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We have identified a Salmonella enterica serotype 4,[5],12:i:- containing a mcr-3.2 in a patient who travelled to Thailand 1 month prior to the identification of it in Canada. The isolate was multidrug resistant, but remained susceptible to the carbapenems, amikacin and piperacillin/tazobactam. The mcr-3.2 was carried on a 261 Kb variant of the IncHI2 pWJ1. This report provides further evidence of the emergence of a ST34 colistin-resistant clone.

This study examined invasive Neisseria meningitidis recovered from invasive meningococcal disease (IMD) cases in Western Canada between 2009 and 2013. A total of 161 isolates from individual IMD cases were analysed for serogroup, serotype, serosubtype, PorA genotype, multi-locus sequence type and nucleotide sequence of their 4CMenB vaccine antigen genes. Sixty-nine isolates were serogroup B (MenB), 47 were serogroup Y (MenY), 22 were serogroup C (MenC), 19 were serogroup W (MenW), three were serogroup E and one was non-encapsulated. MenC, MenY and MenW were mainly clonal, represented primarily by clonal complex (cc) 11, cc23 or cc167, and cc22, respectively. In contrast, MenB were composed of eight different ccs together with 11 isolates not assigned to any known cc. Antigenic analysis and PorA genotyping confirmed the heterogeneity of MenB isolates, while such results supported the clonal nature of most MenC, MenY and MenW isolates. Thirty-four (21.1 %) isolates had at least one gene that encoded one matching vaccine protein component of the 4CMenB vaccine (i.e. PorA P1.4; fHbp variant 1.1; NHBA peptide 2; and NadA-1, -2, or -3). An additional 18 isolates had genes that encoded variant 1 or subfamily B factor H binding proteins of this same vaccine.

The objective of the current study was to determine whether the antimicrobial susceptibility profile or genotype of hospital-acquired isolates of Clostridium difficile differed from isolates causing community-acquired disease. Five hundred diarrhoeal stool samples (one >2 ml sample per patient) from patients across Manitoba, Canada, in 2006–2007 that were reported as C. difficile toxin positive were cultured, resulting in 432 isolates of toxin-positive C. difficile for analysis. Of these 432 isolates, acquisition status could be determined for 235 (54.4 %); 182 (77.4 %) isolates were hospital acquired and 53 (22.6 %) were community acquired. North American pulsotype (NAP) designations based on SmaI PFGE could be defined for 52.3 % of the 432 isolates, with NAP2 (n = 122) being the most common. Ninety-one per cent (71/78) of NAP2 isolates were recovered from patients with hospital-acquired C. difficile disease. Other NAP types and isolates with non-NAP-type PFGE patterns were less frequently associated with hospital-acquired disease. Community-acquired disease (35.3 % of isolates) was associated with a wide variety of NAP types. NAP2 isolates were homogeneous (85.5 % had SmaI PFGE pattern 0003) and demonstrated low susceptibility to moxifloxacin (6.6 %) and clindamycin (1.6 %) compared with non-NAP2 isolates (64.1–93.2 % moxifloxacin susceptible; 14.1–28.2 % clindamycin susceptible). All isolates of C. difficile in Manitoba were susceptible to metronidazole, piperacillin–tazobactam, amoxicillin–clavulanate and meropenem. NAP2 isolates of toxigenic C. difficile were approximately three times more common than NAP1 isolates (28.2 vs 9.1 %) in Manitoba in 2006–2007, and these isolates demonstrated high levels of clonality and multidrug resistance, and were associated with hospital acquisition.