Risk Of Sudden Infant Death Syndrome Research Articles

Supine Sleep-Promoting Baby Mattress: SIDS Prevention and Athlete Injury Relief

Sudden Infant Death Syndrome (SIDS) is a leading cause of death in infants aged one to 12 months, primarily occurring during sleep. Consequently, there is considerable interest among researchers and healthcare professionals regarding the sleeping environment and potential risk factors. One identified risk factor is infants sleeping prone (on their stomach), making supine (on the back) sleeping the recommended position. Associate Research Fellow Shing-Jye Chen from the Department of Sports Science Research at the Taiwan Institute of Sports Science (TISS) is developing a hammock-like air-based baby mattress covered with breathable mesh. This mattress is designed to promote supine sleeping and prevent babies from rolling onto their stomachs during sleep. It features air tubing within tensioned mesh fabric that automatically adjusts to suspend and support the baby’s weight. This design increases the contact surface area between the baby and the mattress, reduces contact pressure, and provides evenly distributed support as the baby grows. Chen takes an interdisciplinary approach, collaborating with experts in baby breathing, sleeping patterns, and biomechanics to develop solutions aimed at reducing the risk of SIDS based on scientific evidence, safety, and effectiveness. In a pilot study, Chen collected data on the mattress’s performance using weights to simulate babies of different ages. His team will explore the relationship between weight and the measured pressure values at different internal air pressures within the inflatable tubing design. The potential application of this product design may extend to injured athletes, particularly in areas where injuries contact the mattress surface, thereby reducing stress.

GFAP expression in the brain during human postnatal development

AbstractGlial fibrillary acidic protein (GFAP) immunohistochemistry was investigated in the developing human brain using two measures; the number of GFAP‐positive cells (density, GFAP+/mm2), and a reactivity score (R‐score), which we recently introduced to indicate astrogliosis, with scores ≥120 indicative of pathological processes. The primary aim was to report on GFAP expression and cell soma size in 26 microscopically defined regions of the amygdala, basal ganglia, cerebellum, hippocampus and medulla, and to determine whether they are affected by postconceptional age (PCA) from 40 to 83 weeks. The secondary aim was to determine if GFAP expression differs according to the classification of sudden infant death syndrome (SIDS) as opposed to infant deaths of known causes, or for the presence of major SIDS risk factors of male sex, cigarette smoke exposure, upper respiratory tract infection (URTI), bed‐sharing and prone sleeping. The cerebellar molecular layer was void of GFAP+ cells, while the internal granular layer (IGL) had the highest density, with >60% of infants having an R‐Score >120. GFAP expression decreased with increasing PCA in the entorhinal and temporal cortex, subiculum and regions of the cerebellum and medulla. GFAP cell soma size corresponded with astrogliosis score and no effect of PCA was evident. Various region‐dependent GFAP expressional differences were seen according to SIDS classification and the risk factors studied. The findings indicate that the density of GFAP decreases in specific regions of the brain within the first year of postnatal development, and that reactive astrocytes are common, particularly within the early postnatal months.

Early Newborn Metabolic Patterning and Sudden Infant Death Syndrome

Sudden infant death syndrome (SIDS) is a major cause of infant death in the US. Previous research suggests that inborn errors of metabolism may contribute to SIDS, yet the relationship between SIDS and biomarkers of metabolism remains unclear. To evaluate and model the association between routinely measured newborn metabolic markers and SIDS in combination with established risk factors for SIDS. This was a case-control study nested within a retrospective cohort using data from the California Office of Statewide Health Planning and Development and the California Department of Public Health. The study population included infants born in California between 2005 and 2011 with full metabolic data collected as part of routine newborn screening (NBS). SIDS cases were matched to controls at a ratio of 1:4 by gestational age and birth weight z score. Matched data were split into training (2/3) and testing (1/3) subsets. Data were analyzed from January 2005 to December 2011. Metabolites measured by NBS and established risk factors for SIDS. The primary outcome was SIDS. Logistic regression was used to evaluate the association between metabolic markers combined with known risk factors and SIDS. Of 2 276 578 eligible infants, 354 SIDS (0.016%) cases (mean [SD] gestational age, 38.3 [2.3] weeks; 220 male [62.1%]) and 1416 controls (mean [SD] gestational age, 38.3 [2.3] weeks; 723 male [51.1%]) were identified. In multivariable analysis, 14 NBS metabolites were significantly associated with SIDS in a univariate analysis: 17-hydroxyprogesterone, alanine, methionine, proline, tyrosine, valine, free carnitine, acetyl-L-carnitine, malonyl carnitine, glutarylcarnitine, lauroyl-L-carnitine, dodecenoylcarnitine, 3-hydroxytetradecanoylcarnitine, and linoleoylcarnitine. The area under the receiver operating characteristic curve for a 14-marker SIDS model, which included 8 metabolites, was 0.75 (95% CI, 0.72-0.79) in the training set and was 0.70 (95% CI, 0.65-0.76) in the test set. Of 32 infants in the test set with model-predicted probability greater than 0.5, a total of 20 (62.5%) had SIDS. These infants had 14.4 times the odds (95% CI, 6.0-34.5) of having SIDS compared with those with a model-predicted probability less than 0.1. Results from this case-control study showed an association between aberrant metabolic analytes at birth and SIDS. These findings suggest that we may be able to identify infants at increased risk for SIDS soon after birth, which could inform further mechanistic research and clinical efforts focused on monitoring and prevention.

Impact of Sudden Infant Death Syndrome Risk Reduction Guidelines on Mothers' Knowledge and Practices and their Infants' Outcome

Impact of Sudden Infant Death Syndrome Risk Reduction Guidelines on Mothers' Knowledge and Practices and their Infants' Outcome

County-Level Structural Vulnerabilities in Maternal Health and Geographic Variation in Infant Mortality

ObjectiveTo evaluate whether community factors that differentially affect the health of pregnant people contribute to geographic differences in infant mortality across the United States. Study designThis retrospective cohort study sought to characterize the association of a novel composite measure of county-level maternal structural vulnerabilities, the Maternal Vulnerability Index (MVI), with risk of infant death. We evaluated 11,456,232 singleton infants born at 22 0/7 through 44 6/7 weeks’ gestation from 2012 to 2014. Using county-level MVI, which ranges from 0-100, multivariable mixed effects logistic regression models quantified associations per 20-point increment in MVI, with odds of death clustered at the county level and adjusted for state, maternal, and infant covariates. Secondary analyses stratified by the social, physical, and health exposures that comprise the overall MVI score. Outcome was also stratified by cause of death. ResultsOdds of death were higher among infants from counties with the greatest maternal vulnerability (0.62% in highest quintile vs 0.32% in lowest quintile, [p<0.001]). Odds of death increased 6% per 20-point increment in MVI (aOR: 1.06, 95% CI 1.04, 1.07). The effect estimate was highest with theme of mental health and substance use (aOR 1.08; 95% CI 1.06, 1.09). Increasing vulnerability was associated with six of seven causes of death. ConclusionsCommunity-level social, physical, and healthcare determinants indicative of maternal vulnerability may explain some of the geographic variation in infant death, regardless of cause of death. Interventions targeted to county-specific maternal vulnerabilities may reduce infant mortality.

Association between risk of infant death and birth-weight z scores according to gestational age: A nationwide study using the Finnish Medical Birth Register.

To investigate the association between infant mortality and birth weight using estimated fetal weight (EFW) versus birth-weight charts, by gestational age (GA). This nationwide population-based study used data from the Finnish Medical Birth Register from 2006 to 2016 on non-malformed singleton live births at 24-41+6 weeks of gestation (N = 563 630). The outcome was death in the first year of life. Mortality risks by birth-weight z score, defined as a continuous variable using Maršál's EFW and Sankilampi's birth-weight charts, were assessed using generalized additive models by GA (24-27+6, 28-31+6, 32-36+6, 37-38+6, 39-41+6 weeks). We calculated z score thresholds associated with a two- and three-fold increased risk of infant death compared with newborns with a birth weight between 0 and 0.675 standard deviations. The z score thresholds (with corresponding centiles in parentheses) associated with a two-fold increase in infant mortality were: -3.43 (<0.1) at 24-27+6 weeks, -3.46 (<0.1) at 28-31+6 weeks, -1.29 (9.9) at 32-36+6 weeks, -1.18 (11.9) at 37-38+6 weeks, and - 1.34 (9.0) at 39-41+6 weeks according to the EFW chart. These values were - 2.43 (0.8), -2.62 (0.4), -1.34 (9.0), -1.37 (8.5), and - 1.43 (7.6) according to the birth-weight chart. The association between birth weight and infant mortality varies by GA whichever chart is used, suggesting that different thresholds for the screening of growth anomalies could be used across GA to identify high-risk newborns.

Gather together in the name of our next generation: A scoping review of the essence and implementation of community baby showers

Introduction: Sudden unexpected infant death (SUID) and sudden infant death syndrome (SIDS) collectively represent one of the leading causes of infant mortality worldwide. There are a range of evidence-based modifiable risk factors for both, particularly related to the infant’s sleep environment. Oftentimes, social determinants of health impact optimization of an infant’s sleep environment, thereby compromising their safety and elevating their risk for SIDS and SUID. Many kinds of community interventions that include campaigns and programs have sought to address these environmental modifiable risk factors that contribute towards heightened risk for SIDS and SUID. However given resource limitations, reach and access considerations, and scarcity of a streamlined harmonized process to draw on the strengths of a community in SUID and SIDS reduction, there is mixed success with these interventions. Methods: Although community baby showers are rising as a trending health promotion intervention to optimize access to care, resources and support to infants and their caregivers as well as optimize infant growth and development, there is no review paper to date that consolidates the strengths and limitations in the quality, delivery and evaluation of community baby showers as a continued focus for future public health interventions surrounding the infant population which informs the development of this scoping review. Results: Specifically, this review synthesizes the commonalities, differences, key findings, intervention components as well as gaps in research and practice on community baby showers across published studies (n=20) and secondary sources (n=4). Conclusion: Clinical and public health implications are also closely examined and further inform recommendations for future directions that draw on the strengths and build off the limitations of findings from this review to heighten the clinical and public health impact and further assess the efficacy of community baby showers as an evidence-based community engagement and health promotion intervention for our next generation of infants and their families.

New Step in Understanding the Pathogenetic Mechanism of Sudden Infant Death Syndrome: Involvement of the Pontine Reticular Gigantocellular Nucleus.

This study aimed to investigate, for the first time, the potential role of the gigantocellular nucleus, a component of the reticular formation, in the pathogenetic mechanism of Sudden Infant Death Syndrome (SIDS), an event frequently ascribed to failure to arouse from sleep. This research was motivated by previous experimental studies demonstrating the gigantocellular nucleus involvement in regulating the sleep-wake cycle. We analyzed the brains of 48 infants who died suddenly within the first 7 months of life, including 28 SIDS cases and 20 controls. All brains underwent a thorough histological and immunohistochemical examination, focusing specifically on the gigantocellular nucleus. This examination aimed to characterize its developmental cytoarchitecture and tyrosine hydroxylase expression, with particular attention to potential associations with SIDS risk factors. In 68% of SIDS cases, but never in controls, we observed hypoplasia of the pontine portion of the gigantocellular nucleus. Alterations in the catecholaminergic system were present in 61% of SIDS cases but only in 10% of controls. A strong correlation was observed between these findings and maternal smoking in SIDS cases when compared with controls. In conclusion we believe that this study sheds new light on the pathogenetic processes underlying SIDS, particularly in cases associated with maternal smoking during pregnancy.

Newborn auditory brainstem response and sudden infant death syndrome.

Sudden infant death syndrome (SIDS)-the sudden and unexplained death of a seemingly healthy infant, <1 year old-may be associated with abnormalities in the brain regions that underlie breathing and arousal during sleep. While post-mortem studies suggest abnormalities in SIDS infants' brainstems, there are no studies of these infants' brainstem function before death. One way to assess the function of the brainstem is with auditory brainstem response (ABR), a routine hearing-screening method that noninvasively measures the brainstem's response to sound. We hypothesize that anomalies in newborns' ABR measures may predict SIDS. Indeed, previous studies identified abnormalities in ABR characteristics in small samples of near-miss SIDS infants hospitalized for infant apnea syndrome. However, there is a need to examine the ABRs of infants who died of SIDS. Therefore, in the current study, we propose integrating two secondary datasets to examine newborns' ABRs (N = 156,972), including those who later died of SIDS (n = ~42; .27 out of every 1000 infants), using existing archived records of neonatal ABR results from a sample of newborns born in Florida. We hypothesize that infants who die from SIDS are more likely than non-SIDS infants to have abnormal ABRs as newborns. Understanding the association between SIDS and ABR may facilitate more accurate identification of an infant's risk for SIDS at birth, enabling increased monitoring, which may facilitate interventions and improve survivorship.

Dysregulation of platelet serotonin, 14–3–3, and GPIX in sudden infant death syndrome

Sudden infant death syndrome (SIDS) is the leading cause of post-neonatal infant mortality, but the underlying cause(s) are unclear. A subset of SIDS infants has abnormalities in the neurotransmitter, serotonin (5-hydroxytryptamine [5-HT]) and the adaptor molecule, 14–3–3 pathways in regions of the brain involved in gasping, response to hypoxia, and arousal. To evaluate our hypothesis that SIDS is, at least in part, a multi-organ dysregulation of 5-HT, we examined whether blood platelets, which have 5-HT and 14–3–3 signaling pathways similar to brain neurons, are abnormal in SIDS. We also studied platelet surface glycoprotein IX (GPIX), a cell adhesion receptor which is physically linked to 14–3–3. In infants dying of SIDS compared to infants dying of known causes, we found significantly higher intra-platelet 5-HT and 14–3–3 and lower platelet surface GPIX. Serum and plasma 5-HT were also elevated in SIDS compared to controls. The presence in SIDS of both platelet and brainstem 5-HT and 14–3–3 abnormalities suggests a global dysregulation of these pathways and the potential for platelets to be used as a model system to study 5-HT and 14–3–3 interactions in SIDS. Platelet and serum biomarkers may aid in the forensic determination of SIDS and have the potential to be predictive of SIDS risk in living infants.

Educational Boost Slashes SIDS Risk Awareness Gap Among Nurses in Iraq

This study evaluates the impact of an educational program on nurses' knowledge of Sudden Infant Death Syndrome (SIDS) risk factors at pediatric teaching hospitals in Baghdad City. Using a quasi-experimental design with fifty nurses divided into a control and a research group, we assessed knowledge levels through pre-tests and two post-tests. Results indicated that the educational intervention significantly improved nurses' knowledge from 60% to 76%, although this effect diminished slightly over time. The study underscores the importance of continuous education in enhancing nurse awareness and the implementation of safe sleep practices to reduce SIDS occurrences. Highlights: Educational Impact: The study demonstrates a significant increase in nurses' knowledge about SIDS risk factors following an educational intervention. Sustained Learning: Knowledge gains were observed to diminish slightly over time, highlighting the need for ongoing educational programs. Practical Implications: Enhanced nurse training supports safer sleep practices, potentially reducing the incidence of SIDS. Keywords: Nurse Education, Knowledge, Risk Factors, Sudden Infant Death Syndrome, Safe Sleep Practices

Respiratory syncytial virus vaccination during pregnancy for improving infant outcomes.

Respiratory syncytial virus vaccination during pregnancy for improving infant outcomes.

Changes in Tryptophan Hydroxylase 2 and 5HT1A Receptor Density May Contribute to Developmental Variation in Response to Serotonin in the in vitro Bullfrog Brainstem

Bullfrog, Lithobates catesbeiana, is a vertebrate animal model that can be used to study toxicology and developmental physiology. Our research is focused on better understanding vulnerability to brainstem respiratory centers in the pathology of sudden infant death syndrome (SIDS). We propose that a link between nicotine exposure during development leads to changes in the serotonergic signaling cascades of respiratory coordinating neurons. Caudal raphe neurons send serotonergic fibers that arborize and terminate directly on or near respiratory neurons in the brainstem. In bullfrogs, serotonin elicits a developmentally dependent effect on respiratory motor output. Late metamorphic tadpoles demonstrate an increase in lung burst activity with exposure to low concentrations of serotonin (≤ 0.5μM 5-hydroxytryptamine; 5-HT) mediated in part by 5-HT1a receptor (5HT1aR) activation. This developmental change in activity may be due to changes in the number of serotonergic fibers and/or 5-HT1a receptor density. Using the NIH Basic Local Alignment Search Tool (BLAST) we compared human and bullfrog 5HT1aR and tryptophan hydroxylase 2 (TH2) protein sequences and found a 34 and 65 percent identity match respectively. Quantitative western blot analysis of both proteins indicates developmental shifts in the serotonergic network during metamorphosis. These results were supported by immunohistochemical staining of 5HT1aR and TH2 in caudal raphe containing brainstem sections from pre-metamorphic tadpoles and post-metamorphic frogs. Impairments in the maturation of this serotonergic network may underlie the toxidrome associated with developmental nicotine exposure and further support the increased risk of SIDS following that exposure. This research was supported by the University of Wisconsin- La Crosse (UWL) through support from the UWL College of Science and Health, two UWL Undergraduate Research Creative Grants and a UWL FY23/24 Faculty Research Grant. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Prenatal and postnatal factors associated with sudden infant death syndrome: an umbrella review of meta-analyses.

Comprehensive quantitative evidence on the risk and protective factors for sudden infant death syndrome (SIDS) effects is lacking. We investigated the risk and protective factors related to SIDS. We conducted an umbrella review of meta-analyses of observational and interventional studies assessing SIDS-related factors. PubMed/MEDLINE, Embase, EBSCO, and Google Scholar were searched from inception until January 18, 2023. Data extraction, quality assessment, and certainty of evidence were assessed by using A Measurement Tool Assessment Systematic Reviews 2 following PRISMA guidelines. According to observational evidence, credibility was graded and classified by class and quality of evidence (CE; convincing, highly suggestive, suggestive, weak, or not significant). Our study protocol was registered with PROSPERO (CRD42023458696). The risk and protective factors related to SIDS are presented as equivalent odds ratios (eORs). We identified eight original meta-analyses, including 152 original articles, covering 12 unique risk and protective factors for SIDS across 21 countries/regions and five continents. Several risk factors, including prenatal drug exposure [eOR = 7.84 (95% CI = 4.81-12.79), CE = highly suggestive], prenatal opioid exposure [9.55 (95% CI = 4.87-18.72), CE = suggestive], prenatal methadone exposure [9.52 (95% CI = 3.34-27.10), CE = weak], prenatal cocaine exposure [4.38 (95% CI = 1.95-9.86), CE = weak], prenatal maternal smoking [2.25 (95% CI = 1.95-2.60), CE = highly suggestive], postnatal maternal smoking [1.97 (95% CI = 1.75-2.22), CE = weak], bed sharing [2.89 (95% CI = 1.81-4.60), CE = weak], and infants found with heads covered by bedclothes after last sleep [11.01 (95% CI = 5.40-22.45), CE = suggestive], were identified. On the other hand, three protective factors, namely, breastfeeding [0.57 (95% CI = 0.39-0.83), CE = non-significant], supine sleeping position [0.48 (95% CI = 0.37-0.63), CE = suggestive], and pacifier use [0.44 (95% CI = 0.30-0.65), CE = weak], were also identified. Based on the evidence, we propose several risk and protective factors for SIDS. This study suggests the need for further studies on SIDS-related factors supported by weak credibility, no association, or a lack of adequate research.

Correlation of gestational age and age at death in sudden infant death syndrome: another pointer to the role of critical developmental period?

Filiano and Kinney proposed a triple-risk model for the sudden infant death syndrome (SIDS) that involves the intersection of three risks: (1) a vulnerable infant, (2) a critical developmental period in homeostatic control, and (3) an exogenous stressor(s). The primary evidence for the role of a critical developmental period in SIDS etiology is the peak of cases around the third month of life. Independently, several studies pointed to correlation between gestational age and age at death in SIDS, but used that to assess the SIDS risk for preterm infants, ignoring further ramifications. We did a detailed analysis of CDC data spanning over two decades (1983-2011). We focused not only on the correlation between two age variables (gestational and age at death), but also on the possibility of misdiagnosis. Also, we attempted to account for potential biases in the data induced by the ICD-9/ICD-190 transition or the "Back to Sleep" campaign. The peak of deaths in the third month of life, that was the main argument for the role of the critical development period, wasn't unique to SIDS. However, we confirmed an almost linear and negative correlation between gestational age and the week of death due to SIDS. This pattern (slope of correlation < 0 and significance of correlation p < 0.05) is characteristic of SIDS among all diseases analyzed in the study. We interpret the results as the evidence of the role of the critical development period in SIDS etiology. Possibly more attention in the future research should be put to theories that are based on homeostatic control.

Progress towards universal health coverage and inequalities in infant mortality: an analysis of 4·1 million births from 60 low-income and middle-income countries between 2000 and 2019

Expanding universal health coverage (UHC) might not be inherently beneficial to poorer populations without the explicit targeting and prioritising of low-income populations. This study examines whether the expansion of UHC between 2000 and 2019 is associated with reduced socioeconomic inequalities in infant mortality in low-income and middle-income countries (LMICs). We did a retrospective analysis of birth data compiled from Demographic and Health Surveys (DHSs). We analysed all births between 2000 and 2019 from all DHSs available for this period. The primary outcome was infant mortality, defined as death within 1 year of birth. Logistic regression models with country and year fixed effects assessed associations between country-level progress to UHC (using WHO's UHC service coverage index) and infant mortality (overall and by wealth quintile), adjusting for infant-level, mother-level, and country-level variables. A total of 4 065 868 births to 1 833 011 mothers were analysed from 177 DHSs covering 60 LMICs between 2000 and 2019. A one unit increase in the UHC index was associated with a 1·2% reduction in the risk of infant death (AOR 0·988, 95% CI 0·981-0·995; absolute measure of association, 0·57 deaths per 1000 livebirths). An estimated 15·5 million infant deaths were averted between 2000 and 2019 because of increases in UHC. However, richer wealth quintiles had larger associated reductions in infant mortality from UHC (quintile 5 AOR 0·983, 95% CI 0·973-0·993) than poorer quintiles (quintile 1 0·991, 0·985-0·998). In the early stages of UHC, UHC expansion was generally beneficial to poorer populations (ie, larger reductions in infant mortality for poorer households [infant deaths per 1000 per one unit increase in UHC coverage: quintile 1 0·84 vs quintile 5 0·59]), but became less so as overall coverage increased (quintile 1 0·64 vs quintile 5 0·57). Since UHC expansion in LMICs appears to become less beneficial to poorer populations as coverage increases, UHC policies should be explicitly designed to ensure lower income groups continue to benefit as coverage expands. UK National Institute for Health and Care Research.

Features of &lt;i&gt;ESCHERICHIA COLI&lt;/i&gt; samples from patients with diarrheal syndrome in the Republic of Guinea

Introduction. Diarrheal diseases are a global public health issue and cause 15% of deaths in children under 5 years old, of which about 80% occur in the regions of Africa and Southeast Asia. According to the Global Enteric Multicentre Study (GEMS) conducted in a number of African countries, one of the leading pathogens of high risk of death in infants and young children is diarrheagenic E. coli (DEC). In recent decades, antimicrobial resistance (AMR) has become globally ubiquitous. The Republic of Guinea urgently needs large-scale studies devoted to assessing DEC distribution and antibiotic resistance. The purpose of the study is to assess the pattern of E. coli infections and to test the susceptibility to antibiotics in strains of diarrheagenic E. coli sampled from individuals residing in the Republic of Guinea.&#x0D; Materials and methods. From 2019 to 2022, we studied 724 samples of faeces of patients with acute diarrhea, among them 72 (9.9%) children aged 1–5 years, 128 (17.7%) children aged 6–17 years, and 524 (72.4%) people aged 18 years and older; a method of polymerase chain reaction (PCR) was applied with the use of the AmpliSense® Escherichioses-FL reagent kit to identify the genetic determinants of DEC: EPEC, EHEC, ETEC, EIEC, and EAgEC (Central Research Institute of Epidemiology of Rospotrebnadzor, Russia). Susceptibility to 15 antimicrobial agents was found by the disc-diffusion method using Mueller–Hinton agar (Russia) and Oxoid discs (UK). Results were interpreted according EUCAST criteria, versions 2019–2022 (https://www.eucast.org/ast_of_bacteria/previous_versions_of_documents).&#x0D; Results. For the period from 2019 to 2022, the percentage of E. coli infections in the etiological pattern of acute intestinal infections amounted to 51.7%. In the age-related manner, DEC was significantly more common in young children aged 0–5 (96.9%, p 0.05) as compared to school age children aged 6–17 (53.9%) and adults (45.6%). In all years of observation, EAgEC strains prevailed, accounting for 38.4%. Other DEC pathotypes, EPEC, ETEC, EIEC and STEC, accounted for 27.2%, 17.5%, 11.8%, and 5.1%, respectively. DEC strains are susceptible to meropenem, amikacin, and nitrofurantoin. The activity of other antibiotics ranged from 11.3% for ampicillin, 28.3% for trimethoprim-sulfamethoxazole, and 34.0% for tetracycline to 73.6% for cephalosporins, 84.0% for aminoglycosides, and 98.1% for fluorinated quinolones.&#x0D; Conclusion. To reduce the burden of diarrheal diseases in the Republic of Guinea, it may be necessary to conduct targeted epidemiological and microbiological studies to identify DEC and monitor the development of antimicrobial resistance of E. coli infection pathogens in the population.

The study of the microbiome in forensic investigations on pediatric deaths.

Sudden infant death syndrome (SIDS) is a tragic and devastating condition whose causes remain largely unknown. Recent studies have shown that the composition of a child's gut flora can play a significant role in the development of SIDS. This work aims to research those factors that influence the composition of the intestinal flora, the role they have in the development of SIDS and the new strategies for preventing SIDS showing a new interpretation through a detailed review of the literature. The gut in physiological conditions is mainly composed of Bacteroidetes, Firmicutes, Actinobacteria, and Proteobacteria, but when there is the presence of dysbiotic or different microbial communities, the onset of the disease is more likely as an altered microbial community can lead to an interruption of the gut-brain axis and an increased risk of SIDS. All this implies that the composition of the microbiome can be modified to reduce the risk of sudden death in newborns. The results of the literature provide valuable information on the potential role of the intestinal microbiome in SIDS even if not all mechanisms are yet clear, especially in the mechanisms of death. Therefore, it is necessary in cases of SIDS when carrying out an autopsy to also investigate this area; to this end, we suggest a questionnaire to be administered to family members to understand the eating habits of the newborn and the family and integrate with microbiological investigations to explore every possible hypothesis.

Evaluation of mothers' knowledge about infant sudden death syndrome and its risk factors.

Sudden infant death syndrome is the third leading cause of infant death in the first year of life and is one of the most important health problems around the world. The exact etiology of this phenomenon is not clear yet, but some risk factors, especially prone sleep positions, have been described. Fortunately, by modifying some environmental factors, the SIDS incidence might be decreased. Mothers' and caregivers' knowledge about this neglected event could be an important factor in determining SIDS prevalence. This cross-sectional study was conducted in the pediatric and neonatal specialty clinic of Bahar Shahroud Hospital in 2020. Five hundred and twenty-seven pregnant women of reproductive age (18 to 45 years) were included in the study. Assessment of mothers' knowledge was done using a sudden infant death syndrome risk questionnaire. Statistical analysis of data was performed using independent t-test, Chi-square, and logistic regression. The number of 527 pregnant women of childbearing age participated in our study. 81.9% were under 35 years old. According to the study, factors such as maternal age, mother's level of education, number of pregnancies, and history of previous infant death syndrome had a significant relationship with the mother's level of knowledge about infant death syndrome. The findings showed that the mother's age is over 35 years old during pregnancy (CI: 0.95-0.46-OR: 1.53) and the level of education under a diploma (CI: 3.13-1.6: 06, OR: 1.86), and increasing parity is associated with a lower level of knowledge about infant death syndrome. According to mothers' lack of knowledge about SIDS and the availability of simple and cost-effective methods to prevent SIDS, improving mothers' knowledge about this important event in pregnancy and postpartum, educational sessions are crucial.

National SIDS Trends in the United States From 2000 to 2019: A Population-Based Study on 80 Million Live Births.

Sudden infant death syndrome (SIDS) is the most common cause of death for infants between 1 month and 1 year of age in the United States. The objective was to examine recent trends in SIDS in the United States, over time and by sex and race. A population-based cross-sectional study was conducted on 80 710 348 live births using data from the Center for Disease Control and Prevention's (CDC) "Birth Data" and "Mortality Multiple Cause" files from 2000 to 2019. Logistic regression examined the effects of sex and race on the risk of SIDS and examined temporal changes in risk across sex and race over the study period. Incidence of SIDS decreased from 6.3 to 3.4/10 000 births from 2000 to 2019, with an overall incidence of 4.9/10 000 births (95% confidence interval [CI] = 4.4-5.3). Male infants were at the greatest risk of SIDS as were black and American Indian infants. Although SIDS incidence decreased by sex and race over time, the decline was smaller among Hispanic and American Indian infants.