Together with plague, smallpox and typhus, epidemics of dysentery have been a major scourge of human populations for centuries(1). A previous genomic study concluded that Shigella dysenteriae type 1 (Sd1), the epidemic dysentery bacillus, emerged and spread worldwide after the First World War, with no clear pattern of transmission(2). This is not consistent with the massive cyclic dysentery epidemics reported in Europe during the eighteenth and nineteenth centuries(1,3,4) and the first isolation of Sd1 in Japan in 1897(5). Here, we report a whole-genome analysis of 331 Sd1 isolates from around the world, collected between 1915 and 2011, providing us with unprecedented insight into the historical spread of this pathogen. We show here that Sd1 has existed since at least the eighteenth century and that it swept the globe at the end of the nineteenth century, diversifying into distinct lineages associated with the First World War, Second World War and various conflicts or natural disasters across Africa, Asia and Central America. We also provide a unique historical perspective on the evolution of antibiotic resistance over a 100-year period, beginning decades before the antibiotic era, and identify a prevalent multiple antibiotic-resistant lineage in South Asia that was transmitted in several waves to Africa, where it caused severe outbreaks of disease.

BackgroundElderly patients are at particular risk for bacteremia and sepsis. Atypical presentation may complicate the diagnosis. We studied patients with bacteremia, in order to assess possible age-related effects on the clinical presentation and course of severe infections.MethodsWe reviewed the records of 680 patients hospitalized between 1994 and 2004. All patients were diagnosed with bacteremia, 450 caused by Escherichia coli and 230 by Streptococcus pneumoniae. Descriptive analyses were performed for three age groups (< 65 years, 65–84 years, ≥ 85 years). In multivariate analyses age was dichotomized (< 65, ≥ 65 years). Symptoms were categorized into atypical or typical. Prognostic sensitivity of CRP and SIRS in identifying early organ failure was studied at different cut-off values. Outcome variables were organ failure within one day after admission and in-hospital mortality.ResultsThe higher age-groups more often presented atypical symptoms (p <0.001), decline in general health (p=0.029), and higher in-hospital mortality (p<0.001). The prognostic sensitivity of CRP did not differ between age groups, but in those ≥ 85 years the prognostic sensitivity of two SIRS criteria was lower than that of three criteria. Classical symptoms were protective for early organ failure (OR 0.67, 95% CI 0.45-0.99), and risk factors included; age ≥ 65 years (OR 1.65, 95% CI 1.09-2.49), comorbid illnesses (OR 1.19, 95% CI 1.02-1.40 per diagnosis), decline in general health (OR 2.28, 95% CI 1.58-3.27), tachycardia (OR 1.50, 95% CI 1.02-2.20), tachypnea (OR 3.86, 95% CI 2.64-5.66), and leukopenia (OR 4.16, 95% CI 1.59-10.91). Fever was protective for in-hospital mortality (OR 0.46, 95% CI 0.24-0.89), and risk factors included; age ≥ 65 years (OR 15.02, 95% CI 3.68-61.29), ≥ 1 comorbid illness (OR 2.61, 95% CI 1.11-6.14), bacteremia caused by S. pneumoniae (OR 2.79, 95% CI 1.43-5.46), leukopenia (OR 4.62, 95% CI 1.88-11.37), and number of early failing organs (OR 3.06, 95% CI 2.20-4.27 per failing organ).ConclusionsElderly patients with bacteremia more often present with atypical symptoms and reduced general health. The SIRS-criteria have poorer sensitivity for identifying organ failure in these patients. Advanced age, comorbidity, decline in general health, pneumococcal infection, and absence of classical symptoms are markers of a poor prognosis.

Antimicrobial resistance (AMR) is a major threat to global health. Understanding the emergence, evolution, and transmission of individual antibiotic resistance genes (ARGs) is essential to develop sustainable strategies combatting this threat. Here, we use metagenomic sequencing to analyse ARGs in 757 sewage samples from 243 cities in 101 countries, collected from 2016 to 2019. We find regional patterns in resistomes, and these differ between subsets corresponding to drug classes and are partly driven by taxonomic variation. The genetic environments of 49 common ARGs are highly diverse, with most common ARGs carried by multiple distinct genomic contexts globally and sometimes on plasmids. Analysis of flanking sequence revealed ARG-specific patterns of dispersal limitation and global transmission. Our data furthermore suggest certain geographies are more prone to transmission events and should receive additional attention.

Our findings strengthen the previous impression of an approximately 3-fold increased preponderance in males, with at least 10-fold increased frequency in CD compared with UC, and with a possible relationship to suppurative complications and extraintestinal manifestations, as well as an increased risk of having a bowel resection. The increased survival seems to be due to the introduction of renal transplantation.

Escherichia albertii is an emerging human enteric pathogen (1). It belongs to the attaching and effacing group of bacteria, which also includes enteropathogenic and Shiga toxin-producing Escherichia coli (EPEC and STEC, respectively). Shiga toxin-producing E. albertii has been described, however, only in association with Shiga toxin (stx) subtype 2f (2). Sporadic infections as well as foodborne outbreaks caused by E. albertii have been reported, although rarely (3, 4). The prevalence, epidemiology, and clinical relevance of E. albertii are poorly understood, probably due to underestimation and misclassification of this pathogen (4). The phenotypic features distinguishing E. albertii from E. coli include a negative indole reaction and an inability to ferment lactose-, Dsorbitol, and D-xylose (1).In Norway, all presumptive enteropathogenic E. coli strains isolated from humans are submitted to the National Reference Laboratory for Enteropathogenic Bacteria for biochemical verification and for classification into well-known pathotypes according to virulence genes present (L. T. Brandal, A. L. Wester, H. Lange, I. Løbersli, B. A. Lindstedt, L. Vold, and G. Kapperud, submitted for publication). For outbreak detection purposes, all E. coli isolates are investigated with a generic multilocus variable-number tandem-repeat analysis (MLVA) (5).By these routine analyses, a nonmotile, ␤-D-glucuronidase-, lactose-, and xylose-negative isolate with eae and stx 2 was identified. This isolate had an MLVA profile often seen in E. albertii (NA-NA-NA-NA-NA-NA-5-X-X-NA, where NA designates a locus not present and X indicates different repeat numbers). A PCR specific for E. albertii was conducted (6), and 16S rRNA sequencing was performed (MicroSEC 500 16S rRNA gene bacterial sequencing kit; Life Technologies), both of which confirmed the isolate as E. albertii. stx 2 was subtyped and sequenced (7), and the expression of the stx 2a gene was verified (ImmunoCard STAT!EHEC; Meridian Bioscience Europe). All E. albertii isolates identified from 2008 to 2014 (n ϭ 39) were examined for the presence of stx 2f (8) and the cytolethal distending toxin B gene (cdtB) (9).Interestingly, the E. albertii isolate identified in the present study carried stx 2a , hitherto never reported in E. albertii. Additionally, we showed that stx 2a was expressed. This indicates that E. albertii is able to transduce not only stx 2f -carrying bacteriophages but also stx 2a -carrying bacteriophages. STEC harboring eae and stx 2a are considered highly virulent and have the ability to induce life-threatening hemolytic uremic syndrome (HUS) in infected patients (10). In contrast, STEC harboring stx 2f are associated with milder symptoms (11) and have, to our knowledge, never previously been detected in HUS patients. The patient infected with stx 2a -positive E. albertii was 48 years old, had bloody diarrhea, and was infected in Norway (Table 1). Domestically acquired E. albertii infection was commonly seen in patients included in the present study; however, the majori...

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In 2011, an outbreak of illness caused by Yersinia enterocolitica O:9 in Norway was linked to ready-to-eat salad mix, an unusual vehicle for this pathogen. The outbreak illustrates the need to characterize isolates of this organism, and reinforces the need for international traceback mechanisms for fresh produce.

Aminoglycosides (AGs) are important antibacterial agents for the treatment of various infections in humans and animals. Following extensive use of AGs in humans, food-producing animals and companion animals, acquired resistance among human and animal pathogens and commensal bacteria has emerged. Acquired resistance occurs through several mechanisms, but enzymatic inactivation of AGs is the most common one. Resistance genes are often located on mobile genetic elements, facilitating their spread between different bacterial species and between animals and humans. AG resistance has been found in many different bacterial species, including those with zoonotic potential such as Salmonella spp., Campylobacter spp. and livestock-associated MRSA. The highest risk is anticipated from transfer of resistant enterococci or coliforms (Escherichia coli) since infections with these pathogens in humans would potentially be treated with AGs. There is evidence that the use of AGs in human and veterinary medicine is associated with the increased prevalence of resistance. The same resistance genes have been found in isolates from humans and animals. Evaluation of risk factors indicates that the probability of transmission of AG resistance from animals to humans through transfer of zoonotic or commensal foodborne bacteria and/or their mobile genetic elements can be regarded as high, although there are no quantitative data on the actual contribution of animals to AG resistance in human pathogens. Responsible use of AGs is of great importance in order to safeguard their clinical efficacy for human and veterinary medicine.