A Nationwide Outbreak of Invasive Pneumococcal Disease in Israel Caused by Streptococcus Pneumoniae Serotype 2

2020 ◽  
Author(s):  
Ron Dagan ◽  
Shalom Ben-Shimol ◽  
Rachel Benisty ◽  
Gili Regev-Yochay ◽  
Stephanie W Lo ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Invasive Pneumococcal Disease ◽  
Pneumococcal Disease ◽  
Large Scale ◽  
Evolutionary Dynamics ◽  
Fold Increase ◽  
Population Based ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Single Locus Variant

Abstract Background Invasive pneumococcal disease (IPD) caused by Streptococcus pneumoniae serotype 2 (Sp2) is infrequent. Large scale outbreaks have not been reported following pneumococcal conjugate vaccine (PCV) implementation. We describe a Sp2 IPD outbreak in Israel, in the 13-valent PCV (PCV13) era, with focus on Sp2 population structure and evolutionary dynamics. Methods The data derived from a population-based, nationwide active surveillance of IPD since 2009. 7-valent PCV (PCV7)/PCV13 vaccines were introduced in July 2009 and November 2010, respectively. Sp2 isolates were tested for antimicrobial susceptibility, Multilocus Sequence Typing (MLST) and Whole Genome Sequencing (WGS) analysis. Results Overall, 170 Sp2 IPD cases were identified during 2009-2019; Sp2 increased in 2015 and caused 6% of IPD during 2015-2019, a 7-fold increase compared with 2009-2014. The outbreak was caused by a previously unreported molecular type (ST-13578), initially observed in Israel in 2014. This clone caused 88% of Sp2 during 2015-2019. ST-13578 is a single-locus variant of ST-1504, previously reported globally, including in Israel. WGS analysis confirmed clonality among the ST-13578 population. Single-nucleotide polymorphisms-dense regions support a hypothesis that the ST-13578 outbreak clone evolved from ST-1504 by recombination. All tested strains were penicillin-susceptible (MIC <0.06 μg/mL). The ST-13578 clone was identified almost exclusively (99%) in the Jewish population and was mainly distributed in 3/7 Israeli districts. The outbreak is still ongoing, although declining since 2017. Conclusions: To the best of our knowledge, this is the first widespread Sp2 outbreak since PCV13 introduction worldwide, caused by the emerging ST-13578 clone.

scholarly journals 1888. A Nationwide Outbreak of Invasive Pneumococcal Disease (IPD) Caused by a Novel Streptococcus Pneumoniae Serotype 2 (SP2) Clone in the PCV13 Era, in Israel

2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S54-S54
Author(s):  
Ron Dagan ◽  
Shalom Ben-Shimol ◽  
Rachel Benisty ◽  
Gili Regev-Yochay ◽  
Merav Ron ◽  
...  
Keyword(s):  
Population Structure ◽  
Jewish Population ◽  
Pneumococcal Disease ◽  
Large Scale ◽  
Evolutionary Dynamics ◽  
Fold Increase ◽  
Population Based ◽  
Whole Genome ◽  
Single Strain ◽  
The Uk

Abstract Background IPD caused by Sp2 (non-PCV13 serotype) is relatively rare. However, Sp2 has a high potential for causing IPD including meningitis. Large-scale outbreaks of Sp2 IPD are rare and were not reported post-PCV implementation. We describe Sp2 IPD outbreak in Israel, in the PCV13 era, caused by a novel clone. Additionally, we analyzed the population structure and evolutionary dynamics of Sp2 during 2006–2018. Methods An ongoing, population-based, nationwide active surveillance, conducted since July 2009. PCV7/PCV13 were implemented in Israel in July 2009 and November 2010, respectively. All isolates were tested for antimicrobial susceptibility, PFGE, MLST and whole-genome sequencing (WGS). Results. Overall, 173 Sp2 IPD cases were identified; all isolates were analyzed by MLST (Figure 1). During 2016–2017, Sp2 caused 7.6% of all-IPD, a 7-fold increase compared with 2006–2015, and ranked second (after serotype 12F causing 12%) among IPD isolates. During 2006–2015, 98% (40/41) Sp2 IPD were caused by the previously reported global ST-1504 clone. The outbreak was caused by a novel clone ST-13578, not previously reported (Figure 2). WGS analysis confirmed that ST-13578 was related, but genetically distinct from ST-1504, observed exclusively before the outbreak. A single strain of clone ST-74 previously globally reported was identified in 2017–2018. An additional case was identified in an adult in the UK, following a family visit from Israel. The ST-13578 clone was identified only in the Jewish population and was mainly distributed in 3 of the 7 Israeli districts. All tested strains were penicillin-susceptible (MIC < 0.06 μg/mL). Conclusion To the best of our knowledge, this is the first widespread Sp2 outbreak since PCV13 introduction worldwide, caused by a novel clone ST-13578. The outbreak is still ongoing, although a declining trend was noted since 2017. Disclosures All Authors: No reported Disclosures.

scholarly journals Different Within-Host Viral Evolution Dynamics in Severely Immunosuppressed Cases with Persistent SARS-CoV-2

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 808
Author(s):  
Laura Pérez-Lago ◽  
Teresa Aldámiz-Echevarría ◽  
Rita García-Martínez ◽  
Leire Pérez-Latorre ◽  
Marta Herranz ◽  
...  
Keyword(s):  
Single Nucleotide Polymorphisms ◽  
Evolutionary Dynamics ◽  
Viral Evolution ◽  
Special Focus ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
New Variant ◽  
History Of ◽  
Evolution Dynamics ◽  
The Uk

A successful Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) variant, B.1.1.7, has recently been reported in the UK, causing global alarm. Most likely, the new variant emerged in a persistently infected patient, justifying a special focus on these cases. Our aim in this study was to explore certain clinical profiles involving severe immunosuppression that may help explain the prolonged persistence of viable viruses. We present three severely immunosuppressed cases (A, B, and C) with a history of lymphoma and prolonged SARS-CoV-2 shedding (2, 4, and 6 months), two of whom finally died. Whole-genome sequencing of 9 and 10 specimens from Cases A and B revealed extensive within-patient acquisition of diversity, 12 and 28 new single nucleotide polymorphisms, respectively, which suggests ongoing SARS-CoV-2 replication. This diversity was not observed for Case C after analysing 5 sequential nasopharyngeal specimens and one plasma specimen, and was only observed in one bronchoaspirate specimen, although viral viability was still considered based on constant low Ct values throughout the disease and recovery of the virus in cell cultures. The acquired viral diversity in Cases A and B followed different dynamics. For Case A, new single nucleotide polymorphisms were quickly fixed (13–15 days) after emerging as minority variants, while for Case B, higher diversity was observed at a slower emergence: fixation pace (1–2 months). Slower SARS-CoV-2 evolutionary pace was observed for Case A following the administration of hyperimmune plasma. This work adds knowledge on SARS-CoV-2 prolonged shedding in severely immunocompromised patients and demonstrates viral viability, noteworthy acquired intra-patient diversity, and different SARS-CoV-2 evolutionary dynamics in persistent cases.

scholarly journals A NOTE ON PHASING LONG GENOMIC REGIONS USING LOCAL HAPLOTYPE PREDICTIONS

2006 ◽  
Vol 04 (03) ◽  
pp. 639-647 ◽  
Author(s):  
ELEAZAR ESKIN ◽  
RODED SHARAN ◽  
ERAN HALPERIN
Keyword(s):  
Large Scale ◽  
Computational Cost ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Novel Approach ◽  
Maximum Likelihood Criterion ◽  
The Common ◽  
Genomic Regions ◽  
High Computational Cost ◽  
Combining Information

The common approaches for haplotype inference from genotype data are targeted toward phasing short genomic regions. Longer regions are often tackled in a heuristic manner, due to the high computational cost. Here, we describe a novel approach for phasing genotypes over long regions, which is based on combining information from local predictions on short, overlapping regions. The phasing is done in a way, which maximizes a natural maximum likelihood criterion. Among other things, this criterion takes into account the physical length between neighboring single nucleotide polymorphisms. The approach is very efficient and is applied to several large scale datasets and is shown to be successful in two recent benchmarking studies (Zaitlen et al., in press; Marchini et al., in preparation). Our method is publicly available via a webserver at .

scholarly journals Coeliac disease and invasive pneumococcal disease: a population-based cohort study

2017 ◽  
Vol 145 (6) ◽  
pp. 1203-1209 ◽  
Author(s):  
A. RÖCKERT TJERNBERG ◽  
J. BONNEDAHL ◽  
M. INGHAMMAR ◽  
A. EGESTEN ◽  
G. KAHLMETER ◽  
...  
Keyword(s):  
Cohort Study ◽  
Coeliac Disease ◽  
Invasive Pneumococcal Disease ◽  
Pneumococcal Disease ◽  
Cox Regression ◽  
Statistical Significance ◽  
Pneumococcal Vaccination ◽  
Population Based ◽  
Increased Risk ◽  
Severe Infections

SUMMARYSevere infections are recognized complications of coeliac disease (CD). In the present study we aimed to examine whether individuals with CD are at increased risk of invasive pneumococcal disease (IPD). To do so, we performed a population-based cohort study including 29 012 individuals with biopsy-proven CD identified through biopsy reports from all pathology departments in Sweden. Each individual with CD was matched with up to five controls (n = 144 257). IPD events were identified through regional and national microbiological databases, including the National Surveillance System for Infectious Diseases. We used Cox regression analyses to estimate hazard ratios (HRs) for diagnosed IPD. A total of 207 individuals had a record of IPD whereas 45/29 012 had CD (0·15%) and 162/144 257 were controls (0·11%). This corresponded to a 46% increased risk for IPD [HR 1·46, 95% confidence interval (CI) 1·05–2·03]. The risk estimate was similar after adjustment for socioeconomic status, educational level and comorbidities, but then failed to attain statistical significance (adjusted HR 1·40, 95% CI 0·99–1·97). Nonetheless, our study shows a trend towards an increased risk for IPD in CD patients. The findings support results seen in earlier research and taking that into consideration individuals with CD may be considered for pneumococcal vaccination.

scholarly journals Evaluating post-vaccine expansion patterns of pneumococcal serotypes

2020 ◽  
Author(s):  
Maile T. Phillips ◽  
Joshua L. Warren ◽  
Noga Givon-Lavi ◽  
Adrienn Tothpal ◽  
Gili Regev-Yochay ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Invasive Pneumococcal Disease ◽  
Jewish Population ◽  
Pneumococcal Disease ◽  
Pneumococcal Serotypes ◽  
Conjugate Vaccines ◽  
Pneumococcal Conjugate Vaccines ◽  
Vaccine Serotypes ◽  
Serotype Replacement ◽  
Disease Understanding

ABSTRACTStreptococcus pneumoniae remains a leading cause of morbidity and mortality. Pneumococcal conjugate vaccines (PCVs) are effective but target only a fraction of the more than 90 pneumococcal serotypes. As a result, the introduction of PCVs has been followed by the emergence of non-vaccine serotypes. With higher-valency PCVs currently under development, there is a need to understand and predict patterns of serotype replacement to anticipate future changes. In this study, we evaluated patterns of change in serotype prevalence post-PCV introduction in Israel. We found that the assumption that non-vaccine serotypes increase by the same proportion overestimates changes in serotype prevalence in Jewish and Bedouin children. Furthermore, pre-vaccine prevalence was positively associated with increases in prevalence over the study period. From our analyses, serotypes 12F, 8, 16F, 33F, 9N, 7B, 10A, 22F, 24F, and 17F were estimated to have gained the most cases of invasive pneumococcal disease through serotype replacement in the Jewish population. However, this model also failed to quantify some additional cases gained, suggesting that changes in carriage in children alone may be insufficient to explain serotype replacement in disease. Understanding of serotype replacement is important as higher-valency vaccines are introduced.

scholarly journals Invasive isolates of Streptococcus pneumoniae in Serbia: Antimicrobial susceptibility and serotypes

2013 ◽  
Vol 141 (1-2) ◽  
pp. 48-53 ◽  
Author(s):  
Ina Gajic ◽  
Vera Mijac ◽  
Lazar Ranin ◽  
Dragana Andjelkovic ◽  
Miroslava Radicevic ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Invasive Pneumococcal Disease ◽  
Antimicrobial Susceptibility ◽  
Pneumococcal Disease ◽  
Medical Problem ◽  
Resistance Rate ◽  
Reference Laboratory ◽  
Susceptibility Pattern ◽  
Antimicrobial Susceptibility Pattern ◽  
Resistance Rates

Introduction. Streptococcus pneumoniae is one of the leading causes of bacterial meningitis and sepsis. Invasive pneumococcal disease is a significant medical problem worldwide, particularly in children, due to a huge increase of pneumococcal resistance to antibiotics. Objective. The aim of the study was to investigate the antimicrobial susceptibility pattern of invasive pneumococcal isolates, as well as to determine whether decreased S. pneumoniae susceptibility to antibiotics was related to a particular serotype. Methods. Antimicrobial susceptibility to 19 antibiotics was determined in 58 invasive pneumococcal strains that were collected from seven regional centers during the period July 2009 to February 2011 in the National Reference Laboratory for streptococci and pneumococci. Results. The overall nonsusceptibility rate to penicillin was detected in 34% of pneumococcal isolates and to erythromycin in 36%. Higher resistance rates were observed among children than among adults. Penicillin resistance rate was 65% in children versus 22% in adults, while erythromycin nonsusceptibility rate was 47% in children versus 32% in adults. Co-resistance to penicillin and erythromycin was detected in 21% strains, mostly isolated from children. Multiresistance was found in one third of isolates. All strains were susceptible to vancomycin, linezolid, fluoroquinolones, telithromycin and rifampicin, while 23 (40%) isolates were susceptible to all tested antibiotics. The most common resistant serotypes were 19F and 14. Conclusion. The study has revealed that penicillin and macrolide resistance among invasive pneumococcal isolates is very high in Serbia. This emphasizes the need for continuous monitoring for invasive pneumococcal disease to document the serotype distribution and antimicrobial susceptibility pattern.

scholarly journals INFLUENCE ON HOMEOSTASIS AS THE CRITERION FOR SELECTING SINGLE NUCLEOTIDE POLYMORPHISMS FOR THE STUDY OF METABOLIC SYNDROM IN THE KAZAKH POPULATION

REPORTS ◽  
2020 ◽  
Vol 5 (333) ◽  
pp. 86-93
Author(s):  
V.V. Benberin ◽  
◽  
T.A. Voshchenkova ◽  
A.A. Nagymtayeva ◽  
A.S. Sibagatova ◽  
...  
Keyword(s):  
Single Nucleotide Polymorphisms ◽  
Traditional Approach ◽  
Population Based ◽  
Malignant Neoplasms ◽  
Nucleotide Polymorphisms ◽  
Genetic Determinants ◽  
Single Nucleotide ◽  
Sequence Of Events ◽  
Kazakh Population ◽  
Symptom Complex

Metabolic syndrome (MS) is increasingly cited as the world's leading health risk. The sequence of events toward multimorbidity in most cases passes through MS. According to the research, MS heritability ranges from 23 to 27% in Europeans, and 51 to 60% in Asians. The purpose of the review: to form a strategy for the selection of single nucleotide polymorphisms (SNPs) for the study of MS in the Kazakh population based on the effect of SNPs on homeostasis indicators The stable symptom complex of MS is a complicated dynamic system of successive accumulations of dysmetabolic disorders of homeostasis. This system starts the development of subsequent age-associated diseases), such as cardiometabolic, neurodegenerative, and malignant neoplasms. The system for selecting SNPs for the MS study, proposed on the basis of the concept of homeostasis dysfunction, assumes, in conditions of limited resources, to see the greatest level of their influence within the conditional framework of three genetic models of homeostasis dysregulation: insulin resistance , oxidative stress, and chronic inflammation. This approach is fundamentally different from the traditional approach involving candidate genes. It is expected that scientific research in this direction will contribute not only to the understanding of general biological processes, but also to the targeted search for genetic determinants and for new opportunities for personalized interventions.

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