During August 1996 (winter) and February 1997 (summer), a total of 180 Campylobacter isolates from a restricted geographical area were obtained from human and veterinary cases, raw milk and chicken, ...

The rate of yersiniosis in New Zealand (NZ) is high compared with other developed countries, and rates have been increasing over recent years. Typically, >99% of human cases in NZ are attributed to Yersinia enterocolitica (YE), although in 2014, a large outbreak of 220 cases was caused by Yersinia pseudotuberculosis. Up until 2012, the most common NZ strain was YE biotype 4. The emergent strain since this time is YE biotype 2/3 serotype O:9. The pathogenic potential of some YE biotypes remains unclear. Most human cases of yersiniosis are considered sporadic without an identifiable source. Key restrictions in previous investigations included insufficient sensitivity for the isolation of Yersinia spp. from foods, although foodborne transmission is the most likely route of infection. In NZ, YE has been isolated from a variety of sick and healthy domestic and farm animals but the pathways from zoonotic reservoir to human remain unproven. Whole-genome sequencing provides unprecedented discriminatory power for typing Yersinia and is now being applied to NZ epidemiological investigations. A “One-Health” approach is necessary to elucidate the routes of transmission of Yersinia and consequently inform targeted interventions for the prevention and management of yersiniosis in NZ

Leptospirosis in New Zealand has been strongly associated with animal-contact occupations and with serovars Hardjo and Pomona. However, recent data suggest changes in these patterns, hence, serovar-specific epidemiology of leptospirosis from 1999 to 2017 was investigated. The 19-year average annual incidence is 2.01/100,000. Early (1999–2007) and late (2008–2017) study period comparisons showed a significant increase in notifications with serovar Ballum (IRR: 1.59, 95% CI: 1.22–2.09) in all cases and serovar Tarassovi (IRR: 1.75, 95% CI: 1.13–2.78) in Europeans and a decrease in notifications with serovars Hardjo and Pomona in all cases. Incidences of Ballum peaked in winter, Hardjo peaked in spring and Tarassovi peaked in summer. Incidence was highest in Māori (2.24/100,000) with dominant serovars being Hardjo and Pomona. Stratification by occupation showed meat workers had the highest incidence of Hardjo (57.29/100,000) and Pomona (45.32/100,000), farmers had the highest incidence of Ballum (11.09/100,000) and dairy farmers had the highest incidence of Tarassovi (12.59/100,000). Spatial analysis showed predominance of Hardjo and Pomona in Hawke’s Bay, Ballum in West Coast and Northland and Tarassovi in Waikato, Taranaki and Northland. This study highlights the serovar-specific heterogeneity of human leptospirosis in New Zealand that should be considered when developing control and prevention strategies.

Incidence of human yersiniosis in New Zealand has increased between 2013 and 2017. For surveillance and outbreak investigations it is essential that an appropriate level of discrimination between pathogenicYersinia enterocoliticaisolates is provided, in order to support epidemiological linking of connected cases. Subtyping of 227Y. enterocoliticaisolates was performed using a range of different typing methods, including biotyping, serotyping and seven loci multiple-locus variable-number tandem-repeat analysis (MLVA). In addition, core genome single-nucleotide polymorphism (core SNP) analysis and multi-locus sequence typing were performed on a subset of 69 isolates. Sixty-seven different MLVA types were identified. One MLVA profile was associated with an outbreak in the Bay of Plenty region, supported by epidemiological data. Core SNP analysis showed that all the outbreak-related isolates clustered together. The subtyping and epidemiological evidence suggests that the outbreak of yersiniosis in the Bay of Plenty region between October and December 2016 could be attributed to a point source. However, subtyping results further suggest that the same clone was isolated from several regions between August 2016 and March 2017. Core SNP analysis and MLVA typing failed to differentiate betweenY. enterocoliticabiotype 2 and biotype 3. For this reason, we propose that these biotypes should be reported as a single type namely:Y. enterocoliticabiotype 2/3 and that the serotype should be prioritised as an indicator of prevalence.

An apparent increase in the incidence of S. Brandenburg in New Zealand, coupled with the possibility that the virulence of the organism may also be changing, prompted this study.Three typing methods: macro-restriction fragment length polymorphism (MRFLP) profiling using pulsed field gel electrophoresis (PFGE), plasmid profiling and antimicrobial susceptibility profiling were used to determine strain diversity amongst 115 recent and historical isolates of S. Brandenburg from both human cases and non-human sources.Antimicrobial resistance was noted only in three isolates. Plasmids of varying sizes were found in 31 isolates. MRFLP analysis resulted in 13 different patterns. Combining the three sets of typing data yielded 24 composite types. Comparison of composite type, isolation date and geographical location of case allowed the retrospective recognition of seven potential clusters during the 5-year study period. Composite types of 24 (80%) of the non-human isolates tested were indistinguishable from human isolates, suggesting that human infection may be via a number of vehicles.Although not cost-effective for routine use on all salmonella isolates, the methods used in this study are an important adjunct to serotyping for discrimination within an emerging serotype.

Introduction: Shiga toxin producing Escherichia coli (STEC) cause significant endemic disease in Aotearoa | New Zealand (NZ) with a 2022 case incidence rate of 19.9/100,000 population. The introduction of culture independent diagnostic testing has been pivotal in elucidating STEC case numbers.Methods: Epidemiological data from 5,769 cases of STEC infection confirmed during the 7-year period 2016-2022 were reviewed in conjunction with epidemiological typing data from 3,746 case isolates (2,939 analyzed via whole genome sequencing).Results and discussion: Severe illness was reported for 25% of all STEC cases, and 23% of cases were hospitalized. All age groups were affected, but the greatest level of morbidity was observed in those less than 5 years old where the hemolytic uremic syndrome (HUS) incidence rate was 2.86/100,000. Serotypes O157:H7 and O26:H11 together accounted for 54% of infections. Other common serotypes differed from those reported as common elsewhere and included O128:H2, O38:H26, O146:H21 and O91:H14. Shiga toxin subtype 2a strains were more associated with serious illness than other subtypes, regardless of eae positivity. Multiple STEC strains were inadvertently identified in 1.2% of culture positive case samples suggesting that carriage of more than one strain could be more prevalent. Single nucleotide polymorphism (SNP) analysis indicated that most STEC cases were sporadic as 5-SNP genomic clusters were uncommon. Infection sources are rarely proven as food and environmental sample data are limited and insufficient to assist in determining pathways to infection. By combining isolate WGS-derived typing data and case epidemiological data we demonstrated the importance of shifting the focus from a select number of STEC serogroups to composite seropathotypes—based on full serotype, ST, cgMLST relatedness and stx sub-toxin profile—to assist in understanding both the role of each type in disease severity, and relationships across historical type groups. This knowledge may be useful in future prioritizing of clinical and public health resources.