What is the most likely cause of a multidrug‑resistant Mycobacterium tuberculosis psoas abscess in a patient with type‑2 diabetes mellitus when vertebral tuberculosis is absent?

MDR-TB Psoas Abscess Without Vertebral Involvement in Type 2 Diabetes

Primary Mechanism

The most likely cause is hematogenous dissemination of MDR-TB from a primary pulmonary focus, with the psoas muscle serving as a site of secondary infection independent of vertebral involvement. 1

Pathophysiologic Explanation

The psoas abscess in this clinical scenario develops through the following mechanism:

• Hematogenous spread from a primary pulmonary or extrapulmonary TB focus is the predominant route when vertebral tuberculosis is absent, as mycobacteria disseminate through the bloodstream and seed the highly vascular psoas muscle tissue 1

• The psoas muscle is particularly susceptible to tuberculous seeding because of its rich blood supply and proximity to retroperitoneal lymphatic drainage, allowing direct hematogenous implantation without requiring contiguous spread from bone 1

• Type 2 diabetes mellitus significantly increases the risk of both TB infection and MDR-TB development through multiple mechanisms: higher baseline mycobacterial loads (increasing mutation probability), impaired immune response with reduced IFN-γ production, compromised innate immunity with decreased IL-12 response, and 53% lower plasma rifampicin levels that create subtherapeutic drug exposure 2

Key Risk Factors for MDR-TB in This Patient

The development of multidrug resistance in this diabetic patient likely resulted from:

• Previous inadequate TB treatment is the most powerful predictor of MDR-TB, including incomplete regimens, addition of single drugs to failing regimens, poor adherence, or unrecognized pre-existing resistance 3, 2

• Diabetes mellitus independently increases MDR-TB risk because higher bacterial loads require longer treatment duration, creating more opportunities for spontaneous mutations under drug selection pressure 2

• The longer time to sputum conversion in diabetic TB patients (often >5 months) extends the period during which resistant mutations can emerge and be selected 2

Clinical Pitfalls to Avoid

Never assume vertebral involvement is required for tuberculous psoas abscess—hematogenous dissemination can create isolated psoas infection without Pott's spine, particularly in immunocompromised hosts like diabetic patients 1

• Obtain drug susceptibility testing immediately to both first- and second-line agents, as empiric treatment decisions depend on resistance patterns 4, 3

• Recognize that diabetes creates a "perfect storm" for MDR-TB: higher bacterial loads increase mutation rates, subtherapeutic drug levels from altered pharmacokinetics promote selection pressure, and impaired immunity allows persistent infection 2

Management Implications

• Immediate referral to an MDR-TB specialist is mandatory, as treatment requires at least 5 effective drugs for 18-24 months after culture conversion, typically including a fluoroquinolone, injectable agent (amikacin/kanamycin/capreomycin), and additional oral agents 4, 3

• Optimize diabetes control aggressively, as poor glycemic control perpetuates the cycle of treatment failure through sustained immunosuppression and altered drug metabolism 2

• Consider surgical drainage of the psoas abscess in conjunction with appropriate MDR-TB chemotherapy, particularly if the collection is large or causing compressive symptoms 1