An outbreak of multiple serotypes of salmonella in New Zealand linked to consumption of contaminated tahini imported from Turkey.

A widespread salmonellosis outbreak linked to consumption of hummus made from contaminated tahini imported from Turkey occurred in New Zealand in November 2012. This article summarizes the outbreak detection, investigation, and control. The New Zealand Enteric Reference Laboratory alerted public health units regarding a cluster of 11 persons with Salmonella Montevideo infection identified from different regions of the North Island of New Zealand. A multiagency outbreak investigation commenced to determine the source of illness and prevent further transmission. Salmonellosis is a notifiable disease in New Zealand. Outbreak cases were identified through routine salmonellosis notifications, and interviewed using a standardized questionnaire to identify common exposures. Clinical and food isolates were initially characterized by serotyping and then further typed by pulsed-field gel electrophoresis (PFGE). PFGE profiles were sent to PulseNet and international alerts were posted. The scope of the investigation widened to include persons with either Salmonella Maastricht and Salmonella Mbandaka infection following detection of these serotypes in tahini epidemiologically linked to laboratory-confirmed cases. All three of the tahini-associated serotypes were detected in people who had consumed tahini, and these were found to have PFGE profiles indistinguishable from the tahini isolates. Twenty-seven salmonellosis cases infected with at least one of the three tahini-associated Salmonella serotypes were detected between September 1 and December 31, 2012; of these, 16 (59%) cases (12 with Salmonella Montevideo, 3 with Salmonella Mbandaka, and 1 with Salmonella Maastricht infection) had PFGE patterns indistinguishable from the outbreak profile. The investigation led to a trade withdrawal and consumer recall for tahini sesame paste from the consignment and products containing this tahini. The outbreak ceased following the recall. The importer of the implicated tahini was reminded of his duties as a food importer, including ensuring appropriate product testing. Changes to New Zealand legislation strengthened food safety responsibilities of food importers.

An outbreak of Salmonella Typhimurium phage type 42 associated with the consumption of raw flour.

A cluster of salmonellosis cases caused by Salmonella Typhimurium phage type 42 (STM42) emerged in New Zealand in October 2008. STM42 isolates from a wheat-based poultry feed raw material (broll; i.e., product containing wheat flour and particles of grain) had been identified in the 2 months prior to this cluster. Initial investigations indicated that eating uncooked baking mixture was associated with illness. A case-control study was conducted to test the hypothesis that there was an association between STM42 cases and consumption of raw flour or other baking ingredients. Salmonella isolates from human and non-human sources were compared using pulsed-field gel electrophoresis (PFGE) and multiple-locus variable number tandem repeat analysis (MLVA). Environmental investigations included testing flour and other baking ingredients from case homes, unopened bags of flour purchased from retail stores, and inspection of an implicated flour mill. A case-control study of 39 cases and 66 controls found cases had 4.5 times the odds of consuming uncooked baking mixture as controls (95% confidence interval [CI] 1.6-12.5, p-value 0.001). Examination of individual baking ingredients found that, after adjusting for eggs, flour had an odds ratio (OR) of 5.7 (95% CI 1.1-29.1, p-value 0.035). After adjusting for flour, eggs had an OR of 0.8 (95% CI 0.2-3.4, p-value 0.762). PFGE patterns were identical for all STM42 isolates tested; however, MLVA distinguished isolates that were epidemiologically linked to the cluster. STM42 was recovered from flour taken from four cases' homes, two unopened packs purchased from retail stores and packs from three batches of retrieved (recalled) product. This outbreak was associated with the consumption of uncooked baking mixture containing flour contaminated with STM42. The implicated flour mill initiated a voluntary withdrawal from sale of all batches of flour thought to be contaminated. Media releases informed the public about implicated flour brands and the risks of consuming uncooked baking mixture.

Interval colorectal cancers after negative faecal immunochemical test in the New Zealand Bowel Screening Pilot.

OBJECTIVE: Evaluate the diagnostic performance of faecal immunochemical test (FIT), identify risk factors for FIT-interval colorectal cancers (FIT-IC) and describe long-term outcomes of participants with colorectal cancers (CRC) in the New Zealand Bowel Screening Pilot (BSP). DESIGN: From 2012 to 2017, the BSP offered eligible individuals, aged 50-74 years, biennial screening using a quantitative FIT with positivity threshold of 15 µg haemoglobin (Hb)/g faeces. Retrospective review of prospectively maintained data extracted from the BSP Register and New Zealand Cancer Registry identified any CRC reported in participants who returned a definitive FIT result. Further details were obtained from hospital records. FIT-ICs were primary CRC diagnosed within 24 months of a negative FIT. Factors associated with FIT-ICs were identified using logistic regression. RESULTS: Of 387 215 individuals invited, 57.4% participated with 6.1% returning positive FIT results. Final analysis included 520 CRC, of which 111 (21.3%) met FIT-IC definition. Overall FIT sensitivity for CRC was 78.7% (95% CI=74.9% to 82.1%), specificity was 94.1% (95% CI=94.0% to 94.2%). In 78 (70.3%) participants with FIT-IC, faecal Hb was reported as undetectable. There were no significant associations between FIT-IC and age, sex, ethnicity and deprivation. FIT-ICs were significantly associated with proximal tumour location, late stage at diagnosis, high-grade tumour differentiation and subsequent round screens. Median follow-up time was 74 (2-124) months. FIT-IC had significantly poorer overall survival. CONCLUSION: FIT sensitivity in BSP compared favourably to published data. FIT-ICs were more likely to be proximal tumours with poor long-term outcomes. Further lowering of FIT threshold would have minimal impact on FIT-IC.

Absence of sustained breast cancer incidence inflation in a national mammography screening programme.

OBJECTIVE: To investigate the impact of population mammography screening on breast cancer incidence trends in New Zealand. METHODS: Trends in age-specific rates of invasive breast cancer incidence (1994-2014) were assessed in relation to screening in women aged 50-64 from 1999 and 45-69 following the programme age extension in mid-2004. RESULTS: Breast cancer incidence increased significantly by 18% in women aged 50-64 compared with 1994-98 (p<0.0001), coinciding with the 1999 introduction of mammography screening, and remained elevated for four years, before declining to pre-screening levels. Increases over 1994-99 incidence occurred in the 45-49 (21%) and 65-69 (19%) age groups following the 2004 age extension (p<0.0001). Following establishment of screening (2006-10), elevated incidence in the screening target age groups was compensated for by lower incidence in the post-screening ⩾70 age groups than in 1994-98. Incidence in women aged ⩾45 was not significantly higher (+5%) after 2006 than in 1994-98. The cumulated risk of breast cancer in women aged 45-84 for 1994-98 was 10.7% compared with 10.8% in 2006-10. CONCLUSIONS: Increases in breast cancer incidence following introduction of mammography screening in women aged 50-64 did not persist. Incidence inflation also occurred after introduction of screening for age groups 45-49 and 65-69. The cumulated incidence for women aged 45-84 over 2006-10 after screening was well established, compared with 1994-98 prior to screening, shows no increase in diagnosis. Over-diagnosis is not inevitable in population mammography screening programmes.

Breast cancer mortality and screening mammography in New Zealand: Incidence-based and aggregate analyses.

OBJECTIVE: To investigate trends in breast cancer mortality in New Zealand women, to corroborate or negate a causal association with service screening mammography. METHOD: Cumulated mortality rates from breast cancer deaths individually linked to incident cases diagnosed before and after screening commencement were compared, in women aged 50-64 (from 2001) and aged 45-49 and 65-69 (from 2006). Trends and differences in aggregate invasive breast cancer mortality (1975-2013) were assessed in relation to introduction of mammography screening targeting women aged 50-64 and 45-69. Joinpoint analysis was also undertaken. RESULTS: The reduction in incidence-based cumulated breast cancer mortality before and after the introduction of screening was -15% (p = 0.006) for women aged 45-69, and 17% (p = 0.005) for those aged 50-64. Aggregate mortality declined by -34% (2005-13 compared with 1992-98) in the age group 50-64, and by -28% among women aged 45-49 and -25% among women aged 65-74. For women aged 50-64 the 2-joinpoint model shows a 1990 turning point, from prior rising mortality to a mean -1.8% decline per annum, coinciding with improvements in primary treatment of breast cancer; and a steepening of the decline (-3.0% p.a.) from the late 1990s, coinciding with the introduction of service mammography screening. CONCLUSION: Breast cancer mortality declines occurring since the advent of screening mammography in New Zealand are consistent with other incidence-based and aggregate studies of screening mammography in populations, individual-based cohort studies, and randomized controlled trials.

Debunking the 'only 50%' myth: prevalence of established risk factors in New Zealanders with self-reported ischaemic heart disease.

OBJECTIVE: To estimate the prevalence of established risk factors for ischaemic heart disease (IHD) in New Zealand adults and compare the prevalence in adults with and without this disease. DESIGN: Data were obtained from the 2002/03 New Zealand Health Survey. Risk factor prevalence was determined by: self-reported doctor diagnosis of high blood pressure, high cholesterol and diabetes; self-report of smoking and physical inactivity; and measurement of obesity. Presence of IHD was based on self-report of heart disease (doctor diagnosed at age 25 years or over) together with current medical or past surgical treatment for this disease. Multiple logistic regression was used to determine prevalence rate ratios (PRRs) for males and females separately, adjusting for age, ethnicity and deprivation. RESULTS: The overall prevalence of IHD was 8%. Overall risk factor prevalences were in the range of 20-25% for each of high blood pressure, high cholesterol, smoking, obesity and physical inactivity, and approximately 5% for diabetes. Overall, 94-97% of adults with IHD had at least one risk factor (depending on how smoking was defined). The PRRs of IHD were highest for cholesterol (about 4.5), followed by blood pressure (about 2.3), with all other risk factors around 1.5. PAF estimates indicate that 80-85% of IHD was attributable to the presence of at least one risk factor for all age, gender and ethnic groups. CONCLUSIONS: Established risk factors account for 80-85% of the non-fatal burden of IHD in New Zealand. Limited research resources would be better used to evaluate which interventions are effective and efficient at reducing exposure of all population groups to known risk factors, rather than on identification of additional risk factors.

Unanswered questions, the epidemiology of a community outbreak: meningococcal C disease in Northland, New Zealand, 2011.

AIM: We describe the epidemiology of a community outbreak of Meningococcal C disease in Northland in 2011, and national trends in serogroup C disease in New Zealand. METHODS: Notification data from EpiSurv for all meningococcal C cases were analysed for 2011 for Northland and for the period 2001-2011 nationally. RESULTS: In 2011, the rate of group C meningococcal disease for the population in the Whangarei district aged less than 20 years was 27.6 cases per 100,000 population (6 cases) compared with 17.6 cases per 100,000 population under 20 years (8 cases) in the Northland District Health Board (DHB). All except one case were under 20 years of age. The case fatality rate was 33%. Nationally the rate of meningococcal C disease has fluctuated over the last decade, with an increasing trend apparent since 2007. There has been a noticeable increase over the last 3 years of group C cases infected with the C:P1.5-1,10-8 strain (including all of the Northland cases). This strain has also been associated with a higher case fatality rate (16% in the period 2007-2011). CONCLUSION: Meningococcal C disease in New Zealand, although still less common than group B, is poorly understood. The relationships between carriage, invasive disease and community outbreaks deserve greater study. Active monitoring of surveillance data is warranted to ensure timely funded introduction of the highly effective meningococcal C conjugate vaccine on to the national immunisation schedule when appropriate, given increasing disease rates, the high case fatality rate and significant Maori non-Maori inequities in disease incidence.

Acute gastrointestinal illness in New Zealand: information from a survey of community and hospital laboratories.

AIM: To describe and quantify laboratory testing of faecal samples for enteric pathogens as a component of the reporting pyramid of acute gastrointestinal illness (AGI) in New Zealand. METHOD: Postal survey of community and hospital laboratories throughout New Zealand conducted in mid-2006, requesting data from the 2005 calendar year. RESULTS: Of the 47 laboratories eligible for the survey, responses were received from 35 (74%, 16 hospital laboratories, 12 community laboratories, five hospital and community laboratories, and two Public Health Laboratories). Based on survey data and extrapolation it was estimated that approximately 250,000 faecal samples were received by New Zealand laboratories in 2005. The majority of these (77%) were requested by primary healthcare providers on people in the community. Routine testing of these samples would include bacteria (Salmonella, Shigella, Campylobacter, Yersinia) and parasites (Cryptosporidium, Giardia) and (depending principally on the age of the patient) rotavirus. Testing for other pathogens was comparatively infrequent. The frequency of detection of a pathogen in community samples was estimated as approximately 20%. CONCLUSION: The positivity rate of 20% for faecal samples from people in the community is consistent with overseas results. Although there was considerable variation in the testing methods employed by the laboratories the methods were considered appropriate based on consultation with ESR Public Health and Reference Laboratory staff. These data on the number and type of samples, and positivity rate , will assist in the determination of a reporting pyramid for AGI in New Zealand.

Surveillance of vaccine breakthrough cases following MeNZB vaccination.

AIM: To describe and investigate epidemic strain serogroup B meningococcal disease in recipients of the meningococcal vaccine, MeNZB. METHOD: Epidemic strain meningococcal disease cases in vaccine recipients were identified by matching disease notification and laboratory data against the National Immunisation Register. Descriptive analyses were undertaken for disease cases aged under 20 years and vaccine breakthrough cases (epidemic strain meningococcal disease cases with onset 28 or more days after receipt of the third MeNZB dose). Questionnaires were sent to hospital clinicians requesting medical histories and laboratory test results for vaccine breakthrough cases. A committee reviewed this information to assess immune competence in these cases. RESULTS: From the start of the meningococcal B immunisation programme in July 2004 to the end of 2006, 34 vaccine breakthrough cases were identified. No underlying host factors were identified that explained disease occurrence for the 30 cases (88.2%) for whom questionnaires were completed. For 12 (35.3%) cases all requested laboratory tests to assess immune competence were performed and these subjects were judged to be immune competent. CONCLUSION: While epidemic strain meningococcal disease incidence has fallen dramatically with the introduction of the vaccine, these early results confirm the expectation that vaccine breakthrough cases will occur in immune competent individuals given the anticipated vaccine effectiveness of approximately 75%.

Post-marketing safety monitoring of a new group B meningococcal vaccine in New Zealand, 2004-2006.

New Zealand introduced a new outer membrane vesicle vaccine in 2004 to combat an epidemic of group B meningococcal disease. An Independent Safety Monitoring Board oversaw intensive safety monitoring, which included hospital surveillance, health professional reporting (passive and active) and mortality monitoring. With over three million doses administered to individuals aged under 20 years, the monitoring results provide consistent evidence supporting the vaccine's safety.

How low can it go? Projecting ischaemic heart disease mortality in New Zealand to 2015.

AIMS: This study aims to identify how ischaemic heart disease (IHD) mortality rates in New Zealand have varied between successive cohorts and time periods. This information is then used to project IHD mortality rates and counts (burdens) out to year 2011-15. METHODS: Age/period/cohort models were constructed (5-year periods and 5-year age groups, generating 10-year overlapping cohorts) using both frequentist and Bayesian methods. Data were available from 1956 for the total population and from 1981 for Maori. The projection period was 2001-5 to 2011-15. Uncertainty was quantified as the Bayesian 90% credible interval. RESULTS: IHD mortality rates for all age by gender groups increased from 1956-60 to peak in 1966-70, then declined by more than 60% to current (1996-2000) levels. However, the decline has been much shallower for Maori. This decline has resulted from increasingly favourable period effects since 1971-75 (less marked for Maori). However, no substantive cohort effects have been seen, at least from the 1891 to the 1951 cohort. Our model suggests that, for the first time, a substantive and unfavourable cohort effect may be emerging among recent birth cohorts. CONCLUSIONS: IHD mortality rates are projected to continue to fall from 2001-05 to 2011-15, albeit more slowly than in the past as the increasing (favourable) period effect is partly offset by an emerging (unfavourable) cohort effect. The result is a relatively small projected decline in absolute IHD mortality burden overall, but an actual increase among Maori.

Proceedings of the Meningococcal Vaccine Strategy World Health Organization satellite meeting, 10 March 2004, Auckland, New Zealand.

From 1991 to the end of 2003 there have been 5293 cases and 216 deaths from meningococcal disease in New Zealand. On 10 March 2004, the New Zealand Ministry of Health hosted a special meeting to release the first results of the clinical trial in 16 to 24 month olds of a new vaccine (MeNZB), which has been tailor-made to provide protection against the New Zealand epidemic strain. These proceedings summarise the key points from the meeting presentations and highlight some of the important issues considered in the subsequent discussion. In the toddler age-group trial, 75% of the MeNZB recipients exhibited a four-fold or greater rise in serum bactericidal antibodies after three doses of MeNZB--compared with 4% of the control vaccine recipients. Local reactions to MeNZB and the control vaccine were common, especially injection site tenderness. These data, along with data from New Zealand clinical trials in four other age groups and efficacy and safety data from the Norwegian parent vaccine, were used to support the application for a licence to use MeNZB in a proposed mass immunisation programme for 0-19 year olds. During the immunisation programme, a comprehensive safety monitoring programme will be in place to monitor for any adverse reactions following MeNZB immunisation. This will include real-time hospital-based monitoring in the regions first to roll out the vaccine.

The New Zealand Meningococcal Vaccine Strategy: a tailor-made vaccine to combat a devastating epidemic.

The New Zealand Meningococcal Vaccine Strategy aims to end the devastating 14-year epidemic of B:4:P1.7b,4 group B meningococcal disease in New Zealand through a mass immunisation programme to all under 20 year olds using a tailor-made vaccine (MeNZB). This paper describes the scientific rationale, development, and key components of the New Zealand Meningococcal Vaccine Strategy. A summary of the efficacy and safety data of existing outer membrane vesicle group B meningococcal vaccines is included as these data critically support the Strategy.