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Background During the COVID-19 pandemic caused by SARS-CoV-2, coinfections with Streptococcus pneumoniae have emerged as a significant public health concern. The impact of these coinfections on disease severity and mortality rates remains underexplored. This study aims to address this gap by analyzing the clinical outcomes of patients coinfected with S. pneumoniae and SARS-CoV-2 at CHU Ibn Rochd in Casablanca, Morocco, between 2020 and 2022. Methods A cohort of 120 hospitalized patients diagnosed with S. pneumoniae infection was studied retrospectively and prospectively. Clinical and demographic data, vaccination status, and infection characteristics were collected. Among these patients, 41 were identified as coinfected with both pathogens. Statistical analyses, including multivariate logistic regression, were performed to assess associations between coinfection and clinical outcomes, such as ICU admission and mortality. Results Compared to non-coinfected patients, those coinfected with SARS-CoV-2 had higher ICU admission (53.7% vs. 24.05%) and mortality (39.02% vs. 13.9%) rates. Multivariate analysis identified coinfection and increasing age as independent predictors of severe outcomes. The most frequent pneumococcal serotypes were 3, 19 A, 6 B, and 9 V, with 31.7% of cases involving non-vaccine types. Most coinfected patients, especially those who died, were unvaccinated against pneumococcus or SARS-CoV-2. Conclusions Coinfection with SARS-CoV-2 significantly increases the risk of severe outcomes in patients with S. pneumoniae infection. These findings highlight the importance of early detection and support the implementation of comprehensive vaccination strategies targeting high-risk populations. Clinical trial number Not applicable.

Background The production of β-lactamases by the Enterobacterales family is currently the leading cause of antibiotic resistance. Urinary tract infections (UTIs) account for 25% of all infections, and UTIs caused by extended-spectrum beta-lactamase-producing Enterobacterales (ESBL-PE) constitute a serious public health concern in children and adult patients. The aim of this study was to describe the antimicrobial susceptibility profiles and molecular characteristics of ESBL-PE isolates from UTIs in Burundi. Methods A laboratory-based cross-sectional study involving 247 isolates of Enterobacterales was carried out at six selected hospital sites in Burundi. The bacterial isolates, which were collected over a nine-month period, were randomly selected from the biobank of isolated and identified enteric gram-negative bacteria from urine samples from UTI patients. The clinical and demographic characteristics of the UTI patients were extracted from the OpenClinic GA Information System via a structured data collection sheet. The ESBL-PEs were confirmed via a double-disk synergy test and PCR methods. The chi-square test was used to determine the relationship between epidemiological and microbiological variables; as well as the presence of ESBL-PE isolates. Results Among the 247 Enterobacterales isolates, Escherichia coli (72.4%) and Klebsiella pneumoniae (14.5%) predominated. Among the isolates, 28.74% were phenotypically positive for ESBL production. The high percentage of resistant isolates to antibiotics were observed for tetracycline (91.5%), amoxycillin-clavulanic acid (72.6%) and cotrimoxazole (65.6%). There was no resistance to either meropenem or imipenem. The most effective antibiotics were nitrofurantoin (91.1%) and amikacin (71.7%). The majority of the bla CTX-M genes (80.28%) were found in ESBL-PE isolates from UTI patients. The percentages of bla TEM and bla SHV genes were 53.52% and 25.35%, respectively. The bla CTX-M and bla TEM genes were the most prevalent coexisting resistance genes (26.8%), followed by the group of bla CTX-M , bla TEM , and bla SHV genes (18.3%). The bla TEM and bla SHV genes did not coexist in this study. Conclusion The bla CTX-M gene is predominant in UTIs, which are caused primarily by the ESBL-PE strains acquired in hospital and community settings. Amikacin, nitrofurantoin, imipenem and meropenem could be the drugs of choice for treating ESBL-PE in Burundi. On the basis of these findings, we suggest the development of infection prevention and control interventions, antibiotic stewardship policies and the establishment of routine surveillance of ESBL-PE in Burundi. The transmission dynamics of TEM - and CTX-M - type ESBL-PE need to be further understood in Burundian hospital and community settings.

Background Sepsis remains a major global health threat, particularly among children under five years in low- and middle-income countries. Africa bears a disproportionate burden of sepsis-related morbidity and mortality. Comprehensive data on the etiology, prevalence, and mortality of pediatric sepsis in Africa remain limited. This systematic review and meta-analysis aimed to determine the causative pathogens, pooled prevalence, mortality, and risk factors of sepsis in African children under five years of age. Methods Following PRISMA guidelines, we conducted a systematic search of PubMed, Web of Science, and Scopus for studies published from January 2000 to December 2024. Studies reporting microbiologically confirmed sepsis in children aged 0 to 60 months in Africa were included. Data were managed with Epi Info (version 7.2.7.0) and analyzed in R (version 4.4.2). Pooled prevalence and mortality were estimated using a random-effects model. Heterogeneity was assessed using I 2 statistics, and publication bias was evaluated via funnel plots, Egger’s test, and the trim-and-fill method. Subgroup analyses were performed to identify sources of heterogeneity. The quality of original studies was assessed using the National Heart, Lung, and Blood Institute’s Quality Assessment Tools. This review was registered in PROSPERO (CRD42024621969). Results Forty-six studies from 19 African countries, including 98,651 children and 59,521 pathogens, were analyzed. The most common pathogens were Klebsiella pneumoniae (25%), Acinetobacter baumannii (14.3%), and Staphylococcus aureus (13.2%). Gram-negative bacteria predominated (58.1%), with regional variations. The pooled prevalence of sepsis was 40.2% (95% CI: 26.8–55.4%), decreasing to 27.1% (95% CI: 15.5–43.0%) after adjustment for publication bias. Pooled mortality among clinically suspected cases was 16.3% (95% CI: 10.6–24.4%). Significant risk factors included prolonged rupture of membranes (OR 2.28; 95% CI: 1.30–4.00, p  < 0.001), low birth weight (OR 2.16; 95% CI: 1.21–3.87, p  < 0.001), and prematurity (OR 3.13; 95% CI: 1.94–5.08, p  < 0.001). Conclusion Sepsis in African children under five is highly prevalent and associated with substantial mortality, driven primarily by Gram-negative bacteria. Regional differences in pathogen distribution highlight the need for tailored antimicrobial strategies. These findings underscore the urgency of improving neonatal and pediatric care, enhancing diagnostic capacity, and implementing targeted prevention and management interventions to reduce sepsis burden in Africa. Clinical trial number Not applicable.

IntroductionAutoantibodies neutralizing type I interferon (AAN-I-IFN) have been found in at least 10-15% of critical COVID-19 pneumonia cases in various studies across North and Latin America, Oceania, Europe, and Asia. We sought to analyze the prevalence of AAN-I-IFN and describe the demographic, clinical, and laboratory characteristics in a Moroccan cohort of patients with life-threatening COVID-19.MethodsWe performed a cross-sectional and multicenter study of patients hospitalized in different university hospitals and clinical centers in Casablanca between November 2020 and December 2021.ResultsOur cohort included 195 patients with proven SARS-CoV-2 infection, 164 (84.1%) of whom developed severe or critical COVID-19 disease requiring hospitalization, and 31 (15.9%) patients developed mild or moderate disease. Patients with moderate or mild COVID-19 did not exhibit detectable levels of AAN-I-IFNs. Among the 20 patients with AAN-I-IFN, most were men (n=16, 80%), and age ranged from 19 to 101 years. 13 (65%) patients with severe COVID-19 and 7 (35%) with critical COVID-19 had AAN-I-IFNs. Twelve patients (60%) had autoantibodies (auto-Abs) neutralizing both high and low concentrations of IFN-α2 and/or IFN-ω, five (25%) had auto-Abs neutralizing only low concentrations of IFN-α2 or IFN-ω, two (10%) had auto-Abs neutralizing IFN-β (1ng/mL) only, and one (5%) had auto-Abs neutralizing high and low concentrations of IFN-α2 and IFN-ω, as well as IFN-β at 1ng/mL, but none neutralized IFN-β at 10 ng/mL.ConclusionOverall, AAN-I-IFNs were detected in 20/195 (10.3%) of Moroccan patients with life-threatening COVID-19 and in 20/164 (12.2%) patients with severe or critical disease, whereas none were detected in patients with mild or moderate COVID-19.

Psoriatic lesions are rarely complicated by recurrent infections. The aim of our study is to determine skin colonisation and nasal carriage of Staphylococcus aureus in patients with psoriasis and in healthy persons. a comparative study that include 33 patients with psoriasis and 33 healthy persons. Samples were taken from lesional and non lesional psoriatic skin and from healthy skin of control group. For S. aureus nasal carriage, we used sterile cotton tipped swabs. Out of 165 samples (66 skin samples and 33 nasal swabs), 26 S. Aureus strains were isolated in 26 persons, 57.69% in the control group and 42.3% in the psoriasis group. S. aureus skin colonization was found in one case (3%) in lesional psoriatic skin vs 9 cases (27.3%) in control skin OR=0.08 IC 95% (0.01-0.70) p=0.02 and in 12,1% in non lesional psoriatic skin vs 27, 3% in control skin (p =0,13). This colonization was less important in lesional psoriatic skin (3%) than in non lesional psoriatic skin (12.1%) p= 0.20. Nasal screening identified (7/33) 21, 21% S. aureus carriers in psoriasis group and in control group. Our results are in consensus with literature findings. They have confirmed the importance of antimicrobial peptides in Innate immunity of human skin. These peptides are normally produced by keratinocytes in response to inflammatory stimuli such as psoriasis. Their high expression in psoriasis skin reduces the risk of skin infection and skin colonization with S. Aureus.

Epidermodysplasia verruciformis (EV) is a rare genodermatosis caused by β-human papillomaviruses (HPV) in immunodeficient patients. EV is characterized by flat warts and pityriasis-like lesions and might be isolated or syndromic, associated with some other infectious manifestations. We report here three patients from two independent families, with syndromic EV for both of them. By whole exome sequencing, we found that the patients carry new homozygous variants in STK4, both leading to a premature stop codon. STK4 deficiency causes a combined immunodeficiency characterized by a broad infectious susceptibility to bacteria, viruses, and fungi. Auto-immune manifestations were also reported. Deep immunophenotyping revealed multiple cytopenia in the three affected patients, in particular deep CD4+ T cells deficiency. We report here the fourth and the fifth cases of the syndromic EV due to STK4 deficiency.

Acute bronchiolitis is the leading cause of infant hospitalization worldwide, with respiratory syncytial virus (RSV) historically predominating. Prospective virological data for the 2025–2026 epidemic season in Morocco were lacking. A prospective observational cohort study was conducted at the Department of Pediatric Infectious Diseases and Clinical Immunology, Casablanca Mother-Child Hospital, from August 2025 through March 2026. Consecutive infants aged 1–24 months hospitalized with acute viral bronchiolitis underwent nasopharyngeal sampling and multiplex rapid antigen testing for RSV, influenza A, influenza B, and SARS-CoV-2. A total of 131 infants were enrolled (median age 4.8 months; male-to-female ratio 0.84:1). At least one virus was identified in 63 patients (48.1%; 95% CI 39.1–57.3%). RSV predominated: 49 sole infections and 2 co-infections with influenza A, totaling 51 positives (80.9% of virus-positive cases; 38.9% of the cohort). Influenza A totaled 8 cases (12.7%), including the 2 co-infections; influenza B accounted for 2 further cases (3.2%). SARS-CoV-2 was not detected. Epidemic activity peaked in January 2026 (65 admissions), declining through February (34) and March (12). All detected pathogens have licensed preventive options, supporting the introduction of nirsevimab, maternal RSV vaccination, and seasonal influenza vaccination as public health priorities in Morocco.

Innate immune deficiencies can impair both cellular and humoral immune responses. In contrast, other immune functions may appear normal, leading to increased susceptibility to specific pathogens, such as severe viral infections or Mendelian Susceptibility to Mycobacterial Disease (MSMD). Studying these deficiencies is essential for understanding the pathophysiology of these infectious diseases. This review highlights the diverse spectrum of genetic mutations contributing to defects in innate and intrinsic immunity, including Mendelian susceptibility to mycobacterial disease (MSMD), chronic mucocutaneous candidiasis, and predispositions to invasive bacterial and viral infections. Identifying key mutations in pathprovideh such as TLR3, IFN signaling, and IL-17A/F immunity provides valuable insights into the pathogenesis of these conditions. Our findings underscore the need for early genetic diagnosis and targeted interventions, particularly in regions with high undiagnosed cases, to reduce the morbidity and mortality associated with defects in innate and intrinsic immunity.

Introduction Viruses are the most common triggering factors for asthma exacerbation during the autumn and winter seasons. Viruses, such as influenza A and rhinovirus, play a major role in the occurrence of severe exacerbation of asthma. This association between viral infection and asthma exacerbation in children is a result of the antiviral response of the immune system and various anti-inflammatory phenomena. In this work, we aimed to identify the virological profile of asthma exacerbation in children and analyze the correlation between viral infection type and the severity of exacerbation. Materials and methods This retrospective study was conducted from January 2016 to January 2024. The study included children hospitalized for asthma exacerbation associated with signs of viral-like respiratory infection with positive virological testing by multiplex real-time polymerase chain reaction or rapid test in the case of influenza A or respiratory syncytial virus (RSV). Data analysis was performed with Microsoft Excel and SPSS software using a previously established data collection sheet Results Thirty cases were collected for the study period. The mean age of the patients was 4 years and 8 months, with a male-to-female ratio of 3.3. Eighteen patients were known to have asthma, of which nine had uncontrolled asthma, and exacerbation was inaugural in 12 patients. Viral shedding was found in 14 patients. A viral agent was found in all patients, with coinfection of two or more viruses in three patients. The viruses found were influenza A (18 cases), coupled rhinovirus/enterovirus (eight cases), RSV (eight cases), human metapneumovirus (three patients), and parainfluenza type IV in only one inaugural patient. Asthma exacerbation was severe in 20 patients, moderate in eight patients, and two patients had severe acute asthma requiring intensive care management. We noted a higher frequency of severe exacerbation among those with an influenza A viral infection. All patients with RSV infection exhibited moderate exacerbation. No other significant correlation between asthma severity and other types of viruses was found. Conclusions Our results demonstrate the major role played by viruses in triggering asthma exacerbation, primarily influenza virus, followed by enterovirus, rhinovirus, RSV, and metapneumovirus. Larger-scale studies should be carried out to establish a more complete virological profile and further investigate the viral factor in the management of asthma in children.

Nouveau-né de sexe féminin, ayant présenté une asphyxie périnatale pour laquelle il a été réanimé. Il a été référé ensuite pour sclérème cutané, constaté par les parents au dixième jour de vie. Les lésions étaient des placards érythémateux nodulaires indurés, évoquant une cytostéatonécrose néonatale au niveau des régions fessières. L''évolution a été notée par une hypercalcémie progressive atteignant 128 mg/L (80-110 mg/L), ce qui a indiqué une ré-hospitalisation à un mois de vie. L'échographie rénale a objectivé une néphrocalcinose médullaire. Le traitement a associé une hyperhydratation, des diurétiques, des corticoïdes et une abstention d'administration de la vitamine D avec une surveillance clinique et biologique de la calcémie. L'évolution a été vers la régression des lésions cutanées et la normalisation de la calcémie un mois après. La surveillance échographique de la néphrocalcinose est toujours en cours.