In response to a surge in clinical notifications in May 2019, we undertook 4 successive multidisciplinary V. parahemolyticus AGE outbreak investigations (Table). This effort required enhanced epidemiologic investigation, establishment of national V. parahemolyticus whole-genome sequencing capability (Appendix), and extensive environmental investigations, including food source traceback, testing of implicated seafoods, sea surface temperature measurements, and seafood supply chain inquiries. During January 2019–May 2022, 136 of the 182 cases entered into the national notifiable disease database had viable V. parahemolyticus isolates referred to the New Zealand Institute for Public Health and Forensic Science: 90 outbreak-related and 46 background isolates (predominantly locally acquired [38/46] owing to COVID-19 border restrictions during the period) (2). We also identified 4 shellfish isolates from outbreak-implicated mussel farms, sampled by the New Zealand Institute for Bioeconomy Science and Ministry for Primary Industries in 2020 and 2021. We subjected all isolates to tdh/trh-toxin gene testing and whole-genome sequencing, comparing New Zealand strains to available international sequences (Appendix).

Figure 1

Figure 1. Maximum-likelihood phylogenetic tree of sequence type 36 isolates for study of emergent Vibrio parahaemolyticusgastroenteritis outbreaks, New Zealand, 2019–2022. Tree was constructed using core-genome single-nucleotide polymorphism alignment of all...

Investigations revealed the first V. parahaemolyticus AGE outbreak was caused by pandemic clone ST36, widely distributed to cases through commercially supplied New Zealand green-lipped mussels (Table). This finding represented Trans-Pacific expansion of tdh+/trh+ ST36 to Oceania; New Zealand isolates clustering (<30–50 single-nucleotide polymorphisms [SNPs]) with a Pacific Northwest/northeast USA lineage detected since 2007 (Figure 1). An ST36 infection occurred in April 2019 in a background case and seafood area distinct from the winter outbreak source. The close clustering (<5 SNPs) of this isolate with outbreak isolates and those causing sporadic illness thereafter demonstrated ST36’s high clonality and wide dispersal in New Zealand. Five closely related clinical isolates were also later reported in Australia in 2021.

Figure 2

Figure 2. Maximum-likelihood phylogenetic tree of sequence type 50 isolates for study of emergent Vibrio parahaemolyticusgastroenteritis outbreaks, New Zealand, 2019–2022. Tree was constructed using core-genome single-nucleotide polymorphism alignment of all...

Two subsequent outbreaks in winter 2020 and summer 2021, also associated with commercially supplied mussels, represented the emergence of pathogenic tdh+/trh+ ST50 in New Zealand (Table; Figure 2). We noted clinical and mussel-derived outbreak isolates to be closely related to background ST50 infections associated with geographically dispersed seafood growing areas, suggesting a bloom of clonal ST50 in New Zealand’s marine environment in 2020 replaced pandemic ST36 predominance. Internationally, ST50 is relatively uncommon, and New Zealand ST50 was genetically distinct from most international isolates, except those later emerging in an Australia oysterborne outbreak (8). Australia’s 2021 samples formed a monophyletic group, with some closely related to New Zealand samples (Figure 2, panel B). Those results are insufficient to demonstrate dispersal from New Zealand because separate incursions from a common source may have occurred. Nevertheless, the genomic epidemiology illustrates the interconnected nature of international marine ecosystems and emerging risks. Suspected mechanisms for the extensive global dispersal of related clones have included the international shellfish trade and contaminated ballast from cargo ships (5). Environmental conditions associated with aquaculture also may promote the evolution of Vibrio spp. virulence (1). Our findings suggest the need for further research into New Zealand ST50’s emergence.

The occurrence of wintertime outbreaks is unusual when compared with similarly temperate areas overseas (1). Sea surface temperatures >15°C, salinity, and rainfall can affect V. parahaemolyticus abundance and pathogenicity in seafood (1,9,10). Rising seawater temperatures in New Zealand may be contributing to recent trends in seafoodborne illness (11); sea surface temperatures recorded at mussel farms during winter outbreaks averaged 16.3°C in 2019 and 18°C in 2020. Some studies have also suggested higher relative prevalence of pathogenic tdh+/trh+ V. parahaemolyticus during colder temperatures (9,12). We identified a third tdh+/trh+ V. parahaemolyticus type during our investigations, ST199, isolated from cases who had consumed mussels associated with sea surface temperatures <16°C, suggesting this strain may have pathogenic preponderance at lower temperatures. Another hypothesized contributor to the occurrence of winter outbreaks is consumption of raw New Zealand green-lipped mussels as a naturopathic arthritis remedy; however, investigators did not collect information from cases related to reasons for mussel consumption (13).

Outbreaks 3 and 4 occurred during more typical summer months. Outbreak 4 showed diversity with regard to both implicated seafood sources and V. parahaemolyticus strains, and cases became predominantly associated with self-collection of wild shellfish (Table). ST50 from those outbreaks showed multiple distinct subclusters embedded within the wider diversity of historical clinical and environmental isolates (Figure 2, panel B). Outbreak 4 was thus likely driven by a surge of ST50 lineages already established across New Zealand, possibly triggered by an environmental amplification event. The summer of 2021–22 was New Zealand’s fifth warmest recorded summer; daily sea surface temperatures reached 4°C–5°C above average (14).

The apparent mix of pathogen-specific virulence and environmental factors in contributing to the emergence of epidemic V. parahaemolyticus disease is in keeping with experiences reported in Peru associated with El Niño (warmer, wetter) climatic events and arrivals of pandemic Vibrio spp. (3). In that context, the expansion of monitoring of harvest sites could support the early detection of pathogenic V. parahaemolyticus events. In response to New Zealand’s outbreaks, the Ministry for Primary Industries amended national regulations for commercial shellfish growing areas (15).

New Zealand’s experience with V. parahaemolyticus–associated outbreaks also has implications for health equity. Outbreaks disproportionately affected persons of Māori ethnicity (45% of cases and 47% of hospitalizations, but 15% of New Zealand’s population), as well as people of lower socioeconomic status (Table). Supporting Māori and local communities in the safe collection of seafood as a cultural activity and inexpensive food source is critical, including exploring novel methods of environmental monitoring and messaging that highlights the diversity of potentially affected seafoods.

We report Trans-Pacific expansion of pandemic ST36 V. parahaemolyticus to Oceania and emergence of pathogenic ST50, during both cold and warm seasons, associated with distributed musselborne outbreaks, a multisource outbreak of ST50, and uncommon STs affecting varied seafoods. Environmental drivers of Vibrio disease emergence, particularly increasing global climatic changes, require enhanced surveillance, policy, and research responses integrating One Health approaches and tailored local community considerations. Further integrated research should explore virulence, risk factors, and novel methods of environmental monitoring .Our investigations led to greater standardization of local diagnostic practices (initially limited by diverse methodologies, culture-free testing, and incomplete referrals for subtyping), investment in prospective genomic V. parahaemolyticus surveillance, environmental surveillance enhancements, and changes to food safety regulations.