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Resistance genomics and molecular epidemiology of high-risk clones of ESBL-producing Pseudomonas aeruginosa in young children
The emergence of multidrug-resistant poses a global threat, but the distribution and resistance profiling are unclear, especially in young children. Infections due to are common, associated with high mortality, and increasingly β-lactam drug resistant. We studied the molecular epidemiology and antib...
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Published in: | Frontiers in cellular and infection microbiology 2023-05, Vol.13, p.1168096-1168096 |
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description | The emergence of multidrug-resistant
poses a global threat, but the distribution and resistance profiling are unclear, especially in young children. Infections due to
are common, associated with high mortality, and increasingly β-lactam drug resistant.
We studied the molecular epidemiology and antibiotic resistance mechanisms in 294 clinicalisolates of
from a pediatric hospital in China. Non-duplicate isolates were recovered from clinical cases and were identified using an API-20 kit followed by antimicrobial susceptibility testing using the VITEK®2 compact system (BioMerieux, France) and also by broth dilution method. In addition, a double-disc synergy test for the ESBL/E-test for MBL was performed. The presence of beta-lactamases, plasmid types, and sequence types was determined by PCR and sequencing.
Fifty-six percent (
= 164) of the isolates were resistant to piperacillin-tazobactam, followed by cefepime (40%;
= 117), ceftazidime (39%;
= 115), imipenem (36%;
= 106), meropenem (33%;
= 97), and ciprofloxacin (32%;
= 94). Forty-two percent (n = 126) of the isolates were positive for ESBL according to the double-disc synergy test. The blaCTX-M-15 cephalosporinase was observed in 32% (n = 40/126), while 26% (n = 33/126) werepositive for blaNDM-1 carbapenemase. Aminoglycoside resistance gene
was observed in 16% (n = 20/126), and glycylcyclines resistance gene tet(A) was observed in 12% (n = 15/126) of the isolates. A total of 23 sequence types were detected, including ST1963 (12%; n = 16), followed by ST381 (11%;
= 14), ST234 (10%;
= 13), ST145 (58%;
= 10), ST304 (57%;
= 9), ST663 (5%; n = 7), and a novel strain. In ESBL-producing
, 12 different Incompatibility groups (Inc) were observed, the most common being IncFI, IncFIS, and IncA/C. The MOBP was the most common plasmid type, followed by MOBH, MOBF, and MOBQ.
Our data suggest that the spread of antibiotic resistance is likely due toclonal spread and dissemination of different clinical strains of
harbouring different plasmids. This is a growing threat in hospitals particularly in young children which needs robust prevention strategies. |
doi_str_mv | 10.3389/fcimb.2023.1168096 |
format | article |
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poses a global threat, but the distribution and resistance profiling are unclear, especially in young children. Infections due to
are common, associated with high mortality, and increasingly β-lactam drug resistant.
We studied the molecular epidemiology and antibiotic resistance mechanisms in 294 clinicalisolates of
from a pediatric hospital in China. Non-duplicate isolates were recovered from clinical cases and were identified using an API-20 kit followed by antimicrobial susceptibility testing using the VITEK®2 compact system (BioMerieux, France) and also by broth dilution method. In addition, a double-disc synergy test for the ESBL/E-test for MBL was performed. The presence of beta-lactamases, plasmid types, and sequence types was determined by PCR and sequencing.
Fifty-six percent (
= 164) of the isolates were resistant to piperacillin-tazobactam, followed by cefepime (40%;
= 117), ceftazidime (39%;
= 115), imipenem (36%;
= 106), meropenem (33%;
= 97), and ciprofloxacin (32%;
= 94). Forty-two percent (n = 126) of the isolates were positive for ESBL according to the double-disc synergy test. The blaCTX-M-15 cephalosporinase was observed in 32% (n = 40/126), while 26% (n = 33/126) werepositive for blaNDM-1 carbapenemase. Aminoglycoside resistance gene
was observed in 16% (n = 20/126), and glycylcyclines resistance gene tet(A) was observed in 12% (n = 15/126) of the isolates. A total of 23 sequence types were detected, including ST1963 (12%; n = 16), followed by ST381 (11%;
= 14), ST234 (10%;
= 13), ST145 (58%;
= 10), ST304 (57%;
= 9), ST663 (5%; n = 7), and a novel strain. In ESBL-producing
, 12 different Incompatibility groups (Inc) were observed, the most common being IncFI, IncFIS, and IncA/C. The MOBP was the most common plasmid type, followed by MOBH, MOBF, and MOBQ.
Our data suggest that the spread of antibiotic resistance is likely due toclonal spread and dissemination of different clinical strains of
harbouring different plasmids. This is a growing threat in hospitals particularly in young children which needs robust prevention strategies.</description><identifier>ISSN: 2235-2988</identifier><identifier>EISSN: 2235-2988</identifier><identifier>DOI: 10.3389/fcimb.2023.1168096</identifier><identifier>PMID: 37293207</identifier><language>eng</language><publisher>Switzerland: Frontiers Media S.A</publisher><subject>Anti-Bacterial Agents - pharmacology ; Anti-Bacterial Agents - therapeutic use ; antimicrobial susceptibility ; beta-Lactamases - genetics ; beta-Lactamases - therapeutic use ; Ceftazidime ; Cellular and Infection Microbiology ; Child ; Child, Preschool ; Clone Cells ; ESBLs ; Genomics ; Humans ; Microbial Sensitivity Tests ; mlst ; MOB typing ; Molecular Epidemiology ; P. aeruginosa ; PBRT ; Pseudomonas aeruginosa - genetics ; Pseudomonas Infections - drug therapy ; Pseudomonas Infections - epidemiology</subject><ispartof>Frontiers in cellular and infection microbiology, 2023-05, Vol.13, p.1168096-1168096</ispartof><rights>Copyright © 2023 Patil, Chen, Dong, Mai, Lopes, Liu and Wen.</rights><rights>Copyright © 2023 Patil, Chen, Dong, Mai, Lopes, Liu and Wen 2023 Patil, Chen, Dong, Mai, Lopes, Liu and Wen</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c469t-25e2e86765b359db8b5dc3ef39b6afcfcba1f29156b5738d86233168728fd5fa3</citedby><cites>FETCH-LOGICAL-c469t-25e2e86765b359db8b5dc3ef39b6afcfcba1f29156b5738d86233168728fd5fa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10244630/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10244630/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27922,27923,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37293207$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Patil, Sandip</creatorcontrib><creatorcontrib>Chen, Xiaowen</creatorcontrib><creatorcontrib>Dong, Shaowei</creatorcontrib><creatorcontrib>Mai, Huirong</creatorcontrib><creatorcontrib>Lopes, Bruno Silvester</creatorcontrib><creatorcontrib>Liu, Sixi</creatorcontrib><creatorcontrib>Wen, Feiqiu</creatorcontrib><title>Resistance genomics and molecular epidemiology of high-risk clones of ESBL-producing Pseudomonas aeruginosa in young children</title><title>Frontiers in cellular and infection microbiology</title><addtitle>Front Cell Infect Microbiol</addtitle><description>The emergence of multidrug-resistant
poses a global threat, but the distribution and resistance profiling are unclear, especially in young children. Infections due to
are common, associated with high mortality, and increasingly β-lactam drug resistant.
We studied the molecular epidemiology and antibiotic resistance mechanisms in 294 clinicalisolates of
from a pediatric hospital in China. Non-duplicate isolates were recovered from clinical cases and were identified using an API-20 kit followed by antimicrobial susceptibility testing using the VITEK®2 compact system (BioMerieux, France) and also by broth dilution method. In addition, a double-disc synergy test for the ESBL/E-test for MBL was performed. The presence of beta-lactamases, plasmid types, and sequence types was determined by PCR and sequencing.
Fifty-six percent (
= 164) of the isolates were resistant to piperacillin-tazobactam, followed by cefepime (40%;
= 117), ceftazidime (39%;
= 115), imipenem (36%;
= 106), meropenem (33%;
= 97), and ciprofloxacin (32%;
= 94). Forty-two percent (n = 126) of the isolates were positive for ESBL according to the double-disc synergy test. The blaCTX-M-15 cephalosporinase was observed in 32% (n = 40/126), while 26% (n = 33/126) werepositive for blaNDM-1 carbapenemase. Aminoglycoside resistance gene
was observed in 16% (n = 20/126), and glycylcyclines resistance gene tet(A) was observed in 12% (n = 15/126) of the isolates. A total of 23 sequence types were detected, including ST1963 (12%; n = 16), followed by ST381 (11%;
= 14), ST234 (10%;
= 13), ST145 (58%;
= 10), ST304 (57%;
= 9), ST663 (5%; n = 7), and a novel strain. In ESBL-producing
, 12 different Incompatibility groups (Inc) were observed, the most common being IncFI, IncFIS, and IncA/C. The MOBP was the most common plasmid type, followed by MOBH, MOBF, and MOBQ.
Our data suggest that the spread of antibiotic resistance is likely due toclonal spread and dissemination of different clinical strains of
harbouring different plasmids. This is a growing threat in hospitals particularly in young children which needs robust prevention strategies.</description><subject>Anti-Bacterial Agents - pharmacology</subject><subject>Anti-Bacterial Agents - therapeutic use</subject><subject>antimicrobial susceptibility</subject><subject>beta-Lactamases - genetics</subject><subject>beta-Lactamases - therapeutic use</subject><subject>Ceftazidime</subject><subject>Cellular and Infection Microbiology</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Clone Cells</subject><subject>ESBLs</subject><subject>Genomics</subject><subject>Humans</subject><subject>Microbial Sensitivity Tests</subject><subject>mlst</subject><subject>MOB typing</subject><subject>Molecular Epidemiology</subject><subject>P. aeruginosa</subject><subject>PBRT</subject><subject>Pseudomonas aeruginosa - genetics</subject><subject>Pseudomonas Infections - drug therapy</subject><subject>Pseudomonas Infections - epidemiology</subject><issn>2235-2988</issn><issn>2235-2988</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNpVkk1v1DAQhiMEolXpH-CAfOSSxR-xY58QVAUqrQTi42w59jjr4tiLvam0B_472e5StXPx6J2ZZyz7bZrXBK8Yk-qdt2EaVhRTtiJESKzEs-acUsZbqqR8_ig_ay5rvcVL9JhKxV42Z6ynilHcnzd_v0MNdWeSBTRCylOwFZnk0JQj2DmagmAbHEwhxzzuUfZoE8ZNW0L9jWzMCepBu_7xcd1uS3azDWlE3yrMLk85mQUGZR5DytWgkNA-z0vdbkJ0BdKr5oU3scLl6bxofn26_nn1pV1__Xxz9WHd2k6oXUs5UJCiF3xgXLlBDtxZBp6pQRhvvR0M8VQRLgbeM-mkoIwtj9JT6R33hl00N0euy-ZWb0uYTNnrbIK-F3IZtSm7YCNo4Mr4ngBwjzujiHLEMwNdLwR3XLqF9f7I2s7DBM5C2hUTn0CfVlLY6DHfaYJp1wmGF8LbE6HkPzPUnZ5CtRCjSZDnqqmknZAdxmJppcdWW3KtBfzDHoL1wQf63gf64AN98sEy9ObxDR9G_v86-wcCerLB</recordid><startdate>20230524</startdate><enddate>20230524</enddate><creator>Patil, Sandip</creator><creator>Chen, Xiaowen</creator><creator>Dong, Shaowei</creator><creator>Mai, Huirong</creator><creator>Lopes, Bruno Silvester</creator><creator>Liu, Sixi</creator><creator>Wen, Feiqiu</creator><general>Frontiers Media S.A</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20230524</creationdate><title>Resistance genomics and molecular epidemiology of high-risk clones of ESBL-producing Pseudomonas aeruginosa in young children</title><author>Patil, Sandip ; Chen, Xiaowen ; Dong, Shaowei ; Mai, Huirong ; Lopes, Bruno Silvester ; Liu, Sixi ; Wen, Feiqiu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c469t-25e2e86765b359db8b5dc3ef39b6afcfcba1f29156b5738d86233168728fd5fa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Anti-Bacterial Agents - pharmacology</topic><topic>Anti-Bacterial Agents - therapeutic use</topic><topic>antimicrobial susceptibility</topic><topic>beta-Lactamases - genetics</topic><topic>beta-Lactamases - therapeutic use</topic><topic>Ceftazidime</topic><topic>Cellular and Infection Microbiology</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Clone Cells</topic><topic>ESBLs</topic><topic>Genomics</topic><topic>Humans</topic><topic>Microbial Sensitivity Tests</topic><topic>mlst</topic><topic>MOB typing</topic><topic>Molecular Epidemiology</topic><topic>P. aeruginosa</topic><topic>PBRT</topic><topic>Pseudomonas aeruginosa - genetics</topic><topic>Pseudomonas Infections - drug therapy</topic><topic>Pseudomonas Infections - epidemiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Patil, Sandip</creatorcontrib><creatorcontrib>Chen, Xiaowen</creatorcontrib><creatorcontrib>Dong, Shaowei</creatorcontrib><creatorcontrib>Mai, Huirong</creatorcontrib><creatorcontrib>Lopes, Bruno Silvester</creatorcontrib><creatorcontrib>Liu, Sixi</creatorcontrib><creatorcontrib>Wen, Feiqiu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Frontiers in cellular and infection microbiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Patil, Sandip</au><au>Chen, Xiaowen</au><au>Dong, Shaowei</au><au>Mai, Huirong</au><au>Lopes, Bruno Silvester</au><au>Liu, Sixi</au><au>Wen, Feiqiu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Resistance genomics and molecular epidemiology of high-risk clones of ESBL-producing Pseudomonas aeruginosa in young children</atitle><jtitle>Frontiers in cellular and infection microbiology</jtitle><addtitle>Front Cell Infect Microbiol</addtitle><date>2023-05-24</date><risdate>2023</risdate><volume>13</volume><spage>1168096</spage><epage>1168096</epage><pages>1168096-1168096</pages><issn>2235-2988</issn><eissn>2235-2988</eissn><abstract>The emergence of multidrug-resistant
poses a global threat, but the distribution and resistance profiling are unclear, especially in young children. Infections due to
are common, associated with high mortality, and increasingly β-lactam drug resistant.
We studied the molecular epidemiology and antibiotic resistance mechanisms in 294 clinicalisolates of
from a pediatric hospital in China. Non-duplicate isolates were recovered from clinical cases and were identified using an API-20 kit followed by antimicrobial susceptibility testing using the VITEK®2 compact system (BioMerieux, France) and also by broth dilution method. In addition, a double-disc synergy test for the ESBL/E-test for MBL was performed. The presence of beta-lactamases, plasmid types, and sequence types was determined by PCR and sequencing.
Fifty-six percent (
= 164) of the isolates were resistant to piperacillin-tazobactam, followed by cefepime (40%;
= 117), ceftazidime (39%;
= 115), imipenem (36%;
= 106), meropenem (33%;
= 97), and ciprofloxacin (32%;
= 94). Forty-two percent (n = 126) of the isolates were positive for ESBL according to the double-disc synergy test. The blaCTX-M-15 cephalosporinase was observed in 32% (n = 40/126), while 26% (n = 33/126) werepositive for blaNDM-1 carbapenemase. Aminoglycoside resistance gene
was observed in 16% (n = 20/126), and glycylcyclines resistance gene tet(A) was observed in 12% (n = 15/126) of the isolates. A total of 23 sequence types were detected, including ST1963 (12%; n = 16), followed by ST381 (11%;
= 14), ST234 (10%;
= 13), ST145 (58%;
= 10), ST304 (57%;
= 9), ST663 (5%; n = 7), and a novel strain. In ESBL-producing
, 12 different Incompatibility groups (Inc) were observed, the most common being IncFI, IncFIS, and IncA/C. The MOBP was the most common plasmid type, followed by MOBH, MOBF, and MOBQ.
Our data suggest that the spread of antibiotic resistance is likely due toclonal spread and dissemination of different clinical strains of
harbouring different plasmids. This is a growing threat in hospitals particularly in young children which needs robust prevention strategies.</abstract><cop>Switzerland</cop><pub>Frontiers Media S.A</pub><pmid>37293207</pmid><doi>10.3389/fcimb.2023.1168096</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Anti-Bacterial Agents - pharmacology Anti-Bacterial Agents - therapeutic use antimicrobial susceptibility beta-Lactamases - genetics beta-Lactamases - therapeutic use Ceftazidime Cellular and Infection Microbiology Child Child, Preschool Clone Cells ESBLs Genomics Humans Microbial Sensitivity Tests mlst MOB typing Molecular Epidemiology P. aeruginosa PBRT Pseudomonas aeruginosa - genetics Pseudomonas Infections - drug therapy Pseudomonas Infections - epidemiology |
title | Resistance genomics and molecular epidemiology of high-risk clones of ESBL-producing Pseudomonas aeruginosa in young children |
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