Neisseria meningitidis
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Classification
| Neisseria meningitidis | ||||||||||||||
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| Scientific classification | ||||||||||||||
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| Binomial name | ||||||||||||||
| Neisseria meningitidis |
Description & Significance
Neisseria meningitidis is a type of gram negative, parasitic, aerobic bacteria included among the proteobacteria. These organisms are extremely oxidase and catalase positive, are nonmotile or endospore forming and are extremely susceptible to drying. N. meningitidis bacteria are also diplococci, and therefore resemble coffee beans somewhat in their shape. *PICTURE* This bacteria has been found to be the causitive agent of bacterial meningitis, a disease that has appeared to date back to the 16th century. However the diease was only first descrined in 1805 by Swiss physician Gaspard Vieusseaux. Following Vieusseaux, Italian pathologists Ettore Marchiafava and Angelo Celli also described the micrococci in a sample of cerebral spinal fluid (CSF). Finally in 1887, the bacteria was isolated by Anton Weichselbaum.
The genome of Neisseria menignitidis, as well as other bacteria, contains its DNA within which its entire hereditary information is encoded. The genome of a 3 of the 13 serotypes have been sequenced. Strain Z2491, belonging to serotype A, was completely sequenced in September of 2001 by the Sanger Institute. The genome of this particular strain was found to be circular, with a nucleotide length of 2,184,406, was found to contain 2,208 genes, 2,049 protein coding genes, 72 structural RNAs, 87 pseudogenes, 1 contig, be 80% codinf and have a GC content of 51%.
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, vaccination and treatment are not only made possible, but more efficient as well.
Cell structure and metabolism
A notable feature of this bacteria are it's prominent antiphagocytic polysaccharide capsule. The 13 known serogroups; A, B, C, H, I, K, L, M, X, Y, Z, 29E and W135; are grouped on the basis of the capsular polysaccharides which envelope them. They are then further classified into 10 serotypes on the basis of class 2 or 3 OMP antigens, as well as 10 subtypes on the basis of class 1 OMP antigens, and finally 13 immunotypes on the basis of lipooligosccharide 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. N. meningitidis 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, mentioned above.
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 13 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 and septicemic 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. There is a 3-30% normal carrier state lasting days to months that provides the reservoir for infection of susceptible persons. Specifically, the bacterium can be found in the nasopharyngeal tract, in its asymptomatic 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.
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, easily passed to individuals via kissing, sexual contact, coughing and sneezing, giving birth and living in crowded conditions such as dormitories. Risk factors for contracting this disease include time of year (most prevalent during late winter/early spring) being male, age, genetics, a weakened immune system due to a condition such as HIV, and living in crowded conditions as for mentioned. If left untreated meningitis could result in meningicoccal septicemia[[2]] and/or death. 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.[[3]] 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.[[4]]
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 http://genomebiology.com/2007/8/7/R136