Epidemiology of Shiga toxin producing Escherichia coli in Australia, 2000-2010

Abstract

BackgroundShiga toxin-producing Escherichia coli (STEC) are an important cause of gastroenteritis in Australia and worldwide and can also result in serious sequelae such as haemolytic uraemic syndrome (HUS). In this paper we describe the epidemiology of STEC in Australia using the latest available data.MethodsNational and state notifications data, as well as data on serotypes, hospitalizations, mortality and outbreaks were examined.ResultsFor the 11 year period 2000 to 2010, the overall annual Australian rate of all notified STEC illness was 0.4 cases per 100,000 per year. In total, there were 822 STEC infections notified in Australia over this period, with a low of 1 notification in the Australian Capital Territory (corresponding to a rate of 0.03 cases per 100,000/year) and a high of 413 notifications in South Australia (corresponding to a rate of 2.4 cases per 100,000/year), the state with the most comprehensive surveillance for STEC infection in the country. Nationally, 71.2% (504/708) of STEC infections underwent serotype testing between 2001 and 2009, and of these, 58.0% (225/388) were found to be O157 strains, with O111 (13.7%) and O26 (11.1%) strains also commonly associated with STEC infections. The notification rate for STEC O157 infections Australia wide between 2001-2009 was 0.12 cases per 100,000 per year. Over the same 9 year period there were 11 outbreaks caused by STEC, with these outbreaks generally being small in size and caused by a variety of serogroups. The overall annual rate of notified HUS in Australia between 2000 and 2010 was 0.07 cases per 100,000 per year. Both STEC infections and HUS cases showed a similar seasonal distribution, with a larger proportion of reported cases occurring in the summer months of December to February.ConclusionsSTEC infections in Australia have remained fairly steady over the past 11 years. Overall, the incidence and burden of disease due to STEC and HUS in Australia appears comparable or lower than similar developed countries.

Geographically Distinct Escherichia coli O157 Isolates Differ by Lineage, Shiga Toxin Genotype, and Total Shiga Toxin Production

“…Although these SNP lineages are common to Australia, a larger set of isolates would need to be tested to confirm these host associations. Nonetheless, we believe that isolates belonging to SNP lineage IVb are likely to result in less frequent and severe disease outcomes (as determined by the frequency of HUS cases) in Australia based on E. coli O157 epidemiological data for this country (29). While compelling data exist to suggest that the pathogenic potential of E. coli O157 is related to the carriage of specific stx variants, additional underlying factors are also likely to influence lineage-associated virulence.…”

“…Similarly, the majority of U.S. cattle and human isolates were shown to belong to SNP lineage Ib, which is frequently associated with clinical disease in the United States (10). In comparison, Australia has a relatively low reported frequency of HUS cases (29) and the incidence of disease associated with E. coli O157 appears to be lower than the global average. Although the predominant SNP lineages identified in Australia have not previously been associated with human sources (10), a significant association of SNP lineage IVb with Australian humans was identified in the current study.…”

“…The occurrence of different predominant and sometimes exclusive phylotypes in each region also supports the global dissemination and subsequent divergent evolution of this organism in each country. Furthermore, the regional dominance of host-related SNP lineages may also provide a possible explanation for the lower disease burden seen in Australia (29) relative to the United States and Argentina (28,30). This study not only provides a strong basis for the further exploration of regional variations in E. coli O157 genotypes and their associated impacts on the regional prevalence and severity of disease but also supports current genomic research in the global evolution and phylogeny of E. coli O157.…”

Characteristics of Emerging Human-Pathogenic Escherichia coli O26:H11 Strains Isolated in France between 2010 and 2013 and Carrying the stx 2d Gene Only

“…However, a growing number of human EHEC infections are caused by non-O157 EHEC strains (1)(2)(3)(4). Among non-O157 EHEC strains, O26:H11 has emerged as the most common serotype associated with severe diarrhea and HUS worldwide (1)(2)(3)(4)(5)(6).…”

Discrimination of Enterohemorrhagic Escherichia coli (EHEC) from Non-EHEC Strains Based on Detection of Various Combinations of Type III Effector Genes

“…In recent years, cumulative evidence from numerous countries has indicated that up to 30 to 60% of human EHEC infections are caused by non-O157 EHEC (5, 6; U.S. Department of Agriculture [USDA] risk profile for pathogenic non-O157 Shiga-toxin producing E. coli, http://www.fsis.usda.gov/wps/wcm/connect/92de0 38d-c30e-4037-85a6-065c3a709435/Non_O157_STEC_Risk_P rofile_May2012.pdf?MODϭAJPERES). Recent studies have shown that the number of non-O157 STEC infections sometimes surpasses the number of STEC O157 infections (7,8). Accordingly, the list of STEC associated with HUS has been extended to include serotypes O26:H11, O45:H2, O103:H2, O111:H8, O121: H19, O145:H28, and O157:H7 and their non-motile derivatives.…”