Enhanced nasopharyngeal infection and shedding associated with an epidemic lineage of emm3 group A Streptococcus

Background: A group A Streptococcus (GAS) lineage of genotype emm3, sequence type 15 (ST15) was associated with a six month upsurge in invasive GAS disease in the UK. The epidemic lineage (Lineage C) had lost two typical emm3 prophages, Φ315.1 and Φ315.2 associated with the superantigen ssa, but gained a different prophage (ΦUK-M3.1) associated with a different superantigen, speC and a DNAse spd1. Methods and Results: The presence of speC and spd1 in Lineage C ST15 strains enhanced both in vitro mitogenic and DNAse activities over non-Lineage C ST15 strains. Invasive disease models in Galleria mellonella and SPEC-sensitive transgenic mice, revealed no difference in overall invasiveness of Lineage C ST15 strains compared to non-Lineage C ST15 strains, consistent with clinical and epidemiological analysis. Lineage C strains did however markedly prolong murine nasal infection with enhanced nasal and airborne shedding compared to non-Lineage C strains. Deletion of speC or spd1 in two Lineage C strains identified a possible role for spd1 in airborne shedding from the murine nasopharynx. Conclusions: Nasopharyngeal infection and shedding of Lineage C strains was enhanced compared to nonLineage C strains and this was, in part, mediated by the gain of the DNase spd1 through prophage acquisition

Circulating serotypes and antimicrobial sensitivity of Streptococcus pyogenes isolates from children in Cyprus

ABSTRACTThe most common T-serotypes among group A streptococci (n = 88) isolated from pharyngeal samples of children referred to a tertiary hospital in Cyprus for pharyngitis or scarlet fever during a 14-month period (2003–2004) were T28 (25%), T8/25/Imp19 (22.7%) and T12 (9.1%). All 88 isolates were sensitive to penicillin and clindamycin, but 1.1% and 18.2% of isolates were resistant to erythromycin and tetracycline, respectively. Macrolide consumption was estimated at 1.7 defined daily doses/1000 inhabitants/day. The low percentage of resistance to macrolides may have been related, at least in part, to the low consumption of macrolides

Polyelectrolyte/surfactant films: from 2D to 3D structural control

Reversible control of the 3D structure of polyelectrolyte/surfactant films at the air/water interface is showcased. A recently discovered mechanism is exploited to form highly efficient, stable and biocompatible films by spreading aggregates composed of poly-L-lysine and sodium dodecyl sulfate on the surface of water. Reversible control of: (1) the surface monolayer coverage, (2) the switching on or off discrete extended structures, and (3) the extended structure coverage is demonstrated for the first time. The intricacy by which the film structures can be controlled is unprecedented and opens exciting potential to optimize film properties by chemical design for novel biomedical transfer applications.We thank the Institut Laue-Langevin for beam time on FIGARO (DOIs: https://doi.org/10.5291/ILL-DATA.9-12-614 and https://doi.org/10.5291/ILL-DATA.9-12-631), Simon Wood for technical assistance and the Partnership for Soft Condensed Matter (PSCM) for lab support. IV acknowledges the financial support from the Hungarian National Research, Development and Innovation Office (NKFIH K116629). AM acknowledges the financial support from MICINN under grant PID2021-129054NA-I00 and the IKUR Strategy of the Basque Government.Peer reviewe

The cross-species immunity during acute Babesia co-infection in mice

Babesiosis causes high morbidity and mortality in immunocompromised individuals. An earlier study suggested that lethal Babesia rodhaini infection in murine can be evaded by Babesia microti primary infection via activated macrophage-based immune response during the chronic stage of infection. However, whether the same immune dynamics occur during acute B. microti co-infection is not known. Hence, we used the mouse model to investigate the host immunity during simultaneous acute disease caused by two Babesia species of different pathogenicity. Results showed that B. microti primary infection attenuated parasitemia and conferred immunity in challenge-infected mice as early as day 4 post-primary infection. Likewise, acute Babesia co-infection undermined the splenic immune response, characterized by the significant decrease in splenic B and T cells leading to the reduction in antibody levels and decline in humoral immunity. Interestingly, increased macrophage and natural killer splenic cell populations were observed, depicting their subtle role in the protection. Pro-inflammatory cytokines (i.e. IFN-γ, TNF-α) were downregulated, while the anti-inflammatory cytokine IL-10 was upregulated in mouse sera during the acute phase of Babesia co-infection. Herein, the major cytokines implicated in the lethality caused by B. rodhaini infection were IFN- γ and IL-10. Surprisingly, significant differences in the levels of serum IFN- γ and IL-10 between co-infected survival groups (day 4 and 6 challenge) indicated that even a two-day delay in challenge infection was crucial for the resulting pathology. Additionally, oxidative stress in the form of reactive oxygen species contributed to the severity of pathology during acute babesiosis. Histopathological examination of the spleen showed that the erosion of the marginal zone was more pronounced during B. rodhaini infection, while the loss of cellularity of the marginal zone was less evident during co-infection. Future research warrants investigation of the roles of various immune cell subtypes in the mechanism involved in the protection of Babesia co-infected hosts

emm typing and validation of provisional M types for group A streptococci.

This report discusses the following issues related to typing of group A streptococci (GAS): The development and use of the 5' emm variable region sequencing (emm typing) in relation to the existing serologic typing system; the designation of emm types in relation to M types; a system for validation of new emm types; criteria for validation of provisional M types to new M-types; a list of reference type cultures for each of the M-type or emm-type strains of GAS; the results of the first culture exchange program for a quality control testing system among the national and World Health Organization collaborating centers for streptococci; and dissemination of new approaches to typing of GAS to the international streptococcal community

Diphtheria in the Postepidemic Period, Europe, 2000–2009

Efforts must be made to maintain high vaccination coverage

Genomic analysis reveals the molecular basis for capsule loss in the group B Streptococcus population

The human and bovine bacterial pathogen Streptococcus agalactiae (Group B Streptococcus, GBS) expresses a thick polysaccharide capsule that constitutes a major virulence factor and vaccine target. GBS can be classified into ten distinct serotypes differing in the chemical composition of their capsular polysaccharide. However, non-typeable strains that do not react with anti-capsular sera are frequently isolated from colonized and infected humans and cattle. To gain a comprehensive insight into the molecular basis for the loss of capsule expression in GBS, a collection of well-characterized non-typeable strains was investigated by genome sequencing. Genome based phylogenetic analysis extended to a wide population of sequenced strains confirmed the recently observed high clonality among GBS lineages mainly containing human strains, and revealed a much higher degree of diversity in the bovine population. Remarkably, non-typeable strains were equally distributed in all lineages. A number of distinct mutations in the cps operon were identified that were apparently responsible for inactivation of capsule synthesis. The most frequent genetic alterations were point mutations leading to stop codons in the cps genes, and the main target was found to be cpsE encoding the portal glycosyl trasferase of capsule biosynthesis. Complementation of strains carrying missense mutations in cpsE with a wild-type gene restored capsule expression allowing the identification of amino acid residues essential for enzyme activity