Updated: Feb 19, 2009
Escherichia coli is one of the most frequent causes of many common bacterial infections, including cholecystitis, bacteremia, cholangitis, urinary tract infection (UTI), and traveler's diarrhea, and other clinical infections such as neonatal meningitis and pneumonia.
The genus Escherichia is named after Theodor Escherich, who isolated the type species of the genus. Escherichia organisms are gram-negative bacilli that exist singly or in pairs. E coli is facultatively anaerobic with a type of metabolism that is both fermentative and respiratory. They are either nonmotile or motile by peritrichous flagella. E coli is a major facultative inhabitant of the large intestine.
Acute bacterial meningitis
The vast majority of neonatal meningitis cases are caused by E coli and group B streptococcal infections (28.5% and 34.1% overall, respectively). Pregnant women are at a higher risk of colonization with the K1 capsular antigen strain of E coli. This strain is also commonly observed in neonatal sepsis, which carries a mortality rate of 8%; most survivors have subsequent neurologic or developmental abnormalities. Low birth weight and a positive cerebrospinal fluid (CSF) culture result portend a poor outcome. In adults, E coli meningitis is rare but may occur following neurosurgical trauma or procedures or complicating Strongyloides stercoralis hyperinfection involving the CNS.
Pneumonia
E coli respiratory tract infections are uncommon and are almost always associated with E coli UTI. No virulence factors have been implicated. E coli pneumonia may also result from microaspiration of upper airway secretions that have been previously colonized with this organism in severely ill patients; hence, it is a cause of nosocomial pneumonia. However, E coli pneumonia may also be community-acquired in patients who have underlying disease such as diabetes mellitus, alcoholism, chronic obstructive pulmonary disease, and E coli UTI. E coli pneumonia usually manifests as a bronchopneumonia of the lower lobes and may be complicated by empyema. E coli bacteremia precedes pneumonia and is usually due to another focus of E coli infection in the urinary or GI tract.
Intra-abdominal infections
E coli intra-abdominal infections often result from a perforated viscus (eg, appendix, diverticulum) or may be associated with intra-abdominal abscess, cholecystitis, and ascending cholangitis. Patients with diabetes mellitus are also at high risk of developing pylephlebitis of the portal vein and liver abscesses (see Image 1).
Intra-abdominal abscesses are usually polymicrobial and can be caused by spontaneous or traumatic GI tract perforation or after anastomotic disruption with spillage of colon contents and subsequent peritonitis. They can be observed in the postoperative period after anastomotic disruption. Abscesses are often polymicrobial, and E coli is one of the more common gram-negative bacilli observed together with anaerobes.
Cholecystitis and cholangitis result from obstruction of the biliary system from biliary stone or sludge, leading to stagnation and bacterial growth from the papilla or portal circulation. When bile flow is obstructed, colonic organisms, including E coli, colonize the jejunum and duodenum. Interestingly, partial obstruction is more likely than complete obstruction to result in infection, bacteremia, bactibilia, and gallstones.
Enteric infections
As a cause of enteric infections, 6 different mechanisms of action of 6 different varieties of E coli have been reported. Enterotoxigenic E coli (ETEC) is a cause of traveler's diarrhea. Enteropathogenic E coli (EPEC) is a cause of childhood diarrhea. Enteroinvasive E coli (EIEC) causes a Shigella -like dysentery. Enterohemorrhagic E coli (EHEC) causes hemorrhagic colitis or hemolytic-uremic syndrome (HUS). Enteroaggregative E coli (EAggEC) is primarily associated with persistent diarrhea in children in developing countries, and enteroadherent E coli (EAEC) is a cause of childhood diarrhea and traveler's diarrhea in Mexico and North Africa. ETEC, EPEC, EAggEC, and EAEC colonize the small bowel, and EIEC and EHEC preferentially colonize the large bowel prior to causing diarrhea.
Urinary tract infections
The urinary tract is the most common site of E coli infection, and more than 90% of all uncomplicated UTIs are caused by E coli infection. The recurrence rate after a first E coli infection is 44% over 12 months. 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 urosepsis. 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.
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 urinary catheters (see Image 2).
E coli bacteremia is usually 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).
E coli is the leading cause of both community-acquired and nosocomial UTI. Up to 50% of females eventually experience at least one episode of UTI. E coli causes 12-50% of nosocomial infections and 4% of cases of diarrheal disease.
In tropical countries, EPEC is an important cause of childhood diarrhea. ETEC causes 11-15% of cases of traveler's diarrhea in persons visiting developing countries and 30-45% of cases of traveler's diarrhea among those visiting Mexico. EAggEC causes 30% of cases of traveler's diarrhea.
Differential Diagnoses of E coli Infection
| Organism | Ind* | Urease | Motility | Glu Ferm† | Lact Ferm‡ | Sucr Ferm§ | Malt Ferm|| | Esc Hyd¶ | Hyd Sulf TSI# | Oxidase | Orn Dec** | Lys Dec†† |
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| E coli | + | - | + | + | + | +/- | + | - | - | - | +/- | + |
| Klebsiella pneumoniae | - | +/- | - | + | + | + | + | + | - | - | - | + |
| P mirabilis | - | + | + | + | - | - | - | - | + | - | + | - |
| Proteus vulgaris | + | + | + | + | - | + | + | +/- | + | - | - | - |
| Pseudomonas aeruginosa | - | +/- | + | + (ox)‡‡ | - | - | - | - | - | + | - | - |
| Enterobacter aerogenes | - | - | + | + | + | + | + | + | - | - | + | + |
| Enterobacter cloacae | - | - | + | + | + | + | + | - | - | - | + | - |
| Salmonella typhi | - | - | + | + | - | - | + | - | + | - | - | + |
| Citrobacter freundii | +/- | - | + | + | + | + | + | - | +/- | - | - | - |
| Serratia marcescens | - | +/- | + | + | - | + | + | + | - | - | + | + |
*Indole
†Glucose fermentation
‡Lactose fermentation
§Sucrose fermentation
||Maltose fermentation
¶Esculin hydrolysis
#Hydrogen sulfite on TSI
**Ornithine decarboxylase
††Lysine decarboxylase
‡‡Oxidative
| Enterobacter Infections | Pseudomonas Aeruginosa Infections |
| Enterococcal Infections | Serratia |
| Klebsiella Infections | Shigellosis |
| Proteus Infections | Streptococcus Group B Infections |
| Providencia Infections |
E coli meningitis requires antibiotics, such as third-generation cephalosporins (eg, ceftriaxone).
E coli pneumonia requires respiratory support, adequate oxygenation, and antibiotics, such as third-generation cephalosporins or fluoroquinolones.
E coli cholecystitis/cholangitis requires antibiotics such as third-generation cephalosporins that cover E coli and Klebsiella organisms. Empiric coverage should also include anti– E faecalis coverage.
For E coli intra-abdominal abscess, antibiotics also must include anaerobic coverage (eg, ampicillin and sulbactam or cefoxitin). In severe infection, piperacillin and tazobactam, imipenem and cilastatin, or meropenem may be used. Combination therapy with antibiotics that cover E coli plus an antianaerobe can also be used (eg, levofloxacin plus clindamycin or metronidazole).
E coli enteric infections require fluid replacement with solutions containing appropriate electrolytes. Antimicrobials known to be useful in cases of traveler's diarrhea include doxycycline, trimethoprim/sulfamethoxazole (TMP/SMZ), fluoroquinolones, and rifaximin. They shorten the duration of diarrhea by 24-36 h. Antibiotics are not useful in enterohemorrhagic E coli (EHEC) infection and may predispose to development of HUS. Antimotility agents are contraindicated in children and in persons with enteroinvasive E coli (EIEC) infection.
Uncomplicated E coli cystitis can be treated with a single dose of antibiotic or 3-d course of a fluoroquinolone, TMP/SMZ, or nitrofurantoin.
Recurrent E coli cystitis (ie, >2 episodes/y) is treated with continuous or postcoital prophylaxis with a fluoroquinolone, TMP/SMZ, or nitrofurantoin.
Patients with complex cases (eg, those with diabetes, >65 y, or recent history of UTI) are treated with a 7- to 14-d course of antibiotics (eg, levofloxacin, third-generation cephalosporins, or aztreonam).
Acute uncomplicated E coli pyelonephritis in young women is treated with fluoroquinolone or TMP/SMZ for 14 d. Patients with vomiting, nausea, or underlying illness (eg, diabetes) should be admitted to the hospital. If fever and flank pain persist for more than 72 h, ultrasonography or CT scanning may be performed.
Treat E coli perinephric abscess or prostatitis with at least 6 wk of antibiotics.
E coli sepsis requires at least 2 wk of antibiotics and identification of the source of bacteremia based on imaging study results.
Empiric antimicrobial therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.
Inhibits protein synthesis and thus, bacterial growth, by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. Used to treat traveler's diarrhea.
100 mg PO q12h for 5 d
<8 years: Not recommended, can cause permanent discoloration of teeth
>8 years and <100 lb: 2 mg/lb PO divided bid on day 1, then 1 mg/lb PO qd or divided bid
>8 years and >100 lb: Administer as in adults
Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; can increase hypoprothrombinemic effects of anticoagulants; can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last half of pregnancy through 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines
Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Used to treat traveler's diarrhea for 5 d, uncomplicated UTI for 3 d, complicated UTI for 10-14 d, and acute prostatitis for 6-12 wk.
160 mg TMP/800 mg SMZ PO/IV q12h
<2 months: Do not administer
>2 months: 8 mg/kg/d TMP/40 mg/kg/d SMZ PO q12h for 10 d
May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly persons; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine
Documented hypersensitivity; megaloblastic anemia due to folate deficiency
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Obtain CBC counts frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, administer 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholism, elderly, anticonvulsant therapy, malabsorption syndrome); hemolysis may occur in G-6-PD deficiency, patients with AIDS may not tolerate or respond to TMP/SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); administer fluids to prevent crystalluria and stone formation; avoid in pregnancy at term and breastfeeding because sulfonamides may cause kernicterus in infants; discontinue at first appearance of skin rash or sign of adverse reaction (eg, Stevens-Johnson syndrome, toxic epidermal necrolysis, agranulocytosis)
Fluoroquinolone that inhibits bacterial DNA synthesis and, consequently, growth. Used to treat mild-to-moderate UTI for 7-14 d, acute uncomplicated cystitis for 3 d, severe-to-complicated UTI for 7-14 d, infectious diarrhea for 5-7 d, and chronic bacterial prostatitis for 4-6 wk.
500 mg PO bid; alternatively, 400 mg IV q12h
<6 years: Not established
>6 years: Administer as in adults
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT); leads to hypoglycemia in patients concurrently receiving glyburide
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy; avoid alkalinizing urine (crystalluria has been reported); caution in seizure disorder; photosensitivity may occur with prolonged exposure to sunlight or tanning equipment
For infections due to multidrug-resistant gram-negative organisms. Used to treat community-acquired pneumonia for 7-14 d, acute pyelonephritis and complicated UTI for 10 d, and traveler's diarrhea for 5 d.
500 mg PO/IV qd
<6 years: Not recommended
>6 years: Not established
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria. Used to treat uncomplicated UTI for 7 d and complicated UTI or pyelonephritis for 10-14 d.
500 mg PO q8h; not to exceed 3 g/d
<20 kg: 40 mg/kg/d PO divided q8h
>20 kg: Administer as in adults
Reduces efficacy of oral contraceptives
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal impairment
Monobactam that inhibits cell wall synthesis during bacterial growth. Active against aerobic gram-negative bacilli. Used to treat complicated UTIs/pyelonephritis and bacteremia for 7-14 d, intra-abdominal infections for 14-21 d, and pneumonia for 14 d.
1-2 g IV q8h
30 mg/kg IV q8h
Tetracyclines may reduce effects
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal insufficiency; caution in hepatic impairment
Drug combination of beta-lactamase inhibitor with ampicillin. Used to treat intra-abdominal infections for 14-21 d.
1.5 (1 g ampicillin + 0.5 g sulbactam) to 3 g (2 g ampicillin + 1 g sulbactam) IV q6h; not to exceed 4 g/d sulbactam or 8 g/d ampicillin
Not established
Probenecid and disulfiram elevate ampicillin levels; allopurinol decreases ampicillin effects and has additive effects on ampicillin rash; may decrease effects of oral contraceptives
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal failure; evaluate rash and differentiate from hypersensitivity reaction
Synthetic nitrofuran that interferes with bacterial carbohydrate metabolism by inhibiting acetylcoenzyme A. Used to treat uncomplicated UTIs for 7 d or for 3 d after urine is sterile.
100 mg PO q12h
<1 month: Not recommended
>1 month: 5-7 mg/kg/d PO divided qid
Anticholinergics may delay gastric emptying and increase absorption, increasing bioavailability; antacids made of magnesium salts may decrease effects by decreasing absorption; high doses of concurrent probenecid decrease renal clearance and increase toxicity of nitrofurantoin
Documented hypersensitivity; renal insufficiency (CrCl <60 mL/min), anuria, oliguria; do not use for pyelonephritis or perinephric abscess
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
May cause severe and irreversible peripheral neuropathy that can be fatal; renal impairment, diabetes, electrolyte imbalance, anemia, and vitamin B deficiency increase risk for adverse effects; prolonged use of antibiotics may result in fungal or bacterial overgrowth of resistant or nonsusceptible organisms; take with food to enhance tolerance and improve absorption; interstitial pneumonitis or pulmonary fibrosis, optic neuritis, and hemolytic anemia may occur
Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell wall synthesis. Effective against most gram-positive and gram-negative bacteria. Used to treat intra-abdominal infections for 14-21 d.
1 g IV q8h
<3 months: Not recommended
>3 months: 20 mg/kg IV q8h
Probenecid may inhibit renal excretion, increasing meropenem levels
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Pseudomembranous colitis and thrombocytopenia may occur, requiring immediate discontinuation of medication
Third-generation cephalosporin that arrests bacterial growth by binding to one or more penicillin-binding proteins. Used to treat meningitis and bacteremia for 14-21 d and pneumonia, complicated UTI, or pyelonephritis for 14 d.
2 g IV divided bid; not to exceed 4 g/d
Neonatal meningitis: 50-75 mg/kg/d IV divided q12h
Probenecid may increase levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections, pseudobiliary lithiasis, non– C difficile diarrhea, and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy; caution in breastfeeding
Antipseudomonal penicillin plus beta-lactamase inhibitor. Inhibits biosynthesis of cell wall mucopeptide and is effective during stage of active multiplication. Used to treat intra-abdominal infections for 14-21 d.
4.5 g IV q8h
<12 years: Not established
>12 years: Administer as in adults
Tetracyclines may decrease effects of piperacillin; high concentrations of piperacillin may physically inactivate aminoglycosides if administered in same IV line; effects are synergistic when administered concurrently with aminoglycosides; probenecid may increase penicillin levels; prolongs neuromuscular blockade of vecuronium if used concomitantly; if used with heparin, monitor coagulation parameters frequently
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Perform CBC counts prior to initiation of therapy and at least weekly during therapy; monitor for liver function abnormalities by measuring AST and ALT during therapy; caution in hepatic disease; perform urinalysis and BUN and creatinine determinations during therapy and adjust dose if values become elevated; monitor blood levels to avoid possible neurotoxic reactions
For treatment of multiple-organism infections in which other agents do not have wide-spectrum coverage or are contraindicated due to potential for toxicity. Used to treat pneumonia and complicated UTI for 14 d, bacteremia for 7 d, and intra-abdominal abscess for 14-21 d.
500 mg IV q6h
<12 years: Not established
>12 years: Administer as in adults
Coadministration with cyclosporine may increase adverse CNS effects of both agents; coadministration with ganciclovir may result in generalized seizures
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Adjust dose in renal insufficiency; caution in CNS disorders (eg, brain lesions, history of seizures); for hemodialysis, use only when benefit outweighs risk of seizures
Nonabsorbed (<0.4%), broad-spectrum antibiotic specific for enteric pathogens of the gastrointestinal tract (ie, gram-positive, gram-negative, aerobic, 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 travelers' diarrhea.
200 mg PO tid
<12 years: Not established
>12 years: Administer as in adults
Induces CYP450 3A4 in vitro; limited data exist; no significant interactions shown in single-dose studies with midazolam and oral contraceptives
Documented hypersensitivity to rifaximin or rifamycin antimicrobial agents (eg, rifampin)
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May promote intestinal bacterial overgrowth and cause superinfection; discontinue if diarrhea persists >24-48 h or worsens; seek immediate medical care if fever and/or bloody stools emerge (tablets not effective); not effective for travelers' diarrhea due to suspected pathogens other than E coli; postmarketing reports include allergic dermatitis, rash, angioneurotic edema, urticaria, and pruritus
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 are commonly used to treat these types of infections (penicillins, cephalosporins) and to antibiotics normally reserved for more severe infections (eg, fluoroquinolones, gentamicin).
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.2
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E coli, Escherichia coli, traveler's diarrhea, traveler diarrhea, E coli cholecystitis, E coli bacteremia, E coli cholangitis, E coli urinary tract infection, E coli UTI, E coli neonatal meningitis, E coli pneumonia, E coli acute bacterial meningitis, E coli nosocomial pneumonia, E coli hospital-acquired pneumonia, E coli nosocomial infection, E coli hospital-acquired infection, E coli bronchopneumonia, enterotoxigenic E coli, ETEC, enteropathogenic E coli, EPEC, enteroinvasive E coli, EIEC, E coli dysentery
enterohemorrhagic E coli, EHEC, E coli hemorrhagic colitis, hemolytic-uremic syndrome, HUS, enteroaggregative E coli, EAggEC, enteroadherent E coli, EAEC, uncomplicated E coli urethritis, uncomplicated E coli cystitis, symptomatic E coli cystitis, E coli pyelonephritis, acute E coli prostatitis, E coli prostatic abscess, E coli urosepsis, E coli septic arthritis, E coli endophthalmitis, E coli suppurative thyroiditis, E coli sinusitis, E coli osteomyelitis, E coli endocarditis, E coli skin infection, E coli diabetic skin infection, E coli soft-tissue infection, E coli diarrheal disease
Tarun Madappa, MD, MPH, Critical Care Fellow, Section of Critical Care Medicine, St Vincent Catholic Medical Center, New York Medical College, New York.
Tarun Madappa, MD, MPH is a member of the following medical societies: American College of Chest Physicians and American Thoracic Society
Disclosure: Nothing to disclose.
Chi Hiong U Go, MD, Assistant Professor, Department of Internal Medicine, Texas Tech University Health Science Center at Odessa
Chi Hiong U Go, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine
Disclosure: Nothing to disclose.
Larry I Lutwick, MD, Professor of Medicine, State University of New York, Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus
Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Charles V Sanders, MD, Edgar Hull Professor and Chairman, Department of Internal Medicine, Professor of Microbiology, Immunology and Parasitology, Louisiana State University School of Medicine at New Orleans; Medical Director, Medicine Hospital Center, Charity Hospital and Medical Center of Louisiana at New Orleans; Consulting Staff, Ochsner Medical Center
Charles V Sanders, MD is a member of the following medical societies: Alliance for the Prudent Use of Antibiotics, Alpha Omega Alpha, American Association for the Advancement of Science, American Association of University Professors, American Clinical and Climatological Association, American College of Physician Executives, American College of Physicians, American Federation for Medical Research, American Foundation for AIDS Research, American Geriatrics Society, American Lung Association, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Association for Professionals in Infection Control and Epidemiology, Association of American Medical Colleges, Association of American Physicians, Association of Professors of Medicine, Infectious Disease Society for Obstetrics and Gynecology, Infectious Diseases Society of America, Louisiana State Medical Society, Orleans Parish Medical Society, Royal Society of Medicine, Sigma Xi, Society of General Internal Medicine, Southeastern Clinical Club, Southern Medical Association, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology
Disclosure: Nothing to disclose.
Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.