Abstract
Most Shiga toxin-producing Escherichia coli (STEC) infections that are associated with severe sequelae such as hemolytic uremic syndrome (HUS) are caused by attaching and effacing pathogens that carry the locus of enterocyte effacement (LEE). However, a proportion of STEC isolates that do not carry LEE have been associated with HUS. To clarify the emergence of LEE-negative STEC, we compared the genetic composition of the virulence plasmids pO113 and pO157 from LEE-negative and LEE-positive STEC, respectively. The complete nucleotide sequence of pO113 showed that several plasmid genes were shared by STEC O157:H7. In addition, allelic profiling of the ehxA gene demonstrated that pO113 belongs to a different evolutionary lineage than pO157 and that the virulence plasmids of LEE-negative STEC strains were highly related. In contrast, multilocus sequence typing of 17 LEE-negative STEC isolates showed several clonal groups, suggesting that pathogenic LEE-negative STEC has emerged several times throughout its evolution.
Highlights
Despite our increasing knowledge of the role of patient race/ethnicity in drug prescribing practice for specific conditions, how or whether these specific effects translate into overall antimicrobial drug use by race/ethnicity remains unclear. We address this gap in knowledge by describing the extent of racial/ethnic disparities in overall antimicrobial drug prescription fill rates in the United States
We found a large disparity in antimicrobial drug fill rates by race/ethnicity: white persons reported making twice as many antimicrobial drug prescription fills as persons who were not white
The survey measures reported antimicrobial drug fills and not actual use [8]; the fill rates we report are substantially lower than those measured by others using sales data [1] or other national surveys [9]
Summary
We aimed to accurately map current and new BU-endemic areas and compare and contrast the changing incidence in these locations, to document disease severity and associate this with diagnostic delay, and to identify times of increased transmission risk. We aimed to clarify year-to-year changes in capsular serotypes, genotypes of penicillin and macrolide resistance, and diversity of sequence types (STs) in all pneumococcal isolates collected throughout Japan during April 2010–March 2017. We aimed to explore the genetic relationships of the 2015 and 2016 isolates from CAR with this reported population structure of NmW/cc. We aimed to estimate the influenza-associated severe acute respiratory infection (SARI) hospitalization using the methods recommended by the World Health Organization (5)
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