Epidemic Meningococcal Disease Research Articles

Neisseria meningitidis Sibling Small Regulatory RNAs Connect Metabolism with Colonization by Controlling Propionate Use.

Neisseria meningitidis (meningococcus) colonizes the human nasopharynx, primarily as a commensal, but sporadically causing septicemia and meningitis. During colonization and invasion, it encounters different niches with specific nutrient compositions. Small noncoding RNAs (sRNAs) are used to fine-tune expression of genes, allowing adaptation to their physiological differences. We have previously characterized sRNAs (Neisseria metabolic switch regulators [NmsRs]) controlling switches between cataplerotic and anaplerotic metabolism. Here, we extend the NmsR regulon by studying methylcitrate lyase (PrpF) and propionate kinase (AckA-1) involved in the methylcitrate cycle and serine hydroxymethyltransferase (GlyA) and 3-hydroxyacid dehydrogenase (MmsB) involved in protein degradation. These proteins were previously shown to be dysregulated in a ΔnmsRs strain. Levels of transcription of target genes and NmsRs were assessed by reverse transcriptase quantitative PCR (RT-qPCR). We also used a novel gene reporter system in which the 5' untranslated region (5' UTR) of the target gene is fused to mcherry to study NmsRs-target gene interaction in the meningococcus. Under nutrient-rich conditions, NmsRs downregulate expression of PrpF and AckA-1 by direct interaction with the 5' UTR of their mRNA. Overexpression of NmsRs impaired growth under nutrient-limiting growth conditions with pyruvate and propionic acid as the only carbon sources. Our data strongly suggest that NmsRs downregulate propionate metabolism by lowering methylcitrate enzyme activity under nutrient-rich conditions. Under nutrient-poor conditions, NmsRs are downregulated, increasing propionate metabolism, resulting in higher tricarboxylic acid (TCA) activities. IMPORTANCE Neisseria meningitidis colonizes the human nasopharynx, forming a reservoir for the sporadic occurrence of epidemic invasive meningococcal disease like septicemia and meningitis. Propionic acid generated by other bacteria that coinhabit the human nasopharynx can be utilized by meningococci for replication in this environment. Here, we showed that sibling small RNAs, designated NmsRs, riboregulate propionic acid utilization by meningococci and, thus, colonization. Under conditions mimicking the nasopharyngeal environment, NmsRs are downregulated. This leads to the conversion of propionic acid to pyruvate and succinate, resulting in higher tricarboxylic acid cycle activity, allowing colonization of the nasopharynx. NmsRs link metabolic state with colonization, which is a crucial step on the trajectory to invasive meningococcal disease.

Population structure of Neisseria meningitidis ST-9493 identified in Colombian isolates

IntroductionNeisseria meningitidis is associated with invasive infections causing high mortality rates. The objective of this study was to describe the population structure of Colombian invasive isolates with ST-9493, a potentially emerging clonal group in the country. MethodsThe complete genomes of 34 invasive isolates of serogroup B with ST-9493 and its variants at one or two loci were sequenced by Illumina to describe the phenotypic and genotypic characteristics of these isolates. ResultsThe relationship of a clonal group associated with ST-136 CC41/44 was phylogenetically established, identifying two main clades composed of isolates from an outbreak or endemic. The most frequent alleles and peptides included porA 17, porB 44, fHbp 2.24, NHBA 10, and the FetA F5-17 variant. Most of the isolates were susceptible to the antibiotics evaluated. ConclusionThis study shows that meningococcal isolates with ST-9493 are an autochthonous clonal group with population dynamics and the capacity to cause endemic and epidemic meningococcal disease in Colombia.

Population structure of Neisseria meningitidis ST-9493 identified in Colombian isolates

IntroductionNeisseria meningitidis is associated with invasive infections causing high mortality rates. The objective of this study was to describe the population structure of Colombian invasive isolates with ST-9493, a potentially emerging clonal group in the country. MethodsThe complete genomes of 34 invasive isolates of serogroup B with ST-9493 and its variants at one or two loci were sequenced by Illumina to describe the phenotypic and genotypic characteristics of these isolates. ResultsThe relationship of a clonal group associated with ST-136 CC41/44 was phylogenetically established, identifying two main clades composed of isolates from an outbreak or endemic. The most frequent alleles and peptides included porA 17, porB 44, fHbp 2.24, NHBA 10, and the FetA F5-17 variant. Most of the isolates were susceptible to the antibiotics evaluated. ConclusionThis study shows that meningococcal isolates with ST-9493 are an autochthonous clonal group with population dynamics and the capacity to cause endemic and epidemic meningococcal disease in Colombia.

Efficacy and Effectiveness of the Meningococcal Conjugate Group A Vaccine MenAfriVac® in Preventing Recurrent Meningitis Epidemics in Sub-Saharan Africa.

For more than a century, epidemic meningococcal disease mainly caused by serogroup A Neisseria meningitidis has been an important public health problem in sub-Saharan Africa. To address this problem, an affordable meningococcal serogroup A conjugate vaccine, MenAfriVac®, was developed specifically for populations in the African meningitis belt countries. MenAfriVac® was licensed based on safety and immunogenicity data for a population aged 1–29 years. In particular, the surrogate markers of clinical efficacy were considered to be the higher immunogenicity and the ability to prime immunological memory in infants and young children compared to a polysaccharide vaccine. Because of the magnitude of serogroup A meningitis epidemics and the high morbidity and mortality burden, the World Health Organization (WHO) recommended the MenAfriVac® deployment strategy, starting with mass vaccination campaigns for 1–29-year-olds to rapidly interrupt serogroup A person-to-person transmission and establish herd protection, followed by routine immunization of infants and toddlers to sustain protection and prevent epidemics. After licensure and WHO prequalification of MenAfriVac®, campaigns began in December 2010 in Burkina Faso, Mali, and Niger. By the middle of 2011, it was clear that the vaccine was highly effective in preventing serogroup A carriage and disease. Post introduction meningitis surveillance revealed that serogroup A meningococcal disease had disappeared from all age groups, suggesting that robust herd immunity had been achieved.

Meningococcal strain evolution, dusty dry air and respiratory tract infections: An explosive relationship.

Meningococcal strain evolution, dusty dry air and respiratory tract infections: An explosive relationship.

Increased Risk of MenB Infection in College Students: Time to Reconsider Vaccine Recommendations?

* Abbreviation: MenB — : serogroup B meningococcal Meningococcal infections can be fulminant and result in death only a few hours after symptom onset. The mortality rate ranges between 10% and 15%, and those who survive can have severe sequelae.1 Globally, it is estimated that 1.2 million cases of invasive meningococcal infections occur annually and result in 135 000 deaths.2 Primary prevention of disease through vaccination is essential for control of endemic and epidemic meningococcal disease. Serogroup B meningococcal (MenB) infections account for 65% of cases in infants in the United States (incidence: 3.3 cases per 100 000) and the majority of cases overall in some European countries, including England.2 In 2014 and 2015, 2 recombinant MenB vaccines were licensed in the United States for individuals 10 to 25 years of age.2 MenB vaccines are currently recommended routinely for high-risk groups in the appropriate age category (Category A recommendation) and may be considered in adolescents and young adults (Category B recommendation). In this issue of Pediatrics , Mbaeyi et al3 used the enhanced meningococcal disease … Address correspondence to Lucila Marquez, MD, MPH, Department of Pediatrics, Baylor College of Medicine, 1102 Bates Ave, Suite 1150, Houston, TX 77030. E-mail: lm043062{at}bcm.edu

Elimination of Epidemic Meningitis in the African Region: Progress and Challenges:2010-2016

Epidemics of meningococcal disease constitute a major public health challenge in Africa, affecting mostly the 24 countries of the meningitis belt. These epidemics led to a call for a call for a safe, effective and affordable conjugate vaccine against the major serogroup responsible for recent epidemics by leaders of the region. This paper documents experiences with efforts at eliminating epidemic meningitis in the African Region. The meningoccocal serogroup A conjugate vaccine was developed, licensed and offered to more than 235 million people through mass vaccination campaigns in 16 countries since 2010. Future plans include providing the vaccine to the remaining countries in the African Meningitis Belt and, to implement the vaccine into routine national infant immunization programme and to organise catch-up immunization campaigns every 5 years for unvaccinated <5 year-olds who had missed their routine vaccinations. The success of the project is evidenced by the large declines in cases of group A meningococcal disease since 2010, with no cases reported in vaccinated persons across the 16 countries, reflecting the highly effective nature of the vaccine. The successful control of serogroup A meningococcal disease has highlighted the need to tackle other meningococcal serogroups through development of polyvalent conjugate vaccines with the aim of eliminating epidemics of meningococcal meningitis in the African region.

Acquisition of virulence genes by a carrier strain gave rise to the ongoing epidemics of meningococcal disease in West Africa.

In the African meningitis belt, a region of sub-Saharan Africa comprising 22 countries from Senegal in the west to Ethiopia in the east, large epidemics of serogroup A meningococcal meningitis have occurred periodically. After gradual introduction from 2010 of mass vaccination with a monovalent meningococcal A conjugate vaccine, serogroup A epidemics have been eliminated. Starting in 2013, the northwestern part of Nigeria has been affected by yearly outbreaks of meningitis caused by a novel strain of serogroup C Neisseria meningitidis (NmC). In 2015, the strain spread to the neighboring country Niger, where it caused a severe epidemic. Following a relative calm in 2016, the largest ever recorded epidemic of NmC broke out in Nigeria in 2017. Here, we describe the recent evolution of this new outbreak strain and show how the acquisition of capsule genes and virulence factors by a strain previously circulating asymptomatically in the African population led to the emergence of a virulent pathogen. This study illustrates the power of long-read whole-genome sequencing, combined with Illumina sequencing, for high-resolution epidemiological investigations.

A Seroepidemiological Study of Serogroup A Meningococcal Infection in the African Meningitis Belt

The pattern of epidemic meningococcal disease in the African meningitis belt may be influenced by the background level of population immunity but this has been measured infrequently. A standardised enzyme-linked immunosorbent assay (ELISA) for measuring meningococcal serogroup A IgG antibodies was established at five centres within the meningitis belt. Antibody concentrations were then measured in 3930 individuals stratified by age and residence from six countries. Seroprevalence by age was used in a catalytic model to determine the force of infection. Meningococcal serogroup A IgG antibody concentrations were high in each country but showed heterogeneity across the meningitis belt. The geometric mean concentration (GMC) was highest in Ghana (9.09 μg/mL [95% CI 8.29, 9.97]) and lowest in Ethiopia (1.43 μg/mL [95% CI 1.31, 1.57]) on the margins of the belt. The force of infection was lowest in Ethiopia (λ = 0.028). Variables associated with a concentration above the putative protective level of 2 μg/mL were age, urban residence and a history of recent vaccination with a meningococcal vaccine. Prior to vaccination with the serogroup A meningococcal conjugate vaccine, meningococcal serogroup A IgG antibody concentrations were high across the African meningitis belt and yet the region remained susceptible to epidemics.

Meningococcal serogroup A, C, W, and Y serum bactericidal antibody profiles in Hajj pilgrims

The religious seasons of Hajj and Umra in the Kingdom of Saudi Arabia (KSA) have historically been associated with epidemics of meningococcal disease. Due to the effective preventive measures taken in recent years, including vaccination, no meningococcal outbreaks have been reported during Hajj or were Hajj-associated. However, little is known about the immunological profile of pilgrims. The aim of this study was to assess the immunological profile of pilgrims on arrival in KSA against the four meningococcal serogroups, A, C, W, and Y, contained within the quadrivalent vaccine. Following consent, socio-demographic factors and health-related information was collected from pilgrims arriving at King Abdul Aziz International Airport and a blood sample taken. Antibodies were quantified by serum bactericidal antibody assay using baby rabbit complement (rSBA) against the four meningococcal serogroups, A, C, W, and Y. Serum samples were collected from 796 pilgrims; rSBA results were obtained for all four serogroups for 741 of these samples. A total of 48 (6.5%) Hajjis had previously attended Hajj, ranging from 1 to 14 times (median 2 times); 98.2% had received meningococcal quadrivalent vaccine in the last 3 years. Of the 13 who had not, all originated from Bangladesh, with four reporting no previous meningococcal vaccination and nine reporting having received the vaccination more than 3 years ago. For serogroup A, only one pilgrim from Indonesia had an rSBA titre <8. For serogroups C, W, and Y, the percentages of pilgrims with rSBA titres <8 were 9.9%, 17.4%, and 9.4%, respectively. Of note was the high prevalence of non-complement-mediated lysis in pilgrims originating from Nigeria (28/47; 59.6%) and Afghanistan (21/47; 44.7%), but not the other countries. This may be a reflection of the type and pattern of antibiotic usage among these communities. The vast majority of pilgrims are vaccinated and protected against meningococcal serogroups A, C, W, and Y.

Prevalence and genetic diversity of two adhesion-related genes, pilE and nadA, in Neisseria meningitidis in China.

The main Neisseria meningitidis adhesion molecules, type IV pili (Tfp) and Neisseria adhesion A (NadA), play important roles in the pathogenesis of invasive meningococcal disease. PilE is the major Tfp subunit. In this study, the prevalence and genetic diversity of pilE and nadA were investigated in the prevalent serogroups and clonal complexes (CC) of N. meningitidis isolated in China. All serogroup A strains belonging to CC1 and CC5 and all CC11 serogroup W135 strains were clustered into class II PilE clades. All serogroup C and most of serogroup B isolates except CC8 and ST5642 were class I PilE clades. Class II pilE sequences were highly conserved. All isolates belonging to class I PilE isolates were nadA negative. However, nadA-positive strains were exclusively found in CC5 and CC11 isolates (class II PilE). This study showed that PilE and NadA may be related to epidemic or endemic meningococcal disease.

Editorial Commentary: The Endgame for Serogroup A Meningococcal Disease in Africa?

Editorial Commentary: The Endgame for Serogroup A Meningococcal Disease in Africa?

Effectively introducing a new meningococcal A conjugate vaccine in Africa: The Burkina Faso experience

A new Group A meningococcal (Men A) conjugate vaccine, MenAfriVac™, was prequalified by the World Health Organization (WHO) in June 2010. Because Burkina Faso has repeatedly suffered meningitis epidemics due to Group A Neisseria meningitidis special efforts were made to conduct a country-wide campaign with the new vaccine in late 2010 and before the onset of the next epidemic meningococcal disease season beginning in January 2011. In the ensuing five months (July–November 2010) the following challenges were successfully managed: (1) doing a large safety study and registering the new vaccine in Burkina Faso; (2) developing a comprehensive communication plan; (3) strengthening the surveillance system with particular attention to improving the capacity for real-time polymerase chain reaction (PCR) testing of spinal fluid specimens; (4) improving cold chain capacity and waste disposal; (5) developing and funding a sound campaign strategy; and (6) ensuring effective collaboration across all partners. Each of these issues required specific strategies that were managed through a WHO-led consortium that included all major partners (Ministry of Health/Burkina Faso, Serum Institute of India Ltd., UNICEF, Global Alliance for Vaccines and Immunization, Meningitis Vaccine Project, CDC/Atlanta, and the Norwegian Institute of Public Health/Oslo). Biweekly teleconferences that were led by WHO ensured that problems were identified in a timely fashion. The new meningococcal A conjugate vaccine was introduced on December 6, 2010, in a national ceremony led by His Excellency Blaise Compaore, the President of Burkina Faso. The ensuing 10-day national campaign was hugely successful, and over 11.4 million Burkinabes between the ages of 1 and 29 years (100% of target population) were vaccinated. African national immunization programs are capable of achieving very high coverage for a vaccine desired by the public, introduced in a well-organized campaign, and supported at the highest political level. The Burkina Faso success augurs well for further rollout of the Men A conjugate vaccine in meningitis belt countries.

Critical episodes in the understanding and control of epidemic meningococcal meningitis

Epidemic meningococcal meningitis continues to be an important worldwide cause of morbidity and mortality, especially in developing countries. Throughout its relatively brief history, especially over the past century, a number of ‘critical episodes’ have occurred that have enhanced our understanding of the disease and allowed for its potential control. This article reviews three such ‘episodes’: the first effective treatment for the disease; the development of the first effective meningococcal vaccine; and the description of its epidemiology in sub-Saharan Africa, where the majority of epidemic meningococcal disease continues to occur. These historical ‘episodes’ have informed current strategies that may lead to eventual control of epidemic meningococcal meningitis.

Invasive meningococcal disease and travel

The epidemiology of invasive meningococcal disease varies geographically and in time and the risk of acquiring the disease varies regionally, as well as with living conditions and behavior. An area, in which meningococcal disease outbreaks have frequently occurred, is the "African meningitis belt", where epidemics of meningococcal disease with a peak incidence as high as 100-800/100,000 population/year have been reported. Another risk factor is mass gatherings including the Islamic pilgrimage to Makkah (Mecca), where outbreaks of meningococcal disease have repeatedly occurred. The latest outbreaks occurred during the Hajj pilgrimages of 2000 and 2001, when a shift from serogroup A disease to serogroup W135 occurred. Vaccination against serogroups A, C, W-135 and Y with novel conjugate vaccines may help protect individuals and reduce the spread of bacterial carriage and disease. Individuals who should be vaccinated include travelers to epidemic or hyperendemic areas (as identified by international health authorities), travelers for Umra or Hajj (Hajj pilgrims), travelers to high risk countries or regions (African meningitis belt) during the dry season or countries in sub-Saharan Africa outside the meningitis belt (where outbreak of meningitis has been reported in the preceding 2-3 years), military recruits or deployed military personnel, immunocompromized travelers and high school and college students. This review presents the global epidemiology of meningococcal disease, and discusses prophylaxis options including meningococcal ACWY vaccines.

The epidemiology of meningococcal disease in India

To undertake a review of the literature on the epidemiology of meningococcal disease in India, with a view to informing future control policies. We searched the PUBMED, EMBASE, Global Health, IMSEAR and MedIND databases for observational studies relating to the burden of endemic meningococcal disease in India, the occurrence and epidemiological characteristics of epidemics, and the prevalence of individual meningococcal serogroups. The relatively few reports identified suggest that the incidence of endemic meningococcal disease in India is low, but that occasional epidemics of meningococcal disease have been recorded for at least 100 years. The larger epidemics have affected mainly the cities of northern India and have almost universally been caused by meningococci belonging to serogroup A. These epidemics have showed a few characteristics, including a marked seasonality, which are similar to those of epidemic meningococcal A disease in Africa. New serogroup A-containing meningococcal conjugate vaccines are now being developed and reaching the market, including an affordable monovalent serogroup A vaccine manufactured in India, but intended primarily for use in Africa. These new tools may have a role in containing future Indian epidemics, but their usefulness is dependent on early identification of epidemics. This will require a functional disease surveillance system with adequate laboratory support throughout India.

Direct Bacterial Profiling by Matrix-Assisted Laser Desorption−Ionization Time-of-Flight Mass Spectrometry for Identification of Pathogenic Neisseria

The present study investigates the suitability of direct bacterial profiling as a tool for the identification and subtyping of pathogenic Neisseria. The genus Neisseria includes two human pathogens, Neisseria meningitidis and Neisseria gonorrhoeae, as well as several nonpathogenic Neisseria species. Here, a matrix-assisted laser desorption/ionization time-of-flight mass spectrometry profiling protocol was optimized using a laboratory strain of E. coli DH5alpha to guarantee high quality and reproducible results. Subsequently, mass spectra for both laboratory and clinical strains of N. gonorrhoeae, N. meningitidis, and several nonpathogenic Neisseria species were collected. Significant interspecies differences but little intraspecies diversity were revealed by means of a visual inspection and bioinformatics examination using the MALDI BioTyper software. Cluster analysis successfully separated mass spectra collected from three groups that corresponded to N. gonorrhoeae, N. meningitidis, and nonpathogenic Neisseria isolates. Requiring only one bacterial colony for testing and using a fast and easy measuring protocol, this approach represents a powerful tool for the rapid identification of pathogenic Neisseria and can be adopted for other microorganisms.

Use of an observational cohort study to estimate the effectiveness of the New Zealand group B meningococcal vaccine in children aged under 5 years

In July 2004 a strain-specific vaccine was introduced to combat an epidemic of group B meningococcal disease in New Zealand. We estimated the effectiveness of this vaccine in pre-school-aged children. We conducted a cohort analysis of all children in New Zealand who were aged 6 months to <5 years at the time the vaccine became available for that age group in their area. We defined cases as children who were diagnosed with laboratory-confirmed epidemic strain meningococcal disease. We calculated person-days-at-risk using data from the National Immunization Register and population estimates from Statistics New Zealand. We estimated vaccine effectiveness as 1--relative risk. Compared with unvaccinated children, fully vaccinated children were five to six times less likely to contract epidemic strain meningococcal disease in the 24 months after they became eligible to receive a full vaccination series, corresponding to an estimated vaccine effectiveness of 80.0% (95% confidence interval: 52.5-91.6) for children aged 6 months to <5 years and 84.8% (95% confidence interval: 59.4-94.3) for children aged 6 months to <3 years. With over 3 million doses administered to individuals aged under 20 years throughout New Zealand, combined evidence from the Phase I and II clinical trials, the descriptive epidemiology of meningococcal disease, and this study provide evidence supporting the effectiveness of this vaccine in the 2 years following vaccination.

Systematic review: Impact of meningococcal vaccination on pharyngeal carriage of meningococci

To investigate the effect of meningococcal vaccines on pharyngeal carriage of meningococci. Systematic review. MEDLINE and EMBASE were searched for relevant studies. Controlled trials and observational studies which used comparison groups or compared carriage rates before and after vaccination were included in the review. Twenty-nine studies satisfied the inclusion criteria. Twenty-five studies reported the effect of a polysaccharide vaccine, one the effect of a serogroup C conjugate vaccine and three the impact of serogroup B outer-membrane vaccines on overall and/or serogroup-specific meningococcal carriage rates. Ten studies of meningococcal polysaccharide vaccines found reduced serogroup-specific carriage; seven of these focussed on high-risk groups and had a short follow-up period. Only one of five studies of civilian populations in Africa showed a significantly reduced carriage. Many studies had methodological shortcomings. The one study which assessed the effect of a meningococcal conjugate vaccine on carriage showed a significant impact. Three studies of serogroup B outer-membrane protein vaccines showed no effect on carriage. A few well-designed trials of the impact of meningococcal vaccines on carriage have been undertaken. Such studies should be an essential component of the evaluation of new meningococcal vaccines, particularly those introduced to control epidemic meningococcal disease in Africa.

Serogroup X in Meningococcal Disease, Western Kenya

To the Editor: Although >12 different serogroups of Neisseria meningitidis exist, most disease outbreaks across the African meningitis epidemic belt are caused by serogroup A and, less frequently, by serogroups C and W135 (1). N. meningitidis serogroup X was first described in the 1960s and has been found to cause a few cases of invasive disease across North America, Europe, and Africa (2). In Africa, small serogroup X outbreaks have been described in Ghana (9 cases over a 2-year period) and in Niger (134 cases between 1995 and 2000) (3,4). In 2006, however, 51% of 1,139 confirmed cases of meningococcal meningitis in Niger were found to be caused by serogroup X (5). Before the 2005-06 meningococcal epidemic season, no published reports had described serogroup X isolates in East Africa. We report the involvement of N. meningitidis serogroup X in an outbreak of meningococcal disease in Western Kenya. In January 2006, the Ministry of Health of Kenya and Medecins sans Frontieres were notified of a suspected meningococcal disease outbreak in West Pokot District, bordering Uganda, in Western Kenya. On the basis of the initial outbreak investigation, the outbreak was assessed to have begun in late December 2005. Subsequent active surveillance, using the same clinical case definition of sudden fever onset with stiff neck, altered mental status, or both, showed 74 suspected cases through mid-March 2006, with a case-fatality rate of 20%. No cases were reported after March 2006. Over the course of the outbreak, cerebrospinal fluid samples were obtained from 18 patients. Due to low population density, poor access to seminomadic populations, and the limited nature of the outbreak (relatively small numbers dispersed over a wide geographic region), obtaining specimens from untreated patients in West Pokot proved difficult. Three of the 5 first samples were found to show gram-negative diplococci on staining, the next 2 were negative on Pastorex rapid latex agglutination test (Bio-Rad Laboratories, Hercules, CA, USA) (during the outbreak investigation), and a subsequent 13 were sent to the African Medical and Research Foundation (AMREF) laboratory in Nairobi, Kenya, for culture and susceptibility testing. From these 13 specimens, 2 yielded a pure growth of N. meningitidis serogroup X, while no growth was observed for the remaining 11 specimens. These 2 cultures were subsequently confirmed as serogroup X by the World Health Organization Collaborating Centre for Meningococci in Oslo, Norway. Multilocus sequence typing and sequencing of the porA and fetA genes as described (http://pubmlst.org/neisseria/), showed that the infecting strain belonged to a new sequence type, ST-5403, and that it was subtype P1.19,26 and FetA type F3-27. This sequence type is unrelated to other serogroup X isolates from Africa, including those from the latest serogroup X outbreak in Niger, but it resembles a sequence type isolated in the United States in the 1970s. In addition to the testing at AMREF and in the Oslo laboratory, the 13 samples were also analyzed by PCR at the US Naval Medical Research Unit No. 3 in Cairo, Egypt. Overall, 5 of these 13 specimens were positive for serogroup X (including the 2 samples found to be serogroup X at AMREF and confirmed by PCR in Oslo) and 1 each was positive for serogroups C, W135, and Y. At the same time as this outbreak in Western Kenya, a meningococcal meningitis outbreak was being monitored across the border in the Karamoja region of northeastern Uganda. Seminomadic populations move freely across the 2 countries, and we can assume that there was 1 meningitis outbreak that started in eastern Uganda and spread to Western Kenya. Although initial laboratory testing in Uganda suggested the presence of serogroup A, among 23 specimens subsequently sent to the Oslo laboratory, 11 were identified as serogroup X by PCR and 3 were serogroup W135 (6). Therefore, the outbreaks in both Kenya and Uganda involved multiple N. meningitidis serogroups. In West Pokot, Kenya, the Ministry of Health and Medecins sans Frontieres conducted a vaccination campaign using the trivalent polysaccharide vaccine against serogroups A, C, and W135. Before 2006, previous disease outbreaks caused by serogroup X had not reached the magnitude of those caused by serogroups A, C, or W135; they tended to evolve independently of the occurrence of both serogroups A and C and to be self-limited (3,4). Although most of Kenya is not included in the African meningitis belt, large epidemics of meningococcal disease have been reported previously (7). In conclusion, we would like to highlight the presence of N. meningitidis serogroup X in East Africa, its potential involvement in disease outbreaks, and the difficulties it may cause for laboratory confirmation and, consequently, for making an appropriate epidemic response.