Mycobacterium abscessus is a bacterium belonging to the group known as non-tuberculous mycobacteria (NTM). It is distantly related to the organisms that cause tuberculosis and leprosy. It is classified as a rapidly growing mycobacterium because it develops visible colonies in laboratory cultures in under seven days. M. abscessus is an opportunistic pathogen, known for its inherent resistance to many common antibiotics. Infections are difficult to treat and often require prolonged therapeutic regimens.
Environmental Presence and Transmission
Mycobacterium abscessus is an environmental bacterium found ubiquitously in soil, dust, and various water sources. It thrives in natural and human-made water systems, frequently colonizing plumbing and forming biofilms on surfaces, including those inside tap water pipes and showerheads. This widespread presence means that human exposure to the bacterium is common, although disease is relatively rare and often requires a host predisposition.
Transmission to humans typically occurs through environmental acquisition or in healthcare settings, rather than through person-to-person spread. Environmental exposure can happen when contaminated water or soil enters a break in the skin, such as an open wound or a site of minor trauma. Inhalation of aerosolized water droplets, such as those generated in showers, is a common route for pulmonary infection in susceptible individuals.
Many infections are acquired in healthcare settings (nosocomial infections). These transmissions occur when contaminated medical equipment, materials, or non-sterile water are used during invasive procedures, injections, or surgery. While person-to-person transmission is uncommon, studies suggest that certain strains can spread between patients in high-risk clinical environments, such as those treating individuals with cystic fibrosis.
Clinical Forms of Infection
Infections caused by M. abscessus manifest in several distinct clinical forms, primarily affecting the lungs and soft tissues. The most common presentation is pulmonary disease, often targeting individuals with underlying structural lung conditions. Patients with cystic fibrosis (CF), bronchiectasis, or chronic obstructive pulmonary disease (COPD) are highly susceptible to chronic colonization and progressive lung destruction by this organism.
Pulmonary infection is characterized by persistent symptoms, including a chronic cough, production of purulent sputum, and sometimes hemoptysis (coughing up blood). Over time, this infection can lead to a decline in lung function. The bacterium is also a frequent cause of skin and soft tissue infections (SSTIs), which usually present as boils, abscesses, or nodules.
These SSTIs often follow a breach of the skin barrier, such as trauma, or are linked to medical or cosmetic procedures like injections, surgery, or tattooing. In patients with severely compromised immune systems, M. abscessus can cause disseminated disease, where the infection spreads to multiple organs and the bloodstream. This disseminated form represents the most severe manifestation and can be life-threatening.
Diagnostic Challenges
Identifying Mycobacterium abscessus presents several challenges that complicate timely diagnosis and treatment. The initial identification of the organism relies on culturing patient samples, such as sputum or tissue biopsies. Since M. abscessus is a rapidly growing mycobacterium, it can be differentiated from the slower-growing species like Mycobacterium tuberculosis by its ability to form colonies in three to seven days.
However, initial culture results only identify the organism as a member of the M. abscessus complex, not the specific subspecies. Distinguishing between the three subspecies (M. abscessus subsp. abscessus, M. abscessus subsp. massiliense, and M. abscessus subsp. bolletii) is crucial because they exhibit different antibiotic susceptibility profiles and treatment outcomes. This differentiation often requires molecular testing, such as gene sequencing.
Following species identification, drug susceptibility testing (DST) is performed to determine which antibiotics might be effective. This process is complex for M. abscessus because it involves detecting an inducible form of macrolide resistance. Standard DST requires a prolonged incubation of up to 14 days to allow the resistance mechanism to fully express, which delays the start of effective therapy.
Treatment Complexity and Drug Resistance
Treating Mycobacterium abscessus infection relies on complex, multi-drug regimens, typically involving a combination of three or more different antimicrobial agents. These regimens are structured into two phases: an initial intensive phase and a prolonged continuation phase. The total duration of therapy is extensive, generally lasting 12 to 18 months after the patient’s cultures have consistently converted to negative.
The intensive phase often involves intravenous (IV) antibiotics, such as amikacin and cefoxitin, administered for several weeks to months to reduce the bacterial load. This is followed by a long-term continuation phase, which consists of oral antibiotics, primarily a macrolide like clarithromycin or azithromycin, combined with other oral agents.
The organism’s unique resistance to macrolide antibiotics, which are considered a cornerstone of therapy, complicates treatment. This resistance is often governed by the presence of a gene known as erm(41), which encodes an enzyme that modifies the bacterial ribosome, preventing the macrolide from binding. The resistance is “inducible,” meaning it is activated only after the bacteria are exposed to the macrolide for several days.
The status of the erm(41) gene is the most significant predictor of treatment success, which is why subspecies identification is important. Strains of M. abscessus subsp. massiliense typically have a non-functional copy of erm(41), resulting in preserved macrolide susceptibility and a better prognosis. Conversely, M. abscessus subsp. abscessus and M. abscessus subsp. bolletii possess a functional erm(41) gene, making them resistant to macrolides.
In cases of localized disease, particularly SSTIs or cavitary lung lesions, surgical intervention is frequently a necessary adjunct to antibiotic therapy. Surgical removal of infected tissue or abscesses can significantly improve treatment outcomes by reducing the total number of bacteria that the antibiotics need to clear. The combination of medical therapy, guided by molecular testing, and surgical debridement offers the best chance for successful management.