Triple infection with pulmonary tuberculosis, chronic hepatitis C and systemic brucellosis in an HIV/AIDS patient: a case report from northwestern China.

BACKGROUND AND

OBJECTIVES

Profound immune suppression in people living with HIV/AIDS predisposes to multiple opportunistic and endemic infections. While HIV/tuberculosis (TB) and HIV/hepatitis C virus (HCV) coinfections are well recognized, simultaneous infection with Mycobacterium tuberculosis, HCV, and Brucella spp. is exceptionally rare. Such triple infection poses substantial diagnostic and therapeutic challenges, especially in endemic settings where overlapping febrile syndromes may obscure multiple concurrent etiologies. We describe a complex case of HIV/TB/HCV/brucellosis coinfection from northwestern China and summarize the diagnostic approach, staged treatment strategy, and long-term outcome.

CASE PRESENTATION: A 43-year-old man with a history of intravenous drug use and poorly controlled HIV infection presented with fatigue and progressive left scrotal swelling. He was found to have advanced HIV disease (CD4+ T-cell count 128/μL; HIV RNA 15,000 copies/mL), pulmonary TB confirmed by bronchoalveolar lavage fluid culture, chronic hepatitis C virus infection, and systemic brucellosis confirmed by blood culture and serology. Baseline liver biochemistry was within normal limits, although imaging suggested underlying chronic hepatic vulnerability. Initial treatment consisted of an individualized anti-tuberculosis regimen with isoniazid, rifampin, ethambutol, and levofloxacin, a 12-week rifampin-levofloxacin regimen for brucellosis, and ART with tenofovir disoproxil fumarate/lamivudine/efavirenz. HCV treatment was deferred because of concern about cumulative hepatotoxicity and contraindication between rifampin and direct-acting antivirals. Poor ART adherence subsequently led to virologic failure and resistance, prompting intensification to bictegravir/emtricitabine/tenofovir alafenamide. After completion of rifampin-based therapy, sofosbuvir/velpatasvir was initiated for HCV.

RESULTS

The patient's course was marked by early treatment interruption, delayed virologic suppression, and later recovery under a simplified, multidisciplinary treatment strategy. At month 33, HIV RNA remained 83,500 copies/mL with a CD4+ T-cell count of 80/μL. By month 35, resistance-associated mutations had been detected and ART was intensified. At month 43, HIV RNA had declined to 79 copies/mL, allowing initiation of HCV treatment. By month 48, HIV RNA was 76 copies/mL, HCV RNA was < 25 IU/mL, and the CD4+ T-cell count had risen to 147/μL. At month 54, the patient had achieved substantial immune recovery (CD4+ T-cell count 520/μL) and durable HIV suppression (HIV RNA < 20 copies/mL), with no clinical or radiologic evidence of relapsed TB or brucellosis.

CONCLUSION

This case highlights the diagnostic complexity of overlapping infectious syndromes in an immunocompromised host from an endemic region and demonstrates that even highly complex coinfections can be successfully managed through timely microbiologic confirmation, individualized sequencing of anti-infective and antiretroviral therapies, careful management of drug-drug interactions, and sustained adherence support.