Clone Of Serogroup Research Articles

Characterization of invasive Neisseria meningitidis strains from Québec, Canada, during a period of increased serogroup B disease, 2009-2013: phenotyping and genotyping with special emphasis on the non-carbohydrate protein vaccine targets.

BackgroundThe epidemiology of invasive meningococcal disease (IMD) in Québec, Canada, has been dominated in the past decade by a clone of serogroup B (MenB) Neisseria meningitidis defined by multi-locus sequence typing (MLST) as sequence type (ST)-269. With the licensure of a new MenB vaccine Bexsero (4CMenB) in Canada, this study characterized invasive N. meningitidis recovered in Québec from 2009 to 2013, with an objective to examine the diversity of the 4CMenB vaccine antigens. Isolates were serogrouped by antisera and genogrouped by PCR, and further typed by whole cell ELISA for serotype and serosubtype antigens. Clonal analysis was done by MLST. Isolates were genotyped by analysis of their 4CMenB vaccine antigen genes of PorA, factor H binding protein (fHbp), Neisserial Heparin Binding Antigen (NHBA), and Neisseria Adhesin A (NadA).ResultsOf the 263 IMD isolates analysed, 229, 16, 10, 7, and 1 belonged to MenB, MenY, MenW, MenC, and MenX, respectively. Of the 229 MenB, 159 (69.4 %) were typed as ST-269 clonal complex (CC); and they possessed a restricted number of three fHbp and five nhba gene alleles. Nine N. meningitidis isolates (eight MenB and one MenY) were found to possess at least one gene that encoded for an antigen that matched exactly with protein variants in the 4CMenB vaccine. Two MenB expressed PorA antigen P1.4 and possessed the nhba gene for peptide 2; four other MenB were predicted to have NHBA peptide 2; another two MenB were predicted to encode fHbp peptide 1.1; and a single MenY was found to have nadA gene for NadA peptide 8. In addition, another 172 isolates were found to possess genes for variant 1 fHbp peptides other than peptide 1.1 or NadA variant 1-2/3 peptides other than peptide 8; and therefore, may potentially be covered by 4CMenB.ConclusionThe most prevalent clone of N. meningitidis in Quebec was ST-269 CC; and 96 % of the isolates in this CC were predicted to be covered by 4CMenB vaccine. Extensive genetic diversity was found in the other IMD isolates in Québec which might suggest a lower coverage by the vaccine when compared to the ST-269 MenB.Electronic supplementary materialThe online version of this article (doi:10.1186/s12866-015-0469-6) contains supplementary material, which is available to authorized users.

Serogroup W135 Meningococcal Meningitis, Northern Cameroon, 2007–2008

We analyzed results of recent microbiologic surveillance of meningitis in northern Cameroon. During the 2007 and 2008 meningitis seasons, all 57 identified meningococcal isolates were serogroup W135. This situation might indicate that the area is experiencing a period between epidemic waves due to 2 different clones of serogroup A meningococci.

Emergence of a new clone of serogroup C Neisseria meningitidis in São Paulo, Brazil.

Serogroup C isolates of Neisseria meningitidis recovered from 121 patients with meningitis or septicemia in Greater São Paulo, Brazil, between 1976 and 1990 were analyzed with respect to serotype and multilocus enzyme genotype. The distribution of serotypes has changed since 1989 when serotype 2b started to replace serotype 2a. There were 48 distinct multilocus genotypes (electrophoretic types [ETs]) and 13 distinct complexes. Among the 41 serotype C:2b:- strains analyzed, 38 (93%) were found in complex 11. The percentage of complex 11 increased from 8% in 1988 to 50 and 66% in 1989 and 1990, respectively. Although we have been in an epidemic situation due to serogroup B:4:P1.15 ET-5 complex since 1988, the appearance and increase of a new unrelated strain, C:2b:- of ET-11 complex, in 1989 and 1990 provide enough data to conclude that the presence of two different complexes, ET-5 and -11, of N. meningitidis were responsible for the high levels of meningococcal disease in Greater São Paulo during this period.

Comparison of epidemic neisseria meningitidis strains by dna restriction endonuclease profile analysis

Meningococcal disease (MD) in Western Australia prior to 1987 was caused by endemic, predominantly serogroup B Neisseria meningitidis strains. In 1987/S3 an epidemic of serogroup A MD occurred in remote outback Aboriginal communities in Western Australia. Comparable epidemiologic features of this epidemic with overseas epidemics suggested spread of a single clone of serogroup A Neisseria meningitidis . DNA analysis of serogroup A strains isolated from MD cases admitted to Princess Margaret Hospital for Children in 1987/88 was undertaken. Chromosomal DNA extraction and restriction endonuclease profiles obtained with EcoRI and Hind III demonstrate that these serogroup A strains are clonal. This indicates that the molecular epidemiology of epidemic serogroup A MD in Western Australia is similar to recent experience in Saudi Arabia, Sudan, Chad and Ethiopia, where spread of single closely related clones has been iesponsible for pandemic waves of MD in the past decade.

Clones of Serogroup B Neisseria meningitidis Causing Systemic Disease in the Netherlands, 1958-1986

Serogroup B isolates of Neisseria meningitidis recovered from 278 patients with systemic disease in the Netherlands between 1958 and 1986 were analyzed with respect to serotype and multilocus enzyme genotype. Of the isolates, 28% were serotype 2b and 53% were neither serotypeable nor serosubtypeable. There were 145 distinct multilocus genotypes (electrophoretic types, ETs), with up to 31 isolates belonging to the same ET. Temporal changes in the genotypic composition of meningococcal populations in the Netherlands were demonstrated by the recent occurrence of disease caused by three clone lineages, I, III, and VI, that were not found before 1975. The epidemic of 1966-1967 and the hyperendemic wave of 1972 were caused, in large part, by two closely related but distinct clones of serotype 2b isolates, ET-11 and ET-17, respectively. Deviations in male-to-female ratio and age distribution of patients were observed for disease caused by isolates of individual clone lineages.

Serogroup A Neisseria meningitidis of Clone III-1 Present in Western Norway as Early as 1969–73

A clone of serogroup A Neisseria meningitidis recognized by multilocus enzyme electrophoresis and designated as clone III-1, has caused major epidemics of meningococcal disease in various parts of the world since the 1970s. In Norway, serogroup B meningococci have been responsible for an epidemic since the mid-1970s. We have studied a sample of 53 meningococci isolated from patients in western Norway prior to the serogroup B epidemic. 22/35 meningococcal isolates collected 1969-73 represented clone III-1, whereas this clone was not found in the 18 isolates from 1962-68. It has been speculated that the epidemic of meningococcal disease in Finland caused by clone III-1 in 1973-75 had spread from an epidemic in USSR that began in 1969. Our findings demonstrate, however, that the clone III-1 was present in Scandinavia in 1969.

Genetic structure of Neisseria meningitidis populations in relation to serogroup, serotype, and outer membrane protein pattern.

The genetic structure of populations of Neisseria meningitidis was examined by an analysis of electrophoretically demonstrable allelic variation at 15 genes encoding enzymes in 650 isolates of eight serogroups (A, B, C, W135, X, Y, Z, and 29E) and 38 nonserogroupable isolates. A total of 331 distinctive multilocus genotypes (electrophoretic types, ETs) was identified, among which mean genetic diversity per locus (H = 0.547) was greater than in Escherichia coli and other bacterial species thus far studied. The intercontinental distribution of some ETs and the recovery of organisms of identical genotype over periods of many years strongly suggest that the genetic structure of N. meningitidis is basically clonal as a consequence of low rates of recombination of chromosomal genes. Variation among strains in serogroup, serotype, and the electrophoretic pattern of the major outer membrane proteins has little relationship to the complex structure of populations revealed by enzyme electrophoresis, which involves 14 major lineages of clones diverging from one another at genetic distances greater than 0.50. Genetic diversity among ETs of isolates of the same serogroup was, on average, 84% of that in the total sample. Clones of serogroup A were unusual in being genotypically less heterogeneous than those of other serogroups and in forming a single phylogenetic group. Isolates of the same serotype or outer membrane protein pattern were also highly heterogeneous; on average, 87 and 97%, respectively, of the total species diversity was represented by ETs of the same serotype or outer membrane protein.