eMedicine Specialties > Infectious Diseases > CNS Infections

Naegleria Infection

Subhash Chandra Parija, MBBS, MD, PhD, FRCPath, Director-Professor of Microbiology, Head of Department of Microbiology, Jawaharlal Institute, Postgraduate Medical Education and Research, India
Michael Stuart Bronze, MD, Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Barnett Gibbs, MD, Assistant Chief, Department of Clinical Trials, Walter Reed Army Institute of Research, Infectious Disease Service, National Capital Consortium; Assistant Professor of Medicine, Uniformed Services University of the Health Sciences; Diane H Johnson, MD, Assistant Director, Assistant Professor, Department of Internal Medicine, Division of Infectious Diseases, Winthrop-University Hospital, State University of New York at Stony Brook School of Medicine

Updated: Aug 3, 2009

Introduction

Background

Naegleria fowleri, a free-living ameba, is the causal agent of primary amebic meningoencephalitis (PAM), which is an acute, fulminant, and rapidly fatal CNS infection. PAM develops within several days of exposure to the contaminated water source and typically causes death within 1–2 weeks after admittance to the hospital. Few individuals survive the infection, partly because of its rapid onset and partly because of delayed diagnosis.

H&E-stained photomicrograph (magnified 125X) that shows the cytoarchitectural histpathology found in a case of primary amoebic meningoencephalitis (PAM), caused by Naegleria gruberi. Courtesy of the CDC/Dr. George R. Healy.

Bull reported the first case of N fowleri meningoencephalitis in the United States and coined the term primary amebic meningoencephalitis to distinguish it from the secondary meningoencephalitis caused by the intestinal ameba Entamoeba histolytica.

Naegleria species are ameboflagellates that are ubiquitous in soil and fresh or brackish water (lakes, rivers, ponds). In general, they are sensitive to environmental conditions such as aridity and pH extremes and cannot survive in sea water. In humans, they are found in the throat and nasal cavity. N fowleri is heat tolerant and is able to survive temperatures up to 45.8°C, preadapting the species to mammalian body temperature. Indeed, an incubation temperature of 45°C is routinely used to isolate N fowleri from water samples while suppressing growth of other amebae in the samples.

Although some 30 species of Naegleria have been recognized based on sequencing data, N fowleri is the only one that has been isolated in cases of amebic meningoencephalitis. Other Naegleria species (Naegleria australiensis, Naegleria italica, Naegleria philippinensis) have been found to be pathogenic in murine models of PAM but have not been identified in any human cases of the infection.¹ Because it grows best at somewhat elevated temperatures, N fowleri has been isolated from warm-water bodies, including man-made lakes and ponds, hot springs, and thermally polluted streams and rivers. In the United States, most N fowleri infections occur in the summer months.²

Life cycle of N fowleri

The life cycle of the ameba has 3 stages: trophozoite, a temporary flagellar stage known as ameboflagellate, and cyst.

The trophozoite is the vegetative or feeding stage of the ameba. In humans, this form is found in CSF or in tissue. It measures 10-20 μm in diameter and has a granular cytoplasm and a distinct ectoplasm. The trophozoite is characterized by a large central nuclear karyosome surrounded by a halo. Trophozoites are actively motile with the help of a broadly rounded, granule-free projection (ie, lobopodium) that originates from the surface. The projection helps to ingest bacteria, yeast cells, and cellular debris and may serve as an organelle of attachment. In tissue, trophozoites ingest red and white blood cells and cause tissue destruction. The trophozoite stage is the only one in which the ameba multiplies via binary fission.

The flagellate stage, also known as the ameboflagellate stage, is a temporary form of the ameba in which it neither feeds nor divides in culture. The ameba progresses to the ameboflagellate stage when the trophozoites form is exposed to a change in ionic concentration, such as in distilled water. During the ameboflagellate stage, the parasite is pear-shaped with a flagellar apparatus at the broader end. The flagellar apparatus consists of two terminal flagella, two basal bodies, microtubules, and a single striated rootlet, or rhizoplast. During the flagellated stage, the parasite may exhibit a rapid forward movement or a slowly spinning circular movement. It reverts back to the trophozoite stage within 24 hours.

The cystic stage represents the resistant form of the parasite, offering protection from desiccation and food shortage. The cyst is round, measures 7-10 μm in diameter, and is surrounded by a smooth double-layered 1-μm wall. The cyst consists of a single nucleus, contractile vacuoles, and food vacuoles. In stained preparations, only the vacuoles can be demonstrated as fine granules, but not the nucleus. Cysts are usually absent in clinical specimens, as the infection is so rapid and fatal that the patient typically dies before the trophozoites encyst.³

Pathophysiology

N fowleri infections in humans occur while swimming or diving in warm water contaminated with the parasite. Human-to-human transmission has never been reported. This parasite invades its host by penetrating the olfactory mucosa. During the initial stages of infection, the host response is initiated by the secretion of mucus that traps the trophozoites. Despite this response, some trophozoites are able to reach, adhere to, and penetrate the epithelium.

Moreover, it secretes a 37-kDa protein with mucinolytic activity.⁴ The gene nfa1 has been isolated from the free-living pathogenic amoeba. The protein Nfa1, which has cytolytic function, is located in pseudopodia and specifically in food-cups. N fowleri trophozoites are neurotrophic.⁵ They enter the nose and invade the olfactory mucosa and bulbs, penetrate the submucosal nervous plexus, invade the cribriform plate, and reach the subarachnoid space. Glucose and protein in the CSF support the growth and multiplication of the amebae. The high content of oxygen in the CSF and in the brain also facilitates growth of the amebae.

The trophozoites enter the ventricular system through the foramen of Luschka and Magendie and reach the choroid plexus. These then destroy the ependymal layer of the third, fourth, and lateral ventricles and produce acute ependymitis. They multiply by a process known as promitosis, during which an intact nuclear membrane (demonstrable on electron microscopy) is present. Only trophozoites are found in pathologic lesions in humans.

Most patients with PAM have a history of swimming or diving in a body of fresh water. In arid climates, some cases of PAM have been attributable to the inhalation of cysts. Trophozoites or cysts, which give rise to trophozoites after they excyst, penetrate the nasal mucosa and ascend along the olfactory nerves after phagocytosis by sustentacular cells of the neuroepithelium. Subsequently, they pass through the cribriform plate to invade brain tissue, with resultant purulent meningitis and encephalitis.

Host immunity

The course of N fowleri infection is fulminant and rapid, and patients with PAM die usually within a short period (5-10 d). Therefore, detectable levels of specific antibodies are not produced in the serum during the disease. The role of the cell-mediated immunity (CMI) in resistance to N fowleri infection is not fully understood.

Frequency

United States

Although isolation of N fowleri from the nares of asymptomatic individuals has been reported, PAM itself is rare in the United States. Only 31 cases were reported to the Centers for Disease Control and Prevention (CDC) from 1989-2002. In 2007, 6 cases of PAM were reported in the United States, and all were fatal.² From 1998-2007, 33 infections were reported in the United States. Thirty-one of the infected individuals had come into contact with recreational water, and two had come into contact with water from a geothermal (naturally hot) water supply.⁶

In a survey of 16 sites from Lake Anna in Virginia, a lake that is used to cool reactors at a nuclear power plant and for recreational activities, sampled during the summer of 2007, 9 were found to be positive for N fowleri by a nested polymerase chain reaction (PCR) assay. However, total ameba counts, inclusive of N fowleri, never exceeded 12/50 mL of lake water at any site. The presence of N fowleri was not found to correlate with the conductivity, dissolved oxygen, temperature, or pH of water. To date, no cases of PAM have been reported from this thermally enriched lake.⁷

In August 2005, two Oklahoma boys, aged 7 and 9 years, died of N fowleri infection after swimming in hot stagnant water in lakes in the Tulsa area. In August 2008, a 9-year-old boy died after acquiring N fowleri infection while swimming several times in Lake Elsinore in California. It was the first-ever confirmed case of N fowleri infection in Riverside County, California.⁸

International

The risk of infection has been estimated at one case per 2.6 million exposures to N fowleri. Approximately 200 cases of PAM have been reported worldwide, with some well-publicized outbreaks related to a single source. Most cases occur during the warm summer months in individuals who swim in freshwater pools or lakes.

Most worldwide cases have been reported in the United States. Other cases of N fowleri infection have been reported in Czechoslovakia, Australia, Mexico, New Zealand, Nigeria, Great Britain, and India. A total of 17 cases have been reported so far from different parts of India.⁹

Mortality/Morbidity

PAM carries a mortality rate of greater than 95%, with death occurring within 4-6 days. PAM was the reported cause of death in 23 people in the United States from 1995 to 2004 and in 6 in 2007. As of 2005, only 8 survivors of PAM had been reported, although N fowleri was not isolated in all of these cases. In the rare cases of survival, PAM was recognized very early, allowing for early institution of aggressive therapy. Most survivors have some residual physical or cognitive impairment. One recent survivor was an 8-month-old male infant from India who was treated vigorously and avoided any neurological deficit.¹⁰

Race

PAM has no racial predilection.

Sex

PAM has a male-to-female ratio of 3:1. Although PAM has no natural sexual predilection, the predominance in males is thought to be secondary to a greater risk of exposure due to behavioral factors.

Age

Most cases of PAM have been reported in children and young adults, presumably because of a greater exposure risk in these populations due to behavioral factors. In addition, the more porous cribriform plate in children and young adults is thought to place these individuals at a higher risk for disease.

Clinical

History

Most cases of primary amebic meningoencephalitis (PAM) involve a history of exposure to fresh warm water. Patients with PAM generally present with a history of bathing in a pond or lake 2-6 days prior to the onset of symptoms of meningeal irritation.

The index of suspicion should be increased in children and young adults who have a history of recently swimming in freshwater lakes, ponds, and pools. Isolated cases of PAM have followed bathing in tap and hot water.

Clusters of cases of PAM have been documented during the summer months when freshwater sources are warm. The higher temperature during the hot summer months facilitates the growth of N fowleri.

Physical

The physical signs of PAM are similar to those of bacterial meningitis, as follows:

• Fever
• Alteration in taste (ageusia) or smell (parosmia)
• Sudden-onset headache (usually frontal or bitemporal)
• High temperature (up to 40°C)
• Nausea, vomiting, or both
• Stiff neck
• Photophobia (later in the course of illness)
• Positive Kernig and Brudzinski signs
• Mental status changes
• Physical findings associated with encephalitis and eventual herniation (cranial nerve palsies, seizures, coma)
• Rapid onset of coma and death (within 2 wk)

Causes

PAM is caused by infection with the ameba N fowleri.

Differential Diagnoses

Other Problems to Be Considered

Bacterial meningoencephalitis
Viral meningoencephalitis
Cryptococcal meningoencephalitis in immunocompromised individuals

Workup

Laboratory Studies

The diagnosis of primary amebic meningoencephalitis (PAM) is always parasitic and is based on detection and identification of N fowleri trophozoites in the CSF or brain biopsy samples.

Specimens

The CSF is the specimen of choice for demonstration of the amebae.

Direct wet-mount microscopy

The CSF is centrifuged at 150 xg for 5 minutes. The supernatant is aspirated, and the sediment is suspended in the remaining fluid. A drop of sediment suspension is kept on a slide and mounted with a coverslip and is examined with compound light microscopy using 10X and 40X objectives. The specimen is best examined with phase contrast microscopy. This may show trophozoites with lobopodia extension and retraction.

The amebae are detected based on their active directional movements. Close observation is important because PAM can be diagnosed based on the observation of trophozoites; however, these have been confused with WBCs in reported cases. Cyst and flagellated stages are not found in CSF samples; if both cysts and trophozoites are found in CSF, it is highly suggestive of Acanthamoeba infection, ruling out Naegleria PAM.

Examination of stained CSF smear

CSF Gram stain findings are usually negative. RBCs are present. Wright-Giemsa–stained CSF may show trophozoites with large karyosome and may show a contractile vacuole. Direct fluorescent antibody staining of CSF smears is useful for demonstrating N fowleri in the CSF.

Culture

Naegleria species can be readily cultivated on either nonnutrient agar or agar media containing low concentrations of nutrients (eg, peptone 0.05%, yeast extract 0.05%, glucose 0.1%) in the presence of living or killed bacteria. In general, the bacteria of choice include nonmucoid strains of Klebsiella pneumoniae, Enterobacter species (Enterobacter aerogenes and Enterobacter cloacae), and Escherichia coli. After several days, the plate is microscopically inspected; Naegleria cysts are identified by trails left by migrating amebae in the lawn of the bacteria. Various molecular methods can be used for final confirmation of the identity of the species.

Serodiagnosis

Serologic testing has no role in the diagnosis of acute PAM, since little time is available from onset to death to mount an antibody response. In one survivor, detectable antibody persisted for more than 4 years.

Molecular diagnosis

PCR is available at some research sites using numerous primers. Molecular characterization of strains is also useful in tracking infections to a source and in recognizing potential risks for swimmers or bathers in particular locales. A species-specific DNA probe is available to identify N fowleri in environmental samples, followed by restriction fragment length polymorphism (RFLP) analyses of whole-cell DNA for confirmation. Epidemiologic typing of N fowleri was used in an analysis of the 5.8S rRNA gene and the internal transcribed spacer (ITS) of clinical isolates. In a study performed in the United States, a rapid, sensitive, and specific assay for the detection of N fowleri was developed using Mp2C15 probe in a nested PCR assay format.¹¹ A nested PCR assay has also been applied to detect the presence of the parasite in domestic water sources.¹²

Recently, flow cytometry has been used for the diagnosis of N fowleri infection.¹³

Histology

Both immunofluorescence and immunoperoxidase methods are useful for demonstrating N fowleri trophozoites in the histologic sections of the brain biopsy samples.

Imaging Studies

Head CT scanning yields nonspecific findings, showing a loss of the subarachnoid space and diffuse gray material enhancement.

Other Tests

CSF studies show the following:

• Sanguinopurulent or bloody CSF, showing a nonspecific polymorphonuclear (PMN) neutrophil–predominant neutrophilia
• Increased opening pressure
• PMN pleocytosis
• Elevated RBC count or frank hemorrhagic CSF
• Normal to low CSF glucose level
• Elevated protein level

Procedures

Lumbar puncture: Wet-mount examination of CSF is the main diagnostic tool in PAN.

Histologic Findings

N fowleri infection produces lesions mainly in the base of the brain, brain stem, and cerebellum. The olfactory mucosa and bulbs are the most commonly affected areas. The lesions consist of an acute necrotizing meningoencephalitis associated with moderately purulent exudates. Only trophozoites are found in the CNS lesions, not cysts.

Treatment

Medical Care

Early diagnosis, treatment, and aggressive supportive care hold the only chance for survival in patients with primary amebic meningoencephalitis (PAM). Very few survivors have been reported, with probably no more than a dozen survivors of an estimated 200 cases.

The best described and authenticated case of successful treatment of PAM involved a 9-year-old girl who was diagnosed early in the disease course and treated with intravenous and intrathecal amphotericin B, intravenous and intrathecal miconazole, and oral rifampin. The patient survived with minimal neurologic sequelae.¹⁴

The variables in determining the survival likelihood include how early the diagnosis is made and treatment initiated, the infectious dose of amebae, the virulence of the infecting strain, and the health of the patient.

Naegleria species are highly sensitive to the antifungal drug amphotericin B, and it has been used as the core antimicrobial in virtually all cases in which recovery occurred. Minimum amebacidal concentrations of amphotericin B were determined to be 0.02–0.078 µg/mL. Ultrastructural examination of amebae treated with amphotericin B revealed membrane distortions, including the nuclear envelope, rough and smooth endoplasmic reticula, and plasma membrane blebbing.

The macrolide antibiotic azithromycin is effective against Naegleria species in vitro and in murine models, but it has been reported to have poor CSF penetrance. Other antimicrobials that have been tested, mostly in vitro, include clotrimazole, itraconazole, fluconazole, and ketoconazole, with varying degrees of efficacy. Differences in reported drug sensitivities are due to the use of different N fowleri strains in different laboratories, which show variation to drugs. However, amphotericin B remains the drug of choice in the treatment of PAM.

Surgical Care

Upon evidence of increased intracranial pressure and possible herniation, emergent consultation with a neurosurgeon is warranted for ventriculostomy.

Consultations

Consult with an infectious disease specialist early in the course of illness.

Medication

The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications.

Amphotericin B offers the only clear evidence for a survival benefit in the treatment of primary amebic meningoencephalitis (PAM).

Antifungals

The mechanism of action usually involves inhibiting pathways (enzymes, substrates, transport) necessary for sterol/cell membrane synthesis or altering the permeability of the cell membrane (polyenes) of the fungal cell.

Amphotericin B (Amphocin, Fungizone)

Polyene antibiotic produced by a strain of Streptomyces nodosus; can be fungistatic or fungicidal. Binds to sterols, such as ergosterol, in the fungal cell membrane, causing intracellular components to leak with subsequent fungal cell death.

Dosing

Adult

25-300 mcg IT q48-72h and increase to 500 mcg as tolerated; alternatively, 0.25-1.5 mg/kg/d IV

Pediatric

25-100 mcg IT q48-72h and increase to 500 mcg as tolerated; alternatively, 0.5-0.7 mg/kg/d IV

Interactions

Antineoplastic agents may enhance the potential of amphotericin B for renal toxicity, bronchospasm, and hypotension; corticosteroids, digitalis, and thiazides may potentiate hypokalemia; the risk of renal toxicity is increased with cyclosporine

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Monitor renal function, serum electrolytes (eg, magnesium, potassium), liver function, CBC, and hemoglobin concentrations; resume the therapy at the lowest level (eg, 0.25 mg/kg) when the therapy is interrupted for more than 7 d; hypoxemia, acute dyspnea, and interstitial infiltrates may occur in neutropenic patients receiving leukocyte transfusions (separate time of amphotericin infusion from time of leukocyte transfusion); fever and chills are not uncommon after first few administrations of drug; rare acute reactions may include hypotension, bronchospasm, arrhythmias, and shock

Follow-up

Further Inpatient Care

Patients with primary amebic meningoencephalitis (PAM) should be monitored in the ICU.

Deterrence/Prevention

• Since N fowleri trophozoites and cysts are susceptible to chlorine, swimming pools should be adequately chlorinated. Case clusters have been reported in association with poorly chlorinated pools.
• Strongly consider closure of a site if a case of PAM occurs.
• Warm water is known to be more at risk of harboring these organisms. Thus, avoiding activities in bodies of warm fresh water, hot springs, and water around power plants, which may be thermally polluted, may be advisable. In addition, when taking part in such activities, it would be better to avoid the accidental entry of water into the nose.

Complications

PAM is typically fatal. Death is due to pulmonary edema or cardiorespiratory arrest within a week of appearance of the first symptoms. Persistent seizures may occur in patients who have otherwise recovered.

Prognosis

PAM carries a very poor prognosis, with a mortality rate of greater than 95%.

Miscellaneous

Medicolegal Pitfalls

Consider primary amebic meningoencephalitis (PAM) in all patients with meningoencephalitis, especially with an appropriate exposure history.

Multimedia

Media file 1: H&E-stained photomicrograph (magnified 125X) that shows the cytoarchitectural histpathology found in a case of primary amoebic meningoencephalitis (PAM), caused by Naegleria gruberi. Courtesy of the CDC/Dr. George R. Healy.

References

1. Schuster FL. Cultivation of pathogenic and opportunistic free-living amebas. Clin Microbiol Rev. Jul 2002;15(3):342-54. [Medline].

2. Centers for Disease Control and Prevention (CDC). Primary amebic meningoencephalitis--Arizona, Florida, and Texas, 2007. MMWR Morb Mortal Wkly Rep. May 30 2008;57(21):573-7. [Medline].

3. Parija SC, Jayakeerthee SR. Naegleria fowleri: a free living amoeba of emerging medical importance. J Commun Dis. Sep 1999;31(3):153-9. [Medline].

4. Cervantes-Sandoval I, Serrano-Luna Jde J, García-Latorre E, Tsutsumi V, Shibayama M. Mucins in the host defence against Naegleria fowleri and mucinolytic activity as a possible means of evasion. Microbiology. Dec 2008;154(Pt 12):3895-904. [Medline].

5. Jung SY, Kim JH, Song KJ, Lee YJ, Kwon MH, Kim K. Gene silencing of nfa1 affects the in vitro cytotoxicity of Naegleria fowleri in murine macrophages. Mol Biochem Parasitol. May 2009;165(1):87-93. [Medline].

6. Factsheet of Naeglaria fowleri. Available at http://www.cdc.gov/ncidod/dpd/parasites/Naegleria/factsht_naegleria.htm.

7. Jamerson M, Remmers K, Cabral G, Marciano-Cabral F. Survey for the presence of Naegleria fowleri amebae in lake water used to cool reactors at a nuclear power generating plant. Parasitol Res. Apr 2009;104(5):969-78. [Medline].

8. Naegleria fowleri. Wikipedia. Available at http://en.wikipedia.org/wiki/Naegleria_fowleri. Accessed 9/25/2008.

9. Parija SC. Amoebae. In: Textbook of Medical Parasitology: Protozoology & Helminthology. 3^rd ed. New Delhi, India: All India Publishers and Distributors; 2006:26-61.

10. Rai R, Singh DK, Srivastava AK, Bhargava A. Primary amebic meningoencephalitis. Indian Pediatr. Dec 2008;45(12):1004-5. [Medline].

11. Réveiller FL, Cabanes PA, Marciano-Cabral F. Development of a nested PCR assay to detect the pathogenic free-living amoeba Naegleria fowleri. Parasitol Res. May 2002;88(5):443-50. [Medline].

12. Marciano-Cabral F, MacLean R, Mensah A, LaPat-Polasko L. Identification of Naegleria fowleri in domestic water sources by nested PCR. Appl Environ Microbiol. Oct 2003;69(10):5864-9. [Medline].

13. Johnson PE, Deromedi AJ, Lebaron P, Catala P, Havens C, Pougnard C. High throughput, real-time detection of Naegleria lovaniensis in natural river water using LED-illuminated Fountain Flow Cytometry. J Appl Microbiol. Sep 2007;103(3):700-10. [Medline].

14. Vargas-Zepeda J, Gómez-Alcalá AV, Vásquez-Morales JA, Licea-Amaya L, De Jonckheere JF, Lares-Villa F. Successful treatment of Naegleria fowleri meningoencephalitis by using intravenous amphotericin B, fluconazole and rifampicin. Arch Med Res. Jan-Feb 2005;36(1):83-6. [Medline].

Keywords

Naegleria fowleri, Naegleria infection, N fowleri, primary amebic meningoencephalitis, PAM, purulent meningoencephalitis, N fowleri meningoencephalitis, Naegleria fowleri meningoencephalitis, Naegleria australiensis, Naegleria italica, Naegleria philippinensis, N australiensis, N italica, N philippinensis

Contributor Information and Disclosures

Author

Subhash Chandra Parija, MBBS, MD, PhD, FRCPath, Director-Professor of Microbiology, Head of Department of Microbiology, Jawaharlal Institute, Postgraduate Medical Education and Research, India
Subhash Chandra Parija, MBBS, MD, PhD, FRCPath is a member of the following medical societies: Indian Academy of Tropical Parasitology, Indian Association of Biomedical Scientists, Indian Association of Medical Microbiologists, Indian Association of Pathologists and Microbiologists, Indian Medical Association, Indian Society for Parasitology, National Academy of Medical Sciences, India, and Royal College of Pathologists
Disclosure: Jawaharlal Institute of Postgraduate Medical education & Research , Pondicherry , India Salary Employment

Coauthor(s)

Michael Stuart Bronze, MD, Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center
Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Association of Professors of Medicine, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

Barnett Gibbs, MD, Assistant Chief, Department of Clinical Trials, Walter Reed Army Institute of Research, Infectious Disease Service, National Capital Consortium; Assistant Professor of Medicine, Uniformed Services University of the Health Sciences
Disclosure: Nothing to disclose.

Diane H Johnson, MD, Assistant Director, Assistant Professor, Department of Internal Medicine, Division of Infectious Diseases, Winthrop-University Hospital, State University of New York at Stony Brook School of Medicine
Diane H Johnson, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Medical Women's Association, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Medical Editor

Daniel R Lucey, MD, MPH, Chief, Fellowship Program Director, Department of Internal Medicine, Division of Infectious Diseases, Washington Hospital Center; Professor, Department of Internal Medicine, Uniformed Services University of the Health Sciences
Daniel R Lucey, MD, MPH is a member of the following medical societies: Alpha Omega Alpha and American College of Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Thomas M Kerkering, MD, Chief of Infectious Diseases, Virginia Tech, Carilion School of Medicine, Roanoke, Virginia
Thomas M Kerkering, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Public Health Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Medical Society of Virginia, and Wilderness Medical Society
Disclosure: Nothing to disclose.

CME Editor

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.

Chief Editor

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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