SummaryAdversity, particularly in early life, can cause illness. Clues to the responsible mechanisms may lie with the discovery of molecular signatures of stress, some of which include alterations to an individual’s somatic genome. Here, using genome sequences from 11,670 women, we observed a highly significant association between a stress-related disease, major depression, and the amount of mtDNA (p = 9.00 × 10−42, odds ratio 1.33 [95% confidence interval [CI] = 1.29–1.37]) and telomere length (p = 2.84 × 10−14, odds ratio 0.85 [95% CI = 0.81–0.89]). While both telomere length and mtDNA amount were associated with adverse life events, conditional regression analyses showed the molecular changes were contingent on the depressed state. We tested this hypothesis with experiments in mice, demonstrating that stress causes both molecular changes, which are partly reversible and can be elicited by the administration of corticosterone. Together, these results demonstrate that changes in the amount of mtDNA and telomere length are consequences of stress and entering a depressed state. These findings identify increased amounts of mtDNA as a molecular marker of MD and have important implications for understanding how stress causes the disease.

Younger children may require a longer isolation period and more aggressive treatment.

Echocardiography, anemia and thrombocytosis are useful early differentiating features between KDSS and TSS patients.

We aimed to evaluate the occurrence, treatment, and outcomes of neurological complications after bacterial meningitis in young infants. A case series study from a retrospective cohort from two tertiary-level medical centers in Taiwan between 2007 and 2016 was conducted. Eighty-five young infants aged < 90 days with bacterial meningitis were identified. 25 (29.4%) were born at preterm. Group B Streptococcus (GBS) and Escherichia coli caused 74.1% of identified cases. Despite the majority (90.6%) initially received microbiologically appropriate antibiotics, 65 (76.5%) had experienced at least one neurological complication identified at a median of 6 days (range: 1–173) after onset of bacterial meningitis. The most common neurological complication was seizure (58.8%), followed by subdural effusion (47.1%), ventriculomegaly (41.2%), subdural empyema (21.2%), hydrocephalus (18.8%), ventriculitis (15.3%), periventricular leukomalacia (11.8%), and encephalomalacia (10.6%). Nine patients (10.6%) died (including 4 had critical discharge on request) and 29/76 (38.2%) of the survivors had major neurological sequelae at discharge. Nighteen (22.4%) received surgical intervention due to these complications. After multivariate logistic regression, initial seizure (adjusted odds ratio [aOR]: 4.76, 95% confidence interval [CI]: 1.7–13.0, P = 0.002) and septic shock (aOR: 6.04; 95% CI: 1.35–27.0, P = 0.019) were independent predictors for final unfavorable outcomes.Conclusions: Neurological complications and sequelae are common in young infants after bacterial meningitis. Patients presented with early seizure or septic shock can be an early predictor of final unfavorable outcomes and require close monitoring. Further research regarding how to improve clinical management and outcomes is warranted.