AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

Section 2 of 11  

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Background

Mycobacterium kansasii is an acid-fast bacillus (AFB) that is readily recognized by its photochromogenicity, which produces a yellow pigment when exposed to light. In 1953, Buhler and Pollack first described the bacterium. Under light microscopy, its appearance is relatively long, thick, and cross-barred.

The most common presentation of M kansasii is a chronic pulmonary infection that resembles pulmonary tuberculosis. It may also infect other organs. Incidence of infection has increased because of the HIV/AIDS epidemic. It is the second most common nontuberculous, opportunistic mycobacterial infection associated with AIDS, surpassed only by Mycobacterium avium complex (MAC).

Pathophysiology

Unlike other nontuberculous mycobacteria (NTM), M kansasii is not readily isolated from environmental sources. However, it has been isolated from a small percentage of specimens obtained from water supplies in areas with high endemicity. Most likely, M kansasii is acquired through either aspiration or local inoculation from the environment. Little evidence exists of person-to-person transmission. Molecular characterization of M kansasii shows that it is a homogeneous group of organisms. Five genotypes or subtypes are described. Types I and II are frequent clinical isolates, while the remaining types (III, IV, V) are recovered from environmental samples only. Type I probably is the most prevalent M kansasii isolate from human sources worldwide.

M kansasii infection of the lung causes a pulmonary disease similar to tuberculosis. Histopathologic appearance is similar to that of tuberculosis and may include acute suppuration, nonnecrotic tubercles, or caseation. In persons with AIDS or in patients with other forms of immunocompromise, many of its characteristic histologic features may be absent.

After skin inoculation, M kansasii can cause local disease of the skin and subcutaneous tissue. It may spread from the local site and cause lymphadenitis, infection of a distant organ, or disseminated disease.

Frequency

United States

M kansasii, an unusual pathogen in the pre-AIDS era, increased with the HIV pandemic. It is the second most common cause of nontuberculous mycobacterial disease in patients with AIDS. Typically, it has been described as a disease of urban dwellers and of patients with high incomes and better standards of living. One study in 3 northern California counties found that M kansasii was more common in census tracts with lower income (median income <$32,000). However, this study consisted of a large proportion of patients with HIV (Bloch, 1998).

The disease occurs throughout the United States, with the highest incidence in the midwest and the southwest regions. The study mentioned above, which was performed in northern California, estimated an overall incidence of 2.4 cases per 100,000 adults per year for the whole population, 115 cases per 100,000 persons who are HIV positive per year, and 647 cases per 100,000 persons with AIDS per year. This incidence is much higher than that determined by a national laboratory surveillance during 1982-1983, which estimated a prevalence of 0.3 cases per 100,000 persons.

International

This disease has been reported from most parts of the world. Incidence appears to be relatively high in England and Wales and among South African gold miners. In the United Kingdom, it has been reported as the most common cause of nontuberculous mycobacterial lung infection in patients who are HIV negative.

Mortality/Morbidity

The mortality from M kansasii depends on various factors, including the presence of comorbid diseases, treatment compliance, rifampicin use, and extent of infection. One US center's experience, which included 302 patients over more than a 50-year period (1952-1995), showed a mortality rate of 11%, but this included both immunocompromised and nonimmunocompromised patients (Maliwan, 2005).

• A retrospective study of South African gold miners treated for M kansasii infection reported mortality rates of 2% in those who were HIV negative and 9% in patients with HIV (Corbett, 1999).
• Untreated pulmonary disease progresses and can lead to death in more than 50% of patients.

Race

No racial differences in prevalence have been noted.

Sex

Men are infected more often than women; the male-to-female ratio is 3:1.

Age

• Infection is more common in the older population; it is rare in children.
• Age shifts correlate with the population infected with HIV.

CLINICAL

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History

Most commonly, M kansasii causes lung disease that is clinically indistinguishable from tuberculosis. Symptoms may be less severe and more chronic compared to infection with Mycobacterium tuberculosis. Asymptomatic infection occurs in a small proportion (16%) of patients (Maliwan, 2005).

• Healthy host
• • Pulmonary infection: The most common symptoms of lung infection include cough (91%), sputum production (85%), weight loss (53%), breathlessness (51%), chest pain (34%), hemoptysis (32%), and fever or sweats (17%) (Evans, 1997).
  • Skin infection resembles sporotrichosis secondary to local lymphatic spread. Cutaneous lesions may include nodules, pustules, verrucous lesions, erythematous plaques, abscesses, and ulcers.
• Immunocompromised host
• • Infection manifests late in the course of HIV disease. The lung is the organ most commonly involved. Commonly reported symptoms include fever, chills, night sweats, productive or nonproductive cough, weight loss, fatigue, dyspnea, and chest pain.
  • Disseminated disease occurs in almost 20% of patients infected with HIV who have M kansasii isolates.
  • Meningitis similar to M tuberculosis meningitis has been reported in patients infected with HIV, and it may have a higher mortality rate despite appropriate antibiotic administration.
  • Bacteremia, pericarditis with cardiac tamponade, oral ulcer, chronic sinusitis, osteomyelitis, and scalp abscess have been reported in patients with AIDS.
  • Disseminated M kansasii has also been reported in other immunocompromised hosts (eg, patients with myelodysplastic syndrome, patients on hemodialysis).
  • Skin infections in hosts who are immunocompromised usually have atypical clinical features (eg, cellulitis, seroma). These features, along with atypical histology (eg, absence of granuloma), may delay diagnosis.

Physical

• Common physical findings include the following:
• • Fever
  • Pulmonary crackles and wheezing
  • Lymphadenopathy
• Analysis of a series of 49 patients coinfected with HIV showed the following physical findings at the time of initial isolation of M kansasii:
• • Pulmonary disease
  • • Fever (45%)
    • Lung crackles (40%)
    • Lymphadenopathy (25%)
    • Wheezes (20%)
    • Hepatosplenomegaly (5%)
  • Disseminated disease
  • • Fever (60%)
    • Hepatosplenomegaly (40%)
    • Lung crackles (25%)
    • Lymphadenopathy (10%)
    • Cutaneous lesions (10%)
    • Wheezes (5%)
• In skin infections, nodules, pustules, verrucous lesions, erythematous plaques, abscesses, or ulcers may be present.
• Other signs depend on the site of infection or dissemination.

Causes

Immunocompromised patients, including patients with HIV/AIDS, are at a high risk for the infection.

• Predisposing conditions for infection include pulmonary conditions resulting from pneumoconioses (especially silicosis, gold mining, and coal mining), healed chronic infections (eg, tuberculosis, mycosis, chronic obstructive lung disease, bronchiectasis), heavy smoking, and chronic obstructive pulmonary disease.
• Other risk factors include cancer, diabetes mellitus, long-term steroid use, alcoholism, peptic ulcer disease, coronary artery disease, and prior pneumonia.

DIFFERENTIALS

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Other Problems to be Considered

Mycobacterium scrofulaceum infection
Bacterial cellulitis

WORKUP

Section 5 of 11  

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Lab Studies

• Diagnosis requires isolation of the organism. Unlike other nontuberculous mycobacteria (NTM), M kansasii is believed to rarely represent colonization or an environmental contaminant.
• Initially, evaluate at least 3 sputum samples by AFB staining and mycobacterial cultures. Bacteriologic examination may include AFB stain and culture of specimens (eg, bronchoalveolar lavage, aspirates from sterile sites, tissues).
• Blood culture may be useful to detect M kansasii bacteremia and to establish diagnosis of disseminated infection. Approximately 10% of patients with HIV who are infected with M kansasii have blood cultures that are positive for M kansasii.
• Nucleic acid probes and polymerase chain reaction (PCR) are useful for early identification of growing colonies. They are highly sensitive and specific, providing species identification using a culture directly from BACTEC broth within 2-4 hours.
• Susceptibility testing: The National Committee for Clinical Laboratory Standards (NCCLS) recommends that all initial isolates of M kansasii should be tested only for rifampin susceptibility. If the isolate is resistant to rifampin, further susceptibility to rifabutin, isoniazid, streptomycin, clarithromycin, amikacin, ciprofloxacin and trimethoprim-sulfamethoxazole should be determined. Such rifampin resistant isolates should be sent to an experienced reference laboratory for further testing (Woods, 2000).
• Interpretation of isoniazid susceptibility may be confusing because most M kansasii organisms show resistance to INH at 1 mcg/mL but are susceptible at 5 mcg/mL. The latter reflects a better correlation with in vivo isoniazid activity.
• The currently available skin test is not helpful in establishing diagnosis.

Imaging Studies

• Approximately 90% of patients with M kansasii disease have cavitary infiltrates on chest radiography. Among patients without cavitary lung lesions, clinical symptoms and high-resolution computed tomography (HRCT) scanning are important adjuncts in defining the presence of lung disease.
• The characteristic radiological feature of M kansasii pulmonary infection has been described as a right-sided, apical or subapical, thin-walled cavitary infiltrate (Maliwan, 2005). In a separate study, which included only patients not infected with HIV, a comparison of chest radiographs of patients with M kansasii infection with that of patients with tuberculosis showed that M kansasii infection occurred more frequently as unilateral, right-sided infiltrates. Cavities were observed in both cases, whereas pleural effusions and air space shadowing involving multiple bronchopulmonary segments were less frequent with M kansasii infection (Evans, 1996).
• Analysis of chest radiographs in a series of 16 patients infected with HIV and M kansasii pulmonary infection showed the following abnormalities (in decreasing order of frequency):
• 1. Alveolar opacities
  2. Cavity
  3. Thoracic lymphadenopathy
  4. Pleural effusions
  5. Interstitial opacities

Other Tests

• Patients with M kansasii infection should be counseled about HIV and tested for HIV infection.
• Baseline laboratory workup should include complete blood cell count (CBC), renal profile, and liver profile. Perform a complete HIV evaluation if the patient tests positive for HIV.

Procedures

• Bronchoscopy, tissue biopsy, thoracentesis, or pericardiocentesis may be needed to recover the pathogen and establish diagnosis. In some cases, transthoracic needle aspiration or open-lung biopsy may be necessary.
• Bone marrow and liver biopsies may be useful in establishing disseminated infection.
• Needle aspiration or biopsy of a skin lesion (eg, nodule) may be useful for establishing M kansasii skin infections.

Histologic Findings

The variable histopathologic findings of M kansasii disease may include acute suppuration, nonnecrotic tubercles, or caseation. In general, the findings are similar to tuberculosis.

Examination of lung tissue and lymph nodes usually shows caseating granulomas. Skin lesions may show granulomas with areas of necrosis or foci of acute and chronic inflammation without well-formed granulomas. Other tissues may show caseating or noncaseating granulomas.

AFB are commonly seen in tissues from lungs and lymph nodes. They are found less commonly in tissues from other sites.

In patients with AIDS or other immunocompromised states, many of the histologic characteristics usually associated with M kansasii infection may be absent. Cytologic and histologic material may show a wide range of inflammatory reactions, including granulomas with and without necrosis, neutrophilic abscesses, spindle-cell proliferation, and focal granular eosinophilic necrosis (Smith, 2003).

Diagnostic Criteria

In 1997, the American Thoracic Society established diagnostic criteria for nontuberculous mycobacterial lung disease, regardless of the host's HIV status. The following criteria apply to symptomatic patients with a nodular or cavitary infiltrate on chest radiograph or HRCT scanning that shows multifocal bronchiectasis or multiple small nodules.

• If at least 3 sputum or bronchial wash results are available from the previous 12 months, diagnosis requires either 3 positive culture results in the setting of negative AFB smear results or 2 positive culture results and 1 positive AFB smear result.
• If only 1 bronchial wash is available, diagnosis requires positive culture results with heavily positive (2+, 3+, or 4+) AFB smear results or heavily positive (2+, 3+, or 4+) growth on solid media.
• If sputum or bronchial wash evaluations are nondiagnostic or if another disease cannot be excluded, diagnosis requires transbronchial or open-lung biopsy that yields an NTM or biopsy findings that show compatible histopathologic features (granulomatous inflammation or AFB) and 1 or more sputum or bronchial washings that are positive for an NTM.
• Many experts advise that M kansasii isolated from lungs or elsewhere almost always warrants treatment, especially in patients with AIDS and other immunocompromised groups.

TREATMENT

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Medical Care

After establishing a diagnosis of M kansasii infection, patients should be treated with at least 3 drugs. The initial drug regimen should consist of rifampin, which has been shown to have low failure rates (1.1%) and low long-term relapse rates ( <1%) (Griffin, 2002). Rifampin is the cornerstone of treatment for this infection.

• In general, M kansasii shows good in vitro susceptibility to rifampin, rifabutin, ethambutol, ethionamide, amikacin, streptomycin, clarithromycin, 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. Isoniazid is useful in treatment of M kansasii irrespective of poor susceptibility in vitro. Pyrazinamide should not be used against M kansasii.
• Treatment duration for M kansasii disease is usually 18 months, which is longer than the usual treatment of tuberculosis (6-9 mo).
• Use of intermittent drug regimens has not been studied enough to recommend it. Unlike tuberculosis, in which directly observed therapy (DOT) is widely practiced, the use of intermittent drug regimens for M kansasii has not been studied adequately.
• In adults, treatment of extrapulmonary disease is identical to treatment of pulmonary disease.

Surgical Care

In the treatment of lymph node disease in children, excise all accessible lymph nodes at initial biopsy because the etiologic agent probably is a nontuberculous bacterium other than M kansasii.

Consultations

• Infectious disease specialist, especially in patients who are co-infected with HIV
• Pulmonary medicine consultation, 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 and should be performed as tolerated.

MEDICATION

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The current recommendation for treatment of pulmonary disease caused by M kansasii in nonimmunocompromised adults is the regimen of rifampin (600 mg), ethambutol (25 mg/kg for 2 mo, then 15 mg/kg), and isoniazid (300 mg) with pyridoxine (50 mg) daily for 18 months, with at least 12 months of negative sputum culture results. Streptomycin (0.5 g IM 3 times/wk) should be added for patients with severe disease. Alternatively, clarithromycin can be used as a substitute for any of the 4 drugs.

Rifampin should not be used concurrently with HIV protease inhibitors or non-nucleoside reverse transcriptase inhibitors (NNRTIs) because rifampin significantly enhances their metabolism; in this setting, substitute rifabutin at a lower dose (150 mg/d) for rifampin in those who are on protease inhibitors.

Patients who are infected with rifampin-resistant M kansasii or who are intolerant to rifampin can be treated with a 4-drug regimen that consists of clarithromycin, isoniazid, ethambutol, and sulfamethoxazole.

Most isolates are pyrazinamide-resistant in vitro. Pyrazinamide is unacceptable as an alternative drug for infection with M kansasii.

Other agents with useful activity against M kansasii include fluoroquinolones (moxifloxacin, sparfloxacin), aminoglycosides (streptomycin, amikacin), sulfamethoxazole, and linezolid.

Drug Category: Antibiotics

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

Drug Name	Isoniazid (INH, Laniazid)
Description	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 Dose	5-10 mg/kg/d PO; usual dose 300 mg/d
Pediatric Dose	5-10 mg/kg/d PO
Contraindications	Documented hypersensitivity; previous INH-associated hepatic injury or other severe adverse reactions
Interactions	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
Pregnancy	C - Safety for use during pregnancy has not been established.
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)

Drug Name	Ethambutol (Myambutol)
Description	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 Dose	15 mg/kg/d PO; not to exceed 2.5 g/d
Pediatric Dose	<12 years: Not recommended, but has been used in tuberculosis with a small chance of ocular toxicity ( <5%) >12 years: Administer as in adults
Contraindications	Documented hypersensitivity; optic neuritis (unless clinically indicated)
Interactions	Aluminum salts may delay and reduce absorption (administer several h before or after EMB dose)
Pregnancy	B - Usually safe but benefits must outweigh the risks.
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

Drug Name	Rifabutin (Mycobutin)
Description	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 Dose	300 mg PO qd
Pediatric Dose	5 mg/kg PO qd
Contraindications	Documented hypersensitivity; WBC <1000/mm3; platelet count <50,000/mm3
Interactions	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
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Caution in patients with liver impairment; perform hematologic studies periodically because of association with neutropenia and, more rarely, thrombocytopenia

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 or 1 g PO qd if Biaxin XL
Pediatric Dose	7.5 mg/kg PO bid
Contraindications	Documented hypersensitivity; coadministration of pimozide
Interactions	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
Pregnancy	C - Safety for use during pregnancy has not been established.
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

Drug Name	Streptomycin
Description	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 Dose	15 mg/kg (usually 1 g) IM, 3-5 doses/wk
Pediatric Dose	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
Contraindications	Documented hypersensitivity; non–dialysis-dependent renal insufficiency
Interactions	Nephrotoxicity may be increased with aminoglycosides, amphotericin B, and loop diuretics
Pregnancy	D - Unsafe in pregnancy
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

Drug Name	Amikacin (Amikin)
Description	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 Dose	500-1000 mg IV, 3-5 doses/wk
Pediatric Dose	Administer as in adults
Contraindications	Documented hypersensitivity; renal insufficiency
Interactions	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
Pregnancy	D - Unsafe in pregnancy
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

FOLLOW-UP

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Further Inpatient Care

• Isolation is not required.

Further Outpatient Care

• Monitor patient care clinically and with chest radiography to assess response to therapy and clinical improvement. Monthly induced sputum samples are very useful.
• Monitor patients for drug toxicity, including periodic monitoring for the following:
• • Visual acuity, visual symptoms, and color vision in patients receiving ethambutol
  • Uveitis from rifabutin, indicated by eye pain, decreased visual acuity, and anterior chamber fluid level
  • Liver enzymes for hepatotoxicity from drugs such as isoniazid, rifampin, rifabutin, and clarithromycin

Transfer

• In treatment-resistant cases, consulting the National Jewish Hospital Medical and Research Center in Denver, Colo; the Centers for Disease Control and Prevention in Atlanta, Ga; or other local experts may be useful.

Deterrence/Prevention

• General HIV prevention recommendations

Prognosis

• In patients receiving no drug treatment, M kansasii shows persistence in sputum and progression of clinical and radiographic disease.
• Before rifampin was available, treatment success rates with antimycobacterial drugs were disappointing when compared to tuberculosis. With the advent of rifampin use, 4-month sputum conversion rates with rifampin-containing regimens were 100% in 180 patients from 3 studies. Researchers report that long-term relapse rates for patients on these regimens are less than 1%.
• In patients infected with HIV, predictors of survival include higher CD4 counts, antiretroviral therapy, negative smear microscopy results, and adequate treatment for M kansasii infection (Marras, 2004).

Patient Education

• Explain medication adverse effects.
• • Visual problems may occur with administration of ethambutol.
  • Rifampin reduces the efficacy of oral contraceptives.
• For excellent patient education resources, visit eMedicine's Lung and Airway Center and Procedures Center. Also, see eMedicine's patient education articles Tuberculosis and Bronchoscopy.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Ethambutol may cause optic neuritis. Monthly monitoring may be useful.
• Medications may cause liver failure. Advise patients to contact their physicians if they experience jaundice, abdominal pain or discomfort.
• Rifampin reduces the efficacy of oral contraceptives.

Special Concerns

• Aminoglycosides are contraindicated in pregnancy.
• Rifampin, ethambutol, and isoniazid are considered safe in pregnancy; termination is not necessary.

MULTIMEDIA

Section 10 of 11  

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Media file 1:  This radiograph of a patient with Mycobacterium kansasii pulmonary infectionshows left lower lung infiltrates.
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Media type:  X-RAY

Media file 2:  This is a chest CT scan of a patient with Mycobacterium kansasii pulmonary infection (see Image 1).
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Media type:  CT

Media file 3:  Chest X-ray of a patient with classic right upper lobe cavitary lung disease secondary to Mycobacterium kansasii infection (see Picture 4 for CT thorax of the same patient) (Courtesy- Raj Sreedhar, MD, SIU School of Medicine, Springfield, IL)
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Media type:  X-RAY

Media file 4:  CT thorax of a patient with classic right upper lobe cavitary lung disease secondary to Mycobacterium kansasii infection (see Picture 3 for the Chest X-ray of the same patient) (Courtesy- Raj Sreedhar, MD, SIU School of Medicine, Springfield, IL)
	View Full Size Image
Media type:  CT

REFERENCES

Section 11 of 11

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• Alcaide F, Benitez MA, Martin R. Epidemiology of Mycobacterium kansasii. Ann Intern Med. Aug 17 1999;131(4):310-1. [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].
• 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].
• Breathnach A, Levell N, Munro C. Cutaneous Mycobacterium kansasii infection: case report and review. Clin Infect Dis. Apr 1995;20(4):812-7. [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].
• 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].
• 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].
• 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].
• 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].
• 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].
• 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].
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Article Last Updated: Apr 19, 2006