Epidemiological patterns of meningococcal meningitis in Niger in 2003 and 2004: under the threat of N. meningitidis serogroup W135

Since the Neisseria meningitidis serogroup W135 epidemic in Burkina Faso in 2002, the neighbouring countries dread undergoing outbreaks. Niger has strongly enhanced the microbiological surveillance, especially by adding the polymerase chain reaction (PCR) assay to the national framework of the surveillance system. During the 2003 epidemic season, 8113 clinically suspected cases of meningitis were notified and nine districts of the 42 crossed the epidemic threshold, while during the 2004 season, the number of cases was 3521 and four districts notified epidemics. In 2003 and 2004, serogroup A was identified in most N. meningitidis from cerebrospinal fluid (CSF) specimens (89.7% of 759 and 87.2% of 406, respectively). Although serogroup W135 represented only 8.3% of the meningococcal meningitis in 2003 and 7.9% in 2004, and was not involved in outbreaks, it was widespread in various areas of the country. In the regions that notified epidemics, the proportion of serogroup W135 was tiny while it exceeded 40% in several non-epidemic regions. Despite the wide distribution of W135 serogroup in Niger and the fears expressed in 2001, the threat of a large epidemic caused by N. meningitidis W135 seems to have been averted in Niger so far. There is no clear indication whether this serogroup will play a lasting role in the epidemiology of meningococcal meningitis or not. As early as in the 1990s, a significant but transient increase in the incidence of N. meningitidis serogroup X was observed. Close microbiological surveillance is crucial for monitoring the threat and for identifying at the earliest the serogroups involved in epidemics.     

Emergence of serogroup C meningococcal disease associated with a high mortality rate in Hefei, China

ABSTRACT: BACKGROUND: Neisseria meningitidis serogroup C has emerged as a cause of epidemic disease in Hefei. The establishment of serogroup C as the predominant cause of endemic disease has not been described. METHODS: We conducted national laboratory-based surveillance for invasive meningococcal disease during 2000--2010. Isolates were characterized by pulsed-field gel electrophoresis and multilocus sequence typing. RESULTS: A total of 845 cases of invasive meningococcal disease were reported. The incidence increased from 1.25 cases per 100,000 population in 2000 to 3.14 cases per 100,000 in 2003 (p < 0.001), and peaked at 8.43 cases per 100,000 in 2005. The increase was mainly the result of an increase in the incidence of serogroup C disease. Serogroup C disease increased from 2/23 (9%) meningococcal cases and 0.11 cases per 100,000 in 2000 to 33/58 (57%) cases and 1.76 cases per 100,000 in 2003 (p < 0.01). Patients infected with serogroup C had serious complications more frequently than those infected with other serogroups. Specifically, 161/493 (32.7%) cases infected with serogroup C had at least one complication. The case-fatality rate of serogroup C meningitis was 11.4%, significantly higher than for serogroup A meningitis (5.3%, p = 0.021). Among patients with meningococcal disease, factors associated with death in univariate analysis were age of 15--24 years, infection with serogroup C, and meningococcemia. CONCLUSIONS: The incidence of meningococcal disease has substantially increased and serogroup C has become endemic in Hefei. The serogroup C strain has caused more severe disease than the previously predominant serogroup A strain.     

Meningitis caused by a serogroup W135 clone of the ET-37 complex of Neisseria meningitidis in West Africa

Summary Meningococci belonging to serogroup W135 caused several cases of meningococcal meningitis in The Gambia in 1995 and were isolated during a serogroup A epidemic in Mali in 1994. The eight isolates tested belonged to the same clone of the ET-37 complex and differed in several bands from the pulsed-field gel electrophoresis restriction pattern of serogroup C meningococci of the ET-37 complex isolated in Mali. Three of 6 patients infected in The Gambia died, indicating that this W135 clone is virulent. Vaccines that protect only against infections with meningococci belonging to serogroups A and C are usually used to control outbreaks in Africa, although vaccines containing the W135 polysaccharide are available. The findings of this study indicate that outbreaks of meningococcal meningitis in Africa can be associated with serogroup W135 infections and that serogrouping is essential before vaccination campaigns are started.     

Another Swedish family with complete properdin deficiency: association with fulminant meningococcal disease in one male family member

Inherited deficiency of the complement component properdin is described in a Swedish family without any previous history of meningococcal infections. The properdin-deficient index patient died from a fulminant infection caused by Neisseria meningitidis serogroup Y. Family investigation revealed properdin deficiency in the patient's half-brother and in the maternal grandfather. The half-brother had a history of pneumococcal pneumonia and meningitis probably caused by Borrelia burgdorferi. Opsonic and bactericidal functions of serum were examined in the half-brother after immunization with tetravalent meningococcal vaccine. Vaccination promoted opsonization of N. meningitidis serogroups C and Y but not of serogroups A and W-135. The serum bactericidal activity increased against serogroup C and to some extent against serogroup W-135. This report emphasizes the importance of investigating the complement system even in families with single cases of fulminant meningococcal disease. Individuals with properdin deficiency might be protected from infection by immunization.     

Neisseria meningitidis serogroups A and W-135: carriage and immunity in Burkina Faso, 2003

OBJECTIVES: We sought to describe Neisseria meningitidis immunity and its association with pharyngeal carriage in Burkina Faso, where N. meningitidis serogroup W-135 and serogroup A disease are hyperendemic and most of the population received polysaccharide A/C vaccine during 2002. METHODS: We collected oropharyngeal swab samples from healthy residents of Bobo-Dioulasso (4-14 years old, n=238; 15-29 years old, n=250) monthly during February-June 2003; N. meningitidis isolates were analyzed using polymerase chain reaction and serogrouped using immune sera. Serum samples were collected at the first and last clinic visit and analyzed for anti-A, anti-C, anti-W-135, and anti-Y immunoglobulin G (IgG) concentrations and anti-A and anti-W-135 bactericidal titers. RESULTS: N. meningitidis was carried at least once by 18% of participants; this carriage included strains from serogroups W-135 (5%) and Y and X (both <1%) but not from serogroups A, B, or C. At baseline, the prevalence of putatively protective specific IgG concentrations (> or =2 microg/mL) and bactericidal titers (> or =8) was 85% and 54%, respectively, against serogroup A, and 6% and 22%, respectively, against serogroup W-135. Putatively protective anti-W-135 IgG concentrations and bactericidal titers were of short duration and were not associated with carriage. CONCLUSION: N. meningitidis serogroup W-135 strains did not induce immunity, despite their circulation. Carriage of serogroup A strains was rare despite the hyperendemic incidence of serogroup A meningitis during 2003 in Bobo-Dioulasso. A vaccine that includes serogroup W-135 antigen and eliminates serogroup A carriage is needed for sub-Saharan Africa.     

Meningococcal disease in urban south western Sydney, 1990–1994

Background: There has been a sustained increase in incidence of meningococcal disease throughout Australia since 1987. In south western Sydney the incidence is higher than the national rate and a cluster of cases occurred in 1991 resulting in a widespread vaccination programme. Aims: To investigate the clinical demographics of patients with meningococcal disease treated in south western Sydney, and to differentiate meningococcal strains to understand better the epidemiology in this urban setting. In addition, to investigate whether delays in diagnosis of meningococcal disease and institution of appropriate treatment were occurring. Methods: Retrospective classification of notified cases as meningitis, septicaemia, meningitis/septicaemia, and other syndromes. Clinical information recorded to establish patterns of disease, delays in diagnosis and appropriate treatment, and outcome. Microbiological classification of organisms isolated by serogroup, serotype and subtype. Results: Meningococcal disease primarily affects young children in winter months in south western Sydney, with a secondary peak of incidence in the 15–20 year old age group. 20.7% presented with meningitis only, 22.4% with septicaemia only, and 53.4% with meningitis/septicaemia. There was a delay in diagnosis and institution of appropriate treatment of more than two hours in 21/58 (36.2%) patients including three of the six who died. No patient had received a parenteral antibiotic prior to coming to hospital - 18.9% had received an oral antibiotic. The use of antibiotics before diagnostic lumbar puncture decreased the number of positive CSF cultures. However, in all but one patient with negative cultures there was other microbiological evidence of meningococcal disease. The mortality rate was highest (30.8%) in patients with septicaemia only, 6.5% in patients with meningitis/septicaemia and 0% in patients with meningitis only. Serogroup C was the predominant organism in all age groups. The predominant serotype was 2b (80% of serogroup C isolates). Subtypes were more variable but P1.2 occurred in 66.7% of serogroup C strains. Conclusions: There is a need for more education in our Health Area to improve the time taken to diagnose and institute appropriate treatment. The predominance of serogroup C is unusual in urban Australia where national data show serogroup B organisms predominate. Meningococci of phenotype C:2b:Pl.2 have continued to cause disease in our Health Area for the past five years. This phenotype is uncommon in other areas of Australia.     

Antigenic shift and increased incidence of meningococcal disease

BACKGROUND: The incidence of serogroup C and Y meningococcal disease increased in the United States during the 1990s. The cyclical nature of endemic meningococcal disease remains unexplained. The purpose of this study was to investigate the mechanisms associated with the increase in the incidence of meningococcal disease. METHODS: We characterized an increasing incidence of invasive serogroup C and Y meningococcal disease using population-based surveillance from 1992 through 2001. Isolates were characterized by multilocus sequence typing and antigen sequence typing of 3 outer membrane protein (OMP) genes: porA variable regions (VRs) 1 and 2, porB, and fetA VR. RESULTS: For both serogroups, OMP antigenic shifts were associated with increased incidence of meningococcal disease. For serogroup Y, antigenic shift occurred through amino acid substitutions at all 3 OMPs--PorA VR 1 and 2, PorB, and FetA VR. For serogroup C, antigenic shift involved amino acid substitutions at FetA VR and, in some cases, deletion of the porA gene. On the basis of deduced amino acid sequences, the antigenic changes likely occurred by horizontal gene transfer. CONCLUSIONS: Antigenic shifts were associated with increased incidence of serogroup C and serogroup Y meningococcal disease. For serogroup Y, the changes involved all OMP genes that were studied. Increases in the incidence of meningococcal disease may be caused, in part, by antigenic shift.     

Association of respiratory tract infection symptoms and air humidity with meningococcal carriage in Burkina Faso

Objectives To evaluate risk factors for meningococcal carriage and carriage acquisition in the African meningitis belt, comparing epidemic serogroup A (NmA) to non‐epidemic serogroups. Methods During the non‐epidemic meningitis season of 2003, pharyngeal swabs were taken at five monthly visits in a representative population sample (N = 488) of Bobo‐Dioulasso, Burkina Faso (age 4–29 years) and analysed by culture. Standardized questionnaires were administered. In 2006, a similar study was performed in 624 individuals (age 1–39 years) during an NmA meningitis epidemic. We evaluated serogroup‐specific risk factors for carriage, carriage acquisition and clearance using multivariate logistic and Poisson regression, and a Cox proportional hazard model. Results The prevalence of NmA carriage (current or recent pharyngitis or rhinitis) was 16% (31%) vs. 0% (9%) in the epidemic vs. the hyperendemic setting. During the epidemic situation, NmA carriage was significantly associated with recent sore throat (adjusted odds ratio (OR), 3.41) and current rhinitis (OR 2.65). During the non‐epidemic meningitis season in 2003, air humidity (20–39% and ≥40%, compared to <20%) during the month before swabbing was significantly and positively associated with carriage acquisition of non‐groupable meningococci (OR 2.18 and 1.55) and inversely with carriage clearance (hazard ratio 0.61 and 0.27, respectively). Conclusion Respiratory tract infections may increase meningococcal carriage, and thus contribute to epidemic risk, in addition to seasonality in the meningitis belt. Humid climate may favour carriage of unencapsulated meningococci. These findings may help identifying interventions against epidemic and hyperendemic meningococcal meningitis due to non‐vaccine serogroups.     

The changing epidemiology of meningococcal disease in the United States, 1992-1996

New meningococcal vaccines are undergoing clinical trials, and changes in the epidemiologic features of meningococcal disease will affect their use. Active laboratory-based, population-based US surveillance for meningococcal disease during 1992-1996 was used to project that 2400 cases of meningococcal disease occurred annually. Incidence was highest in infants; however, 32% of cases occurred in persons >/=30 years of age. Serogroup C caused 35% of cases; serogroup B, 32%; and serogroup Y, 26%. Increasing age (relative risk [RR], 1.01 per year), having an isolate obtained from blood (RR, 4.5), and serogroup C (RR, 1.6) were associated with increased case fatality. Among serogroup B isolates, the most commonly expressed serosubtype was P1.15; 68% of isolates expressed 1 of the 6 most common serosubtypes. Compared with cases occurring in previous years, recent cases are more likely to be caused by serogroup Y and to occur among older age groups. Ongoing surveillance is necessary to determine the stability of serogroup and serosubtype distribution.     

Prospective study of a serogroup X Neisseria meningitidis outbreak in northern Ghana

After an epidemic of serogroup A meningococcal meningitis in northern Ghana, a gradual disappearance of the epidemic strain was observed in a series of five 6-month carriage surveys of 37 randomly selected households. As serogroup A Neisseria meningitidis carriage decreased, an epidemic of serogroup X meningococcal carriage occurred, which reached 18% (53/298) of the people sampled during the dry season of 2000, coinciding with an outbreak of serogroup X disease. These carriage patterns were unrelated to that of Neisseria lactamica. Multilocus sequence typing and pulsed-field gel electrophoresis of the serogroup X bacteria revealed strong similarity with other strains isolated in Africa during recent decades. Three closely related clusters with distinct patterns of spread were identified among the Ghanian isolates, and further microevolution occurred after they arrived in the district. The occurrence of serogroup X outbreaks argues for the inclusion of this serogroup into a multivalent conjugate vaccine against N. meningitidis.     

Microheterogeneity of serogroup A (subgroup III) neisseria meningitidis during an outbreak in northern ghana

During a meningitis outbreak in the eastern subdistrict of the Kassena-Nankana District of the Upper East Region of Ghana, we analysed cerebrospinal fluid from suspected meningitis cases for the most common causative organisms. In 50 of 92 samples analysed, serogroup A Neisseria meningitidis were detected. The ages of serogroup A N. meningitidis patients ranged from 4 months to 64 years. The case fatality ratio was 20%. Coma or stupor on presentation worsened the prognosis. All serogroup A N. meningitidis isolates recovered revealed the A: 4: P1.9, 20 phenotype characteristic for the subgroup III clonal grouping. No evidence for resistance to penicillin G, chloramphenicol, cefotaxime, ciprofloxacin, rifampicin or tetracycline was found. All strains were resistant to sulphadiazine. Restriction analysis patterns of opa, iga and ingA genes were characteristic for the majority of N. meningitidis serogroup A subgroup III bacteria isolated in Africa after the 1987 epidemic in Mecca. Differences in pulsed-field gel electrophoresis patterns of NheI and SpeI digested DNA revealed microheterogeneity among the Ghanaian isolates.     

Conjugate vaccine introduction in the African meningitis belt: meeting surveillance objectives

The epidemiology of bacterial meningitis will change with introduction of meningococcal and pneumococcal conjugate vaccines in the African meningitis belt. The principal objectives of surveillance are to evaluate the impact of vaccination, to detect and investigate epidemics and provide material for research. The capacity of existing surveillance activities in the meningitis belt to meet these objectives varies due to infrastructural and financial constraints. Impact assessment of conjugate vaccine against meningococcal serogroup A will be limited to comparing incidence trends from a few surveillance sites with data obtained before vaccine introduction and to comparing trends in the incidence of suspected cases or localised epidemics in most other settings. The timeliness of detection of epidemics and identification of epidemic meningococcal serogroups could be improved in most countries by analysing suspected case data in health centre level resolution and by investigating outbreaks with mobile teams. For research and impact assessment of pneumococcal conjugate vaccines, several surveillance sites covering at least 0.5 million inhabitants should be maintained which undertake exhaustive case finding and systematic laboratory confirmation of meningitis and pneumonia. Molecular diagnostics will facilitate surveillance in remote areas, but the available techniques should be evaluated for diagnostic performance in the field and long‐term sustainability.     

Meningococcal vaccine in travelers

PURPOSE OF REVIEW: New vaccines to prevent meningococcal disease have been licensed in recent years. It is therefore timely to discuss current vaccine strategies pertinent to international travelers in relation to the changing epidemiology. RECENT FINDINGS: Serogroup W135 achieved epidemic status in Africa in 2002, and then largely disappeared over a short time period. The year 2006 saw a marked epidemic rise in meningitis attack rates across the meningitis belt in Africa. This rise was mainly due to a new serogroup A strain, indicating that a new meningitis epidemic wave is beginning in Africa. Epidemics are also spreading south of the meningitis belt, including the Greater Lakes Area (Burundi, Rwanda, Republic of Tanzania). The new quadrivalent conjugate meningococcal vaccine is now licensed in North America but not elsewhere. In most other industrialized countries, the serogroup C conjugate vaccine is licensed. Plain polysaccharide quadrivalent vaccines are available almost worldwide. SUMMARY: Quadrivalent meningococcal vaccination is a visa requirement for Hajj and Umrah pilgrims to Saudi Arabia. Travelers to the meningitis belt during the dry season should be advised to receive meningococcal vaccine that covers all four serogroups. This recommendation should be extended to the Greater Lake Area, because of recent epidemics. Vaccine choices depend on availability.     

Emergence of endemic serogroup W135 meningococcal disease associated with a high mortality rate in South Africa.

BACKGROUND: In the African meningitis belt, Neisseria meningitidis serogroup W135 has emerged as a cause of epidemic disease. The establishment of W135 as the predominant cause of endemic disease has not been described. METHODS: We conducted national laboratory-based surveillance for invasive meningococcal disease during 2000-2005. The system was enhanced in 2003 to include clinical data collection of cases from sentinel sites. Isolates were characterized by pulsed-field gel electrophoresis and multilocus sequence typing. RESULTS: A total of 2135 cases of invasive meningococcal disease were reported, of which 1113 (52%) occurred in Gauteng Province, South Africa. In this province, rates of disease increased from 0.8 cases per 100,000 persons in 2000 to 4.0 cases per 100,000 persons in 2005; the percentage due to serogroup W135 increased from 7% (4 of 54 cases) to 75% (221 of 295 cases). The median age of patients infected with serogroup W135 was 5 years (interquartile range, 2-23 years), compared with 21 years (range, 8-26 years) for those infected with serogroup A (P<.001). The incidence of W135 disease increased in all age groups. Rates were highest among infants (age, <1 year), increasing from 5.1 cases per 100,000 persons in 2003 to 21.5 cases per 100,000 persons in 2005. Overall case-fatality rates doubled, from 11% in 2003 to 22% in 2005. Serogroup W135 was more likely to cause meningococcemia than was serogroup A (82 [28%] of 297 cases vs. 11 [8%] of 141 cases; odds ratio, 8.9, 95% confidence interval, 2.2-36.3). A total of 285 (95%) of 301 serogroup W135 isolates were identified as 1 clone by pulsed-field gel electrophoresis; 7 representative strains belonged to the ST-11/ET-37 complex. CONCLUSIONS: Serogroup W135 has become endemic in Gauteng, South Africa, causing disease of greater severity than did the previous predominant serogroup A strain.     

Incidence, serogroups and case-fatality rate of invasive meningococcal infections in a Swedish region 1975-1989.

In a retrospective study of invasive meningococcal infections in Greater Gothenburg, Sweden, 213 cases of culture-verified meningitis or septicaemia were identified during the 15-year period 1975-1989. The annual incidence was 2.0/100,000. Cases were seen in all age-groups with the highest rates in the 0-4 and 15-19 year-old groups, 9.5 and 6.2/100,000 respectively. 20% of the patients were less than 2 years. 91% of the patients had no known risk factors. In only 10 cases (5%) was contact with another case of meningococcal infection known. The main clinical manifestations were meningitis (57%), septicaemia with no sign of focal infection (25%) and septic shock (17%). The case-fatality rate for all the patients was 6.6% and did not change during the 15-year period. One-third of the patients who presented with septic shock died. The serogroup was known for strains from 192 patients. 51% of the strains belonged to serogroup B, 10% to group A and 23% to group C. In conclusion, the incidence of meningococcal infection was low but the relatively high case-fatality rate warrants a search for effective prophylaxis. About 30% of the cases were potentially preventable by the currently available tetravalent (A, C, Y and W135) polysaccharide vaccine, which is immunogenic in children greater than 2 years. Widespread use of antibiotic prophylaxis to close contacts of known cases would not lower the incidence markedly.     

Genotype-specific carriage of Neisseria meningitidis in Georgia counties with hyper- and hyposporadic rates of meningococcal disease

Carriage of Neisseria meningitidis in a Georgia county with hypersporadic incidence of meningococcal disease ("hypersporadic county") and in a county with no cases of meningococcal disease was determined by a cross-sectional pharyngeal culture study of high school students. Among 2730 students from whom culture samples were obtained, meningococcal carriage was 7.7% (140/1818) in the hypersporadic county and 6.1% (56/912) in the comparison county. Carriage rates by serogroup and genetic type (i.e., electrophoretic type [ET]) did not differ significantly between counties, but apartment or mobile home residency was a risk factor for carriage in the hypersporadic county. Although most cases of meningococcal disease in the hypersporadic county were caused by members of the serogroup C ET-37 clonal group, no ET-37 meningococcal isolates were recovered from carriers in this county. However, 38% of all meningococcal isolates recovered from carriers in both counties were members of the serogroup Y ET-508 clonal group, an emerging cause of meningococcal disease in Georgia and throughout the United States during 1996-2001. Shifts in carriage and transmission of meningococcal strains with different pathogenic potential are important determinants of meningococcal disease incidence.     

Meningococcal disease: risk for international travellers and vaccine strategies

International travel and migration facilitate the rapid intercontinental spread of meningococcal disease. Serogroup A and, less so serogroup C, have been responsible for epidemics in the past (mainly in Africa). In recent years, W135 has emerged (first in Saudi Arabia, then in West Africa) as a serogroup that requires attention. Serogroups X and Y are infrequent, but associated with slowly rising trends. There are significant variations in the incidence of meningococcal disease and the distribution of serogroups responsible for meningococcal disease, both geographically and with time. Vaccine strategies need to address this variation, and broad coverage against all serogroups for which vaccines are currently available should be offered to travellers. Tetravalent polysaccharide meningococcal vaccines are limited by their poor immunogenicity in small infants and by the lack of long-term protection. In contrast, the novel tetravalent conjugate vaccine that is currently only available in North America is immunogenic in young infants, induces long-term protection and reduces nasopharyngeal carriage. The tetravalent conjugate meningococcal vaccine will be a leap forward in the control of meningococcal epidemics in affected countries. It will also boost the uptake of meningococcal vaccines in travellers because the duration of protection is longer and it eliminates the problem of immune hyporesponsiveness of serogroup C with repeated dosing. Current vaccine recommendations are to vaccinate all Hajj pilgrims, all travellers to areas with current outbreaks, travellers to the SubSaharan meningitis belt, and individuals with certain medical conditions.     

ST2859 serogroup A meningococcal meningitis outbreak in Nouna Health District, Burkina Faso: a prospective study

We analysed cerebrospinal fluid samples from suspected meningitis cases in Nouna Health District, Burkina Faso, during the meningitis seasons of 2004-2006. Serogroup A ST2859 meningococci belonging to the ST5 clonal complex of subgroup III meningococci were the predominant causative agent. ST2859 bacteria were associated with focal outbreaks in the north of the district. While >10% of the population of an outbreak village carried ST2859, the population in the south of the district was predominantly colonised by serogroup Y ST4375 meningococci, which were associated with only sporadic cases of meningitis. Colonisation with the less virulent Y meningococci may interfere with the spread of the ST2859 to the south of the district, but there are concerns that this serogroup A clone may cause a third wave of subgroup III meningococcal disease in the African Meningitis Belt.     

Emergence of W135 meningococcal meningitis in Ghana

Neisseria meningitidis serogroup W135, well known for a long time as a cause of isolated cases of meningococcal meningitis, has recently increasingly been associated with disease outbreaks of considerable magnitude. Burkina Faso was hit by W135 epidemics in the dry seasons of 2002-2004, but only four W135 meningitis cases were recorded between February 2003 and March 2004 in adjoining Ghana. This reconfirms previous findings that bottlenecks exist in the spreading of new epidemic N. meningitidis clones within the meningitis belt of sub-Saharan Africa. Of the four Ghanaian W135 meningitis patients one died and three survived, of whom one had profound neurosensory hearing loss and speech impairment. All four disease isolates were sensitive to penicillin G, chloramphenicol, ciprofloxacin and cefotaxime and had the multi-locus sequence type (ST) 11, which is the major ST of the ET-37 clonal complex. Pulsed-field gel electrophoresis (PFGE) profiles of the Ghanaian disease isolates and recent epidemic isolates from Burkina Faso were largely identical. We conducted meningococcal colonization surveys in the home communities of three of the patients and in the Kassena Nankana District located at the border to Burkina Faso. W135 carriage rates ranged between 0% and 17.5%. When three consecutive surveys were conducted in the patient community with the highest carrier rate, persistence of W135 colonization over a period of 1 year was observed. Differences in PFGE profiles of carrier isolates taken at different times in the same patient community were indicative of rapid microevolution of the W135 bacteria, emphasizing the need for innovative fine typing methods to reveal the relationship between W135 isolates.     

Distribution of serogroups of Neisseria meningitidis and antigenic characterization of serogroup Y meningococci in Canada,January 1, 1999 to June 30, 2001

The relative frequency of serogroups of Neisseria meningitidis associated with meningococcal disease in Canada during the period January 1, 1999 to June 30, 2001 was examined. Of the 552 strains of N meningitidis collected from clinical specimens of normally sterile sites, 191 (34.6%), 276 (50.0%), 61 (11.1%) and 23 (4.2%) were identified by serological and molecular methods as serogroups B, C, Y and W135, respectively. About half (50.8%) of the serogroup Y isolates were isolated in the province of Ontario. The two most common serotypes found were 2c and 14. Most of the serogroup Y strains isolated from patients in Ontario were serotype 2c, while serotype 14 was the most common serotype associated with disease in the province of Quebec. The two most common serosubtypes found among the serogroup Y meningococci were P1.5 and P1.2,5. Laboratory findings, based on antigenic analysis, did not suggest that these serogroup Y strains arise by capsule switching from serogroups B and C strains. This study documented a higher incidence of finding serogroup Y meningococci in clinical specimens from patients in Ontario compared to the rest of Canada, and parallels the increase in serogroup Y meningococcal disease reported in some parts of the United States.Key Words: Meningococcal disease, Neisseria meningitidis, SerogroupsInvasive meningococcal disease (IMD) is a notifiable communicable disease that is monitored by a national surveillance program coordinated by the Division of Disease Surveillance and the Division of Respiratory Diseases, Centre for Infectious Disease Prevention and Control, Health Canada. Starting in 1971 and with the help of provincial public health officials, Health Canada began to collect data on the serogroup information on IMD cases. Also, isolates of meningococci collected from patients are routinely sent to Health Canada''s National Microbiology Laboratory (NML) in Winnipeg for further antigenic and genetic analyses.IMD is a serious disease globally but the serogroups of meningococci causing diseases in various countries may vary in frequency. For example, serogroup A is a major cause of disease in Africa and China (1), while serogroups B and C meningococci are the most frequent cause of IMD in Western countries (2). In Canada, most IMD cases are caused by meningococci belonging to serogroups B, C, Y and W135. Serogroups B and C account for over 75% of the isolates collected from patients (3).In the past decade, Neisseria meningitidis serogroup Y has emerged as a frequent cause of IMD in the United States (4,5). In view of these findings, it is important to monitor the incidence of serogroup Y disease. This report presents the frequency of isolation of serogroups of meningococci in normally sterile clinical specimens collected from patients (likely to be presented as IMD) in various parts of Canada and describes the distribution of serotypes and serosubtypes found among the serogroup Y isolates.