Disseminated Nocardia farcinica with multiple cerebral abscesses in a patient receiving induction immunosuppression for autoimmune hepatitis: case report

Abstract

Background Nocardiosis is an opportunistic infection caused by aerobic, Gram-positive actinomycetes of the genus Nocardia that most often affects patients with impaired cell-mediated immunity, including those receiving corticosteroids or other immunosuppressive therapies. Disseminated disease frequently involves the central nervous system, where a systematic review reported an overall case fatality rate of 22.8%, and Nocardia farcinica is the most commonly identified species. We report a case of disseminated Nocardia farcinica with multiple cerebral abscesses in a patient receiving induction immunosuppressive therapy for autoimmune hepatitis. Case report A 55-year-old man with a history of autoimmune hepatitis and occupational soil exposure presented with 4–5 week history of progressive cognitive impairment, dysarthria, and right upper extremity weakness. Two months earlier, he had been treated with high-dose corticosteroids and azathioprine and prescribed trimethoprim-sulfamethoxazole (TMP-SMX) prophylaxis, which had been interrupted for an estimated 2–4 weeks before presentation during ongoing corticosteroid therapy. Upon admission, laboratory tests demonstrated neutrophil-predominant leukocytosis with lymphopenia, and liver function tests showed substantial improvement compared to his initial presentation of autoimmune hepatitis. Neuroimaging revealed multiple ring-enhancing intracerebral lesions with surrounding vasogenic edema. Stereotactic aspiration of a cerebral abscess and drainage of a concurrent retroperitoneal collection grew Nocardia farcinica, confirming disseminated nocardiosis. Antimicrobial therapy was transitioned to imipenem-cilastatin and TMP-SMX based on susceptibility testing. During infection management, azathioprine was paused, and prednisone was continued at a dose of 25 mg/day, followed by a biochemical autoimmune hepatitis flare requiring hepatology-guided monitoring. The patient demonstrated gradual neurologic improvement and was discharged to inpatient rehabilitation after an 18-day hospitalization. Conclusion Disseminated nocardiosis should be considered for immunosuppressed patients with autoimmune hepatitis presenting with subacute neurological decline and ring-enhancing brain lesions, particularly during outpatient immunosuppression transitions when antimicrobial prophylaxis may be interrupted or incompletely reconciled. The patient demonstrated progressive neurological improvement and radiographic abscess reduction after 3 months of susceptibility-guided combination therapy, reinforcing the importance of early tissue diagnosis and neurosurgical intervention in this population.