Multimorbidity, the presence of two or more non-communicable diseases (NCD), is a costly and complex challenge for health systems globally. Patients with NCDs incur high levels of out-of-pocket expenditure (OOPE), often on medicines, but the literature on the association between OOPE on medicines and multimorbidity has not been examined systematically.

The global threat of antimicrobial resistance (AMR) has arisen through a network of complex interacting factors. Many different sources and transmission pathways contribute to the ever-growing burden of AMR in our clinical settings. The lack of data on these mechanisms and the relative importance of different factors causing the emergence and spread of AMR hampers our global efforts to effectively manage the risks. Importantly, we have little quantitative knowledge on the relative contributions of these sources and are likely to be targeting our interventions suboptimally as a result. Here we propose a systems mapping approach to address the urgent need for reliable and timely data to strengthen the response to AMR.

The rate of infection by methicillin-resistant (MRSA) has declined over the past decade, but it is unclear whether this represents a decline in infections overall. To evaluate the trends in the annual rates of infection by subtypes and mean antibiotic resistance, we conducted a 15-year retrospective observational study at two tertiary care institutions in Boston, MA, of 31,753 adult inpatients with isolated from clinical specimens. We inferred the gain and loss of methicillin resistance through genome sequencing of 180 isolates from 2016. The annual rates of infection by declined from 2003 to 2014 by 4.2% (2.7% to 5.6%), attributable to an annual decline in MRSA of 10.9% (9.3% to 12.6%). Penicillin-susceptible (PSSA) increased by 6.1% (4.2% to 8.1%) annually, and rates of methicillin-susceptible penicillin-resistant (MSSA) did not change. Resistance in decreased from 2000 to 2014 by 0.8 antibiotics (0.7 to 0.8). Within common MRSA clonal complexes, 3/14 MSSA and 2/21 PSSA isolates arose from the loss of resistance-conferring genes. Overall, in two tertiary care institutions in Boston, MA, a decline in infections has been accompanied by a shift toward increased antibiotic susceptibility. The rise in PSSA makes penicillin an increasingly viable treatment option.

International and domestic funding for malaria is critically important to achieve the Sustainable Development Goals. Its equitable distribution is key in ensuring that the available, scarce, resources are deployed efficiently for improved progress and a sustained response that enables eradication.

While the majority of veteran suicides involve firearms, no contemporary data describing firearm ownership among US veterans are available. This study uses survey data to describe the prevalence of firearm ownership among a nationally representative sample of veterans, as well as veterans’ reasons for firearm ownership.

, typically a resident of the oro- or nasopharynx and the causative agent of meningococcal meningitis and meningococcemia, is capable of invading and colonizing the urogenital tract. This can result in urethritis, akin to the syndrome caused by its sister species, , the etiologic agent of gonorrhea. Recently, meningococcal strains associated with outbreaks of urethritis were reported to share genetic characteristics with the gonococcus, raising the question of the extent to which these strains contain features that promote adaptation to the genitourinary niche, making them gonococcus-like and distinguishing them from other strains. Here, we analyzed the genomes of 39 diverse isolates associated with urethritis, collected independently over a decade and across three continents. In particular, we characterized the diversity of the nitrite reductase gene (), the factor H-binding protein gene (), and the capsule biosynthetic locus, all of which are loci previously suggested to be associated with urogenital colonization. We observed notable diversity, including frameshift variants, in and and the presence of intact, disrupted, and absent capsule biosynthetic genes, indicating that urogenital colonization and urethritis caused by are possible across a range of meningococcal genotypes. Previously identified allelic patterns in urethritis-associated strains may reflect genetic diversity in the underlying meningococcal population rather than novel adaptation to the urogenital tract.