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👨‍⚕️ Appreciation Post to Dr Mustafa Fadhil Mohammed.

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👨‍⚕️ Appreciation Post to Dr Mustafa Fadhil Mohammed.

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We would like to dedicate this appreciation to our lecturer, Dr Mustafa Fadhil Mohammed, lecturer that taught us for this subject which is "Communicable Disease". We honestly believe it was your innovative, hands-on approach to this subject that made us enjoy this subject so much. You truly know how to make learning fun. We enjoyed being taught by you immensely, you're an excellent teacher and have inspired us to continue learning with an open mind and enthusiastic about something. We appreciate all your hard work, it means so much to us. Once again, thank you so much for your expertise, time and patience.

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Gonorrhea is one of the most common sexually transmitted infections (STIs), especially among young people in the 15-24 age group. While there is a cure, the infection can cause serious complications if it’s not treated properly. Learn more about gonorrhea, including what symptoms to watch for, how the infection is treated, and how to protect yourself.

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A sexually transmitted disease (STI) that known as “the clap” or “the drip”.

Called as STI because it undergoes process of transmission – moves from one person to another person.

It can both infects both female and males.

Most people have no symptoms but it is notifiable.

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Caused by Neiserria gonorrhoeae.

Commonly referred as gonococcus; sphere/ball

Thrive in a warm, moist environment that can affect any mucous membrane.

Affects the urethra, rectum, throat, cervix, vagina, penis and eyes (rare).

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1. Sexual Contact.

Touch on infected area (another person).

Main ways to get gonorrhea – vaginal sex, anal sex and oral sex.

Spread when semen, pre-cum and vaginal fluids get on or inside the genitals, anus or mouth.

2. Childbirth.

Pass to the baby during vaginal delivery.

The baby comes contact with the mother’s genital secretions.

Prevent by C-section delivery.

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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 and aerobic, and it survives within neutrophils. Culturing 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 polymerase chain reaction testing 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 co-infection.

species are fastidious, Gram-negative cocci that require nutrient supplementation to grow in laboratory cultures. Neisseria spp. are facultatively intracellular and typically appear in pairs (diplococci), resembling the shape of coffee beans. Nesseria is non-spore-forming, capable of moving using twitching motility, 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 and N. meningitidis is one cause of bacterial meningitis.

N. 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 agar 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.

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 bacterium is unable to cause infection. To move, individual bacteria use their pili like a grappling hook: first, they are extended from the cell surface and attach to a substrate. Subsequent pilus retraction drags the cell forward. The resulting movement is referred to as twitching motility. N. gonorrhoeae is able to pull 100,000 times its own weight, and the pili used to do so are the amongst the strongest biological motors known to date, exerting one nanonewton. The PilF and PilT ATPase proteins are responsible for powering the extension and retraction of the type IV pilus, respectively. The adhesive functions of the gonococcal pilus play a role in microcolony aggregation and biofilm formation.

Surface proteins called Opa proteins can be used to bind to receptors on immune cells and prevent an immune response. At least 12 Opa proteins are known and the many permutations of surface proteins make recognizing N. gonorrhoeae and mounting a defense by immune cells more difficult.

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.

N. gonorrhoeae evades the immune system through a process called antigenic variation. This process allows N. gonorrhoeae to recombine its genes and alter the antigenic determinants (sites where antibodies bind), such as the Type IV pili, that adorn its surface. Simply stated, the chemical composition of molecules is changed due to changes at the genetic level. N. gonorrhoeae is able to vary the composition of its pili, and LOS; of these, the pili exhibit the most antigenic variation due to chromosomal rearrangement. The PilS gene is an example of this ability to rearrange as its combination with the PilE gene is estimated to produce over 100 variants of the PilE protein. These changes allow for adjustment to the differences in the local environment at the site of infection, evasion of recognition by targeted antibodies, and contribute to the lack of an effective vaccine.

In addition to the ability to rearrange the genes it already has, it is also naturally competent to acquire new DNA (via plasmids), 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 also impeded vaccine development.

Phase variation is similar to antigenic variation, but instead of changes at the genetic level altering the composition of molecules, these genetic changes result in the turning on or off of a gene. Phase variation most often arises from a frameshift in the expressed gene. The Opacity, or Opa, proteins of N. gonorrhoeae rely strictly on phase variation. Every time the bacteria replicate, they may switch multiple Opa proteins on or off through slipped-strand mispairing. That is, the bacteria introduce frameshift mutations that bring genes in or out of frame. The result is that different Opa genes are translated every time. Pili are varied by antigenic variation, but also phase variation. Frameshifts occur in both the pilE and pilC genes, effectively turning off the expression of pili in situations when they are not needed, such as after colonization when N. gonorrhoeae survives within cells as opposed to on their surfaces.

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 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 is 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 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 open reading frames (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.

In 2011, researchers at Northwestern University found evidence of a human DNA fragment in a N. gonorrhoeae genome, the first example of horizontal gene transfer from humans to a bacterial pathogen.

Symptoms of infection with N. gonorrhoeae differ depending on the site of infection and many infections are asymptomatic independent of sex. 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. It is important to note that depending on the route of transmission, N. gonorrhoeae may cause infection of the throat ( pharyngitis) or infection of the anus/rectum ( proctitis).

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 gonococcal infections can occur when N. gonorrhoeae enters the bloodstream, often spreading to the joints and causing a rash (dermatitis-arthritis syndrome). Dermatitis-arthritis syndrome results in joint pain ( arthritis), tendon inflammation ( tenosynovitis), and painless non- pruritic (non-itchy) dermatitis. Disseminated infection and pelvic inflammatory disease in women tend to begin after menses due to reflux during menses, facilitating spread. In rare cases, disseminated infection may cause infection of the meninges of the brain and spinal cord ( meningitis) or infection of the heart valves ( endocarditis).

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 bacterium was thought to move attached to spermatozoa, 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 use pili to anchor onto proteins in the sperm and move through coital liquid.

For N. gonorrhoeae, the first step after successful transmission is adherence to the epithelial cells found at the mucosal site that is infected. The bacterium relies on type IV pili that attach and retract, pulling N. gonorrhoeae toward the epithelial membrane where its surface proteins, such as opacity proteins, can interact directly. After adherence, N. gonorrhoeae replicates itself and forms microcolonies. While colonizing, N. gonorrhoeae has the potential to transcytose across the epithelial barrier and work its way in to the bloodstream. During growth and colonization, N. gonorrhoeae stimulates the release of cytokines and chemokines from host immune cells that are pro-inflammatory. These pro-inflammatory molecules result in the recruitment of macrophages and neutrophils. These phagocytic cells typically take in foreign pathogens and destroy them, but N. gonorrhoeae has evolved many mechanisms that allow it to survive within these immune cells and thwart the attempts at elimination.

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.

The current treatment recommended by the CDC is a dual antibiotic therapy. This includes an injected single dose of ceftriaxone (a third-generation cephalosporin) along with azithromycin administered orally. Azithromycin is preferred for additional coverage of gonorrhea that may be resistant to cephalosporins but susceptible to macrolides. Sexual partners (defined by the CDC as sexual contact within the past 60 days) should also be notified, tested, and treated. It is important that if symptoms persist after receiving treatment of N. gonorrhoeae infection, a reevaluation should be pursued.

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 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, Australia 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, genes exist 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.

As a gram negative bacteria, N. gonorrhoeae requires defense mechanisms to protect itself against the complement system (or complement cascade), whose components are found with human serum. There are three different pathways that activate this system however, they all result in the activation of complement protein 3 (C3). A cleaved portion of this protein, C3b is deposited on pathogenic surfaces and results in opsonization as well as the downstream activation of the membrane attack complex. N. gonorrhoeae has several mechanisms to avoid this action. As a whole, these mechanisms are referred to as serum resistance.

Neisseria gonorrhoeae is named for Albert Neisser, who isolated it as the causative agent of the disease gonorrhea in 1878. 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.

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 taken from a patient with gonorrhea. He erroneously concluded that both syphilis and gonorrhea were indeed the same disease when the man developed the copper-colored rash that is classic for syphilis. 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. One researcher, Ricord, took the initiative to perform 667 inoculations of gonorrheal pus on patients of a mental hospital, with zero cases of syphilis. Notably, the advent of penicillin in the 1940s made effective treatments for gonorrhea available.

1. "^ Neisseria". In: List of Prokaryotic Names with Standing in Nomenclature (LPSN). Created by J.P. Euzéby in 1997. Curated by A.C. Parte since 2013. Available on: http://www.bacterio.net. Retrieved 7 July 2017.

2. Neisser, A. Ueber eine der Gonorrhoe eigentümliche Micrococusform. ^ Centralblatt für die medizinischen Wissenschaften 17 (28): 497-500. link.

3. https://www.cdc.gov/std/tg2015/clinical.htm section on prevention methods

4. Levinson, Warren (1 July 2014). Review of medical microbiology and immunology (Thirteenth ed.). New York. ISBN 9780071818117. OCLC 871305336.

5. "Gonococcal Infections - 2015 STD Treatment Guidelines". 4 January 2018.

6. ^ Birgit., MacKenzie, Colin R. Henrich (2012). Diagnosis of sexually transmitted diseases : methods and protocols. Humana Press. ISBN 9781617799365. OCLC 781681739.

7. ^ Merz, A. J.; So, M.; Sheetz, M. P. (7 September 2000). "Pilus retraction powers bacterial twitching motility". Nature. 407 (6800): 98-102. Bibcode:2000Natur.407...98M. doi:10.1038/35024105. ISSN 0028-0836. PMID 10993081.

8. ^ Freitag, NE; Seifert, HS; Koomey, M (May 1995). "Characterization of the pilF-pilD pilus-assembly locus of Neisseria gonorrhoeae" (PDF). Molecular Microbiology. 16 (3): 575-86. doi:10.1111/j.1365-2958.1995.tb02420.x. PMID 7565116.

9. ^ STI Awareness: Gonorrhea. Planned Parenthood Advocates of Arizona. 11 April 2011. Retrieved 31 August 2011.

10. ^ Stern, Anne; Brown, Melissa; Nickel, Peter; Meyer, Thomas F. (1986). "Opacity genes in Neisseria gonorrhoeae: Control of phase and antigenic variation". Cell. 47 (1): 61-71. doi:10.1016/0092-8674(86)90366-1. PMID 3093085.

11. ^ Aas, Finn Erik; Wolfgang, Matthew; Frye, Stephan; Dunham, Steven; Løvold, Cecilia; Koomey, Michael (2002). "Competence for natural transformation in Neisseria gonorrhoeae: Components of DNA binding and uptake linked to type IV pilus expression". Molecular Microbiology. 46 (3): 749-60. doi:10.1046/j.1365-2958.2002.03193.x. PMID 12410832.

12. ^ Michod, Richard E.; Bernstein, Harris; Nedelcu, Aurora M. (2008). "Adaptive value of sex in microbial pathogens" (PDF). Infection, Genetics and Evolution. 8 (3): 267-85. doi:10.1016/j.meegid.2008.01.002. PMID 18295550.

13. ^ Detels, Roger; Green, Annette M.; Klausner, Jeffrey D.; Katzenstein, David; Gaydos, Charlotte; Hadsfield, Hunter; Peqyegnat, Willo; Mayer, Kenneth; Hartwell, Tyler D.; Quinn, Thomas . (2011). "The Incidence and Correlates of Symptomatic and Asymptomatic Chlamydia trachomatis and Neisseria gonorrhoeae Infections in Selected Populations in Five Countries". Sex. Transm. Dis. 38 (6): 503-509. PMC . PMID 22256336.

14. ^ Caini, Saverio; Gandini, Sara; Dudas, Maria; Bremer, Viviane; Severi, Ettore; Gherasim, Alin (2014). "Sexually transmitted infections and prostate cancer risk: A systematic review and meta-analysis". Cancer Epidemiology. 38 (4): 329-338. doi:10.1016/j.canep.2014.06.002. ISSN 1877-7821. PMID 24986642.

15. ^ Nwokolo, Nneka C; Dragovic, Bojana; Patel, Sheel; Tong, CY William; Barker, Gary; Radcliffe, Keith (1 March 2016). "2015 UK national guideline for the management of infection with Chlamydia trachomatis" (PDF). International Journal of STD & AIDS. 27 (4): 251-267. doi:10.1177/0956462415615443. ISSN 0956-4624. PMID 26538553.

16. STI Awareness: Antibiotic-Resistant Gonorrhea. Planned Parenthood Advocates of Arizona. 6 March 2012. Retrieved 6 March 2012.

17. ^ Charles A Janeway, Jr; Travers, Paul; Walport, Mark; Shlomchik, Mark J. (2001). "The complement system and innate immunity". Immunobiology: The Immune System in Health and Disease. 5th Edition.

18. ^ Gladstein, J. (1 July 2005). "Hunter's Chancre: Did the Surgeon Give Himself Syphilis?". Clinical Infectious Diseases. 41 (1): 128, author reply 128-9. doi:10.1086/430834. ISSN 1058-4838. PMID 15937780.

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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.

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Epidemiology and Risk Factors of Gonorrhea.

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Epidemiology and Risk Factors of Gonorrhea.

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People can contract and transmit sexually transmitted diseases (STDs) through several types of sexual contact.
Unlike some other conditions, a person’s sex, ethnicity, or age do not affect the likelihood that they will contract an STI. Since STIs occur due to sexual contact with others, anyone who is sexually active is at risk of contracting an STI.
There are several potential risk factors for contracting an STI. People should take steps to avoid risks when engaging in sexual activity.

Adolescence. (15 years old to 24 years old).

Reported that gonorrhea cases increases for men and women at the age of adolescent. Female is at higher risk compared to male.

History of Pelvic Inflammatory Disease. (PID).

PID happens when bacteria travels from vagina and cervix to other parts of the body where it can lead to chronic health problems such as infertility. If it is left untreated it will cause  infection and leads to bacterial vaginosis.

Multiple Sex Partners.

Sexually active person can be affected by gonorrhea through unprotected vaginal, anal or oral sex. The risk will be higher when having multiple sex partner.

Oral Contraceptive Use.

The usage of oral or injection hormonal contraception will increase the risk of gonorrhea. Therefore, the usage of condom consistently is protective against sexual transmitted disease.

Male Homosexuality.

Gay/ Bisexual and other men who have sex intercourse with men is one of the risk factor of getting STD and gonorrhea infection. In men the most common gonorrhea are known as inflammation of epididymis that increases the risk of prostate cancer.

Insertion of IUD (Intrauterine Disease).

Studies shows that women with chlamydia and gonorrhea infection during the insertion of the IUD will increase the risk of  pelvic inflammatory disease.

Low Socioeconomic Status.

Lower socioeconomic status plays an important role in spreading gonorrhea. For example, poverty, lower educational achievement, and poor health.

Antibiotic Resistant Gonorrhea.

Untreated gonorrhea due to resistant towards bacteria as gonorrhea has developed resistance to nearly all of the antibiotics used for its treatment.

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The common method of transmission is by sexual intercourse.

The risk of men contracting infection varies with the number of exposures with infectious females. It has been estimated 19% for one exposure and rising 57% for >= to 4 exposures.

The risk of infection to female from infected male have been thoroughly investigated but it have been found in those who have been exposed on more than one occasion have infection rates of between 92% - 59%.

Similarly, it has also been found that males were probably at greatest risk from menstruating females.

Once the gonococci is sexually transferrred, it attaches to the mucosal cells rapidly.

Micturition after intercourse do not remove them.

Due to the presence of pilli a special feature in the organisms allows movement and show marked ability to adhere to the human cells, especially to the squamocolumnar cells of the uterine cervix. It have been found that pilli present in the infectious gonococci can overcome the electrostatic force of repulsions between the negatively charged bacterial surface and the sialic acid on the surface of host cells and bind the organisms loosely to the cell surface.

When organisms are loosely attached to the host cells, many other factors come into play. These include non specific mechanisms such as the mutual attraction of hydrophobic moieties on cell and bacterial surfaces, and more specific mechanisms.

Gonococcal outer membrane protein II occurs in the cell membrane and helps in this process. The presence and absence of which produces different types of colonies and virulence. A single strain of gonococcus can produce many different variants and this helps the organisms to spread to different types as it colonizes.

Hence, the organisms produce endotoxin and attaches itself to the microvilli of the cell membrane and starts multiplying as a result  of phagocytosis.

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To prevent further infection, the defense system of the infected women's body releases WBC to attack and swallow the gonococci. WBC attacks the pathogen by swallowing the proteins on the gonococci to provide antibodies to attack the pathogen and to act as a defense system during future exposure, which is also known as formation of immunological memory.

But, immunological memory doesn't develop for gonococci.
As the WBC attacks and swallows the gonococci, they latch through their OPA receptors and these receptors prevents the process of developing immunological memory due to binding of OPA proteins.

Although immunological memory doesn't develop, the organisms still die and they enter the subepithelial tissue upon death.

The phagocytosed gonococci are then found as pus in the urethral and cervical region.

The gonococci are found inside the phagosomes, degranulated, with dead cells in the vacuoles.

However in some polymorphs, large number of viable organisms are found which damage the polymorphs and are called as the "infectious units". These are protected from host attack and can invade epithelial cells.

In female the spread to the fallopian tubes occurs mainly at the time of menstruation.

Certain strains of gonococci seem to have particular abilities to spread to distant sites, so producing the Disseminated gonorrheal infection syndromes.

They show the resistance to the killing action of complement.

Below attached is a mind map of the pathogenesis of Gonorrhea :

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In some cases, gonorrhea causes no symptoms. In fact, you could be infected and not realize it. When symptoms do appear, they usually occur in the genital area.

Men are more likely to experience symptoms from gonorrhea, and those symptoms typically include:

Pain or burning sensation with urination

Pus-like discharge from the tip of the penis

Pain or swelling in the testicles

In women, symptoms are less likely, but when they do appear they’re usually noticeable within about a week of infection. Symptoms of gonorrhea in women include:

Pain or burning sensation with urination

Increased vaginal discharge that may be bloody or yellowish

Painful intercourse

Vaginal bleeding between periods, including after vaginal intercourse

Abdominal or pelvic pain

When gonorrhea occurs in other parts of the body, these are symptoms you might experience in those areas:

Rectum: Anal itching, pus-like anal discharge, straining during bowel movements, and spots of blood on your toilet paper

Throat: Sore throat and swollen lymph nodes in the neck

Eyes: Pus-like eye discharge, eye pain, and sensitivity to light

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First of all, if you develop any symptoms of Gonnorhea; especially if you recently had unprotected sex or had multiple sex partner, do seek for medical help.

The doctors would perform history taking on you. Here the doctors would ask about your sexual life. No worries, all information collected from you will be private and confidential.

The doctors will then do physical examination with your consent. The examination involves your pelvic area. Doctors will try to look if there is any redness or swelling in your genital area.

Urine test will be done to help identify the bacteria in your urethra.

Swab of affected area. A swab of your throat, urethra, vagina or rectum can collect bacteria that can be identified in a lab. Take smear for gram staining - gram -ve diplococci can be seen.

NAAT  assay is a serological test that will be performed to detect the DNA and RNA of Neisseria Gonnorhea.

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Gonorrhea treatment in adults and babies will be the same.

Antibiotics such as ceftriaxone is  given as an injection with oral azithromycin (Zithromax).

For those who develop allergic reaction to Ceftriaxone, other medications such as  Oral gemifloxacin (Factive) or injectable gentamicin and oral azithromycin. would be given.

To learn more on how they administrate the medications in patients, click the link above! Wish you all happy reading.

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Gonorrhoea is usually treated with a short course of antibiotics.
Antibiotics are usually recommended if:

tests have shown you have gonorrhoea

there's a high chance you have gonorrhoea, even though your test results have not come back yet

your partner has been diagnosed with gonorrhoea

In most cases, treatment involves having an antibiotic injection (usually in the buttocks or thigh) followed by 1 antibiotic tablet. It's sometimes possible to have another antibiotic tablet instead of an injection, if you prefer.

If you have any symptoms of gonorrhoea, these will usually improve within a few days, although it may take up to 2 weeks for any pain in your pelvis or testicles to disappear completely.

Bleeding between periods or heavy periods should improve by the time of your next period.

Attending a follow-up appointment a week or two after treatment is usually recommended, so another test can be carried out to see if you're clear of infection.

You should avoid having sex until you, and your partner, have been treated and given the all-clear, to prevent re-infection or passing the infection on to anyone else.

If your symptoms do not improve after treatment or you think you've been infected again, see your doctor or nurse. You may need repeat treatment or further tests to check for other problems.

Sexual partners

Gonorrhoea is easily passed on through intimate sexual contact. If you're diagnosed with it, anyone you've recently had sex with may have it too.

It's important that your current partner and any other recent sexual partners are tested and treated.

Your local genitourinary medicine (GUM) or sexual health clinic may be able to help by notifying any of your previous partners on your behalf.

A contact slip can be sent to them explaining that they may have been exposed to a sexually transmitted infection (STI) and suggesting they go for a check-up. The slip will not have your name on it, so your confidentiality is protected.

Treating babies with gonorrhoea

Babies with signs of a gonorrhoea infection at birth, or who have an increased risk of infection because their mother has gonorrhoea, will usually be given antibiotics immediately after they're born.

This does not harm the baby, and helps prevent blindness and other complications of gonorrhoea.

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Gonorrhoea is usually treated with a short course of antibiotics. Antibiotics are usually recommended if: tests have shown you have gonorrhoea there's a high chance you have gonorrhoea, even though your test results have not come back yet your partner has been diagnosed with gonorrhoea In most cases, treatment involves having an antibiotic injection (usually in the buttocks or thigh) followed by 1 antibiotic tablet.

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Complication and Prevention of Gonorrhea.

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Complication and Prevention of Gonorrhea.

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1. Complication.

Infertility in both women and men.

Females may have pelvic inflammatory disease (PID) whereas in males, they may have epididymitis.

Increased risk of having HIV/AIDS

Pregnant women have high risk of experiencing ectopic pregnancy and miscarriage

Complications in babies

Newborn babies coming through the infected birth canal may have complications like blindness.

2. Prevention.

Doing screening test

Avoid doing sexual relationship with multiple partners

Do not engage do any sexual activities with someone that have sexually transmitted infection or as long as the infection is not treated

Practice safe sex

Erythomycin can help prevent blindness

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Let's test your understanding about gonorrhea. Open the link above and answer the questions given. Good luck!!🤩🤩🤩🤩🤩

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Too many words!!!!😵😵😵😵😵 Don't worry we have video for you too watch. Hope u guys enjoy and understand it.😎😎

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Gram Negative Bacteria: Neisseria gonorrhoeae

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You all can refer to this slides for this Gonorrhea summarization.

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Thank you for reading our padlet, feel free to use this as your reference, hope it helps!