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In 2019, pneumonia caused 740,180 deaths in children under five years of age, representing 22% of global mortality in this age group. During the COVID-19 pandemic, public health interventions markedly reduced the circulation of most respiratory viruses other than SARS-CoV-2, leading to significant post-pandemic shifts in respiratory pathogen epidemiology. This study aimed to characterize the epidemiology, clinical features, and risk factors associated with respiratory viruses and bacteria causing pneumonia in Mexican children during the late pandemic and post pandemic periods. Children younger than 14 years with pneumonia were recruited from seven hospitals in Mexico. Demographic and clinical data were collected, and nasopharyngeal swabs were analyzed using a multiplex PCR panel detecting 19 viruses and 7 bacteria. Univariate, bivariate, and logistic regression analyses were performed (SPSS v25). A total of 1715 children were included: 704 during the pandemic (2021-2023) and 1011 post-pandemic (2023-2025). Co-infections (72% vs. 65%, p < 0.001), virus-virus co-infections (25% vs. 11%, p < 0.001), and single viral infections (20% vs. 15%, p = 0.007) were more frequent during the pandemic. Pathogen detection was high in both periods, though negative samples increased post-pandemic (5.4% vs. 15%, p < 0.001). During the pandemic, the 5 most frequently detected pathogens were rhinovirus (66%), RSV A and B (38%), Streptococcus pneumoniae (30%), Haemophilus influenzae (28%), human metapneumovirus (13%). In the post-pandemic period, the 5 most frequently detected pathogens were rhinovirus (52%), Haemophilus influenzae (36%), Streptococcus pneumoniae (35%), RSV A and B (28%), metapneumovirus (11%). Rhinovirus and RSV predominated during the pandemic, whereas Haemophilus influenzae, Streptococcus pneumoniae, parainfluenza viruses, Bordetella pertussis, and Mycoplasma pneumoniae significantly increased post-pandemic. Pediatric pneumonia epidemiology shifted from a predominantly viral profile during the pandemic to increased bacterial detections and virus-bacteria co-infections post-pandemic, alongside re-emergence of typical RSV and influenza seasonality. Higher mean age and rhinovirus as the most frequent pathogen persist after the pandemic. Sustained molecular surveillance and reinforced vaccination programs remain essential in the post-pandemic era.

To evaluate clinical outcomes, treatment response and predictors of seizure freedom after vagus nerve stimulation in patients with drug-resistant epilepsy in a Mexican cohort. We conducted a retrospective multicenter cohort across 13 epilepsy centers in Mexico (2003-2024) including patients aged ≥4 years with drug-resistant epilepsy or epileptic encephalopathy. Treatment response was defined as at least 50% seizure reduction and Engel outcomes. Logistic regression identified predictors of seizure freedom. Model performance was assessed with receiver operating characteristic analysis, area under the curve, Hosmer-Lemeshow test, and a confusion matrix. Ninety-three patients (51 children, 42 adults) were included. At 1 year, median monthly seizure frequency decreased by 82.5% (40-7; p < .001). The incidence of status epilepticus declined by 92.8%, acute prolonged seizures by 80.9%, the burden of antiseizure medications by 25%, and epilepsy-related hospitalizations by 100% (all p < .001). Overall, 68.8% achieved ≥50% reduction and 11.8% became seizure-free. On univariate analysis, comorbidities, multiple seizure types, higher baseline seizure frequency, greater number of antiseizure medications, and magnet use were inversely related to seizure freedom, while normal brain MRI showed a direct relationship. On multivariable analysis, only baseline seizure frequency ≥30/month independently predicted seizure freedom (p = .047), corresponding to 97.7% lower odds. A predictive model incorporating comorbidities and number of antiseizure medications improved discrimination (p < .001) with 86.6% sensitivity and 81.8% specificity. Vagus nerve stimulation was associated with substantial seizure frequency reduction, lower morbidity, and less healthcare utilization, with a favorable safety profile. Baseline seizure burden emerged as the key predictor of seizure freedom and may guide patient selection, supporting earlier vagus nerve stimulation consideration in drug-resistant epilepsy.

Primary Sjögren's syndrome (pSS) is an autoimmune disease characterized by inflammation and damage to salivary and lacrimal glands. Its etiology involves both genetic and environmental factors. Among susceptibility genes, IRF5 has been highlighted in European populations, but evidence in non-European groups remains limited. This study evaluated whether IRF5 variants rs2004640G/T, rs2070197T/C, rs10954213G/A, and rs59110799G/T are associated with pSS susceptibility, clinical manifestations, or the presence of autoantibodies in a Mexican population. The diagnosis was confirmed by rheumatologists using the 2016 ACR-EULAR classification criteria for pSS. Genotyping was performed using TaqMan probes in 231 controls and 132 pSS patients from central Mexico. Associations were analyzed through binary logistic regression under different genetic models, adjusting for age and geographic origin. Clinical correlations were examined with SNPStats, and haplotypes were constructed using Haploview. Results showed that all four IRF5 variants were significantly associated with pSS susceptibility. Moreover, rs2004640, rs2070197, and rs10954213 variants were associated with arthritis, a frequent clinical manifestation in pSS patients. This represents the first evidence in a Latin American population demonstrating that IRF5 variants contribute to increased risk of developing pSS. These findings suggest ethnicity-specific genetic influences and highlight the importance of expanding research beyond European cohorts. Replication in larger samples and functional analyses are needed to confirm these associations and clarify their biological relevance.

BackgroundHuman papillomavirus (HPV) is the most frequent sexually transmitted virus, with high importance due its oncogenic risk. Previous studies have reported an association between genital dysbiosis and HPV infection in women and also in men co-infected with HPV and HIV. However, it remains to be determined whether penile skin dysbiosis is associated with HPV infection in men who are HIV-negative. This study characterizes the penile skin microbiota (PSM) of HPV-positive and HPV-negative men, hypothesizing that HPV infection is linked to dysbiotic anaerobic-dominated communities.MethodsA cross-sectional study was conducted on 103 sexually active HIV-negative men (70 HPV-negative, 33 HPV-positive). Those who tested HPV-positive were genotyped. The PSM of all samples was analyzed using 16S rRNA sequencing of the V4 region. Alpha and beta diversity were compared. Community State Types (CSTs) were identified using hierarchical clustering. Associations between CSTs and HPV status were tested adjusting for sexual preference.ResultsHPV-positive men exhibited significantly higher microbial richness than HPV-negative men (Chao1 p = .02), particularly those with high-risk genotypes (Chao1 p = .03). Five CSTs were identified, with CST-5 (dominated by Finegoldia and other anaerobes) showing a three-fold higher likelihood of HPV positivity (OR = 3.11, 95% CI: 1.22-8.22) compared to other CSTs. CST-5 also displayed reduced abundance of commensals like Corynebacterium and Staphylococcus.ConclusionsSubclinical HPV infection in HIV-negative men was associated with a dysbiotic PSM, characterized by an increased abundance of anaerobic bacteria alongside with a reduced proportion of facultative anaerobic genera. These findings suggest that PSM composition may influence HPV susceptibility or persistence. Longitudinal studies are needed to explore causality.

&lt;p&gt;&lt;strong&gt;Background. &lt;/strong&gt;Rickettsioses are zoonoses caused by pathogenic bacteria of the genus &lt;em&gt;Rickettsia &lt;/em&gt;transmitted through bites or feces of ectoparasites (ticks, fleas, lice, and hematophagous mites). Rodents and dogs play a role in the transmission of pathogenic species. However, little is known about the factors associated with the chances of infections and their spatial distribution at the local scale. &lt;strong&gt;Objective.&lt;/strong&gt; To determine the frequency of &lt;em&gt;Rickettsia&lt;/em&gt; Spotted Fever group (SFG) and Typhus group (TG) in dogs and rodents, their spatial distribution, and the factors associated with the &lt;em&gt;Rickettsia&lt;/em&gt; infection at the local scale. &lt;strong&gt;Methods.&lt;/strong&gt; DNA was obtained from 64 dog blood samples and 36 rodent spleens from 48 dwellings in Ucú, Yucatan, Mexico. &lt;em&gt;Rickettsia&lt;/em&gt; was determined by multiplex semi-nested PCR (snPCR). The predictor variables for infection in dogs and rodents were analyzed using generalized linear models (GLM) (p&amp;lt;0.05). &lt;strong&gt;Results.&lt;/strong&gt; SnPCR revealed &lt;em&gt;Rickettsia&lt;/em&gt; in 28.1 % (18/64, 95 % CI 17.6 %-40.8 %) of the dogs and 27.8 % (10/36, 95 % CI 14.2 %-45.2 %) of the rodents. &lt;em&gt;Rickettsia&lt;/em&gt; SFG was detected in dogs; rodents hosted both &lt;em&gt;Rickettsia &lt;/em&gt;TG and SFG. According to the corresponding GLM, dogs living in the interior area of Ucú had a lower chance of infection by &lt;em&gt;Rickettsia&lt;/em&gt; SFG (OR = 0.14) than those living in the other regions. The presence of opossums (&lt;em&gt;Didelphis&lt;/em&gt; spp.) in dwelling premises increases the chances of &lt;em&gt;Rickettsia&lt;/em&gt; TG infection in rodents (OR = 14), and the presence of SFG-infected dogs in dwelling premises increases the chances of &lt;em&gt;Rickettsia&lt;/em&gt; SFG infection in rodents (OR = 21). &lt;strong&gt;Implications.&lt;/strong&gt; The spatial distribution of &lt;em&gt;Rickettsia&lt;/em&gt; hosts was assessed at Ucú. The specific &lt;em&gt;Rickettsia&lt;/em&gt; species were not identified, nor were the probable vectors evaluated. While the results provide a local overview, they do not accurately represent the epidemiological conditions at other sites. The information is valuable and should be considered in developing prevention measures for Rickettsiosis. &lt;strong&gt;Conclusions.&lt;/strong&gt; Statistical modelling revealed that the spatial location of the dwelling, the presence of infected dogs, and the presence of opossums in the same dwelling serve as proxies for the &lt;em&gt;Rickettsia&lt;/em&gt; infection in the captured rodents.&lt;/p&gt;

The use of cannabidiol (CBD) as an alternative pharmacological approach for the symptomatic management of epilepsy has gained attention due to its potential efficacy, particularly in drug-resistant cases of epilepsy. Although multiple studies have described that CBD reduces neuronal hyperexcitability, the mechanistic basis of CBD remains a topic of ongoing research. In this study, we provide an electrophysiological portrayal of CBD’s effects on the glutamatergic transmission and intrinsic excitability of layer V pyramidal neurons of the human neocortex resected from drug-resistant epilepsy patients. The perfusion of CBD transiently depressed the field excitatory potential amplitude elicited in layer I/II and recorded in layer V without altering the paired-pulse ratio, suggesting a postsynaptic locus of action for CBD. Cortical slices perfused with 4-aminopyridine exhibited an increased number of spontaneous synaptic events that were abolished in the presence of CBD. At the cellular level, whole-cell patch-clamp recordings showed that CBD decreased the excitability of layer V pyramidal neurons, as evidenced by changes in the somatic input resistance, the membrane time constant, the hyperpolarization-induced “sag” conductance, the rheobase current needed to elicit an action potential, and the firing discharge in response to depolarizing current steps. Consistent with the last observation, CBD decreased the amplitude of the TTX-sensitive inward currents without altering the kinetics of the macroscopic outwardly directed currents. CBD washout restored the passive and active electrophysiological properties of pyramidal neurons. Collectively, these experiments demonstrate that CBD decreases the neuronal excitability of human cortical neurons from patients with drug-resistant epilepsy.