Small aerobic gram negative cocci, coffee bean like diplococci or in clumps.

It is an encapsulated bacteria primarily targeted by the body’s complement system.

Two medically important agents Neisseria meningitidis and N. gonorrhoeae.

Both agents are oxidase positive.

N. meningitidis colonizes the nasopharynx in approximately 10% of healthy persons, and less frequently, also colonizes  other mucosal sites, such as the cervix urethra and rectum.

N. meningitidis is differentiated from N. gonorrhoeae by a polysaccharide capsule that impairs phagocytosis and it metabolizes both glucose and maltose and N. gonorrhoeae metabolizes only glucose.

N meningitides and N gonorrhoeae have similar virulence factors including: pili that mediate mucosal surface attachment, Por proteins form outer membrane pores that allow passage of nutrients and waste material, and may prevent complement dependent bacterial destruction, Opa proteins are involved in surface adhesion and LOS(lipo-oligosaccharide) a variant of gram negative endotoxin, IgA proteases that cleave the immunoglobulin IgA into its inactive components, and Siderphores allowing collection of iron from iron binding proteins.

Neisseria gonorrhoeae, also known as gonococci or gonococcus is a species of Gram-negative coffee bean-shaped diplococci bacteria responsible for the sexually transmitted infection gonorrhea.

Neisseria are fastidious Gram-negative cocci.

Requires nutrient supplementation to grow in laboratory cultures on chocolate agar with carbon dioxide.

These cocci are facultatively intracellular

Apppear in pairs (diplococci), in the shape of coffee beans.

Eleven species of Neisseria that colonize humans, only two are pathogens.

N. gonorrhoeae is the causative agent of gonorrhea, and is transmitted via sexual contact.

Usually isolated on Thayer-Martin agar or VPN agar, an agar plate containing vancomycin, colistin, nystatin, and TMP-SMX.

Testing to differentiate the species includes testing for oxidase and the carbohydrates maltose, sucrose, and glucose test.

N. gonorrhoeae are motile and possess type IV pili to adhere to surfaces.

N. gonorrhoeae has surface proteins called Opa proteins, which bind to receptors on immune cells.

Opa proteins on N. gonorrhoeae are able to prevent an immune response and immunological memory so that future reinfection is possible.

N. gonorrhoeae can evade the immune system through antigenic variation of its antigenic determinants on its surface, making it more difficult for immune cells to recognize N. gonorrhoeae and mount a defense.

N. gonorrhoeae has the ability to undergo DNA conformational changes that can lead to antibiotic resistance.

10% of infected males and 80% of infected females are asymptomatic.

Infection of the genitals can result in a purulent discharge from the genitals which may be foul smelling.

Infection symptoms may include inflammation, redness, swelling of genitalia, and dysuria.

N. gonorrhoeae can also cause conjunctivitis, pharyngitis, proctitis, urethritis, prostatitis and orchitis.

Conjunctivitis is common in neonates such that 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 result in endocarditis, meningitis or gonococcal dermatitis-arthritis syndrome.

Disseminated gonococcal infection is a complication of sexually transmitted :N. Gonorrheaebwhich affects approximately 1–3% of the estimated 550,000 individuals infected with gonorrhea in the United States annually.

62% of cases with disseminated gonococcal infection have an arthritic form of disease characterized by migratory arthritis, hemorrhagic vesicular pustules and tenosynovitis, as well as mono articular septic joint form at 38%.

Dermatitis-arthritis syndrome presents with arthralgia, tenosynovitis and painless non-pruritic dermatitis.

Infection of the genitals in females with N. gonorrhoeae can result in pelvic inflammatory disease.

Pelvic inflammatory disease, if left untreated, 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 with an infertility risk to 10 to 20% of the females infected with N. gonorrhoeae.

If N. gonorrhoeae is resistant to the penicillin, then ceftriaxone is often used.

Sexual partners should also be notified and treated.

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.

N. gonorrhoeae has a high affinity for horizontal gene transfer, however, antibiotic-resistant gonorrhea is seen as an emerging public health threat.

Patients should also be tested for other sexually transmitted infections, especially Chlamydia infections, since co-infection is seen in up to 50% of cases, and antibacterial coverage is often included for Chlamydia because of this.

Transmission can be reduced by the usage of condoms or dental dams, during intercourse, oral and anal sex, and by limiting sexual partners.

The exudates from infected individuals contain many polymorphonuclear leukocytes (PMN) with ingested gonococci, which stimulate the PMN to release reactive oxygen species in order to kill the gonococci.

A significant fraction of the gonococci can resist killing and are able to reproduce within the PMN phagosomes.

Bacterial RecA protein mediates recombinational repair of DNA damage, and plays an important role in gonococcal survival.

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