In the last 10–15 years, there has been a global resurgence of scarlet fever, an infection historically associated with significant morbidity and mortality. It is unknown whether scarlet fever incidence has increased in Australia. We aimed to examine the incidence, predictors and severity of scarlet fever in the state of Victoria, Australia from 2007 to 2017, analyzing scarlet fever emergency department (ED) presentations, hospitalizations and deaths. Of the 1 578 scarlet fever cases during the study period, most occurred in children aged <10 years (1 344, 85%), in males (882, 56%), and during winter and spring months (918, 57%). There were no deaths with scarlet fever, however, 374 cases (24%) were admitted to hospital. The annual incidence of scarlet fever was stable during the study period (mean, 2.5; range, 1.9–3.1 cases per 100 000). Annual incidence was highest in children aged <5 years (19.3 per 100 000), and was 21% higher in males than females, adjusting for age and year (incidence rate ratio, 1.21, 95%CI 1.09–1.34). Whilst scarlet fever ED presentations and hospitalizations were stable in Victoria from 2007 to 2017, the recent identification of a Streptococcus pyogenes variant in Australia associated with epidemic scarlet fever overseas highlights the risk of future outbreaks.

Commercial point-of-care (POC) diagnostic tests for Group A Streptococcus, Streptococcus pneumoniae, and influenza virus have large potential diagnostic and financial impact. Many published reports on test performance, often funded by diagnostics companies, are prone to bias. The Standards for Reporting of Diagnostic Accuracy (STARD 2015) are a protocol to encourage accurate, transparent reporting. The Quality Assessment of Diagnostic Accuracy Studies (QUADAS-2) tool evaluates risk of bias and transportability of results. We used these tools to evaluate diagnostic test accuracy studies of POC studies for three respiratory pathogens. For the 96 studies analysed, compliance was <25% for 14/34 STARD 2015 standards, and 3/7 QUADAS-2 domains showed a high risk of bias. All reports lacked reporting of at least one criterion. These biases should be considered in the interpretation of study results.

A 60-year-old male presented to an emergency department (ED) with priapism following a sore throat illness. He did not have typical findings of sepsis. The patient then developed severe headache, mental status changes, and hypertension, then suffered a cardiopulmonary arrest. Autopsy showed group A streptococcal (GAS) sepsis, disseminated intravascular coagulation (DIC), and a septic thrombosis to the penile vein. This is the first known case of priapism being the presenting symptom of DIC.

Group A Streptococcus (GAS) are globally distributed bacterial pathogens. We examined the emm genotypes, which are important indicators of virulence, of 349 clinical GAS isolates collected using two surveillance systems, i.e. Invasive Bacterial Infection Surveillance (IBIS) from 2010 to 2011 (234 isolates) and routine surveillance of clinically isolated bacteria from various hospitals during 1996–2011 (115 isolates) in Thailand. The major emm genotypes in IBIS samples were emm44 (12·0%), emm104 (6·8%), emm22 (5·6%), and emm81 (5·6%), whereas only one isolate (0·4%) had the emm1 genotype, which is significantly more common in invasive cases in the Western world. In samples collected during routine surveillance, emm238 (10·4%), emm44 (8·7%), and emm165 (7·0%) were dominant. The major superantigen gene profiles were similar between the groups, and 30·1% of isolates did not possess the phage-encoded superantigens (speA, speC, speH, speI, speK, speL, speM, ssa). Although most isolates exhibited limited gene profiles, emm44 isolates had highly variable gene profiles (15 patterns). We conclude that emm44 is the predominant GAS genotype in Thailand, and isolates varied in superantigen gene profiles.

Streptococcal toxic shock syndrome (STSS) is a severe invasive infection characterized by the sudden onset of shock, multi-organ failure, and high mortality. In Japan, appropriate notification measures based on the Infectious Disease Control law are mandatory for cases of STSS caused by β-haemolytic streptococcus. STSS is mainly caused by group A streptococcus (GAS). Although an average of 60–70 cases of GAS-induced STSS are reported annually, 143 cases were recorded in 2011. To determine the reason behind this marked increase, we characterized the emm genotype of 249 GAS isolates from STSS patients in Japan from 2010 to 2012 and performed antimicrobial susceptibility testing. The predominant genotype was found to be emm1, followed by emm89, emm12, emm28, emm3, and emm90. These six genotypes constituted more than 90% of the STSS isolates. The number of emm1, emm89, emm12, and emm28 isolates increased concomitantly with the increase in the total number of STSS cases. In particular, the number of mefA-positive emm1 isolates has escalated since 2011. Thus, the increase in the incidence of STSS can be attributed to an increase in the number of cases associated with specific genotypes.

The epidemiology and clinical features of invasive group A streptococcal (iGAS) disease in Queensland children was investigated in response to anecdotal evidence of an increase in frequency and severity of this condition. A retrospective review of clinical records of all cases of iGAS disease notified to Queensland Health aged 0–18 years during a 5-year period was conducted. The annualized incidence of iGAS was 3·5/100 000 for the total population aged 0–18 and 13·2/100 000 for the Indigenous population of similar age. The annualized incidence was highest in Indigenous infants but no increase in frequency or severity of iGAS infections was observed. Findings included an increased prevalence in Indigenous children particularly in those aged <1 year, a significant male preponderance, lack of seasonal variation and an association with blunt trauma. Further studies are required to confirm and investigate these findings and to define specific risk factors in high-risk groups.

Molecular mimicry between streptococcal and human proteins has been proposed as the triggering factor leading to autoimmunity in rheumatic fever (RF) and rheumatic heart disease (RHD). This article summarises studies on genetic susceptibility markers involved in the development of RF/RHD. It also focuses on the molecular mimicry in RHD mediated by the responses of B and T cells of peripheral blood, and T cells infiltrating heart lesions, against streptococcal antigens and human tissue proteins. The molecular basis of T-cell recognition is assessed through the definition of heart-crossreactive antigens. The production of cytokines from peripheral and heart-infiltrating mononuclear cells suggests that T helper 1 (Th1)-type cytokines are the mediators of RHD heart lesions. An insufficiency of interleukin 4 (IL-4)-producing cells in the valvular tissue might contribute to the maintenance and progression of valve lesions.