Open AccessEmerging carbapenem-resistant Klebsiella pneumoniae sequence type 16 causing multiple outbreaks in a tertiary hospital in southern Vietnam
Author(s) -
To Nguyen Thi Nguyen,
Phung Kim Phi Nguyen,
Ngan Thi Quynh Le,
Lan Phu Huong Nguyen,
Thuy Bich Duong,
Nghia Dang Trung Ho,
Quynh Nguyen,
Trung Duc Pham,
Anh Tuan Tran,
Hien Nguyen,
Chau Nguyen,
Guy Thwaites,
Maia A. Rabaa,
Duy Pham
Publication year - 2021
Publication title -
microbial genomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.476
H-Index - 28
ISSN - 2057-5858
DOI - 10.1099/mgen.0.000519
Subject(s) - outbreak , klebsiella pneumoniae , colistin , infection control , biology , drug resistance , carbapenem , transmission (telecommunications) , clone (java method) , microbiology and biotechnology , medicine , virology , intensive care medicine , antibiotics , gene , escherichia coli , genetics , electrical engineering , engineering
The emergence of carbapenem resistance in Klebsiella pneumoniae represents a major global public health concern. Nosocomial outbreaks caused by multidrug-resistant K. pneumoniae are commonly reported to result in high morbidity and mortality due to limited treatment options. Between October 2019 and January 2020, two concurrent high-mortality nosocomial outbreaks occurred in a referral hospital in Ho Chi Minh City, Vietnam. We performed genome sequencing and phylogenetic analysis of eight K. pneumoniae isolates from infected patients and two environmental isolates for outbreak investigation. We identified two outbreaks caused by two distinct lineages of the international sequence type (ST) 16 clone, which displayed extensive drug resistance, including resistance to carbapenem and colistin. Carbapenem-resistant ST16 outbreak strains clustered tightly with previously described ST16 K. pneumoniae from other hospitals in Vietnam, suggesting local persistence and transmission of this particular clone in this setting. We found environmental isolates from a hospital bed and blood pressure cuff that were genetically linked to an outbreak case cluster, confirming the potential of high-touch surfaces as sources for nosocomial spread of K. pneumoniae . Further, we found colistin resistance caused by disruption of the mgrB gene by an IS L3 -like element, and carbapenem resistance mediated by a transferable IncF/ bla OXA-181 plasmid carrying the IS L3 -like element. Our study highlights the importance of coordinated efforts between clinical and molecular microbiologists and infection control teams to rapidly identify, investigate and contain nosocomial outbreaks. Routine surveillance with advanced sequencing technology should be implemented to strengthen hospital infection control and prevention measures.