Neisseria is a large genus ofbacteria that colonize themucous membranes of many animals. Of the 11 species that colonize humans, only two arepathogens:N. meningitidis andN. gonorrhoeae.
Neisseria species areGram-negative bacteria included among thePseudomonadota, a large group of Gram-negative forms.Neisseriadiplococci resemblecoffee beans when viewed microscopically.[1]
Pathogenesis and classification
editPathogens
editSpecies of this genus (family Neisseriaceae) of parasitic bacteria grow in pairs and occasionally fours, and thrive best at 98.6 °F (37 °C) in the animal body or serum media.
The genus includes:
- N. gonorrhoeae (also called thegonococcus) causesgonorrhea.
- N. meningitidis (also called the meningococcus) is one of the most common causes of bacterialmeningitis and the causative agent of meningococcalsepticaemia.
The immune system'sneutrophils are restricted in function due to the ability ofNeisseria to evadeopsonization by antibodies, and to replicate within neutrophils despitephagocytosis.Neisseria species are also able to alter their antigens to avoid being engulfed by a process calledantigenic variation, which is observed primarily in surface-located molecules. Thepathogenic species along with somecommensal species, havetype IV pili which serve multiple functions for this organism. Some functions of the type IV pili include: mediating attachment to various cells and tissues, twitching motility, natural competence,microcolony formation, extensive intrastrain phase, and antigenic variation.
Neisseria bacteria have also been shown to be an important factor in the early stages of canine plaque development.[2]
Nonpathogens
editThis genus also contains several, believed to be commensal, or nonpathogenic, species:
- Neisseria bacilliformis
- Neisseria cinerea
- Neisseria elongata
- Neisseria flavescens
- Neisseria lactamica
- Neisseria macacae
- Neisseria mucosa
- Neisseria oralis
- Neisseria polysaccharea
- Neisseria sicca
- Neisseria subflava
- Neisseria flava
However, some of these can be associated with disease.[4]
Biochemical identification
editAll the medically significant species ofNeisseria are positive for bothcatalase andoxidase. DifferentNeisseria species can be identified by the sets of sugars from which they will produce acid. For example,N. gonorrhoeae makes acid from onlyglucose, butN. meningitidis produces acid from both glucose andmaltose.
Polysaccharide capsule.N. meningitidis has apolysaccharide capsule that surrounds the outer membrane of the bacterium and protects against solubleimmune effector mechanisms within theserum. It is considered to be an essentialvirulence factor for the bacteria.[5]N. gonorrhoeae possesses no such capsule.
Unlike most other Gram-negative bacteria, which possesslipopolysaccharide (LPS), both pathogenic and commensal species ofNeisseria have alipooligosaccharide (LOS) which consists of acore polysaccharide andlipid A. It functions as anendotoxin, protects againstantimicrobial peptides, and adheres to theasialoglycoprotein receptor onurethralepithelium. LOS is highly stimulatory to the human immune system. LOSsialylation (by the enzyme Lst) preventsphagocytosis byneutrophils and complement deposition. LOS modification byphosphoethanolamine (by the enzyme LptA) provides resistance to antimicrobial peptides and complement. Strains of the same species have the ability to produce different LOSglycoforms.[6]
History
editThegenusNeisseria is named after the German bacteriologistAlbert Neisser, who in 1879 discovered its first example,Neisseria gonorrhoeae, the pathogen which causes the human disease gonorrhea. Neisser also co-discovered the pathogen that causesleprosy,Mycobacterium leprae. These discoveries were made possible by the development of new staining techniques which he helped to develop.
Genomes
editThe genomes of at least 10Neisseria species have been completely sequenced.[3] The best-studied species areN.meningitidis with more than 70 strains andN. gonorrhoeae with at least 10 strains completely sequenced. Other complete genomes are available forN. elongata,N. lactamica,[7] andN. weaveri. Whole genome shotgun sequences are available for hundreds of other species and strains.[8]N.meningitidis encodes 2,440 to 2,854 proteins whileN. gonorrhoeae encodes from 2,603 to 2,871 proteins.N. weaveri (strain NCTC 13585) has the smallest known genome with only 2,060 encoded proteins[9] althoughN. meningitidis MC58 has been reported to have only 2049 genes.[3] The genomes are generally quite similar. For example, when the genome ofN. gonorrhoeae (strain FA1090) is compared to that ofN. meningitidis (strain H44/76) 68% of their genes are shared.[8]
Genome properties ofNeisseria sp.[3] | ||
---|---|---|
species | Size (bp) | gene number |
N. elongata | 2,260,105 | 2589 |
N. sicca | 2,786,309 | 2842 |
N. mucosa | 2,542,952 | 2594 |
N. subflava | 2,288,219 | 2303 |
N. flavescens | 2,199,447 | 2240 |
N. cinerea | 1,876,338 | 2050 |
N. polysaccharea | 2,043,594 | 2268 |
N. lactamica 23970 | 2,148,211 | 2359 |
N. gonorrhoeae FA1090 | 2,153,922 | 2002 |
N. meningitidis MC58 | 2,184,406 | 2049 |
Vaccine
editDiseases caused byN. meningitidis andN. gonorrhoeae are significant health problems worldwide, the control of which is largely dependent on the availability and widespread use of comprehensive meningococcal vaccines. Development of neisserial vaccines has been challenging due to the nature of these organisms, in particular theheterogeneity, variability and/or poorimmunogenicity of their outer surface components. As strictly human pathogens, they are highly adapted to the host environment, but have evolved several mechanisms to remain adaptable to changing microenvironments and avoid elimination by the hostimmune system. Currently,serogroup A, B, C, Y, and W-135 meningococcal infections can be prevented by vaccines.[10] However, the prospect of developing a gonococcal vaccine is remote.[11]
Antibiotic resistance
editThe acquisition of cephalosporin resistance inN. gonorrhoeae, particularly ceftriaxone resistance, has greatly complicated the treatment of gonorrhea, with the gonococcus now being classified as a "superbug".[12]
Genetic transformation
editGenetic transformation is the process by which a recipient bacterial cell takes up DNA from a neighboring cell and integrates this DNA into the recipient’sgenome byrecombination. InN. meningitidis andN. gonorrhoeae, DNA transformation requires the presence of short DNA sequences (9-10 monomers residing in coding regions) of the donor DNA. These sequences are calledDNA uptake sequences (DUSs). Specific recognition of DUSs is mediated by a type IV pilin.[13] Davidsen et al.[14] reported that inN. meningitidis andN. gonorrhoeae, DUSs occur at a significantly higher density in genes involved inDNA repair andrecombination (as well as inrestriction-modification andreplication) than in other annotated gene groups. These authors proposed that the over-representation of DUS in DNA repair and recombination genes may reflect the benefit of maintaining the integrity of the DNA repair and recombination machinery by preferentially taking up genome maintenance genes that could replace their damaged counterparts in the recipient cell. Caugant and Maiden noted that the distribution of DUS is consistent with recombination being primarily a mechanism for genome repair that can occasionally result in generation of diversity, which even more occasionally, is adaptive.[15] It was also suggested by Michod et al.[16] that an important benefit of transformation inN. gonorrhoeae is recombinational repair of oxidative DNA damages caused by oxidative attack by the host’sphagocytic cells.
International PathogenicNeisseria Conference
editTheInternational PathogenicNeisseria Conference (IPNC), occurring every two years, is a forum for the presentation of cutting-edge research on all aspects of the genusNeisseria. This includes immunology, vaccinology, and physiology and metabolism ofN. meningitidis,N. gonorrhoeae and the commensal species. The first IPNC took place in 1978, and the most recent one was in September 2016. Normally, the location of the conference switches between North America and Europe, but it took place in Australia for the first time in 2006, where the venue was located inCairns.[17]
References
edit- ^Ryan KJ; Ray CG, eds. (2004).Sherris Medical Microbiology (4th ed.). McGraw Hill.ISBN 978-0-8385-8529-0.
- ^Early Canine Plaque Biofilms: Characterization of Key Bacterial Interactions Involved in Initial Colonization of Enamel. Lucy J. Holcombe, Niran Patel, Alison Colyer, Oliver Deusch, Ciaran O’Flynn, Stephen Harris. PLOS One, 2014.
- ^abcdMarri, Pradeep Reddy; Paniscus, Mary; Weyand, Nathan J.; Rendón, María A.; Calton, Christine M.; Hernández, Diana R.; Higashi, Dustin L.; Sodergren, Erica; Weinstock, George M. (2010-07-28)."Genome Sequencing Reveals Widespread Virulence Gene Exchange among Human Neisseria Species".PLOS ONE.5 (7): e11835.Bibcode:2010PLoSO...511835M.doi:10.1371/journal.pone.0011835.ISSN 1932-6203.PMC 2911385.PMID 20676376.
- ^Tronel H, Chaudemanche H, Pechier N, Doutrelant L, Hoen B (May 2001)."Endocarditis due toNeisseria mucosa after tongue piercing".Clin. Microbiol. Infect.7 (5):275–6.doi:10.1046/j.1469-0691.2001.00241.x.PMID 11422256.
- ^Ullrich, M, ed. (2009).Bacterial Polysaccharides: Current Innovations and Future Trends. Caister Academic Press.ISBN 978-1-904455-45-5.
- ^Wilson, Brenda A.; Winkler, Malcolm E.; Ho, Brian Thomas (2019).Bacterial pathogenesis: a molecular approach (4th ed.). Washington, DC: ASM Press. p. 161.ISBN 978-1-55581-940-8.
- ^Minogue, T. D.; Daligault, H. A.; Davenport, K. W.; Bishop-Lilly, K. A.; Bruce, D. C.; Chain, P. S.; Chertkov, O.; Coyne, S. R.; Freitas, T. (2014-09-25)."Draft Genome Assembly of Neisseria lactamica Type Strain A7515".Genome Announcements.2 (5): e00951–14.doi:10.1128/genomeA.00951-14.PMC 4175205.PMID 25291770.
- ^ab"Neisseria in the PATRIC database".PATRIC. 2017-02-26. Retrieved2017-02-26.
- ^Alexander, Sarah; Fazal, Mohammed-Abbas; Burnett, Edward; Deheer-Graham, Ana; Oliver, Karen; Holroyd, Nancy; Parkhill, Julian; Russell, Julie E. (2016-08-25)."Complete Genome Sequence of Neisseria weaveri Strain NCTC13585".Genome Announcements.4 (4): e00815–16.doi:10.1128/genomeA.00815-16.PMC 5000823.PMID 27563039.
- ^"meningococcal group B vaccine".Medscape. WebMD. RetrievedDecember 16, 2015.
- ^Seib KL, Rappuoli R (2010). "Difficulty in Developing a Neisserial Vaccine".Neisseria: Molecular Mechanisms of Pathogenesis. Caister Academic Press.ISBN 978-1-904455-51-6.
- ^Unemo M, Nicholas RA (December 2012)."Emergence of multidrug-resistant, extensively drug-resistant and untreatable gonorrhea".Future Microbiol.7 (12):1401–1422.doi:10.2217/fmb.12.117.PMC 3629839.PMID 23231489.
- ^Cehovin A, Simpson PJ, McDowell MA, Brown DR, Noschese R, Pallett M, Brady J, Baldwin GS, Lea SM, Matthews SJ, Pelicic V (2013)."Specific DNA recognition mediated by a type IV pilin".Proc. Natl. Acad. Sci. U.S.A.110 (8):3065–70.Bibcode:2013PNAS..110.3065C.doi:10.1073/pnas.1218832110.PMC 3581936.PMID 23386723.
- ^Davidsen T, Rødland EA, Lagesen K, Seeberg E, Rognes T, Tønjum T (2004)."Biased distribution of DNA uptake sequences towards genome maintenance genes".Nucleic Acids Res.32 (3):1050–8.doi:10.1093/nar/gkh255.PMC 373393.PMID 14960717.
- ^Caugant DA, Maiden MC (2009)."Meningococcal carriage and disease--population biology and evolution".Vaccine.27 (Suppl 2): B64–70.doi:10.1016/j.vaccine.2009.04.061.PMC 2719693.PMID 19464092.
- ^Michod RE, Bernstein H, Nedelcu AM (2008). "Adaptive value of sex in microbial pathogens".Infect. Genet. Evol.8 (3):267–85.doi:10.1016/j.meegid.2008.01.002.PMID 18295550.
- ^"IPNC - Neisseria.org".neisseria.org. Retrieved2021-01-02.