All sudden unexplained infant respiratory deaths may result from the same underlying mechanism
The Sudden Infant Death Syndrome (SIDS) was defined in 1969 by Beckwith as sudden death of an infant or young child, unexpected by medical history, remaining unexplained after thorough autopsy/death-scene investigation. Recently researchers have used the general terms Sudden Unexplained Death in Infancy (SUDI) and Sudden Unexpected Infant Death (SUID) as "umbrella-terms" covering unexplained deaths (SIDS); sudden deaths for which SIDS risk factors present but insufficient cause is found; and sudden deaths for which sufficient cause is found. A characteristic feature of such deaths is that, 24-hours before death (or unexpected collapse that led to death), the caregivers were unaware that the baby was at increased risk of dying. The explainable cases include deaths from several recognized causes including infection, metabolic conditions, accidental and non-accidental injury, and various genetic or cardiac conditions as well as "Accidental Suffocation and Strangulation in Bed (ASSB)." SIDS is characterized by a ~50% male excess common to all respiratory infant deaths and a 4-parameter lognormal age distribution - thought to be unique and SIDS main distinguishing characteristic. In this article we model these data for age and/or gender distributions of SUDI/SUID and SIDS reported from the U.K., U.S., Norway and Germany. When pooled together with SIDS, these explained SUDI/SUID data on infant ages and gender have the same distributions as SIDS, indicating that the final mode of death for all SUDI or SUID may be a consequence of different paths to the same biological phenomena as for SIDS, though the mechanism of death remains unclear.
Recent studies have described a number of fatalities due to methicillin-resistant Staphylococcus aureus (MRSA) and influenza virus co-infection. MRSA isolates provide a challenge to caregivers due to inherent wide range antibiotic resistance. Many facilities have instituted screening methods, based on the presence of antibiotic resistance genes, to identify MRSA positive patients upon admission. However, the resistance profile of the pathogen does not necessarily determine the severity of disease caused by that organism.We describe a fatal case of necrotizing pneumonia in a patient co-infected with Influenza B and a community-associated, PVL-positive methicillin-susceptible Staphylococcus aureus (MSSA).
Objectives. To estimate excess all-cause mortality in Philadelphia, Pennsylvania, during the COVID-19 pandemic and understand the distribution of excess mortality in the population. Methods. With a Poisson model trained on recent historical data from the Pennsylvania vital registration system, we estimated expected weekly mortality in 2020. We compared these estimates with observed mortality to estimate excess mortality. We further examined the distribution of excess mortality by age, sex, and race/ethnicity. Results. There were an estimated 3550 excess deaths between March 22, 2020, and January 2, 2021, a 32% increase above expectations. Only 77% of excess deaths (n=2725) were attributed to COVID-19 on the death certificate. Excess mortality was disproportionately high among older adults and people of color. Sex differences varied by race/ethnicity. Conclusions. Excess deaths during the pandemic were not fully explained by COVID-19 mortality; official counts significantly undercount the true death toll. Far from being a great equalizer, the COVID-19 pandemic has exacerbated preexisting disparities in mortality by race/ethnicity. Public Health Implications. Mortality data must be disaggregated by age, sex, and race/ethnicity to accurately understand disparities among groups. (Am J Public Health. Published online ahead of print June 10, 2021: e1–e6. https://doi.org/10.2105/AJPH.2021.306285 )
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