eMedicine Specialties > Infectious Diseases > Mycobacterial Infections
Mycobacterium Kansasii: Treatment & Medication
Updated: Mar 18, 2009
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Treatment
Medical Care
In general, M kansasii shows good in vitro susceptibility to rifampin, rifabutin, ethambutol, ethionamide, amikacin, streptomycin, clarithromycin, sulfamethoxazole, and ciprofloxacin. Rifampin-resistant strains are usually cross-resistant to rifabutin and, therefore, need separate susceptibility testing. In vitro susceptibility of isoniazid should be interpreted carefully, as it does not correlate with clinical outcome. In patients with no prior exposure to isoniazid, the drug is useful in the treatment of M kansasii infection, regardless of poor susceptibility results. Isoniazid susceptibility testing in laboratories is performed at lower concentrations (0.2 or 1 mcg/mL), which were designed for M tuberculosis, whereas M kansasii susceptibility requires a higher concentration (5 mcg/mL) . Pyrazinamide should not be used to treat M kansasii infection.
Patients in whom M kansasii infection is diagnosed should be treated with at least 3 drugs. The initial drug regimen should include rifampin, which has been shown to yield low failure rates (1.1%) and low long-term relapse rates (<1%).12 Rifampin is the cornerstone of treatment for M kansasii infection.
The 2007 ATS/IDSA guidelines for nontuberculous mycobacterial (NTM) infections recommend the following regimens for treatment of M kansasii infection:11
- First-line regimen: This consists of rifampin (10 mg/kg/day; maximum, 600 mg) plus ethambutol (15 mg/kg/day) plus isoniazid (5 mg/kg/day; maximum 300 mg) plus pyridoxine (50 mg/day), with the treatment duration continuing until sputum culture results are negative for 12 months.
- Alternative regimen: In patients with rifampin-resistant M kansasii disease, a 3-drug regimen should be used based on in vitro susceptibilities. These 3 drugs should include clarithromycin or azithromycin, moxifloxacin, ethambutol, sulfamethoxazole, or streptomycin.
Patients with M kansasii pulmonary infection should be closely monitored with routine clinical examinations and regular sputum for AFB smears and cultures for mycobacteria during the treatment period. The antimycobacterials can be stopped after AFB sputum results are negative for at least 12 months.
Patients with extrapulmonary and disseminated M kansasii infections should be treated in a similar manner to those with pulmonary disease.
Surgical Care
Surgical treatment is unnecessary in M kansasii infection, as it responds very well to antimycobacterial therapy.
Consultations
- Infectious disease specialist, especially in patients who are co-infected with HIV
- Pulmonologist if bronchoscopy with bronchoalveolar lavage and transbronchial biopsies are needed
- Dermatologist if skin is involved and biopsy is desired
- Thoracic surgeon if open-lung biopsy is necessary (rare)
Diet
A dietitian should evaluate malnourished patients.
Activity
Activity is not limited in patients with M kansasii infection and should be performed as tolerated.
Medication
The 2007 ATS/IDSA guideline for the treatment of M kansasii pulmonary disease recommends a regimen containing rifampin (600 mg), ethambutol (15 mg/kg) and isoniazid (300 mg) with pyridoxine (50 mg) daily for a total duration that includes at least 12 months of negative sputum culture results.
Patients with severe M kansasii infections and disseminated infections should also be treated with 3-drug regimens similar to that instituted for pulmonary infection . Rifampin should not be used concurrently with HIV protease inhibitors or nonnucleoside reverse transcriptase inhibitors (NNRTIs) because rifampin significantly enhances their metabolism. Rifabutin at a lower dose (150 mg/d) should be substituted for rifampin in patients receiving protease inhibitors.
Patients who are infected with rifampin-resistant M kansasii or who are intolerant to rifampin should be treated with a 3-drug regimen based on susceptibility results. For example, rifampin-resistant M kansasii can be treated with a combination of clarithromycin or azithromycin and moxifloxacin with ethambutol or sulfamethoxazole.
Most M kansasii isolates are pyrazinamide-resistant in vitro. Pyrazinamide is unacceptable as an alternative drug for M kansasii infection.
Other agents with useful activity against M kansasii include fluoroquinolones (moxifloxacin, sparfloxacin), aminoglycosides (streptomycin, amikacin), sulfamethoxazole, and linezolid.13
Antibiotics
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
Rifampin (Rifadin, Rimactane)
Considered the most important drug. Inhibits DNA-dependent bacterial but not mammalian RNA polymerase. Cross-resistance may occur. Treat for 6-9 mo or until 6 mo have elapsed from conversion to sputum culture negativity.
Adult
10 mg/kg/d PO/IV
Pediatric
10-20 mg/kg/d PO/IV
Induces microsomal enzymes, which may decrease effects of acetaminophen, PO anticoagulants, barbiturates, benzodiazepines, beta-blockers, chloramphenicol, PO contraceptives, corticosteroids, mexiletine, cyclosporine, digitoxin, disopyramide, estrogens, hydantoins, methadone, clofibrate, quinidine, dapsone, tazobactam, sulfonylureas, theophyllines, tocainide, and digoxin; blood pressure may increase with coadministration of enalapril; coadministration with INH may result in higher rate of hepatotoxicity than with either agent alone (discontinue 1 or both agents if alterations in LFT results occur)
Documented hypersensitivity
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
Obtain CBCs and baseline clinical chemistries prior to and throughout therapy; in liver disease, weigh benefits against risk of further liver damage; interruption of therapy and high-dose intermittent therapy are associated with thrombocytopenia that is reversible if therapy is discontinued as soon as purpura occurs; if treatment is continued or resumed after appearance of purpura, cerebral hemorrhage or death may occur
Isoniazid (INH, Laniazid)
Best combination of effectiveness, low cost, and minor adverse effects. First-line drug unless known resistance or another contraindication is present. Therapeutic regimens of <6 mo demonstrate unacceptably high relapse rate.
Coadministration of pyridoxine is recommended if peripheral neuropathies secondary to INH therapy develop. Prophylactic doses of 6-50 mg of pyridoxine daily are recommended.
Adult
5-10 mg/kg/d PO; usual dose 300 mg/d
Pediatric
5-10 mg/kg/d PO
Higher incidence of INH-related hepatitis can occur with alcohol ingestion on daily basis; aluminum salts may decrease INH serum levels (administer 1-2 h before taking aluminum salts); may increase anticoagulant effects with coadministration; may inhibit metabolic clearance of benzodiazepines; carbamazepine toxicity or INH hepatotoxicity may result from concurrent use (monitor carbamazepine concentrations, 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
Documented hypersensitivity; previous INH-associated hepatic injury or other severe adverse reactions
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 renal and hepatic impairment because severe or fatal hepatitis may develop; hepatotoxicity is increased in patients with preexisting alcoholic liver disease, pregnancy, and when used in combination with acetaminophen; periodic ophthalmologic examinations during INH therapy are recommended, even when visual symptoms do not occur; pyridoxine (10-50 mg/d) is recommended for prevention of peripheral neuropathy (especially in patients with poor nutrition, alcoholism, diabetes mellitus, uremia, and children with low milk or meat intake)
Ethambutol (Myambutol)
Impairs cell metabolism by inhibiting synthesis of 1 or more metabolites, which in turn, causes cell death. No cross-resistance demonstrated.
Mycobacterial resistance is frequent with previous therapy. Use in combination with second-line drugs that have not been administered previously.
Administer q24h until permanent bacteriologic conversion and maximal clinical improvement are observed. Absorption is not significantly altered by food.
Adult
15 mg/kg/d PO; not to exceed 2.5 g/d
Pediatric
<12 years: Not recommended, but has been used in tuberculosis with a small chance of ocular toxicity ( <5%)
>12 years: Administer as in adults
Aluminum salts may delay and reduce absorption (administer several h before or after EMB dose)
Documented hypersensitivity; optic neuritis (unless clinically indicated)
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Use only in children in whom visual acuity can be monitored; reduce dose in impaired renal function; has visual adverse effects that are reversible if promptly discontinued
Rifabutin (Mycobutin)
Ansamycin antibiotic derived from rifamycin S. Inhibits DNA-dependent RNA polymerase, preventing chain initiation, in susceptible strains of Escherichia coli and Bacillus subtilis but not in mammalian cells. If GI upset occurs, administer dose bid with food.
Adult
300 mg PO qd
Pediatric
5 mg/kg PO qd
Inducer of hepatic microsomal enzymes leading to reduction in plasma concentrations of many drugs, including barbiturates, chloramphenicol, corticosteroids, cyclosporine, digoxin, fluconazole, itraconazole, ketoconazole, methadone, PO anticoagulants, PO contraceptives, quinidine, halothane, theophylline, and verapamil; microsomal enzyme inhibitors (eg, fluconazole, protease inhibitors, clarithromycin) increase plasma rifabutin concentrations; in patients infected with HIV who are on protease inhibitors, rifabutin (150 mg/d) should be used as alternative for rifampin; has less effect than rifampin on metabolism of protease inhibitors
Documented hypersensitivity; WBC <1000/µL; platelet count <50,000/µL
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in patients with liver impairment; perform hematologic studies periodically because of association with neutropenia and, more rarely, thrombocytopenia
Clarithromycin (Biaxin)
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Adult
500 mg PO bid or 1 g PO qd if Biaxin XL
Pediatric
7.5 mg/kg PO bid
Toxicity increases with coadministration of fluconazole and pimozide; clarithromycin effects decrease and GI adverse effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, and HMG CoA-reductase inhibitors; serious cardiac arrhythmia may occur with coadministration of cisapride; plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmia and increase in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents
Documented hypersensitivity; coadministration of pimozide
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
Coadministration with ranitidine or bismuth citrate is not recommended with CrCl <25 mL/min; administer half dose or increase dosing interval if CrCl <30 mL/min; diarrhea may be sign of pseudomembranous colitis; superinfections may occur with prolonged or repeated antibiotic therapies
Streptomycin
Recommended by some experts during the initial phase, especially with positive sputum smear results and positive blood cultures. For treatment of susceptible mycobacterial infections.
Use in combination with other antituberculous drugs (eg, INH, EMB, rifampin).
Adult
15 mg/kg (usually 1 g) IM, 3-5 doses/wk
Pediatric
20-40 mg/kg/d IM for 7-14 d or until patient is afebrile for 5-7 d; not to exceed 0.75-1 g/d
Nephrotoxicity may be increased with aminoglycosides, amphotericin B, and loop diuretics
Documented hypersensitivity; non–dialysis-dependent renal insufficiency
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Narrow therapeutic index; not intended for long-term therapy; caution in renal failure (patient not taking dialysis); caution with myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission
Amikacin (Amikin)
Occasionally necessary during initial treatment phase, especially with positive sputum smear results. Irreversibly binds to 30S subunit of bacterial ribosomes. Blocks recognition step in protein synthesis. Causes growth inhibition. Use patient's IBW for dosage calculation.
Adult
500-1000 mg IV, 3-5 doses/wk
Pediatric
Administer as in adults
Coadministration with other aminoglycosides and amphotericin B increases nephrotoxicity; enhances effects of neuromuscular blocking agents; causes respiratory depression; irreversible hearing loss may occur with coadministration of loop diuretics
Documented hypersensitivity; renal insufficiency
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 (patient not taking dialysis), hypocalcemia, myasthenia gravis, and conditions that depress neuromuscular transmission
Moxifloxacin (Avelox)
Inhibits bacterial DNA synthesis and growth. Activity is similar to that of ciprofloxacin and levofloxacin.
Adult
400 mg PO/IV qd for 10 d
Pediatric
<18 years: Not recommended
>18 years: Administer as in adults
Antacids, electrolyte supplements reduce absorption; loop diuretics, probenecid, cimetidine increase serum levels; NSAIDs enhance CNS stimulating effect
May increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT); ferrous sulfate decreases bioavailability (administer moxifloxacin 4 h prior or 8 h following ferrous sulfate); coadministration with drugs that prolong QTc interval (quinidine, procainamide, amiodarone, sotalol, erythromycin, tricyclic antidepressants) increase risk of life-threatening arrhythmia
Documented hypersensitivity; known QT prolongation, concurrent administration of drugs that cause QT prolongation
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
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); superinfections may occur with prolonged or repeated antibiotic therapy; fluoroquinolones have induced seizures in CNS disorders and caused tendinitis or tendon rupture
More on Mycobacterium Kansasii |
| Overview: Mycobacterium Kansasii |
| Differential Diagnoses & Workup: Mycobacterium Kansasii |
 Treatment & Medication: Mycobacterium Kansasii |
| Follow-up: Mycobacterium Kansasii |
| Multimedia: Mycobacterium Kansasii |
| References |
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References
Bloch KC, Zwerling L, Pletcher MJ. Incidence and clinical implications of isolation of Mycobacterium kansasii: results of a 5-year, population-based study. Ann Intern Med. Nov 1 1998;129(9):698-704. [Medline].
Corbett EL, Churchyard GJ, Hay M. The impact of HIV infection on Mycobacterium kansasii disease in South African gold miners. Am J Respir Crit Care Med. Jul 1999;160(1):10-4. [Medline].
Evans AJ, Crisp AJ, Hubbard RB. Pulmonary Mycobacterium kansasii infection: comparison of radiological appearances with pulmonary tuberculosis. Thorax. Dec 1996;51(12):1243-7. [Medline].
Maliwan N, Zvetina JR. Clinical features and follow up of 302 patients with Mycobacterium kansasii pulmonary infection: a 50 year experience. Postgrad Med J. 2005;81:530-33. [Medline].
Evans SA, Colville A, Evans AJ. Pulmonary Mycobacterium kansasii infection: comparison of the clinical features, treatment and outcome with pulmonary tuberculosis. Thorax. Dec 1996;51(12):1248-52. [Medline].
Witzig RS, Fazal BA, Mera RM. Clinical manifestations and implications of coinfection with Mycobacterium kansasii and human immunodeficiency virus type 1. Clin Infect Dis. Jul 1995;21(1):77-85. [Medline].
National Committee for Clinical Laboratory Standards. Susceptibility Testing of Mycobacteria, Nocardiae, and Other Aerobic Actinomycetes; Approved Standard. M24-A. Wayne, PA: National Committee for Clinical Laboratory Standards; 2003.
Woods GL. Susceptibility testing for mycobacteria. Clin Infect Dis. 2000;31:1209-1. [Medline].
Smith MB, Molina CP, Schnadig VJ. Pathologic features of Mycobacterium kansasii infection in patients with acquired immunodeficiency syndrome. Arch Pathol Lab Med. 2003;127:554-60. [Medline].
American Thoracic Society. Diagnosis and treatment of disease caused by nontuberculous mycobacteria. This official statement of the American Thoracic Society was approved by the Board of Directors, March 1997. Medical Section of the American Lung Association. Am J Respir Crit Care Med. Aug 1997;156(2 Pt 2):S1-25. [Medline].
Griffith DE, Aksamit T, Brown-Elliott BA, Catanzaro A, Daley C, Gordin F, et al. An official ATS/IDSA statement: diagnosis, treatment, and prevention of nontuberculous mycobacterial diseases. Am J Respir Crit Care Med. Feb 15 2007;175(4):367-416. [Medline].
Griffith DE. Management of disease due to Mycobacterium kansasii. Clin Chest Med. 2002;23:613-21. [Medline].
Guna R, Munoz C, Dominguez V. In vitro activity of linezolid, clarithromycin and moxifloxacin against clinical isolates of Mycobacterium kansasii. J Antimicrob Chemother. 2005;55:950-53. [Medline].
Marras TK, Morris A, Gonzalez LC. Mortality prediction in pulmonary Mycobacterium kansasii infection and human immunodeficiency virus. Am J Respir Crit Care Med. 2004;170:793-98. [Medline].
Alcaide F, Benitez MA, Martin R. Epidemiology of Mycobacterium kansasii. Ann Intern Med. Aug 17 1999;131(4):310-1. [Medline].
Breathnach A, Levell N, Munro C. Cutaneous Mycobacterium kansasii infection: case report and review. Clin Infect Dis. Apr 1995;20(4):812-7. [Medline].
Davidson PT. The diagnosis and management of disease caused by M. avium complex, M. kansasii, and other mycobacteria. Clin Chest Med. Sep 1989;10(3):431-43. [Medline].
Fishman JE, Schwartz DS, Sais GJ. Mycobacterium kansasii pulmonary infection in patients with AIDS: spectrum of chest radiographic findings. Radiology. Jul 1997;204(1):171-5. [Medline].
O'Brien RJ. The epidemiology of nontuberculous mycobacterial disease. Clin Chest Med. Sep 1989;10(3):407-18. [Medline].
Wolinsky E. Mycobacterial diseases other than tuberculosis. Clin Infect Dis. Jul 1992;15(1):1-10. [Medline].
Woods GL, Meyers WM. Mycobacterial Diseases. In: Damjanov I, Linder J, eds. Anderson's Pathology. Vol 10. St. Louis, Mo: Mosby; 1996:843-55.
Further Reading
Keywords
Mycobacterium kansasii, M kansasii, acid-fast bacillus, AFB, nontuberculous mycobacterial infection, NTM infection, AIDS, Mycobacterium avium complex, MAC, M kansasii chronic pulmonary disease, pulmonary tuberculosis, cutaneous M kansasii infection, M kansasii nodule, M kansasii pustule, M kansasii verrucous lesion, M kansasii erythematous plaque, M kansasii abscess, M kansasii ulcer, M kansasii bacteremia, M kansasii pericarditis, M kansasii oral ulcer, chronic M kansasii sinusitis, M kansasii osteomyelitis, M kansasii scalp abscess
