出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/08/05 23:35:32」(JST)
| Neisseria gonorrhoeae | |
|---|---|
| Neisseria gonorrhoeae cultured on two different media types. | |
| Scientific classification | |
| Kingdom: | Bacteria |
| Phylum: | Proteobacteria |
| Class: | Beta Proteobacteria |
| Order: | Neisseriales |
| Family: | Neisseriaceae |
| Genus: | Neisseria |
| Species: | N. gonorrhoeae |
| Binomial name | |
| Neisseria gonorrhoeae Zopf, 1885 |
|
| Synonyms | |
|
Gonococcus Neisser 1879 |
|
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. gonorrhoeae was first described by Albert Neisser in 1879.
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") 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 non-motile 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 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.[7]
The genomes of several strains of N. gonorrhoeae have been sequenced. Most of them are about 2.1 Mb in size and encode 2,100 to 2,600 proteins (although most seem to be in the lower range).[8] For instance, strain NCCP11945 consists of one circular chromosome (2,232,025 bp) encoding 2,662 predicted ORFs and one plasmid (4,153 bp) encoding 12 predicted ORFs. The estimated coding density over the entire genome is 87%, and the average G+C content is 52.4%, values that are similar to those of strain FA1090. The NCCP11945 genome encodes 54 tRNAs and four copies of 16S-23S-5S rRNA operons.[9]
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.[10][11]
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.[12]
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.[13] Men who have had a gonorrhea infection have a significantly increased risk of having prostate cancer.[14]
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.[citation needed]
N. gonorrhoeae can also cause conjunctivitis, pharyngitis, proctitis or urethritis, prostatitis, and orchitis.[citation needed]
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.[citation needed]
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.[citation needed]
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 females infected with N. gonorrhoeae.[citation needed]
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.[15]
Antibiotic resistance in gonorrhea has been noted by beginning in the 1940s, when gonorrhea was treated with penicillin, but doses had to be continually increased in order to remain effective. By the 1970s, 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.”[16]
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. gonorrhoeae’s high affinity for horizontal gene transfer, however, antibiotic-resistant gonorrhea is seen as an emerging public health threat.[16]
Patients should also be tested for other sexually transmitted infections (there is a fivefold increase of HIV transmission[17]), especially Chlamydia infections, since co-infection is frequent (up to 50% of cases). Antibacterial coverage is often included for Chlamydia because of this.[citation needed]
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.[citation needed]
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.[18]
The exudates from infected individuals contain many polymorphonuclear leukocytes (PMN) with ingested gonococci. These gonococci stimulate the PMN to release an internal oxidative burst involving reactive oxygen species in order to kill the gonococci.[19] 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.[20] 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.[21]
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| リンク元 | 「結膜炎」「淋菌性結膜炎」 |
| 拡張検索 | 「neonatal gonococcal conjunctivitis」 |
see. マイナーエマージェンシー第1版 p.65 SOP.174
| 疾患名 | 病原体 | 潜伏期 | 病型 | 症状、経過 | |||
| 感染性結膜炎 | 流行性角結膜炎 | epidemic keratoconjunctivitis | はやりめ | アデノウイルス8,19,37型(ときに4型) | 7-14日 | 急性濾胞性結膜炎 | 眼脂、流涙、羞明。眼瞼腫瘤、結膜充血、浮腫、結膜の小出血斑。耳前リンパ節の腫脹と圧痛。2-4週間で消退。発症後10日後に角膜に点状上皮化混濁。 |
| 咽頭結膜熱 | pharyngoconjunctival fever | プール熱 | アデノウイルス3型(ときに4,7型) | 5-6日 | 急性結膜炎 | 急性結膜炎、咽頭炎、発熱。点状上皮化混濁は少ない。 | |
| 急性出血性結膜炎 | acute hemorrhagic conjunctivitis | エンテロウイルス70型 | 1日 | 球結膜下出血。眼球は浮腫状、結膜充血、濾胞形成は軽度。耳前リンパ節腫脹軽度。発症より3-4日にびまん性の多発性びらん。眼痛、異物感、羞明。約1週間で治癒。罹患後2,3週間後に四肢の弛緩性の運動麻痺や脳神経麻痺があり得る。 | |||
| トラコーマ | trachoma | ||||||
| 封入体結膜炎 | inclusion conjunctivitis | ||||||
| 新生児封入体結膜炎 | neonatal inclusion conjunctivitis | ||||||
| 細菌性結膜炎 | bacterial conjunctivitis | ||||||
| 淋菌性結膜炎 | gonococcal conjunctivitis | ||||||
| 新生児膿漏眼 | blennorrhea of the newborn | ||||||
| アレルギー性結膜疾患 | アレルギー性結膜炎 | allergic conjunctivitis | |||||
| 春季カタル | vernal conjunctivitis | ||||||
| その他の結膜炎 | フリクテン性結膜炎 | phlyctenular conjunctivitis | 束状結膜炎 | ||||
| 慢性濾胞性結膜炎 | chronic follicular conjunctivitis | ||||||
| Stevens-Johnson症候群 | Stevens-Johnson syndrome | ||||||
| 眼類天疱瘡 | ocular pemphigoid | ||||||
| 結膜弛緩症 | conjunctivochalasis | ||||||