eMedicine Specialties > Infectious Diseases > Bacterial Infections

Nocardiosis

Ronald A Greenfield, MD, Professor, Department of Internal Medicine, Section of Infectious Diseases, University of Oklahoma College of Medicine

Updated: Oct 14, 2008

Introduction

Background

Nocardiosis is an acute, subacute, or chronic infectious disease that occurs in cutaneous, pulmonary, and disseminated forms. Primary cutaneous nocardiosis manifests as cutaneous infection (cellulitis or abscess), lymphocutaneous infection (sporotrichoid nocardiosis), or subcutaneous infection (actinomycetoma). Pleuropulmonary nocardiosis manifests as an acute, subacute, or chronic pneumonitis, usually in immunocompromised hosts, although isolated cases have been reported in immunocompetent hosts. Disseminated nocardiosis may involve any organ; lesions in the brain or meninges are most common.

Pathophysiology

Members of the genus Nocardia are aerobic actinomycetes that are ubiquitous saprophytes in soil, decaying organic matter, and water. At least 30 species of the genus Nocardia have been identified, and at least 13 of these are reported to cause human disease. New Nocardia species continue to be identified.¹ Nocardia asteroides is responsible for most cases of Nocardia disease among humans in the United States; various other Nocardia species are dominant in other parts of the world. Nocardia species also cause infections in animals, including bovine mastitis and sporotrichoid nocardiosis in horses.

When observed microscopically, either in Gram-stained smears of clinical specimens or cultures or on histopathology in tissues, Nocardia organisms are branching, beaded, filamentous, gram-positive bacteria with a characteristic morphology to a trained observer.

High-power microscopic appearance of Nocardia. Image courtesy of CDC.

The cutaneous, lymphocutaneous, and subcutaneous forms of nocardiosis arise from local traumatic inoculation. These infections are not necessarily associated with immunocompromised host states, but dissemination from these sites of inoculation is more likely in immunocompromised hosts. Pleuropulmonary nocardiosis presumably arises from inhalation exposure. Disseminated nocardiosis results from hematogenous dissemination, usually from a pulmonary focus. Most persons with disseminated nocardiosis have underlying immunocompromising disease or are receiving immunosuppressive therapy.

Photomicrograph of tissue biopsy stained with Gomori methenamine silver demonstrating acute inflammatory response and organisms compatible with Nocardia.

Frequency

United States

In the 1970s, a survey estimated the incidence of nocardiosis in the United States at 500-1000 cases per year (0.4 cases per 100,000 population per year). However, with the increased prevalence of impaired cell-mediated immunity since then, the incidence of nocardiosis has likely also increased.³

Clusters of nocardiosis have been described in hospitalized patients, related to contaminated fomites from construction or contaminated hands of staff.¹

International

No reliable estimates on the international frequency of nocardiosis are available.

Mortality/Morbidity

Nocardiosis has a variable prognosis, depending on the site of infection, extent of infection, and underlying host factors.⁴

• Cure rates with appropriate therapy are approximately 100% in skin and soft-tissue infections.
• Ninety percent of pleuropulmonary infections can be cured with appropriate therapy.
• The cure rate in disseminated nocardiosis falls to 63%, while only half of patients with brain abscess can be cured with therapy.

Race

Nocardiosis has no apparent racial predilection.

Sex

Nocardiosis is more common in males than in females, with a male-to-female ratio of 3:1. This difference may be related to exposure frequency rather than a gender difference in susceptibility.

Age

All ages are susceptible to nocardiosis. The mean age at diagnosis is in the fourth decade of life.

Clinical

History

Clinical manifestations of nocardiosis depend on the site of infection.^{5,6,7,8,9,10,11,12,13,14,15,16}

• Primary cutaneous nocardiosis may present as cutaneous infection, lymphocutaneous infection, or subcutaneous infection.
  • Cutaneous nocardiosis generally manifests as either cellulitis or, more likely, single or multiple nontender erythematous nodule(s) at the site of traumatic inoculation. These nodules occasionally drain purulent material.
  • Lymphocutaneous nocardiosis manifests as similar lesions accompanied by ascending regional lymphadenopathy. The lymphadenopathy may also occasionally drain purulent material.
  • Nocardial species can cause mycetoma, a chronic, swollen, purulence-draining, subcutaneous infection of the extremities, typically encountered in tropical areas of the world.¹⁵
• Postoperative wound infections due to Nocardia species are rare.
• Traumatic inoculation nocardial arthritis has occurred but is rare. This presents as a subacute or chronic monarthritis, typically involving the knee.
• Traumatic inoculation nocardial endophthalmitis has also occurred in rare instances.
• Pulmonary disease is the predominant clinical finding in most patients with nocardiosis.^8,16
  • Pulmonary nocardiosis may be acute, subacute, or chronic.
  • Clinical manifestations include inflammatory endobronchial masses or localized or diffuse pneumonias, which may be accompanied by cavitation, abscess formation, pleural effusion, or empyema.
  • Symptoms in patients with nocardiosis are indistinguishable from those in patients with similar pulmonary infections of other microbial etiology. Cough with sputum production and fever are the dominant symptoms.
  • At least 40% of patients with disseminated nocardiosis have pulmonary infection; therefore, the clinical presentation may be dominated by the pulmonary symptoms.
• Patients with nocardiosis may present with deep abscess at any site, particularly in the lower extremities or the CNS. In patients with extra-CNS abscesses, fever and local symptoms predominate.
  • Up to 25% of nocardiosis cases (other than those involving mycetoma) involve the CNS. When occurring in isolation, CNS nocardiosis manifests as a slowly progressive mass lesion, with a host of specific neurologic findings related to the specific location of the abscess.
  • CNS nocardiosis is detected in 20-40% of disseminated nocardial infections. In two thirds of patients with CNS nocardiosis, clinical findings indicate abscess with or without meningitis, including fever, headache, stiff neck, and/or altered mental status.

Physical

The physical findings of nocardiosis also vary based on the site of infection.

• Patients with primary cutaneous nocardiosis present with cellulitis, cutaneous nodules, nodules with ascending lymphadenopathy, or with a mycetoma that is clinically indistinguishable from similar infections due to other pathogens.
• Patients with pulmonary nocardiosis present with findings of pulmonary consolidation with or without evidence of pleural effusions.
• The presentation of disseminated nocardiosis depends on the sites of infection.
  • Pulmonary findings frequently predominate.
  • Local findings associated with metastatic abscesses may be present at almost any site but are typically in the lower extremities. The combination of pneumonia and lower-extremity abscess is particularly suggestive of nocardiosis, although this is not seen exclusively in nocardiosis.
  • Patients with brain abscess may present with altered mental status, personality changes, or various localizing neurologic findings.
  • Patients with meningitis present with fever, altered consciousness, and meningismus.

Causes

Pulmonary and disseminated nocardiosis are clearly associated with immunocompromising conditions, with approximately 60% of cases of nocardiosis other than mycetoma occurring in individuals with some compromise of host defense systems. Conditions associated with an increased risk of pulmonary and disseminated nocardiosis include the following:

• Chronic pulmonary disease: Although pulmonary nocardiosis has been described in association with various chronic pulmonary diseases, patients with pulmonary alveolar proteinosis are at particular risk.
• Alcoholism
• Cirrhosis
• Lymphoreticular malignancy
• Solid-organ transplantation¹⁷
• Bone marrow or stem cell transplantation
• Long-term corticosteroid use or Cushing syndrome
• Systemic lupus erythematosus
• Systemic vasculitis
• Ulcerative colitis
• Sarcoidosis
• Renal failure
• Whipple disease
• Hypogammaglobulinemia
• Treatment with anti–tumor necrosis factor antibody
• HIV infection and AIDS: Nocardiosis in individuals with advanced HIV disease usually presents as a relentlessly progressive infiltrative pulmonary infection. The median CD4 count in patients infected with HIV who develop nocardiosis is approximately 50 cells/µL.¹³

Differential Diagnoses

Workup

Laboratory Studies

• The diagnosis of nocardiosis is established with culture of the causative organism from the infection site(s). Because nocardiae grow slower than common bacteria, the microbiology laboratory should always be notified when nocardiosis is clinically suspected. This is particularly true when sputum is the submitted specimen. Respiratory secretions, skin biopsy samples, and aspirates from abscesses are the most common specimens from which Nocardia species are identified. Direct smears or histopathologic stains of these specimens can be highly suspicious, as noted above. Nocardia species can usually be isolated in 3-5 days.
• Blood cultures are positive for Nocardia organisms in a minority of patients, but they always should be obtained when pulmonary or disseminated nocardiosis is suspected.
• Immunodominant antigens of Nocardia species have been identified and used in serological assays. However, no serologic technique or molecular technique is yet available for routine clinical use. Similarly, nucleic acid amplification assays have been described but are not available for routine clinical use.

Imaging Studies

• Plain chest radiography and, often, CT chest scanning are useful in evaluating pulmonary nocardiosis and in monitoring the course of the infection. However, no characteristic radiographic findings have been described. Radiographic findings may include irregular nodules (which may cavitate), reticulonodular or diffuse alveolar pulmonary infiltrates, lung abscess formation, and pleural effusion.
  
  

  

  Plain chest radiograph in a patient with nocardiosis. Image courtesy of Applied Radiology, Anderson Publishing, LTD.

  
  
• 
  
  

  

  Chest CT scan in a patient with pleuropulmonary nocardiosis. Image courtesy of Applied Radiology, Anderson Publishing, LTD.

  
  

• All patients with nocardiosis, except those with mycetoma, should undergo brain imaging with either CT scanning or MRI (likely preferred). Intracranial abscess is the most common abnormality found. Spread of intracranial abscesses to contiguous structures is particularly suggestive of nocardiosis.
  
  

  

  Brain CT scan in a patient with nocardial brain abscess. Image courtesy of Applied Radiology, Anderson Publishing, LTD.

  
  
• Localized symptoms other than pulmonary or CNS should be evaluated with appropriate site-specific imaging.

Other Tests

• If meningitis is suspected, cerebrospinal fluid (CSF) should be obtained for analysis unless this is contraindicated by mass effect on brain imaging. Nocardial meningitis typically results in findings typical of bacterial meningitis (ie, neutrophilic pleocytosis, hypoglycorrhachia, and a mildly elevated CSF protein level).

Procedures

• Biopsy of skin lesions or aspiration of deep abscesses may be required for diagnosis of nocardiosis.
• Similarly, in patients with pulmonary nocardiosis, bronchoalveolar lavage and/or transbronchial lung biopsy may be required if the microbial etiology is not definitively established based on examination and culture of expectorated sputum.

Histologic Findings

Suppurative infection with organisms of characteristic morphology and staining attributes is the typical histopathologic finding in nocardiosis. Granulomatous infection is occasionally encountered.

Treatment

Medical Care

• Protracted specific antimicrobial therapy is the mainstay of medical care for nocardiosis. Therapy is generally recommended for at least 6 months.¹
• In patients who require immunosuppressive therapy, such therapy can generally be continued while appropriate specific therapy for nocardiosis is administered.

Surgical Care

• For lesions outside the CNS, surgical management is the same as standard recommendations for other infections; that is, localized abscesses generally require prompt surgical therapy.
• In patients with nocardial brain abscesses, surgery should be performed if the lesions are large, if they are readily accessible, or if they progress beyond 2 weeks of antimicrobial therapy.⁹

Consultations

An infectious diseases specialist is recommended for coordinating protracted antimicrobial therapy. Depending on the infection site(s), consultation with a pulmonologist, thoracic surgeon, general surgeon, and/or neurosurgeon may be appropriate.

Diet

No specific dietary recommendations are warranted.

Activity

Activity can be as tolerated by the patient.

Medication

Sulfonamides have long been the first-line antimicrobial therapy for nocardiosis. Among the sulfonamides, sulfadiazine is generally preferred because of its CNS and CSF penetration. Trimethoprim-sulfamethoxazole (TMP-SMX) is considered by most an acceptable alternative to sulfadiazine. The addition of trimethoprim has not been shown convincingly to enhance the efficacy of sulfonamide. Therefore, this drug must be dosed to provide a dose of sulfamethoxazole equivalent to that given with sulfadiazine alone. TMP-SMX may be the preferred therapy when parenteral therapy is required because it is generally the only available parenteral sulfonamide agent.

In patients who are unable to take sulfonamides, therapy may be guided by in vitro susceptibility testing, although such testing for Nocardia species is difficult technically, poorly standardized, and not fully correlated with in vivo results of therapy. No data exist from comparative clinical trials to guide the choice among alternative therapies.

In Vitro Susceptibility Data¹

Alternative oral therapies include minocycline and amoxicillin/clavulanate. These may be used initially in mild to moderately severe disease or as sequential therapy after an induction course of parenteral therapy. Modern fluoroquinolones often have demonstrable in vitro activity against Nocardia species but have failed therapeutically.

Antibiotics

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

Sulfadiazine (Microsulfon)

Exerts its bacteriostatic action by competitive antagonism of paraaminobenzoic acid (PABA). Microorganisms that require exogenous folic acid and do not synthesize folic acid are not susceptible to the action of sulfonamides. In difficult cases, may be important to document peak serum levels (2 h after PO dose are 100-150 mg/L).

Dosing

Adult

6-12 g/d PO divided q4-6h

Pediatric

<2 months: 100 mg/kg/d PO divided q6h
>2 months: 75 mg/kg loading dose PO followed by maintenance dose of 120-150 mg/kg/d PO divided q4-6h

Interactions

Increases effect of oral anticoagulants and oral hypoglycemic agents; sulfadiazine effects are decreased when administered concurrently with PABA or PABA metabolites of drugs such as proparacaine, tetracaine, sunscreens, and procaine

Contraindications

Documented hypersensitivity

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

Caution in impaired renal or hepatic function or G-6-PD deficiency; dose should be adjusted in renal insufficiency; maintain adequate intravascular fluid volume to reduce the risk of crystalluria

Trimethoprim-sulfamethoxazole (Bactrim, Septra)

Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.

Dosing

Adult

10-15 mg/kg/d TMP and 50-75 mg/kg/d SMX PO/IV divided bid/qid

Pediatric

<2 months: Do not administer
>2 months: Not established

Interactions

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; 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

Contraindications

Documented hypersensitivity; megaloblastic anemia due to folate deficiency

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

Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBCs 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, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholism, elderly, anticonvulsant therapy, malabsorption syndrome); hemolysis may occur in G-6-PD deficient individuals; patients with AIDS may not tolerate or respond to TMP-SMX; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation

Meropenem (Merrem IV)

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-negative organisms and slightly decreased activity against staphylococci and streptococci compared to imipenem.

Dosing

Adult

1 g IV q8h

Pediatric

40 mg/kg IV q8h

Interactions

Probenecid may increase serum levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Pseudomembranous colitis and thrombocytopenia may occur, requiring immediate discontinuation of medication

Cefotaxime (Claforan)

Third-generation cephalosporin with gram-negative spectrum. Lower efficacy against gram-positive organisms. Arrests bacterial cell wall synthesis, which in turn inhibits bacterial growth.

Dosing

Adult

Moderate to severe infections: 1-2 g IM/IV q6-8h
Life-threatening infections: 1-2 g IM/IV q4h

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

Probenecid may increase levels; coadministration with furosemide and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Adjust dose in severe renal impairment; associated with severe colitis

Ceftriaxone (Rocephin)

Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin-binding proteins.

Dosing

Adult

1-2 g IV qd or divided bid; not to exceed 4 g/d

Pediatric

>7 days: 25-50 mg/kg/d IV; not to exceed 125 mg/d
Infants and children: 50-75 mg/kg/d IV divided q12h; not to exceed 2 g/d

Interactions

Probenecid may increase levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Adjust dose in renal impairment; caution in women who are breastfeeding and in people allergic to penicillin

Amikacin (Amikin)

For gram-negative bacterial coverage of infections resistant to gentamicin and tobramycin. Effective against Pseudomonas aeruginosa.
Irreversibly binds to 30S subunit of bacterial ribosomes and blocks recognition step in protein synthesis, which causes growth inhibition. Use patient's IBW for dosage calculation.

Dosing

Adult

10-15 mg/kg/d IV/IM divided bid

Pediatric

Administer as in adults

Interactions

Coadministration with other aminoglycosides, penicillins, cephalosporins, and amphotericin B increases nephrotoxicity; enhances effects of neuromuscular blocking agents; causes respiratory depression; irreversible hearing loss may occur with coadministration of loop diuretics

Contraindications

Documented hypersensitivity

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

Not intended for long-term therapy; caution in patients with renal failure (not on dialysis), hypocalcemia, myasthenia gravis, and conditions that depress neuromuscular transmission

Minocycline (Minocin)

Treats infections caused by susceptible gram-negative and gram-positive organisms, in addition to infections caused by susceptible Chlamydia, Rickettsia, and Mycoplasma.

Dosing

Adult

100 mg PO bid

Pediatric

<8 years: Not recommended
>8 years: 4 mg/kg PO initially, followed with 2 mg/kg q12h

Interactions

Bioavailability decreases minimally with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate

Contraindications

Documented hypersensitivity; severe hepatic dysfunction

Precautions

Pregnancy

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

Precautions

Photosensitivity may occur rarely; last one half of pregnancy through age 8 y can cause permanent discoloration of teeth; blue/black discoloration of the skin may occur with prolonged use

Amoxicillin and clavulanate (Augmentin)

Drug combination treats bacteria resistant to beta-lactam antibiotics. In children >3 mo, base dosing protocol on amoxicillin content. Because of different amoxicillin/clavulanic acid ratios in 250-mg tab (250/125) vs 250-mg chewable tab (250/62.5), do not use 250-mg tab until child weighs >40 kg.

Dosing

Adult

500-875 mg PO q8-12h

Pediatric

<40 kg: 20-40 mg/kg/d PO divided bid
>40 kg: Administer as in adults

Interactions

Coadministration with warfarin or heparin increases risk of bleeding

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Linezolid (Zyvox)

Prevents formation of functional 70S initiation complex, which is essential for bacterial translation process. Bacteriostatic against enterococci and staphylococci and bactericidal against most strains of streptococci. Used as alternative in patients allergic to vancomycin and for treatment of vancomycin-resistant enterococci.

Dosing

Adult

600 mg PO/IV q12h

Pediatric

Preterm neonate <7 days: 10 mg/kg PO/IV q12h
Term neonates-12 years: 10 mg/kg PO/IV q8h
>12 years: Administer as in adults

Interactions

May cause hypertension when used concomitantly with adrenergic agents including pseudoephedrine, sympathomimetic agents, vasopressor or dopaminergic agents (reduce dose of dopamine or epinephrine if concurrent use required); serotonin syndrome may occur if used concomitantly with serotonergic agents including tricyclic antidepressants, meperidine, dextromethorphan, trazodone, venlafaxine, and selective serotonin reuptake; may cause myelosuppression or pseudomembranous colitis inhibitors

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

Precautions

Has mild MAO inhibitor properties and has potential to have same interactions as other MAO inhibitors; caution in uncontrolled hypertension, pheochromocytoma, carcinoid syndrome, or untreated hyperthyroidism, and patients who are at increased risk for bleeding, have preexisting thrombocytopenia, receive concomitant medications that may decrease platelet count or function, or who may require > 2 wk of therapy (monitor platelet counts); unnecessary use may lead to development of resistance to drug; may cause peripheral or optic neuropathy or lactic acidosis with prolonged use (>4 wk)

Follow-up

Inpatient & Outpatient Medications

• Antimicrobial therapy for pulmonary or disseminated nocardiosis should be continued for 6-12 months and at least 1 month following resolution of all evidence of infection.
• Follow-up radiographic studies should be obtained to monitor treatment.
• Follow-up laboratory studies are required to monitor for adverse effects of prolonged antimicrobial therapy.

Deterrence/Prevention

Although not clearly established, prophylactic therapy for Pneumocystis jiroveci pneumonia (PCP) with TMP-SMX in patients with AIDS whose CD4 count is less than 200 cells/µL probably decreases the likelihood of nocardiosis. (For an excellent discussion of PCP prophylaxis, see the eMedicine article Prevention of Opportunistic Infections in Patients Infected With HIV.) Similarly, TMP-SMX prophylaxis in solid-organ transplant or hematopoietic stem cell transplant recipients may decrease the likelihood of nocardiosis. However, prophylaxis is not fully effective in either circumstance.

Patient Education

• Patients with nocardiosis must be educated about the need for protracted antimicrobial therapy.
• Patients with nocardiosis should be informed of the potential adverse effects of protracted antimicrobial therapy and which circumstances require reporting to their physician promptly.

Multimedia

Media file 1: High-power microscopic appearance of Nocardia. Image courtesy of CDC.

Media file 2: Photomicrograph of tissue biopsy stained with Gomori methenamine silver demonstrating acute inflammatory response and organisms compatible with Nocardia.

Media file 3: Plain chest radiograph in a patient with nocardiosis. Image courtesy of Applied Radiology, Anderson Publishing, LTD.

Media file 4: Chest CT scan in a patient with pleuropulmonary nocardiosis. Image courtesy of Applied Radiology, Anderson Publishing, LTD.

Media file 5: Brain CT scan in a patient with nocardial brain abscess. Image courtesy of Applied Radiology, Anderson Publishing, LTD.

References

1. Sorrell TC, Mitchell DH, Iredell JR. Nocardia species. In: Mandell, Bennett, Dolin. Principles and Practice of Infectious Diseases. volume 2. 6^th edition. Churchill Livingstone; 2005.

2. Beaman BL, Beaman L. Nocardia species: host-parasite relationships. Clin Microbiol Rev. Apr 1994;7(2):213-64. [Medline].

3. McNeil MM, Brown JM. The medically important aerobic actinomycetes: epidemiology and microbiology. Clin Microbiol Rev. Jul 1994;7(3):357-417. [Medline].

4. Smego RA Jr, Moeller MB, Gallis HA. Trimethoprim-sulfamethoxazole therapy for Nocardia infections. Arch Intern Med. Apr 1983;143(4):711-8. [Medline].

5. Boiron P, Locci R, Goodfellow M, et al. Nocardia, nocardiosis and mycetoma. Med Mycol. 1998;36 Suppl 1:26-37. [Medline].

6. Castro JG, Espinoza L. Nocardia species infections in a large county hospital in Miami: 6 years experience. J Infect. Apr 2007;54(4):358-61. [Medline].

7. Filice GA. Nocardiosis in persons with human immunodeficiency virus infection, transplant recipients, and large, geographically defined populations. J Lab Clin Med. Mar 2005;145(3):156-62. [Medline].

8. Hui CH, Au VW, Rowland K, et al. Pulmonary nocardiosis re-visited: experience of 35 patients at diagnosis. Respir Med. Jun 2003;97(6):709-17. [Medline].

9. Kilincer C, Hamamcioglu MK, Simsek O, et al. Nocardial brain abscess: review of clinical management. J Clin Neurosci. May 2006;13(4):481-5. [Medline].

10. Lederman ER, Crum NF. A case series and focused review of nocardiosis: clinical and microbiologic aspects. Medicine (Baltimore). Sep 2004;83(5):300-13. [Medline].

11. Lerner PI. Nocardiosis. Clin Infect Dis. Jun 1996;22(6):891-903; quiz 904-5. [Medline].

12. Matulionyte R, Rohner P, Uckay I, et al. Secular trends of nocardia infection over 15 years in a tertiary care hospital. J Clin Pathol. Aug 2004;57(8):807-12. [Medline].

13. Pintado V, Gomez-Mampaso E, Cobo J, et al. Nocardial infection in patients infected with the human immunodeficiency virus. Clin Microbiol Infect. Jul 2003;9(7):716-20. [Medline].

14. Saubolle MA, Sussland D. Nocardiosis: review of clinical and laboratory experience. J Clin Microbiol. Oct 2003;41(10):4497-501. [Medline].

15. Pilsczek FH, Augenbraun M. Mycetoma fungal infection: multiple organisms as colonizers or pathogens?. Rev Soc Bras Med Trop. Jul-Aug 2007;40(4):463-5. [Medline].

16. Martinez Tomas R, Menendez Villanueva R, Reyes Calzada S, et al. Pulmonary nocardiosis: risk factors and outcomes. Respirology. May 2007;12(3):394-400. [Medline].

17. Peleg AY, Husain S, Qureshi ZA, et al. Risk factors, clinical characteristics, and outcome of Nocardia infection in organ transplant recipients: a matched case-control study. Clin Infect Dis. May 15 2007;44(10):1307-14. [Medline].

18. Jodlowski TZ, Melnychuk I, Conry J. Linezolid for the treatment of Nocardia spp. infections. Ann Pharmacother. Oct 2007;41(10):1694-9. [Medline].

19. Sridhar MS, Gopinathan U, Garg P, et al. Ocular nocardia infections with special emphasis on the cornea. Surv Ophthalmol. Mar-Apr 2001;45(5):361-78. [Medline].

Keywords

nocardiosis, nocardiasis, Nocardia infection, pulmonary nocardiosis, acute nocardiosis, subacute nocardiosis, chronic nocardiosis, cutaneous nocardiosis, pulmonary nocardiosis, disseminated nocardiosis, primary cutaneous nocardiosis, lymphocutaneous nocardiosis, cutaneous nocardiosis, subcutaneous nocardiosis, CNS nocardiosis, cellulitis, sporotrichoid, actinomycetes, actinomycetoma, Nocardia asteroides, Nocardia brasiliensis, Nocardia farcinica, Nocardia nova, Nocardia transvalensis, Nocardia otitidiscaviarum, N asteroides, N brasiliensis, N farcinica, N nova, N transvalensis, N otitidiscaviarum, pleuropulmonary nocardiosis

Contributor Information and Disclosures

Author

Ronald A Greenfield, MD, Professor, Department of Internal Medicine, Section of Infectious Diseases, University of Oklahoma College of Medicine
Ronald A Greenfield, MD is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Central Society for Clinical Research, Infectious Diseases Society of America, Medical Mycology Society of the Americas, Phi Beta Kappa, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology
Disclosure: Pfizer Honoraria Speaking and teaching; Gilead Honoraria Speaking and teaching; Ortho McNeil Honoraria Speaking and teaching; Wyeth Honoraria Speaking and teaching; Abbott Honoraria Speaking and teaching; Astellas Honoraria Speaking and teaching; Cubist  Speaking and teaching

Medical Editor

Thomas J Marrie, MD, Chair, Professor, Department of Medicine, Division of Infectious Diseases, University of Alberta College of Medicine
Thomas J Marrie, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society for Microbiology, Canadian Infectious Disease Society, and Royal College of Physicians and Surgeons of Canada
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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