المؤلفون: Lo, Stephanie W, Gladstone, Rebecca A, Tonder, Andries J van, Plessis, Mignon Du, Cornick, Jennifer E, Hawkins, Paulina A, Madhi, Shabir A, Nzenze, Susan A, Kandasamy, Rama, Ravikumar, K L, Elmdaghri, Naima, Kwambana-Adams, Brenda, Almeida, Samanta Cristine Grassi, Skoczynska, Anna, Egorova, Ekaterina, Titov, Leonid, Saha, Samir K, Paragi, Metka, Everett, Dean B, Antonio, Martin

المصدر: Journal of Antimicrobial Chemotherapy (JAC); Mar2020, Vol. 75 Issue 3, p512-520, 9p

مصطلحات موضوعية: TETRACYCLINES, DRUG resistance in bacteria, PNEUMOCOCCAL vaccines, GENES, STREPTOCOCCUS pneumoniae, PENICILLIN, RESEARCH, SEQUENCE analysis, RESEARCH methodology, MEDICAL cooperation, EVALUATION research, STREPTOCOCCUS, SEROTYPES, COMPARATIVE studies, RESEARCH funding, DRUG resistance in microorganisms, ANTIBIOTICS, PHARMACODYNAMICS

مصطلحات جغرافية: SOUTH Africa

مستخلص: Objectives: We reported tet(S/M) in Streptococcus pneumoniae and investigated its temporal spread in relation to nationwide clinical interventions.Methods: We whole-genome sequenced 12 254 pneumococcal isolates from 29 countries on an Illumina HiSeq sequencer. Serotype, multilocus ST and antibiotic resistance were inferred from genomes. An SNP tree was built using Gubbins. Temporal spread was reconstructed using a birth-death model.Results: We identified tet(S/M) in 131 pneumococcal isolates and none carried other known tet genes. Tetracycline susceptibility testing results were available for 121 tet(S/M)-positive isolates and all were resistant. A majority (74%) of tet(S/M)-positive isolates were from South Africa and caused invasive diseases among young children (59% HIV positive, where HIV status was available). All but two tet(S/M)-positive isolates belonged to clonal complex (CC) 230. A global phylogeny of CC230 (n=389) revealed that tet(S/M)-positive isolates formed a sublineage predicted to exhibit resistance to penicillin, co-trimoxazole, erythromycin and tetracycline. The birth-death model detected an unrecognized outbreak of this sublineage in South Africa between 2000 and 2004 with expected secondary infections (effective reproductive number, R) of ∼2.5. R declined to ∼1.0 in 2005 and <1.0 in 2012. The declining epidemic could be related to improved access to ART in 2004 and introduction of pneumococcal conjugate vaccine (PCV) in 2009. Capsular switching from vaccine serotype 14 to non-vaccine serotype 23A was observed within the sublineage.Conclusions: The prevalence of tet(S/M) in pneumococci was low and its dissemination was due to an unrecognized outbreak of CC230 in South Africa. Capsular switching in this MDR sublineage highlighted its potential to continue to cause disease in the post-PCV13 era. [ABSTRACT FROM AUTHOR]

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المؤلفون: Azarian, Taj, Mitchell, Patrick K., Georgieva, Maria, Thompson, Claudette M., Ghouila, Amel, Pollard, Andrew J., von Gottberg, Anne, du Plessis, Mignon, Antonio, Martin, Kwambana-Adams, Brenda A., Clarke, Stuart C., Everett, Dean, Cornick, Jennifer, Sadowy, Ewa, Hryniewicz, Waleria, Skoczynska, Anna, Moïsi, Jennifer C., McGee, Lesley, Beall, Bernard, Metcalf, Benjamin J.

المصدر: PLoS Pathogens; 11/26/2018, Vol. 14 Issue 11, p1-26, 26p

مصطلحات موضوعية: STREPTOCOCCUS pneumoniae, SEROTYPES, MICROORGANISMS, ANTIGENS, POLYSACCHARIDES

مستخلص: Streptococcus pneumoniae serotype 3 remains a significant cause of morbidity and mortality worldwide, despite inclusion in the 13-valent pneumococcal conjugate vaccine (PCV13). Serotype 3 increased in carriage since the implementation of PCV13 in the USA, while invasive disease rates remain unchanged. We investigated the persistence of serotype 3 in carriage and disease, through genomic analyses of a global sample of 301 serotype 3 isolates of the Netherlands³–31 (PMEN31) clone CC180, combined with associated patient data and PCV utilization among countries of isolate collection. We assessed phenotypic variation between dominant clades in capsule charge (zeta potential), capsular polysaccharide shedding, and susceptibility to opsonophagocytic killing, which have previously been associated with carriage duration, invasiveness, and vaccine escape. We identified a recent shift in the CC180 population attributed to a lineage termed Clade II, which was estimated by Bayesian coalescent analysis to have first appeared in 1968 [95% HPD: 1939–1989] and increased in prevalence and effective population size thereafter. Clade II isolates are divergent from the pre-PCV13 serotype 3 population in non-capsular antigenic composition, competence, and antibiotic susceptibility, the last of which resulting from the acquisition of a Tn916-like conjugative transposon. Differences in recombination rates among clades correlated with variations in the ATP-binding subunit of Clp protease, as well as amino acid substitutions in the comCDE operon. Opsonophagocytic killing assays elucidated the low observed efficacy of PCV13 against serotype 3. Variation in PCV13 use among sampled countries was not independently correlated with the CC180 population shift; therefore, genotypic and phenotypic differences in protein antigens and, in particular, antibiotic resistance may have contributed to the increase of Clade II. Our analysis emphasizes the need for routine, representative sampling of isolates from disperse geographic regions, including historically under-sampled areas. We also highlight the value of genomics in resolving antigenic and epidemiological variations within a serotype, which may have implications for future vaccine development. [ABSTRACT FROM AUTHOR]

: Copyright of PLoS Pathogens is the property of Public Library of Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)