eMedicine Specialties > Dermatology > Mycobacterial Infections

Atypical Mycobacterial Diseases

Noah S Scheinfeld, MD, JD, FAAD, Assistant Clinical Professor, Department of Dermatology, Columbia University; Consulting Staff, Department of Dermatology, St Luke's Roosevelt Hospital Center, Beth Israel Medical Center, New York Eye and Ear Infirmary; Private Practice

Updated: Mar 21, 2008

Introduction

Background

Investigators have defined 30 facultative saprophytes and entities that are acid-fast mycobacteria but do not cause tuberculosis or leprosy. These mycobacteria or atypical mycobacteria (ATM) exist in almost all habitats. The most common infection is the so-called case of fish tank granuloma, which is caused by Mycobacterium marinum. Mycobacterium avium-intracellulare is the most common etiology of systemic disease in humans. Other types of mycobacteria have been discussed in different eMedicine articles (see Mycobacterium Fortuitum, Mycobacterium gordonae, Mycobacterium Avium-Intracellulare Infection, and Mycobacterium Marinum Infection of the Skin. Other types of mycobacteria are discussed here.

Runyon proposed the following schema:

• Group 1 - Photochromogens (eg, Mycobacterium kansasii, M marinum, Mycobacterium simiae)
• Group 2 - Scotochromogens (eg, Mycobacterium scrofulaceum, Mycobacterium szulgai, Mycobacterium gordonae)
• Group 3 - Nonphotochromogens (eg, Mycobacterium malmoense, Mycobacterium xenopi, M avium-intracellulare)
• Group 4 - Fast growers (3-5 d) (eg, Mycobacterium fortuitum, Mycobacterium chelonae, Mycobacterium abscessus)

M chelonae is an atypical fast-growing mycobacteria that is a rare cause of human infection.

In 1996, Horsburgh¹ noted clinically important nontuberculous mycobacteria (NTMB), including M kansasii, M genavense, M marinum, M simiae, M scrofulaceum, M szulgai, M avium, M haemophilum, M intracellulare, M malmoense, Mycobacterium ulcerans, M xenopi, M abscessus, M chelonae, M fortuitum, and (rarely) Mycobacterium smegmatis.

Four clinical syndromes comprise nearly all cases: pulmonary disease, lymphadenitis, skin or soft tissue disease, and disseminated disease in AIDS. M avium and M intracellulare (known together as M avium-intracellulare complex) are the most common causes of pulmonary disease, lymphadenitis, and disseminated disease. All 4 clinical syndromes seem to be increasing in frequency, particularly in immunosuppressed hosts. Specific reservoirs of these organisms leading to human disease are still being found.

NTMB are acquired from the environment, but M abscessus is a rapidly growing mycobacterium found in soil and water throughout the world. Disease in patients who are immunocompetent usually consists of localized skin and soft tissue infections.

M kansasii occurs most commonly in Kansas, Texas, Illinois, England, and urban settings.

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

Infections with ATM usually occur in immunocompromised hosts due to host immunity and resistance factors. Pulmonary infections can occur in patients with impaired ventilation systems. These infections can also be introduced after surgery and through contaminated injections because ATM do not have the ability to pass through the mucosa or the integument.

Frequency

International

Cutaneous infections with ATM are rare in the United States and worldwide. They are much more common in immunocompromised hosts, in particular those with HIV or leukemia or those undergoing immunosuppressive therapy.

Mortality/Morbidity

ATM infections cause little mortality. They can cause morbidity, especially when they are not diagnosed and not treated effectively. Often times, cutaneous ATM infection can resolve on its own without intervention. In children, cervical lymphadenitis caused by ATM can result in facial nerve injury, and the incidence of hypertrophic scarring varies among the different treatments.

Race

No apparent difference in race exists on the course of ATM infection.

Sex

ATM infection is more common in men than in women. M kansasii infection is much more common in men than in women.

Age

ATM infections are more commonly reported in older patients. This probably relates to the decline in health in such patients (eg, older patients who have smoked have poorer pulmonary function).

• ATM diseases tend to affect adults and can rarely affect children. For example, a 6-year-old girl with a primary cutaneous form of M kansasii infection has been reported. She was successfully treated with surgical excision and oral erythromycin.
• The median age of patients with M kansasii infection is 43 years.

Clinical

History

Underlying diseases contribute to ATM infections, including pulmonary emphysema, diabetes mellitus, leukemia, collagen diseases, lung cancer, chronic kidney diseases, systemic lupus erythematosus (SLE),^2,3 carcinomatous pleurisy, bronchiectasis, and previously treated tuberculosis. For example, most patients with M malmoense infections are old people with lung disease. Cutaneous M chelonae infection occurred in a patient who underwent a liver transplant.

• Some patients give a history of surgery. Surgery can provide a portal of entry of such infections. Procedures include cosmetic liposuction,⁴ liposculpture,⁴ breast augmentation mammaplasty, or median sternotomy.
• In 2007, Sañudo et al⁵ described nontuberculous mycobacterial infection after mesotherapy in 15 patients.
• Breast implant infection with M fortuitum group was reported by Vinh et al⁶ ; it required removal of the implant and a prolonged course of antibiotics. After the infection resolved, a new implant was successfully placed.
• Infections with ATM following trauma have been reported.
• In 2007, Murdoch and McDonald⁷ reported M avium-intracellulare cellulitis occurring with septic arthritis after joint injection.
• Nosocomial disease has become increasingly important; pseudoepidemics associated with contaminated, automated endoscopic washing machines are the most recently described manifestation.
  • M chelonae has been found in the colonic mucous membranes, the respiratory tracts, and as a contaminant in the tap water used for diluting concentrated chlorhexidine. The organism happened to be isolated with the mucous membranes that were picked up while using the washed fiberscope in the colons of 6 patients.
  • These findings suggest that M fortuitum and M chelonae groups, in spite of the fact that they rarely cause infection, have a significant risk of infecting older patients (those >60 y) in general hospitals with various underlying diseases attributable to infections.
• Two patients were infected with M smegmatis after self-injection with a veterinary-grade anabolic steroid.
• Most patients with M kansasii infection have some alteration of their immune status, but disseminated infection is relatively uncommon.
• Patients can report systemic and constitutional symptoms that include productive cough/purulent sputum, hemoptysis, weight loss, weakness, fever, and night sweats.
• Injection abscesses due to M chelonei var abscessus have been reported in a patient with diabetes. M chelonae wound infections after plastic surgery using contaminated gentian violet skin-marking solution has also been reported.⁸ Infection with M abscessus associated with intramuscular injection of adrenal cortex extract has been reported.⁹ Skin lesions due to M chelonae subsp abscessus associated with injections of lidocaine (lignocaine) given by a bioenergetic (a practitioner of alternative medicine) in Colombia have been reported. Megaesophagus and pulmonary infection with rapidly growing mycobacteria have been reported.¹⁰ M chelonae often occurs after puncture wounds and is a community-acquired disease. Infection can occur from scratches; road traffic accidents; and other trauma, such nails or wire.
• A patient with M gordonae infection reported a rat bite.
• In 2003, Sungkanuparph et al¹¹ reported a retrospective study of a series of patients infected with rapidly growing mycobacteria in Ramathibodi Hospital (Bangkok, Thailand) from January 1993 to June 1999. The following was reported:
  • Eighteen patients had no underlying disease, and 2 were infected with HIV. Reported physical findings were lymphadenitis (7), skin and subcutaneous abscess (7), eye infection (4), pulmonary infection (1), and chronic otitis media (1). Sweet syndrome manifested in 4 of 7 patients with lymphadenitis. The organisms isolated included M chelonae/M abscessus group (17 cases) and M fortuitum group (3 cases).
  • The ATM were susceptible to amikacin, netilmicin, and imipenem. The M fortuitum group was susceptible to more antibiotics than the M chelonae/M abscessus group.
  • Histology findings demonstrated pathology that ranged from nonspecific to suppurative or caseous granulomas.
  • Antimicrobial susceptibility defined the clinical response, which was good. A combination of 2 or more drugs provided effective therapy. Surgical resection was performed in apposite cases to reduce the load of the organism. Surgery was almost always used in cases with infections involving pan-resistant ATM.
• Redboard et al¹²  noted 4 cases of M fortuitum complex furunculosis after pedicures (in Cincinnati, Ohio and northern Kentucky) that manifested as nonhealing furuncles on the lower leg.
• In 2007, Hoetzenecker et al¹³ described dissemination of a localized cutaneous infection with M chelonae in a patient undergoing immunosuppressive treatment.

Physical

The lesions of ATM infection manifest in a variety of fashions. They can manifest with lymphadenitis, especially cervical lymphadenitis. Multiple or isolated skin nodules can present in a linear distribution. In this way, ATM infections can resemble sporotrichosis. This section reviews case reports related to specific types of ATM.

• M genavense has caused disseminated disease in patients who are HIV positive.
• In preschool-aged children who are immunocompetent, cervical lymphadenitis has been caused by M malmoense. It has caused cutaneous nodules on the hands.
• Cutaneous infection has been caused by M szulgai in a boy who underwent a bone marrow transplantation with marrow from a matched unrelated donor.¹⁴ M szulgai has caused cellulitis, draining nodules, and plaques. It has also been related to bursitis and pneumonia.
  • Only a handful of case reports on M szulgai have been published. A patient with SLE developed a cutaneous nodule caused by M szulgai. Another patient was on long-term corticosteroid therapy for sarcoidosis and exhibited multicentric, purely cutaneous infection.
  • Another patient had disseminated disease involving the skin, the bones, and the lungs and was shown to have a diminished proportion of T lymphocytes and a suppressed response to mitogens. Another patient had multiple inflammatory skin lesions and osteomyelitis and had been receiving prednisone therapy for desquamate interstitial pneumonitis. Finally, a patient aged 6 months with a carbuncle over the angle of the jaw has been reported.
• M scrofulaceum is a slow-growing atypical mycobacteria that is found in environmental water sources, tap water, and the human respiratory tract. It causes scrofula, a granulomatous cervical adenitis in children and pulmonary disease in adults. It is usually unilateral. Few reports of it causing skin disease exist. It has caused an isolated red nodule on the finger. In 1987, Murray-Leisure et al¹⁵ described a man with SLE who developed cutaneous abscesses due to M scrofulaceum. In 1982, Sowers¹⁶ reported a case in which M scrofulaceum caused sporotrichoid infection of the hands of a woman who regularly cleaned fish aquariums.
• A case series of disseminated M simiae infection with blood, pulmonary, and cutaneous localization has been reported.
  • From the 11-year period from 1983-1993, 137 clinical isolates of M simiae were obtained from 75 patients at a university hospital in San Antonio, Texas.
  • The sites of isolation of the 137 specimens varied. Of the isolates, 128 (93%) were from a pulmonary source, 4 (3%) were from a hematologic source, 1 (0.8%) was from a skin source, 1 (0.8%) was from urine, 1 (0.8%) was from a lymph node, 1 (0.8%) was from bone marrow, and 1 (0.8%) was from the brain.
  • Of 62 patients in this series, 6 (10%) had definite infection, 9 (14%) had probable disease, and 48 (76%) were thought to be colonized.
  • During the last 2 years of the study, 1992-1993, M simiae became the second most frequently isolated NTMB at this university hospital in San Antonio, Texas. The only ATM that infected more patients were of the M avium complex species.
• M smegmatis has been linked to cutaneous disease.
• M kansasii presents clinically in a manner most resembling tuberculosis. Most patients who present with localized primary cutaneous M kansasii infection are immunocompetent, whereas most patients with disseminated or pulmonary infection are immunocompromised. It may resemble cellulitis or sporotrichosis.
  • M kansasii flexor tenosynovitis caused the development of carpal tunnel syndrome.¹⁷ The diagnosis was made from synovial tissue specimens. It has also caused granulomatous synovitis and bursitis.
  • M kansasii infection has been limited to the skin in a patient with AIDS with intracutaneous abscess formation and regional lymph node enlargement.
  • M kansasii infection has presented as cellulitis in a patient with SLE.
  • Cutaneous and mediastinal lymphadenitis due to M kansasii is reported.
  • M kansasii can cause septic arthritis.¹⁸ About 50 cases have been published. Risk factors include local trauma; local or systemic corticosteroid therapy; chronic skin psoriasis; and immunodepression, especially that due to HIV infection.
  • A clinical presentation similar to that expected in lupus profundus has been reported. Cutaneous M kansasii infection associated with a papulonecrotic tuberculid reaction¹⁹ and ulcerative perineal lesions²⁰ due to M kansasii have been reported.
• Cutaneous M chelonae infection has occurred with a bilateral linear distribution that resembled sporotrichosis.²¹
• M gordonae has caused granulomatous synovitis and bursitis. It is sometimes called tap water scotochromogen. It has also caused granulomatous nodules on the back of the hand.
• M haemophilum can cause multiple, tender, cutaneous nodules. They can be purple and develop into ulcers or abscesses. They are often situated over the joints of the limbs. Wasting, tenosynovitis, and joint effusions can occur.
• M fortuitum, M chelonae, and M abscessus can present as painful papular lesions, epitrochlear adenopathies, and erythematous nodular and ulcerating skin nodules.
  • In people with end-stage renal disease who are on hemodialysis, ATM infection manifests as multiple abscesses on the lower legs.
  • A dermatosis with a linear distribution, which resembles the dermatitis caused by sporotrichosis, and is caused by M abscessus has been reported. Disseminated nodules are rare.
  • An infection due to ATM, acquired from a public bath, has been reported.²²
  • Cold abscesses can be present.
  • Erythema at the site of a puncture wound can also occur as an initial manifestation of an ATM infection.
  • Other findings present in patients infected with ATM can include osteomyelitis, lymphadenitis, and endocarditis.
  • ATM infections can result is keratitis and corneal ulcerations.

Causes

Exposure to contaminated water, injections, surgical procedures, and trauma has been linked to infection with ATM. Immunosuppression predisposes patients to infections with ATM.

• In a hospital in Taiwan,²³ 12 cockroaches (Periplaneta americana) were found to be infected with the following organisms:
  • Four with M kansasii
  • Three with M xenopi
  • Two with M gordonae
  • One with M haemophilum
  • One with M fortuitum
  • One with M avium
• Because cockroach infestation commonly occurs in the hospital environment, cockroaches might be implicated as a cause of hospital-acquired infections due to ATM.

Differential Diagnoses

Other Problems to Be Considered

In 2007, Perrin²⁴ described a patient with AIDS and a cutaneous M avium-intracellulare infection mimicking histoid leprosy.

Workup

Laboratory Studies

• The optimal way to diagnosis ATM is by performing a culture of tissue. This should be performed at multiple temperatures 25°, 37°, and 42° to ensure that the cultures grow out all possible pathogens.
• The development of DNA fingerprinting technology, especially pulsed-field gel electrophoresis, has been suggested as a diagnostic tool. Polymerase chain reaction has been used to aid in diagnosing these conditions.

Imaging Studies

• In 1999, Erasmus et al²⁵ noted that the radiologic manifestations of pulmonary ATM infection are protean and include consolidation, cavitation, fibrosis, nodules, bronchiectasis, and adenopathy.
  • Pulmonary ATM infection has 5 distinct clinicoradiologic manifestations: classic infection, nonclassic infection, nodules in patients who are asymptomatic, infection in patients with achalasia, and infection in patients who are immunocompromised. Although classic ATM infection may be indistinguishable from active tuberculosis, it is usually more indolent.
  • The characteristic radiologic features of nonclassic ATM infection include bronchiectasis and centrilobular nodules isolated to or most severe in the lingula and the middle lobe. In patients with acquired immunodeficiency syndrome, mediastinal or hilar adenopathy is the most common radiographic finding.

Other Tests

• The purified protein derivative test result is usually negative in infections with ATM.

Procedures

• A biopsy of the skin, the cervical nodes, and the lung can be used to diagnose ATM. The tissue obtained can be used for cultures of the tissue and for histopathologic examination.

Histologic Findings

Histopathologic examination of tissue can reveal tuberculoid, palisading, and sarcoidlike granulomas; a diffuse infiltrate of histiocytic foamy cells; acute and chronic panniculitis; nonspecific chronic inflammation; cutaneous abscesses; suppurative granulomas; and necrotizing folliculitis. Suppurative granulomas are the most characteristic feature in skin biopsy specimens from cutaneous ATM infections. The evolution of the disease and the immunologic status of the host may explain this spectrum of morphologic changes.

Some authorities note severe inflammatory lesions involved with the dermis and the hypodermis; these can have 3 main histopathologic patterns: granulomatous nodular or diffuse inflammation with mixed granulomas, prevailing abscesses with mild granulomatous reaction, and deep dermal and subcutaneous granulomatous inflammation with no neutrophil component.

Treatment

Medical Care

• Infections with ATM can be treated with a variety of antibiotics. Some infections can be resistant, and proper sensitivities must be obtained.
• Effective treatment of M kansasii infection can usually be accomplished with a rifampin-based regimen, or a rifabutin-based regimen can be used for patients who are HIV seropositive and receiving antiretroviral therapy.
• Jousse-Joulin et al²⁶ described skin and joint infection by M chelonae treated with rescue treatment with interferon gamma.
• Han et al²⁷ analyzed clinical and microbiologic features of 115 cases involving rapidly growing mycobacteria isolated at the University of Texas M.D. Anderson Cancer Center from 2000-2005. Antimicrobial susceptibility test results demonstrated that M abscessus was the most resistant species and that Mycobacterium mucogenicum was most susceptible.

Surgical Care

• A combined therapeutic approach, including surgical drainage, debridement, and prolonged (>3 mo) treatment with combined antimicrobial agents, has been used in some cases of ATM.
• In some cases based on clinical assessment, successful treatment requires aggressive debridement of all infected subcutaneous tissues and skin.
• Split-thickness skin grafting has been successfully used to cover large wounds. Grafting did not appear to foster recurrent infection.

Consultations

Consultations with infectious disease specialists, surgeons, dermatologists, and pulmonary specialists may be necessary.

Medication

The drug of choice depends on the sensitivity of an organism. M kansasii is most susceptible to antituberculosis medications and can be treated with minocycline. M scrofulaceum is not sensitive to medications, and surgical removal is often required. Combinations of medications based on sensitivities should also be used. M szulgai is sensitive to medications. M haemophilum may be sensitive to p- aminosalicylic acid and rifampin or rifabutin. For M fortuitum and M abscessus, combinations of medications that include ciprofloxacin, clarithromycin, amikacin, cefoxitin, and tobramycin among others have been used.

Antimycobacterial agents

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

Isoniazid (Nydrazid, Laniazid)

Used in isolation for prevention of tuberculosis and in combination to treat tuberculosis and mycobacterial infections.

Dosing

Adult

300 mg PO/IV qd
15 mg/kg PO 2-3 times/wk; not to exceed 900 mg/d

Pediatric

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

Interactions

Higher incidence of isoniazid-related hepatitis can occur with alcohol ingestion on daily basis; aluminum salts may decrease serum levels (administer 1-2 h before taking aluminum salts); may increase anticoagulants effects with coadministration; may inhibit metabolic clearance of benzodiazepines; carbamazepine toxicity or isoniazid hepatotoxicity may result from concurrent use (monitor carbamazepine concentrations and liver function); coadministration with cycloserine may increase CNS adverse effects (eg, dizziness); acute behavioral and coordination changes may occur with coadministration of disulfiram; coadministration with rifampin after halothane anesthesia may result in hepatotoxicity and hepatic encephalopathy; may inhibit hepatic microsomal enzymes and increase toxicity of hydantoin

Contraindications

Documented hypersensitivity; previous isoniazid-associated hepatic injury or other severe adverse reactions

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 patients with history of liver disease in black or Hispanic women, in women in the postpartum period, or in patients >50 y because risk of drug-induced hepatitis is greatest in these populations; patients with malnutrition, diabetes, or alcoholism have increased risk of neuropathy; pyroxidine may be used concurrently to prevent neuropathy

Clarithromycin (Biaxin)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Dosing

Adult

500 mg PO bid

Pediatric

7.5 mg/kg PO q12h

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

Contraindications

Documented hypersensitivity; concurrent use of cisapride or pimozide; caution in severe liver or renal impairment

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

Advise patients to notify health care professionals if fever and diarrhea develop (diarrhea may be sign of pseudomembranous colitis); coadministration with ranitidine or bismuth citrate is not recommended with CrCl <25 mL/min; give half dose or increase dosing interval if CrCl <30 mL/min; superinfections may occur with prolonged or repeated antibiotic therapies

Streptomycin sulfate

Used in combination with other drugs in the treatment of MAI.

Dosing

Adult

1g IM qd initially, then decrease to 1 g 2-3 times/wk

Pediatric

20 mg/kg/d IM; not to exceed 1 g

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 may occur with other nephrotoxic drugs

Contraindications

Documented hypersensitivity; non–dialysis-dependent renal insufficiency

Precautions

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 patients who are obese, use ideal body weight to calculate dosage; caution in patients with myasthenia gravis and neonates because risk of neuromuscular blockade is increased; cross-sensitivity among aminoglycosides may occur

Ciprofloxacin (Cipro)

Used in combination with other agents in the treatment of MAI.

Dosing

Adult

500-750 mg PO bid

Pediatric

<18 years: Not recommended
>18 years: Administer as in adults

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

Contraindications

Documented hypersensitivity; children <18 y

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

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; cross-sensitivity among similar agents may occur

Rifabutin (Mycobutin)

Used for prevention of DMAI in patients with HIV.

Dosing

Adult

300 mg PO qd

Pediatric

Not established

Interactions

Decreases plasma concentration of methadone, verapamil, cyclosporine, digoxin, corticosteroids, oral anticoagulants, barbiturates, theophylline, quinidine, halothane, protease inhibitors, non-nucleoside reverse transcriptase inhibitors, oral contraceptives, ketoconazole, and chloramphenicol; toxicity increases when administered concurrently with indinavir, ketoconazole, itraconazole, ritonavir, erythromycin, or protease inhibitors

Contraindications

Documented hypersensitivity; white blood cell count <1000/µL or platelet count <50,000/µL

Precautions

Pregnancy

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

Precautions

Do not administer to patients with active tuberculosis; no evidence rifabutin is effective in prophylaxis against M tuberculosis; may give isoniazid and rifabutin concurrently in patients requiring prophylaxis against both M tuberculosis and M avium complex; perform hematologic studies periodically in patients receiving prophylaxis due to association with neutropenia and more rarely thrombocytopenia

Minocycline (Dynacin, Minocin)

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

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 with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy; tetracyclines can increase hypoprothrombinemic effects of anticoagulants

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 with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines; hepatitis or lupuslike syndromes may occur

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; blocks recognition step in protein synthesis; causes growth inhibition. Use IBW of patient for dosage calculation.

Dosing

Adult

15 mg/kg/d IV/IM divided bid/tid; not to exceed 1.5 g/d regardless of higher BW

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

D - Fetal risk shown in humans; use only 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

Para-aminosalicylate sodium (Sodium P.A.S.)

Bacteriostatic agent useful against M tuberculosis. Inhibits onset of bacterial resistance to streptomycin and isoniazid. Administer aminosalicylate sodium with other antituberculous drugs.

Dosing

Adult

14-16 g/d PO divided bid/tid

Pediatric

275-420 mg/kg/d PO tid/qid

Interactions

Oral absorption of digoxin may be reduced, causing a reduction in serum levels when administered concurrently with P.A.S; an increase in digoxin dosing may be necessary; a deficiency in vitamin B-12 (oral) may be induced because of P.A.S interference of its GI absorption; parenteral vitamin B-12 supplementation may be required

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 gastric ulcer and history of congestive heart failure; avoid situations in which excess sodium is potentially harmful

Cefoxitin (Mefoxin)

Second-generation cephalosporin indicated for gram-positive cocci and gram-negative rod infections. Infections caused by cephalosporin- or penicillin-resistant gram-negative bacteria may respond to cefoxitin. Higher doses for severe or serious infections required.

Dosing

Adult

1-2 g IV q6-8h; not to exceed 12 g/d

Pediatric

Infants and children: 80-160 mg/kg/d IV divided q4-6h

Interactions

Probenecid may increase effects; coadministration with aminoglycosides or furosemide may increase nephrotoxicity (closely monitor renal function)

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 insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy

Follow-up

Further Inpatient Care

• Patients with ATM can be treated as outpatients after appropriate surgery has been performed.

Further Outpatient Care

• Patients sometimes must take prolonged courses of antibiotics and must be aware of this.

Inpatient & Outpatient Medications

• Inpatient and outpatient medications include appropriate antibiotics based on sensitivities.

Deterrence/Prevention

• Patients should avoid contaminant material and injections with contaminated materials. Patients should also avoid contaminated water.

Complications

• Scarring and nerve damage can occur from long-standing untreated infections.

Prognosis

• The prognosis is good with proper medical and surgical treatment.

Patient Education

• Patients should avoid exposure to ATM by contaminated injections or materials.

Miscellaneous

Medicolegal Pitfalls

• Confusion of ATM with tuberculosis and overtreating it is a pitfall.
• Failing to diagnosis these infections, especially in children, and allowing them to progress is a pitfall.
• Allowing local infections to spread by not diagnosing this condition is a pitfall.
• Ali et al²⁸  described M fortuitum infection masquerading as an orbital mass.

References

1. Horsburgh CR Jr. Epidemiology of disease caused by nontuberculous mycobacteria. Semin Respir Infect. Dec 1996;11(4):244-51. [Medline].

2. Czelusta A, Moore AY. Cutaneous Mycobacterium kansasii infection in a patient with systemic lupus erythematosus: case report and review. J Am Acad Dermatol. Feb 1999;40(2 Pt 2):359-63. [Medline].

3. Hsu PY, Yang YH, Hsiao CH, Lee PI, Chiang BL. Mycobacterium kansasii infection presenting as cellulitis in a patient with systemic lupus erythematosus. J Formos Med Assoc. Aug 2002;101(8):581-4. [Medline].

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Keywords

atypical mycobacterial infection, ATM, AMI, nontypical mycobacterial infections, NTM, NTMI, Mycobacterium kansasii, M kansasii, Mycobacterium genavense, M genavense, Mycobacterium marinum, M marinum, Mycobacterium simiae, M simiae, Mycobacterium scrofulaceum, M scrofulaceum, Mycobacterium szulgai, M szulgai, Mycobacterium avium, M avium, Mycobacterium haemophilum, M haemophilum, Mycobacterium intracellulare, M intracellulare, Mycobacterium malmoense, M malmoense, Mycobacterium ulcerans, M ulcerans, Mycobacterium xenopi, M xenopi, Mycobacterium abscessus, M abscessus, Mycobacterium chelonae, M chelonae, Mycobacterium fortuitum, M fortuitum, Mycobacterium smegmatis, M smegmatis, Mycobacterium avium-intracellulare complex, M avium-intracellulare complex

Contributor Information and Disclosures

Author

Noah S Scheinfeld, MD, JD, FAAD, Assistant Clinical Professor, Department of Dermatology, Columbia University; Consulting Staff, Department of Dermatology, St Luke's Roosevelt Hospital Center, Beth Israel Medical Center, New York Eye and Ear Infirmary; Private Practice
Noah S Scheinfeld, MD, JD, FAAD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Optigenex Consulting fee Independent contractor

Medical Editor

Takeji Nishikawa, MD, Emeritus Professor, Department of Dermatology, Keio University School of Medicine; Director, Samoncho Dermatology Clinic; Managing Director, The Waksman Foundation of Japan Inc
Disclosure: Nothing to disclose.

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Director, Division of Dermatology, Scott and White Clinic; Director Dermatology Residency Training Program, Scott and White Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: 3M Pharmaceutical Grant/research funds Other; Graceway Pharmaceuticals Grant/research funds Other

Managing Editor

Jeffrey P Callen, MD, Professor of Medicine, Chief, Division of Dermatology, University of Louisville School of Medicine
Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and American College of Rheumatology
Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Electrical Optical Sciences Honoraria Consulting; Centocor Honoraria Consulting

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

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