Paul Southwell

There are few data describing the microbiology and genetic typing of Staphylococcus aureus that cause infections in developing countries. In this study we observed S. aureus infections in Pacific Island nation of Fiji in both the community and hospital setting with an emphasis on clonal complex (CC) genotyping and antimicrobial susceptibility. S. aureus was commonly found in impetigo lesions of school children and was recovered from 57% of impetigo lesions frequently in conjunction with group A streptococcal infection. Methicillin-resistant S. aureus (MRSA) comprised 7% (20/299) of isolates and were all non-multi-resistant and all genotyped as CC1. In contrast, there was a diverse selection of 17 CCs among the 105 genotyped methicillin-susceptible S.aureus (MSSA) strains. Isolates of the rare, phylogenetically divergent and non-pigmented CC75 lineage (also called S.argenteus) were found in Fiji. From hospitalized patients the available 36 MRSA isolates from a 9-month period were represented by five CCs. The most common CCs were CC1 and CC239. CC1 is likely to be a community-acquired strain, reflecting what was found in the school children, whereas the CC239 is the very successful multi-drug resistant MRSA nosocomial lineage. Of 17 MSSA isolates, 59% carried genes for Panton-Valentine leukocidin. The S. aureus bacteraemia incidence rate of 50 per 100,000 population is among the highest reported in the literature and likely reflects the high overall burden of staphylococcal infections in this population. S. aureus is an important cause of disease in Fiji and there is considerable genotypic diversity in community skin infections in Fijian schoolchildren. Community acquired- (CA)- MRSA is present at a relatively low prevalence (6.7%) and was solely to CC1 (CA-MRSA). The globally successful CC239 is also a significant pathogen in Fiji.

In 2010 there were 214 laboratory-confirmed cases of invasive meningococcal disease analysed by the National Neisseria Network, a nationwide network of reference laboratories. One hundred and twenty-four isolates of Neisseria meningitidis from invasive cases of meningococcal disease were available for which the phenotypes (serogroup, serotype and serosubtype) and/ or genotype and antibiotic susceptibility were determined. An additional 90 cases were confirmed by non-culture based methods (77 by nucleic acid amplification testing and 13 by serology), and where possible, serotyping was determined. Nationally 167 (78%) laboratory-confirmed cases, where a serogroup was determined, were infected with serogroup B, 16 (7.5%) with serogroup C, 9 (4.2%) with serogroup W135 and 7 (3.3%) with serogroupY meningococci. The national total of confirmed cases has decreased since 2004, but the number of cases may vary between jurisdictions each year. New South Wales had the highest number of recorded cases in 2010. Typical primary and secondary disease peaks were observed in those aged 4 years or less and in adolescents and young adults respectively. Serogroup B cases predominated in all age groups and jurisdictions. The common phenotype circulating in Australia continues to be B: 15: P1.7, corresponding to the porA genotype P1.7,16-26. Serogroup C cases were again numerically low, as were serogroups W135 and Y. Eighty per cent of all isolates showed decreased susceptibility to the penicillin group of antibiotics (minimal inhibitory concentration (MIC) 0.06-0.5 mg/L). All isolates remained susceptible to ceftriaxone. One isolate had reduced susceptibility to ciprofloxacin, and none to rifampicin.

In 2009 there were 233 laboratory-confirmed cases of invasive meningococcal disease (IMD) analysed by the National Neisseria Network, Australia, a nationwide network of reference laboratories. One hundred and thirty-five isolates of Neisseria meningitidis from invasive cases of meningococcal disease were available for which the phenotypes (serogroup, serotype and serosubtype) and/or genotype and antibiotic susceptibility were determined. An additional 98 cases were confirmed by non-culture-based methods (92 by nucleic acid amplification testing (NAAT) and six by serology), and where possible serotyping was determined. Nationally, 194 (83%) laboratory-confirmed cases where a serogroup was determined were infected with serogroup B and 13 (5.6%) serogroup C meningococci. The national total of confirmed cases has remained relatively stable since 2006, but the number of cases may vary between jurisdictions each year. New South Wales had the highest number of recorded cases in 2009. Typical primary and secondary disease peaks were observed in those aged 4 years or less and in adolescents and young adults respectively. Serogroup B cases predominated in all age groups and jurisdictions. The common phenotypes circulating in Australia continue to be B:15:P1.7 and B:4:P1.4. Although serogroup C cases were low, phenotype C:2a:P1.5 again predominated in this group. No evidence of meningococcal capsular 'switching' was detected. Approximately two-thirds of all isolates showed decreased susceptibility to the penicillin group of antibiotics (MIC 0.06 to 0.5 mg/L). All isolates remained susceptible to ceftriaxone. Four isolates had reduced susceptibility to ciprofloxacin, and none to rifampicin.

In 2008, there were 260 laboratory-confirmed cases of invasive meningococcal disease (IMD) analysed by the National Neisseria Network, a nationwide network of reference laboratories. One hundred and forty-nine isolates of Neisseria meningitidis from invasive cases of meningococcal disease were available for which the phenotypes (serogroup, serotype and serosubtype) and antibiotic susceptibility were determined. An additional 111 cases were confirmed by nonculture based methods. Nationally, 223 (85%) laboratory-confirmed cases where a serogroup was determined were infected with serogroup B and 17 (6.5%) infected with serogroup C meningococci. Nationally, the total number of confirmed cases has remained relatively stable since 2006, but the number of cases in each jurisdiction may vary from year to year. Queensland had the highest number of recorded cases in 2008. Typical primary and secondary disease peaks were observed in those aged 4 years or less and in adolescents and young adults respectively. Serogroup B cases predominated in all age groups and jurisdictions. The common phenotypes circulating in Australia were again B: 15: P1.7 and B: 4: P1.4. Although serogroup C cases were numerically low, phenotype C: 2a: P1.5 predominated in this group. No evidence of meningococcal capsular ` switching' was detected. About three-quarters of all isolates showed decreased susceptibility to the penicillin group of antibiotics (MIC 0.06-0.5 mg/L). All isolates remained susceptible to ceftriaxone. One isolate had reduced susceptibility to rifampicin and two to ciprofloxacin.