Introduction: Despite the advances in its prevention, invasive meningococcal disease (IMD) remains a serious health problem worldwide due to its high morbidity and mortality, including in Romania, with 22% mortality rate. The objectives were to describe the trends of IMD cases admitted to a tertiary care hospital in Romania, over 24 years, and the case fatality rate (CFR) by age, year of admission, and Neisseria meningitidis serogroups. Materials and Methods: A retrospective study was conducted in IMD patients admitted to the National Institute for Infectious Diseases “Prof. Dr. Matei Bals”, Bucharest, Romania, between 2001 and 2024. Results: A total of 256 IMD patients were admitted, 171 under fourteen years, out of which 75 were infants. Most cases were reported before 2008. The case distribution showed 90 patients (35%) with meningitis, 84 (32%) with meningococcaemia, and 82 (32%) with an association of both. Serogroup B was the most frequently and steadily found (58 cases). The overall CFR was 12%. CFR was highest in infants younger than 6 months (19%) and meningococcaemia cases (29%). Conclusions: In our study, IDM had the highest frequency and CFR in infants and meningococcaemia cases. The trends showed a decline in cases after 2008. Serogroup B was the most prevalent and stable strain over 24 years.

Sepsis is a life-threatening syndrome driven by a dysregulated host response to infection and is frequently complicated by sepsis-associated encephalopathy (SAE), which contributes to long-term cognitive and neuropsychiatric sequelae. Despite advances in critical care, effective targeted therapies for SAE remain limited. Aquaporin-4 (AQP4), the predominant astrocytic water channel, plays a central role in cerebral water homeostasis, neuroinflammatory signaling, and blood–brain barrier integrity, suggesting its potential involvement in sepsis-induced cerebral dysfunction and neurorepair processes. Polymicrobial sepsis was induced in C57BL/6J mice using the cecal ligation and puncture (CLP) model. AQP4 activity was pharmacologically modulated through either inhibition or facilitation following sepsis induction. Disease severity was assessed using physiological parameters and a modified murine sepsis score. Neurological outcomes were evaluated through standardized behavioral tests assessing locomotor activity, motor coordination, cognitive performance, and depressive-like behavior. Neuroinflammatory and neuronal changes were examined by immunohistochemical analyses of microglial activation (Iba1), astroglial reactivity (GFAP), neuronal integrity (NeuN), and AQP4 expression. Compared with AQP4 facilitation, pharmacological inhibition of AQP4 was associated with a more favorable clinical recovery profile, reflected by lower sepsis severity scores and a more favorable body weight trajectory during the recovery phase. Behavioral analyses demonstrated preserved cognitive function, enhanced motor coordination, and reduced depressive-like behavior in AQP4 inhibitor-treated mice compared with animals receiving AQP4 facilitation. At the histological level, the inhibitor-treated group showed lower microglial and astroglial activation and better preservation of neuronal markers than the facilitator-treated group, whereas AQP4 facilitation exacerbated neuroinflammatory responses and neuronal alterations. These findings highlight a dual, context-dependent role of AQP4 in sepsis-associated cerebral dysfunction. These findings suggest that AQP4 modulation influences sepsis-associated cerebral dysfunction in a context-dependent manner. Within our experimental design, AQP4 facilitation was associated with worse outcomes, whereas AQP4 inhibition was associated with a comparatively more favorable neurobehavioral and histological profile.