Tuberculosis is the most frequent cause of death in humans from a single infectious agent. Due to low numbers of bacteria present in sputum during early infection, diagnosis does not usually occur until >3 to 4 months after symptoms develop. We created a new more sensitive diagnostic that can be carried out in 10 min with no processing or technical expertise.

It is now clear that parental histories of drug use, toxicant exposure, and social stress all have a significant influence on the health and development of the next generation. However, the ability of epigenetic parental life memories to interact with subsequent gestational exposures and cumulatively modify the developmental trajectory of the offspring remains an unexplored perspective in toxicology. Studies from our laboratory have identified male-specific postnatal growth restriction in a mouse model of chronic, preconception paternal alcohol exposure. The goal of the current study was to determine if paternal alcohol use, before conception, could modify the susceptibility of the offspring to a completely separate exposure encountered by the mother during pregnancy. In independent experiments, we previously identified altered developmental programming and increased markers of severe asthma induced by gestational exposure to particulate air pollution. In this study, male mice were exposed to either the control or alcohol preconception treatments, then mated to naive females, which we subsequently exposed to an ultrafine mixture of particulate matter via inhalation. Individually, neither preconception paternal drinking nor gestational exposures to particulate air pollution impacted the postnatal growth of female offspring. However, when both exposures were combined, females displayed a 30% reduction in weight gain. Unexpectedly, this exposure paradigm resulted in a dramatic postnatal increase in litter loss due to maternal cannibalism, which prevented additional measures of offspring health. These preliminary studies provide evidence of a complex interplay between preconception life history and intrauterine environmental factors in the control of postnatal growth.

AimTo quantify changes on RSV- associated hospitalizations during COVID-19 pandemic, among children four years of age or younger at the state and county levels of Texas using routinely acquired hospital admission records.MethodsWe used the Texas Public Use Data Files (PUDF) of the Department of State Human Services (DSHS) to obtain hospital admissions and healthcare outcomes from 2006 to 2021. We used the 2006–2019 period to estimate a long-term temporal trend and predict expected values for 2020–2021. Actual and predicted values were used to quantify changes in seasonal trends of the number of hospital admissions and mean length of hospital stay. Additionally, we calculated hospitalization rates and assessed their similarity to rates reported in the RSV Hospitalization Surveillance Network (RSV-NET).ResultsAn unusually low number of hospitalizations in 2020 was followed by an unusual peak in the third quarter of 2021. Hospital admissions in 2021 were approximately twice those in a typical year. The mean length of hospital stay typically followed a seasonal trend before COVID-19, but increased by a factor of ∼6.5 during the pandemic. Spatial distribution of hospitalization rates revealed localized healthcare infrastructure overburdens during COVID-19. RSV associated hospitalization rates were, on average, two times higher than those of RSV-NET.ConclusionHospital admission data can be used to estimate long-term temporal and spatial trends and quantify changes during events that exacerbate healthcare systems, such as pandemics. Using the mean difference between hospital rates calculated with hospital admissions and hospital rates obtained from RSV-NET, we speculate that state-level hospitalization rates for 2022 could be at least twice those observed in the two previous years, and the highest in the last 17 years.

Background Interactions between air pollution and infectious agents are increasingly recognized and critical to identify, especially to protect vulnerable populations. Pregnancy represents a vulnerable period for influenza infection and air pollution exposure, yet interactions during pregnancy remain unclear. Maternal exposure to ultrafine particles (UFPs, $$\le$$ ≤ 100 nm diameter), a class of particulate matter ubiquitous in urban environments, elicits unique pulmonary immune responses. We hypothesized that UFP exposure during pregnancy would lead to aberrant immune responses to influenza enhancing infection severity. Results Building from our well-characterized C57Bl/6N mouse model employing daily gestational UFP exposure from gestational day (GD) 0.5–13.5, we carried out a pilot study wherein pregnant dams were subsequently infected with Influenza A/Puerto Rico/8/1934 (PR8) on GD14.5. Findings indicate that PR8 infection caused decreased weight gain in filtered air (FA) and UFP-exposed groups. Co-exposure to UFPs and viral infection led to pronounced elevation in PR8 viral titer and reduced pulmonary inflammation, signifying potential suppression of innate and adaptive immune defenses. Pulmonary expression of the pro-viral factor sphingosine kinase 1 (Sphk1) and pro-inflammatory cytokine interleukin-1β (IL-1$$\beta$$ β ) was significantly increased in pregnant mice exposed to UFPs and infected with PR8; expression correlated with higher viral titer. Conclusions Results from our model provide initial insight into how maternal UFP exposure during pregnancy enhances respiratory viral infection risk. This model is an important first step in establishing future regulatory and clinical strategies for protecting pregnant women exposed to UFPs.