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.

Complement component C5 and C6 mutation screening indicated in meningococcal disease in South Africa.

BACKGROUND: Invasive meningococcal disease (MD), caused by Neisseria meningitidis infection, is endemic in South Africa, with a seasonal peak in winter and spring. There were 2 432 laboratory-confirmed cases between 2006 and 2010. Human deficiency of the fifth complement component (C5D) or complete absence of the sixth component (C6Q0) leads to increased risk of MD, which is often recurrent. All attacks are serious and can lead to death or severe long-term consequences. OBJECTIVE: To determine the frequency of specific disease-associated C5 and C6 gene mutations in patients presenting with MD in the Western Cape. RESULTS: In 109 patients with confirmed invasive MD investigated for local mutations known to cause C5D and C6Q0, 3 were C5D and 11 were C6Q0. In 46 black patients tested, 3 were C5D and 7 were C6Q0. In 63 coloured patients, none were C5D and 4 were C6Q0. All deficient patients were followed up and offered prophylaxis. CONCLUSION: C5D and C6Q0 are not rare genetic diseases in South Africa and affected patients are susceptible to repeated MD; 12.8% of MD patients tested were C5D or C6Q0. Blacks were at greatest risk with 21.7% being either C5D or C6Q0. We strongly recommend diagnostic testing for complement C5 and C6 deficiency in the routine work-up of all MD cases in South Africa. Prophylactic treatment should be started in susceptible individuals.

Reducing inequalities with vaccines: New Zealand's MeNZB vaccine initiative to control an epidemic.

Disadvantaged children of Maori and Pacific origin in New Zealand carry an inequitable burden of infectious diseases, many of which are preventable, some by vaccine. Immunisation is recognised in the developing world as a cheap, effective and efficient means of reducing inequalities. The MeNZB immunisation programme delivered in 2004-2006 towards the expected natural end of a projected 15-year epidemic appears to have had an effect (difficult to prove conclusively) on reducing the disproportionate burden of meningococcal disease carried by this group of children. It was delayed by the late engagement of the New Zealand Ministry of Health, fully briefed from 1996, leading to unnecessary and potentially avoidable deaths and sequelae, many lifelong. Further, failure to adequately assess vaccine effectiveness means that the contribution of MeNZB to the observed reduction in disease, particularly in those aged less than five years, will never be reliably known. However, the MeNZB campaign has at least left a legacy: the National Immunisation Register, which should enable New Zealand to minimise the 'vaccine inverse care law' and contribute to reducing ethnic inequity in the burden of vaccine preventable diseases.

Hajj-associated outbreak strain of Neisseria meningitidis serogroup W135: estimates of the attack rate in a defined population and the risk of invasive disease developing in carriers.

An outbreak of disease due to Neisseria meningitidis serogroup W135 (W135) occurred in 2000 and 2001 among pilgrims returning from the annual Islamic pilgrimage to Saudi Arabia (the Hajj) and in their contacts. For the Hajj in 2000, the attack rate of W135 disease was 25 cases per 100,000 pilgrims. After the introduction of quadrivalent meningococcal vaccine for the Hajj in 2001, no pilgrim developed W135 disease. The estimated attack rates for household contacts of returning pilgrims were 18 cases and 28 cases per 100,000 contacts for the years 2000 and 2001, respectively. On the basis of rates of transmission of W135 carriage and national epidemiological data, the risk that an unvaccinated household contact who had acquired W135 carriage would develop invasive meningococcal disease was estimated to be 1 case per 70 acquisitions. Public health policies to protect household contacts of Hajj pilgrims need to be implemented.

Meningococcal disease among children of Indian subcontinent ethnic origin.

The rate of meningococcal septicaemia and meningitis was significantly lower in children of Indian subcontinent ethnic origin than in children of other origins over 12 years in the Blackburn area of the UK.

Control of group C meningococcal disease in Australian aboriginal children by mass rifampicin chemoprophylaxis and vaccination.

An outbreak of 12 cases of meningitis, 11 caused by Neisseria meningitidis serogroup C, occurred at Doomadgee from September, 1990, to April, 1991. The incidence of meningitis was 17.55/10(3) person-years. Only children aged 1-10 years were affected. In October, 1990, or shortly thereafter, 473/509 children aged between 1 and 15 years inclusive had one dose of Mencevax AC. From the time of vaccination until April, 1991, a further eight cases occurred, six in vaccinated children. Vaccine efficacy in 1-15 year olds was calculated as 77%. Despite this, in April, 1991, the prevalence of antibody to group C polysaccharide in vaccinated children (78%) was not significantly different from that in unvaccinated children and adults. 46 nonresponders were revaccinated, and, in February, 1992, 78% had antibodies to group C polysaccharide. In April, 1991, an estimated 3.0% of the population had group C organisms, carriage being directly related to household crowding. In June, 1991, 2 months after mass prophylaxis with rifampicin, none of these individuals were carriers. In October, 1991, the carriage rate of group C organisms was 0.64%. There have been no further cases caused by the epidemic strain. Although uncrowded housing is a basic need, mass chemoprophylaxis and two doses of vaccine for children should be used in similar outbreaks.

Epidemiology of pediatric meningitis caused by Haemophilus influenzae B, Streptococcus pneumoniae and Neisseria meningitidis in Israel.

Bacterial meningitis remains a serious cause of morbidity and mortality in childhood. We report 3 year data on meningitis caused by Haemophilus influenzae b, Streptococcus pneumoniae and Neisseria meningitidis in Israeli children younger than 13 years of age. The data were obtained prospectively through an active surveillance system involving all 25 centers in which children are hospitalized. A case was defined by: a) culture positive cerebrospinal fluid; or b) positive blood culture with > 10 cells. During the study period, 482 cases of meningitis due to the three organisms were identified. Of these, 58%, 20% and 22% were caused by H. influenzae b, S. pneumoniae and N. meningitidis, respectively. The male/female ratio was 1.5:1. An over-representation of the non-Jewish population was seen only in cases caused by S. pneumoniae. The median age was 11 months and 59% of all cases occurred by the age of 12 months. The median age was 10, 12 and 36 months and the age-specific incidence for children aged 0-4 years was 18.5, 5.3 and 5.2 per 100,000, respectively, for H. influenzae b, S. pneumoniae and N. meningitidis. The chance of being hospitalized with meningitis during the first 5 years of life was estimated at 146.2 per 100,000. Meningitis was seasonal: 59% al all cases occurred during fall and winter and only 18% during summer. A total of 2,097 hospitalization days were required when extrapolated to a population in which 100,000 live births occur yearly. The case fatality rate was 2.2%, 5.9% and 6.3% for H. influenzae b, S. pneumoniae and N. meningitidis, respectively, with a higher fatality in females and non-Jews.

Epidemiology of pediatric meningitis caused by Haemophilus influenzae type b, Streptococcus pneumoniae, and Neisseria meningitidis in Israel: a 3-year nationwide prospective study. Israeli Pediatric Bacteremia and Meningitis Group.

In a 3-year nationwide prospective study on pediatric meningitis caused by Haemophilus influenzae type b, Streptococcus pneumoniae, and Neisseria meningitidis in Israel, 1258 invasive infections with a known focus were observed. Meningitis was found in 482 (38%): 56%, 16%, and 76% of all infections by H. influenzae type b, S. pneumoniae, and N. meningitidis, respectively. The incidence of meningitis during the first year of life was 67.1, 17.5, and 9.5/100,000 for H. influenzae type b, S. pneumoniae, and N. meningitidis, respectively, and in children < 5 years old it was 18.5, 5.3, and 5.2. Extrapolated for a population in which 100,000 live births occur yearly, 2097 hospital days were required. The case fatality rate was 2.2%, 5.9%, and 6.3% for H. influenzae type b, S. pneumoniae, and N. meningitidis, respectively. Boys were affected significantly more often than girls, but mortality was higher among girls. On the basis of the observed serotypes and age distribution, even with optimal vaccine development in the next 5 years, it is not likely that > 50% of all cases will be prevented.

Differences in the epidemiology of childhood community-acquired bacterial meningitis between two ethnic populations cohabiting in one geographic area.

A comparison of the epidemiology of community-acquired bacterial meningitis between Jewish and Bedouin populations cohabiting one geographical area is reported here. During the years 1981 to 1985, 100 children younger than 13 years old with community-acquired bacterial meningitis were hospitalized. Seventy-one patients were younger than 12 months. The principal bacteria isolated were Haemophilus influenzae 42%; Streptococcus pneumoniae 29% and Neisseria meningitidis 20%. The case fatality rate was 12%. The chance of acquiring meningitis during the first 5 years of life was twice as common among Bedouins than among Jews (328/100,000 vs. 173/100,000, respectively; P less than 0.0001). The most common cause of meningitis during the first year of life was S. pneumoniae among Bedouins and H. influenzae among Jews. Meningitis caused by H. influenzae and S. pneumoniae was usually associated with respiratory morbidity during fall and winter among Jews, but with diarrheal morbidity during summer and fall among Bedouins. Since the most prevalent type of morbidity among Jews results from respiratory infections and among Bedouins from diarrhea, our findings suggest that community-acquired bacterial meningitis is associated with the type of morbidity most prevalent in the community at any given season rather than with a specific type of infection.