|
Variable |
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.
| Outcome |
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) |
| Sequelae | |
| 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%).
| Variable |
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.
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New Zealand (Aotearoa) experienced a Neisseria meningitidis serogroup B epidemic during 1991–2006, and incidence remains twice that of other high-income countries. We reviewed clinical, laboratory, and immunization data for children <15 years of age with laboratory-confirmed invasive meningococcal disease in Auckland, New Zealand, during January 1, 2004–December 31, 2020. Of 319 cases in 318 children, 4.1% died, and 23.6% with follow-up data experienced sequelae. Children of Māori and Pacific ethnicity and those living in the most deprived areas were overrepresented. Eighty-one percent were positive for N. meningitidis serogroup B, 8.6% for serogroup W, 6.3% for serogroup C, and 3.7% for serogroup Y. Seventy-nine percent had bacteremia, and 63.9% had meningitis. In New Zealand, Māori and Pacific children are disproportionately affected by this preventable disease. N. meningitidis serogroup B vaccine should be included in the New Zealand National Immunization Schedule to address this persistent health inequity.
Invasive meningococcal disease (IMD) is a bacterial infection with typically rapid onset. In children, infection is associated with high (7%–9%) case-fatality rates (CFRs) and serious long-term sequelae[1,2]. Infants and young children have the highest incidence of disease; a second peak occurs during adolescence[3]. IMD inequitably affects Indigenous populations and persons living in areas of deprivation[3,4].
The bacterium Neisseria meningitidis is categorized into serogroups based on its polysaccharide capsule; 6 serogroups (A, B, C, W, X, and Y) are responsible for nearly all IMD cases worldwide[5]. The major clinical manifestations of IMD are meningitis and sepsis. Early recognition is critical because sepsis can rapidly progress to multiorgan dysfunction and death[6]. A leading cause of admission to pediatric intensive care units (ICUs) throughout Australasia[7], IMD can lead to disabling, long-term sequelae for approximately one third of surviving children, including hearing loss, neurodevelopmental impairment, limb or digit loss, and scarring[2,8,9]. Those sequelae heavily affect healthcare resources and the quality of life of affected children and their families[2,9].
The global incidence of IMD has declined over the past 20 years, partly because of the availability of safe, effective vaccines for all major disease-causing serogroups and successful vaccination programs[5]. Overall incidence of IMD in most high-income countries is well under 1.5 per 100,000 per year[5]. In contrast, New Zealand (Aotearoa) reports the highest rate of N. meningitidis serogroup B (MenB) disease in the world[3,5,10]. During 1991–2006, New Zealand experienced a prolonged MenB epidemic caused by the B:P1.7–2,4 strain[11]. The epidemic peaked in 2001, with an incidence of 17.4 cases/100,000 persons in the overall population and 212 cases/100,000 infants[11]. In response, MeNZB, a strain-specific outer membrane vesicle (OMV) vaccine, was developed and delivered nationally in 3 doses to persons <20 years of age during 2004–2006 and in 4 doses to infants during 2006–2008[11]. Overall vaccination coverage was 80%, and coverage was higher among Pacific peoples compared with those of other ethnicities. The vaccine effectiveness of MeNZB against the epidemic strain was estimated at 68%–77% and was associated with the waning of the epidemic[4,11].
Since that time, regional outbreaks of N. meningitidis serogroup C (MenC) and serogroup W (MenW) disease have been associated with high CFRs, prompting emergency targeted vaccination programs in 2011 and 2018[12,13]. However, since 2014, the incidence of IMD in NZ has been increasing, up to an overall rate of 2.8 cases/100,000 persons in 2019[3]. Almost half of cases in 2019 occurred in children <15 years of age, and the highest rates in infants <1 year of age (51.5/100,000 infants). As observed internationally, an increasing proportion of IMD caused by MenW has occurred in New Zealand, accounting for 30% of the country’s cases in 2019[3,5]. Auckland, New Zealand’s largest city, has a pediatric (<15 years of age) population of ≈320,000, which makes up 34% of the total New Zealand pediatric population[14]. Ethnic groups in Auckland include Māori (18%), Pacific peoples (19%), and those of Asian (25%) and European (34%) heritage.
A 4-component MenB vaccine, 4CMenB (Bexsero; GlaxoSmithKline), was developed using 3 subcapsular antigens and the NZ MeNZB OMV vaccine[15]. Vaccine effectiveness data from Australia, Canada, Italy, and the United Kingdom show reductions in MenB of 71%–100% in eligible cohorts 2–5 years after 4CMenB was introduced[15]. Although there is no evidence that 4CMenB reduces N. meningitidis carriage[16], OMV meningococcal vaccines appear to provide some protection against IMD caused by non-MenB serogroups, as well as against N. gonorrhoeae[17,18]. Although 4CMenB and MenACWY vaccines are funded in New Zealand for a small number of persons with high-risk medical conditions and, recently, for adolescents in certain collective residences, no meningococcal vaccines are universally funded in the National Immunization Schedule. We aimed to describe the experience of pediatric IMD in Auckland during 2004–2020—including demographic factors; clinical, microbiological, and laboratory features; treatment; and outcomes—to demonstrate the impact of IMD on children in New Zealand and to highlight the need for funding of meningococcal vaccines.
