VIM-2 metallo- -lactamase-producing Pseudomonas aeruginosa causing an outbreak in South Africa

Jacobson, Rachael; Minenza, Nadia; Nicol, Mark P.; Bamford, Colleen

doi:10.1093/jac/dks100

Cited by 35 publications

(21 citation statements)

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“…Sixty percent of the isolates carried identical bla VIM sequences (which, based on the amplicon sequence, were consistent with bla VIM-2 or four other, less frequently observed variants: bla VIM-10 , bla , bla , and bla VIM-30 ), and 40% of the isolates were found to contain bla DIM-1 . While bla VIM (and especially bla VIM-2 ) is acknowledged as one of the most commonly isolated MBLs in Africa and throughout the world (19)(20)(21)(22), the presence of bla DIM-1 has been reported only once before, for a Pseudomonas stutzeri isolate from The Netherlands (23). In this study, bla DIM-1 was found in hospital isolates belonging to the families Enterobacteriaceae, Pseudomonadaceae, Burkholderiaceae, and Comamonadaceae.…”

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confidence: 62%

Identification of bla _OXA-51-like , bla _OXA-58 , bla _DIM-1 , and bla _VIM Carbapenemase Genes in Hospital Enterobacteriaceae Isolates from Sierra Leone

et al. 2013

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fWe describe the results of a molecular epidemiological survey of 15 carbapenemase-encoding genes from a recent collection of clinical isolates from Mercy Hospital in Bo, Sierra Leone. The most salient findings revealed that (i) 60% of the isolates harbored multiple carbapenemase genes; (ii) the bla DIM-1 gene, which has previously only been reported in The Netherlands, is also circulating in this environment; and (iii) bla OXA-51-like and bla OXA-58 genes, which were thought to reside exclusively in Acinetobacter species, can also be found in members of the Enterobacteriaceae. Carbapenem antibiotics are currently the most potent ␤-lactam antibiotics clinically available and are used as a last resort to treat infections caused by multidrug-resistant Gram-negative pathogens. The significance and usage of this family of antibiotics have risen dramatically over the last decade, especially in hospital settings, due to the global spread and increasing prevalence of bacterial pathogens that harbor extended-spectrum ␤-lactamase genes that confer resistance to all ␤-lactam compounds except for carbapenems (1). Not surprisingly, the positive selection pressure provided by the increased usage of carbapenems has resulted in the emergence and expansion of carbapenem resistance in a number of common nosocomial pathogenic species (1).Carbapenem resistance is mediated mostly by ␤-lactamase enzymes that are capable of hydrolyzing carbapenem compounds (carbapenemases) and often differ in host microorganism range, substrate specificity, and ␤-lactamase inhibitor sensitivity (2, 3). Furthermore, carbapenemases are frequently found in pathogenic strains that contain additional genetic determinants that confer resistance to aminoglycosides, tetracyclines, ␤-lactams, and fluoroquinolones and can result in intractable infections with high mortality rates (4, 5). The spread of Ambler class A, B, and D carbapenemase genes, which were encountered only rarely less than 2 decades ago, has been facilitated by conjugative plasmids, transposons, and integrons to such an extent that carbapenemase genes have now been reported worldwide (2). Despite this fact and the clinical impact of these genes, the true incidence and prevalence of carbapenem resistance and carbapenemase genes are still unknown, as many countries do not track and report antibiotic resistance rates; this is particularly true in many African countries (1).To better understand the level, distribution, and evolution of multidrug resistance in environments that currently lack a national antibiotic stewardship policy, we initiated a molecular epidemiology surveillance program at Mercy Hospital in Bo, Sierra Leone. The preliminary evidence, obtained using an antimicrobial resistance determinant microarray as a screening tool (6), indicated the presence of class B metallo-␤-lactamase (MBL) and class D carbapenem-hydrolyzing ␤-lactamase (CHDL) genes in this environment. In this study, we utilized PCR and DNA sequencing to target 15 carbapenemase genes (bla , bla , bla OXA-48 ,

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confidence: 62%

Identification of bla _OXA-51-like , bla _OXA-58 , bla _DIM-1 , and bla _VIM Carbapenemase Genes in Hospital Enterobacteriaceae Isolates from Sierra Leone

et al. 2013

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“…VIM-2-producing P. aeruginosa isolates have been observed in Tunisia (6)(7)(8), Kenya (9), the Ivory Coast (10), Algeria (11), and South Africa (12). Further, reports have shown the import of P. aeruginosa with VIM-2 from African countries (Ghana, Tunisia, and Egypt) into Europe (13)(14)(15).…”

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confidence: 99%

Identification of VIM-2-Producing Pseudomonas aeruginosa from Tanzania Is Associated with Sequence Types 244 and 640 and the Location of bla _VIM-2 in a TniC Integron

Moyo

Haldorsen

Aboud

et al. 2015

Antimicrob Agents Chemother

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e Epidemiological data on carbapenemase-producing Gram-negative bacteria on the African continent are limited. Here, we report the identification of VIM-2-producing Pseudomonas aeruginosa isolates in Tanzania. Eight out of 90 clinical isolates of P. aeruginosa from a tertiary care hospital in Dar es Salaam were shown to harbor bla VIM-2 . The bla VIM-2 -positive isolates belonged to two different sequence types (ST), ST244 and ST640, with bla VIM-2 located in an unusual integron structure lacking the 3= conserved region of qac⌬E1-sul1. Pseudomonas aeruginosa is an opportunistic pathogen associated with a number of nosocomial infections. Carbapenems (i.e., meropenem and imipenem) are often the treatment of choice for infections caused by P. aeruginosa that is resistant to other antipseudomonal ␤-lactams (1). However, the emergence and spread of acquired carbapenemases, particularly metallo-␤-lactamases (MBLs), among P. aeruginosa are threatening the usefulness of carbapenems (2). Resistance to carbapenems in P. aeruginosa can also occur due to impermeability, efflux mechanisms, and other ␤-lactamases, including overexpression of the chromosomal AmpC (3).Several acquired MBLs have been identified in P. aeruginosa, including the VIM, IMP, SPM, GIM, AIM, FIM, and NDM enzymes (2, 4). The genes encoding these MBLs are associated with mobile genetic elements, such as insertion sequence common region (ISCR) elements, transposons, and plasmids, and as gene cassettes in integron structures. The dissemination of the various MBLs among P. aeruginosa isolates has been shown to occur in many different genetic backgrounds (5). However, two major clonal complexes (CC), CC235 and CC111, predominate, particularly with respect to the dissemination of VIM enzymes (5).On the African continent, an increasing number of reports indicates that MBL-producing, and in particular VIM-2-producing, P. aeruginosa is widespread in Africa. VIM-2-producing P. aeruginosa isolates have been observed in Tunisia (6-8), Kenya (9), the Ivory Coast (10), Algeria (11), and South Africa (12). Further, reports have shown the import of P. aeruginosa with VIM-2 from African countries (Ghana, Tunisia, and Egypt) into Europe (13-15).(Part of this study was presented at the 22nd European Congress of Microbiology and Infectious Diseases, 31 March to 3 April 2012, London, United Kingdom.)The aim of this study was to determine the occurrence and molecular epidemiology of MBL-producing P. aeruginosa isolates identified from clinical specimens at a tertiary hospital in Dar es Salaam, Tanzania. This was a cross-sectional study conducted at the Central Pathology Laboratory, Muhimbili National Hospital (MNH), Dar es Salaam, Tanzania. MNH is the largest tertiary health care facility in Tanzania and serves as a university teaching and referral hospital to the population of Dar es Salaam and the whole country. The study included 90 clinical isolates of P. aeruginosa consecutively collected from May 2010 to July 2011. Duplicate isolates were excluded from the study. Only i...

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“…For instance, The CAPITAL surveillance program tested the susceptibility of 2,722 P. aeruginosa isolates, which revealed that the rates of resistance to imipenem, meropenem, and ceftazidime were 21.9, 15.4, and 15.2%, respectively (10). MLST (multilocus sequence typing) is an unambiguous molecular typing method that is used mostly to assess local outbreaks of infections (11)(12)(13). Study of population genetic backgrounds is also an application for MLST.…”

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Multilocus Sequence Typing Reveals Genetic Diversity of Carbapenem- or Ceftazidime-Nonsusceptible Pseudomonas aeruginosa in China

Wang

Zhou

et al. 2013

Antimicrob Agents Chemother

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It is unclear whether the genetic background of drug-resistant Pseudomonas aeruginosa was disseminated from a certain clone. Thus, we performed MLST (multilocus sequence typing) of 896 P. aeruginosa isolates that were nonsusceptible to imipenem, meropenem, or ceftazidime. This revealed 254 sequence types (STs), including 104 new STs and 34 STs with novel alleles. Thirtythree clonal complexes and 404 singletons were found. In conclusion, drug-resistant P. aeruginosa clones can be developed from diverse genetic backgrounds. Pseudomonas aeruginosa is one of the most common opportunistic pathogens and can cause severe diseases in humans, especially patients in intensive care units, burn centers, and cystic fibrosis centers (1-4). Infections caused by P. aeruginosa are often difficult to treat and are a great challenge to physicians and patients, raising morbidity and mortality rates (5, 6). Previous studies have revealed that the number of drug-resistant P. aeruginosa strains is increasing and the rate of resistance to carbapenems goes up every year (7-9). For instance, The CAPITAL surveillance program tested the susceptibility of 2,722 P. aeruginosa isolates, which revealed that the rates of resistance to imipenem, meropenem, and ceftazidime were 21.9, 15.4, and 15.2%, respectively (10). MLST (multilocus sequence typing) is an unambiguous molecular typing method that is used mostly to assess local outbreaks of infections (11-13). Study of population genetic backgrounds is also an application for MLST. For example, previous studies have indicated that the P. aeruginosa population structure is nonclonal (14-17). Specifically, Kidd et al. collected 501 P. aeruginosa isolates from an extensive region and various sources and identified 274 different sequence types (STs) that were confirmed as nonclonal (18). Some studies have focused on different geographic areas, but the samples used were of limited size or from the environment (16,18). A large-scale epidemiological study of drug-resistant P. aeruginosa based on MLST has not been conducted in China. This study was conducted in order to investigate the drug resistance of P. aeruginosa in China and its genetic background based on MLST.A total of 2,818 P. aeruginosa isolates were collected in 2010 from 65 hospitals in 22 regions of China. Susceptibilities to 16 antimicrobial agents were evaluated by the disk diffusion method. The results were interpreted according to the 2012 Clinical and Laboratory Standards Institute (CLSI) guidelines (19), and P. aeruginosa ATCC 27853 was used as the control. The results showed that carbapenems (imipenem and meropenem), cephalosporins (cefepime and ceftazidime), penicillins (piperacillin and tazobactam-piperacillin), quinolones (ciprofloxacin), and aminoglycosides (amikacin and gentamicin) were more active than other drugs, with susceptibility rates ranging from 71.2 to 85.2%. The rates of isolate resistance to imipenem, meropenem, and ceftazidime were 23.1, 18.1, and 15.3%, respectively. Cefoperazone, sulbactam-cefoperazone, and aztre...

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VIM-2 metallo- -lactamase-producing Pseudomonas aeruginosa causing an outbreak in South Africa

Cited by 35 publications

References 5 publications

Identification of bla _OXA-51-like , bla _OXA-58 , bla _DIM-1 , and bla _VIM Carbapenemase Genes in Hospital Enterobacteriaceae Isolates from Sierra Leone

Identification of bla _OXA-51-like , bla _OXA-58 , bla _DIM-1 , and bla _VIM Carbapenemase Genes in Hospital Enterobacteriaceae Isolates from Sierra Leone

Identification of VIM-2-Producing Pseudomonas aeruginosa from Tanzania Is Associated with Sequence Types 244 and 640 and the Location of bla _VIM-2 in a TniC Integron

Multilocus Sequence Typing Reveals Genetic Diversity of Carbapenem- or Ceftazidime-Nonsusceptible Pseudomonas aeruginosa in China

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VIM-2 metallo- -lactamase-producing Pseudomonas aeruginosa causing an outbreak in South Africa

Cited by 35 publications

References 5 publications

Identification of bla OXA-51-like , bla OXA-58 , bla DIM-1 , and bla VIM Carbapenemase Genes in Hospital Enterobacteriaceae Isolates from Sierra Leone

Identification of bla OXA-51-like , bla OXA-58 , bla DIM-1 , and bla VIM Carbapenemase Genes in Hospital Enterobacteriaceae Isolates from Sierra Leone

Identification of VIM-2-Producing Pseudomonas aeruginosa from Tanzania Is Associated with Sequence Types 244 and 640 and the Location of bla VIM-2 in a TniC Integron

Multilocus Sequence Typing Reveals Genetic Diversity of Carbapenem- or Ceftazidime-Nonsusceptible Pseudomonas aeruginosa in China

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Identification of bla _OXA-51-like , bla _OXA-58 , bla _DIM-1 , and bla _VIM Carbapenemase Genes in Hospital Enterobacteriaceae Isolates from Sierra Leone

Identification of bla _OXA-51-like , bla _OXA-58 , bla _DIM-1 , and bla _VIM Carbapenemase Genes in Hospital Enterobacteriaceae Isolates from Sierra Leone

Identification of VIM-2-Producing Pseudomonas aeruginosa from Tanzania Is Associated with Sequence Types 244 and 640 and the Location of bla _VIM-2 in a TniC Integron