Alainna Jamal , MD-PhD Candidate 1 , Brenda Coleman , PhD 2 , Jennie Johnstone , MD, FRCPC, PhD 2 , Kevin Katz , MD, MSc, FRCPC 3 , Matthew P Muller , MD, FRCPC, PhD 4 , Samir Patel , PhD, FCCM (D), ABMM 5 , Roberto Melano , MSc, PhD 6 , Anu Rebbapragada , PhD, D(ABMM), FCCM, CIC 7 , David Richardson , MD, FRCPC 8 , Alicia Sarabia , MD, FRCPC 9 , Samira Mubareka , MD, FRCPC 10 , Susan Poutanen , MD, MPH, FRCPC 2 , Zoe Zhong , PhD 2 , Philipp Kohler , MD, MSc 11 , Allison McGeer , MSc, MD, FRCPC, FSHEA 1
23 October 2019
Though CPE in Canada are mainly acquired abroad, outbreaks/transmission in Canadian hospitals have been reported. We determined the incidence of HA CPE in southern Ontario, Canada, to inform prevention and control programs.
Toronto Invasive Bacterial Diseases Network (TIBDN) has performed population-based surveillance for CPE in the Toronto area/Peel region of southern Ontario, Canada, since CPE were first identified in October 2007. Clinical microbiology laboratories report all CPE isolates to TIBDN; annual lab audits are performed. Incidence calculations used first isolates as numerator; denominator (patient-days/fiscal year for Toronto/Peel hospitals) was from the Ontario Ministry of Health and Long-Term Care.
The incidence of HA CPE has risen from 0 in 2007/2008 to 0.45 and 0.28 per 100,000 patient-days for all and clinical cases, respectively, in 2017/2018 (Figure, P < 0.0001). 190/790 (24%) incident cases of CPE colonization/infection in southern Ontario from October 2007 to December 2018 were likely HA (hospitalized in Ontario with no history of hospitalization abroad/high-risk travel). Eighty (25%) were female and the median age was 73 years (IQR 57–83 years). 157 (83%) had no prior travel abroad and 33 (17%) had prior low-risk travel. 122 (64%) had their CPE identified >72 hours post-admission (of which 83 also had ≥1 other prior Ontario hospitalization); 68 (36%) had their CPE identified at admission but had recent prior Ontario hospitalization. HA cases vs. foreign acquisitions were significantly more likely K. pneumoniae (48% vs. 38%, P = 0.02) and Enterobacter spp. (20% vs. 7%, P < 0.0001) and less likely E. coli (20% vs. 48%, P < 0.0001). Genes of HA vs. foreign acquisitions were significantly more likely bla KPC (34% vs. 12%, P < 0.0001) and bla VIM (12% vs. 2%, P < 0.0001) and less likely bla NDM±OXA (38% vs. 56%, P < 0.0001) and bla OXA (13% vs. 27%, P = 0.0001). 36 (19%) HA cases had a negative CPE screen before their first positive CPE test (10/36 (28%) were on admission). The median incidence of HA CPE per 100,000 patient-days at each hospital was 0.44 (IQR 0.15–0.68) ( P < 0.0001).
A quarter of CPE cases in southern Ontario were HA and the incidence of HA cases is increasing. Most cases were admitted to >1 Ontario hospital. Strategies to control transmission are critical.