Practice Essentials
Mycobacterium kansasii is known to cause a chronic pulmonary infection that closely resembles pulmonary tuberculosis. [1, 2] The most common symptoms associated with pulmonary M kansasii infection include cough, sputum production, weight loss, breathlessness, chest pain, hemoptysis, and fever or sweating. Additionally, cutaneous M kansasii infection can spread locally into the lymphatics, mimicking sporotrichosis, and is characterized by nodules, pustules, verrucous lesions, erythematous plaques, abscesses, and ulcers.
In advanced HIV-infected or other immunocompromised patients, M kansasii infection may manifest as disseminated disease, affecting multiple systems and potentially leading to conditions such as meningitis, pericarditis, osteomyelitis, and scalp abscesses. Diagnosis of M kansasii infection hinges on the isolation of the organism from sputum or other clinical samples. Unlike other nontuberculous mycobacteria (NTM), M kansasii is seldom considered a mere colonization or environmental contaminant.
Before initiating antimicrobial therapy, it is crucial to test all clinical isolates of M kansasii for susceptibility to rifampin and clarithromycin. For patients with rifampin-susceptible M kansasii, the first-line treatment regimen includes rifampin and ethambutol, supplemented with either isoniazid or a macrolide such as clarithromycin or azithromycin. Conversely, for patients with rifampin-resistant M kansasii or those intolerant to rifampin, an alternative regimen based on in vitro susceptibility should be employed. This regimen typically comprises a fluoroquinolone, ethambutol, and a macrolide, with the option to substitute isoniazid in place of the macrolide.
Treatment for M kansasii should continue for at least 12 months. However, extended treatment may be necessary for patients who do not achieve sputum conversion within 4 months. This approach ensures comprehensive management of the infection, aiming to mitigate the risk of persistent or recurrent disease.
Background
Mycobacterium kansasii is an acid-fast bacillus (AFB) that is readily recognized based on its characteristic photochromogenicity, which produces a yellow pigment when exposed to light. In 1953, Buhler and Pollack first described the bacterium. Under light microscopy, M kansasii appears relatively long, thick, and cross-barred.
The most common presentation of M kansasii infection is a chronic pulmonary infection that resembles pulmonary tuberculosis. However, it may also infect other organs. Mycobacterium kansasii infection became the second-most-common nontuberculous opportunistic mycobacterial infection associated with AIDS, surpassed only by Mycobacterium avium complex (MAC) infection. The incidence of M kansasii infection increased with the burgeoning of the HIV/AIDS epidemic. However, with better control of HIV/AIDS with antiretroviral therapy (ART), there has been a declining trend in most of world.
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. Mycobacterium kansasii is acquired via 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. Seven genotypes, or subtypes (I to VII), are described. Types I and II are common clinical isolates, with type I being the most prevalent M kansasii isolate from human sources worldwide. The remaining types (III-VII) mostly are recovered from environmental samples only and very rarely are found in human samples. [1]
Mycobacterium kansasii infection of the lung causes a pulmonary disease similar to tuberculosis. Its 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. [2]
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. [3]
Epidemiology
Frequency
United States
The prevalence of M kansasii, an unusual pathogen in the pre-AIDS era, increased with the HIV pandemic. With the advent of HIV/AIDS in the United States, M kansasii became the second-most-common cause of NTM disease in patients with AIDS. Mycobacterium kansasii infection typically has been described as a disease of urban dwellers and of patients with high incomes and better standards of living. A 5-year study of 3 northern California counties in the 1990s found that M kansasii infection was more common in census tracts with a lower median income. [4] This study estimated an overall incidence of 2.4 cases per 100,000 adults per year in the general population of northern California, 115 cases per 100,000 persons with HIV infection per year, and 647 cases per 100,000 persons with AIDS per year.
M kansasii infection occurs throughout the United States, with the highest incidence in the Midwest and the Southwest. A national laboratory surveillance from 1982-1983 estimated the prevalence of M kansasii infection to be 0.3 case per 100,000 persons. This was confirmed by another laboratory-based data analysis at San Francisco General Hospital, which showed a decrease in NTM infection from 319 cases in 1993 to 59 in 2001 (P< 0.001). [5] A 2017 review of a US national hospitalization database found that M kansasii made up only 3% of all clinical isolates of NTM, with a higher frequency of isolation in the western states. [6]
International
Mycobacterium kansasii infection has been reported in most areas of the world. The incidence appears to be relatively high in England and Wales and among South African gold miners. [7] In the United Kingdom, it has been reported as the most common cause of NTM lung infection in patients without HIV infection. [8] Based on the analysis of identification data received by the NTM-Network European Trials Group (NET) for 20,182 patients in 30 countries across 6 continents in 2008, M kansasii was the sixth most common NTM isolated from pulmonary samples. Mycobacterium avium complex (MAC) was the most common NTM in most countries. [9]
An increasing incidence of NTM infections has been reported in other countries, including Israel, Korea, Spain, Portugal, France, Brazil, and Japan. [2] However, recent reports suggest downward trends of M kansasii in several countries. M kansasii was found to be the most common cause of NTM pulmonary disease in sub-Saharan Africa. [10]
Mortality/Morbidity
The likelihood of mortality associated with M kansasii infection depends on various factors, including the presence of comorbid diseases, treatment compliance, rifampin 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. [11] Estimates for NTM disease in Ontario, Canada, from 2001-2013 found 1-year and 5-year survival rates for M kansasii infection to be 84% and 64%, respectively. [12] A retrospective study of South African gold miners treated for M kansasii infection reported mortality rates of 2% in those without HIV infection and 9% in patients with HIV infection. [7]
Untreated pulmonary M kansasii disease progresses and can lead to death in more than 50% of infected individuals.
Race
M kansasii infection has no reported racial predilection.
Sex
M kansasii infection is more common in men, with a male-to-female ratio of 3:1.
Age
M kansasii infection is more common in the older population and is rare in children.
The age predilection shifts in conjunction with age predilections of HIV infection.
Prognosis
Untreated M kansasii infection persists in sputum and progresses both clinically and radiographically. Untreated pulmonary M kansasii disease progresses and can lead to death in more than 50% of infected individuals.
Before rifampin was available, treatment success rates with antimycobacterial drugs were disappointing when compared to tuberculosis. With the advent of rifampin, 4-month sputum conversion rates with rifampin-containing regimens were 100% in 180 patients from 3 studies. Researchers report that long-term relapse rates in patients on these regimens are less than 1%. A systemic review and meta-analysis of 24 studies showed a post-treatment sputum conversion rate of 80.2% (95% CI= 58.4%-95.2%) among patients with M kansassii infection. [13]
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. [14, 15]
Patients with cavitary lung disease have a slower response to treatment. Patients with CNS infection have high rates of morbidity and mortality despite appropriate treatment.
Patient Education
The adverse effects of any medications used for treatment are as follows:
-
Visual problems may occur with administration of ethambutol.
-
Rifampin has drug interactions with other drugs which are metablised in the liver, such as oral contraceptives, and reduces their efficacy . Therefore, it is important to ask the physician about any need to adjust the dose of any other concomitantly used drugs.
-
Chest radiograph in a patient with Mycobacterium kansasii pulmonary infection shows left lower lung infiltrates.
-
Chest CT scan in a patient with Mycobacterium kansasii pulmonary infection.
-
Chest radiograph in a patient with classic right upper lobe cavitary lung disease secondary to Mycobacterium kansasii infection. Courtesy of Raj Sreedhar, MD, SIU School of Medicine, Springfield, IL.
-
CT thorax of a patient with classic right upper lobe cavitary lung disease secondary to Mycobacterium kansasii infection. Courtesy of Raj Sreedhar, MD, SIU School of Medicine, Springfield, IL.
