Meningococcal carriage in the African Meningitis Belt
ABSTRACT In the African meningitis belt, epidemics of meningococcal disease occur periodically, although unpredictably, every few years. These epidemics continue to cause havoc but new efforts to control the disease, through the use of conjugate vaccines, are being made. Conjugate vaccines are likely to reduce meningococcal carriage, thus generating herd immunity, but to understand their potential impact we need to know more about the epidemiology of meningococcal carriage in Africa. We review published studies of meningococcal carriage in the African meningitis belt. A wide range of carriage prevalences has been reported, from 3% to over 30%, and the serogroup distribution has been variable. Factors influencing carriage include age, contact with a case, and the epidemic/endemic situation; however, season and immunisation with polysaccharide vaccine have little effect. Since the dynamics of carriage within a population are complex, longitudinal carriage studies are of great value; however, few such studies have been done. Carefully designed carriage studies are needed to measure and interpret the impact of meningococcal group A conjugate vaccines in Africa.
Full-textDOI: · Available from: Caroline L Trotter, Sep 04, 2015
- SourceAvailable from: Martin C J Maiden
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- "At the time of writing, the continued rollout of MenAfriVac across the meningitis belt has presented the prospect of the elimination of epidemic serogroup A meningococcal disease . For the maintenance of vaccine effectiveness, however, it is important know the rates and dynamics of carriage across the meningitis belt, which remains poorly understood and which is unlike meningococcal carriage in high-income countries [101,106]. The MenAfriCar consortium (http://www.menafricar.org) "
ABSTRACT: The development and implementation of conjugate polysaccharide vaccines against invasive bacterial diseases, specifically those caused by the encapsulated bacteria Neisseria meningitidis, Haemophilus influenzae and Streptococcus pneumoniae, has been one of the most effective public health innovations of the last 25 years. These vaccines have resulted in significant reductions in childhood morbidity and mortality worldwide, with their effectiveness due in large part to their ability to induce long-lasting immunity in a range of age groups. At the population level this immunity reduces carriage and interrupts transmission resulting in herd immunity; however, these beneficial effects can be counterbalanced by the selection pressures that immunity against carriage can impose, potentially promoting the emergence and spread of virulent vaccine escape variants. Studies following the implementation of meningococcal serogroup C vaccines improved our understanding of these effects in relation to the biology of accidental pathogens such as the meningococcus. This understanding has enabled the refinement of the implementation of conjugate polysaccharide vaccines against meningitis-associated bacteria, and will be crucial in maintaining and improving vaccine control of these infections. To date there is little evidence for the spread of virulent vaccine escape variants of the meningococcus and H. influenzae, although this has been reported in pneumococci.Philosophical Transactions of The Royal Society B Biological Sciences 08/2013; 368(1623):20120147. DOI:10.1098/rstb.2012.0147 · 6.31 Impact Factor
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- "Bacteria are transmitted from person-to-person through droplets of respiratory or throat secretions, primarily from asymptomatic carriers. Invasive disease is a rare outcome, while carriage prevalence estimates of N. meningitidis in the meningitis belt range from 3% to 30%, varying by age and season , . "
ABSTRACT: The optimal long-term vaccination strategies to provide population-level protection against serogroup A Neisseria meningitidis (MenA) are unknown. We developed an age-structured mathematical model of MenA transmission, colonization, and disease in the African meningitis belt, and used this model to explore the impact of various vaccination strategies. The model stratifies the simulated population into groups based on age, infection status, and MenA antibody levels. We defined the model parameters (such as birth and death rates, age-specific incidence rates, and age-specific duration of protection) using published data and maximum likelihood estimation. We assessed the validity of the model by comparing simulated incidence of invasive MenA and prevalence of MenA carriage to observed incidence and carriage data. The model fit well to observed age- and season-specific prevalence of carriage (mean pseudo-R2 0.84) and incidence of invasive disease (mean R2 0.89). The model is able to reproduce the observed dynamics of MenA epidemics in the African meningitis belt, including seasonal increases in incidence, with large epidemics occurring every eight to twelve years. Following a mass vaccination campaign of all persons 1-29 years of age, the most effective modeled vaccination strategy is to conduct mass vaccination campaigns every 5 years for children 1-5 years of age. Less frequent campaigns covering broader age groups would also be effective, although somewhat less so. Introducing conjugate MenA vaccine into the EPI vaccination schedule at 9 months of age results in higher predicted incidence than periodic mass campaigns. We have developed the first mathematical model of MenA in Africa to incorporate age structures and progressively waning protection over time. Our model accurately reproduces key features of MenA epidemiology in the African meningitis belt. This model can help policy makers consider vaccine program effectiveness when determining the feasibility and benefits of MenA vaccination strategies.PLoS ONE 05/2013; 8(5):e63605. DOI:10.1371/journal.pone.0063605 · 3.23 Impact Factor
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- "Globally, N. meningitidis causes an estimated 1.2 million cases and 135,000 deaths each year [1-3]. In Africa, N. meningitidis is the leading cause of severe, life-threatening meningitis and is responsible for thousands of cases and scores of deaths across sub-Saharan “meningitis belt” countries [4-7]. Moreover, N. meningitidis serogroups A and W-135 have been exported from Asia to other regions . "
ABSTRACT: Background To understand epidemiologic patterns of meningococcal disease in Asia, we performed a retrospective molecular analysis of cerebrospinal fluid (CSF) specimens collected in prospective surveillance among children aged < 5 years of age in China, South Korea, and Vietnam. Methods A total of 295 isolates and 2,302 CSFs were tested by a meningococcal species- and serogroup-specific polymerase chain reaction (PCR) assay targeting the Neisseria meningitidis (Nm) ctrA gene. Multi-locus sequence typing (MLST) was performed in Nm gene amplification analysis and incidence rates for meningococcal meningitis were estimated. Results Among 295 isolates tested, 10 specimens from Vietnam were confirmed as serogroup B and all were Sequence Type (ST) 1576 by MLST. Among the 2,032 CSF specimen tested, 284 (14%) were confirmed by PCR (ctrA gene), including 67 (23.6%) from China, 92 (32.4%) from Korea, and 125 (44.0%) from Vietnam. Neonates and infants aged < 6 months of age accounted for more than 50% of Nm-PCR positive CSF. Two CSF specimens from Vietnam were identified as serogroup B using MLST. In addition, 44 specimens underwent sequencing to confirm meningococcal serogroup; of these, 21 (48%) were serogroup C, 12 (27%) were serogroup X, 9 (20%) were serogroup Y and 2 (5%) were serogroup B. The incidence rates of meningococcal meningitis among children < 5 years of age was highest in Vietnam (7.4/100,000 [95% CI, 3.6—15.3] followed by Korea (6.8/100,000 [95% CI, 3.5-13.5] and China (2.1/100,000) [95% CI, 0.7-6.2]). Conclusions These results suggest that there is a previously undetected, yet substantial burden of meningococcal meningitis among infants and young children. Standardized, sensitive and specific molecular diagnostic assays with Nm serogrouping capacity are needed throughout Asia to understand the true burden of N. meningitidis disease.BMC Infectious Diseases 11/2012; 12(1):310. DOI:10.1186/1471-2334-12-310 · 2.61 Impact Factor