Escherichia coli (E coli) Infections

Background

Escherichia coli (E coli) are facultative anaerobic gram-negative bacteria that are part of the normal gastrointestinal system.^[1] These organisms mainly are found within the large intestine and frequently are implicated as causes of bacterial infections. These infections can stem from disruption of the gut mucosal membrane leading to local tissue invasion and potential distant tissue seeding through bacteremia. Urinary tract infections are thought to occur via bacterial migration proximally up the ureter, causing colonization and potential infection of the bladder and more proximal structures. Common infections with E coli as a pathogen include cholecystitis, bacteremia, cholangitis, urinary tract infection (UTI), traveler's diarrhea, pneumonia, and neonatal meningitis.

The genus Escherichia is named after Theodor Escherich, the individual who isolated the type species of the genus. These organisms are gram-negative facultatively anaerobic bacilli, may exist singly or in pairs, utilize both fermentative and respiratory metabolism for energy, and either are nonmotile or motile by peritrichous flagella. E coli has a rapid reproduction time as low as 20 minutes in laboratory conditions, and virulence depends on what types of capsular antigens, flagellar antigens, and somatic polysaccharides each strain possesses.^[2]

See Travelers' Diarrhea: Antimicrobial Therapy and Chemoprevention for more detail.

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Pathophysiology

Acute bacterial meningitis

Most cases of neonatal meningitis are caused by group B streptococcal infections and E coli (50% and 20% respectively). Pregnant individuals are at a higher risk for colonization with the K1 capsular antigen strain of E coli. Approximately 80% of the E coli strains that cause neonatal meningitis feature the K1 capsular antigen. This K1 capsular antigen is similar to the group B Neisseria meningitidis capsule, which provides protection from phagocytosis.^[3] This strain commonly is observed in neonatal sepsis, which carries a mortality rate of up to 50% if untreated and up to 10% if treated.

Some 25-50% of survivors have subsequent neurologic deficits and up to 20% demonstrated developmental abnormalities at 5 years post infection. Low birth weight and a positive cerebrospinal fluid (CSF) culture result portend a poor outcome.^[4] In adults, E coli meningitis is rare but occasionally can be seen in those with neurosurgical trauma or complications of neurosurgical procedures with prosthetic device infections. E coli meningitis in an individual with no significant medical comorbidities or those receiving immunosuppression, particularly steroids, should raise suspicion of Strongyloides stercoralis.^[5]

Pulmonary (lung) infections

E coli respiratory tract infections are extremely uncommon due to this bacteria’s normal habitat of the large intestine being located remotely from the lungs. E coli pneumonia is thought to be secondary to aspiration or microaspiration, which can be seen in those with neurological disorders that affect the swallowing mechanism and protection of the airway.^[6]  Due to the structure of the lungs, predominant lung fields affected are the lower lobes with right greater than left affected. If an individual aspirates while supine, the right upper field may develop pneumonia due to the change in dependent area of the airways.

A parapneumonic effusion and empyema may be secondary to an untreated E coli pneumonia. Lung abscesses from septic emboli may develop from an E coli bacteremia. This mechanism is different from a pneumonia, as the primary route of infection is seeding the lungs through the blood stream and not an infection through the alveoli as seen in pneumonia. The primary etiology of the bacteremia generally is pyelonephritis or intraabdominal infection.

Unless from a sputum culture isolated during pneumonia, blood culture during bacteremia, or wound culture aspirated from a lung abscess that identifies E coli, it is impossible to distinguish lung pathology caused by this organism from other enteric gram-negative organisms.

Intra-abdominal Infections

E coli intra-abdominal infections often result from damage to the gut mucosal barrier.^[7] This leads to localized infections (eg, diverticulitis, appendicitis) or geographically distant infections (transient splanchnic vein bacteremia leading to pyogenic liver abscesses) (see image below). Complete disruption of the gastrointestinal tract can be spontaneous, traumatic, or anastomotic (prior surgical reconnection site of bowel with failure to heal) in origin with subsequent spillage of gastrointestinal contents, subsequent peritonitis, and complicated by abscess formation. Intra-abdominal abscesses often are polymicrobial as they derive mainly from the gastrointestinal tract that harbors millions of different gram-positive, gram-negative, and anaerobic species. Therefore, E coli plays a component role in these infections but is not the sole cause unless isolated via culture from a sterile space.

Obstruction of flow of different parts of the gastrointestinal system can lead to subsequent bacterial superinfection (eg, cholecystitis, ascending cholangitis) leading to severe illness and sepsis.

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Escherichia coli liver abscess.

Enteric infections

E coli enteric infections are molecularly and clinically identified through their pathogenicity mechanisms. These strains generally only can be differentiated through molecular mechanisms or presumed through the patient’s clinical syndrome. In total, there are 6 different distinct mechanisms for which E coli can be differentiated – enterotoxigenic E coli (ETEC), Shiga toxin-producing E coli (STEC), enteropathogenic E coli (EPEC), enteroinvasive E coli (EIEC), enteroaggregative E coli (EAEC), and diffusely adherent E coli (DAEC).^[8]

Despite naming conventions, there are no differences in antimicrobial susceptibilities of these different E coli bacteria. Thus, antibiotics that target E coli would treat all these organisms if they were identified in the same patient. Care must be given in identifying hematochezia or gross blood in the stool, as this may be secondary to dysentery caused by STEC with lysis of these bacteria through antibiotic treatment potentially leading to release of their toxins and clinical deterioration of the patient.

As a cause of enteric infections, 6 different mechanisms of action of 6 different varieties of E coli have been reported. ETEC is a cause of traveler's diarrhea^[1] ; EPEC is a cause of childhood diarrhea; EIEC causes a Shigella-like dysentery; STEC causes hemorrhagic colitis that can lead to a diffuse systemic illness of hemolytic-uremic syndrome (HUS); EAEC primarily is associated with persistent diarrhea in children in developing countries, and DAEC is a cause of childhood diarrhea and traveler's diarrhea in Mexico and North Africa. ETEC, EPEC, EAEC, and DAEC colonize the small bowel, and EIEC and STEC preferentially colonize the large bowel prior to causing diarrhea.

STEC is among the most common causes of foodborne diseases. This organism is responsible for several GI illnesses, including nonbloody and bloody diarrhea. Patients with these diseases, especially children, may be affected by neurologic and renal complications, including HUS. Strains of STEC serotype O157:H7 have caused numerous outbreaks and sporadic cases of bloody diarrhea and HUS.

Kappeli et al looked at 97 non-O157 STEC strains in patients with diarrhea and found that HUS developed in 40% of patients; serotype O26:H11/H most often was associated with this syndrome.^[2] Although strains associated with HUS were more likely to harbor STX 2 and EAE compared with those associated with bloody diarrhea, only 5 of the 8 patients with HUS had the STX2 gene; among the 3 patients with EAE -negative, STX2 -negative strains, only STX1 or STX1 and EHXA caused the HUS.

Urinary tract infections

The urinary tract is the most common site of E coli infection, and more than 90% of all uncomplicated urinary tract infections (UTIs) are caused by E coli infection. E coli UTIs are caused by uropathogenic strains of E coli. E coli causes a wide range of UTIs, including uncomplicated urethritis cystitis, symptomatic cystitis, pyelonephritis, acute prostatitis, prostatic abscess, and sepsis from an ascending urinary tract infection. Uncomplicated cystitis occurs primarily in females who are sexually active and are colonized by a uropathogenic strain of E coli. Subsequently, the periurethral region is colonized from contamination of the colon, and the organism reaches the bladder during sexual intercourse. The recurrence rate after a first E coli infection is 44% over 12 months.^[9]

Uropathogenic strains of E coli have an adherence factor called P fimbriae, or pili, which binds to the P blood group antigen. These P fimbriae mediate the attachment of E coli to uroepithelial cells. Thus, patients with intestinal carriage of E coli that contains P fimbriae are at greater risk of developing UTI than the general population. Complicated UTI and pyelonephritis are observed in elderly patients with structural abnormalities or obstruction such as prostatic hypertrophy or neurogenic bladders or in patients with indwelling urinary catheters. E coli right sided pyelonephritis is visualized in the image below.

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Escherichia coli right pyelonephritis.

E coli bacteremia usually is associated with UTIs, especially in cases of urinary tract obstruction of any cause. The systemic reaction to endotoxin (cytokines) or lipopolysaccharides can lead to disseminated intravascular coagulation and death. E coli is a leading cause of nosocomial bacteremia from a GI or genitourinary source.

Other infections

Other miscellaneous E coli infections include septic arthritis, endophthalmitis, suppurative thyroiditis, sinusitis, osteomyelitis, endocarditis, and skin and soft-tissue infections (especially in patients with diabetes).

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Epidemiology

Frequency

United States

E coli is the leading cause of both community-acquired and nosocomial UTI.^[10] Up to 50% of females eventually experience at least 1 episode of UTI, and up to 10% of post-menopausal individuals report having a UTI within the past year. E coli causes 12-50% of nosocomial infections and 4% of cases of diarrheal disease.

International

E coli is the most common cause of traveler’s diarrhea. The attack rate is 10-40% among travelers. Worldwide, ETEC causes 30-60% of all cases of traveler's diarrhea and is the most isolated pathogen. EAEC also has been implicated, but less frequently. ^[11]

Mortality/Morbidity

E coli neonatal meningitis carries a mortality rate of up to 10%, and most survivors have neurological or developmental abnormalities.

The mortality and morbidity associated with E coli bacteremia is the same as that for other aerobic gram-negative bacilli.

Race

E coli infections have no recognized racial predilection. 

Sex

E coli UTI is more common in females than in males because of differences in anatomic structure and changes during sexual maturation, pregnancy, and childbirth.

Men older than 45 years with prostatic hypertrophy are at an increased risk for UTI due to related bladder stasis.

Among neonates, E coli UTI is more common in boys than in girls, but circumcision reduces the risk.

Age

E coli is an important cause of meningitis in neonates. 

Children are at high risk for traveler’s diarrhea due to oral sensory seeking and indiscretion with personal hygiene.^[11]

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History

Acute bacterial meningitis

Newborns with Escherichia coli (E coli) meningitis present with fever and failure to thrive or abnormal neurologic signs. Other findings in neonates include jaundice, decreased feeding, periods of apnea, and listlessness.

Patients younger than 1 month present with irritability, lethargy, vomiting, lack of appetite, and seizures.

Those older than 4 months have neck rigidity, tense fontanels, and fever.

Older children and adults with acute E coli meningitis may develop headache, vomiting, confusion, lethargy, seizures, and fever.^{[3, 12]}

In rare instances, E coli, or other gram-negative meningitis, may occur in the setting of Strongyloides hyperinfection. Individuals from a community where Strongyloides is endemic or an individual who traveled through an endemic region may develop S stercoralis hyperinfection if infected with the parasite and given immunosuppression, specifically high dose steroids. This then leads to translocation across the gut barrier, causing an E coli bacteremia and potential seeding of the meninges.

Persons with a history of open CNS trauma may develop a contiguous infection from a surgical site infection. E coli meningitis in isolation is due only to open CNS trauma or neurosurgical procedures. Because patients who have undergone neurosurgical procedures frequently have headaches, nuchal rigidity, and a decreased level of consciousness secondary to the surgery, it may be difficult to identify a concurrent active infection.

The differential diagnoses of acute E coli meningitis include bacterial meningitis (most common H influenza, N meningitidis, and S pneumoniae), viral meningitis, sepsis, seizure disorder, brain abscess, ruptured aneurysm, and neonatal tetanus.

Pneumonia

Patients with E coli pneumonia usually present with fever, shortness of breath, increased respiratory rate, increased respiratory secretions, and crackles upon auscultation.^[6]

Findings include bronchopneumonia on chest radiography, commonly in the lower lobes. If patient is limited to the supine position, pneumonia may present in the upper lobes (right upper favored over left upper lobe). Many patients are intubated, have fever, an increased respiratory rate, and increased purulent respiratory secretions.

The differential diagnoses of E coli pneumonia include congestive heart failure, pulmonary embolism, other bacterial pneumonias, and viral pneumonias. Other pneumonias caused by gram-negative bacilli are difficult to distinguish clinically and require a sputum culture to identify a causative organism.

Intra-abdominal infections

Patients with E coli cholecystitis or cholangitis develop right upper quadrant (RUQ) pain, fever, and jaundice (Charcot’s Triad). In severe cases, hypotension and confusion also develop (Raynaud’s Pentad).^[7]

Cholecystitis may be difficult to distinguish from cholangitis, however both may manifest with significant fever (>102*F), and cholangitis may be more severe with shaking chills (rigors), and cholangitis due to obstruction of the common bile duct could be complicated by hepatic abscess.

Patients with E coli intra-abdominal abscesses generally present as an abscess that is a combination of other enteric organisms to include potential anaerobic bacteria. Individuals may have low-grade fevers, but the clinical spectrum of presentations range from nonspecific abdominal examination findings to septic shock. If the infection is contained, the patient may not have peritonitis. Peritonitis manifests as diffuse abdominal pain with rebound tenderness on palpation and fever.

The differential diagnoses include other intraabdominal infections such as appendicitis, diverticulitis, septic thrombophlebitis, retroperitoneal hematoma.

Enteric infections

Patients with E coli traveler's diarrhea (ETEC or EAEC) present with watery diarrhea and may appear dehydrated. Traveler's diarrhea commonly affects individuals from developed countries traveling to underdeveloped or undeveloped countries, especially in tropical climates. The differential diagnoses of E coli traveler's diarrhea include rotavirus infection, Norwalk virus infection, Salmonella infection, and Campylobacter diarrhea.

Patients with E coli childhood diarrhea (EAEC or EPEC) also present with watery diarrhea and may appear to be dehydrated. These infections produce a noninflammatory watery diarrhea observed especially in children of tropical countries. The differential diagnoses of E coli childhood diarrhea include Vibrio cholerae infection and rotavirus infection.

In May, June, and July, 2011 an outbreak of gastroenteritis caused by Shiga toxin-producing E coli was seen in Germany. Most patients were adults, and 22% of the cases developed hemolytic-uremic syndrome (HUS). The outbreak strain was typed as an enteroaggregative Shiga toxin-producing E coli O104:H4, producing extended-spectrum beta-lactamase. The consumption of sprouts was identified as the most likely vehicle of infection. This outbreak was different as it was caused by EAEC that produced a Shiga toxin and it exemplifies the threat posed by foodborne pathogens with their propensity to cause large common-source outbreaks.^{[13, 14]}

Patients with E coli dysentery (caused by STEC or EIEC) have fever, bloody diarrhea, and dehydration. Intestinal mucosa produces a significant inflammatory response. Clinically, patients with E coli dysentery present with fever and have blood and PMN leukocytes in their stool. The differential diagnoses of E coli dysentery include shigellosis, typhoid fever, and amebic dysentery.

Patients with E coli HUS (caused by STEC) have fever, bloody diarrhea, dehydration, hemolysis, thrombocytopenia, and uremia. The hemolysis may lead to deposition of the remnants of the red blood cells into the kidney, causing oxidative destruction, and potentially requiring dialysis. Symptoms of E coli HUS range from nonbloody to bloody diarrhea, however generally have systemic findings due to the systemic cascade that occurs in the setting of bacterial toxin related hemolysis. This includes renal failure, microangiopathic hemolytic anemia, thrombocytopenia, and CNS manifestations. The differential diagnoses of E coli HUS include Shigella infections, Clostridium difficile enterocolitis, ulcerative colitis/Crohn disease, ischemic colitis, diverticulosis, and appendicitis.

Urinary tract infections

Acute E coli cystitis manifests with dysuria, increased urinary frequency, urinary urgency, and rarely may present with a low grade fever.^{[15, 16]} Less commonly, patients have may develop urinary tract infections secondary to other enteric organisms such as Klebsiella, Proteus mirabilis, or Enterococcus. Approximately 15% of cases are culture-negative; these are due to Chlamydia trachomatis, Ureaplasma urealyticum, or Mycoplasma hominis infection. Staphylococcus saprophyticus urinary tract infection is a rare infection observed in 5-10% of cases, especially in sexually active women, associated with alkaline pH and microscopic hematuria.

Patients with E coli pyelonephritis or complicated UTI present with localized flank or low back pain, high fever (>102°F), urinary frequency, and urgency. Due to the systemic nature of this more severe infection, other symptoms may include rigors, sweating, headache, nausea, and vomiting. Untreated or severe infections can be complicated by necrotizing intrarenal or perinephric abscess, which may manifest as a bulging flank mass or pyelonephritis that does not respond to antibiotics. Patients with diabetes or urinary tract obstruction also can develop bacteremia and septicemia. The differential diagnoses include psoas abscess appendicitis, ectopic pregnancy, and ruptured ovarian cyst.

Patients with E coli acute prostatitis or prostatic abscess have chills, sudden fever (>102°F), and perineal and back pain with a tender, swollen, indurated, and hot prostate. Acute prostatitis also manifests as dysuria, urgency, and frequent voiding. Some patients may have myalgia, urinary retention, malaise, and arthralgias. If the patient does not respond to antibiotics, consider prostatic abscess and confirm it with imaging studies. Treatment consists of open surgical or percutaneous drainage. Patients with E coli prostatic abscess, which manifests as a complication of acute prostatitis, have a high fever despite adequate antimicrobial therapy and fluctuance of the prostate upon rectal examination. The differential diagnoses of E coli acute prostatitis or prostatic abscess can include chronic bacterial prostatitis, which usually is asymptomatic; some patients may have frequency, dysuria, and nocturia with pain and discomfort in the perineal, suprapubic, penile, scrotal, or groin region. Also included are infected prostatic calculi, which can cause recurrent UTIs and should be surgically removed.^[9] Finally, nonbacterial prostatitis also is a differential diagnostic possibility and manifests as perineal, suprapubic scrotal, low back, or urethral tip pain.

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Physical

Acute bacterial meningitis

E coli is a common cause of meningitis in newborns and is associated most frequently with prematurity.

E coli meningitis can be acquired during birth or can develop secondarily after infection in another body site, such as in cases of omphalitis, upper respiratory tract infection, or infected circumcision wound.

In adults, E coli meningitis is not uncommon in those who have undergone multiple neurological procedures or who have had open CNS trauma.

Immunosuppressed patients receiving corticosteroid therapy and those with S stercoralis hyperinfection also are at risk for E coli meningitis.

Pneumonia

E coli pneumonia often is preceded by colonization of the upper respiratory tract (eg, nasopharynx), however this is rare in the general population and seen more in individuals with cystic fibrosis, intubation, or those with chronic aspiration.^[6]

Community-acquired E coli pneumonia has been reported in rare cases.

Intra-abdominal infections

Along with Enterococcus faecalis and Klebsiella species, E coli is one of the most common organisms associated with cholecystitis/cholangitis and intra-abdominal abscesses, as part of polymicrobial flora including anaerobes.^[7]

E coli cholecystitis/cholangitis manifests as the classic Charcot triad of fever, pain, and jaundice in 70% of cases. Fever is the most common finding (95%). RUQ pain and jaundice may be absent if no obstruction is present.

In late stages, hypotension, confusion, and renal failure are observed.

Liver abscess can develop as a complication of an E coli biliary tract infection.

The findings of E coli intra-abdominal abscesses are less conspicuous than those of diffuse peritonitis. The patient may have only low-grade fever, generalized malaise, and anorexia. In the postoperative patient who may have a distended and tender abdomen, clinical diagnosis of E coli intra-abdominal abscess may be difficult.

Enteric infections

Traveler's diarrhea usually occurs in persons from industrialized countries who visit tropical or subtropical regions and develop abdominal cramps and frequent explosive bowel movements 1-2 days after exposure to contaminated food or water.^[11]

E coli enterotoxin acts on the GI mucosa, leading to an outpouring of copious fluid from the small bowel.

The symptoms usually last 3-4 days and are self-limited.

Large fluid loss may result in dehydration.

EIEC infections are rare and manifest as bloody diarrheal stool containing PMN leukocytes. Patients usually have fever, abdominal cramping, and tenesmus lasting 5-7 days.

Childhood diarrhea is due to EPEC strains and usually occurs in underdeveloped countries or nursery outbreaks. The volume of diarrhea is less than that with ETEC strains, and no inflammatory cells are found in the diarrheal fluid. The child may experience fever, and diarrhea lasts longer than 2 weeks in some cases.

Infection with STEC strains of the serotype 0157:H7 begins as watery diarrhea followed by grossly bloody stool without inflammatory PMN cells and results in HUS in 10% of cases, characterized by hemolysis, thrombocytopenia, uremia (possibly requiring dialysis), and death in some cases.

EAEC and DAEC cause clinical illnesses that are not yet well characterized and are associated with persistent diarrhea in children.

Urinary tract infections

E coli is the leading cause of community-acquired and nosocomial UTI.^{[9, 10]}

Females are predisposed to UTI because of their anatomy and changes in hormones during sexual maturation, pregnancy, and childbirth.^[16] Post-menopausal females are at high risk for urinary tract infections due to loss of protective vaginal bacteria that rely on estrogen for growth and thus decrease in the absence of significant estrogen production after menopause.

Young boys with posterior urethral valves and elderly men with prostatic hypertrophy are predisposed to urinary tract infections due to the obstructive nature of these disease processes leading to stasis of urine and potential for infection to develop.

Other risk factors for the development of UTIs include catheterization or mechanical manipulation leading to introduction of a foreign body that can become colonized easier or potentially introduce bacteria upon placement. Other mechanisms that cause obstruction can lead to urine stasis and increase risk for the subsequent fluid to become infected. Diabetes may increase risk through glycosuria thereby providing nutrients the bacteria need to grow faster and develop an infection.

Patients with E coli UTI present with a wide spectrum of symptoms, ranging from asymptomatic cystitis to pyelonephritis/perinephric abscess.

Uncomplicated E coli acute cystitis may manifest as suprapubic pain, dysuria, and increased urinary frequency. Fever may be present but is suggestive of a developing complicated UTI or pyelonephritis.

Acute pyelonephritis generally manifests with nausea, fever, and costovertebral tenderness.

Acute prostatitis manifests as a sudden onset of fever and chills with perineal pain, and the individual may have concurrent low back pain.

Perinephric abscess may manifest as a bulging flank mass. GI symptoms such as nausea and vomiting are more likely in elderly persons. Patients with bacteremia secondary to an obstructed urinary catheter may present with decreased urine output.

Prostatic abscess can occur as a complication of acute prostatitis, notably in patients with diabetes mellitus, and should be considered in patients with acute prostatitis or UTI that is not improving with adequate antimicrobial therapy.

Other infections

E coli bacteremia can lead to septic shock, manifesting as hypotension and fever (in some cases, with hypothermia rather than fever). It may be complicated by a multisystem organ failure to include acute renal failure, uremia, hepatic failure, acute respiratory distress syndrome, neurologic dysfunction such as stupor or coma, and death. Non–life-threatening E coli bacteremia may manifest as a sudden onset of fever and chills, tachycardia, tachypnea, and mental confusion. In cases of E coli UTI with urinary tract obstruction, bacteremia or septicemia may ensue.

A retrospective study determined risk factors for mortality in patients with fluoroquinolone-resistant E coli. Results show fluoroquinolone resistance, cirrhosis, and cardiac dysfunction independently predicted mortality.^{[17, 18]}

Several cases of E coli endophthalmitis have been reported in patients with diabetes who have UTI or pyelonephritis.^[19]

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Laboratory Studies

All patients with suspected Escherichia coli (E coli) infection should undergo laboratory analysis based on the clinical syndrome suspected.^{[1, 7, 8, 6, 20]}  Routine CBC count with differential to evaluate for leukocytosis may be helpful in isolating a systemic infection but may be normal in isolated cystitis or non-invasive E coli diarrheal diseases.

Microbiological cultures with gram stain from regions of suspected infection can be helpful.

E coli is a gram-negative bacillus that grows well on commonly used media. It is lactose-fermenting and beta-hemolytic on blood agar. Most E coli strains are nonpigmented on blood agar. If additional agars are used, it will grow pink on MacConkey’s agar, and may have a darker color around the colony due to secretion of the bile salts. The image below shows Escherichia coli as a gram-negative (red appearing – safranin counterstain) bacillus (rod shape) on Gram staining.

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Escherichia coli on Gram stain. Gram-negative bacilli.

In the image below Escherichia coli can be seen growing on MacConkey agar.

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Escherichia coli culture on MacConkey agar.

Definitive diagnosis is based on the isolation of the organism in the microbiology laboratory from clinical specimens. Specimens may be blood, urine, sputum, or other fluids such as cerebrospinal fluid, pleural fluid, abscesses, and peritoneal fluid.

Recovery of the organism in contaminated sites, such as sputum and wounds, must be analyzed in the context of the patient's clinical state to determine if it represents colonization or infection. Recovery from normally sterile sites, such as the CSF, should be considered diagnostic of infection.

Lumbar puncture and a CSF culture positive for E coli establish the diagnosis of acute E coli meningitis; however, lumbar puncture is not justified in all babies presenting with sepsis.^{[1, 6, 7, 8, 20]} Indications for lumbar puncture include positive blood culture results, abnormal neurological signs, and detection of bacterial antigens in the urine.

Individuals with pneumonia generally do not need sputum cultures or blood cultures unless their pneumonia is severe. Patients with severe community acquired pneumonia (CAP) should have sputum cultures performed and have blood cultures performed if septic. These cultures are ideally obtained pre-antibiotic treatment, however antibiotics should not be withheld if cultures cannot be obtained in a timely manner. Factors that favor obtaining sputum cultures are intubated patients, being treated for MRSA/Pseudomonas, previously infected with these prior organisms, or recently hospitalized and received parenteral antibiotics within the past 90 days.^[6]

A sputum culture with gram stain is considered a good specimen if there are many leukocytes observed with few squamous cells, representing infection without significant oropharyngeal contamination.

In enteric infections, the causative organism is suggested based on the clinical presentation and the characteristic of the patient's stool.^{[1, 6, 7, 8, 20]} ETEC, EPEC, EAEC, and DAEC infections produce watery stools without inflammatory cells. EIEC infection produces dysentery-type stools, and STEC infection produces hemorrhagic-type stools. If available, a diarrhea panel polymerase chain reaction (PCR) test on stool can assist in discriminating between the different types of E coli. Use of these tests generally is not indicated for acute uncomplicated diarrhea but may be helpful in distinguishing hemorrhagic strains from non-hemorrhagic strains as well as assessing for outbreaks of disease. Recognize that stool culture in the absence of fever, ≥5 episodes of diarrhea per day, and high C-reactive protein (CRP) are of very low diagnostic yield.^[20]  

Besides PCR tests, other types of E coli can be identified from older tests that are not performed routinely, are difficult to interpret, and require trained microbiology personnel.^{[1, 6, 7, 8, 20]} EPEC can be identified based on findings from serotyping, assays of adherence, and DNA probes. For DAEC and EAEC, serotyping is not useful, and these strains are identified based on their adherence pattern on tissue culture cells. STEC can be identified by looking for the major serotype involved, 0157:H7. Recognize there are other hemolytic strains that do not possess this serotype. STEC strains are cultured in a sorbitol MacConkey agar. Strains that are sorbitol-negative then are serotyped with 0157:H7 antisera.

In UTIs, a urine dipstick test may be utilized to rapidly determine if the patient has pyuria (white blood cells) or nitrate reducing bacteriuria (many enteric gram-negative bacteria) based on the detection of leukocyte esterase and nitrites.^{[1, 6, 7, 8, 20]} Definitive diagnosis is based on urine culture results, with a normal individual requiring >100,000 colony forming units (CFUs) of bacteria to be considered an infection, whereas this number is less in a catheterized patient.

Collect the specimen from a midstream clean void or from the superior access area of a urinary catheter in patients with an indwelling Foley catheter. Recognize longstanding Foley catheters may have colonization and may not represent a true infection. If this is the case, it is reasonable to replace the Foley catheter and then draw a urine culture specimen. Do not draw urine cultures on those without symptoms, as there may be bacterial growth >100,000 CFUs, that represents asymptomatic bacteriuria, which only requires treatment in pregnancy and in those undergoing urologic procedures.^[21]

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Imaging Studies

In suspected pneumonia, chest imaging such as chest radiography is indicated.^[8] A CT may be indicated to further delineate potential cause of pneumonia or if used in combination with CT angiography to assess for a pulmonary embolism in the setting of shortness of breath.

In cholecystitis/cholangitis, a right upper quadrant ultrasound is indicated to assess for inflammation and dilation of the gallbladder and bile ducts. CT scans can be utilized to further visualize the inflammation as well as to assess for alternative causes of intraabdominal pain.

In intra-abdominal abscesses, a CT scan with and without IV contrast is indicated to assess for intraabdominal abscesses. Sonograms may be missed due to depth of the lesion as well as bowel air obstructing the sound waves of the ultrasound,

In UTI, a bilateral renal ultrasound is useful to assess for hydronephrosis and inflammation suggestive of obstruction versus pyelonephritis. If clinically indicated, a CT scan may be indicated to assess for obstruction, nephrolithiasis, or intraparenchymal abscesses.

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Procedures

The following procedures may be indicated:

• Meningitis -Lumbar puncture with CSF Gram stain/culture. Blood cultures to assess for bacteremic seeding of CSF.
• Pneumonia – Sputum cultures, bronchoscopy
• Lung Abscess – Blood cultures, thoracentesis with gram stain / wound culture, sputum culture
• Cholecystitis/cholangitis - Decompression of biliary system through endoscopic drainage, sphincterotomy for stone extraction, or endoscopic cholangiography
• Intra-abdominal abscess - Aspiration and drainage. Depending on the size of the abscess, a drain may need to be left to ensure resolution of the abscess.
• UTI - In cases of ureteral obstruction, placement of stent or stone extraction. Lithotripsy may be required to eliminate a nephrolithiasis, as these can become seeded in UTIs and infection persists until the infected source is removed.
• Prostatic hypertrophy - Transurethral prostatectomy or transurethral resection of the prostate (TURP)
• Prostatic abscess – Surgical drainage

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Medical Care

Medical care of Escherichia coli (E coli) infection is based on the clinical syndrome and severity of the infection.^[1]

In addition to antibiotics, provide supportive care, such as hydration, adequate oxygenation, and blood pressure support, if indicated.

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Surgical Care

Surgical drainage/decompression may be indicated in patients with cholecystitis or cholangitis.^[8]

Surgical drainage or debridement may be indicated for those patients with intra-abdominal abscess with ultimate surgical choice depending on size and location of the abscess. For surgical drainage, interventional radiology may assist with aspiration and drain placement. Generally antibiotics need to be continued to treat an intraabdominal infection for at least 4-7 days post-surgical source control.^[7]

In patients with urinary tract obstruction, such as prostatic hypertrophy, TURP may be indicated to relieve the continued bladder outlet obstruction and urinary retention. In some cases, ureteral stents may need to be placed for decompression of the renal pelvis for obstructing renal stones. Antibiotics are needed in addition to the stents; however, place these stents as soon as possible with urological services assisting with stone removal. Institute adequate surgical drainage for prostatic abscesses using transurethral unroofing or a perineal incision.

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Diet

Oral food and liquids should be cautiously withheld in suspected cases of aspiration pneumonia in individuals with altered mental status, stroke, or prior intubation who have not yet been evaluated by a speech-language pathologist.

Food, hydration, and electrolyte containing solutions should be given to prevent malnutrition during an E coli diarrheal episode.

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Activity

Activity can be continued as tolerated by the patient.

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Consultations

Consultation with an infectious disease provider is recommended to treat infections that require long-term IV antibiotics and monitoring.^{[1, 8]} Some infections that require multi-week antimicrobial therapy are pyogenic liver abscesses, multiple intraabdominal abscesses that are not source controlled/surgically drained, empyema, and perinephric abscesses.

• References

Long-Term Monitoring

Generally, no long-term monitoring for E coli related infections is required once the initial infection is identified and treated. Weekly safety lab monitoring may be needed if the patient is on long term IV antibiotic therapy to treat the infection.

• References

Guideline Summary

International clinical practice guidelines for the treatment of acute uncomplicated cystitis and pyelonephritis in women were updated in 2010 by  the Infectious Diseases Society of America and the European Society for Microbiology and Infectious Diseases.^[15]

A clinical practice guideline for the management of asymptomatic bacteriuria by the Infectious Diseases Society of America (IDSA) was updated in 2019.^[21]

Guidance on the Treatment of Antimicrobial-Resistant Gram-Negative Infections was published by the Infectious Diseases Society of America (IDSA) in 2024.^[22]  

These guidelines are summarized below. Please see the complete guidelines for more detail.

• References

International clinical practice guidelines for the treatment of acute uncomplicated cystitis and pyelonephritis in women updated in 2010 by IDSA and the ESMID

International clinical practice guidelines for the treatment of acute uncomplicated cystitis and pyelonephritis in women were updated in 2010 by  the Infectious Diseases Society of America (IDSA) and the European Society for Microbiology and Infectious Diseases (ESMID); they are summarized below^[15] :

• Nitrofurantoin and trimethoprim-sulfamethoxazole are recommended as first-line treatments for acute uncomplicated cystitis due to their proven effectiveness in numerous clinical trials and low rates of resistance among uropathogens.
• Fosfomycin and pivmecillinam are also viable options, but may have slightly lower efficacy compared to the first-line choices.
• Fluoroquinolones and β-lactam agents should be reserved for cases where other options are not available, as they carry a risk of collateral damage and may have inferior efficacy.
• Amoxicillin and ampicillin are not recommended for empirical treatment due to their poor effectiveness and high prevalence of resistance globally.
• Urine culture and susceptibility testing should always be conducted in patients suspected of having pyelonephritis to tailor initial empirical therapy based on the infecting uropathogen.
• Oral ciprofloxacin is appropriate for treating pyelonephritis in non-hospitalized patients if fluoroquinolone resistance is below 10%. An initial intravenous dose of a long-acting antimicrobial is recommended if resistance exceeds 10%.
• Once-daily oral fluoroquinolones like ciprofloxacin or levofloxacin are suitable for non-hospitalized patients if fluoroquinolone resistance is not above 10%. If resistance is higher, an initial intravenous dose of a long-acting antimicrobial is recommended.
• Oral trimethoprim-sulfamethoxazole is appropriate if the uropathogen is known to be susceptible, otherwise, an initial intravenous dose of a long-acting antimicrobial is recommended.
• Oral β-lactam agents are less effective for treating pyelonephritis. If they are used, an initial intravenous dose of a long-acting antimicrobial is recommended.
• Hospitalized women with pyelonephritis should be treated with an intravenous antimicrobial regimen based on local resistance data and tailored to susceptibility results.

• References

A clinical practice guideline for the management of asymptomatic bacteriuria by the Infectious Diseases Society of America (IDSA) updated in 2019

A clinical practice guideline for the management of asymptomatic bacteriuria by the Infectious Diseases Society of America (IDSA) was updated in 2019; it is summarized below^[21] : 

• Pediatric patients should not be screened for or treated for asymptomatic bacteriuria.
• Healthy nonpregnant women also should not be screened for or treated for asymptomatic bacteriuria.
• Pregnant women should be screened for and treated for asymptomatic bacteriuria, with a recommended duration of 4-7 days of antibiotic therapy.
• Functionally impaired older individuals and residents of long-term care facilities should not be screened for or treated for asymptomatic bacteriuria.
• In older patients with cognitive impairment and bacteriuria but without symptoms, careful assessment for other causes is recommended instead of antimicrobial treatment.
• Patients with diabetes do not require screening or treatment for asymptomatic bacteriuria.
• Renal transplant recipients one month post-surgery should not be screened or treated for asymptomatic bacteriuria.
• Patients with nonrenal solid organ transplants should not undergo screening or treatment for asymptomatic bacteriuria.
• High-risk neutropenic patients and those with spinal cord injuries should not be screened or treated for asymptomatic bacteriuria.
• Short-term indwelling catheter patients should not be screened or treated for asymptomatic bacteriuria.
• Long-term indwelling catheter patients should also not be screened or treated for asymptomatic bacteriuria.
• Patients undergoing elective nonurologic surgery do not require screening or treatment for asymptomatic bacteriuria.
• Patients undergoing urological procedures with mucosal trauma should be screened and treated for asymptomatic bacteriuria.
• Patients undergoing urologic device implantation or living with such devices should not be screened or treated for asymptomatic bacteriuria.

• References

2024 Guidance on the Treatment of Antimicrobial-Resistant Gram-Negative Infections by the Infectious Diseases Society of America (IDSA)

Infectious Diseases Society of America 2024 Guidance on the Treatment of Antimicrobial-Resistant Gram-Negative Infections is summarized below^[22] :

• Fosfomycin is not suggested for use in pyelonephritis or cUTI, but additional doses may have uncertain benefits based on recent data.
• Amoxicillin-clavulanic acid is not preferred for uncomplicated ESBL-producing cystitis, but may be considered in specific cases where other options are limited.
• Piperacillin-tazobactam is not the first choice for treating pyelonephritis or cUTI; continued use should be decided cautiously if clinical improvement is observed, despite potential risks of microbiological failure.
• Ceftolozane-tazobactam is considered effective against ESBL-E, but is recommended for treating DTR P. aeruginosa or polymicrobial infections.
• Mechanistic details explaining why piperacillin-tazobactam may not be effective for ESBL-E infections are outlined.
• With an increasing prevalence of CRE isolates producing metallo-beta-lactamases, testing methods and dosing recommendations for ceftazidime-avibactam in combination with aztreonam have been updated.
• Traditional β-lactams administered via high-dose extended-infusion are suggested for DTR P aeruginosa infections, with considerations for differences in activity across available agents.
• Sulbactam-durlobactam combined with meropenem or imipenem-cilastatin is now the preferred treatment for CRAB infections, with revised dosing recommendations for high-dose ampicillin-sulbactam.
• Recommendations for S maltophilia treatment prioritize agents in order of preference, and testing methods for ceftazidime-avibactam and aztreonam are discussed in detail.

• References

Medication Summary

Escherichia coli (E coli) meningitis requires antibiotics, such as third generation cephalosporins (eg, ceftriaxone) due to its excellent CNS penetration.

E coli pneumonia requires respiratory support, adequate oxygenation, and antibiotics, such as third generation cephalosporins or fluoroquinolones. If an individual is particularly ill, it is reasonable to use a fourth generation cephalosporine (cefepime) or extended spectrum penicillin (eg, piperacillin/tazobactam) while waiting cultures and susceptibilities.

E coli cholecystitis/cholangitis requires antibiotics such as third-generation cephalosporins that cover E coli and Klebsiella organisms. Empiric coverage should of a community acquired intraabdominal infection does not need to include empiric coverage of enterococcus species (eg, E faecalis).However, if enterococcus is identified on culture from an intraabdominal infection, recognize that enterococci are intrinsically resistant to cephalosporins, and antibiotics would need to be altered.

For E coli intra-abdominal abscess, antibiotics must include anaerobic coverage (eg, ampicillin/sulbactam or metronidazole). In severe infection, piperacillin/tazobactam, ertapenem, or meropenem may be used. Combination therapy with antibiotics that cover E coli plus an antianaerobe can also be used (eg, levofloxacin plus metronidazole). Due to anaerobic evolving resistance patterns, cefoxitin, clindamycin, and moxifloxacin have fallen out of favor to cover for anaerobes.

E coli enteric infections may present with septic shock or severe dehydration and require crystalloid fluid replacement. Antimicrobials known to be useful in cases of traveler's diarrhea include azithromycin, fluoroquinolones, and rifaximin. They shorten the duration of diarrhea by 24-36 hours. Antibiotics should not be used in STEC infection as they may lyse the bacteria leading to release of Shiga toxin and may predispose to development of HUS. Antimotility agents are contraindicated in children and in persons with EIEC infection.

Uncomplicated E coli cystitis can be treated with a single dose of oral fosfomycin, a three day course of a fluoroquinolone or TMP/SMX, or five day course of nitrofurantoin.^{[15, 16]}

Acute uncomplicated E coli pyelonephritis in young women is treated with fluoroquinolone for five days or trimethoprimsulfamethoxazole (TMP/SMX) for 14 days. Of note, nitrofurantoin is ineffective for treatment of pyelonephritis and thus cannot be used if this diagnosis is suspected based on clinical evaluation. Patients with vomiting, nausea, inability to tolerate oral medications, or underlying comorbidities at risk for clinical deterioration, should be admitted to the hospital. If fever and flank pain persist for more than 72 hours, it is reasonable to pursue ultrasonography or CT scanning to assess for secondary complications like perinephric abscess that may require surgical intervention. Culture data should alter antimicrobial administration if resistance to current antibiotics is detected.

Treat E coli perinephric abscess or prostatitis with at least six weeks of antibiotics.

E coli bacteremia requires at least seven days of antibiotics and identification of the source of bacteremia based on clinical examination, imaging studies as indicated, and laboratory analysis. Seven days of antibiotic treatment is non-inferior to 14 days (E Coli), however if the patient were to have a clinical syndrome that would require antibiotic treatment longer than seven days, the longer of the 2 durations of antibiotics should be pursued.

McGannon et al found that antibiotics that target DNA synthesis, such as ciprofloxacin (CIP) and TMP/SMZ, showed increased Shiga toxin production, whereas antibiotics that target the cell wall, transcription, or translation did not.^[23] Remarkably, high levels of Shiga toxin were detected even when growth of O157:H7 was completely suppressed by CIP. In contrast, azithromycin significantly reduced Shiga toxin levels even when O157:H7 viability remained high.

Since the late 1990s, multidrug-resistant Enterobacteriaceae (mostly E coli) that produce extended-spectrum beta-lactamases (ESBLs), such as the CTX-M enzymes, have emerged within the community setting as an important cause of UTIs. These bacteria are resistant to the groups of antibiotics that commonly are used to treat these types of infections (penicillins, cephalosporins) and to antibiotics normally reserved for more severe infections (eg, fluoroquinolones, gentamicin). Enterobacterales are inferred to produce ESBL enzymes when susceptibility to ceftriaxone (CTX) has a minimum inhibitory concentration (MIC) of ≥2 µg/mL.

The spread of CTX-M–positive bacteria considerably changes how the treatment of community-acquired infections is approached and limits the oral antibiotics that may be administered. This finding has major implications for treating individuals who do not clinically respond to first-line antibiotics. ^[12]

In one study, mortality following bacteremic infection caused by ESBL producing E coli was significantly higher than non–ESBL-producing E coli. These findings have serious implications for antibiotic prescription, as cephalosporins are ineffective treatment for many E coli infections.^[24]

Infections due to ESBL-producing E coli largely have been regarded as a healthcare-associated phenomenon. However, reports of community-associated infections caused by ESBL-producing E coli have begun to emerge, and this occurrence of community-associated infections due to extended-spectrum β-lactamase (ESBL)–producing Escherichia coli has been recognized among patients without discernible healthcare-associated risk factors in the United States. Most (54.2%) ESBL-producing strains that cause community-associated episodes belonged to ST131 or its related sequence types. Among these strains, all except one produced CTX-M–type ESBL, in particular CTX-M-15.^[25]

According to the 2024 IDSA guidelines for the treatment of antimicrobial-resistant gram-negative infections, the preferred treatment of infections by ESBL E coli, nitrofurantoin and TMP-SMX are preferred for the treatment of uncomplicated cystitis; TMP-SMX, ciprofloxacin, or levofloxacin are preferred for the treatment of complicated cystitis or pyelonephritis; and meropenem, imipenem-cilastatin, or ertapenem are preferred for the treatment of infections outside the urinary tract. If piperacillin-tazobactam or cefepime is empirically started for the treatment of uncomplicated cystitis and the organism is later identified as ESBL E coli and clinical improvement occurred, a change of antibiotics is not necessary.^[22]

• References

Nitrofurantoin (Macrodantin)

• Dosing, Interactions, etc.

Clinical Context:  Nitrofurantoin is synthetic nitrofuran and interferes with bacterial carbohydrate metabolism by inhibiting acetylcoenzyme A. It is used to treat uncomplicated UTIs for five days in females and 7 days in males.

• References

Rifaximin

• Dosing, Interactions, etc.

Clinical Context:  Rifaximin is a nonabsorbed (< 0.4%), broad-spectrum antibiotic specific for enteric pathogens of the GI tract (ie, gram-positive, gram-negative, aerobic, anaerobic). It is a rifampin structural analog, and it binds to the beta-subunit of bacterial DNA-dependent RNA polymerase, thereby inhibiting RNA synthesis. It is indicated for E coli (enterotoxigenic and enteroaggregative strains) associated with travelers' diarrhea.

• References

Class Summary

Empiric antimicrobial therapy must be comprehensive and cover all likely pathogens in the context of the clinical setting. However, given the broad use of antibiotics in hospitals, a study was performed to determine the relationship between hospital use of 16 classes of antibacterial agents and the incidence of quinolone-resistant E coli isolates. The results revealed that although the level of hospital use of quinolones influenced the incidence of quinolone resistance in E coli hospital isolates, the consumption of 2 other classes of antibiotics, cephalosporins and tetracyclines, is also associated with quinolone resistance.^[18]

Recent data from the Canadian national surveillance study, CANWARD, revealed that 868 urine isolates of E coli collected from 2010-2013 were sensitive to fosfomycin using the Clinical and Laboratory Standards Institute (CLSI) agar dilution method, with minimum inhibitory concentrations (MICs) interpreted using CLSI M100-S23 (2013) criteria. The concentrations of fosfomycin inhibiting 50% (MIC ₅₀ ) and 90% (MIC ₉₀ ) of isolates were 1 or less and 4 μg/mL, respectivelyl; 99.4% of isolates were susceptible to fosfomycin.^[16]

• References

Ceftriaxone (Rocephin)

• Dosing, Interactions, etc.

Clinical Context:  Ceftriaxone is a third-generation cephalosporin that arrests bacterial growth by binding to one or more penicillin-binding proteins. It is used to treat pneumonia for 5 days, bacteremia for 7 days, pyelonephritis for 14 days and meningitis from 7-21 days depending on the organism identified and clinical response. Ceftriaxone has excellent CNS penetration and may be paired with metronidazole to cover intraabdominal infections.

• References

Ceftazidime/avibactam (Avycaz)

• Dosing, Interactions, etc.

Clinical Context:  A third generation pseudomonally active cephalosporin with broad gram negative activity paired with a beta lactamase inhibitor that extends the spectrum of gram negative activity to bacteria that may not be generally susceptible to ceftazidime. Generally one of the last antimicrobial lines of defense for antimicrobial resistant infections. Duration is 5-14 days depending on clinical indication with generally used for bacterial pneumonia, UTIs, and intraabdominal infections.

• References

Ampicillin and sulbactam (Unasyn)

• Dosing, Interactions, etc.

Clinical Context:  Ampicillin and sulbactam is a drug combination of a beta-lactamase inhibitor with ampicillin. It is used to treat pyelonephritis for 14 days and intra-abdominal infections, duration based on the clinical syndrome, generally ranging from 4-14 days or longer if infection does not have source control.

• References

Piperacillin and tazobactam (Zosyn)

• Dosing, Interactions, etc.

Clinical Context:  Piperacillin and tazobactam is an antipseudomonal penicillin plus beta-lactamase inhibitor that covers some gram positives, gram negatives, and anaerobes. It inhibits biosynthesis of cell wall mucopeptide and is effective during the stage of active multiplication. It is broader in spectrum than Ceftriaxone and it is used when infection is thought to be polymicrobial. It is utilized to treat intra-abdominal infections, with the duration pending on the clinical syndrome, with antibiotics generally utilized for 4-7 days if source control is thought to be achieved.  

• References

Ciprofloxacin (Cipro)

• Dosing, Interactions, etc.

Clinical Context:  Ciprofloxacin is a fluoroquinolone that binds DNA gyrase and leading DNA strand breakage and death of the bacteria (bactericidal). Acute uncomplicated cystitis in women may be treated for three days, pyelonephritis for 5 days, bacteremia for 7 days, and prostatitis for 6 weeks. 

• References

Levofloxacin (Levaquin)

• Dosing, Interactions, etc.

Clinical Context:  Levofloxacin is used for infections due to multidrug-resistant gram-negative organisms. It is used to treat community-acquired pneumonia for 7 days, acute pyelonephritis and complicated UTI for 5 days, and traveler's diarrhea for 5 days.

• References

Eravacycline (Xerava)

• Dosing, Interactions, etc.

Clinical Context:  Flurocycline within the tetracycline class that disrupts bacterial protein synthesis through binding of the 30S ribosomal subunit, thus preventing elongation of peptide chains. Used for complicated intraabdominal infections for 4-14 days, depending on indication, and is generally favored for use in for antimicrobial resistant infections.

• References

Trimethoprim/sulfamethoxazole (Bactrim, Bactrim DS, Septra DS, Sulfatrim)

• Dosing, Interactions, etc.

Clinical Context:  Trimethoprim/sulfamethoxazole inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid. It is used to treat uncomplicated UTI for 3 days, pyelonephritis for 14 days, and acute prostatitis for 6 weeks.

• References

Aztreonam (Azactam)

• Dosing, Interactions, etc.

Clinical Context:  Aztreonam is a monobactam that inhibits cell wall synthesis during bacterial growth. It is active against aerobic gram-negative bacilli. This medication is intravenous only and generally utilized in those with penicillin allergies due to minimal cross reactivity between Aztreonam, pencillins, and cephalosporins. It is used to treat complicated UTIs/pyelonephritis and bacteremia for 7 days, pneumonia for 7 days, and intra-abdominal infections based on the clinical syndrome identified.

• References

Meropenem (Merrem IV)

• Dosing, Interactions, etc.

Clinical Context:  Meropenem is a bactericidal broad-spectrum carbapenem antibiotic that inhibits cell wall synthesis. Other carbapenems in the class include Ertapenem and Imipenem paired with Cilastatin. It is effective against most gram-positive and gram-negative bacteria. Carbapenems are spared for severe infections, such as septic shock, or where resistant gram-negative organisms are suspected. Meropenem and Imipenem are utilized if Pseudomonas aeruginosa is required to be covered empirically, else Ertapenem is more narrow in spectrum. Carbapenems are drugs of choice in ESBL bacterial infections and demonstrated a mortality benefit over Piperacillin/tazobactam. Duration of antimicrobial therapy depends on the clinical syndrome with pyelonephritis treated for 5 days, bacteremia for 7 days, and multiple uncontrolled infections for potentially longer.

• References

Further Outpatient Care

Supportive care and rehabilitation should be provided to persons with meningitis who develop neurologic sequelae.

• References

Further Inpatient Care

Further inpatient care includes the following:

• Supportive and symptomatic care
• Adequate hydration and oxygenation
• Periodic neurological test for meningitis

• References

Inpatient & Outpatient Medications

Most severe Escherichia coli (E coli) infections warrant hospitalization due to the potential for rapid clinical deterioration.^{[1, 8]} These include meningitis, pneumonia, cholecystitis/cholangitis, intra-abdominal abscess, and some cases of complicated UTI and pyelonephritis.

In patients with pyelonephritis, a switch to oral medications should be made as soon as the patient is able to tolerate oral intake.

The duration of therapy depends on the type of infection and clinical syndrome.

In cases of STEC diarrhea, antibiotics are contraindicated; treatment is supportive and symptomatic in nature.

• References

Complications

HUS may complicate STEC infection. E coli meningitis in neonates usually results in neurologic sequelae.

• References

Prognosis

The prognosis depends on the specific diagnosis; therefore, no generalizations can be made.

• References

Patient Education

Patients should be instructed on personal hygiene, such as washing hands and improving food preparation techniques.

When individuals travel abroad to tropical and subtropical areas and are unable to determine adequate sanitation of water systems, measures should be undertaken to avoid contamination of food and water. These include drinking bottled water, avoidance of drinking tap water, avoidance of  drinks with ice (possible contamination), avoidance of fruits / vegetables that cannot be peeled (possible water contamination), and avoidance of street vendor foods (possible fecal contamination while handling food).

Prophylactic antibiotics are not warranted for most individuals to prevent travelers’ diarrhea. Only high-risk individuals with multiple comorbidities should be considered for any preventative therapy due to potential risk for side effects and antimicrobial resistance.

Advise patients to cook meat appropriately and to prevent STEC/ETEC infections caused by cross contamination of cutting surfaces in the kitchen. This can be accomplished by utilizing different cutting boards when cutting meats and vegetables and will decrease the risk for hemorrhagic colitis and HUS.

• References