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Table 1.  


Total no. (missing data)

No. (%) cases/y

Average incidence, cases/100,000 population/y

Age, y 319 (0)    
   <1 y   118 (37.0) 31.5
   1–4   120 (37.6) 8.2
   5–9   46 (14.4) 2.6
   10–14   35 (11.0) 2.0
Sex 319 (0)    
   F   125 (39.2) 4.8
   M   194 (60.8) 7.0
Ethnicity, prioritized 319 (0)    
   Māori   114 (35.7) 11.6
   Pacific   140 (43.9) 13.4
   Non-Māori, non-Pacific   65 (20.4) 1.9
New Zealand Index of Deprivation Quintile† 317‡    
   1   11 (3.5) NA
   2   21 (6.6) NA
   3   42 (13.2) NA
   4   54 (17.0) NA
   5   189 (59.6) NA
Clinical manifestations 319 (0)    
   Bacteremia only   108 (33.9) NA
   Meningitis only   63 (19.7) NA
   Meningitis with bacteremia   138 (42.3) NA
   Septic arthritis only   5 (1.6) NA
   Septic arthritis with bacteremia   2 (0.6) NA
   Meningitis and septic arthritis with bacteremia   3 (0.9) NA
Vital signs on first presentation      
   Temperature >38·5°C or <36°C 314 (5) 150 (47.7) NA
   Systolic hypotension for age 218 (101) 84 (38.5) NA
   Impaired level of consciousness 291 (28) 99 (34.0) NA
Clinical signs at first presentation      
   Rash in cases with bacteremia 248 (3) 213 (85.9) NA
   Includes purpura 213 (3) 108 (50.7) NA
   Includes petechiae without purpura 213 (3) 86 (40.4) NA
   Blanching only 213 (3) 19 (8.9) NA
   Meningism in cases with meningitis 184 (20) 111 (60.3) NA
   Bulging fontanelle in infants with meningitis 43 (39) 19 (44.2) NA
   Arthritis during admission 314 (5) 19 (6.1) NA
   Arthralgia during admission 314 (5) 23 (7.3) NA

Table 1. Demographic and clinical factors of 319 confirmed cases of invasive meningococcal disease in children <15 years of age, Auckland, New Zealand, 2004–2020*

*NA, not applicable.
†Each NZDep quintile contains ≈20% of the population. 1 = least deprived; 5 = most deprived.
‡Two overseas cases were excluded.

Table 2.  


No. cases/total no. (%)

Died 13/319 (4.1)
Cure, complete outcome data 258/306 (84.3)
Cure, incomplete outcome data 48/306 (15.6)
Cure without sequelae 197/258 (76.4)
Cure with sequelae 61/258 (23.6)
   Neurodevelopmental 35/258 (13.6)
   Sensorineural hearing loss 32/258 (12.4)
   Skin scarring 16/258 (6.2)
   Loss of limbs or digits 7/258 (2.7)
   Chronic kidney disease 1/258 (0.4)
   Other sequelae* 5/258 (1.9)
Neurodevelopmental sequelae
   Delayed development 20/258 (7.8)
   Cerebral ischemia 13/258 (5)
   Epilepsy 8/258 (3.1)
   Learning, concentration, behavior, psychological 8/258 (3.1)
   Other† 10/258 (3.9)

Table 2. Outcomes of 319 confirmed cases of invasive meningococcal disease in children <15 years of age, Auckland, New Zealand, 2004–2020

*Other: bone growth arrest 2/258 (0.8%); cardiomyopathy 1/258 (0.4%); gastrointestinal hemorrhage 1/258 (0.4%); panniculitis 1/258 (0.4%). †Other neurodevelopmental: chronic hydrocephalus 2/258 (0.8%); autism spectrum disorder 1/258 (0.4%); ataxia 1/258 (0.4%); carotid artery narrowing 1/258 (0.4%); chronic headache 1/258 (0·4%); cranial nerve palsy 1/258 (0.4%); encephalomalacia 1/258 (0.4%); hypertonia 1/258 (0.4%); syringomyelia 1/258 (0.4%).

Table 3.  


No. cases (%)

OR (95% CI)

p value

Ethnicity, compared with non-Māori, non-Pacific population
   Pacific 38/118 (32.2) 2.91 (1.31–7.18) 0.0128
   Māori 28/96 (29.2) 2.52 (1.10–6.35) 0.0366
Reduced penicillin susceptibility 12/64 (18.8) 0.548 (0.25–1.14) 0.117
NZDep quintile† 271 1.21 (0.95–1.58) 0.142
Age, mo† 271 0.996 (0.99–1.00) 0.157
Serogroup, compared with MenB
   MenC 7/18 (38.9) 1.80 (0.64–4.82) 0.247
   MenW 6/25 (24.0) 0.89 (0.31–2.24) 0.822
   MenY 3/8 (37.5) 1.70 (0.34–7.16) 0.478
Male sex, compared with female 50/168 (29.8) 1.39 (0.80–2.48) 0.248
Season, compared with autumn
   Spring 23/76 (30.3) 1.47 (0.64–3.60) 0.374
   Summer 11/35 (31.4) 1.56 (0.57–4.31) 0.386
   Winter 30/116 (25.9) 1.19 (0.54–2.79) 0.683
MeNZB vaccination, compared with fully vaccinated
   Unvaccinated 43/166 (25.9) 0.76 (0.39–1.51) 0.425
   Partially vaccinated 12/41 (29.3) 0.90 (0.37–2.17) 0.817
Prehospital parenteral antibiotic treatment 10/44 (22.7) 0.79 (0.35–1.64) 0.537
Sepsis criteria 39/145 (26.9) 1.14 (0.51–2.77) 0.751

Table 3. Univariate logistic regression for combined outcome of death or sequelae in 271 confirmed cases of invasive meningococcal disease in children <15 years of age, Auckland, New Zealand, 2004–2020*

*Men, Neisseria meningitidis serogroup; OR, odds ratio; NZDep, New Zealand Index of Deprivation
†Continuous variable; OR represents increase in odds for each unit increase in variable.


A New Study Highlights the Need for the Meningitis B Vaccine for Children in New Zealand

  • Authors: Cameron Burton, MBChB; Emma Best, MBChB; Matthew Broom, MBChB; Helen Heffernan, BSc (Hons 1); Simon Briggs, MBChB; Rachel Webb, MD
  • CME / ABIM MOC Released: 3/16/2023
  • Valid for credit through: 3/16/2024, 11:59 PM EST
Start Activity

  • Credits Available

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    • Letter of Completion
    • ABIM MOC points

Target Audience and Goal Statement

This activity is intended for primary care physicians, pediatricians, infectious disease specialists, and other clinicians who treat and manage children at risk for infection with Neisseria meningitidis.

The goal of this activity is for learners to be better able to evaluate the epidemiology, clinical features, and outcomes of pediatric invasive meningococcal disease.

Upon completion of this activity, participants will:

  • Assess the global epidemiology of invasive meningococcal disease
  • Analyze the epidemiology of invasive meningococcal disease among children in Aotearoa New Zealand
  • Evaluate clinical features of invasive meningococcal disease in the current study
  • Distinguish outcomes of invasive meningococcal disease in the current study


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  • Cameron Burton, MBChB

    Te Whatu Ora Counties Manukau
    University of Auckland 
    Auckland, New Zealand

  • Emma Best, MBChB

    Te Whatu Ora Te Toka Tumai Auckland
    University of Auckland
    Auckland, New Zealand

  • Matthew Broom, MBChB

    Te Whatu Ora Te Toka Tumai Auckland
    University of Auckland
    Auckland, New Zealand

  • Helen Heffernan, BSc (Hons 1)

    Institute of Environmental Science and Research
    Wellington, New Zealand

  • Simon Briggs, MBChB

    Te Whatu Ora Te Toka Tumai Auckland
    University of Auckland
    Auckland, New Zealand

  • Rachel Webb, MD

    Te Whatu Ora Te Toka Tumai Auckland
    University of Auckland
    Auckland, New Zealand

CME Author

  • Charles P. Vega, MD

    Health Sciences Clinical Professor of Family Medicine
    University of California, Irvine School of Medicine
    Irvine, California


    Charles P. Vega, MD, has the following relevant financial relationships:
    Consultant or advisor for: GlaxoSmithKline; Johnson & Johnson Pharmaceutical Research & Development, L.L.C.


  • Cheryl Salerno, BA

    Emerging Infectious Diseases


    Cheryl Salerno, BA, has no relevant financial relationships.

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    Associate Director, Accreditation and Compliance, Medscape, LLC


    Yaisanet Oyola, MD, has no relevant financial relationships.

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A New Study Highlights the Need for the Meningitis B Vaccine for Children in New Zealand: Discussion



Key Findings

Despite a reduction in the number of cases of IMD since the MenB epidemic, the incidence of IMD in New Zealand remains double that of other high-income countries[3,5]. Although MenB remains the most common serogroup in children, the epidemic B:P1.7–2,4 strain no longer dominates in the Auckland region. Rates of pediatric IMD increased in Auckland and nationally in 2014–2019, partly because of an observed global increase in MenW[3,5]. Mirroring international trends in invasive bacterial disease during the COVID-19 pandemic[26–28], there was a sharp decrease in cases of pediatric IMD in NZ in 2020 after national COVID-19 control measures began, and that decrease continued through 2021[29]. Future patterns of pediatric IMD remain uncertain; however, there is a risk of resurgent disease exacerbated by rising poverty and socioeconomic inequity[30].

Our findings highlight the severity of IMD. One third of the cases we studied included admission to an ICU, comparable with data for international cohorts[8,31]. Over half of those cases required invasive ventilation or inotropic/vasopressor support. The CFR in our cohort was 4.1%, which compares to rates for other high-income settings of 2%–12%[1]. Sequelae occurred in 23.6% of survivors. Because outcome was classified as unknown for 48 cases that lacked audiologic data but had no other reported sequelae, we might have overestimated the proportion of survivors with sequelae. Our study revealed that 1 in 4 children did not receive an audiology assessment after meningococcal meningitis. Given this finding, we strongly recommend that children in New Zealand who are diagnosed with meningococcal meningitis receive audiology assessment before hospital discharge. Active follow-up for survivors of IMD should focus on confirming audiology assessment and screening for neurologic, developmental, and psychological effects[2,9]. Our lack of access to mental health and educational data and shorter follow-up durations of ≥3 months might have underestimated the prevalence of long-term neurocognitive and psychological effects. Urgent action is needed to honor the nation’s commitment to Te Tiriti o Waitangi, the 1840 founding document that established bicultural partnership between indigenous Māori and the British Crown.

Our data demonstrate the usefulness of PCR for diagnosing culture-negative IMD[32,33]. Blood culture results were negative in 79% of children who received prehospital antibiotics. However, when performed, N. meningitidis blood PCR was positive in all those cases. Drew et al. similarly reported positive blood PCR in 25 of 28 IMD cases that had a negative blood culture after intramuscular penicillin[32]. We suggest that clinicians consider using N. meningitidis PCR testing, especially in the context of prior antibiotic administration. We found no statistically significant differences in clinical outcomes between children who received prehospital parenteral antibiotics and those who did not; however, our study was not powered to detect a difference in those outcomes.

In our cohort, bacteremia and meningitis coexisted in 44.2% of cases; we propose that CSF testing be carefully considered for those with proven meningococcal bacteremia, especially in infants. In cases with bacteremia, 85.9% had a rash at first examination; rash characteristics included purpura (50.7%), petechiae without purpura (40.4%), and blanching only (8.9%), findings similar to those reported for a pediatric cohort in Ireland[9]. Whereas a classic purpuric or petechial rash can suggest IMD, rash at presentation might be nonspecific or absent. It is therefore important for clinicians to maintain a high index of suspicion of IMD in children with suspected sepsis without rash.

In our cohort, we noted an increase over time in the proportion of isolates with reduced penicillin susceptibility. Similar trends have been reported among adults in Auckland, as well as in Spain and Australia[34–36]. Earlier literature reported an association between reduced penicillin susceptibility and increased complications[37]; however, no difference in outcomes were noted for our pediatric cohort or for the Auckland adult cohort[34]. New Zealand guidelines recommend a third-generation cephalosporin for empiric treatment of sepsis in children[38]. Because all isolates we studied were ceftriaxone-susceptible, reduced penicillin susceptibility is unlikely to have clinical significance for empiric therapy in New Zealand.

Our study illustrates the considerable inequity of IMD in the Auckland region of New Zealand. Māori and Pacific children had disproportionately higher rates of IMD and were more likely to experience complications. All but 1 death occurred in Māori or Pacific children. Children living in Auckland’s most deprived 20% of neighborhoods had rates of IMD 17 times higher than those in the least deprived 20% of neighborhoods. The relationship between ethnicity, socioeconomic deprivation, and the risk of severe childhood infections is not well understood but is likely rooted in the ongoing effects of colonization and structural racism[39]. Recent findings from a nationally representative longitudinal study, Growing Up in New Zealand[40], indicate that disparities in infectious disease hospitalizations among infants of Māori or Pacific peoples can be only partly explained by socioeconomic deprivation factors. Nonetheless, household crowding has been shown to be strongly associated with epidemic IMD in New Zealand[41].

Addressing the upstream determinants of health is important, but vaccination remains the best strategy to control IMD and is a key method for reducing inequity[4,5,42]. Although New Zealand’s universal vaccination programs have not yet resulted in equitable uptake, prioritizing delivery and implementation might improve coverage and outcomes for those most at risk[43]. Despite having the highest rate of MenB in the world and some prior success with MeNZB immunization, New Zealand has not yet included 4CMenB in the National Immunization Schedule nor funded vaccine for children at highest risk of disease. The real-world evidence for 4CMenB is clear and demonstrates that control of IMD in New Zealand is within reach[15].

In conclusion, IMD remains a severe, life-threatening disease in young children in New Zealand; Māori and Pacific infants and those living in areas of socioeconomic deprivation are at greatest risk. The recent increase in incidence of MenB IMD highlights the urgent case for inclusion of 4CMenB in the National Immunization Schedule. Using N. meningitidis PCR to aid diagnosis of culture-negative, clinically suspected IMD, along with routine inpatient audiology assessment after cases of meningococcal meningitis, may improve clinical outcomes.