Background: Neonatal bullous pneumopathy is a severe complication of staphylococcal respiratory infection, traditionally attributed to strains producing Panton-Valentine leukocidin (PVL). Clinically indistinguishable disease nonetheless arises with PVL-negative strains, creating a diagnostic paradox with immediate therapeutic consequences. Methods: We report an index case of PVL-negative bullous pneumopathy in an infant born at 32 weeks’ gestation and analyze it through 5 falsifiable mechanistic hypotheses, derived from a structured literature synthesis (72 sources, updated June 29, 2026) and Monte Carlo modeling (10,000 iterations), organized as a Lakatosian research program and appraised against independent datasets. Results: The analysis indicates that alpha-hemolysin (Hla; ∼95% of strains vs. 2% to 5% for PVL) is the principal alternative effector of injury; that neonatal NLRP3 inflammasome hyperactivation amplifies tissue destruction; that preterm surfactant deficiency removes a protective barrier; that phenol-soluble modulins contribute to necrosis; and that PVL detection can generate false negatives. Modeling estimated the probability of severe disease at 0.73 (95% CI: 0.68-0.78), with mortality falling from 25.6% without antitoxin therapy to 5.5% with a protein-synthesis inhibitor plus intravenous immunoglobulin. Conclusions: A negative PVL test must not reassure the clinician facing neonatal necrotizing pneumonia; toxin-suppressive therapy should be considered irrespective of PVL status, within a multimarker diagnostic strategy.
Background: Dengue is a widespread mosquito-borne illness across tropical and subtropical areas. Leukopenia is a common hematological abnormality in dengue infection; however, the association between dengue serological markers and white blood cell (WBC) count has not been well characterized. Objective: To evaluate the association between dengue nonstructural protein 1 (NS1) antigen positivity, dengue immunoglobulin M (IgM) antibody positivity, and WBC count categories among serologically confirmed dengue patients. Materials and Methods: A retrospective observational study was conducted among 457 serologically confirmed dengue patients attending a tertiary care teaching hospital between October and December 2025. Demographic characteristics, dengue NS1 antigen status, dengue IgM antibody status, and WBC counts were obtained from laboratory records. WBC counts were categorized as leukopenia (<4000 cells/mm 3 ), normal (4000 to 11,000 cells/mm 3 ), or leukocytosis (>11,000 cells/mm 3 ). Associations between serological markers and WBC count categories were analyzed using Pearson’s chi-square test. Odds ratios (ORs) with 95% CIs were calculated where appropriate. Results: Among the 457 patients, leukopenia was observed in 145 (31.7%), while 305 (66.7%) had normal counts and 7 (1.5%) had leukocytosis. NS1 antigen was positive in 288 patients (63.0%) and dengue IgM antibody in 264 (57.8%). Leukopenia was present in 128 of 288 NS1 antigen-positive patients (44.4%) compared with 17 of 169 NS1 antigen-negative patients (10.1%) (Fisher exact test, P < 0.001; OR: 7.15; 95% CI: 4.12-12.43). As a marker of NS1 antigen positivity, leukopenia showed a specificity of 89.9% (95% CI: 84.5-93.6) and a positive predictive value of 88.3% (95% CI: 82.0-92.5), but a sensitivity of only 44.4% (95% CI: 38.8-50.2). Dengue IgM antibody positivity showed the opposite relationship: leukopenia was present in 63 of 264 IgM-positive patients (23.9%) compared with 69 of 177 IgM-negative patients (39.0%) (Fisher exact test, P < 0.001; OR: 0.49; 95% CI: 0.32-0.74). Leukopenia was most frequent in the small group with equivocal IgM results (13/16, 81.2%). Conclusions: Leukopenia was markedly more frequent among NS1 antigen-positive patients and markedly less frequent among IgM antibody-positive patients, indicating that leukopenia clusters in the early viremic phase of dengue infection and resolves as the antibody response develops. Leukopenia was specific but insensitive as a marker of the NS1 antigen-positive phase, so its principal practical value may lie in informing the choice and timing of serological testing rather than in confirming a diagnosis already established by NS1 antigen detection. Prospective multicenter studies recording the day of illness at presentation, serial hematological measurements, quantitative NS1 antigen levels, and clinical outcomes are warranted to validate these findings.
Background: Mycoplasma pneumoniae is a well-established pathogen that affects both the upper and lower respiratory tracts in children and adolescents. It can also affect the skin, mucous membranes, central nervous system, and other tissues. Epidemics occur every 3 to 5 years and by the end of 2023, a resurgence of cases was reported, suggesting a new epidemic. This study aimed to characterize the pediatric M. pneumoniae cases over the past 14 years. Methods: We reviewed medical records of patients aged 0 to 18, evaluated in the emergency department or hospitalized, with a positive PCR result for M. pneumoniae from respiratory specimens between 2011 and 2024. Results: A total of 270 patients with a positive PCR for M. pneumoniae were included. Three outbreaks were identified: 2015 to 2016, 2018 to 2019, and 2024, with the latter being the most significant, comprising 40.3% of the study population. The median age at presentation was 7 years (IQR: 3.8 to 11), with 37% of patients under 5 years; 25% aged 2 to 5 years, and 12% were under 2 years old. Seventy-four patients (27.4%) had a history of severe comorbidities. Two hundred five patients (76%) presented with pneumonia, 78 (29%) with asthma exacerbations, and 45 (16.7%) with extrapulmonary manifestations. Fourteen patients (5.2%) required pediatric intensive care, and only 22 of them required mechanical ventilation. No mortalities occurred. Conclusion: Our data highlights a substantial burden of M. pneumoniae in children under 5 years old. This underscores the importance of maintaining a high index of suspicion and considering this pathogen in young children during outbreaks, ensuring timely diagnosis and appropriate management.
Opportunistic infections remain a major cause of morbidity and mortality in individuals with advanced human immunodeficiency virus (HIV) disease. Although central nervous system opportunistic infections are common, simultaneous infection by multiple nonbacterial pathogens is rare. We report a 46-year-old man with advanced HIV disease and profound immunosuppression who presented with gastrointestinal symptoms and altered mental status. Brain magnetic resonance imaging initially suggested cerebral toxoplasmosis; however, persistent symptoms and new lesions despite trimethoprim-sulfamethoxazole prompted further investigation. Cerebrospinal fluid analysis and stereotactic brain biopsy confirmed concurrent central nervous system coinfection with Toxoplasma gondii , Cryptococcus neoformans , and cytomegalovirus. Extraneurological involvement included cytomegalovirus colitis and chorioretinitis. Combination therapy with ganciclovir, amphotericin B, fluconazole, and trimethoprim-sulfamethoxazole resulted in marked clinical improvement, allowing discharge after 59 days. This case highlights the importance of maintaining a broad differential diagnosis and pursuing advanced diagnostics when empiric therapy fails in advanced HIV disease.
