Genetic mechanisms for loss of encapsulation in polysialyltransferase-gene-positive meningococci isolated from healthy carriers

Weber, Martin V. R.; Claus, Heike; Maiden, Martin C. J.; Frosch, Matthias; Vogel, Ulrich

doi:10.1016/j.ijmm.2006.05.004

Cited by 33 publications

(26 citation statements)

References 26 publications

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“…We have recently demonstrated the high rate of capsule synthesis gene-silencing events in carried meningococci, which, however, are not fixed in the population (20). We have now analyzed the same strain collection for the frequency of fetA deletion by using dot blot hybridization and, in the case of negative results, by PCR.…”

Section: Resultsmentioning

confidence: 99%

Deletion of the MeningococcalfetAGene Used for Antigen Sequence Typing of Invasive and Commensal Isolates from Germany: Frequencies and Mechanisms

et al. 2007

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Antigen sequence typing (ST) of FetA is part of the molecular typing scheme of Neisseria meningitidis. Among invasive meningococcal isolates from 2,201 patients in Germany, we identified 11 strains lacking the fetA gene because of deletions mediated by repeat arrays flanking the gene, i.e., Correia elements, repeat sequence 13 (RS13), and duplicated RS3. Geographic mapping and multilocus ST of invasive isolates revealed that fetA deletion was a sporadic event without genetic fixation. Among 821 carrier strains, 12 strains lacked fetA, suggesting that fetA is maintained during asymptomatic carriage. Interestingly, most of these isolates belonged to the multilocus ST-35 clonal complex (cc). ST-35 cc strains and the recently published ST-192 strains from Burkina Faso may benefit from loss of fetA, but their infrequent occurrence among invasive isolates currently does not affect fetA antigen ST.

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Section: Resultsmentioning

confidence: 99%

Deletion of the MeningococcalfetAGene Used for Antigen Sequence Typing of Invasive and Commensal Isolates from Germany: Frequencies and Mechanisms

et al. 2007

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“…Thirty-nine (67%) of the 58 isolates were ctrA negative; of those, 32 isolates lacked capsule biosynthesis and capsule transport genes and thus were classified as capsule operon-null (cnl) isolates (83,84). Fifteen isolates had insertions bearing coding sequences from IS1301 (80)(81)(82), including nine in cssF (MnW) and three each in cssA (MnY) and csb (MnB). An additional isolate had an IS30-family insertion sequence associated with truncation of the cssA gene (MnY) (85) (see Table S1 in the supplemental material).…”

Section: Genotypic Characterization By Wgsmentioning

confidence: 99%

Comparison of Phenotypic and Genotypic Approaches to Capsule Typing of Neisseria meningitidis by Use of Invasive and Carriage Isolate Collections

Mohamed

Rojas

et al. 2016

J Clin Microbiol

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e Neisseria meningitidis serogroup B (MnB) is a leading cause of bacterial meningitis; however, MnB is most commonly associated with asymptomatic carriage in the nasopharyngeal cavity, as opposed to the disease state. Two vaccines are now licensed for the prevention of MnB disease; a possible additional benefit of these vaccines could be to protect against disease indirectly by disrupting nasopharyngeal carriage (e.g., herd protection). To investigate this possibility, accurate diagnostic approaches to characterize MnB carriage isolates are required. In contrast to invasive meningococcal disease (IMD) isolates, which can be readily serogrouped, carriage isolates often lack capsule expression, making standard phenotypic assays unsuitable for strain characterization. Several antibody-based methods were evaluated for their abilities to serogroup isolates and were compared with two genotyping methods (real-time PCR [rt-PCR] and whole-genome sequencing [WGS]) to identify which approach would most accurately ascertain the polysaccharide groups associated with carriage isolates. WGS and rt-PCR were in agreement for 99% of IMD isolates, including those with coding sequences for MnB, MnC, MnW, and MnY, and the phenotypic methods correctly identified serogroups for 69 to 98% of IMD isolates. In contrast, only 47% of carriage isolates were groupable by genotypic methods, due to mutations within the capsule operon; of the isolates identified by genotypic methods, <43% were serogroupable with any of the phenotypic methods tested. These observations highlight the difficulties in the serogrouping and capsular genogrouping of meningococcal carriage isolates. Based on our findings, WGS is the most suitable approach for the characterization of meningococcal carriage isolates. N eisseria meningitidis, a Gram-negative bacterium that causes both epidemic and endemic life-threatening disease, is also an obligate human commensal organism that colonizes the nasopharyngeal mucosa with no or minimal harm to the host, a phenomenon known as carriage (1). Asymptomatic pharyngeal colonization with N. meningitidis in young adults is relatively common, and these asymptomatic carriers represent a potential reservoir for the transmission of pathogenic isolates in the community (2, 3). The rates of asymptomatic carriage in the United States and Europe are highest among adolescents and young adults, peaking at the age of 19 years, and are estimated to be 10% to 35% (4-6). Rates of transmission and carriage are higher in closed and semiclosed populations, such as university students living in dormitories and military recruits housed in barracks (7). Higher rates of carriage are also found among people in close contact with patients with active meningococcal infections (8). For the majority of people, carriage is an immunizing process that results in systemic, serogroup-specific, protective antibody responses (9, 10). Invasive meningococcal disease (IMD) usually occurs shortly after the onset of colonization of a susceptible host, when the bacteria ...

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“…Sixteen percent of meningococcal isolates during a very large carriage survey conducted in Bavaria, Germany, were constitutively unencapsulated [2]. Furthermore, of 538 strains harboring a capsule polymerase gene of serogroups B, C, W-135, and Y, 166 (31%) were unencapsulated due to reversible or irreversible genetic events [28]. These Wndings imply that lacking a capsule might be a selective advantage for some lineages (capsule null locus meningococci), whilst for others within host evolution frequently implies adaptive mutation toward loss of encapsulation.…”

Section: Neisseria Meningitidismentioning

confidence: 99%

Biofilm formation by the human pathogen Neisseria meningitidis

Lappann

Vogel

2010

Med Microbiol Immunol

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The past decade has seen an increasing interest in biofilm formation by Neisseria meningitidis, a human facultative pathogen causing life-threatening childhood disease commencing from asymptomatic nasopharyngeal colonization. Studying the biology of in vitro biofilm formation improves the understanding of inter-bacterial processes in asymptomatic carriage, of bacterial aggregate formation on host cells, and of meningococcal population biology. This paper reviews publications referring to meningococcal biofilm formation with an emphasis on the role of motility and of extracellular DNA. The theory of sub-dividing the meningococcal population in settler and spreader lineages is discussed, which provides a mechanistic framework for the assumed balance of colonization efficacy and transmission frequency.

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Genetic mechanisms for loss of encapsulation in polysialyltransferase-gene-positive meningococci isolated from healthy carriers

Cited by 33 publications

References 26 publications

Deletion of the MeningococcalfetAGene Used for Antigen Sequence Typing of Invasive and Commensal Isolates from Germany: Frequencies and Mechanisms

Deletion of the MeningococcalfetAGene Used for Antigen Sequence Typing of Invasive and Commensal Isolates from Germany: Frequencies and Mechanisms

Comparison of Phenotypic and Genotypic Approaches to Capsule Typing of Neisseria meningitidis by Use of Invasive and Carriage Isolate Collections

Biofilm formation by the human pathogen Neisseria meningitidis

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