A 40-year-old Caucasian woman with 22-year history of anorexia nervosa was brought to a community hospital after being found unresponsive at home. She was generally well until three months prior to admission, when she developed progressive weight loss, fatigue and weakness that limited her ability to walk. Two weeks prior to presentation, she developed a dry cough. She had no dyspnea, hemoptysis, pleuritic chest pain, fevers, chills or night sweats, nausea, vomiting or diarrhea, arthralgias, or rashes.
She was noted to be hypothermic, hypotensive, and tachycardic on arrival. She was cachectic on exam, weighing 43 kg with body mass index (BMI) of 16.8. Chest x-ray and computed tomography (CT) of the chest revealed bilateral thick-walled upper lobe cavitary lesions (see image below). She was started on broad-spectrum antibiotics with vancomycin, piperacillin-tazobactam and levofloxacin for septic shock. She was placed on airborne isolation and a bronchoscopy was performed. A bronchoalveolar lavage (BAL) specimen revealed 4+ acid fast bacilli (AFB) on auramine-rhodamine stain. Empiric anti-tuberculosis therapy with rifampin, isoniazid, pyrazinamide, ethambutol and pyridoxine was initiated. She developed progressive respiratory failure six days later, requiring intubation and mechanical ventilatory support, and was subsequently transferred to our hospital for further care.
At our institution, azithromycin was added to treat for the possibility of NTM infection. Laboratory studies were notable for: white blood cell (WBC) count 15.7 K/mcL, absolute lymphocyte count 330/mcL, hemoglobin 9.4 g/dL, platelets 60 K/mcL, and non-reactive human immunodeficiency virus (HIV) antigen/antibody test. Immunologic tests included normal total immunoglobulin G (IgG) 1079 mg/dL (700-1600). AFB blood cultures were negative. QuantiFERON(R)-TB gold (QIAGEN(R), Germantown, MD) was indeterminate as the patient's mitogen response was <0.5IU/mL. DNA probes for M. tuberculosis complex, M. avium complex and M. kansasii were negative, and the organism was speciated as M. szulgai at 28 days. Pyrazinamide and azithromycin were discontinued. She subsequently developed elevated AST on rifampin, isoniazid and ethambutol. After consultation with National Jewish, the patient was switched to moxifloxacin, ethambutol and rifabutin. She was discharged to an acute rehabilitation facility after 65 days of hospitalization, weighing 27 kg (BMI 10.5).
At a subsequent outpatient infectious disease clinic visit, the patient had gained 6 kg but had developed a drug rash. AFB culture susceptibilities returned and the isolate was found to be resistant to ciprofloxacin and rifampin (Table 1). The patient was then started on clarithromycin and amikacin but was unable to tolerate that regimen. Therapy was changed by an outpatient provider to isoniazid, rifabutin, and pyrazinamide due to limited options secondary to adverse reactions. Her course was then complicated by drug-induced dermatological skin eruption and hepatotoxicity, the latter of which required readmission and cessation of therapy. Her weight increased to 29 kg with nasogastric feeds and she was transferred to an eating disorders unit at a psychiatric hospital. She was subsequently lost to follow-up.