Neisseria gonorrhoeae - wikipedia Neisseria gonorrhoeae Neisseria gonorrhoeae Gram - stain of gonococcal urethritis. Note distribution in neutrophils and presence of both intracellular and extracellular bacteria. ( CDC ) Scientific classification Domain : Bacteria Phylum : Proteobacteria Class : Betaproteobacteria Order : Neisseriales Family : Neisseriaceae Genus : Neisseria Species : N. gonorrhoeae Binomial name Neisseria gonorrhoeae ( Zopf 1885 ) Trevisan 1885 Synonyms Micrococcus der Gonorrhoe Neisser 1879 Gonococcus neisseri Lindau 1898 Neisseria gonorrhoeae, also known as gonococcus ( singular ), or gonococci ( plural ) is a species of gram - negative diplococci bacteria isolated by Albert Neisser in 1879. It causes the sexually transmitted genitourinary infection gonorrhea as well as other forms of gonococcal disease including disseminated gonococcemia, septic arthritis, and gonococcal ophthalmia neonatorum. It is oxidase positive, aerobic, and it survives within neutrophils. To culture, it requires carbon dioxide supplementation and enriched agar ( chocolate agar ) with various antimicrobials ( Thayer - Martin ). It exhibits antigenic variation through recombination of its pili and surface proteins that interact with the immune system. Sexual transmission is possible through vaginal, anal, or oral sex. Sexual transmission may be prevented through the use of barrier protection. Perinatal transmission may occur during childbirth, and may be prevented by antibiotic treatment of the mother before birth and the application of antibiotic eye gel on the eyes of the newborn. After an episode of gonococcal infection, infected persons do not develop immunity to future infections. Reinfection is possible due to N. gonorrhoeae 's ability to evade the immune system by varying its surface proteins. N. gonorrhoeae can cause infection of the genitals, throat, and eyes. Asymptomatic infection is common in males and females. Untreated infection may spread to the rest of the body ( disseminated gonorrhea infection ), especially the joints ( septic arthritis ). Untreated infection in women may cause pelvic inflammatory disease and possible infertility due to the resulting scarring. Diagnosis is through culture, gram stain, or PCR of a urine sample, urethral swab, or cervical swab. Chlamydia co-testing and testing for other STI 's is recommended due to high rates of coinfection. Due to resistance to penicillins, standard treatment is with the third generation cephalosporin ceftriaxone. Antibiotic resistance is a growing problem due to N. gonnorhoeae 's recombinant abilities. There is currently no vaccine available for N. gonorrhoeae although efforts are underway to develop one. Because it is possible to contract gonorrhea multiple times from the same partner ( who may or may not be symptomatic ) notification and treatment of sexual partners is recommended. Contents 1 Microbiology 1.1 Culture and identification 1.2 Surface proteins 1.3 Antigenic variation 1.4 Survival of gonococci 2 Genome 2.1 Horizontal gene transfer 3 Transmission 4 Disease 4.1 Diagnosis 4.2 Prevention 4.3 Treatment 4.4 Antibiotic resistance 4.5 Vaccine 5 History 5.1 Name origin 5.2 Discovery 6 See also 7 References 8 External links Microbiology. Neisseria species are fastidious Gram - negative cocci that require nutrient supplementation to grow in laboratory cultures. Neisseria are facultatively intracellular and typically appear in pairs ( diplococci ), resembling the shape of coffee beans. Nesseria is non-spore forming, non-motile and an obligate aerobe ( requires oxygen to grow ). Of the 11 species of Neisseria that colonize humans, only two are pathogens. N. gonorrhoeae is the causative agent of gonorrhea ( also called `` the clap '' ) and N. meningitidis is the causative agent of meningitis. Culture and identification Thayer - Martin Agar is selective for growth of Neisseria species. Further testing ( oxidase, gram stain, carbohydrate utilization ) is needed to differentiate N. gonorrhoeae from meningitidis Carbohydrate utilization of Neisseria gonorrhoeae. N. gonorrhoeae will oxidise glucose, not maltose, sucrose, or lactose ; N. meningitidis ferments glucose and maltose. Neisseria gonorrhoeae is usually isolated on Thayer - Martin agar ( or VPN ) agar in an environment enriched with 3 - 7 % carbon dioxide. Thayer - Martin agar is a chocolate agar plate ( heated blood agar ) containing nutrients and antimicrobials ( vancomycin, colistin, nystatin, and trimethoprim ). This agar preparation facilitates the growth of Neisseria species while inhibiting the growth of contaminating bacteria and fungi. Martin Lewis and New York City are other types of selective chocolate agar commonly used for neisseria growth. N. gonorrhoeae is oxidase positive ( possessing cytochrome c oxidase ) and catalase positive ( able to convert hydrogen peroxide to oxygen ). When incubated with the carbohydrates lactose, maltose, sucrose, and glucose, N. gonorrhoeae will oxidize only the glucose. Surface proteins On its surface, N. gonorrhoeae bears hair - like pili, surface proteins with various functions, and sugars called lipooligosaccharides. The pili mediate adherence, movement, and DNA exchange. The Opa proteins interact with the immune system, as do the Porins. Lipooligosaccharide ( LOS ) is an endotoxin that provokes an immune response. All are antigenic and all exhibit antigenic variation ( see below ). The pili exhibit the most variation. The pili, Opa proteins, porins, and even the LOS have mechanisms to inhibit the immune response, making asymptomatic infection possible. Dynamic polymeric protein filaments called type IV pili allow N. gonorrhoeae to adhere to and move along surfaces. To enter the host the bacteria uses the pili to adhere to and penetrate mucosal surfaces. The pili are a necessary virulence factor for N. gonorrhoeae ; without them, the bacteria is unable to cause infection. To move, the bacteria uses the type IV pili like a grappling hook, extending and retracting it for movement. Pili extend and attach to a substrate that signals the pilus to retract, dragging the cell forward. The resulting movement is referred to as t witching motility. N. gonorrhoeae is able to pull 100,000 times its 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. A set of ATPase proteins power the pulling actions of the type IV pilus : Pil F ( extension ) and Pil T ( retraction ). The adhesive functions of the gonococcal pilus plays a role in microcolony aggregation and biofilm formation. This illustration depicts a Gram - stain of a urethral exudate showing typical intracellular gram - negative diplococci, and pleomorphic extracellular gram - negative organisms, which is diagnostic for gonococcal urethritis. Surface proteins called Opa proteins can be used to bind to receptors on immune cells and prevent an immune response. There are at least 12 Opa proteins and the many permutations of surface proteins make it more difficult for immune cells to recognize N. gonorrhoeae and mount a defense. Lipooligosaccharide ( LOS ) is a low - weight version of lipopolysaccharide present on the surfaces of most other gram negative bacteria. It is a sugar ( saccharide ) side chain attached to lipid A ( thus `` lipo - '' ) in the outer membrane coating the cell wall of the bacteria. The root `` oligo '' refers to the fact that it is a few sugars shorter than the typical lipopolysaccharide. As an endotoxin LOS provokes inflammation. The shedding of LOS by the bacteria is responsible for local injury in, for example, pelvic inflammatory disease. Although its main function is as an endotoxin, LOS may disguise itself with host sialic acid and block initiation of the complement cascade. Antigenic variation N. gonorrhoeae evades the immune system through a process called antigenic variation, in which the N. gonorrhoeae bacterium is able to recombine its genes and alter the antigenic determinants ( sites where antibodies bind ) such as the Opa proteins and Type IV pili that adorn its surface. It is able to vary the composition of its pili, Opa proteins, and lipooligosaccharides ( LOS ) ; of these, the pili exhibit the most antigenic variation due to chromosomal rearrangement. Every time the bacteria replicate they may switch multiple Opa proteins on or off through slipped - strand mispairing. That is, the bacteria introduces frameshift mutations that bring genes in or out of frame. The result is that different Opa genes are translated every time. In addition to the ability to rearrange the genes it already has, it is also naturally competent to acquire new DNA, via its type IV pilus, specifically proteins Pil Q and Pil T. These processes allow N. gonorrhoeae to acquire / spread new genes, disguise itself with different surface proteins, and prevent the development of immunological memory -- an ability which has led to antibiotic resistance and has made vaccine development difficult. Survival of gonococci After gonococci invade and transcytose the host epithelial cells they land in the submucosa, where neutrophils promptly consume them. The pili and Opa proteins on the surface may interfere with phagocytosis, but most gonococci end up in neutrophils. The exudates from infected individuals contain many neutrophils with ingested gonococci. Neutrophils release an oxidative burst of reactive oxygen species in their phagosomes in order to kill the gonococci. However, a significant fraction of the gonococci can resist killing through the action of their catalase which breaks down reactive oxygen species and are able to reproduce within the neutrophil phagosomes. Stohl and Seifert showed that the bacterial RecA protein, which mediates repair of DNA damage, plays an important role in gonococcal survival. Michod et al. have suggested that N. gonorrhoeae may replace DNA damaged in neutrophil phagosomes with DNA from neighboring gonococci. The process in which recipient gonococci integrate DNA from neighboring gonococci into their genome is called transformation. The growth of Neisseria gonorrhoeae colonies on New York City medium agar, a specialised and selective media for Gonococci Genome 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 ). 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. Horizontal gene transfer 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. Transmission N. gonorrhoeae may be transmitted through vaginal, oral, or anal sex ; nonsexual transmission is unlikely in adult infection. It can also be transmitted to the newborn during passage through the birth canal if the mother has untreated genitourinary infection. Given the high rate of asymptomatic infection, all pregnant women should be tested for gonorrhea infection. 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. Disease Main article : Gonorrhoea Symptoms of infection with N. gonorrhoeae differ, depending on the site of infection. Note also that many infected men are asymptomatic and most infected females ( 50 - 80 % ) are asymptomatic. In symptomatic men, the primary symptom of genitourinary infection is urethritis -- burning with urination ( dysuria ), increased urge to urinate, and a pus - like ( purulent ) discharge from the penis. The discharge may be foul smelling. If untreated, scarring of the urethra may result in difficulty urinating. Infection may spread from the urethra in the penis to nearby structures including the testicles ( epididymitis / orchitis ), or to the prostate ( prostatitis ). Men who have had a gonorrhea infection have a significantly increased risk of having prostate cancer. In symptomatic women, the primary symptoms of genitourinary infection are increased vaginal discharge, burning with urination ( dysuria ), increased urge to urinate, pain with intercourse, or menstrual abnormalities. Pelvic inflammatory disease results if N. gonorrhoeae ascends into the pelvic peritoneum ( via the cervix, endometrium and fallopian tubes ). The resulting inflammation and scarring of the fallopian tubes can lead to infertility and increased risk of ectopic pregnancy. Pelvic inflammatory disease develops in 10 to 20 % of the females infected with N. gonorrhoeae. N. gonorrhoeae may cause infection of the throat ( pharyngitis ) through oral sex. Infected persons may experience sore throat and swollen lymph nodes, or may be asymptomatic. N. gonorrhoeae may cause infection of the anus / rectum ( proctitis ) through anal sex. Infected persons may experience blood or a pus - like discharge, or may be asymptomatic. In perinatal infection, the primary manifestation is infection of the eye ( neonatal conjunctivitis or ophthalmia neonatorum ) when the newborn is exposed to N. gonorrhoeae in the birth canal. The eye infection can lead to corneal scarring or perforation, ultimately resulting in blindness. If the newborn is exposed during birth, conjunctivitis occurs within 2 -- 5 days after birth and is severe. Gonococcal ophthalmia neonatorum, once common in newborns, is prevented by the application of erythromycin ( antibiotic ) gel to the eyes of babies at birth as a public health measure. Silver nitrate is no longer used in the United States. Disseminated N. gonorrhoeae infections can occur in which gonococci enter the bloodstream, often spreading to the joints and causing a rash ( dermatitis - arthritis syndrome ). Dermatitis - arthritis syndrome presents with joint pain ( arthritis ), tendon inflammation ( tenosynovitis ), and painless non-pruritic ( non-itchy ) dermatitis. Disseminated infection and PID tend to begin after menses due to reflux during menses, facilitating spread. Rarely, disseminated infection may cause infection of the meninges of the brain and spinal cord ( meningitis ) or infection of the heart valves ( endocarditis ). Diagnosis Tests that use polymerase chain reaction ( PCR, aka nucleic acid amplification ) to identify genes unique to N. gonorrhoeae are recommended for screening and diagnosis of gonorrhea infection. These PCR - based tests require a sample of urine, urethral swabs, or cervical / vaginal swabs. Culture ( growing colonies of bacteria in order to isolate and identify them ) and gram - stain ( staining of bacterial cell walls to reveal morphology ) can also be used to detect the presence of N. gonorrhoeae in all specimen types except urine. If gram - negative, oxidase - positive diplococci are visualized on direct gram stain of urethral pus ( male genital infection ), no further testing is needed to establish the diagnosis of gonorrhea infection. However, in the case of female infection direct gram stain of cervical swabs is not useful because the N. gonorrhoeae organisms are less concentrated in these samples. The chances of false positives are increased as gram - negative diplococci native to the normal vaginal flora can not be distinguished from N. gonorrhoeae. Thus, cervical swabs must be cultured under the conditions described above. If oxidase positive, gram - negative diplococci are isolated from a culture of a cervical / vaginal swab specimen, then the diagnosis is made. Culture is especially useful for diagnosis of infections of the throat, recutum, eyes, blood, or joints -- areas where PCR - based tests are not well established in all labs. Culture is also useful for antimicrobial sensitivity testing, treatment failure, and epidemiological purposes ( outbreaks, surveillance ). In patients who may have disseminated gonococcal infection ( DGI ), all possible mucosal sites should be cultured ( e.g., pharynx, cervix, urethra, rectum ). Three sets of blood cultures should also be obtained. Synovial fluid should be collected in cases of septic arthritis. Patients should also be tested for other sexually transmitted infections including chlamydia, syphilis, and HIV. Studies have found co-infection with chlamydia ranging from 46 to 54 % in young people with gonorrhea. For this reason, gonorrhea and chlamydia testing are often combined. Patients diagnosed with gonorrhea infection have a fivefold increase risk of HIV transmission. Additionally, infected persons who are HIV positive are more likely to shed and transmit HIV to uninfected partners during an episode of gonorrhea. Prevention Transmission can be reduced by using latex barriers ( e.g. condoms or dental dams ) during sex and by limiting sexual partners. Condoms and dental dams should be used during oral and anal sex as well. Spermicides, vaginal foams, and douches are not effective for prevention of transmission. Treatment Ceftriaxone ( a third - generation cephalosporin ) is the first line treatment. Because co-infection with chlamydia is so common, people are often treated for both by combining ceftriaxone with azithromycin or doxycycline. Azithromycin is preferred for additional coverage of resistant gonorrhea. Sexual partners ( defined by the CDC as sexual contact within the past 60 days ) should also be notified, tested, and treated. Antibiotic resistance Antibiotic resistance in gonorrhea has been noted beginning in the 1940s. Gonorrhea was treated with penicillin, but doses had to be progressively 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 ''. 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. However, because of N. gonorrhoeae 's high affinity for horizontal gene transfer, antibiotic - resistant gonorrhea is seen as an emerging public health threat. Vaccine Due to the relative frequency of infection and the rapid evolution of antibiotic resistance in strains of N. gonorrhoeae, vaccines are thought to be an important goal in the prevention of infection. Development of a vaccine has been complicated by the ongoing evolution of resistant strains and antigenic variation ( the ability of N. gonorrhoeae to disguise itself with different surface markers to evade the immune system ). History Name origin Neisseria gonnorhoeae is named for Albert Neisser who isolated it as the causative agent of the disease gonorrhea in 1978. Galen ( 130 AD ) coined the term `` gonorrhea '' from the Greek gonos which means `` seed '' and rhoe which means `` flow ''. Thus gonorrhea means `` flow of seed '', a description referring to the white penile discharge, assumed to be semen, seen in male infection. Discovery In 1878 Albert Neisser isolated and visualized N. gonorrhoeae diplococci in samples of pus from 35 men and women with the classic symptoms of genitourinary infection with gonorrhea -- two of whom also had infections of the eyes. In 1882, Leistikow and Loeffler were able to grow the organism in culture. Then in 1883 Max Bockhart proved conclusively that the bacterium isolated by Albert Neisser was the causative agent of the disease known as gonorrhea by inoculating the penis of a healthy man with the bacteria. The man developed the classic symptoms of gonorrhea days after -- satisfying the last of Koch 's postulates. Until this point researchers debated whether syphilis and gonorrhea were manifestations of the same disease or two distinct entities. One such 18th century researcher, John Hunter, tried to settle the debate in 1767 by inoculating a man with pus from a patient with gonorrhea. He erroneously concluded that both disease were indeed the same when the man developed the copper - colored rash classic syphilis, respectively. Although many sources repeat that Hunter inoculated himself, others have argued that it was in fact another man. After Hunter 's experiment other scientists sought to disprove his conclusions by inoculating other male physicians, medical students, and incarcerated men with gonorrheal pus, who all developed the burning and discharge of gonorrhea. 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Gonorrhea in women. W. B Saunders Co. ^ Jump up to : Ligon, B. Lee ( October 2005 ). `` Albert Ludwig Sigesmund Neisser : discoverer of the cause of gonorrhea ''. Seminars in Pediatric Infectious Diseases. 16 ( 4 ) : 336 -- 341. doi : 10.1053 / j. spid. 2005.07. 001. ISSN 1045 - 1870. PMID 16210113. ^ Jump up to : Singal, Archana ; Grover, Chander ( 2016 - 02 - 12 ). Comprehensive Approach to Infections in Dermatology. JP Medical Ltd. ISBN 9789351527480. ^ Jump up to : Ross, John J. ( 2005 - 12 - 01 ). `` Book Review ''. New England Journal of Medicine. 353 ( 22 ) : 2412 -- 2413. doi : 10.1056 / NEJM200512013532221. ISSN 0028 - 4793. Jump up ^ Gladstein, J. ( 2005 - 07 - 01 ). `` Hunter 's Chancre : Did the Surgeon Give Himself Syphilis ? ''. Clinical Infectious Diseases. 41 ( 1 ) : 128 -- 128. doi : 10.1086 / 430834. ISSN 1058 - 4838. External links Todar, Kenneth. `` Pathogenic Neisseriae : Gonorrhea, Neonatal Ophthalmia and Meningococcal Meningitis ''. Todar 's Online Textbook of Bacteriology. Gonorrhea at eMedicine `` Neisseria gonorrhoeae ''. NCBI Taxonomy Browser. 485. Type strain of Neisseria gonorrhoeae at BacDive -- the Bacterial Diversity Metadatabase Diseases of the skin and appendages by morphology Growths Epidermal wart callus seborrheic keratosis acrochordon molluscum contagiosum actinic keratosis squamous - cell carcinoma basal - cell carcinoma Merkel - cell carcinoma nevus sebaceous trichoepithelioma Pigmented Freckles lentigo melasma nevus melanoma Dermal and subcutaneous epidermal inclusion cyst hemangioma dermatofibroma ( benign fibrous histiocytoma ) keloid lipoma neurofibroma xanthoma Kaposi 's sarcoma infantile digital fibromatosis granular cell tumor leiomyoma lymphangioma circumscriptum myxoid cyst Rashes With epidermal involvement Eczematous contact dermatitis atopic dermatitis seborrheic dermatitis stasis dermatitis lichen simplex chronicus Darier 's disease glucagonoma syndrome langerhans cell histiocytosis lichen sclerosus pemphigus foliaceus Wiskott -- Aldrich syndrome Zinc deficiency Scaling psoriasis tinea ( corporis cruris pedis manuum faciei ) pityriasis rosea secondary syphilis mycosis fungoides systemic lupus erythematosus pityriasis rubra pilaris parapsoriasis ichthyosis Blistering herpes simplex herpes zoster varicella bullous impetigo acute contact dermatitis pemphigus vulgaris bullous pemphigoid dermatitis herpetiformis porphyria cutanea tarda epidermolysis bullosa simplex Papular scabies insect bite reactions lichen planus miliaria keratosis pilaris lichen spinulosus transient acantholytic dermatosis lichen nitidus pityriasis lichenoides et varioliformis acuta Pustular acne vulgaris acne rosacea folliculitis impetigo candidiasis gonococcemia dermatophyte coccidioidomycosis subcorneal pustular dermatosis Hypopigmented tinea versicolor vitiligo pityriasis alba postinflammatory hyperpigmentation tuberous sclerosis idiopathic guttate hypomelanosis leprosy hypopigmented mycosis fungoides Without epidermal involvement Red Blanchable Erythema Generalized drug eruptions viral exanthems toxic erythema systemic lupus erythematosus Localized cellulitis abscess boil erythema nodosum carcinoid syndrome fixed drug eruption Specialized urticaria erythema ( multiforme migrans gyratum repens annulare centrifugum ab igne ) Nonblanchable Purpura Macular thrombocytopenic purpura actinic / solar purpura Papular disseminated intravascular coagulation vasculitis Indurated scleroderma / morphea granuloma annulare lichen sclerosis et atrophicus necrobiosis lipoidica Miscellaneous disorders Ulcers Hair telogen effluvium androgenic alopecia alopecia areata systemic lupus erythematosus tinea capitis loose anagen syndrome lichen planopilaris folliculitis decalvans acne keloidalis nuchae Nail onychomycosis psoriasis paronychia ingrown nail Mucous membrane Aphthous stomatitis oral candidiasis lichen planus leukoplakia pemphigus vulgaris mucous membrane pemphigoid cicatricial pemphigoid herpesvirus coxsackievirus syphilis systemic histoplasmosis squamous - cell carcinoma Infectious diseases Bacterial disease : Proteobacterial G − primarily A00 -- A79, 001 -- 041, 080 -- 109 α Rickettsiales Rickettsiaceae / ( Rickettsioses ) Typhus Rickettsia typhi Murine typhus Rickettsia prowazekii Epidemic typhus, Brill -- Zinsser disease, Flying squirrel typhus Spotted fever Tick - borne Rickettsia rickettsii Rocky Mountain spotted fever Rickettsia conorii Boutonneuse fever Rickettsia japonica Japanese spotted fever Rickettsia sibirica North Asian tick typhus Rickettsia australis Queensland tick typhus Rickettsia honei Flinders Island spotted fever Rickettsia africae African tick bite fever Rickettsia parkeri American tick bite fever Rickettsia aeschlimannii Rickettsia aeschlimannii infection Mite - borne Rickettsia akari Rickettsialpox Orientia tsutsugamushi Scrub typhus Flea - borne Rickettsia felis Flea - borne spotted fever Anaplasmataceae Ehrlichiosis : Anaplasma phagocytophilum Human granulocytic anaplasmosis, Anaplasmosis Ehrlichia chaffeensis Human monocytotropic ehrlichiosis Ehrlichia ewingii Ehrlichiosis ewingii infection Rhizobiales Brucellaceae Brucella abortus Brucellosis Bartonellaceae Bartonellosis : Bartonella henselae Cat - scratch disease Bartonella quintana Trench fever Either B. henselae or B. quintana Bacillary angiomatosis Bartonella bacilliformis Carrion 's disease, Verruga peruana β Neisseriales M+ Neisseria meningitidis / meningococcus Meningococcal disease, Waterhouse -- Friderichsen syndrome, Meningococcal septicaemia M − Neisseria gonorrhoeae / gonococcus Gonorrhea ungrouped : Eikenella corrodens / Kingella kingae HACEK Chromobacterium violaceum Chromobacteriosis infection Burkholderiales Burkholderia pseudomallei Melioidosis Burkholderia mallei Glanders Burkholderia cepacia complex Bordetella pertussis / Bordetella parapertussis Pertussis γ Enterobacteriales ( OX − ) Lac+ Klebsiella pneumoniae Rhinoscleroma, Klebsiella pneumonia Klebsiella granulomatis Granuloma inguinale Klebsiella oxytoca Escherichia coli : Enterotoxigenic Enteroinvasive Enterohemorrhagic O157 : H7 O104 : H4 Hemolytic - uremic syndrome Enterobacter aerogenes / Enterobacter cloacae Slow / weak Serratia marcescens Serratia infection Citrobacter koseri / Citrobacter freundii Lac − H2S+ Salmonella enterica Typhoid fever, Paratyphoid fever, Salmonellosis H2S − Shigella dysenteriae / sonnei / flexneri / boydii Shigellosis, Bacillary dysentery Proteus mirabilis / Proteus vulgaris Yersinia pestis Plague / Bubonic plague Yersinia enterocolitica Yersiniosis Yersinia pseudotuberculosis Far East scarlet - like fever Pasteurellales Haemophilus : H. influenzae Haemophilus meningitis Brazilian purpuric fever H. ducreyi Chancroid H. parainfluenzae HACEK Pasteurella multocida Pasteurellosis Actinobacillus Actinobacillosis Aggregatibacter actinomycetemcomitans HACEK Legionellales Legionella pneumophila / Legionella longbeachae Legionnaires ' disease Coxiella burnetii Q fever Thiotrichales Francisella tularensis Tularemia Vibrionaceae Vibrio cholerae Cholera Vibrio vulnificus Vibrio parahaemolyticus Vibrio alginolyticus Plesiomonas shigelloides Pseudomonadales Pseudomonas aeruginosa Pseudomonas infection Moraxella catarrhalis Acinetobacter baumannii Xanthomonadaceae Stenotrophomonas maltophilia Cardiobacteriaceae Cardiobacterium hominis HACEK Aeromonadales Aeromonas hydrophila / Aeromonas veronii Aeromonas infection ε Campylobacterales Campylobacter jejuni Campylobacteriosis, Guillain -- Barré syndrome Helicobacter pylori Peptic ulcer, MALT lymphoma, Gastric cancer Helicobacter cinaedi Helicobacter cellulitis Biology portal Retrieved from `` https://en.wikipedia.org/w/index.php?title=Neisseria_gonorrhoeae&oldid=821925529 '' Categories : Bacterium - related cutaneous conditions Gram - negative bacteria Infections with a predominantly sexual mode of transmission Pathogenic bacteria Neisseriales Infectious causes of cancer Hidden categories : Wikipedia articles needing page number citations from February 2015 Articles with ' species ' microformats Use dmy dates from December 2010 Talk Contents About Wikipedia Wikispecies Afrikaans Català Čeština Deutsch Español Euskara فارسی Français Galego 한국어 Italiano Latviešu Magyar Nederlands 日本 語 Norsk Polski Português Русский Suomi Svenska Türkçe Українська 中文 Edit links This page was last edited on 23 January 2018, at 12 : 05. 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Question: give two reasons neisseria gonorrhoeae is able to re-infect individuals after treatment
Answer: infected persons do not develop immunity to future infections