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Case report reveals severe co-infection of Mycobacterium kansasii and Salmonella Typhimurium following immunosuppression in an adult, highlighting diagnostic urgency.
Disseminated Mycobacterium kansasii and Salmonella Typhimurium co-infection is exceptionally rare, particularly in patients without overt immunodeficiency. This case describes a unique disease progression and iatrogenic drivers in such co-infections. A 61-year-old male with uncontrolled diabetes presented with recurrent fever accompanied by axillary lymph node enlargement. Elevated inflammatory markers were noted. Brain magnetic resonance imaging (MRI) revealed a right parietal abscess with subdural empyema. Blood cultures and metagenomic Next-Generation Sequencing (mNGS) of blood and cerebrospinal fluid (CSF) confirmed Salmonella Typhimurium infection. Chest computed tomography (CT) demonstrated bilateral pulmonary inflammation. Contrast-enhanced CT/MRI of the spleen showed splenomegaly with heterogeneous enhancement and diffuse small enhancing nodules. Ultrasound revealed generalized lymph node enlargement, particularly axillary. Right axillary lymph node excision pathology, culture and mNGS confirmed Mycobacterium kansasii . The patient was diagnosed with disseminated Mycobacterium kansasii (lymph nodes, lungs, and spleen) and Salmonella Typhimurium (bloodstream, brain) co-infection. HIV testing was negative, while anti-interferon-γ autoantibodies and interferon-γ levels were within normal ranges. Clinical trajectory suggested initial Mycobacterium kansasii pulmonary and lymphatic infection, followed by Salmonella bacteremia after ingesting raw pig gallbladders. Subsequent immunosuppression (cyclosporine/prednisone) triggered disseminated co-infection (brain, lymph nodes, spleen). Prolonged antimicrobial therapy achieved remission. This case describes a rare disseminated co-infection with Mycobacterium kansasii and Salmonella Typhimurium, initially presenting with non-tuberculous mycobacterium infection and subsequently complicated by salmonellosis due to raw porcine gallbladder ingestion, with dissemination of both pathogens driven by immunosuppression. It highlights the need for suspicion of atypical pathogens and cautious use of immunosuppressive therapy.
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Huang et al. (2026) studied this question.
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