Background:Hypervirulent Klebsiella pneumoniae (hvKp) can cause invasive community-acquired infections in healthy adults. HvKp is usually susceptible to most antibiotics; however, multi-drug resistance, including to carbapenems, is emerging. This is especially concerning due to the combination of disease severity and antibiotic resistance. Recent reports of the ST23 lineage of hvKp has raised alarms globally, making reporting of these cases significant. Methods:Carbapenemase-producing K. pneumoniae (CP-Kp) in Alberta, Canada were screened for the presence of hypervirulence genes associated with the hypervirulent phenotype. A hypermucoviscous string test was performed on all isolates, and genomes were sequenced using both Illumina NextSeq and Oxford Nanopore Technologies platforms. The presence of hypervirulence-associated genes (ybt, clb, iuc, iro, rmpA/A2) in the assembled genomes was determined. Results:Eight different sequence types (ST) were observed among the 16 cases identified, including several global high-risk lineages (ST11, ST15, ST231, ST147, and ST395) and one hypervirulent lineage (ST23). Carbapenemase genes included bla NDM-1 (n = 1), bla OXA-48-type (n = 7), or both bla NDM + bla OXA-48-type (n = 8). The ST23 isolate harboured ybt and clb on the chromosome, iro and iuc on a 229.9 kb IncFIB,IncHI1B virulence plasmid, and bla OXA-48 on a 92.3 kb IncFIA,IncFII plasmid. Almost half of the isolates co-harboured virulence genes and a carbapenemase (bla NDM-1, n = 4 or bla NDM-5, n = 3) on the same plasmid, creating hybrid plasmids. Phenotypically, however, 81% of isolates (n = 13) were string test-negative. Conclusion:These data highlights the presence of high-risk lineages of hvKp in the Canadian landscape, as well as the first report of ST23 in Canada.

Obesity, and the associated metabolic syndrome, is a risk factor for increased disease severity with a variety of infectious agents, including influenza virus. Yet, the mechanisms are only partially understood. As the number of people, particularly children, living with obesity continues to rise, it is critical to understand the role of host status on disease pathogenesis. In these studies, we use a diet-induced obese ferret model and tools to demonstrate that, like humans, obesity resulted in notable changes to the lung microenvironment, leading to increased clinical disease and viral spread to the lower respiratory tract. The decreased antiviral responses also resulted in obese animals shedding higher infectious virus for a longer period, making them more likely to transmit to contacts. These data suggest that the obese ferret model may be crucial to understanding obesity’s impact on influenza disease severity and community transmission and a key tool for therapeutic and intervention development for this high-risk population.

This study investigated the mechanism of carbapenem resistance in an Enterobacter cloacae complex positive by the modified carbapenem inactivation method (mCIM) but negative by the Rosco Neo-Rapid Carb Kit, β CARBA, and conventional PCR for common carbapenemase genes (KPC, NDM, OXA-48, IMP, VIM, GES, and IMI/NMC). Using whole genome sequencing (WGS) data we confirmed the identification of Enterobacter asburiae (ST1639) and the presence of blaFRI-8 located on a 148kb IncFII(Yp) plasmid. This is the first occurrence of a clinical isolate harboring the FRI-8 carbapenemase and the second occurrence of FRI in Canada. This study highlights the need to use both WGS and phenotypic screening methods for detection of carbapenemase-producing strains if we consider the growing diversity of carbapenemases.

Infection prevention and control measures are used to contain outbreaks of carbapenemase-producing Enterobacteriaceae. We report the absence of transmission of Klebsiella pneumoniae carrying New Delhi metallo-β-lactamase and oxacillinase-48 genes among 19 screened contacts of an index case after 14 months of routine practices in a long-term care facility.

Although the respiratory tract is the primary site of SARS-CoV-2 infection and the ensuing immunopathology, respiratory immune responses are understudied and urgently needed to understand mechanisms underlying COVID-19 disease pathogenesis. We collected paired longitudinal blood and respiratory tract samples (endotracheal aspirate, sputum or pleural fluid) from hospitalized COVID-19 patients and non-COVID-19 controls. Cellular, humoral and cytokine responses were analysed and correlated with clinical data. SARS-CoV-2-specific IgM, IgG and IgA antibodies were detected using ELISA and multiplex assay in both the respiratory tract and blood of COVID-19 patients, although a higher receptor binding domain (RBD)-specific IgM and IgG seroconversion level was found in respiratory specimens. SARS-CoV-2 neutralization activity in respiratory samples was detected only when high levels of RBD-specific antibodies were present. Strikingly, cytokine/chemokine levels and profiles greatly differed between respiratory samples and plasma, indicating that inflammation needs to be assessed in respiratory specimens for the accurate assessment of SARS-CoV-2 immunopathology. Diverse immune cell subsets were detected in respiratory samples, albeit dominated by neutrophils. Importantly, we also showed that dexamethasone and/or remdesivir treatment did not affect humoral responses in blood of COVID-19 patients. Overall, our study unveils stark differences in innate and adaptive immune responses between respiratory samples and blood and provides important insights into effect of drug therapy on immune responses in COVID-19 patients.

In 2018 to 2019, PCR for carbapenemases in routine Gram-negative isolates submitted to the National Microbiology Laboratory revealed an increase in IMP-type metalloenzyme-positive isolates, mostly among Morganellaceae Whole-genome sequencing revealed that 23 Morganellaceae harbored blaIMP-27 within a chromosomal Tn7 element. Phylogenomics indicated diversity of isolates but also the presence of a few clonal isolates dispersed geographically. These isolates may be difficult to detect due to carbapenem susceptibility and false-negative results in phenotypic testing.IMPORTANCE Over the last decade or so, the frequency of isolation of clinical carbapenemase-producing organisms (CPOs) has increased among health care-associated infections. This may seriously compromise antimicrobial therapy, as carbapenems are considered the last line of defense against these organisms. The ability of carbapenemases to hydrolyze most β-lactams in addition to the co-occurrence of mechanisms of resistance to other classes of antimicrobials in CPOs can leave few options for treating infections. The class B metalloenzymes are globally distributed carbapenemases, and the most commonly found include the NDM, VIM, and IMP types. Our study describes a sudden emergence of IMP-27-harboring Morganellaceae during 2018 to 2019 in Canada. There is a paucity of literature on IMP-27 isolates, and our data bolster the information on the genetic context, antimicrobial profiles, and phylogenomics of this group of CPOs.

In the context of a recent rise in prevalence of NDM-encoding carbapenemase-producing Enterobacterales (CPE) in the province of QC, Canada, the genetic environment of blaNDM- 1 was investigated. Three NDM-producing clinical isolates of Enterobacter hormaechei recovered from hospitalized patients involved in a putative outbreak were further characterized by whole-genome sequencing (WGS). Two isolates were confirmed by pulsed-field gel electrophoresis and WGS to be closely related. In addition to a similar to 128 kb IncFII conjugative multidrug-resistance (MDR) plasmid, these isolates possessed a similar to 45 kb mobilizable IncR MDR plasmid containing 2 MDR regions: a complex class 1 integron harboring blaNDM- 1 and 7 other AMR genes, and the IS26-mph(A)-mrx-mphR(A)-IS6100 azithromycin resistance unit. The predicted antimicrobial resistance (AMR) genes correlated with the antimicrobial susceptibility testing results. The multidrug-resistant phenotype in addition to the presence of two important mobile genetic elements, suggest a potent role as a reservoir of antibiotic resistance for such a small IncR plasmid. IMPORTANCE Analyzing the genetic environment of clinically relevant MDR genes can provide information on the way in which such genes are maintained and disseminated. Understanding this phenomenon is of interest for clinicians as it can also provide insight on where these genes might have been sourced, possibly supporting outbreak investigations.

Background: Carbapenemase-producing Enterobacterales (CPE) have rapidly become a global health concern and are associated with substantial morbidity and mortality due to limited treatment options. Travel to endemic areas, especially healthcare exposure in these areas, is an important risk factor for acquisition. We describe the evolving epidemiology, molecular features, and outcomes of CPE in Canada through surveillance by the Canadian Nosocomial Infection Surveillance Program (CNISP). Methods: CNISP has conducted surveillance for CPE among inpatients and outpatients of all ages since 2010. Participating acute-care facilities submit eligible specimens to the National Microbiology Laboratory for detection of carbapenemase production, and epidemiological data are collected. Incidence rates per 10,000 patient days are calculated based on inpatient data. Results: In total, 59 CNISP hospitals in 10 Canadian provinces representing 21,789 beds and 6,785,013 patient days participated in this surveillance. From 2010 to 2018, 118 (26%) CPE-infected and 547 (74%) CPE-colonized patients were identified. Few pediatric cases were identified (n = 18). Infection incidence rates remain low and stable (0.02 per 10,000 patient days in 2010 to 0.03 per 10,000 patient days in 2018), and colonization incidence rates have increased by 89% over the surveillance period. Overall, 92% of cases were acquired in a healthcare facility: 61% (n = 278) in a Canadian healthcare facility and 31% (n = 142) in a healthcare facility outside Canada. Of the 8% of cases not acquired in a healthcare facility, 50% (16 of 32) reported travel outside of Canada in the 12 months prior to positive culture. The distribution of carbapenemases varied by region; New Delhi metallo-B-lactamase (NDM) was dominant (59%) in western Canada and Klebsiella pneumoniae carbapenemase (KPC) (66%) in central Canada. NDM and class D carbapenemase OXA-48 were more commonly identified among those who traveled outside of Canada, whereas KPC was more commonly identified among patients without travel. In addition, 30-day all-cause mortality was 14% (25 of 181) among CPE infected patients and 32% (14 of 44) among those with bacteremia. Conclusions: CPE rates remain low in Canada; however, national surveillance data suggest that the increase in CPE in Canada is now being driven by local nosocomial transmission as well as travel and healthcare within endemic areas. Changes in screening practices may have contributed to the increase in colonizations; however, these data are currently lacking and will be collected moving forward. These data highlight the need to intensify surveillance and coordinate infection control measures to prevent further spread of CPE in Canadian acute-care hospitals.Funding: NoneDisclosures: Susy Hota reports contracted research for Finch Therapeutics. Allison McGeer reports funds to her institution for projects for which she is the principal investigator from Pfizer and Merck, as well as consulting fees from the following companies: Sanofi-Pasteur, Sunovion, GSK, Pfizer, and Cidara.

Abstract Background The hospital water environment is a CPE reservoir, and transmission of CPE from drains to patients is a risk. Methods We cultured sink and shower drains in patient rooms and communal shower rooms that were exposed to inpatients with CPE colonization/infection from October 2007 to December 2017 at 10 hospitals. We compared patient room drain CPE to prior room occupant CPE using Illumina and MinION whole-genome sequencing. Results Three-hundred and ten inpatients exposed 1,209 drains, of which 53 (4%) yielded 62 CPE isolates at 7 (70%) hospitals. Compared to room occupant CPE isolates, drain CPE isolates were more likely Enterobacter spp. (6, 10% vs. 25, 51%, p< 0.0001) or KPC-producers (9, 15% vs. 23, 47%, p=0.0002). Of the 49 CPE isolates in patient room drains, 4 (8%) were linked to a prior room occupant (Table), 24 (49%) had the same carbapenemase as a prior room occupant but isolates/carbapenemase gene-containing plasmids that were unrelated, and 21 (43%) did not share a carbapenemase with a prior room occupant. The 4 drains linked to prior room occupants were likely contaminated by these room occupants, who were CPE-colonized prior to drain exposure. Despite few links between drain and room occupant CPE, there were 10 isolates harbouring related blaNDM-1-containing IncHI2A/HI2-type plasmids in 8 rooms on two units at one hospital. Nine of these were Enterobacter hormaechei ST66 isolates that were 0 to 6 SNVs apart and one was a Klebsiella oxytoca STnovel isolate. Table. Four patient room drain CPE isolates (D1b, D4, D5, D12) and isolates from prior room occupants that they were related to by whole-genome sequencing. Conclusion It was uncommon for drain CPE to be linked to prior patient exposure. This suggests contamination of most drains by undetected colonized patients and a need for more aggressive patient screening in our hospitals. This may also suggest retrograde (drain-to-drain) transmission, especially considering the 10 isolate drain cluster at one hospital. Reasons for the preponderance of Enterobacter spp. in drains requires further study. Disclosures Allison McGeer, MD, FRCPC, GlaxoSmithKline (Advisor or Review Panel member, Research Grant or Support)Merck (Advisor or Review Panel member, Research Grant or Support)Pfizer (Research Grant or Support)

Background. Data on household transmission of carbapenemase-producing Enterobacterales (CPE) remain limited. We studied risk of CPE household co-colonization and transmission in Ontario, Canada. Methods. We enrolled CPE index cases (identified via population-based surveillance from January 2015 to October 2018) and their household contacts. At months 0, 3, 6, 9, and 12, participants provided rectal and groin swabs. Swabs were cultured for CPE until September 2017, when direct polymerase chain reaction (PCR; with culture of specimens if a carbapenemase gene was detected) replaced culture. CPE risk factor data were collected by interview and combined with isolate whole-genome sequencing to determine likelihood of household transmission. Risk factors for household contact colonization were explored using a multivariable logistic regression model with generalized estimating equations. Results. Ninety-five households with 177 household contacts participated. Sixteen (9%) household contacts in 16 (17%) households were CPE-colonized. Household transmission was confirmed in 3/177 (2%) cases, probable in 2/177 (1%), possible in 9/177 (5%), and unlikely in 2/177 (1%). Household contacts were more likely to be colonized if they were the index case's spouse (odds ratio [OR], 6.17; 95% confidence interval [CI], 1.05-36.35), if their index case remained CPE-colonized at household enrollment (OR, 7.00; 95% CI, 1.92-25.49), or if they had at least 1 set of specimens processed after direct PCR was introduced (OR, 6.46; 95% CI, 1.52-27.40). Conclusions. Nine percent of household contacts were CPE-colonized; 3% were a result of household transmission. Hospitals may consider admission screening for patients known to have CPE-colonized household contacts.

BackgroundHospital drains may be an important reservoir for carbapenemase-producing Enterobacterales (CPE).AimTo determine prevalence of CPE in hospital drains exposed to inpatients with CPE, relatedness of drain and patient CPE, and risk factors for drain contamination.MethodsSink and shower drains in patient rooms and communal shower rooms exposed to 310 inpatients with CPE colonization/infection were cultured at 10 hospitals. Using short- and long-read whole-genome sequencing, inpatient and corresponding drain CPE were compared. Risk factors for drain contamination were assessed using multi-level modelling.FindingsOf 1209 exposed patient room and communal shower room drains, 53 (4%) yielded 62 CPE isolates in seven (70%) hospitals. Of 49 CPE isolates in patient room drains, four (8%) were linked to prior room occupants. Linked drain/room occupant pairs included Citrobacter freundii ST18 isolates separated by eight single nucleotide variants (SNVs), related blaKPC-containing IncN3-type plasmids (different species), related blaKPC-3-containing IncN-type plasmids (different species), and related blaOXA-48-containing IncL/M-type plasmids (different species). In one hospital, drain isolates from eight rooms on two units were Enterobacter hormaechei separated by 0–6 SNVs. Shower drains were more likely to be CPE-contaminated than hand hygiene (odds ratio: 3.45; 95% confidence interval: 1.66–7.16) or patient-use (13.0; 4.29–39.1) sink drains. Hand hygiene sink drains were more likely to be CPE-contaminated than patient-use sink drains (3.75; 1.17–12.0).ConclusionDrain contamination was uncommon but widely dispersed. Drain CPE unrelated to patient exposure suggests contamination by undetected colonized patients or retrograde (drain-to-drain) contamination. Drain types had different contamination risks.

PurposeAntimicrobial resistance (AMR), especially multidrug resistance, is one of the most serious global threats facing public health. The authors proof‐of‐concept study assessing the suitability of shotgun proteomics as an additional approach to whole‐genome sequencing (WGS) for detecting AMR determinants.Experimental DesignPreviously published shotgun proteomics and WGS data on four isolates of Campylobacter jejuni are used to perform AMR detection by searching the Comprehensive Antibiotic Resistance Database, and their detection ability relative to genomics screening and traditional phenotypic testing measured by minimum inhibitory concentration is assessed.ResultsBoth genomic and proteomic approaches identify the wild‐type and variant molecular determinants responsible for resistance to tetracycline and ciprofloxacin, in agreement with phenotypic testing. In contrast, the genomic method identifies the presence of the β‐lactamase gene, blaOXA‐61, in three isolates. However, its corresponding protein product is detected in only a single isolate, consistent with results obtained from phenotypic testing.

Objectives: To investigate a persistent multispecies OXA-204 outbreak occurring simultaneously in multiple distant hospitals in the province of Quebec, Canada. Methods: OXA-204 carbapenemase-producing Enterobacterales (CPE) isolated from multiple hospitals between January 2016 and October 2018 were included in the study. An epidemiological inquiry was conducted in order to elucidate possible transmission routes and a putative source. Isolates were characterized by standardized antibiotic susceptibility testing and by WGS, using Illumina short-read data and MinION long-read data. Results: The outbreak comprised 65 patients and 82 isolates from four hospital sites. Most patients were >= 65years old, had multiple comorbidities and had received antibiotics recently. The infection to colonization ratio was 1:20. No persistent environmental reservoir was identified. The most frequent organism was Citrobacter freundii (n=78), followed by Klebsiella spp. (n=3) and Escherichia coli (n=1). WGS analysis showed 77/78 C. freundii isolates differing by 0-26 single nucleotide variants (SNVs). Results of WGS analysis showed bla(OXA-204) was present on three plasmids types (IncX1, IncA/C-2 and IncFII/FIB/A/C-2) and on a prophage. All C. freundii isolates harboured multiple copies of bla(OXA-204), both on the chromosome and a plasmid. Plasmid IncFII/FIB/A/C-2 was observed in all three species. Conclusions: Transfer of OXA-204 plasmids likely occurred between species within the same patient, highlighting the plasticity of these plasmids and potential for widespread dissemination. OXA-204 carbapenemase has been introduced into Quebec and has rapidly disseminated. Although the infection to colonization ratio was low in this outbreak, this carbapenemase has been associated with severe infection elsewhere.

Among 162 isolates of extended-spectrum beta-lactamase-(ESBL)-producing Escherichia coli recovered from the urine of Canadian patients (2007-2017), five (3.1%) were not susceptible in vitro to fosfomycin (MIC >= 128 mu g/mL). These isolates underwent whole genome sequencing to assess for the presence of fos genes. The fosA3 gene was detected in one isolate. (C) 2019 Elsevier Inc. All rights reserved.

Abstract Background Hospital wastewater environments are recognized as reservoirs for multi-drug-resistant bacteria, and sink drains in ICUs have been implicated in numerous outbreaks. The mechanism of pathogen transmission to patients, and the best approach to risk mitigation remains unclear. We tested a new copper alloy sink drain for its effect on detection of gammaproteobacteria in sink drains and adjacent aerosols. Methods We randomized 90 sinks in 76 ICU rooms/bedspaces in 7 ICUs to new standard chrome or copper alloy drains. We sampled sinks on 4 occasions over 4 months. Drain tailpieces were sampled using cotton swabs of 140 cm2 of the interior surface, inserted into 1mL of Dey-Engley neutralizing broth, and cultured semi-quantitatively for gammaproteobacteria on Mac3CV. 850L samples of air adjacent to sinks were obtained by impaction onto Mac3CV. Faucet swabs were also cultured. Multivariable analysis adjusting for factors associated with growth in air and drains used conditional logistic regression, GEE with an exchangeable correlation matrix, a robust estimate of variance, negative binomial distribution and log link function. Results Gammaproteobacteria were detected in 247/424 (58%) tailpiece swabs, 137/456 (30%) air samples, and 31/456 (7%) faucet swabs. In multivariable analysis, growth was less likely from air adjacent to sinks with copper vs. chrome drains [IRR 0.50 (95% CI 0.35, 0.73), P < 0.0001], with reduced effect size observed when drain growth was included in the model [IRR 0.64 (95% CI 0.43, 0.94)], P = 0.025]. Growth in air was more likely when drain growth was 1–899 cfu/cm2 [IRR 2.38 (95% CI 1.46, 3.88), P = 0.001] or ≥900 cfu/cm2 [IRR 3.55 (95% CI 1.87, 6.86), P < 0.001] vs. no growth. Tailpiece swab growth was more likely if rooms were occupied compared with empty [IRR 1.85 (95% CI 1.25, 2.76), P = 0.002], and less likely from copper drains compared with swabs from chrome drains [IRR 0.51 (95% CI 0.47, 0.75), P ≤ 0.001]. Conclusion Sinks with new copper drains are less likely to have detectable gammaproteobacteria in adjacent air when compared with standard chrome drains, and results suggest this is mediated through reduced bacterial growth in the drains. Ongoing study is needed to determine whether this influences patient risk for hospital-acquired infection. Disclosures All authors: No reported disclosures.

Abstract Background Hospital drains may be a source of CPE in patients. We determined prevalence of and risk factors for CPE contamination of hospital drains exposed to patients with CPE colonization/infection. Methods We cultured hand hygiene and patient use sink as well as tub/shower drains exposed to 310 inpatients colonized/infected with CPE in 10 Ontario hospitals. A multi-level logistic regression model was fitted to determine whether type of drain/room/unit was associated with CPE drain contamination. Drain and room occupant CPE isolates underwent Illumina whole-genome and MinION sequencing. Single nucleotide variant (SNV) phlogenomic analyses and plasmid characterization were performed. Results 53/ Of the 1,209 drains, 53 (4%) at 7 (70%) hospitals yielded CPE. Patient room shower drains were significantly more likely to yield CPE than hand hygiene sink (OR 3.35, 95% CI 1.61–6.97) and patient use sink (OR 10.89, 95% CI 3.62–32.80) drains. Hand hygiene sink drains were significantly more likely to yield CPE than patient use sink drains (OR 3.26, 95% CI 1.05–10.13). 8 (15%) drain isolates matched the room occupant CPE gene/species; 24 (44%) matched the gene but not species, and 23 (42%) matched neither gene nor species. Among 13 drain/11 room occupant pairs with molecular comparisons to date, only 1/13 (8%) drain isolates matched the respective room occupant carbapenemase allele and replicon harboring the carbapenemase gene (IncN replicon harboring blaKPC-3). In addition, one drain isolate had a plasmid highly related to plasmids of 2 isolates from a patient occupying a room in an adjacent unit (IncN3 replicons harboring blaKPC-2). At another hospital, all 6 drain isolates were located on one unit and had an IncHI2A/HI2/TrfA replicon harboring blaNDM-1; 5 of these were E. cloacae ST66, with 0–3 SNV differences observed between isolates. Conclusion Different drain types have different risks of CPE contamination. In our setting, most drain contamination was not caused by recognized room occupants. Further investigation is needed to understand the sources of hospital drain CPE contamination. Disclosures All authors: No reported disclosures.

Objectives: Globally there is an increased prevalence of carbapenem-resistant Acinetobacter spp, (CRAs) and carbapenemase-producing Acinetobacter spp. (CPAs) in the hospital setting. This increase prompted the Canadian Nosocomial Infection Surveillance Program (CNISP) to conduct surveillance of CRA colonizations and infections identified from patients in CNISP-participating hospitals between 2010 and 2016, Methods: Participating acute care facilities across Canada submitted CRAs from 1 January 2010 to 31 December 2016. Patient data were collected from medical records using a standardized questionnaire. WGS was conducted on all CRAs and data underwent single nucleotide variant analysis, resistance gene detection and MLST. Results: The 7 year incidence rate of CRA was 0.02 per 10 000 patient days and 0.015 per 1000 admissions, with no significant increase observed over the surveillance period (P>0.73). Ninety-four CRA isolates were collected from 58 hospitals, of which 93 (98.9%) were CPA. Carbapenemase OXA-235 group (48.4%) was the most common due to two separate clusters, followed by the OXA-23 group (41,9%), Patients with a travel history were associated with 38.8% of CRA cases. The all-cause 30 day mortality rate for infected cases was 24.4 per 100 CPA cases. Colistin was the most active antimicrobial agent (95.8% susceptibility). Conclusions: CRA remains uncommon in Canadian hospitals and the incidence did not increase from 2010 to 2016. Almost half of the cases were from two clusters harbouring OXA-235-group enzymes. Previous medical treatment during travel outside of Canada was common.

This report describes two hypervirulent Klebsiella pneumoniae isolates that produced K. pneumoniae carbapenemase (KPC), which were identified from a rectal swab and a urine culture upon hospital admission. The patient had recently traveled to Greece, where he was hospitalized. The isolates were sequence type 86 and contained an IncHI1B IncFIBK hypervirulent plasmid and an IncFIIK plasmid harboring KPC.

OBJECTIVES To identify the β-lactamase responsible for the positive detection of carbapenemase production in four clinical isolates of Pseudomonas aeruginosa that were negative by PCR for KPC, OXA-48, NDM, VIM, IMP, GES and NMC/IMI carbapenemase genes. METHODS WGS using short-read and long-read methods was used to characterize the isolates. Bioinformatic analysis was used to identify the potential gene encoding a carbapenemase. Cloning, antimicrobial susceptibility testing and biochemical and phenotypic characterization were used to determine metallo-enzyme activity. Single-nucleotide variant (SNV) typing was used to determine strain relatedness. Conjugation experiments were used to determine transmissibility of the novel carbapenemase-encoding gene. RESULTS WGS analysis revealed a novel class B β-lactamase gene, blaCAM-1 (Central Alberta Metallo-β-lactamase), located in a 73 kb integrative element, named IMEPaCAM-1, in the chromosome of four clinical isolates of P. aeruginosa. The cloned blaCAM-1 gene conferred carbapenem resistance to Escherichia coli TOP10. The four isolates, which were all closely related, were from three patients, all of whom spent time in the same hospital in 2008 and/or 2009. IMEPaCAM-1 could not be transferred by conjugation. CONCLUSIONS A novel metallo-enzyme, CAM-1, is encoded on an integrative element, IMEPaCAM-1, located in the chromosome of clinical isolates of P. aeruginosa. No additional isolates harbouring CAM-1 have been identified in Alberta since 2007.