Neisseria meningitidis
Articles that lack this notice, including many Eduzendium ones, welcome your collaboration! |
Classification
Neisseria meningitidis | ||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Scientific classification | ||||||||||||||
| ||||||||||||||
Binomial name | ||||||||||||||
Neisseria meningitidis |
Description & Genome Structure
Neisseria meningitidis is a type of gram negative, aerobic bacteria included among the proteobacteria. These organisms are extremely oxidase and catalase positive, have an oxidative metabolism and are extremely susceptible to drying. N. meningitidis bacteria are also diplococci, and therefore resemble coffee beans somewhat in their shape. *PICTURE* This bacteria also contains an outer membrane integral protein known as OpcA. This protein's purpose has been linked to cell adhesion of Neisseria meningitidis to epithelial, as well as endothelial cells via binding to vitronectin and proteoglycan cell-surface receptors located within the host. The Opca protein has been found to function independently of pilus based adhesion.
The genome of Neisseria menignitidis, as well as other bacteria, contains its DNA within which its entire hereditary information is encoded. DNA from a number of the 12 serotypes strains have been sequenced.
The 2,272,351-base pair genome of Neisseria meningitidis strain MC58 (serogroup B), a causative agent of meningitis and septicemia, contains 2158 predicted coding regions, 1158 (53.7%) of which were assigned a biological role. Three major islands of horizontal DNA transfer were identified; two of these contain genes encoding proteins involved in pathogenicity, and the third island contains coding sequences only for hypothetical proteins. Insights into the commensal and virulence behavior of N. meningitidis can be gleaned from the genome, in which sequences for structural proteins of the pilus are clustered and several coding regions unique to serogroup B capsular polysaccharide synthesis can be identified. Finally, N. meningitidis contains more genes that undergo phase variation than any pathogen studied to date, a mechanism that controls their expression and contributes to the evasion of the host immune system.
[[1]]
Clearly, the information provided by the genomic sequencing of MC58 as well as serogroup C strain FAM18, among others, has enabled researches to discover the means by which this bacteria invade and infect their hosts. Furthermore, without this molecular level understanding, treatment of meningitis would be difficult.
Cell structure and metabolism
Neisseria meningitidis, is a gram-negative diplococcal bacterium. A notable feature of this bacterium is its prominent antiphagocytic polysaccharide capsule. The 12 strains that have been identified are grouped on the basis of their capsular polysaccharides; which in certain cases can be further subdivided according to the presence of outer membrane protein and lipopolysaccharide antigens. Neisseria meningitidis cell surface also posseses type IV pili, which are retractile fibers that serve in their attachment to epithelial cells during host colonization and invasion. As far as sources of energy are concerned, glucose and lactose are believed to be essential for successful colonization.
Ecology
Neisseria is strictly found in human hosts- no animal hosts are known to exist. Naturally, a small percentage of the population are carriers for the asymptomatic form of the bacteria. Consequently, Neisseria meningitidis impose no detrimental affects on their hosts as long as they remain in the nasopharyngeal tract. Neisseria provide no direct benefits to their human hosts either.
Pathology
As mentioned earlier, there are approximately 12 serogroups of Neisseria meningiditis. Among these known strains, serogroups A, B, and C have been found to be those responsible for 90% of meningococcal meningitis cases. Specifically, serogroup A has been implicated in meningitis epidemics in developing countries, while serogroups B and C have been implicated in meningitis epidemics in already developed countries.
Neisseria meningitidis is only found in human hosts of which 5-15% of the population are carriers. Specifically, the bacterium can be found in the nasopharyngeal tract, in its non-detrimental form. Transformation from it's initial asymptomatic form into meningitis arises when the bacterium crosses the mucosal barrier via type IV pili, and enters the blood stream. Once in the blood stream they are free to travel to the cerebral spinal fluid or the meninges, tissues that surround the brain and spinal cord. Accordingly, this infection of the meninges results in bacterial meningitis, which mainly affects adults, and should not be confused with viral meningitis which affects babies and young children.
Meningitis results in the swelling of the meninges and causes flu-like such as high fever, severe headache, and neck stiffness and pain that make touching your chin to your chest difficult. It is also highly contagious and could result in death if left untreated. Fortunately, antibiotics and steriod medications can be used to cure the disease and treat inflammation, respectively.
Application to Biotechnology
Does this organism produce any useful compounds or enzymes? What are they and how are they used?
Current Research
A vast amount of research is being performed on Neisseria meningitidis in order to gain further insight into a varitey of different areas. In one study, researchers have used serogroup B Neisseria meningitidis as a means of assertaining the effect that luxS has on virulence. LuxS is required for autoindicer-2 (AI-2) production. Autoinducer-2 is a boron-based molecule that is produced by bacteria, such as N. meninigitidis, that controls the signals in the quorum sensing process by which biofilms establish a network of communication between them.[[2]] Numerous bacteria have been found to posses luxS. In this particular study reseachers have discovered that serotype B Neisseris meningitidis posses a functional copy of luxS that is vital for full meningococcal virulence. Consequently, strains that lack luxS (due to a deletion) are defective to bacteremia, a precursor of meningococcal pathogenesis.[[3]]
References
http://en.wikipedia.org/wiki/Neisseria_meningitidis http://www.brown.edu/Courses/Bio_160/Projects1999/bmenin/nmenin.html http://www.sanger.ac.uk/Projects/N_meningitidis http://www.webmd.com/a-to-z-guides/meningitis-cause http://en.wikipedia.org/wiki/Genomes http://www.sciencemag.org/cgi/content/abstract/sci;287/5459/1809 http://www.cehs.siu.edu/fix/medmicro/neiss.htm