Ákos Vince Andrejkovits

Background/Objectives: Listeria monocytogenes is an uncommon but potentially life-threatening cause of central nervous system infection, predominantly affecting older adults and immunocompromised patients. Neurolisteriosis may present with nonspecific neurological manifestations, and the absence of classical meningeal signs may delay diagnosis. We report a case of L. monocytogenes meningoencephalitis in an elderly patient without known immunosuppression, with rapid cerebrospinal fluid (CSF) molecular testing facilitating early diagnosis and appropriate antimicrobial treatment. Case presentation: A 76-year-old man with significant cardiovascular comorbidities was admitted with a 3-day history of fever, headache, nausea, vomiting, fatigue, and gait instability. He was alert on admission, with only mild meningeal signs, and initial cranial computed tomography showed no acute intracranial abnormalities. CSF analysis revealed inflammatory changes. Empirical ceftriaxone therapy was supplemented with vancomycin, followed by the initiation of intravenous ampicillin and gentamicin after molecular identification of L. monocytogenes. The diagnosis was subsequently confirmed by CSF culture, while blood cultures remained negative. Clinical and laboratory parameters improved progressively, accompanied by marked improvement in CSF findings on follow-up examination. The patient was discharged in stable condition after 18 days of hospitalization. Conclusions: Neurolisteriosis should be considered in elderly patients presenting with fever and neurological symptoms, even in the absence of overt immunosuppression or prominent meningeal signs. This case highlights the diagnostic value of rapid CSF molecular testing, particularly when blood cultures are negative and the initial clinical presentation is nonspecific. Early recognition of L. monocytogenes infection and timely initiation of targeted antimicrobial therapy are essential to improving outcomes.

Background: Recurrent malaria refers to repeated episodes of the disease in the same individual. Plasmodium vivax is known for its ability to relapse due to dormant liver-stage hypnozoites and poses a particular risk to travelers returning from endemic areas. Prompt diagnosis and treatment are crucial to prevent recurrences. Case Presentation: We present the case of a 41-year-old man from Romania who developed Plasmodium vivax malaria after traveling through Southeast Asia without chemoprophylaxis. He presented with fever, chills, myalgia, headache, vomiting, and abdominal pain. Clinical findings included mild jaundice and slight neurological signs. Laboratory tests showed severe thrombocytopenia, elevated bilirubin, inflammatory markers, and borderline creatinine levels. Malaria was confirmed by a rapid diagnostic test and blood smear microscopy. The patient was treated with doxycycline and atovaquone–proguanil. He improved and was discharged, but experienced two relapses, both confirmed as Plasmodium vivax by RT-PCR. Despite receiving primaquine as radical cure after the first Plasmodium vivax malaria relapse, a second relapse occurred. Each episode was managed with blood-stage antimalarial therapy, leading to full clinical and biological recovery. Conclusions: Malaria rarely occurs in non-endemic areas; it should be considered in patients with compatible travel history and symptoms. Given the high relapse potential of Plasmodium vivax, accurate species identification is critical to guide appropriate long-term management.

Studies suggest that the dynamic changes in cellular response might correlate with disease severity and outcomes in SARS-CoV-2 patients. The study aimed to investigate the dynamic changes of lymphocyte subsets in patients with COVID-19. In this regard, 53 patients with COVID-19 were prospectively included, classified as mild, moderate, and severe. The peripheral lymphocyte profiles (LyT, LyB, and NK cells), as well as CD4+/CD8+, CD3+/CD19+, CD3+/NK and CD19+/NK ratios, and their dynamic changes during hospitalization and correlation with disease severity and outcome were assessed. We found significant differences in CD3+ lymphocytes between severity groups (p < 0.0001), with significantly decreased CD3+CD4+ and CD3+CD8+ in patients with severe disease (p < 0.0001 and p = 0.048, respectively). Lower CD3+/CD19+ and CD3+/NK ratios among patients with severe disease (p = 0.019 and p = 0.010, respectively) were found. The dynamic changes of lymphocyte subsets showed a significant reduction in NK cells (%) and a significant increase in CD3+CD4+ and CD3+CD8+ cells in patients with moderate and severe disease. The ROC analysis on the relationship between CD3+ cells and fatal outcome yielded an AUC of 0.723 (95% CI 0.583–0.837; p = 0.007), while after addition of age and SpO₂, ferritin and NLR, the AUC significantly improved to 0.927 (95%CI 0.811–0.983), p < 0.001 with a sensitivity of 90.9% (95% CI 58.7–99.8%) and specificity of 85.7% (95% CI 69.7–95.2%). The absolute number of CD3+ lymphocytes might independently predict fatal outcomes in COVID-19 patients and T-lymphocyte subset evaluation in high-risk patients might be useful in estimating disease progression.

We thank Patrick Chambers for his interest

The aim of the study was to evaluate the vitamin D status in hospitalized COVID-19 patients and the correlation with C reactive protein (CRP), ferritin, fibrinogen, and peripheral blood leukocytes, as well as inflammatory derived indices. A prospective study was performed on 203 COVID-19 hospitalized patients, classified by disease severity. Blood was collected after admission, and inflammatory biomarkers and vitamin D status were assessed using routine laboratory procedures. No significant correlation was found between vitamin D serum levels and disease severity stratified by different age groups. However, the highest vitamin D levels were found in patients with mild disease: median 29.39 (IQR 12.12–44.02) ng/mL, while for moderate and severe forms the serum levels were significantly lower: median 15.10 (IQR 9.56–24.11) ng/mL for moderate, and 18.86 (IQR 12.50–27.88) ng/mL for severe; p = 0.009. Patients with no comorbidities showed a significantly higher level of vitamin D median 24.72 (IQR 16.05–31.52) ng/mL compared to subjects with at least one comorbidity: median 16.02 (IQR 9.81–25.22) ng/mL, p = 0.004. We did not find an association between vitamin D levels and inflammatory biomarkers except for significantly lower vitamin D levels in moderate and severe COVID-19 compared to mild disease forms.