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Susceptibility-guided combination therapy improves neurological status and reduces abscess size in a patient with nocardiosisCase report: Brain infection in autoimmune hepatitis patient

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Key Takeaway
Consider disseminated nocardiosis in immunocompromised patients with autoimmune hepatitis and subacute neurological decline.

This case report details the clinical course of a 55-year-old man with autoimmune hepatitis and occupational soil exposure who presented with subacute neurological decline and ring-enhancing brain lesions. The authors describe the patient's management using imipenem-cilastatin and trimethoprim-sulfamethoxazole based on susceptibility testing, while azathioprine was paused and prednisone continued at 25 mg/day.

The primary finding is that the patient experienced gradual neurologic improvement and radiographic abscess reduction after 3 months of the specified combination therapy. The report highlights the clinical progression from initial presentation to recovery over a 3-month follow-up period.

A significant limitation of this evidence is the single-patient sample size, which precludes broader generalizations about treatment efficacy or safety profiles for nocardiosis. However, the case underscores the importance of susceptibility-guided therapy in immunocompromised patients with neurological involvement. Clinicians should consider disseminated nocardiosis as a potential cause for subacute neurological decline and ring-enhancing lesions in patients with autoimmune hepatitis.

How this fits prior evidence

This case report addresses a gap in clinical management for specific opportunistic infections in immunocompromised patients. While previous coverage noted that corticosteroid, IVIG, antibiotic, and mechanical ventilation are associated with higher odds of invasive pulmonary aspergillosis in SFTS patients, this report focuses on the treatment of nocardiosis in an autoimmune hepatitis patient. It does not directly relate to the findings regarding anti-VEGF therapy for retinal diseases or belimumab for systemic lupus erythematosus.

A case report describes a 55-year-old man with autoimmune hepatitis who developed a rare brain infection called nocardiosis. He had been taking corticosteroids and azathioprine for his liver condition and had a history of occupational soil exposure. He presented with subacute neurological decline and ring-enhancing brain lesions.

Doctors paused his azathioprine and continued prednisone at 25 mg per day. Based on susceptibility testing, they treated him with a combination of imipenem-cilastatin and trimethoprim-sulfamethoxazole. After three months, he showed gradual neurological improvement and reduction of brain abscesses on imaging.

This is a single-patient case report, so the findings cannot be generalized. No adverse events were reported, but the patient's azathioprine was paused during treatment. The report highlights that disseminated nocardiosis should be considered in immunosuppressed patients with autoimmune hepatitis who develop neurological symptoms and brain lesions.

For readers, this is a reminder that rare infections can occur in people on immunosuppressive therapy. If you or a loved one has autoimmune hepatitis and experiences new neurological symptoms, discuss them with your doctor. This case does not change standard treatment recommendations.

What this means for you:
Rare brain infections can occur in immunosuppressed patients; prompt diagnosis and targeted antibiotics are key.

Common questions

What is nocardiosis?

Nocardiosis is a rare bacterial infection that often affects the lungs or brain. It usually occurs in people with weakened immune systems, such as those on long-term steroids or other immunosuppressants.

How was this patient treated?

The patient was treated with a combination of antibiotics: imipenem-cilastatin and trimethoprim-sulfamethoxazole, chosen based on lab tests. His azathioprine was paused, but he continued prednisone at 25 mg per day.

What were the results of treatment?

After three months of treatment, the patient showed gradual improvement in neurological symptoms and reduction of brain abscesses on scans. No side effects were reported in the case report.

Is this treatment recommended for all patients?

No. This is a single case report, so the findings may not apply to everyone. Treatment decisions should be made by a doctor based on individual circumstances and susceptibility testing.

Study Details

Study typeMeta analysis
EvidenceLevel 1
PublishedJul 2026
View Original Abstract ↓
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. 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. 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.
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