5/12/14, 9:17 PM Neisseria gonorrhoeae - Wikipedia, the free encyclopedia

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Neisseria gonorrhoeae
Neisseria gonorrhoeae, also known as gonococci (plural), or gonococcus (singular), is a
species of Gram-negative coffee bean-shaped diplococci bacteria responsible for the sexually
transmitted infection gonorrhea.
[1]
N. gonorrhoea was first described by Albert Neisser in 1879.
Microbiology
Neisseria are fastidious Gram-negative cocci that require nutrient supplementation to grow in
laboratory cultures. To be specific, they grow on chocolate agar with carbon dioxide. These cocci are
facultatively intracellular and typically appear in pairs (diplococci), in the shape of coffee beans. Of
the eleven species of Neisseria that colonize humans, only two are pathogens. N. gonorrhoeae is the
causative agent of gonorrhea (also called "The Clap," which is derived from the French word
"clapier," meaning "brothel") and is transmitted via sexual contact.
[2]
Neisseria is usually isolated on Thayer-Martin agar (or VPN agar)an agar plate containing
antibiotics (vancomycin, colistin, nystatin, and trimethoprim) and nutrients that facilitate the growth
of Neisseria species while inhibiting the growth of contaminating bacteria and fungi. Further testing
to differentiate the species includes testing for oxidase (all clinically relevant Neisseria show a
positive reaction) and the carbohydrates maltose, sucrose, and glucose test in which N. gonorrhoeae
will oxidize (that is, utilize) only the glucose.
N. gonorrhoeae are motile (twitching motility) and possess type IV pili to adhere to surfaces. The
type IV pili operate mechanistically similar to a grappling hook. Pili extend and attach to a substrate
that signals the pilus to retract, dragging the cell forward. N. gonorrhoeae are able to pull 100,000
times their own weight, and it has been claimed that the pili used to do so are the strongest biological
motor known to date, exerting one nanonewton.
[3]
N. gonorrhoeae has surface proteins called Opa proteins, which bind to receptors on immune cells.
In so doing, N. gonorrhoeae is able to prevent an immune response. The host is also unable to
develop an immunological memory against N. gonorrhoeae which means that future reinfection is
possible. N. gonorrhoeae can also evade the immune system through a process called antigenic
variation, in which the N. gonorrhoeae bacterium is able to alter the antigenic determinants (sites
where antibodies bind) such as the Opa proteins
[4]
and Type IV pili
[5]
that adorn its surface. The
many permutations of surface proteins make it more difficult for immune cells to recognize N.
gonorrhoeae and mount a defense.
[6]
N. gonorrhoeae is naturally competent for DNA transformation as well as being capable of
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conjugation. These processes allow for the DNA of N. gonorrhoeae to acquire or spread new genes.
Especially dangerous from the aspect of healthcare is the ability to conjugate, since this can lead to
antibiotic resistance.
In 2011, researchers at Northwestern University found evidence of a human DNA fragment in a
Neisseria gonorrhoeae genome, the first example of horizontal gene transfer from humans to a
bacterial pathogen.
[7][8]
Transmission
N. gonorrhoeae is transmitted from person to person during sexual relations. Traditionally, the
bacteria was thought to move attached to spermatozoon, but this hypothesis did not explain female
to male transmission of the disease. A recent study suggests that rather than surf on wiggling
sperm, N. gonorrhoeae bacteria uses hairlike structures called pili to anchor onto proteins in the
sperm and move through coital liquid.
[9]
Disease
Main article: Gonorrhoea
Symptoms of infection with N. gonorrhoeae differ, depending on the site of infection. Note also that
10% of infected males and 80% of infected females are asymptomatic.
[citation needed]
Infection of the genitals can result in a purulent (or pus-like) discharge from the genitals, which may
be foul-smelling. Symptoms may include inflammation, redness, swelling, and dysuria
N. gonorrhoeae can also cause conjunctivitis, pharyngitis, proctitis or urethritis, prostatitis, and
orchitis.
Conjunctivitis is common in neonates (newborns), and silver nitrate or antibiotics are often applied
to their eyes as a preventive measure against gonorrhoea. Neonatal gonorrheal conjunctivitis is
contracted when the infant is exposed to N. gonorrhoeae in the birth canal and can lead to corneal
scarring or perforation, resulting in blindness in the neonate.
Disseminated N. gonorrhoeae infections can occur, resulting in endocarditis, meningitis or
gonococcal dermatitis-arthritis syndrome. Dermatitis-arthritis syndrome presents with arthralgia,
tenosynovitis, and painless non-pruritic (non-itchy) dermatitis.
Infection of the genitals in females with N. gonorrhoeae can result in pelvic inflammatory disease if
left untreated, which can result in infertility. Pelvic inflammatory disease results if N. gonorrhoeae
travels into the pelvic peritoneum (via the cervix, endometrium and fallopian tubes). Infertility is
caused by inflammation and scarring of the fallopian tube. Infertility is a risk to 10 to 20% of the
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females infected with N. gonorrhoeae.
Treatment and prevention
If N. gonorrhoeae is resistant to the penicillin family of antibiotics, then ceftriaxone (a third-
generation cephalosporin) is often used. Sexual partners should also be notified and treated.
[10]
Antibiotic-resistant gonorrhea has been noted by epidemiologists; beginning in the 1940s, gonorrhea
was treated with penicillin, but doses had to be continually increased in order to remain effective,
and, by the 70s, penicillin- and tetracycline-resistant gonorrhea emerged in the Pacific Basin. These
resistant strains then spread to Hawaii, California, the rest of the United States, and Europe.
Fluoroquinolones were the next line of defense, but soon resistance to this antibiotic emerged as
well. Since 2007, standard treatment has been third-generation cephalosporins, such as ceftriaxone,
which are considered to be our last line of defense.
[11]
Recently, a high-level ceftriaxone-resistant strain of gonorrhea, called H041, was discovered in
Japan. Lab tests found it to be resistant to high concentrations of ceftriaxone, as well as most of the
other antibiotics tested. Within N. gonorrhoeae, there are genes that confer resistance to every single
antibiotic used to cure gonorrhea, but thus far they do not coexist within a single gonococcus.
Because of N. gonorrhoeaes high affinity for horizontal gene transfer, however, antibiotic-resistant
gonorrhea is seen as an emerging public health threat.
[11]
Patients should also be tested for other sexually transmitted infections, especially Chlamydia
infections, since co-infection is frequent (up to 50% of cases). Antibacterial coverage is often
included for Chlamydia because of this.
Transmission can be reduced by the usage of latex barriers, such as condoms or dental dams, during
intercourse, oral and anal sex, and by limiting sexual partners.
Vaccine
Due to the relative frequency of infection and the emerging development of antibiotic resistance in
strains of N. gonorrhoeae, vaccines are thought to be an important goal in the prevention of
infection. However, there has been a relatively low emphasis on research to such a vaccine in the
medical literature and few human clinical trials for prospective vaccines. The ability to develop an
effective vaccine has been limited by the lack of acquired immunity to infection to model a vaccine
after and the current lack of commitment in effort and resources.
[12]
Survival of gonococci
The exudates from infected individuals contain many polymorphonuclear leukocytes (PMN) with
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ingested gonococci. These gonococci stimulate the PMN to release an internal oxidative burst
involving reactive oxygen species in order to kill the gonococci.
[13]
However, a significant fraction of
the gonococci can resist killing and are able to reproduce within the PMN phagosomes.
Stohl and Seifert showed that the bacterial RecA protein, that mediates recombinational repair of
DNA damage, plays an important role in gonococcal survival.
[14]
The protection afforded by RecA
protein may be linked to transformation, the process by which recipient gonococci take up DNA from
neighboring gonococci and integrate this DNA into the recipient genome through recombination.
Michod et al. have suggested that an important benefit of transformation in N. gonorrhoeae may be
recombinational repair of oxidative DNA damages caused by oxidative attack by the hosts phagocytic
cells.
[15]
See also
Neisseria meningitidis
References
1. ^ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill.
ISBN 0-8385-8529-9.
2. ^ Genco, C; Wetzler, L (editors) (2010). Neisseria: Molecular Mechanisms of Pathogenesis.
Caister Academic Press. ISBN 978-1-904455-51-6.
3. ^ "Mighty microbe pulls 100,000 times its bodyweight". New Scientist. 19 April 2008. Retrieved
2009-07-01.
4. ^ Stern, Anne; Brown, Nickel, Meyer (10 October 1986). "Opacity genes in Neisseria
gonorrhoeae: Control of phase and antigenic variation". Cell 47 (1).
5. ^ Cahoon, Laty; Seifert (4 August 2011). "Focusing homologous recombination: pilin antigenic
variation in the pathogenic Neisseria". Mol. Microbiol. 81 (5): 11361143. doi:10.1111/j.1365-
2958.2011.07773.x.
6. ^ STI Awareness: Gonorrhea. Planned Parenthood Advocates of Arizona. 11 April 2011.
Retrieved 31 August 2011.
7. ^ "Gonorrhea Acquires a Piece of Human DNA: First Evidence of Gene Transfer from Human
Host to Bacterial Pathogen". ScienceDaily.com. 13 February 2011. Retrieved 15 February 2011.
8. ^ Anderson, Mark T.; H. Steven Seifert (15 Feb 2011). "Opportunity and Means: Horizontal
Gene Transfer from the Human Host to a Bacterial Pathogen". MBio 2 (1): e0000511.
doi:10.1128/mBio.00005-11. PMC 3042738. PMID 21325040.
9. ^ Anderson, Mark T. (2014). "Seminal Plasma Initiates a Neisseria gonorrhoeae Transmission
State". mBio 5 (2): e01004-13. doi:10.1128/mBio.01004-13.
10. ^ "UK doctors advised gonorrhoea has turned drug resistant". BBC News. 10 October 2011.
11. ^
a

b
STI Awareness: Antibiotic-Resistant Gonorrhea. Planned Parenthood Advocates of
5/12/14, 9:17 PM Neisseria gonorrhoeae - Wikipedia, the free encyclopedia
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Arizona. 6 March 2012. Retrieved 6 March 2012.
12. ^ Zhu W, Chen CJ, Thomas CE, Anderson JE, Jerse AE, Sparling PF (2011). "Vaccines for
gonorrhea: can we rise to the challenge?". Front Microbiol 2: 124.
doi:10.3389/fmicb.2011.00124. PMC 3109613. PMID 21687431.
13. ^ Simons MP, Nauseef WM, Apicella MA (2005). Interactions of Neisseria gonorrhoeae with
adherent polymorphonuclear leukocytes. Infect Immun 73(4):1971-1977. PMID 1578453
14. ^ Stohl EA, Seifert HS (2006). Neisseria gonorrhoeae DNA recombination and repair enzymes
protect against oxidative damage caused by hydrogen peroxide. J Bacteriol 188(21):7645-7651.
PMID 16936020
15. ^ Michod RE, Bernstein H, Nedelcu AM (2008). Adaptive value of sex in microbial pathogens.
Infect Genet Evol 8(3):267-285. Review. PMID 18295550
http://www.hummingbirds.arizona.edu/Faculty/Michod/Downloads/IGE%20review%20sex.pdf
External links
Todar's Online Textbook of Bacteriology
eMedicine: Gonococcal Infections