The bacterium Mycobacterium abscessus belongs to a group known as nontuberculous mycobacteria (NTM), which are distantly related to the organisms causing tuberculosis and leprosy. It is classified as a rapidly growing mycobacterium, though its growth in a laboratory setting still takes several days. This organism is a ubiquitous environmental microbe found globally in water, soil, and dust. M. abscessus is one of the most drug-resistant mycobacteria, causing severe, chronic infections, especially in susceptible individuals. Its resistance profile and difficulty of eradication pose a significant threat to vulnerable patient populations.
What is Mycobacterium Abscessus?
Mycobacterium abscessus is an environmental organism that is part of the MABC complex. It is a resilient microbe capable of forming biofilms, allowing it to persist in plumbing systems, water distribution networks, and hospital environments. While most people who encounter this bacteria never develop an illness, it becomes problematic when it enters the body through wounds or is inhaled by individuals with compromised defenses.
The infection manifests in humans through two main clinical presentations: pulmonary disease and skin or soft tissue infections (SSTI). Pulmonary infection is the most severe and common form, typically causing a chronic cough, sputum production, and progressive lung damage. SSTI are often characterized by boils, pus-filled blisters, or abscesses at the site of entry, frequently linked to healthcare-associated exposure.
Factors Driving Severe Illness and Mortality
While a healthy person is unlikely to die from an M. abscessus infection, the risk of severe illness and mortality increases sharply among those with pre-existing conditions. The infection poses a significant threat to patients with underlying structural lung diseases, such as bronchiectasis or chronic obstructive pulmonary disease (COPD). Patients with cystic fibrosis (CF) are particularly vulnerable, as M. abscessus can cause a progressive, destructive lung infection that accelerates the decline of respiratory function.
Immunocompromised individuals, including those on long-term steroid therapy or with hematologic malignancies, are also at high risk for disseminated disease. In these cases, the infection can spread beyond the lungs or skin to almost any organ, leading to bacteremia and systemic failure. Studies tracking patients with nontuberculous mycobacterial lung disease (NTM-LD) have shown that the M. abscessus complex is associated with a significantly increased risk of death compared to other NTM species.
This elevated mortality risk is due to the infection itself and the progressive destruction of lung tissue. This destruction often results in cavitary lesions and fibrocavitary disease, which is a marker of advanced lung damage strongly linked to a higher risk of death in NTM patients.
How Mycobacterium Abscessus is Contracted
Acquisition of M. abscessus is primarily environmental, as the bacteria are naturally found in soil, water, and household dust. The most common route of infection involves the inhalation of aerosolized particles from contaminated water sources, such as showerheads, nebulizers, or plumbing systems. Skin and soft tissue infections occur when the bacteria enter the body through a break in the skin exposed to contaminated soil or water.
A major concern is iatrogenic transmission, meaning infection resulting from medical procedures. Outbreaks have been traced to contaminated medical devices, improperly sterilized surgical instruments, or injections using contaminated solutions. While M. abscessus is generally not transmitted person-to-person, specific circumstances, particularly within cystic fibrosis clinics, suggest a potential for indirect cross-transmission via fomites or shared equipment.
Challenges in Eradicating the Infection
Treatment of M. abscessus infection is notoriously difficult due to the organism’s intrinsic and acquired resistance to many common antibiotics. The primary hurdle is a mechanism known as inducible macrolide resistance, which is conferred by the presence of the erm(41) gene. This gene acts as a ribosomal methylase, chemically modifying the bacterial ribosome and preventing macrolide antibiotics like clarithromycin from binding effectively.
The presence of a functional erm(41) gene means that bacteria, even if initially susceptible to a macrolide, can rapidly develop resistance once treatment begins. This mechanism is most pronounced in two of the three main subspecies: M. abscessus subspecies abscessus and M. abscessus subspecies bolletii. Conversely, the M. abscessus subspecies massiliense has a non-functional erm(41) gene, making it more susceptible to macrolides and associated with better treatment outcomes.
Eradication requires a highly complex, multidrug regimen. Treatment often begins with an intensive phase involving intravenous (IV) antibiotics, such as amikacin and cefoxitin. This IV therapy is followed by a prolonged oral regimen, and the total duration typically lasts a minimum of 12 months after a patient achieves negative culture results. The necessary combination of drugs is often associated with significant side effects, frequently leading to changes in the treatment plan and a high rate of treatment failure or relapse.