Human metapneumovirus (hMPV), a member of the Pneumoviridae subfamily, has emerged as a significant etiological agent of acute respiratory tract infections across diverse age groups, particularly affecting infants, the elderly, and immunocompromised individuals. Since its initial identification in 2001, hMPV has been recognized globally for its seasonal circulation pattern, predominantly in late winter and spring. hMPV is a leading etiological agent, accounting for approximately 5% to 10% of hospitalizations among pediatric patients with acute respiratory tract infections. hMPV infection can result in severe bronchiolitis and pneumonia, particularly in young children, with clinical manifestations often indistinguishable from those caused by human RSV. Primary hMPV infection typically occurs during early childhood; however, re-infections are frequent and may occur throughout an individual’s lifetime. hMPV is an enveloped, negative-sense RNA virus transmitted through respiratory droplets and aerosols, with a 3–5-day incubation period. The host immune response is marked by elevated pro-inflammatory cytokines, which contribute to disease severity. Advances in molecular diagnostics, particularly reverse transcription–quantitative polymerase chain reaction (RT-qPCR) and metagenomic next-generation sequencing (mNGS), have improved detection accuracy and efficiency. Despite these advancements, treatment remains largely supportive, as no specific antiviral therapy has yet been approved. Promising developments in vaccine research, including mRNA-based candidates, are currently undergoing clinical evaluation. This review synthesizes current knowledge on hMPV, highlighting its virological, epidemiological, and clinical characteristics, along with diagnostic advancements and emerging therapeutic strategies, while underscoring the critical role of continued research and sustained preventive measures—including vaccines, monoclonal antibodies, and non-pharmaceutical interventions—in mitigating the global burden of hMPV-related disease.

(1) Background: The importance of group A streptococcus (GAS) infection severity has been recognized in children and adults. However, to our knowledge, there have been no systematic reviews or pooled assessments of the incidence and outcome of invasive GAS (iGAS) disease in neonates, a potentially high-risk population. Therefore, we performed a systematic review of available data regarding the risk factors, clinical presentation, and outcome of GAS infection in neonates. (2) Methods: An electronic search of the existing literature was carried out during the period July 2023–September 2023 in the PubMed and Scopus databases, considering studies referring to GAS infection in the neonatal population. (3) Results: Overall, 39 studies met all the inclusion criteria and were included in this review, evaluating data from 194 neonates. Unfortunately, there were a lot of missing data among the retrieved studies. Our systematic review highlighted the presence of differences with regards to clinical presentation, infection sites, and outcome of GAS invasive disease between neonates with early-onset (EOS) or late-onset sepsis (LOS). Common characteristics of EOS included respiratory distress, rapid deterioration, and high mortality rate irrespective of the infection site, while rash, gastrointestinal tract symptoms, and fever appeared to be the most frequent symptoms/clinical signs and manifestations of LOS disease. The management of severe invasive iGAS disease consists mainly of specific antimicrobial treatment as well as supportive care with fluids and electrolyte supplementation, minimizing or counteracting the effects of toxins. Furthermore, a mortality rate of approximately 14% was recorded for iGAS disease in the total of all studies’ neonates. (4) Conclusions: Although iGAS is a rare entity of neonatal infections, the potential severity of the disease and the rapid deterioration requires the development of quick analysis methods for the detection of GAS allowing the prompt diagnosis and administration of the indicated antibiotic treatment. Furthermore, given the exceptional risk for both the pregnant woman and the neonate, it is very important to raise awareness and create easily accessible guidelines that could facilitate the prevention and management of maternal as well as the subsequent neonatal severe iGAS disease.

The COVID-19 pandemic has raised significant concerns regarding its potential impact on maternal and neonatal health. This study aimed to investigate the immunologic and hemostatic profiles of neonates exposed to SARS-CoV-2 during the peripartum period (0–14 days prior to delivery). This retrospective study included 28 neonates born to COVID-19-positive mothers during the peripartum period and a control group of 54 neonates born to mothers who never tested positive for SARS-CoV-2 during pregnancy. Arterial blood samples were collected from all neonates on the second day of life for the simultaneous assessment of full blood count, C-reactive protein (CRP), serum interleukin-6 (IL-6), and Interferon gamma-induced protein 10 (IP-10) levels, as well as Rotational Thromboelastometry (ROTEM) tests (EXTEM, INTEM, and NATEM). Neonates born to COVID-19-positive mothers and those born to COVID-19-negative mothers exhibited similar coagulation profiles based on ROTEM analysis. Multiple linear regression analysis revealed that peripartum COVID-19 infection was associated with higher IP-10 levels in neonates (coefficient: +16.8, 95% CI: +9.0 to +24.6, p < 0.0001). Our study findings suggest that the presence of immunologic disturbance in neonates is related to recent peripartum exposure to maternal SARS-CoV-2 infection, as evidenced by increased IP-10 levels in blood samples obtained from neonates born to SARS-CoV-2-positive mothers. However, peripartum exposure to maternal SARS-CoV-2 did not appear to disrupt the hemostatic profile of the exposed newborns based on ROTEM test results.

Blau syndrome (BS) is a rare, autosomal dominant monogenic autoinflammatory disease, usually presenting as a triad of symptoms (granulomatous dermatitis, uveitis, and nonerosive arthritis) and caused by gain-of-function mutations in the nucleotide oligomerization domain 2 (NOD2) gene. However, very few reports in children of copresence of BS with large vessel vasculitis exist. We hereby describe a case of BS associated with clinical features of Takayasu arteritis. An 8.5-year-old boy presented with hypertension, cardiac insufficiency, arthritis, and ocular disease. Among other investigations, he underwent cervical and chest computed tomography and computed tomography angiography scans that revealed the presence of type IIa Takayasu arteritis lesions. Genetic analysis revealed a heterozygous mutation of NOD2 gene leading to the amino acid exchange Arg-587-Cys in the NACHT domain of the NOD2 protein (R587C) as pathogenic cause of BS. He received treatment with prednisolone, methotrexate, and infliximab (antitumor necrosis factor-α) in addition to antihypertensive medication with a favorable clinical response. Cases of BS should be investigated for the coexistence of Takayasu arteritis. However, further research is required to delineate a possible common pathogenic mechanism between the two clinical entities.

Background/Objectives: Perinatal asphyxia constitutes a major complication of the perinatal period with well-described effects on multiple organs and systems of the neonate; its impact, though, on the ovaries is hardly known. The objective of the present study was to investigate potential histological alterations of the ovaries in an animal model of perinatal asphyxia with or without resuscitation. Methods: This was a prospective, randomized animal study; 26 female Large White/Landrace piglets, aged 1–4 days, were the study subjects and were randomly allocated in 3 groups. In Group A (control), the animals had their ovaries surgically removed without any manipulation other than the basic preparation and mechanical ventilation. The other 2 groups, B (asphyxia) and C (asphyxia/resuscitation), underwent asphyxia until bradycardia and/or severe hypotension occurred. At the hemodynamic compromise, animals in group B had their ovaries surgically removed, while animals in group C were resuscitated. Following return of spontaneous circulation (ROSC), the latter were left for 30 min to stabilize and subsequently had their ovaries surgically removed. The ovarian tissues were assessed by the pathologists for the presence of apoptosis, balloon cells, vacuolated oocytes, and hyperplasia of the stroma. The histological parameters were graded from 0 (absence) to 3 (abundant presence). Results: The presence of balloon cells and apoptosis was found to be more prominent in the ovaries of animals in groups B and C, compared to that of the control group at a statistically significant degree (p = 0.0487 and p = 0.036, respectively). A significant differentiation in balloon cell presence was observed in cases with higher grading (2–3) in the asphyxia group (with or without resuscitation) (p value: 0.0214, OR: 9, 95% CI: 1.39–58.4). Although no statistically significant difference was noted regarding the other 2 histological parameters that were studied, there was a marked negative correlation between the duration of asphyxia and grade of vacuoles in oocytes when the potential effect of the duration of asphyxia or resuscitation on the histological findings was investigated (r = −0.54, p = 0.039). Conclusions: We aimed at investigating the potential effect on the neonatal ovaries in our animal model of perinatal asphyxia. Given that the presence of apoptosis and balloon cells was more prominent in cases of asphyxia, it can be speculated that perinatal asphyxia might have an impact on the neonatal ovaries in addition to the other, better-studied systemic effects. More research is needed in order to clarify the potential effect of perinatal asphyxia on the ovaries.