for enteric pathogens of the GI tract (ie, gram-positive, gram-negative, aerobic and anaerobic). Rifampin structural analog. Binds to beta-subunit of bacterial DNA-dependent RNA polymerase, thereby inhibiting RNA synthesis. Indicated for E coli (enterotoxigenic and enteroaggregative strains) associated with traveler's diarrhea.

Ceftazidime/avibactam (Avycaz)

Indicated for adults and pediatric patients aged 3 months or older for complicated intra-abdominal infections (cIAIs) in combination with metronidazole and for complicated urinary tract infections (cUTIs) including pyelonephritis caused by certain susceptible Gram-negative microorganisms, including Escherichia coli.



Further Outpatient Care

See the list below:

  • Monitor patients with Escherichia coli infection for postinfectious functional GI disorders such as irritable bowel syndrome.[36]

Further Inpatient Care

See the list below:

  • Admit for fluid resuscitation and intravenous antibiotic administration any child who is significantly dehydrated, is persistently vomiting, or who has evidence of pyelonephritis.

  • Children with suspected or confirmed sepsis, meningitis, or hemolytic-uremic syndrome (HUS) require skilled inpatient management. HUS may progress to renal failure, which requires meticulous fluid electrolyte management and may require dialysis.


See the list below:

  • Arrange transfer to a tertiary care facility if HUS is suspected. These patients may require dialysis and should be managed by a team that includes a pediatric intensivist, nephrologist, and infectious disease specialist.


See the list below:

  • Traveler's diarrhea

    • Drink only carbonated beverages and boiled or bottled water (preferably carbonated). Consider bringing supply of bottled water or premixed infant formula.

    • Travelers should avoid ice, raw salads, and any fruits they do not peel themselves. Consume foods while they are steaming hot.

    • Prophylactic antibiotic treatment is not recommended for infants and children. Parents should carry packets of oral rehydration salts when traveling outside the United States.

    • Promising data have been reported in a patch vaccine containing heat-labile toxin from E coli.[37, 38]

  • Thoroughly cooking ground beef is the most effective measure to prevent hemorrhagic colitis caused by E coli 0157:H7.

  • Although an National Institutes of Health (NIH) investigational vaccine for E coli O157:H7 has been found to be immunogenic in young children, sporadic outbreaks could limit its use on a broad scale.[39] Priority has been placed on vaccination strategies to reduce the carriage of these organisms in the principal reservoir of this pathogen (ie, cattle).[22]

Patient Education

See the list below:

  • Advise parents of children diagnosed with hemorrhagic colitis to observe their child closely for signs of HUS (eg, oliguria or anuria, pallor, irritability).

  • Make parents of children diagnosed with urinary tract infection (UTI) aware of the possibility that UTI may be the cause of future episodes of fever, particularly fever without apparent source. Parents should be reminded to inform treating physicians of the child's history of UTI and to discuss indications for obtaining a urine culture.