Updated: Jun 17, 2008
Clinically significant anaerobic cocci include Peptostreptococcus species, Veillonella species (gram-negative cocci), and microaerophilic streptococci (aerotolerant). Anaerobic gram-positive cocci include various clinically significant species of the genus Peptostreptococcus.1
Peptostreptococcus infections can occur in all body sites, including the CNS, head, neck, chest, abdomen, pelvis, skin, bone, joint, and soft tissues. Inadequate therapy against these anaerobic bacteria may lead to clinical failures. Because of their fastidiousness, peptostreptococci are difficult to isolate and are often overlooked. Isolating them requires appropriate methods of specimen collection, transportation, and cultivation. Their slow growth and increasing resistance to antimicrobials, in addition to the polymicrobial nature of the infection, complicate treatment.2
Peptostreptococcus is the only genus among anaerobic gram-positive cocci encountered in clinical infections. This group also includes species within the genus formerly known as Peptococcus, with the exception of Peptococcus niger. This change in taxonomy was based on the results of a guanine-plus-cytosine content analysis. Additionally, Gaffkya anaerobia was renamed Peptostreptococcus tetradius. The species of anaerobic gram-positive cocci isolated most commonly include Peptostreptococcus magnus,3 Peptostreptococcus asaccharolyticus, Peptostreptococcus anaerobius, Peptostreptococcus prevotii, and Peptostreptococcus micros.4,5,6,7
Anaerobic gram-positive cocci that produce large amounts of lactic acid during the process of carbohydrate fermentation were reclassified as Streptococcus parvulus and Streptococcus morbillorum from Peptococcus or Peptostreptococcus. Most of these organisms are anaerobic, but some are microaerophilic.
Based on DNA homology and whole-cell polypeptide-pattern study findings supported by phenotypic characteristics, the DNA homology group of microaerobic streptococci that was formerly known as Streptococcus anginosus or Streptococcus milleri is now composed of 3 distinct species: S anginosus, Streptococcus constellatus, and Streptococcus intermedius.8 The microaerobic species S morbillorum was transferred into the genus Gemella. A new species within the genus Peptostreptococcus is Peptostreptococcus hydrogenalis; it contains the indole-positive, saccharolytic strains of the genus.9
Peptostreptococcus organisms are part of the normal florae of human mucocutaneous surfaces, including the mouth, intestinal tract, vagina, urethra, and skin.2 They are isolated with high frequency from all specimen sources. Anaerobic gram-positive cocci are the second most frequently recovered anaerobes and account for approximately one quarter of anaerobic isolates. Anaerobic gram-positive cocci are usually recovered mixed with other anaerobic or aerobic bacteria from infections at different sites of the body.
Many of these infections are synergistic. Bacterial synergy, the presence of which is determined by mutual induction of sepsis enhancement, increased mortality, increased ability to induce abscesses, and enhancement of the growth of the bacterial components in mixed infections, is found between anaerobic gram-positive cocci and their aerobic and anaerobic counterparts.10 The ability of anaerobic gram-positive cocci and microaerophilic streptococci to produce capsular material is an important virulence mechanism, but other factors may also influence the interaction of these organisms in mixed infections.11
The exact frequency of Peptostreptococcus infections is difficult to calculate because of inappropriate methods of collection, transportation, and cultivation of specimens. These infections are found more commonly in patients with chronic infections. Recovery rates in blood cultures are 2-5% and are higher in patients who have predisposing conditions. In 1974, Martin reported that anaerobic cocci were isolated in 8.5-31% of clinical specimens that yielded any anaerobic bacteria at the Mayo Clinic.6
In 2 studies published in 1988 and 1989, Brook reported that anaerobic gram-positive cocci accounted for 26% of all anaerobic bacteria recovered at BethesdaNavyHospital and WalterReedArmyHospital from 1973-1985. The infected sites where the organisms predominated were ears (53% of all anaerobic isolates), cysts (40%), bones (39%), and obstetrical and gynecological sites (35%). They were occasionally found in the CNS, abdomen, lymph nodes, bile, and eyes. Most isolates were found in abscesses, wounds, and obstetrical and gynecological infections.
The recovery rates differed for the different anaerobic gram-positive cocci. In descending order of frequency, the most common anaerobic gram-positive cocci were P magnus (18% of all anaerobic gram-positive cocci and microaerophilic streptococci), P asaccharolyticus (17%), P anaerobius (16%), P prevotii (13%), P micros (4%), Peptostreptococcus saccharolyticus (3%), and Peptostreptococcus intermedius (2%).5,12
The highest recovery rates of P magnus were in bone and chest infections. The highest recovery rate of P asaccharolyticus and P anaerobius were with obstetrical/gynecological and respiratory tract infections and wounds. Isolates of each of the most frequently recovered anaerobic gram-positive cocci were recovered from abscesses, wounds, and obstetrical and gynecological infections.5
Although most of the infections were polymicrobial when anaerobic and facultative cocci were recovered, these organisms were isolated in pure culture in 45 (8%) of 559 patients who had infections involving anaerobic gram-positive cocci, in 12 (10%) of 121 individuals who had infections due to microaerophilic streptococci, and in 15 (9%) of 176 patients who had P magnus infection.7 The most frequent types of infections from which anaerobic gram-positive cocci were isolated in pure culture were soft tissue infections, osteomyelitis, arthritis (especially in the presence of a prosthetic implant), and bacteremia. Most patients from whom microaerophilic streptococci were recovered in pure culture had abscesses (eg, dental, intracranial, pulmonary), bacteremia, meningitis, or conjunctivitis.
P magnus is the most commonly isolated anaerobic cocci.3 It is most often recovered in pure culture. The most common peptostreptococci in the different infectious sites are P anaerobius in oral infections; P magnus and P micros in respiratory tract infections; P magnus, P micros, P asaccharolyticus, Peptostreptococcus vaginalis, and P anaerobius in skin and soft tissue infections; P magnus and P micros in deep organ abscesses; P magnus, P micros, and P anaerobius in gastrointestinal tract–associated infections; P magnus, P micros, P asaccharolyticus, P vaginalis, P tetradius, and P anaerobius in female genitourinary infections; and P magnus, P asaccharolyticus, P vaginalis, and P anaerobius in bone and joint infections and leg and foot ulcers.8
The frequency of these infections appears to be higher in developing countries, where therapy is often inadequate or delayed.
Mortality has decreased over the past 3 decades.
Peptostreptococcus infections can occur in patients of all ages; however, head and neck infections occur more frequently in children than in adults.1
Although anaerobic cocci can be isolated from infections at all body sites, a predisposition for certain sites has been observed. In general, Peptostreptococcus species, particularly P magnus, have been recovered more often from subcutaneous and soft tissue abscesses and diabetes-related foot ulcers than from intra-abdominal infections.1 Peptostreptococcus infections occur more often in chronic infections and in association with the predisposing conditions below.
A patient's recovery from anaerobic infection depends on prompt and proper treatment according to the following principles: (1) neutralizing toxins produced by anaerobes, (2) preventing local bacterial proliferation by changing the environment, and (3) limiting the spread of bacteria.
In most cases, surgical therapy is critically important. Surgical therapy includes (1) draining abscesses, (2) debriding necrotic tissues, (3) decompressing closed-space infections, and (4) relieving obstructions. If surgical drainage is not used, the infection may persist and serious complications may develop.
Clinical judgment, personal experience, safety, and expected level of patient compliance should direct the physician in the choice of antimicrobial agents. When choosing antimicrobials for the therapy of mixed infections, their aerobic and anaerobic antibacterial spectrum and their availability in oral or parenteral form should be considered. Some antimicrobials have a limited range of activity.
Aside from susceptibility patterns, other factors influencing the choice of antimicrobial therapy include the pharmacologic characteristics of the various drugs, their toxicity, their effect on the normal florae, and their bactericidal activity. Although identification of the infecting organisms and their antimicrobial susceptibility may be needed for selection of optimal therapy, the clinical setting and gram-stain preparation of the specimen may indicate the types of anaerobes present in the infection and may indicate the nature of the infectious process.
Although the duration of therapy for anaerobic infections is generally longer than for aerobic and facultative infections, the duration must be individualized depending on the patient's response to the therapy. In some cases, the patient may require a 6- to 8-week course. However, therapy may be shortened after proper surgical drainage.19
Because peptostreptococci are often mixed with other aerobic and anaerobic bacteria in the infectious process, broader antimicrobial coverage is often necessary. Furthermore, because of the difficulty in recovering other fastidious anaerobic organisms, they may not be recovered even when cultures are taken.
Antimicrobial agents with broader coverage against anaerobic bacteria, including peptostreptococci, include cefoxitin, clindamycin, carbapenem (eg, imipenem, meropenem, ertapenem), tigecycline, the combination of a penicillin (eg, ticarcillin) with a beta-lactamase inhibitor (ie, clavulanate), and quinolones with anti-anaerobic activity (ie, moxifloxacin).19
An anti–gram-negative enteric agent is generally added to treat Enterobacteriaceae when treating intra-abdominal infections.
Penicillin is added to metronidazole to cover microaerophilic streptococci, peptostreptococci, Actinomyces species, and Arachnia species when treating intracranial and dental infections.
Penicillin is the antimicrobial of choice for bacteremia caused by non beta-lactamase producers; however, if other organisms may be involved in another site, broader coverage is needed.
A macrolide or amoxicillin is added to metronidazole to treat S aureus and aerobic streptococci in upper respiratory tract infections.
Doxycycline is effective against chlamydial and mycoplasmal infections and is added to most regimens when treating pelvic infections.
Oral therapy for peptostreptococci is often substituted for parenteral therapy. Oral agents include clindamycin, amoxicillin and clavulanate, and chloramphenicol.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
Interferes with synthesis of cell-wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms (beta-lactam).
10-28 million U/d IV q4h in 6 divided doses
50,000-100,000 U/d IV
Probenecid can increase effects; coadministration with tetracyclines can decrease effects
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in impaired renal function; may cause angioedema, pruritic rash, delayed rash, and gastrointestinal intolerance
Second-generation cephalosporin indicated for gram-positive cocci and gram-negative rod infections. Infections caused by cephalosporin- or penicillin-resistant gram-negative bacteria may respond.
2 g IV q6h
40 mg/kg/d IV q6h
Probenecid may increase effects; coadministration with aminoglycosides or furosemide may increase nephrotoxicity (closely monitor renal function)
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged use or repeated treatment; caution in previously diagnosed colitis
Second-generation cephalosporin indicated for management of infections caused by susceptible gram-positive cocci and gram-negative rods.
2 g IV q12h
20-40 mg/kg IV q12h for 5-10 d
Consumption of alcohol within 72 h of administration may produce disulfiramlike reactions; may increase hypoprothrombinemic effects of anticoagulants
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Reduce dosage by half with CrCl <10-30 mL/min and by one fourth with CrCl <10 mL/min; bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged or repeated therapy
Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
150-300 mg PO q6h
600 mg IV q8h
20-30 mg/kg/d PO divided q6h
25-40 mg/kg/d IV
Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption
Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis
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 severe hepatic dysfunction; no adjustment necessary in renal insufficiency; commonly associated with Clostridium difficile diarrhea; associated with severe and possibly fatal colitis
Treat bacteria resistant to beta-lactam antibiotics.
500 mg PO q8h
875 mg PO q12h
40 mg/kg/d PO q8h (tid formulation)
45 mg/kg/d PO q12h (bid formulation)
Coadministration with warfarin or heparin increases risk of bleeding
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Administer for a minimum of 10 d to eliminate organism and prevent sequelae (endocarditis, rheumatic fever); following treatment, perform cultures to confirm eradication of streptococci
Inhibit biosynthesis of cell-wall mucopeptide and are effective during stage of active growth. Contains 4.7-5 mEq of Na+/g.
3.1 g IV q4-6h
200-300 mg/kg/d IV q4-6h
Tetracyclines may decrease effects; high concentrations of ticarcillin may physically inactivate aminoglycosides if administered in same IV line; effects are synergistic when administered concurrently with aminoglycosides; probenecid may increase penicillin levels
Documented hypersensitivity; severe pneumonia, bacteremia, pericarditis, emphysema, meningitis, and purulent or septic arthritis should not be treated with oral penicillin during acute stage
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; exercise caution in hepatic insufficiency; perform urinalysis, BUN, and creatinine determinations during therapy, and adjust dose if values become elevated; monitor blood levels to avoid possible neurotoxic reactions
Binds to 50S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. Effective against gram-negative and gram-positive bacteria.
500 mg to 1 g IV q6h; not to exceed 4 g/d
80-100 mg/kg/d IV
Concurrently with barbiturates, serum levels may decrease while barbiturate levels may increase, causing toxicity; manifestations of hypoglycemia may occur with sulfonylureas; rifampin may reduce serum levels, presumably through hepatic enzyme induction; may increase effects of anticoagulants; may increase serum hydantoin levels, possibly resulting in toxicity; hydantoins may either increase or decrease levels
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
Use only for indicated infections; rarely, serious or fatal blood dyscrasias (aplastic anemia, hypoplastic anemia, thrombocytopenia, granulocytopenia) can occur; leukopenia, thrombocytopenia, and anemia are dose-related effects; adjust dose in severe liver or kidney dysfunction; caution in pregnancy at term or during labor because of potential toxic effects on fetus (gray baby syndrome)
For treatment of multiorganism infections in which other agents do not have wide-spectrum coverage or are contraindicated because of potential for toxicity.
500-750 mg IV q6h; not to exceed 3 g/d
15-25 mg/kg/d IV q6h; not to exceed 2 g/d
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; high doses can cause seizures and renal failure, especially in elderly patients and those with prior seizure disorders
Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis. Effective against most gram-positive and gram-negative bacteria. Has slightly increased activity against gram-negatives and slightly decreased activity against staphylococci and streptococci compared with imipenem.
1 g IV q8h
<3 months: Not recommended
>3 months: 40 mg/kg IV q8h
Probenecid may inhibit renal excretion, increasing levels
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
Pseudomembranous colitis and thrombocytopenia may occur, requiring immediate discontinuation of medication
Bactericidal activity results from inhibition of cell wall synthesis and is mediated through ertapenem binding to penicillin-binding proteins. Stable against hydrolysis by a variety of beta-lactamases, including penicillinases, cephalosporinases, and extended-spectrum beta-lactamases. Hydrolyzed by metallo-beta-lactamases.
1 g/d for 14 d if given IV and for 7 d if given IM; infuse over 30 min if given IV
Not established
Probenecid may reduce renal clearance and increase half-life but benefit is minimal and does not justify coadministration
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Pseudomembranous colitis may occur; seizures and adverse CNS reactions may occur; when using with lidocaine to administer IM, avoid inadvertent injection into blood vessel
Inhibits the A subunits of DNA gyrase, resulting in inhibition of bacterial DNA replication and transcription.
400 mg PO/IV qd
<18 years: Not recommended
>18 years: Administer as in adults
Antacids and electrolyte supplements reduce absorption; loop diuretics, probenecid, and cimetidine increase serum levels; NSAIDs enhance CNS stimulating effect
May increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT); ferrous sulfate decreases bioavailability (administer moxifloxacin 4 h prior or 8 h following ferrous sulfate); coadministration with drugs that prolong QTc interval (quinidine, procainamide, amiodarone, sotalol, erythromycin, tricyclic antidepressants) increase risk of life-threatening arrhythmia
Documented hypersensitivity; known Q-T prolongation; concurrent administration of drugs that cause Q-T prolongation
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
In prolonged therapy, periodically evaluate organ system functions (eg, renal, hepatic, hematopoietic); superinfections may occur with prolonged or repeated antibiotic therapy; fluoroquinolones have induced seizures in CNS disorders and caused tendinitis or tendon rupture
A glycylcycline antibiotic that is structurally similar to tetracycline antibiotics. Inhibits bacterial protein translation by binding to 30S ribosomal subunit, and blocks entry of amino-acyl tRNA molecules in ribosome A site. Complicated intra-abdominal infections caused by C freundii, E cloacae, E coli, K oxytoca, K pneumoniae, E faecalis (vancomycin-susceptible isolates only), S aureus (methicillin-susceptible isolates only), S anginosus group (includes S anginosus, S intermedius, and S constellatus), B fragilis, B thetaiotaomicron, B uniformis, B vulgatus, C perfringens, and P micros.
Infuse each dose over 30-60 min
100 mg IV once, then 50 mg IV q12h
Severe hepatic impairment (ie, Child Pugh class C): 100 mg IV once, then 25 mg IV q12h
<18 years: Not established
>18 years: Administer as in adults
Coadministration decreases warfarin clearance and increases warfarin Cmax and AUC (monitor aPTT and INR); coadministration of antibiotics with oral contraceptives may decrease contraceptive effect
Documented hypersensitivity
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in severe hepatic impairment (reduce dose); may adversely effect tooth development; may permit clostridial overgrowth, resulting in antibiotic-associated colitis; may have adverse effects similar to those of tetracyclines (eg, photosensitivity, pseudotumor cerebri, pancreatitis, antianabolic action)
Brook I. Anaerobic Infections. In: Diagnosis and Management. 4th Edition. New York: Informa Healthcare USA inc; 2007.
Finegold SM. Anaerobic Bacteria in Human Disease. Orlando, Fla: Academic Press; 1977.
Bourgault AM, Rosenblatt JE, Fitzgerald RH. Peptococcus magnus: a significant human pathogen. Ann Intern Med. Aug 1980;93(2):244-8. [Medline].
Bartlett JG. Anaerobic bacterial infections of the lung and pleural space. Clin Infect Dis. Jun 1993;16 Suppl 4:S248-55. [Medline].
Brook I. Recovery of anaerobic bacteria from clinical specimens in 12 years at two military hospitals. J Clin Microbiol. Jun 1988;26(6):1181-8. [Medline].
Martin WJ. Isolation and identification of anaerobic bacteria in the clinical laboratory. A 2-year experience. Mayo Clin Proc. May 1974;49(5):300-8. [Medline].
Brook I. Peptostreptococcal infection in children. Scand J Infect Dis. 1994;26(5):503-10. [Medline].
Murdoch DA. Gram-positive anaerobic cocci. Clin Microbiol Rev. Jan 1998;11(1):81-120. [Medline].
Jousime-Somers H, Summanen P, Citron DM, et al. Wadsworth-KTL Anaerobic Bacteriology Manual. 6th ed. Belmont, Calif: Star Publishing; 2002.
Araki H, Kuriyama T, Nakagawa K, Karasawa T. The microbial synergy of Peptostreptococcus micros and Prevotella intermedia in a murine abscess model. Oral Microbiol Immunol. Jun 2004;19(3):177-81. [Medline].
Brook I, Walker RI. Pathogenicity of anaerobic gram-positive cocci. Infect Immun. Aug 1984;45(2):320-4. [Medline].
Brook I. Anaerobic bacterial bacteremia: 12-year experience in two military hospitals. J Infect Dis. Dec 1989;160(6):1071-5. [Medline].
Saini S, Gupta N, Aparna, Seema, Sachdeva OP. Bacteriological study of paediatric and adult chronic suppurative otitis media. Indian J Pathol Microbiol. Jul 2005;48(3):413-6. [Medline].
Brook I. Microbiology of acute and chronic maxillary sinusitis associated with an odontogenic origin. Laryngoscope. May 2005;115(5):823-5. [Medline].
Blairon L, De Gheldre Y, Delaere B, Sonet A, Bosly A, Glupczynski Y. A 62-month retrospective epidemiological survey of anaerobic bacteraemia in a university hospital. Clin Microbiol Infect. Jun 2006;12(6):527-32. [Medline].
Song Y, Liu C, McTeague M, Vu A, Liu JY, Finegold SM. Rapid identification of Gram-positive anaerobic coccal species originally classified in the genus Peptostreptococcus by multiplex PCR assays using genus- and species-specific primers. Microbiology. Jul 2003;149:1719-27. [Medline].
Aldridge KE, Ashcraft D, Cambre K, Pierson CL, Jenkins SG, Rosenblatt JE. Multicenter survey of the changing in vitro antimicrobial susceptibilities of clinical isolates of Bacteroides fragilis group, Prevotella, Fusobacterium, Porphyromonas, and Peptostreptococcus species. Antimicrob Agents Chemother. Apr 2001;45(4):1238-43. [Medline].
Wexler HM, Finegold SM. Current susceptibility patterns of anaerobic bacteria. Yonsei Med J. Dec 1998;39(6):495-501. [Medline].
Brook I. Treatment of anaerobic infection. Expert Rev Anti Infect Ther. Dec 2007;5(6):991-1006. [Medline].
Malik NN, Goh D, McLean C, Huchzermeyer P. Orbital cellulitis caused by Peptostreptococcus. Eye. Jun 2004;18(6):643-4. [Medline].
Peptostreptococcus infection, anaerobic cocci, anaerobic gram-positive cocci, peptococci, peptostreptococci, Peptococcus, microaerophilic streptococci, Peptostreptococcus magnus, P magnus, Peptostreptococcus asaccharolyticus, P asaccharolyticus, Peptostreptococcus anaerobius, P anaerobius, Peptostreptococcus prevotii, P prevotii, Peptostreptococcus micros, P micros, Streptococcus anginosus, S anginosus, Streptococcus milleri, S milleri, Streptococcus constellatus, S constellatus, Streptococcus intermedius, S intermedius, Streptococcus morbillorum, S morbillorum, Peptostreptococcus hydrogenalis, P hydrogenalis, Staphylococcus aureus, S aureus, Streptococcus, Veillonella, Fusobacterium, Porphyromonas, Prevotella, Prevotella bivia, P bivia, Prevotella disiens, P disiens, Escherichia coli, E coli, Bacteroides fragilis, B fragilis
Itzhak Brook, MD, MSc, Professor, Department of Pediatrics, Georgetown University School of Medicine
Itzhak Brook, MD, MSc is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Armed Forces Infectious Diseases Society, Association of Military Surgeons of the US, Infectious Diseases Society of America, International Immunocompromised Host Society, International Society for Infectious Diseases, Medical Society of the District of Columbia, New York Academy of Sciences, Pediatric Infectious Diseases Society, Society for Ear, Nose and Throat Advances in Children, Society for Experimental Biology and Medicine, Society for Pediatric Research, Southern Medical Association, and Surgical Infection Society
Disclosure: Nothing to disclose.
Douglas A Drevets, MD, Assistant Professor, Department of Medicine, Section of Infectious Disease, Oklahoma University Health Sciences Center
Douglas A Drevets, MD is a member of the following medical societies: American Association of Immunologists, American Society for Microbiology, Central Society for Clinical Research, and Christian Medical & Dental Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Aaron Glatt, MD, Professor of Clinical Medicine, New York Medical College; President and CEO, Former Chief Medical Officer, Departments of Medicine and Infectious Diseases, New Island Hospital
Aaron Glatt, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Infectious Diseases Society of America, International AIDS Society, and Society for Healthcare Epidemiology of America
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.
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