AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Mycobacterium avium-intracellulare (MAI, or MAC) is the atypical Mycobacterium most commonly associated with human disease. It is primarily a pulmonary pathogen that affects individuals with immune compromise secondary to AIDS, hairy cell leukemia, and immunosuppressive chemotherapy. In this clinical setting, MAI has been associated with osteomyelitis; tenosynovitis; synovitis; and disseminated disease involving the lymph nodes, the CNS, the liver, the spleen, and the bone marrow. Although the prevalence of MAI infection has increased following the AIDS epidemic, it remains a rare cause of skin disease. However, MAI has been found to cause cutaneous disease in individuals with immunocompetence and immunosuppression.
 
The eMedicine Infectious Diseases article Mycobacterium Avium-Intracellulare may provide additional information. Medscape CME courses that might be of interest are Nontuberculous Mycobacteria: Update on Diagnosis and Treatment and Infectious Complications Associated With Immunomodulating Monoclonal Antibodies Used in the Treatment of Hematologic Malignancy.

Pathophysiology

MAI is an acid-fast atypical Mycobacterium. The organism is ubiquitous in the environment, and it is the most common bacteria isolated from patients with AIDS. MAI causes cutaneous disease by 3 separate mechanisms, which occur in unique patient populations with different morphologic manifestations. MAI infection may involve the skin primarily via posttraumatic inoculation, secondarily as a manifestation of disseminated Mycobacterium avium-intracellulare (DMAI) systemic disease, and by direct extension as a complication of cervical lymphadenitis.

Primary cutaneous MAI infection generally occurs in hosts who are immunocompetent after traumatic introduction into the soft tissue. Local disease ensues, manifested primarily as nodules that may progress to ulcers. One case report described primary MAI infection resulting in a clinical picture resembling lupus vulgaris.¹ Disseminated disease most commonly occurs in individuals who are immunosuppressed, and hematogenous seeding of the skin may result in a wide variety of skin lesions, including nodules and abscesses, panniculitis,² folliculitis, and acute disease with hemorrhagic pustules.

MAI is the most common cause of pediatric cervical adenitis. Skin involvement in this setting is not uncommon and includes sinus track and abscess formation. Cervical adenitis rarely involves deeper structures, but it may result in extensive superficial destruction with cosmetic deformity.

Frequency

United States

In the United States, MAI infection is considered a nonreportable infectious disease. The US Centers for Disease Control and Prevention surveillance data from Houston and Atlanta suggest an incidence of 1 case per 100,000 persons per year. In 1994, the highest incidence of DMAI, 37,000 cases, was measured. Because DMAI infection often occurs in association with HIV, this was not surprising. Thus, the 1994 peak was coincident with the peak in the AIDS epidemic. One case series revealed cutaneous involvement in 6 of 30 cases of DMAI infection.

US Centers for Disease Control and Prevention data suggest that the incidence of MAI infection may be decreasing as a result of highly active antiretroviral therapy and antimicrobial prophylaxis. Primary cutaneous MAI infection is rare, with 12 cases reported in the literature prior to 1997. The degree to which skin involvement occurs as a sequela of cervical adenitis has not been well studied; however, the literature suggests that the risk of skin involvement increases with advanced disease.

Mortality/Morbidity

• Primary cutaneous involvement does not usually result in systemic disease and most often occurs in otherwise healthy individuals; therefore, the prognosis is favorable because treatment is generally curative.
• Disseminated disease resulting in cutaneous MAI infection occurs in individuals with underlying illnesses and may significantly increase morbidity in this population. Controversy remains regarding the impact of DMAI infection on life expectancy in patients with AIDS. However, untreated DMAI infection in this population is clearly associated with an increased mortality rate.
• Cervical adenitis may cause local destruction of superficial structures and may result in cosmetic and functional impairment without treatment, but dissemination beyond the primary site is rare.

Race

No racial predilection has been noted.

Sex

No sexual predilection has been noted.

Age

Cutaneous MAI infection has been reported in all age groups.

• Cervical adenitis most commonly affects children. One chart review series of 47 children with cervical adenitis revealed a median age of 3 years when the MAI infection was diagnosed by doctors.
• Most case reports of primary cutaneous MAI infection have been in individuals aged 2-10 years, although adult cases have been described.
• A literature review of 8 cases of cutaneous MAI infection occurring secondary to disseminated disease found a median patient age of 22.2 years, with a range of 2-28 years.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

Any history of the introduction of a foreign object (eg, needle, splinter) should be sought if MAI infection is suspected.

• Cutaneous MAI infection should be suspected when an individual who is immunocompromised presents with obscure skin lesions. Additional symptoms, including fatigue, fever, diarrhea, weight loss, back or bone pain, shortness of breath, and/or cough may suggest disseminated disease.
• Patients with MAI cervical adenitis may present with an indolent course of a unilaterally expanding mass in the neck.
• Fever and other constitutional symptoms are generally absent.
• Primary cutaneous MAI infection is most often the result of traumatic inoculation, although a specific history of trauma is generally absent.
• Patients may describe the development of a single nodule or multiple nodules progressing over time into ulcerative lesions with or without serosanguineous exudates. Nodules may be tender.
• Cutaneous MAI infection in an HIV-positive patient mimicking histoid leprosy has been reported.³
• Henoch-Schönlein purpura associated with pulmonary MAI complex infection has been noted.⁴
• MAI can be associated with osteomyelitis. Primary nontraumatic MAI complex osteomyelitis of the distal phalanx has occurred.⁵ Multifocal osteomyelitis caused by nontuberculous mycobacteria in patients with a genetic defect of the interferon-gamma receptor has been noted.
• Subcutaneous and muscular abscesses due to MAI can occur as a manifestation of immune restoration in patients with AIDS.
• Murdoch and McDonald⁶ reported MAI cellulitis occurring with septic arthritis after joint injection.

Physical

• Examination in the case of disseminated disease may reveal a patient who is febrile with positive findings on lung examination and with findings of hepatosplenomegaly; lymphadenopathy; swollen, tender joints or focal neurologic deficits in the setting of painful, erythematous, indurated subcutaneous plaques; painful nodules and ulcers; folliculitis; or hemorrhagic pustules.
• Patients with cervical adenitis due to MAI usually present with enlarged submandibular or submaxillary nodes.
• Skin abscess and sinus tracks may be present. Sporotrichoid spread of cutaneous MAI complex infection can occur.⁷
• Primary cutaneous MAI infection generally results in painful subcutaneous nodules and ulcers that occur on the extremities and the trunk. Lesions may be present in multiple stages of development, and nodules have been described as both flesh colored and purple-red.

Causes

MAI is the most common organism isolated from patients with AIDS.

• Immunosuppression is a risk factor for disseminated disease.
• Patients who are immunosuppressed and at risk for DMAI disease include those on immunosuppressive agents after undergoing transplantation and patients with leukemia and lymphoma.
• No risk factors for primary cutaneous MAI infection or cervical adenitis are known.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to Be Considered

In 2007, Perrin⁸ noted a patient with AIDS and a cutaneous MAI infection mimicking histoid leprosy.

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• If MAI or DMAI infection is suspected, an HIV test should be performed. To evaluate the disease of MAI infection itself, a CBC count with differential should be performed. Disseminated disease can cause blood abnormalities. These abnormalities include anemia, leukocytosis, leukopenia, and hypogammaglobulinemia. Alkaline phosphatase levels can be elevated in persons with DMAI infection.
• A urinalysis should be performed.
• A liver function panel should be obtained.
• Cultures should be obtained. MAI is classified as a nonchromogen. It is slow growing, and colonies may not appear for 2-4 weeks. Culture sites should include cutaneous lesions, blood, sputum, and urine if DMAI disease is suspected. Stool cultures can be collected if diarrhea is present.
• Polymerase chain reaction studies of tissue may yield organism identification in 24 hours.

Imaging Studies

• Chest radiography is indicated to assess pulmonary involvement if disseminated disease is suspected. One series found that 8 of 11 cases of DMAI infection with cutaneous involvement had positive results on chest radiographs.

Procedures

• Biopsy should be performed. Tissue samples of cutaneous lesions may be obtained for histopathologic evidence of mycobacterial infection, and staining with Ziehl-Neelsen stain may reveal acid-fast bacilli.

Histologic Findings

A spectrum of histologic findings is present in skin infection with MAI. This is not surprising because tissue pathology varies with the stage of the disease and the host's immune status.

Granulomas are often present in tissue infected with MAI. Tuberculid, palisading, and sarcoidlike granulomas can be found in the context of a diffuse infiltrate of foamy histiocytic cells. Other nonspecific findings include panniculitis, chronic inflammation, cutaneous abscesses, necrotizing folliculitis, and suppurative granulomas.

Liou et al⁹ noted that spindle cell pseudotumors due to mycobacterial infection may occur in immunocompromised hosts. They reported a case of spindle cell pseudotumor in a 37-year-old man with AIDS. The tumor manifested as a firm nodule on the right arm. Histologically, the tumor was composed of spindle cells mixed with histiocytes and inflammatory cells. Ziehl-Neelsen stain revealed many acid-fast bacilli. The bacilli were identified as MAI. Culture and sequencing of the polymerase chain reaction product of the mycobacterial 65-kd heat-shock protein gene helped to establish the diagnosis. Immunohistochemically, the spindle cells stained with CD68, a marker found on active tissue macrophages.

In 2007, Shiomi et al¹⁰ reported a 58-year-old Japanese woman with systemic lupus erythematosus and interstitial pneumonia for 17 years. She had been treated with prednisolone and azathioprine, as well as insulin treatment for diabetes mellitus. She had a nodule in the deep dermis with extension into the subcutaneous fat tissue. The nodule was composed of spindle cells focally showing a vaguely storiform pattern, with focal foam cells, epithelioid histiocytes, and multinucleated giant cells. Ziehl-Neelsen staining showed numerous acid-fast bacilli within the spindle cells and epithelioid histiocytes, which were determined to be MAI after culture and polymerase chain reaction testing.

Staging

MAI is described as either localized or disseminated. A staging system is not applicable.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

A standard chemotherapy regimen has not been established for MAI infection because of significant resistance to antimycobacterial drugs. MAI is usually resistant to single-drug therapy and must be treated with multiple antitubercular medications. Sparfloxacin has good antimicrobial activity against several acid-fast bacteria and is expected to be an effective drug for treating mycobacteriosis.

• Cervical adenitis¹¹
• • The mainstay of treatment is surgical excision, with chemotherapy as primary treatment mainly reserved for cases with surgical contraindications. The relative infrequency of this condition has precluded clinical trials; therefore, treatment schedules are derived from anecdotal evidence.
  • Macrolides should be used in combination with rifamycin or ethambutol. Combination therapy with clarithromycin, ethambutol, and rifamycin has also been used.
• Disseminated MAI infection
• • Prophylaxis in patients who are immunosuppressed: Combination therapy for primary prevention is not currently recommended. Patients with HIV infection and CD4 counts of less than 100 should receive lifetime prophylaxis with rifabutin (300 mg qd).
  • Treatment: No agent is currently approved by the US Food and Drug Administration for the specific treatment of DMAI infection. Recommendations state that at least 2 drugs should be used simultaneously, one of which should be either azithromycin or clarithromycin. Many experts choose ethambutol as a second agent.
• Primary cutaneous MAI infection
• • Pediatric patients: In a 9-year-old patient, treatment with a combination of surgery and cycloserine (500 mg/d), isoniazid (200 mg/d), and clarithromycin (150 mg/d) following susceptibility testing resulted in complete clearance after 2 months of medical therapy, followed by surgical excision.
  • Adult patients: Streptomycin (1 g IM qd for 3 mo), isoniazid (300 mg/d), and rifampicin (600 mg/d for 9 mo) have been used as treatment.

Surgical Care

Surgical excision is the primary treatment for cervical adenitis, and it is often combined with chemotherapy for the treatment of primary MAI infections (see Medical Care above). Vuppalapati et al¹² noted MAI infection involving skin and soft tissues of the hand treated with radical debridement and reconstruction in addition to multidrug chemotherapy.

Consultations

• Consult an infectious diseases specialist to confirm the diagnosis and to assist with the selection of an appropriate treatment regimen based on local resistance patterns.
• Consult a general surgeon or an ear, nose, and throat (ENT) specialist for cervical adenitis.

Diet

No dietary restrictions are necessary.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

A standard chemotherapy regimen has not been established for MAI infection because of significant resistance to antimycobacterial drugs. The goals of pharmacotherapy are to eradicate the infection, reduce morbidity, and prevent complications.

Drug Category: Antibiotics

Therapy must cover all likely pathogens in the context of this clinical setting.

Drug Name	Ethambutol (Myambutol)
Description	Used for MAI infection in combination with other agents.
Adult Dose	15-25 mg/kg/d PO, 50 mg/kg PO 2 times/wk, or 25-30 mg/kg PO 3 times/wk
Pediatric Dose	<13 years: Not recommended >13 years: Administer as in adults
Contraindications	Documented hypersensitivity; optic neuritis
Interactions	Neurotoxicity may be additive with other neurotoxic agents
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Dose reduction required in renal and hepatic disease; can cause optic neuritis and peripheral neuritis; visual acuity monitoring is recommended; may precipitate gout by elevating serum uric acid levels

Drug Name	Isoniazid (Nydrazid, Laniazid)
Description	Used in isolation for prevention of tuberculosis and in combination for tuberculosis and MAI infections.
Adult Dose	300 mg PO/IV qd 15 mg/kg PO 2-3 times/wk; not to exceed 900 mg/d
Pediatric Dose	10-20 mg/kg PO; not to exceed 300 mg/d 20-30 mg/kg PO 2-3 times/wk; not to exceed 900 mg/d
Contraindications	Documented hypersensitivity; acute liver disease; previous hepatitis from isoniazid
Interactions	Aluminum-containing antacids may inhibit absorption; psychotic reactions and coordination difficulties may occur with disulfiram; BCG vaccine may not be effective during therapy; CNS toxicity is additive with other antitubercular agents; inhibits metabolism of phenytoin and may increase serum levels; concurrent use with carbamazepine is associated with increased risk of hepatotoxicity; severe reactions may occur with ingestion of foods containing tyramine
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 patients with history of liver disease, in black or Hispanic women, in women in the postpartum period, or in patients >50 y because the risk of drug-induced hepatitis is greatest in these populations; patients with malnutrition, diabetes, or alcoholism have an increased risk of neuropathy; pyroxidine may be used concurrently to prevent neuropathy

Drug Name	Clarithromycin (Biaxin)
Description	Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Adult Dose	500 mg PO bid
Pediatric Dose	7.5 mg/kg PO q12h
Contraindications	Documented hypersensitivity; concurrent use of cisapride or pimozide; caution in severe liver or renal impairment; dosage adjustment required if CrCl <30 mL/min
Interactions	May increase risk of arrhythmias with cisapride or pimozide; increases serum levels of carbamazepine, digoxin, or theophylline; increases levels of HMG-CoA reductase inhibitors; may increase risk of rhabdomyolysis; may increase effects of warfarin; may decrease effects of zidovudine; delavirdine increases blood levels
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	Advise patients to notify health care professionals if fever and diarrhea develop; caution regarding possibility of superinfection; zidovudine and clarithromycin

Drug Name	Streptomycin (Amikin, Garamycin)
Description	Used in combination with other drugs in the treatment of MAI infection.
Adult Dose	1g IM qd initially, then decrease to 1 g 2-3 times/wk
Pediatric Dose	20 mg/kg/d IM; not to exceed 1 g
Contraindications	Documented hypersensitivity; cross-sensitivity among aminoglycosides may occur
Interactions	Inactivated by penicillins and cephalosporins when coadministered to patients with renal insufficiency; possible respiratory paralysis with inhalation anesthetics or neuromuscular blockage; concurrent loop diuretic use increases risk of ototoxicity; increased incidence of nephrotoxicity with other nephrotoxic drugs
Pregnancy	D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions	Caution in renal impairment; blood level monitoring may be useful in preventing ototoxicity and nephrotoxicity; caution in geriatric and neonatal patients; in obese patients, ideal body weight should be used to calculate dosage; caution in patients with myasthenia gravis and neonates because risk of neuromuscular blockade is increased

Drug Name	Ciprofloxacin (Cipro)
Description	Used in combination with other agents in the treatment of MAI infection.
Adult Dose	500-750 mg PO bid
Pediatric Dose	<18 years: Not recommended >18 years: Administer as in adults
Contraindications	Documented hypersensitivity; cross-sensitivity among agents may occur; children <18 y; pregnancy
Interactions	Increases theophylline levels; administration with iron salts, bismuth salts, and zinc salts may decrease absorption; may increase effects of warfarin; serum levels may be decreased by antineoplastic agents; cimetidine may interfere with elimination; beneficial effects may be antagonized by nitrofurantoin; probenecid decreases renal elimination; may increase nephrotoxicity with cyclosporine; concurrent foscarnet may increase risk of seizures; concurrent therapy with corticosteroids may increase risk of tendon rupture; concurrent tube feeding impairs absorption; should not be taken with milk or yogurt alone because absorption may be decreased
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	Encourage patients to maintain a fluid intake of 1.5 L/d to prevent crystalluria; may cause dizziness or drowsiness; can result in pseudomembranous colitis; may cause photosensitivity, rash, tendonitis, or tendon rupture; hypersensitivity reactions include anaphylaxis and Stevens-Johnson syndrome

Drug Name	Rifabutin (Mycobutin)
Description	Used for prevention of DMAI infection in patients with HIV infection.
Adult Dose	300 mg PO qd
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; cross-sensitivity with other rifamycins; contraindicated in active tuberculosis and with concomitant ritonavir
Interactions	Increases metabolism of corticosteroids, disopyramide, quinidine, opiates, oral hypoglycemic agents, warfarin, estrogens, oral contraceptive pills containing estrogen, phenytoin, verapamil, fluconazole, theophylline, zidovudine, and chloramphenicol; ritonavir increases blood levels
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	May turn bodily fluids orange; can cause hepatitis, altered taste, dyspnea, skin rash/discoloration, hemolysis and neutropenia, and thrombocytopenia; may result in a flulike syndrome

Drug Name	Sparfloxacin (Zagam)
Description	Has excellent bioavailability and a large volume of distribution. Elimination is almost exclusively by hepatic metabolism and biliary excretion. Only an oral formulation is available.
Adult Dose	400 mg PO on day 1, followed by 200 mg/d PO for 10 d
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; children, unless benefits outweigh risks (as cystic fibrosis)
Interactions	Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations May increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Pregnancy	D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions	In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy; prolonged Q-T interval on ECG, and ventricular arrhythmias may occur

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Patients hospitalized with DMAI disease require inpatient care.
• Primary cutaneous MAI infection and cervical adenitis may be treated in an outpatient setting if patients are medically compliant.

Further Outpatient Care

• In cases of cervical adenitis and primary cutaneous MAI infection, follow-up care is required to assess for toxicity due to therapeutic agents and to monitor patients for possible disease recurrence or surgical complications.
• Patients with DMAI disease may need to be started on a prophylactic regimen for MAI infection prevention, and they may need to be monitored for recurrence.

In/Out Patient Meds

• See Treatment.

Deterrence/Prevention

• Medical prophylaxis with rifabutin (300 mg PO qd) is indicated for patients who are immunosuppressed.
• Prevention of primary cutaneous MAI infection has not been addressed in the literature because the disease is rare.

Complications

• Cervical adenitis can be complicated by local destruction of an overlying structure. Furthermore, the proximity to the trachea and the oropharynx may result in airway compromise and should be considered when evaluating patients with cervical adenitis.
• Patients receiving treatment for DMAI infection are often on multiple medications, and care should be taken to address possible interactions before initiating pharmacotherapy.

Prognosis

• The relationship between cutaneous lesions and mortality in DMAI infection is unknown.
• If untreated, DMAI disease is associated with an increased mortality rate in patients with AIDS.
• Primary cutaneous MAI infection and atypical Mycobacterium-induced cervical adenitis are responsive to combined surgical and medical treatment and may result in significant cosmetic deformity and/or scarring.

Patient Education

• Patients receiving prophylaxis with rifabutin should be educated regarding the purpose of the therapy and the potential adverse effects.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to consider cutaneous infection with MAI in patients with antibiotic-resistant cellulitis, in those with nonhealing nodules and ulcers, and in patients who are immunosuppressed with evidence of DMAI infection is a pitfall. Primary cutaneous infection is rare, but it does not necessarily mandate a workup for immunosuppression. Of note, isoniazid is a first-line agent in the treatment of M tuberculosis, but it is ineffective for DMAI infection.
• Failure to refer cases of cervical adenitis to a surgeon is a pitfall. Surgical referral for all cases of cervical adenitis is appropriate.
• MAI infection can be related to infliximab use.¹³

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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22. Inwald D, Nelson M, Cramp M, Francis N, Gazzard B. Cutaneous manifestations of mycobacterial infection in patients with AIDS. Br J Dermatol. Jan 1994;130(1):111-4. [Medline].
23. Kerlikowske KM, Katz MH, Chan AK, Perez-Stable EJ. Antimycobacterial therapy for disseminated Mycobacterium avium complex infection in patients with acquired immunodeficiency syndrome. Arch Intern Med. Apr 1992;152(4):813-7. [Medline].
24. Maltezou HC, Spyridis P, Kafetzis DA. Nontuberculous mycobacterial lymphadenitis in children. Pediatr Infect Dis J. Nov 1999;18(11):968-70. [Medline].
25. Marinho RO, Hutchison IL. Facial infection caused by Mycobacterium avium-intracellulare. J Oral Maxillofac Surg. Jun 2000;58(6):668-70. [Medline].
26. Masur H. Recommendations on prophylaxis and therapy for disseminated Mycobacterium avium complex disease in patients infected with the human immunodeficiency virus. Public Health Service Task Force on Prophylaxis and Therapy for Mycobacterium avium Complex. N Engl J Med. Sep 16 1993;329(12):898-904. [Medline].
27. Palenque E. Skin disease and nontuberculous atypical mycobacteria. Int J Dermatol. Sep 2000;39(9):659-66. [Medline].
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Article Last Updated: Mar 28, 2008