Mycobacterium abscessus is a rapidly growing member of the non-tuberculous mycobacteria (NTM) group, responsible for serious chronic infections, primarily affecting the lungs or skin and soft tissues. The organism possesses inherent resistance to many common antibiotics, making treatment intensive, multi-drug, and prolonged. Achieving a definitive “cure” is complex and depends heavily on the bacteria’s biology and the patient’s overall health. Treatment success is often measured by sustained clinical and microbiological control rather than immediate clearance.
What is Mycobacterium Abscessus?
Mycobacterium abscessus is a species of bacteria classified as a rapid-growing mycobacterium (RGM). Unlike the mycobacteria that cause tuberculosis, this organism is not typically transmitted person to person. It is commonly found in the environment, residing naturally in water, soil, and dust. Infections usually occur after environmental exposure or via contaminated medical equipment.
Infections most frequently manifest as a chronic lung disease, particularly in individuals with pre-existing conditions like cystic fibrosis or bronchiectasis. The organism can also cause skin and soft tissue infections, often following surgery or trauma where the skin barrier is compromised. Clinicians must differentiate between the three main subspecies—abscessus, massiliense, and bolletii—because their genetic differences directly impact treatment planning and prognosis.
The Challenge of Intrinsic Antibiotic Resistance
The difficulty in treating M. abscessus stems from its intrinsic resistance mechanisms. The mycobacterium is protected by a thick, waxy cell wall, rich in mycolic acids, which acts as a barrier to limit antibiotic entry. This defense is supplemented by drug efflux pumps and drug-modifying enzymes that actively neutralize or expel antibiotics.
A major factor in treatment failure is the presence of the erm(41) gene, which confers inducible resistance to macrolide antibiotics like clarithromycin. This gene encodes a ribosomal methylase enzyme that is activated by drug exposure, causing resistance after several days of treatment. The functional status of this gene is subspecies-dependent.
The abscessus and bolletii subspecies carry a functional version, making them highly macrolide-resistant, while massiliense often has a truncated, non-functional gene, making it susceptible to macrolides. The erm(41) gene status determines the entire treatment regimen and is a major predictor of outcome. The organism also possesses the beta-lactamase enzyme BlaMab, which breaks down many penicillin-related antibiotics. This high level of resistance necessitates using a combination of multiple drugs, often including agents with significant toxicity.
Defining Treatment Success and Prognosis
The definition of a “cure” for M. abscessus infection is complex and rarely involves swift eradication. Treatment success is generally defined by achieving sustained sputum culture conversion (SCC). This requires that a patient’s respiratory samples be consistently negative for the bacteria for a minimum of 12 months after all antibiotic treatment has been discontinued.
Success rates are highly variable and depend on the specific subspecies. Patients infected with the macrolide-susceptible M. massiliense typically have significantly better outcomes, with reported SCC rates ranging from 54% to over 80%. In contrast, those infected with the highly resistant M. abscessus subspecies often have much lower success rates, sometimes in the range of 23% to 34%.
The risk of relapse is a constant concern, with recurrence rates being higher for the abscessus subspecies. For patients with chronic lung disease, such as cystic fibrosis, the goal shifts from complete eradication to long-term disease management and suppression. Factors that worsen the prognosis include advanced underlying lung disease, disseminated disease, and poor adherence to the demanding treatment regimen.
Current Treatment Strategies
Treatment for M. abscessus is a prolonged, intensive, and multi-phase process tailored to the individual patient and the specific subspecies. The first step is determining macrolide susceptibility, which dictates the core antibiotic combination. This is based on genetic testing for the erm(41) gene or prolonged drug susceptibility testing.
Initial Intensive Phase
The initial intensive phase typically lasts between two and four weeks and requires a combination of intravenous (IV) and oral antibiotics. This phase commonly includes a macrolide (clarithromycin or azithromycin) combined with two or more IV agents, such as amikacin, cefoxitin, imipenem, or tigecycline. The goal is to rapidly reduce the bacterial load and prevent the development of further resistance.
Continuation Phase
Following the initial phase, patients transition to a continuation phase. This involves a long-term regimen of primarily oral antibiotics, usually for 12 to 18 months after culture conversion is achieved. This phase typically includes the macrolide, if the strain is susceptible, paired with one or two other oral agents, such as clofazimine or linezolid. The total duration of therapy often exceeds 18 months and is associated with a high rate of drug-related side effects, which can complicate adherence.
Adjuvant Surgery
In cases of localized disease, especially nodular lung infections or persistent soft tissue abscesses that do not respond to drug therapy, adjuvant surgery is often required. Surgical resection of the infected tissue is considered a definitive treatment option for refractory disease. Combining aggressive antibiotic therapy and surgical intervention offers the best chance for a successful outcome in localized, difficult-to-treat infections.