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Shiga toxin-producing Escherichia coli (STEC) is a major cause of serious human gastrointestinal illness and has the potential to cause life-threatening complications, such as hemolytic uremic syndrome (HUS) (1). An [...]

Pharyngeal diphtheria caused by toxigenic Corynebacterium diphtheriae is well-controlled in Australia due to a vaccine administered as part of the national immunization program. Rare cases of cutaneous and pharyngeal diphtheria [...]

A new variant of Streptococcus pyogenes serotype M1 (designated 'M1UK') has been reported in the United Kingdom, linked with seasonal scarlet fever surges, marked increase in invasive infections, and exhibiting enhanced expression of the superantigen SpeA. The progenitor S. pyogenes 'M1global' and M1UK clones can be differentiated by 27 SNPs and 4 indels, yet the mechanism for speA upregulation is unknown. Here we investigate the previously unappreciated expansion of M1UK in Australia, now isolated from the majority of serious infections caused by serotype M1 S. pyogenes. M1UK sub-lineages circulating in Australia also contain a novel toxin repertoire associated with epidemic scarlet fever causing S. pyogenes in Asia. A single SNP in the 5' transcriptional leader sequence of the transfer-messenger RNA gene ssrA drives enhanced SpeA superantigen expression as a result of ssrA terminator read-through in the M1UK lineage. This represents a previously unappreciated mechanism of toxin expression and urges enhanced international surveillance. A variant of group A Streptococcus serotype M1 (UK) has been increasingly reported and can be differentiated from the global variant by its overexpression of the superantigen SpeA. Here, Davies et al probe the mechanism behind enhanced SpeA expression and demonstrate that a SNP in the 5' leader sequence of ssrA is responsible for this virulence phenotype. [ABSTRACT FROM AUTHOR]

We report the recent emergence of invasive meningococcal disease due to serogroup E in Queensland, Australia, in previously healthy patients. Molecular typing revealed the genotype of these strains to be E:P1.21-7,16:F5-36:ST-1157 (cc1157); when analyzed phylogenetically, compared with international cc1157 strains, they were relatively unrelated to each other. [ABSTRACT FROM AUTHOR]

Objectives: The objective of this study was to develop a real-time PCR assay targeting the gonococcal porB gene (PorB-PCR) for predicting susceptibility of Neisseria gonorrhoeae to penicillin. This complements a previously described PCR assay for detecting penicillinase-producing N. gonorrhoeae (PPNG) developed by our laboratory (PPNG-PCR).Methods: The PorB-PCR assay was designed using six probes to characterize various combinations of amino acids at positions 101 and 102 of the PorB1b class protein, including the WT G101/A102 and mutant G101K/A102D, G101K/A102N and G101K/A102G sequences, as well as the PorB1a sequence. The ability of these sequences to predict penicillin susceptibility was initially assessed using 2307 N. gonorrhoeae isolates from throughout Australia for which phenotypic susceptibility data were available. The assay was then applied to N. gonorrhoeae-positive clinical specimens (n = 70). Specificity was assessed by testing commensal Neisseria strains (n = 75) and N. gonorrhoeae-negative clinical specimens (n = 171).Results: Testing of the 2307 N. gonorrhoeae isolates using PorB-PCR to detect G101/A102 and PorB1a sequences identified a total of 78.4% (61.2% and 17.2%, respectively) of penicillin-susceptible isolates with specificities of 97.4% and 99.3% and positive predictive values of 98.8% and 98.9%, where PPNG strains were simultaneously identified and excluded. Similar performance data were obtained when the PorB-PCR assay was applied to the N. gonorrhoeae-positive clinical specimens. No false-positive results were observed for the N. gonorrhoeae-negative samples and no cross-reactions were observed with the non-gonococcal species.Conclusions: When used in parallel with the previously described PPNG-PCR, the PorB-PCR approach has the potential to facilitate individualized treatment of gonorrhoea using penicillin. [ABSTRACT FROM AUTHOR]

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The article analyzes the prevalence of invasive pneumococcal disease (IPD) among non-indigenous people before and after the provision of pneumococcal vaccines in north Queensland. Remarkable decline in average annual cases of IPD and serotype IPD was reported after the introduction of vaccines. A 91 percent reduction was observed in children aged 5 years and below while 62 percent for adults aged 15-64 years old. Newly created conjugate vaccines could help reduce more IPD cases in the country.

A recent analysis of group A Streptococcus (GAS) invasive infections in Australia has shown a predominance of M4 GAS, a serotype recently reported to lack the antiphagocytic hyaluronic acid (HA) capsule. Here, we use molecular genetics and bioinformatics techniques to characterize 17 clinical M4 isolates associated with invasive disease in children during this recent epidemiology. All M4 isolates lacked HA capsule, and whole genome sequence analysis of two isolates revealed the complete absence of the hasABC capsule biosynthesis operon. Conversely, M4isolates possess a functional HA-degrading hyaluronate lyase (HylA) enzyme that is rendered nonfunctional in other GAS through a point mutation. Transformation with a plasmid expressing hasABC restored partial encapsulation in wild-type (WT) M4 GAS, and full encapsulation in an isogenic M4 mutant lacking HylA. However, partial encapsulation reduced binding to human complement regulatory protein C4BP, did not enhance survival in whole human blood, and did not increase virulence of WT M4 GAS in a mouse model of systemic infection. Bioinformatics analysis found no hasABC homologs in closely related species, suggesting that this operon was a recent acquisition. These data showcase a mutually exclusive interaction of HA capsule and active HylA among strains of this leading human pathogen. [ABSTRACT FROM AUTHOR]

Escherichia coli O157 is a food-borne pathogen whose major reservoir has been identified as cattle. Recent genetic information has indicated that populations of E. coli O157 from cattle and humans can differ genetically and that this variation may have an impact on their ability to cause severe human disease. In addition, there is emerging evidence that E. coli O157 strains from different geographical regions may also be genetically divergent. To investigate the extent of this variation, we used Shiga toxin bacteriophage insertion sites (SBI), lineage-specific polymorphisms (LSPA-6), multilocus variable-number tandem-repeat analysis (MLVA), and a tir 255T > A polymorphism to examine 606 isolates representing both Australian and U.S. cattle and human pop ulations. Both uni- and multivariate analyses of these data show a strong association between the country of origin and multilocus genotypes (P < 0.0001). In addition, our results identify factors that may play a role in virulence that also differed in isolates from each country, including the carriage of sfce, in the argW locus uniquely observed in Australian isolates and the much higher frequency of sfcc2-positive (also referred to as stx2J strains in the U.S. isolates (4% of Australian isolates versus 72% of U.S. iso lates). LSPA-6 lineages differed between the two continents, with the majority of Australian isolates belonging to lineage I/II (LI/ II) (LI, 2%; LI/II, 85%; LII, 13%) and the majority of U.S. isolates belonging to LI (LI, 60%; LI/II, 16%; LII, 25%). The results of this study provide strong evidence of phylogeographic structuring of E. coli 0157 populations, suggesting divergent evolution of enterohemorrhagic E. coli 0157 in Australia and the United States. [ABSTRACT FROM AUTHOR]

Abstract: Molecular testing for stx1 and/or stx2 is a reliable way of detecting Shiga toxigenic Escherichia coli (STEC) when faecal specimens can be cultured; however, detection of Shiga toxin in unculturable specimens is also of public health importance. The Meridian Premier EHEC assay was evaluated against the gold standard Vero cell cytotoxic assay for Shiga toxin detection in direct faecal specimens. An initial study of 817 patient specimens submitted for routine STEC detection was conducted, evaluating positive faeces detected by the Meridian assay with the Vero cell assay. Twenty-nine percent of 136 Meridian-positive faeces were confirmed as containing Shiga toxin. A further 62 faecal specimens were evaluated for statistical purposes, with all specimens tested by both Meridian and Vero cell assays. On direct faeces, the Meridian assay gave high specificity (76.95%) but low sensitivity (40%). This study confirmed that testing by Meridian assay on cultures is preferential to testing direct faeces for Shiga toxin. [Copyright &y& Elsevier]

Background: Toxigenic Corynebacterium ulcerans is an emerging zoonosis globally, causing both cutaneous and respiratory diphtheria-like illness. In Queensland, human infection with toxigenic C. ulcerans is rare, with only three cases reported before October 2015. This case series describes five subsequent cases of toxigenic C. ulcerans in Queensland with links to companion animals., Methods: All data were collected as part of routine public health response, and strains were whole genome sequenced for further characterisation. Household contacts were screened, treated with appropriate antibiotics, and received a diphtheria toxoid-containing vaccine if more than five years had elapsed since their last dose., Findings: No epidemiological or genomic links could be established between any of the five patients, including between the two cases notified from the same locality within eight days of each other. The C. ulcerans strains from Cases Two, Four and Five were closely related to the strains isolated from their respective pets by whole genome sequencing. Domestic dogs were identified as the most likely mode of transmission for Cases One and Three; however, this was unable to be laboratory confirmed, since Case One's dog was treated with antibiotics before it could be tested, and Case Three's dog was euthanised and cremated prior to case notification., Interpretation: These are the first reported Australian cases of this emerging zoonosis with links to companion animals. These cases demonstrate the likely transmission route between companion animals and humans, with no evidence of human-to-human transmission. The existing requirement in the Queensland Health Public Health Management Guidelines, of restrictions on cases and some contacts while awaiting swab results, is currently under review., (© Commonwealth of Australia CC BY-NC-ND)

In September 2016, an invasive group A streptococcal disease outbreak occurred among residents of a residential aged care facility. An expert advisory group recommended mass prophylaxis for residents and staff in addition to strict infection control practices to prevent further spread. Whole genome sequencing confirmed the cases were related., (© Commonwealth of Australia CC BY-NC-ND)

While the differential association of Escherichia coli O157 genotypes with animal and human hosts has recently been well documented, little is known about their distribution between countries and how this might affect regional disease rates. Here, we used a 48-plex single nucleotide polymorphism (SNP) assay to segregate 148 E. coli O157 isolates from Australia, Argentina, and the United States into 11 SNP lineages. We also investigated the relationship between SNP lineages, Shiga toxin (Stx) gene profiles, and total Stx production. E. coli O157 isolates clearly segregated into SNP lineages that were differentially associated with each country. Of the 11 SNP lineages, seven were detected among isolates from a single country, two were detected among isolates from all three countries, and another two were detected only among U.S. and Argentinean isolates. A number of Australian (30%) and Argentinean (14%) isolates were associated with novel, previously undescribed SNP lineages that were unique to each country. Isolates within SNP lineages that were strongly associated with the carriage of stx2a produced comparatively more Stx on average than did those lacking the stx2a subtype. Furthermore, the proportion of isolates in stx2a-associated SNP lineages was significantly higher in Argentina and the United States than Australia (P < 0.05). This study provides evidence for the geographic divergence of E. coli O157 and for a prominent role of stx2a in total Stx production. These results also highlight the need for more comprehensive studies of the global distribution of E. coli O157 lineages and the impacts of regionally predominant E. coli O157 lineages on the prevalence and severity of disease., (Copyright © 2015, American Society for Microbiology. All Rights Reserved.)

Background: QT interval prolongation on the electrocardiogram (ECG) may be drug-induced and is traditionally associated with torsades des pointes. A better predictor of torsades des pointes is the time interval between the peak and the end of the T-wave (Tp-e). Older studies of propofol's effect on the corrected interval (QTc) are conflicting and confounded by polypharmacy. It was recently shown that target-controlled infusion of propofol at 3 microg/mL has no effect on QTc or Tp-e. This plasma concentration of propofol is at the extreme lower end of the range for surgical anesthesia. In this randomized, double-blind, clinical study, we investigated the dose-response relationship between propofol, QTc, and Tp-e in a range of doses clinically relevant for surgical anesthesia., Methods: Sixty healthy unpremedicated children, aged 3-10 yr, were recruited. Subjects were randomized to receive target-controlled infusions of propofol, to achieve 1 of 3 plasma concentrations: 3, 4.5, and 6 microg/mL. A preoperative 12 lead ECG was performed and repeated 5 min after induction. Two investigators, blinded to group allocation and to the timing of the ECG traces, independently measured QTc and Tp-e within and between each group. Paired t-tests were used to compare QTc and Tp-e within groups. One-way analysis of variance was used for intergroup analysis. The primary outcome measure was a change of >25 ms in Tp-e both within and between groups., Results: ECG recordings were obtained in 51 children. There were no demographic or ECG differences at baseline, at which time QTc and Tp-e values were within normal limits. There were no differences in QTc or Tp-e after induction within or between the three different groups., Discussion: Propofol has no effect on myocardial repolarization in healthy children at clinically relevant doses. This suggests that propofol would be a rational choice for children with a preexisting repolarization abnormality.

A comprehensive invasive pneumococcal disease (IPD) laboratory surveillance program was carried out in Australia in 2003. This program provided data on the prevalence of pneumococcal serotypes and antimicrobial resistance. There were 1,995 isolates tested with 34 per cent (683) from children aged less than five years and 27 per cent (535) from the elderly aged more than 65 years. One thousand eight hundred and sixty were isolates from blood, 79 from CSF and 56 from other sterile sites. In young children, 84 per cent of isolates were a serotype and 92 per cent a serogroup in the 7-valent pneumococcal conjugate vaccine (7vPCV). Of penicillin resistant isolates in children less than five years of age 85 per cent and 98 per cent were a serotype and serogroup in the 7vPCV respectively. When the universal 7vPCV vaccine program in young children is introduced in 2005, a proportion of cases of IPD should also be prevented in young adults (estimated reduction of 54 cases annually) and elderly Australians (an estimated reduction of 110 cases annually) as a result of improved herd immunity. Pneumococcal serotypes with higher rates of penicillin resistance (19F, 14 and 6B) were more prevalent in the elderly than in young children. In contrast, erythromycin resistance was more common in children less than five years of age (24%) compared to the elderly (15%). The predominant serotype with erythromycin resistance in Australia was serotype 14 and thus there is likely to be a major reduction in erythromycin resistance as a result of 7vPCV vaccination. Continued surveillance of pneumococcal serotype distribution and antibiotic susceptibility will be essential in order to identify serotype replacement by non-vaccine serotypes and to monitor the overall impact of current and future vaccine programs on invasive pneumococcal disease in Australia, not only in young children but also in other age groups.

The management of an organisational outbreak of meningococcal disease using the national Guidelines for the early clinical and public health management of meningococcal disease in Australia (the Guidelines), could be considered a relatively straightforward task. Nevertheless, discretional judgements are often still required by the outbreak control team, as no guidelines can fully cover every eventuality. The greatest challenges generated by this outbreak did not result from the magnitude of the intervention, but from the difficulties in defining the margins of the intervention in the face of heightened community and professional concern. Also Public Health decisions and communication strategies needed to be responsive to these concerns.

This paper reports the results of comprehensive laboratory surveillance of invasive pneumococcal disease (IPD) in Australia during 2001 and 2002. The 7-valent conjugate pneumococcal vaccine was introduced for high risk paediatric groups, including Indigenous children, in late 2001. Of 1,355 isolates from non-Indigenous children, 86 per cent belonged to serotypes and 93 per cent to serogroups represented in the 7-valent pneumococcal conjugate vaccine. Thirteen per cent and 24 per cent of isolates had reduced susceptibility to penicillin and erythromycin, respectively and of these, more than 99 per cent belonged to serogroups represented in the 7-valent vaccine. Of the 1,504 isolates from non-Indigenous adults, 96 per cent belonged to serotypes included in the 23-valent polysaccharide vaccine; 14 per cent and 15 per cent had reduced susceptibility to penicillin and erythromycin, respectively and more than 95 per cent of these belonged to serotypes included in the 7-valent conjugate vaccine. In Western Australia and the Northern Territory (the only states for which Indigenous status was consistently available), there were 29 cases of IPD in Indigenous children, of which 21 were due to 7-valent vaccine serotypes in 2001, compared with 24 cases, including 10 due to vaccine serotypes, in 2002. This represents a statistically significant increase in the proportion of total isolates due to non-vaccine serotypes (chi2 = 3.93, p = 0.048) following the introduction of the 7-valent conjugate vaccine, principally due to serotypes 7F and 12F. The number of episodes due to penicillin resistant isolates decreased from nine in 2001 to two in 2002. Ninety per cent of isolates from Indigenous adults were included in the 23-valent polysaccharide vaccine and six per cent and five per cent had reduced susceptibility to penicillin and erythromycin, respectively. Conjugate pneumococcal vaccines can be expected to reduce the incidence of IPD due to vaccine serotypes in vaccinated children and potentially, their adult contacts. It may also impact favourably on the incidence of IPD due to penicillin and erythromycin resistant strains. Continued surveillance of both serotype distribution and antibiotic susceptibility are required to identify serotype replacement by non-vaccine serotypes and to monitor the overall impact of current and future vaccine programs on invasive pneumococcal disease in Australia.

This study describes all episodes of invasive meningococcal disease (n=120) acquired in north Queensland over the 5 year period 1995 to 1999. Indigenous people had a 3-fold greater risk than others of acquiring invasive meningococcal disease. There were 7 deaths, six in non-indigenous people. The majority (72.4%) of identified isolates were serogroup B. We found no evidence of significant resistance to the antibiotics recommended for treatment or chemoprophylaxis. Two outbreaks of disease were identified, one serogroup B and one serogroup C. Compared to the previous 5 years (1990 to 1994) there were far fewer cases of serogroup C disease and a lower incidence and risk of invasive meningococcal disease among indigenous people.