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Gonorrhea

  • Author: Brian Wong, MD; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
 
Updated: Mar 15, 2016
 

Practice Essentials

Gonorrhea is a purulent infection of the mucous membrane surfaces caused by Neisseria gonorrhoeae. N gonorrhoeae is spread by sexual contact or through transmission during childbirth. The Centers for Disease Control (CDC) recommends that all patients with gonorrheal infection also be treated for presumed co-infection with Chlamydia trachomatis.[1] See the image below.

This patient presented with gonococcal urethritis, This patient presented with gonococcal urethritis, which became systemically disseminated, leading to gonococcal conjunctivitis of the right eye. Courtesy of the CDC/Joe Miller, VD.

See 20 Signs of Sexually Transmitted Infections, a Critical Images slideshow, to help make an accurate diagnosis.

Signs and symptoms

History

In women, the major genitourinary symptoms of gonorrhea include the following:

  • Vaginal discharge: The most common presenting symptom of gonorrhea, vaginal discharge from endocervicitis is usually described as thin, purulent, and mildly odorous; however, many patients have minimal or no symptoms from gonococcal cervicitis
  • Dysuria
  • Intermenstrual bleeding
  • Dyspareunia (painful intercourse)
  • Mild lower abdominal pain

If the infection progresses to pelvic inflammatory disease (PID), symptoms may include the following:

  • Lower abdominal pain: Most consistent symptom of PID
  • Increased vaginal discharge or mucopurulent urethral discharge
  • Dysuria: Usually without urgency or frequency
  • Cervical motion tenderness
  • Adnexal tenderness (usually bilateral) or adnexal mass
  • Intermenstrual bleeding
  • Fever, chills, nausea, and vomiting (less common)

In males, the major genitourinary symptoms of gonorrhea include the following:

  • Urethritis: The major manifestation of gonococcal infection in men; initial characteristics include burning upon urination and a serous discharge; a few days later, the discharge usually becomes more profuse, purulent, and, at times, tinged with blood
  • Acute epididymitis: Usually unilateral and often occurs in conjunction with a urethral exudate
  • Urethral strictures: Have become uncommon in the antibiotic era, but they can present with a decreased and abnormal urine stream, as well as with the secondary complications of prostatitis and cystitis
  • Rectal infection: May present with pain, pruritus, discharge, or tenesmus

In males and females, the classic presentation of disseminated gonococcal infection (DGI) is an arthritis-dermatitis syndrome. Joint or tendon pain is the most common presenting complaint in the early stage of infection. The second stage of DGI is characterized by septic arthritis. The knee is the most common site of purulent gonococcal arthritis.

In neonates, in whom bilateral conjunctivitis (ophthalmia neonatorum) often follows vaginal delivery from an untreated mother with a gonococcal infection, symptoms of gonococcal conjunctivitis include the following:

  • Eye pain
  • Redness
  • Purulent discharge

Physical examination

Look for the following genitourinary symptoms during physical examination in females:

  • Mucopurulent or purulent vaginal, urethral, or cervical discharge
  • Vaginal bleeding; vulvovaginitis in children
  • Cervical friability - Tendency to bleed upon manipulation
  • Cervical motion tenderness during bimanual pelvic examination
  • Fullness and/or tenderness of the adnexa, unilateral or bilateral (eg, ovaries, fallopian tubes)
  • Lower abdominal pain/tenderness, with or without rebound tenderness
  • Possible low back pain - More common in progression to PID
  • Upper right abdominal tenderness (with perihepatitis)

Look for the following genitourinary symptoms during physical examination in males:

  • Mucopurulent or purulent urethral discharge: Obtained by milking the urethra along the shaft of the penis
  • Possible epididymitis: Unilateral epididymal tenderness and edema, with or without penile discharge or dysuria
  • Penile edema without other overt inflammatory signs
  • Urethral stricture: Uncommon; more often seen in the preantibiotic era with urethral irrigation using caustic liquids

See Clinical Presentation for more detail.

Diagnosis

Culture is the most common diagnostic test for gonorrhea, followed by the deoxyribonucleic acid (DNA) probe and then the polymerase chain reaction (PCR) assay and ligand chain reaction (LCR). The DNA probe is an antigen detection test that uses a probe to detect gonorrhea DNA in specimens.

Specific culture of a swab from the site of infection is a criterion standard for diagnosis at all potential sites of gonococcal infection. Cultures are particularly useful when the clinical diagnosis is unclear, when a failure of treatment has occurred, when contact tracing is problematic, and when legal questions arise.

In patients who may have DGI, all possible mucosal sites should be cultured (eg, pharynx, cervix, urethra, rectum), as should blood and synovial fluid (in cases of septic arthritis). Three sets of blood cultures should also be obtained.

See Workup for more detail.

Management

For uncomplicated urogenital, anorectal, and pharyngeal gonococcal infection, a drug regimen using ceftriaxone plus either azithromycin or doxycycline may be used. Antimicrobial drugs used alone or in various combinations in other gonococcal infections include the following:

  • Gonococcal arthritis: Ceftriaxone
  • Gonococcal conjunctivitis: Ceftriaxone
  • Gonorrhea contributing to PID: Cefoxitin, ceftriaxone, doxycycline, metronidazole, cefotetan, clindamycin, gentamicin
  • Gonococcal epididymitis: Ceftriaxone, doxycycline
  • DGI: Ceftriaxone, cefotaxime, ceftizoxime
  • Gonococcal meningitis and endocarditis: Ceftriaxone

See Treatment and Medication for more detail.

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Background

Gonorrhea, an important public health problem and the second most common notifiable disease in the United States, is a purulent infection of mucous membrane surfaces caused by the gram-negative diplococcus Neisseria gonorrhoeae. Although gonorrhea (known colloquially as the clap and the drip) is most frequently spread during sexual contact, it can also be transmitted from the mother's genital tract to the newborn during birth, causing ophthalmia neonatorum and systemic neonatal infection. (See Etiology.)

In women, the cervix is the most common site of gonorrhea, resulting in endocervicitis and urethritis, which can be complicated by pelvic inflammatory disease (PID). In men, gonorrhea causes anterior urethritis. Gonorrhea can also spread throughout the body to cause localized and disseminated disease. Complications also include ectopic pregnancy and increased susceptibility to human immunodeficiency virus (HIV) infection. Most commonly, the term gonorrhea refers to urethritis and/or cervicitis in a sexually active person. (See Pathophysiology, Prognosis, Presentation, and Workup.)

Gonococcal infections following sexual and perinatal transmission are a major source of morbidity worldwide. In the developed world, where prophylaxis for neonatal eye infection is standard, the vast majority of infections follow genitourinary mucosal exposure. (See Pathophysiology, Etiology, and Prognosis, and Treatment.]

In the pediatric population, the importance of gonorrhea is 3-fold, as follows:

  • As a common and preventable sexually transmitted disease (STD) in the sexually active teenage population
  • As a perinatal infection at childbirth
  • As a forensic aid in investigating sexual abuse

Gonococcemia

Gonococcemia is defined as the presence of N gonorrhoeae in the bloodstream, which can lead to the development of disseminated gonococcal infection (DGI). Gonococcemia occurs in about 0.5-3% of patients with gonorrhea (see the image below). (See Pathophysiology and Prognosis.)

This patient presented with gonococcal urethritis, This patient presented with gonococcal urethritis, which became systemically disseminated, leading to gonococcal conjunctivitis of the right eye. Courtesy of the CDC/Joe Miller, VD.

The clinical manifestations of this process are biphasic, with an early bacteremic phase consisting of tenosynovitis, arthralgias,[2] and dermatitis, followed by a localized phase consisting of localized septic arthritis. Other potentially severe clinical complications include osteomyelitis, meningitis, endocarditis, adult respiratory distress syndrome (ARDS),[3, 4] and fatal septic shock.[5] Polymyositis is also a rare complication of gonococcemia. (See Pathophysiology, Prognosis, and Presentation.)

Patients who are pregnant or menstruating may be particularly prone to gonococcemia. Other populations at risk of infection include women and individuals with complement deficiencies, HIV disease, or systemic lupus erythematosus (SLE). DGI is an important, potentially life-threatening, and easily treatable clinical entity that remains the most common cause of acute septic arthritis in young, sexually active adults.

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Pathophysiology

The pathophysiology of N gonorrhoeae and the relative virulence of different subtypes depend on the antigenic characteristics of the respective surface proteins. Certain subtypes are able to evade serum immune responses and are more likely to lead to disseminated (systemic) infection.

Well-characterized plasmids commonly carry antibiotic-resistance genes, most notably penicillinase. Plasmid and nonplasmid genes are transmitted freely between different subtypes. The ensuing exchange of surface protein genes results in high host susceptibility to reinfection. The exchange of antibiotic resistance genes has led to extremely high levels of resistance to beta-lactam antibiotics. Fluoroquinolone resistance has also been documented on multiple continents and in widespread populations within the United States.[6]

Infection of the lower genital tract, the most common clinical presentation, primarily manifests as male urethritis and female endocervicitis. Infection of the pharynx, rectum, and female urethra occur frequently but are more likely to be asymptomatic or minimally symptomatic. Retrograde spread of the organisms occurs in as many as 20% of women with cervicitis, often resulting in pelvic inflammatory disease (PID), with salpingitis, endometritis, and/or tubo-ovarian abscess. Retrograde spread can lead to frank abdominal peritonitis and to a perihepatitis known as Fitz-Hugh-Curtis syndrome.

Long-term sequelae of PID, such as tubal factor infertility, ectopic pregnancy, and chronic pain, may occur in up to 25% of affected patients. Epididymitis or epididymo-orchitis may occur in men after gonococcal urethritis. Lower genital infection is a risk factor for the presence of other sexually transmitted diseases (STDs), including human immunodeficiency virus (HIV).

Conjunctivitis can occur in adults, as well as children, following direct inoculation of organisms (usually as a result of hand-eye inoculation in adults) and can lead to blindness.

Disseminated gonococcal infection

Disseminated gonococcal infection (DGI) occurs following approximately 1% of genital infections. Patients with DGI may present with symptoms of rash, fever, arthralgias, migratory polyarthritis, septic arthritis, tendonitis, tenosynovitis, endocarditis, or meningitis.

N gonorrhoeae organisms spread from a primary site, such as the endocervix, the urethra, the pharynx, or the rectum, and disseminate to the blood to infect other end organs. Usually, multiple sites, such as the skin and the joints, are infected. Neisserial organisms disseminate to the blood due to a variety of predisposing factors, such as host physiologic changes, virulence factors of the organism itself, and failures of the host's immune defenses.[7]

For example, changes in the vaginal pH that occur during menses and pregnancy and the puerperium period make the vaginal environment more suitable for the growth of the organism and provide increased access to the bloodstream. (Three fourths of the cases of DGI occur in women; susceptibility is increased if the primary mucosal infection occurs during menstruation or pregnancy.)[8, 9]

Defects in the host's immune defenses are also involved in the pathophysiology, with certain patients more likely to develop bacteremia. Specifically, patients with deficiency in terminal complement components are less able to combat infection, as complement plays an important role in the killing of neisserial organisms. As many as 13% of patients with DGI have a complement deficiency.

A study of 22 patients with DGI revealed that total serum complement activity was greater than 25% below the normal mean. Other causes of immunocompromise (eg, HIV, SLE) also predispose to dissemination of infection.

In addition, certain strains of gonorrhea causing asymptomatic genital infections are seen in association with DGI.[10]

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Etiology

N gonorrhoeae is a gram-negative, intracellular, aerobic diplococcus; more specifically, it is a form of diplococcus known as the gonococcus. N gonorrhoeae is spread by sexual contact or through vertical transmission during childbirth. It mainly affects the host’s columnar or cuboidal epithelium. Virtually any mucous membrane can be infected by this microorganism. The physiologic ectopy of the squamocolumnar junction onto the ectocervix in the adolescent female is one factor that causes particular susceptibility to this infection.

Many factors influence the manner in which gonococci mediate their virulence and pathogenicity. Pili help in attachment of gonococci to mucosal surfaces and contribute to resistance by preventing ingestion and destruction by neutrophils. Opacity-associated (Opa) proteins increase adherence between gonococci and phagocytes, promote invasion into host cells, and possibly down-regulate the immune response.

Porin channels (porA, porB) in the outer membrane play key roles in virulence. Gonococcal strains with porA may have inherent resistance to normal human serum and an increased ability to invade epithelial cells, explaining their association with bacteremia.

Certain acquired plasmids and genetic mutations enhance virulence. TEM-1–type beta-lactamase (penicillinase) affects penicillin binding and efflux pumps and confers resistance to penicillin.[11, 12] TetM protects the ribosome and confers resistance to tetracycline. Alterations in gyrA and parC genes result in fluoroquinolone resistance by efflux activation and decreased antibiotic cell permeation.[11]

Gonococci attach to the host mucosal cell (pili and Opa proteins play major roles) and, within 24-48 hours, penetrate through and between cells into the subepithelial space. A typical host response is characterized by invasion with neutrophils, followed by epithelial sloughing, formation of submucosal microabscesses, and purulent discharge. If left untreated, macrophage and lymphocyte infiltration replaces the neutrophils. Some gonococcal strains cause an asymptomatic infection, leading to an asymptomatic carrier state in persons of either sex.

The ability to grow anaerobically allows gonococci, when mixed with refluxed menstrual blood or attached to sperm, to secondarily invade lower genital structures (vagina and cervix) and progress to upper genital organs (endometrium, salpinx, ovaries).

Gonococcal infection usually follows mucosal inoculation during vaginal, anal, or oral sexual contact or perinatally.

Sexually transmitted infection

Gonococcal infection usually follows mucosal inoculation during vaginal, anal, or oral sexual contact. It also may be caused by inoculation of mucosa by contaminated fingers or other objects. Transmission through penile-rectal contact is fairly efficient.

The risk of transmission of N gonorrhoeae from an infected woman to the urethra of her male partner is approximately 20% per episode of vaginal intercourse and rises to 60-80% after 4 or more exposures. In contrast, the risk of male-to-female transmission approximates 50-70% per contact, with little evidence of increased risk with more sexual exposures.

Persons who have unprotected intercourse with new partners frequently enough to sustain the infection in a community are defined as core transmitters.

Neonatal and pediatric gonococcal infection

Neonatal gonococcal infection may follow conjunctival infection, which is obtained during passage through the birth canal. In addition, direct infection may occur through the scalp at the sites of fetal monitoring electrodes.

In children, infection may occur from sexual abuse by an infected individual or possibly nonsexual contact in the child's household or in institutional settings.

Autoinoculation

Autoinoculation can occur when a person touches an infected site (genital organ) and contacts skin or mucosa.

Risk factors

Risk factors for gonorrhea include the following:

  • Sexual exposure to an infected partner without barrier protection (eg, failure to use a condom or condom failure) [13]
  • Multiple sex partners
  • Male homosexuality
  • Low socioeconomic status
  • Minority status - Blacks, Hispanics, and Native Americans have the highest rates in the United States
  • History of concurrent or past STDs
  • Exchange of sex for drugs or money
  • Use of crack cocaine
  • Early age of onset of sexual activity
  • Pelvic inflammatory disease (PID) - Use of an intrauterine device (IUD)
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Epidemiology

Occurrence in the United States

An estimated 700,000 new gonococcal infections occur annually in the United States, with less than half being reported.[14, 15, 16] In 2009, 301,174 cases of gonorrhea were reported to the US Centers for Disease Control and Prevention (CDC).[17, 18, 19, 16] The national average in 2009 was 99.1 cases per 100,000 population, a 10.5% decrease from 2008, with considerable state-to-state variation (see the figure below).[18, 16] Some experts estimate the annual cost of gonorrhea and its complications to be $1.1 billion.

Gonorrhea rates, United States, 1941-2009. Centers Gonorrhea rates, United States, 1941-2009. Centers for Disease Control and Prevention.

In the United States, the number of gonococcal infections peaked in the 1970s, the era of the sexual revolution. With the onset of the HIV epidemic and the practicing of safe sex techniques, the incidence dramatically decreased from 468 cases per 100,000 population in 1975 to 100-150 cases per 100,000 population at the turn of the century. The incidence of disseminated gonococcal infection (DGI) naturally parallels the incidence of gonococcal infection.[20]

Within the United States, carriage rates highly depend on the geographic area, the racial and ethnic group, and sexual preferences. The rate of gonorrhea is much higher in African Americans than in other racial groups[21] and is much higher in the rural southeastern United States and in inner cities, presumably because of an association with socioeconomic and behavioral factors, as well as with social networks.

Rates of infection range from about 246.4 cases per 100,000 population in Mississippi to 8 cases per 100,000 population in Vermont. The CDC began a campaign (Healthy People 2010: http://www.cdc.gov/nchs/healthy_people.htm) that targeted an incidence rate of 19 cases per 100,000 population. According to 2009 data from the CDC, the only states with incidences below that target were Utah, Montana, Idaho, Wyoming, Maine, Vermont, and New Hampshire, along with Puerto Rico (see the image below).[18, 16] Healthy People 2020 is in the process of being developed (http://healthypeople.gov/2020/default.aspx).

Rates of gonococcal infection per 100,000 by state Rates of gonococcal infection per 100,000 by state and outlying regions (2009). Data from the Centers for Disease Control and Prevention (CDC):

In children who have been sexually abused, rates of recovery of gonorrhea range from 1% to 30%. In female adolescents who are sexually active, asymptomatic carriage of gonorrhea occurs in 1-5%.

The incidence of antibiotic-resistant strains of N gonorrhoeae has been rising since the late 1940s. Of greatest concern is the rise in the percentage of cases due to penicillinase-producing N gonorrhoeae.

International occurrence

An estimated 200 million new cases of gonorrhea occur annually. In 1999, the number of new cases of gonococcal infection diagnosed in North America was 1.56 million; in Western Europe, 1.11 million; in South and Southeast Asia, 27.2 million; and in Latin America and the Caribbean, 7.27 million.

Gonorrhea was the most common STD worldwide for at least most of the 20th century, although since the mid-1970s, public health initiatives in the industrialized world have resulted in declining incidence of the disease. As noted earlier, however, gonococcal infection is still the second most common notifiable disease in the United States, and Western European rates approximate those in the United States.[22, 23, 24]

Although the frequency data are unknown in most developing nations, these countries are considered to have the highest rates of gonorrhea and its complications. Gonococcal infection rates in pregnant women in the Central African Republic and South Africa were found to be 3.1% and 7.8%, respectively.

The incidence of antibiotic-resistant strains has been rising since the late 1940s. Of greatest concern historically has been the high percentage of cases due to penicillinase-producing N gonorrhoeae. However, fluoroquinolone resistance has increased rapidly over the past decade on most continents and within the United States. The CDC reported fluoroquinolone resistance in 6.8% of 2004 isolates, 9.4% of 2005 isolates, and 13.3% of 2006 isolates.[6]

Race-related demographics

All sexually active populations are at risk for gonococcal infection, and the level of risk rises with the number of sexual partners and the presence of other STDs.

Although race has no intrinsic effect on susceptibility to gonorrhea, the frequency of gonorrhea in the United States is increased among urban dwellers, individuals of lower socioeconomic status, and minorities of any population. This may be due to decreased access to diagnosis and treatment; lack of adequate care (ie, education, diagnosis, and treatment), leading to increased transmission rates; and/or reflection bias due to data collection site preference (eg, urban emergency departments [EDs] and STD clinics), as well as true differences in prevalence.

Overall, the African American–to–white ratio of gonococcal infections declined from 23:1 in 2002 to 18:1 in 2006. Infection rates have been trending downward since 1998. However, between 2005 and 2006, the CDC noted a 6.3% increase in the rate of gonococcal infections in African Americans. Subsequently, rates have begun to downtrend once again. (See the figure below.)

Gonorrhea rates by race/ethnicity, United States, Gonorrhea rates by race/ethnicity, United States, 2000-2009. Centers for Disease Control and Prevention.

Similarly, in other ethnic groups, rates increased from 2002 to 2006, including by 22.8% in American Indian/Alaskan Natives, by 17.7% in whites, and by 11.8% in Hispanics. On the other hand, the rate decreased by 1.4% in Asian/Pacific Islanders.

Sex-related demographics

The male-to-female ratio for gonorrhea is approximately 1:1.2; however, females may be asymptomatic, whereas males are rarely asymptomatic. Women younger than 25 years are at the highest risk for gonococcal infection.

Men who have sex with men are much more likely to acquire and carry gonorrhea and have far higher rates of antibiotic-resistant bacteria.

Serious sequelae are much more common in women, in whom pelvic inflammatory disease (PID) may lead to ectopic pregnancy or infertility and in whom DGI is more likely, owing to menstruation, pregnancy, and a higher incidence in occult infection.

Age-related demographics

The highest incidence of gonococcal infection in the United States is among persons aged 15-24 years.[18, 16] This is likely due to the following (see the figure below):

  • Increased numbers of sexual partners
  • Decreased access to or use of health care
  • Physiologic ectopy of the squamocolumnar junction in females
  • Decreased use of barrier contraceptives
    Gonorrhea rates by age and sex, United States, 200 Gonorrhea rates by age and sex, United States, 2009. Centers for Disease Control and Prevention.

Infection in children is a marker for child sexual abuse and should be reported as such, although a 2007 review provided some support for nonsexual transmission between children and for transmission from adults to children related to poor hand hygiene.[25, 26]

Gonococcemia remains an important disease in the adolescent and young adult population, with a peak incidence in males aged 20-24 years and in females aged 15-19 years.

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Prognosis

With adequate early therapy, complete cure and return to normal function are the rule. Most gonococcal infections respond quickly to cephalosporin therapy. Late, delayed, or inappropriate therapy may lead to significant morbidity or, on rare occasions, death.

Complications in males

Urethral strictures secondary to gonococcal infection in men are less common than previously thought. Some strictures in the preantibiotic era likely resulted from treatment by urethral irrigation using caustic compounds rather than from the gonorrhea itself.

Other complications, such as penile lymphangitis, periurethral abscess, acute prostatitis, seminal vesiculitis, and infection of the Tyson and Cowper glands, are now rare.

Complications in females

Tubal scarring and infertility are the major complications of gonococcal infection in females. The incidence of involuntary infertility is estimated at 15% after one attack of pelvic inflammatory disease (PID) and approximately 50%-80% after 3 attacks. (However, infertility may be more common after chlamydial PID than after gonococcal PID, presumably because the more acute inflammatory signs associated with gonorrhea prompt women to seek diagnosis and treatment sooner.)

Failure to diagnose PID can result in acute morbidity, including tuboovarian abscess, endometritis, Fitz-Hugh-Curtis syndrome (perihepatitis), and other chronic sequelae. Perihepatitis secondary to gonorrhea presents as right upper quadrant pain and nausea.

The incidence of ectopic pregnancy is increased from 7-fold to 10-fold in women with previous salpingitis, with resultant increased fetal and maternal mortality rates.

Gonococcal infections in women may also manifest as gonococcal urethritis or infection of periurethral (Skene) or Bartholin glands.

Pelvic inflammatory disease

PID is generally the most feared complication of gonococcal infection, because it is one of the leading causes of female infertility and often leads to hospitalization. This can be devastating to any woman, especially an adolescent who potentially has many years of childbearing ahead of her. In a 2011 study, female adolescents with PID were more likely than older women to have a rapid recurrence of PID or to become pregnant despite reporting more consistent condom use.[27]

Tubo-ovarian abscess and, rarely, tubal perforation with peritonitis and death, can occur, especially if the tubo-ovarian abscess was recurrent. Females with recurrent PID have high rates of ectopic pregnancy and infertility.

Epididymitis and orchitis

Epididymitis and orchitis occur infrequently in males who go untreated. These conditions usually respond well to the same antibiotics used for uncomplicated urethritis, but the drugs are administered for a longer course.

Arthritis

Gonorrhea is the most common cause of arthritis in the adolescent. However, arthritis (septic or reactive) is a rare complication of this disease.

Because it mimics septic arthritis, excluding the possibility of gonococcal infection in any adolescent with acute onset of pyogenic arthritis is important. Adequate diagnosis may require culturing extraarticular sites for N gonorrhoeae.

Additional complications

Complications of gonococcal infections also include the following[28] :

  • Corneal scarring after ocular gonococcal infections
  • Destruction of cardiac valves in gonococcal endocarditis
  • Death from congestive heart failure related to endocarditis
  • Central nervous system (CNS) complications of gonococcal meningitis

It has been suggested that a person with a gonococcal infection may be at a 3- to 5-fold increased risk of acquiring HIV infection, if exposed to the virus.

DGI is an acute illness that causes fever, asymmetrical polyarthralgias, and skin pustules overlying small joints in patients with gonorrhea. Disseminated infection may also lead to meningitis or endocarditis.

In newborns, vertical transmission can cause conjunctivitis, known as ophthalmia neonatorum, and permanent damage and blindness, if untreated.

Oral sex with an infected partner can result in pharyngitis, and, similarly, anal infection can arise from anal sex or local spread from a vaginal source.

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Patient Education

Discuss safe sexual practices with all individuals in whom gonorrhea is suspected. Proper education to prevent gonorrhea may be more effective than simplistic instructions to avoid sex, especially in the teenaged population. Teenagers involved with abstinence-only campaigns have unchanged STD rates and disproportionately acquire anal and oral infections, rather than vaginal infections (the perception being that if an activity is not vaginal sex, it is not sex). Stress that oral or anal sex can also transmit disease.

Patients should know the method of disease transmission and the adverse impact of recurrent infections on future fertility, they should be counseled about the risks of complications following gonococcal infection and the risk of other STDs, and they should always be instructed to refer any sex partners for prompt evaluation and treatment.

In addition, these individuals should be aware that they should avoid sexual contact until medication is finished and until their partners are fully evaluated and treated. Thereafter, they should avoid unprotected contact.

The discussion of responsible sexual behavior should not be limited or withheld because of personal religious or moral views, because these may not be shared by the patient, and teenagers are notorious for sexual experimentation; evidence suggests that offering only limited discussion does the teenage population a huge disservice. This advice is especially pertinent in states where sexual education is almost nonexistent in the school system because of abstinence-only teaching, which is misleading and factually inaccurate.

In one study in Peru, a bundle of interventions that included extensive public health efforts, including training of local medical personnel, specific and presumptive treatment, outreach to female sex workers, and supply of barrier contraception, may have been effective at reducing the prevalence of several STDs, although the effect did not reach statistical significance overall.

The effects were more greatly pronounced (and significant) among female sex workers and young adult women. The study was hampered by several methodologic limitations, such as comparing different cities as controls, which made drawing conclusions from the data difficult.[29]

Abstinence education

Although the most effective STD prevention is abstinence from sex, this is oftentimes an unrealistic expectation, especially in the teenaged population. In fact, 88% of teenagers who pledged abstinence in middle and high school still engaged in premarital sex. Moreover, they tend to have riskier, unprotected sex because of their lack of education. Those who pledge before having sex have been found to have a 33% higher prevalence rate of STDs than have those who had sex and then retrospectively pledged, with nonpledgers falling in between. This is despite a lower number of partners and an older age at first intercourse in pledgers.

Moreover, pledgers are less likely to be aware of their STD status and are less likely to seek testing, even if their STD rates are similar overall (again, highlighting a lack of appropriate sexual education).

Of course, abstinence should be explained to be the best option, but a more practical expectation is abstinence from sex with someone known or suspected of having an STD until treatment is obtained and completed. In light of the difficulty of knowing a potential partner's sexual history (or honesty), strongly recommend the use of condoms as a reasonable alternative to abstinence.[13]

Risks of unprotected sex

Patients should also be counseled about the additional risks of unprotected sex, including the acquisition of more serious or lifelong infections such as herpes, hepatitis B, and HIV, and, of course, about the risks of pregnancy. The emotional aspect of sexual relationships may also need to be addressed, especially in teenage girls. Teenagers are vulnerable in that they are sexually mature but not yet emotionally mature.

For patient education information, see the Sexual Health Center, as well as Sexually Transmitted Diseases, Gonorrhea, and Chlamydia.

Patient education materials are also available at The Centers for Disease Control and Prevention (CDC) Website (Sexually Transmitted Diseases – Gonorrhea) and from many local public health departments.

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Contributor Information and Disclosures
Author

Brian Wong, MD Assistant Professor of Medicine, Division of Infectious Diseases, Loma Linda University Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Chief of Infectious Disease, Program Director of Infectious Disease Fellowship, Department of Internal Medicine, Wayne State University School of Medicine

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, International Immunocompromised Host Society, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Neal Ammar, MD Staff Physician, Department of Dermatology, UMDNJ-New Jersey Medical School

Neal Ammar, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, and Sigma Xi

Disclosure: Nothing to disclose.

Mounir Bashour, MD, CM, FRCS(C), PhD, FACS Assistant Professor of Ophthalmology, McGill University; Clinical Assistant Professor of Ophthalmology, Sherbrooke University; Medical Director, Cornea Laser and Lasik MD

Mounir Bashour, MD, CM, FRCS(C), PhD, FACS is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American College of International Physicians, American College of Surgeons, American Medical Association, American Society of Cataract and Refractive Surgery, American Society of Mechanical Engineers, American Society of Ophthalmic Plastic and Reconstructive Surgery, Biomedical Engineering Society, Canadian Medical Association,Canadian Ophthalmological Society, Contact Lens Association of Ophthalmologists, International College of Surgeons US Section, Ontario Medical Association, Quebec Medical Association, and Royal College of Physicians and Surgeons of Canada

Nicholas John Bennett, MB, BCh, PhD, Assistant Professor in Pediatrics, Division of Infectious Diseases, Connecticut Children's Medical Center

Nicholas John Bennett, MB, BCh, PhD, is a member of the following medical societies: Alpha Omega Alpha and American Academy of Pediatrics

Disclosure: Nothing to disclose.

John L Brusch, MD, FACP Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

David F Butler, MD Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Sanda Cebular, MD Fellow, Department of Medicine, Section of Infectious Diseases, State University of New York at Brooklyn

Sanda Cebular, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine and American Medical Association

Disclosure: Nothing to disclose.

Joseph Domachowske, MD Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York Upstate Medical University

Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Dirk M Elston, MD Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Renuka Heddurshetti, MD Fellow in Infectious Diseases, Department of Internal Medicine, State University of New York at Brooklyn

Renuka Heddurshetti, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Rajendra Kapila, MD, MBBS Associate Professor, Department of Medicine, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Rajendra Kapila, MD, MBBS is a member of the following medical societies: American College of Physicians, American Medical Association, Infectious Diseases Society of America, and Infectious Diseases Society of New Jersey

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Larry I Lutwick, MD Professor of Medicine, State University of New York Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus

Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD Assistant Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society

Disclosure: Nothing to disclose.

Fernando H Murillo-Lopez, MD Senior Surgeon, Unidad Privada de Oftalmologia CEMES

Fernando H Murillo-Lopez, MD is a member of the following medical societies: American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Christopher J Rapuano, MD Professor, Department of Ophthalmology, Jefferson Medical College of Thomas Jefferson University; Co-Chairman of the Cornea Service, Co-Chairman of Refractive Surgery Department, Wills Eye Institute

Christopher J Rapuano, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, Cornea Society, Eye Bank Association of America, International Society of Refractive Surgery, and Pan-American Association of Ophthalmology

Disclosure: Allergan Honoraria Speaking and teaching; Allergan Consulting fee Consulting; Alcon Honoraria Speaking and teaching; Inspire Honoraria Speaking and teaching; RPS Ownership interest Other; Vistakon Honoraria Speaking and teaching; EyeGate Pharma Consulting; Inspire Consulting fee Consulting; Bausch & Lomb Honoraria Speaking and teaching

Gregory J Raugi, MD, PhD Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle School of Medicine; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle

Gregory J Raugi, MD, PhD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Robert W Tolan Jr, MD Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: Novartis Honoraria Speaking and teaching

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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This patient presented with gonococcal urethritis, which became systemically disseminated, leading to gonococcal conjunctivitis of the right eye. Courtesy of the CDC/Joe Miller, VD.
Gonorrhea rates, United States, 1941-2009. Centers for Disease Control and Prevention.
Gonorrhea rates by race/ethnicity, United States, 2000-2009. Centers for Disease Control and Prevention.
Gonorrhea rates by age and sex, United States, 2009. Centers for Disease Control and Prevention.
Rates of gonococcal infection per 100,000 by state and outlying regions (2009). Data from the Centers for Disease Control and Prevention (CDC):
Disseminated gonococcemia, acral pustules.
Cytologic smear of cutaneous acral pustule showing gram-negative, intracellular diplococci.
 
 
 
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