Gonococcal Infections 

  • Author: Brian Wong, MD; Chief Editor: Burke A Cunha, MD   more...
 
Updated: Aug 18, 2011
 

Background

Gonorrhea (also called the clap and the drip), which is caused by Neisseria gonorrhoeae, is an important public health problem and is the second most common reportable bacterial sexually transmitted infection. Gonorrhea is most frequently spread during sexual contact. However, it can also be transmitted from the mother's genital tract to the newborn during birth, causing ophthalmia neonatorum and systemic neonatal infection. The incubation period is usually 2-8 days.

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.

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Pathophysiology

N gonorrhoeae is a gram-negative, intracellular, aerobic diplococcus. It mainly affects the host’s columnar or cuboidal epithelium.

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 killing 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 into 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.[1, 2]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.[1]

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 attachment to sperm, to secondarily invade lower genital structures (vagina and cervix) and progress to upper genital organs (endometrium, salpinx, ovaries).

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Epidemiology

Frequency

United States

An estimated 700,000 new gonococcal infections occur annually in the United States.[3] In 2009, 301,174 cases of gonorrhea were reported to the US Centers for Disease Control and Prevention (CDC).[4] In the United States, the rate of gonorrhea was approximately 115 cases per 100,000 population between 1996 and 2006. Since the 1970s, the overall incidence of gonococcal infections has declined considerably in modern Western countries. See the figure below.

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

The rate of gonorrhea is much higher in African Americans than in other racial groups[5] 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 social networks. Some experts estimate the annual cost of gonorrhea and its complications at $1.1 billion.

International

In 1999, an estimated 62.35 million cases of gonococcal infection were diagnosed, predominantly in males.[6] In a report by the World Health Organization, it is now estimated that gonorrhea accounts for 88 million infections each year worldwide.[7] Although the frequency data are unknown in most developing countries, gonococcal infection rates in pregnant women in the Central African Republic and South Africa were found to be 3.1% and 7.8%, respectively. In 1999, the number of new cases of gonococcal infection diagnosed in North America was 1.56 million, 1.11 million in Western Europe, 27.2 million in South and Southeast Asia, and 7.27 million in Latin American and the Caribbean. Developing countries have the highest rates of gonorrhea and its complications.[8]

Mortality/Morbidity

  • Symptomatic and asymptomatic gonococcal infection in women may lead to tubal scarring and infertility. The incidence of involuntary infertility is estimated to be 15% after one attack of PID and approximately 50%-80% after 3 attacks. The incidence of ectopic pregnancy is increased 7-fold to 10-fold in women with previous salpingitis, increasing both fetal and maternal mortality rates. Failure to diagnose PID can result in acute morbidity, including tuboovarian abscess, endometritis, or Fitz-Hugh-Curtis syndrome (perihepatitis), and the chronic sequelae noted above.
  • Gonococcal infections in women may also manifest as gonococcal urethritis or infection of periurethral (Skene) or Bartholin glands.
  • Infertility may be more common after chlamydial PID than after gonococcal PID, possibly because the significant acute inflammatory signs associated with gonorrhea prompt women to seek a diagnosis, thereby leading to sooner treatment.
  • Urethral strictures caused by gonorrhea in men are less common than once believed. Some strictures in the preantibiotic era likely resulted from treatment by urethral irrigation using caustic compounds rather than from the actual gonorrhea infection.
  • 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.

Race

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 sexually transmitted diseases (STDs).

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 an increased rate of gonococcal infections in African Americans by 6.3%. 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 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

  • Since 1987, infection rates have downtrended in the United States in both males and females.
  • An asymptomatic carrier state can occur in both sexes but is believed to occur more frequently in females than in males. Symptomatic gonococcal disease, found more often in males than in females, prompt many men to obtain prompt curative treatment, usually preventing permanent sequelae.
  • Serious complications of gonococcal infection are much more common in women than in men. PID in women may lead to ectopic pregnancy or infertility. Females may be more likely than males to develop disseminated gonococcal infection (DGI) possibly because of hormonal differences, menstruation, and alteration in vaginal pH. Women younger than 25 years are at the highest risk for gonococcal infection.

Age

In the United States, the highest rates of gonorrhea are found in young (15-30 y) unmarried persons and in groups of low educational and socioeconomic status.[9] See the figure below.

Gonorrhea rates by age and sex, United States, 200Gonorrhea rates by age and sex, United States, 2009. Centers for Disease Control and Prevention.

Infection in children is a marker for child sexual abuse.

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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.

Coauthor(s)

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.

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.

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.

Specialty Editor Board

Kenneth C Earhart, MD  Deputy Head, Disease Surveillance Program, United States Naval Medical Research Unit #3

Kenneth C Earhart, MD is a member of the following medical societies: American College of Physicians, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and Undersea and Hyperbaric Medical Society

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

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.

Eleftherios Mylonakis, MD  Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital

Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

References
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  2. Palmer HM, Young H, Graham C, Dave J. Prediction of antibiotic resistance using Neisseria gonorrhoeae multi-antigen sequence typing. Sex Transm Infect. Aug 2008;84(4):280-4. [Medline].

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  9. Department of Health and Human Services, Centers for Disease Control and Prevention. STD Surveillance 2006: Trends in Reportable Sexually Transmitted Diseases in the United States, National Surveillance Data for Chlamydia, Gonorrhea, and Syphilis. Available at http://www.cdc.gov/std/stats/trends2006.htm.

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  14. McNally LP, Templeton DJ, Jin F, Grulich AE, Donovan B, Whiley DM, et al. Low positive predictive value of a nucleic acid amplification test for nongenital Neisseria gonorrhoeae infection in homosexual men. Clin Infect Dis. Jul 15 2008;47(2):e25-7. [Medline].

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  19. CDC. Update to CDC's sexually transmitted diseases treatment guidelines, 2006: fluoroquinolones no longer recommended for treatment of gonococcal infections. MMWR Morb Mortal Wkly Rep. Apr 13 2007;56(14):332-6. [Medline]. [Full Text].

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  22. Ota KV, Fisman DN, Tamari IE, et al. Incidence and treatment outcomes of pharyngeal Neisseria gonorrhoeae and Chlamydia trachomatis infections in men who have sex with men: a 13-year retrospective cohort study. Clin Infect Dis. May 1 2009;48(9):1237-43. [Medline].

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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.
 
 
 
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