Furthermore, genomic sequences indicated the isolates from Western Australia were within the same United Kingdom–South America cluster as isolates from the eastern coast of Australia ( 13).įigure 1. All isolates had the same PorA:FetA profile (P1.5,2:F1–1) as that identified in the MenW:cc11 collection responsible for outbreaks in South America and the United Kingdom ( 8).
Raw reads were assembled, auto-tagged, and curated by using the BIGSdb genomics platform on the PubMLST website ( ) ( 12). We further characterized isolates by using whole-genome sequencing with the Miseq Platform (Illumina, San Diego, CA, USA). All isolates less susceptible to or resistant to penicillin were identified in 2016. All isolates were susceptible to ciprofloxacin (MIC 0.5 mg/L). MIC results were interpreted according to Clinical Laboratory Standard Institute ( ) breakpoints. We performed drug susceptibility testing by using the Etest (bioMérieux, Marcy l’Etoile, France). The 19 MenW:cc11 strains isolated during January 1, 2013–December 31, 2016, were assessed for susceptibility to penicillin, ciprofloxacin, ceftriaxone, and rifampin. Three deaths were caused by MenW:cc11 infection, 1 in 2015 and 2 in 2016. Since that time, an additional 18 MenW:cc11 laboratory-confirmed cases have been reported, representing 11% (n = 2) of all IMD cases in 2014, 27% (n = 3) in 2015, and 67% (n = 13) in 2016, a significant increase from 2014 through 2016 (p = 0.0004, by Fisher exact test). The first laboratory-confirmed MenW:cc11 case in Western Australia was recorded in April 2013 and was the only MenW case for that year. In concordance with the national trend, there has been a shift in the predominant serogroup in Western Australia MenW was responsible for most IMD cases in 2016. However, it has a population of only 2.5 million persons. Western Australia is the largest state in Australia (land area 1.02 million square miles). We report recent emergence and clonal expansion of a phylogenetically related cluster of penicillin-resistant MenW:cc11 isolates in Western Australia. The mechanism of relative resistance in these isolates involves expression of altered forms of 1 of 4 penicillin-binding proteins (PBPs) that are involved in peptidoglycan biosynthesis during bacterial growth and cell division ( 10).Īlthough treatment with penicillin is still effective against these penicillin-intermediate strains, low-dose treatment regimens may fail for cases involving penicillin-resistant isolates (MIC >0.5 mg/L) ( 11).
Conversely, isolates conferring intermediate resistance to penicillin (MIC 0.12-0.25 mg/L) are uncommon but the frequency of these isolates varies geographically. For meningococci, a penicillin MIC >2 mg/L is caused by plasmid-mediated β-lactamase-production but is extremely rare ( 9). Although extensive core-genome analyses of these MenW:cc11 strains have been reported ( 7, 8), antimicrobial drug susceptibility of these clinical isolates has not been generally reported.Īlthough penicillin has been used for control of IMD, clinical isolates relatively resistant to this drug have been reported worldwide. meningitidis strains in the cc11 lineage (MenW:cc11) ( 5, 6), which have also been reported worldwide. However, during 2016, the prevalence of serogroup W disease increased because of N. In Australia, after introduction of serogroup C conjugate vaccine in the national immunization program in 2003, incidence of serogroup C has decreased serogroup B predominated during 2004–2015. Serogroups B, C, and Y continue to predominate in the United States, Europe, Asia, and Australia ( 3, 4). Until recently, serogroup A was the major cause of disease in Africa ( 2). IMD is most commonly caused by isolates expressing a serogroup A, B, C, W, X, or Y polysaccharide capsule. Similar STs are grouped into the same clonal complex (cc). Meningococcal strains can be classified into 12 serogroups phenotypically and into sequence types (STs) by multilocus sequence typing ( 1). The main manifestations of this disease are septicemia or meningitis. Invasive meningococcal disease (IMD) is caused by a meningococcus, Neisseria meningitidis.