eMedicine Specialties > Infectious Diseases > Skin and Soft-Tissue Infections

Catscratch Disease

Stephen J Nervi, MD, Staff Physician, Department of Dermatology, University of Medicine and Dentistry of New Jersey, New Jersey School of Medicine
Rajendra Kapila, MD, MBBS, Associate Professor, Department of Medicine, UMDNJ, New Jersey Medical School; Roseanne A Ressner, DO, Fellow, Department of Infectious Diseases, Brooke Army Medical Center; Lynn L Horvath, MD, Clinical Assistant Professor of Medicine/Infectious Disease, University of Texas Health Science Center; Consulting Staff, Department of Infectious Disease, Brooke Army Medical Center; Joyce R Drayton, MD, Assistant Professor, Department of Internal Medicine, Division of Infectious Disease, Morehouse School of Medicine

Updated: Jan 26, 2009

Introduction

Background

Catscratch disease (CSD) is a bacterial infection caused by Bartonella henselae, a gram-negative rod. It is associated with a self-limited subacute solitary or regional lymphadenopathy. Patients with catscratch disease usually have a history of sustaining a scratch or bite from a cat or kitten.

Pathophysiology

The hallmark of catscratch disease is regional adenopathy proximal to the site of inoculation.

In immunocompetent patients, Bartonella infection causes a granulomatous and suppurative response. In immunocompromised patients, the response can be vasculoproliferative with neovascularization.

Bartonella is able to promote angioproliferation through adhesion A, which is observed in bacillary angiomatosis, peliosis, and verruga peruana.

Nine outer membrane proteins (OMP) of B henselae have been identified. The 43-kD OMP is a major protein capable of binding endothelial cells; further investigation is needed to clarify its role in the pathogenesis of catscratch disease.

Frequency

United States

An estimated 9.3 cases of catscratch disease per 100,000 population occur each year, with 22,000 cases annually and approximately 2,000 hospitalizations per year in the United States. The median age among individuals who develop catscratch disease is 15 years.

Most cases of catscratch disease occur in the fall and winter.

International

Catscratch disease has been reported worldwide; however, the international incidence is unknown. The disease is more prevalent in areas with warm humid climates.

Mortality/Morbidity

Catscratch disease is typically benign and self-limited in immunocompetent people. Symptoms usually resolve within 2-4 months.

Of affected patients, 5-25% experience a course complicated by involvement of sites other than regional lymph nodes. Patients may also present with constitutional symptoms.

Reynolds et al found that the catscratch disease–associated hospitalization rate in the United States was 0.60 per 100,000 patients younger than 18 years (95% CI, 0.49-0.72) and 0.86 per 100,000 patients younger than 5 years.¹

Patients older than 60 years are more likely to present with atypical features of catscratch disease.

Immunocompromised hosts may develop more serious forms of infection with B henselae or Bartonella quintana, such as bacillary angiomatosis, bacillary peliosis, or bacteremia.

Race

Catscratch disease is reported more commonly in whites.

Sex

Catscratch disease is reported more commonly in males, who account for approximately 60% of all cases.

Age

In a database analysis by Jackson et al, 55% of patients with catscratch disease were aged 18 years or younger.² More adults may develop catscratch disease than previously recognized, as most studies on the disease have focused primarily on pediatric populations. For additional information on pediatric catscratch disease, see the article Catscratch Disease in eMedicine’s Pediatrics: General Medicine volume.

Clinical

History

• Most patients with catscratch disease (CSD) report a history of exposure to cats (eg, recent cat scratch, bite, lick).
• Most persons with catscratch disease develop one or more 3- to 5-mm red-brown nontender papules the site of inoculation 3-10 days after the bacteria are introduced.
• Within 1-3 weeks, lymphadenopathy develops in the nodal group, draining the inoculum site. Lymphadenopathy often consists of a single node and can be moderately tender, with erythema and increased warmth of the overlying skin. Lymphadenopathy should resolve within 2-4 months but lasts up to 6-12 months in rare cases.
• Up to 10% of nodes may suppurate, requiring needle aspiration.
• Other symptoms of catscratch disease might include the following:
  • Malaise/fatigue (29.4%)
  • Fever (28%)
  • Anorexia (14.5%)
  • Headache (13%)
  • Sore throat (7%)
  • Arthralgia (2.5%)

Physical

• Fever may be present. In one series of 1200 cases of catscratch disease, only 9% of patients had a fever higher than 39°C.
• In 1-3 weeks, the inoculum-site lesions evolve through erythematous, vesicular, and papular-crusted changes.
• When patients present with painful adenopathy, the original site of inoculation may not be apparent.
• Nodes draining the site of inoculation enlarge within 1-3 weeks of contact with the kitten or cat. The upper extremities are the most common location (46% axillary and epitrochlear nodes), followed by the neck and jaw region (26% cervical and submandibular nodes), the groin (17.5% femoral and inguinal), preauricular region (7%), and clavicular region (2%). In 10-20% of cases, more than one region is affected. Node size is typically 1-5 cm but may enlarge to 8-10 cm.
• The following are forms of atypical catscratch disease, accounting for 5-25% of cases:
  • Parinaud oculoglandular syndrome: This syndrome affects 5-10% of patients with catscratch disease and is the most common form of atypical catscratch disease. Parinaud syndrome is characterized by ipsilateral preauricular lymphadenopathy and unilateral granulomatous conjunctivitis. Although this syndrome can be caused by other infections, B henselae is the most common etiologic agent.
  • Neuroretinitis: Unilateral painless vision loss occurs with central scotoma, optic disc swelling, or a macular star referred to as Leber neuroretinitis or idiopathic stellate neuroretinitis. The patient’s vision usually recovers completely within 1-3 months.
  • Acute encephalopathy: The predominant symptom is rapid progression of headache to lethargy and coma. Seizures and even status epilepticus can occur in these patients. The CSF may be normal or may have a lymphocytic pleocytosis. CT scanning and MRI findings are usually normal, and the course is generally self-limited without neurologic sequelae. However, persistent cognitive impairment and death have been reported in some cases. Myelitis, radiculitis, compression neuropathy, and cerebellar ataxia have been reported.
  • Bartonella endocarditis: This condition should be considered in patients with manifestations of endocarditis and negative blood culture results who have regular contact with cats. Possible risk factors include alcoholism, homelessness, and body louse infestation. Patients with Bartonella endocarditis often require valve replacement.
  • Visceral involvement: This usually entails systemic symptoms combined with multiple hypoechogenic-hypodense hepatic or splenic lesions. The liver is described as having a nutmeg appearance with stellate necrotizing granulomata on the histologic examination. This syndrome may develop in the absence of lymphadenopathy.
  • Bone and joint involvement: Osteolytic lesions may develop at various sites, and vertebral osteomyelitis with epidural abscess may occur in these cases. Catscratch disease–associated arthropathy may also occur.
  • Skin: Various skin manifestations occur in approximately 5% of patients with catscratch disease. These manifestations include nonspecific rashes, erythema nodosum, and leukocytoclastic vasculitis. For additional information on cutaneous manifestations of catscratch disease, see the article Catscratch Disease in eMedicine’s Dermatology volume.
• Immunocompromised patients (eg, those with cancer, persons who have undergone transplantation, and persons with HIV infection) may develop bacillary angiomatosis, bacillary peliosis, or persistent or relapsing fever with bacteremia.
  • Bacillary angiomatosis: This vasculoproliferative disease mostly involves the skin but can involve the other organs. It manifests as numerous brown to violaceous tumors of the skin and subcutaneous tissues. Without antibiotic therapy, the disease progresses with dissemination. The lesions are very similar to verruga peruana, the chronic form of Carrión disease (Oroya fever) from Bartonella bacilliformis infection.
  • Bacillary peliosis: This condition involves the solid internal organs with reticuloendothelial elements (usually the liver, but the spleen, abdominal lymph nodes, and bone marrow may also be involved). Vasculoproliferation of sinusoidal hepatic capillaries may result in blood-filled spaces in the liver.
  • Persistent or relapsing fever with bacteremia: This is another distinct clinical syndrome in immunocompromised individuals.

Causes

• Catscratch disease is usually caused by B henselae, formerly known as Rochalimaea henselae. In the genus Bartonella, B bacilliformis, B quintana, Bartonella elizabethae, Bartonella vinsonii, and Bartonella koehlerae are also responsible for human disease.
• In 1993, Dolan et al isolated B henselae from lymph nodes of patients with catscratch disease. Bartonella species are small pleomorphic, fastidious, facultative, gram-negative, and intracellular bacilli. Infection appears to confer lifelong immunity, as reports of recurrences of clinical catscratch disease are rare.³
• Domestic cats are the natural reservoir and vectors of B henselae. In cats, B henselae infection is asymptomatic. Fleas are believed to transmit the bacteria between cats, and seroprevalence in cats is highest in warm or humid climates, where prevalence of flea infestation among cats is higher.
• The transmission of B henselae from cats to humans occurs via a scratch or bite when the bacterium is present on the cat’s claws or oral cavity. Kittens younger than 12 months are 15 times more likely to transmit the disease than adult cats. Kittens are more likely to be bacteremic with B henselae and are more likely to scratch. Individuals who have been scratched or bitten by a kitten are 27 times more likely to become infected, and people who have at least one kitten with fleas are 29 times more likely to become infected than people whose animals were free of fleas.
• Human-to-human transmission has not been reported, and no data support transmission from fleas to humans.

Differential Diagnoses

Other Problems to Be Considered

Lymphoma
Histiocytic necrotizing lymphadenitis (Kikuchi-Fujimoto disease)
Nontuberculous mycobacterial infection
Bacterial adenitis
Cutaneous anthrax
Erysipelothrix rhusiopathiae infection
Viral infections: orf (parapoxvirus), cowpox (orthopoxvirus)

Workup

Laboratory Studies

• In addition to lymphadenopathy 10 mm or larger that persists for 3 or more weeks, 3 of 4 of the following criteria confirm the diagnosis of catscratch disease (CSD). In an atypical case, all 4 of the following criteria may be needed:
  • Contact with a cat, with or without a scratch mark or a regional inoculation lesion (skin papule, eye granuloma, mucous membrane)
  • Laboratory and radiology findings: Purified protein derivative (PPD) or serology negative for other infectious causes of adenopathy; sterile pus aspirated from node; polymerase chain reaction (PCR) assay positive for Bartonella; CT scan that reveals liver or spleen abscesses
  • Enzyme-linked immunosorbent assay (ELISA) positive for serum antibody to B henselae or indirect fluorescent antibody (IFA) assay serology test greater than 1:64; a 4-fold rise in titer between acute- and convalescent-phase specimens
  • Biopsy of node, skin, liver, bone, or eye granuloma showing granulomatous inflammation compatible with catscratch disease; positive Warthin-Starry silver stain finding
• IFA testing (96% sensitive) and ELISA (71% sensitive) are used to detect serum antibody to B henselae. An antibody titer that exceeds 1:64 suggests recent Bartonella infection. Paired acute and convalescent sera (drawn 6 wk apart) showing a 4-fold or greater increase is confirmatory. With IFA and ELISA tests, some cross-reactivity may occur between Bartonella species (especially B henselae and B quintana) and other bacteria such as Chlamydia psittaci.
• PCR is the most sensitive test and is able to differentiate between different Bartonella species, as well as subspecies and strains. However, this test is not readily available.
• A presumptive diagnosis of infection with catscratch disease bacilli can be made with Warthin-Starry and Brown-Hopps gram-stained tissues.
• Studies to rule out other common causes of regional adenopathy should be performed.

Imaging Studies

• In patients with disseminated catscratch disease and persistent high fever, abdominal pain, and severe systemic symptoms, abdominal CT scanning may be helpful. Multiple hypodense lesions of the liver and spleen are the major manifestations seen on such scans. These lesions resolve or calcify after weeks to months.

Other Tests

• Bartonella species are fastidious and difficult to culture. They can be isolated in either cell cultures or axenic media with blood-enriched agar plates.
• The catscratch disease skin test is no longer recommended. The test is less sensitive, less specific, poorly standardized, not readily available, not approved by the FDA, and considered by some to be unsafe.

Procedures

• If suppuration occurs, lymph node aspiration may be required. Avoid incision and drainage of nodes because chronic draining sinuses may result.

Histologic Findings

The primary inoculation lesion site consists of acellular areas of necrosis in the dermis with surrounding histiocytes and epithelioid cells. Lymphocytes and multinucleated giant cells can be found surrounding the histiocytes.

Findings in involved lymph nodes can be nonspecific but include lymphoid hyperplasia followed by stellate granulomas. The centers are acellular and necrotic with surrounding histiocytes and lymphocytes. Microabscesses can develop and become confluent at later stages.

Warthin-Starry staining of involved lymph nodes or primary inoculation skin sites may reveal chains, clumps, or clusters of pleomorphic B henselae bacilli.

Treatment

Medical Care

Most cases of catscratch disease (CSD) require only supportive and symptomatic care. Occasionally, lymph node aspiration is indicated for symptomatic relief. Antibiotics may be unnecessary for typical catscratch disease in immunocompetent individuals.

Consultations

Consultation with an infectious disease specialist should be sought in cases of atypical catscratch disease or in cases of catscratch disease in immunocompromised patients.

Medication

Analgesics are often used for localized discomfort.

Currently, only limited and/or anecdotal evidence supports the use of antibiotics in the treatment of typical catscratch disease (CSD) in immunocompetent hosts. B henselae is susceptible to many antibiotics in vitro. However, the susceptibility patterns do not predict efficacy in vivo.

Immunocompetent patients with mild-to-moderate catscratch disease may not need antibiotics. Needle aspiration and azithromycin may be considered in patients with extensive symptomatic lymphadenopathy.⁴

A prospective, randomized, double-blind, placebo-controlled study by Bass et al showed that azithromycin administered for 5 days decreased lymph node volume as measured by ultrasonography within the first month of treatment. No other differences in clinical outcome were noted.⁵

Bartonella is an intracellular bacterium and responds poorly to penicillin derivatives in vivo despite susceptibility in vitro.

Musso et al⁶ found that aminoglycosides were bactericidal and Ives et al⁷ showed that clarithromycin and azithromycin were also efficacious in catscratch disease. Gentamicin, trimethoprim-sulfamethoxazole, rifampin, and ciprofloxacin have been reported anecdotally as reasonable choices for antibiotic therapy.

A single treatment for all Bartonella -related diseases has not been identified, so treatment must be tailored to specific situations.

Immunocompromised patients tend to develop more-severe Bartonella infections and may require prolonged antibiotic treatment.

Some patients, usually who are immunocompromised, develop a Jarisch-Herxheimer–like reaction shortly after receiving antibiotic therapy.

Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Azithromycin (Zithromax)

Inhibits RNA-dependent protein synthesis at the chain elongation step; binds to the 50S ribosomal subunit resulting in blockage of transpeptidation.

Dosing

Adult

500 mg PO on day 1 followed by 250 mg PO on days 2-5

Pediatric

10 mg/kg PO on day 1 followed by 5 mg/kg PO on days 2-5

Interactions

May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine

Contraindications

Documented hypersensitivity to azithromycin, other macrolide antibiotics, or any component of the formulation

Precautions

Pregnancy

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

Precautions

Use with caution in patients with hepatic dysfunction; hepatic impairment with or without jaundice has occurred chiefly in older children and adults; it may be accompanied by malaise, nausea, vomiting, abdominal colic, and fever; discontinue use if these occur; may mask or delay symptoms of incubating gonorrhea or syphilis, so appropriate culture and susceptibility tests should be performed prior to initiating azithromycin; pseudomembranous colitis has been reported with use of macrolide antibiotics; use caution with renal dysfunction; prolongation of the QTc interval has been reported with macrolide antibiotics; use caution in patients at risk of prolonged cardiac repolarization; susp (IR and ER) are not interchangeable

Doxycycline (Doryx, Bio-Tab, Doxy, Periostat, Vibramycin)

Inhibits protein synthesis by binding with the 30S and possibly the 50S ribosomal subunit(s) of susceptible bacteria; may also cause alterations in the cytoplasmic membrane.

Dosing

Adult

100 mg PO bid

Pediatric

<8 years (<45 kg): Not established
>8 years (>45kg): Administer as in adults

Interactions

Antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate decrease bioavailability; can increase hypoprothrombinemic effects of anticoagulants; can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy; CYP3A4 inducers may decrease levels (barbiturates, carbamazepine, phenytoin)

Contraindications

Documented hypersensitivity to doxycycline, tetracycline, or any component of the formulation; children <8 y; severe hepatic dysfunction; pregnancy

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Do not use during pregnancy -- use of tetracyclines during tooth development may cause permanent discoloration of the teeth and enamel hypoplasia; prolonged use may result in superinfection, including oral or vaginal candidiasis; photosensitivity reaction may occur with this drug; avoid prolonged exposure to sunlight or tanning equipment; avoid in children <8 y

Ciprofloxacin (Cipro)

Inhibits DNA-gyrase in susceptible organisms; inhibits relaxation of supercoiled DNA and promotes breakage of double-stranded DNA.

Dosing

Adult

500 mg PO bid

Pediatric

<12 years: Not recommended
>12 years: 20-30 mg/kg/d PO bid

Interactions

Metal cations (aluminum, calcium, iron, magnesium, and zinc) bind quinolones in GI tract and inhibit absorption; may increase theophylline levels; hypoprothrombinemic effect of warfarin may be enhanced by ciprofloxacin; may decrease renal secretion of methotrexate, decrease phenytoin levels, decrease the metabolism of ropivacaine, increase effect of glyburide, and decrease metabolism of caffeine

Contraindications

Documented hypersensitivity to ciprofloxacin, any component of the formulation, or other quinolones

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

CNS stimulation may occur (tremor, restlessness, confusion, and, very rarely, hallucinations or seizures); use with caution in patients with known or suspected CNS disorder; prolonged use may result in superinfection; tendon inflammation and/or rupture have been reported with ciprofloxacin and other quinolone antibiotics; risk may be increased with concurrent corticosteroids, particularly in the elderly; discontinue at first sign of tendon inflammation or pain; adverse effects, including those related to joints and/or surrounding tissues are increased in pediatric patients; rare cases of peripheral neuropathy may occur; severe hypersensitivity reactions, including anaphylaxis, have occurred with quinolone therapy; quinolones may exacerbate myasthenia gravis, use with caution (rare, potentially life-threatening weakness of respiratory muscles may occur); caution in renal impairment; avoid excessive sunlight; may cause moderate-to-severe phototoxicity reactions

Rifampin (Rifadin, Rimactane, Rifadin IV)

Inhibits bacterial RNA synthesis by binding to the beta subunit of DNA-dependent RNA polymerase, blocking RNA transcription

Dosing

Adult

300 mg PO bid

Pediatric

10 mg/kg/d PO (maximum 600 mg/d)

Interactions

Potent CYP450 inducer with multiple drug-drug interactions; of note, decreases activity of protease inhibitors and nonnucleoside reverse transcriptase inhibitors; effectiveness of oral contraceptives impaired; would evaluate for possible drug interactions when placing a patient on rifampin

Contraindications

Documented hypersensitivity to rifampin, any rifamycins, or any component of the formulation; concurrent use of amprenavir, saquinavir/ritonavir (possibly other protease inhibitors)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use with caution and modify dosage in patients with liver impairment; observe for hyperbilirubinemia; discontinue therapy if this in conjunction with clinical symptoms or any signs of significant hepatocellular damage develop; since rifampin has enzyme-inducing properties, porphyria exacerbation is possible; use with caution in patients with porphyria; use with caution in patients receiving concurrent medications associated with hepatotoxicity (particularly with pyrazinamide), or in patients with history of alcoholism (even if ethanol consumption is discontinued during therapy)
Monitor for compliance and effects including hypersensitivity, thrombocytopenia in patients on intermittent therapy; urine, feces, saliva, sweat, tears, and CSF may be discolored to red/orange; do not administer IV form via IM or SC routes; restart infusion at another site if extravasation occurs; remove soft contact lenses during therapy since permanent staining may occur; regimens of 600 mg once or twice weekly have been associated with high incidence of adverse reactions including a flulike syndrome

Erythromycin (E.E.S., E-Mycin, Eryc, Erythrocin)

Inhibits RNA-dependent protein synthesis at the chain elongation step; binds to the 50S ribosomal subunit, resulting in blockage of transpeptidation

Dosing

Adult

500 mg PO qid

Pediatric

Erythromycin ethylsuccinate PO at 40 mg/kg total/d in 4 divided doses (max total daily dose 2 g/d)

Interactions

Increases levels of theophylline, warfarin, carbamazepine, cyclosporine, triazolam, alfentanil, bromocriptine, and statin drugs; may increase digoxin levels; serious arrhythmias have occurred with concurrent cisapride use

Contraindications

Documented hypersensitivity to erythromycin or any component of the formulation; preexisting liver disease (erythromycin estolate); concomitant use with ergot derivatives, pimozide, or cisapride

Precautions

Pregnancy

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

Precautions

Systemic: Use caution if hepatic impairment with or without jaundice has occurred; it may be accompanied by malaise, nausea, vomiting, abdominal colic, and fever; discontinue use if these occur; avoid using erythromycin lactobionate in neonates since formulations may contain benzyl alcohol, which is associated with toxicity in neonates; observe for superinfections; use in infants has been associated with infantile hypertrophic pyloric stenosis (IHPS); macrolides have been associated with rare QT prolongation and ventricular arrhythmias, including torsade de pointes; elderly persons may be at increased risk of adverse events, including hearing loss and/or torsade de pointes when dosage 4 g/d, particularly if concurrent renal/hepatic impairment

Follow-up

Further Inpatient Care

• Depending on severity, immunocompromised patients or patients with atypical manifestations of catscratch disease (CSD) may require hospitalization.

Further Outpatient Care

• Patients should be instructed to return for a follow-up evaluation to ensure resolution of lymphadenopathy in 2-4 months.
• Patients should return to care if their condition worsens or the lymph node starts to suppurate.

Prognosis

• Catscratch disease is usually self-limiting and carries an excellent prognosis.
• Complications and sequelae are rare in typical catscratch disease.
• Severe encephalitis and other disseminated forms of B henselae infection can lead to long-term sequelae.
• The disease is very rare.

Miscellaneous

Medicolegal Pitfalls

• Symptoms of catscratch disease (CSD) that do not resolve and persistent lymphadenopathy should be re-evaluated for other infectious etiologies and lymphoma.
• Failure to have the patient follow up for resolution of symptoms and to rule out other etiologies may result in adverse outcomes.
• If antibiotics are administered, monitor for adverse reactions. Dose adjustments may be necessary in children and in cases of renal insufficiency and hepatic disease.

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Keywords

catscratch disease, cat scratch disease, CSD, cat scratch fever, catscratch fever, Bartonella henselae infection, B henselae infection, Bartonella infection, bacillary angiomatosis, peliosis, verruga peruana, Parinaud's oculoglandular syndrome, Parinaud oculoglandular syndrome, Parinaud syndrome, neuroretinitis, acute encephalopathy, endocarditis, Bartonella endocarditis, subacute regional lymphadenitis, bartonellosis, catscratch antigen, CSA, atypical catscratch disease, atypical cat scratch disease, Rochalimaea henselae, R henselae

Contributor Information and Disclosures

Author

Stephen J Nervi, MD, Staff Physician, Department of Dermatology, University of Medicine and Dentistry of New Jersey, New Jersey School of Medicine
Stephen J Nervi, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Sigma Xi
Disclosure: Nothing to disclose.

Coauthor(s)

Rajendra Kapila, MD, MBBS, Associate Professor, Department of Medicine, UMDNJ, New Jersey Medical School
Rajendra Kapila, MD, MBBS is a member of the following medical societies: American College of Physicians, American Medical Association, Infectious Diseases Society of America, and Infectious Diseases Society of New Jersey
Disclosure: Nothing to disclose.

Roseanne A Ressner, DO, Fellow, Department of Infectious Diseases, Brooke Army Medical Center
Roseanne A Ressner, DO is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, Armed Forces Infectious Diseases Society, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Lynn L Horvath, MD, Clinical Assistant Professor of Medicine/Infectious Disease, University of Texas Health Science Center; Consulting Staff, Department of Infectious Disease, Brooke Army Medical Center
Lynn L Horvath, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Society for Microbiology, Armed Forces Infectious Diseases Society, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Joyce R Drayton, MD, Assistant Professor, Department of Internal Medicine, Division of Infectious Disease, Morehouse School of Medicine
Joyce R Drayton, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Preventive Medicine, American Holistic Medical Association, Infectious Diseases Society of America, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Medical Editor

John M Leedom, MD, Professor of Medicine, Keck School of Medicine, University of Southern California; Chief, Division of Infectious Diseases, Department of Internal Medicine, Los Angeles County, University of Southern California Medical Center
John M Leedom, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Society for Microbiology, Infectious Diseases Society of America, International AIDS Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

John W King, MD, Professor of Medicine, Section of Infectious Diseases, Louisiana State University Health Sciences Center; Director, Viral Therapeutics Clinics for Hepatitis; Consulting Staff, Department of Infectious Diseases, Overton Brook Veterans Affairs Medical Center
John W King, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Association of Subspecialty Professors, Infectious Diseases Society of America, and Sigma Xi
Disclosure: emedicine $50.00 author of chapter

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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