Diagnosis of neurosyphilis is currently based on the cerebrospinal fluid (CSF) assessments and CSF-Venereal Disease Research Laboratory (CSF-VDRL) is the traditional “gold standard.” In the real world, CSF assessments and CSF-VDRL are not always available. This study aimed to identify noninvasive predictors of neurosyphilis based on real-world clinical parameters and diagnostic criteria in populations with different HIV status. In this retrospective cohort study, syphilis patients with different HIV statuses hospitalized for neurosyphilis screening were retrospectively recruited at an infectious disease hospital. Neurosyphilis was defined by real-world diagnostic criteria. Logistic regression and receiver operating characteristic curve analysis were used to investigate and evaluate predictors of neurosyphilis. In total, 528 patients were enrolled, including 143 syphilis patients without HIV infection and 385 HIV/syphilis-co-infected patients. One hundred twelve and 304 neurosyphilis patients were identified in the HIV-negative and HIV-positive groups, respectively. A high serum toluidine red unheated serum test (TRUST) titer was a robust predictor of neurosyphilis in all participants. An age ≥50 years old [adjusted odds ratio (aOR) = 5.062, 95% confidence interval (CI), 1.449–17.680] in the HIV-negative group and CD4 ⁺ T cell count <330/μL (<300 as reference, aOR = 0.552, 95% CI, 0.315–0.966) in the HIV-positive group were predictors of asymptomatic neurosyphilis. In real-world situations, for asymptomatic syphilis patients, relatively old age and a high serum TRUST titer in HIV-negative populations, and CD4 ⁺ T cells 1:64 in HIV-positive populations might predict neurosyphilis.

Progressive multifocal leukoencephalopathy (PML) is a rare demyelinating disease of the central nervous system caused by JC virus (JCV) and is difficult to diagnose. We report on a male HIV-positive patient with PML finally diagnosed by 3 times lumbar punctures and 2 times brain biopsies. Negative results of JCV-PCR in cerebrospinal fluid (CSF) do not rule out the diagnosis of PML when clinical manifestations and neuroimaging features suspected PML. It is necessary to obtain new CSF and make repeat tests and even perform brain biopsy.

Background: Mycobacterium avium complex (MAC) is an uncommon clinical pathogen, especially in the central nervous system (CNS), and carries a poor prognosis. MAC infections commonly present as immune reconstitution disease (IRD) in HIV patients. Herein, we report a case of intracranial infection caused by MAC in an AIDS patient without disseminated MAC (DMAC) and immune reconstitution inflammatory syndrome (IRIS). Case presentation: A 31-year-old HIV-positive male presented us with progressively worsening CNS symptoms, and neuroimaging revealed ring-enhancing lesions. The intracranial lesions worsened after the empirical therapy for toxoplasma encephalitis and fungal infection. Due to the rapid progression of the disease, the patient died. Mycobacterium avium was the only pathogen in brain tissue after cultures and molecular biology tests. Conclusion: MAC infection in CNS is challenging to diagnose in HIV patients. Our findings emphasize that obtaining tissue samples and applying molecular biology methods is essential to help diagnose the patient as soon as possible to receive adequate treatment.

Talaromyces marneffei is a common cause of opportunistic infections in people with advanced acquired immunodeficiency syndrome. This infection is characterized by complex and diverse clinical manifestations. Patients with acute human immunodeficiency virus infection typically present with self-limiting viremia symptoms and relatively preserved immune function. Herein, we report the first documented case of disseminated Talaromyces marneffei infection in a 16-year-old male patient, occurring within 2 months of human immunodeficiency virus (HIV-1) exposure and accompanied by a CD4+ T-cell count of 3/μL. After the administration of aggressive antifungal therapy and antiretroviral therapy, the patient exhibited a significant improvement in clinical symptoms, and he was subsequently discharged from the hospital.

To characterise T‐cell immunity and inflammatory profiles in HIV patients with mycobacterial co‐infections. This study enrolled 41 HIV patients co‐infected with Mycobacterium tuberculosis (HIV‐TB, n = 27) or non‐tuberculous mycobacteria (HIV‐NTM, n = 14), along with 30 controls (20 HIV‐monoinfected, 10 post‐treatment) from a single centre. Flow cytometry quantified T‐cell subsets (CD3 + CD4+, CD3 + CD8+, CD28+ subsets), mitochondrial parameters (mass [MM], low membrane potential [MMP‐low%]) and cytokines (IFN‐γ, IL‐2/4/6/10/17A, TNF‐α). Co‐infected groups showed reduced T‐cell counts versus HIV‐monoinfected controls ( p < 0.05). Elevated MMP‐low% in CD3 + CD4+/CD28+ T cells indicated mitochondrial dysfunction in co‐infected patients ( p < 0.05). HIV‐TB patients exhibited higher CD3 + CD4+/CD28+/CD8+ T‐cell MM than HIV‐NTM ( p < 0.05), while HIV‐NTM demonstrated greater MMP‐low% ( p < 0.05). Proinflammatory cytokines (IFN‐γ, IL‐6, IL‐17A) inversely correlated with CD4+ counts and MM, but positively with CD8 + CD28+ MMP‐low%. MMP‐low% in CD3 + CD4 + CD28+ T cells and IL‐2 differentiated IRIS/non‐IRIS cases ( p < 0.05), with combined AUC = 0.834 for IRIS prediction ( p = 0.001). HIV/mycobacterial co‐infection exacerbates T‐cell depletion and mitochondrial dysfunction, with HIV‐NTM showing more severe impairment. MMP‐low% and IL‐2 may serve as biomarkers for IRIS risk stratification.