Gonococcal Arthritis 

  • Author: Michael P Keith, MD, FACP, FACR; Chief Editor: Herbert S Diamond, MD   more...
 
Updated: Aug 19, 2011
 

Background

Gonococcal arthritis is caused by infection with the gram-negative diplococcus Neisseria gonorrhoeae. In the United States, gonococcal arthritis is the most common form of septic arthritis.[1] This is in contrast to Western Europe, where gonococcal arthritis is uncommon,[2] likely owing to a 70% decline in gonococcal infections over the last 2 decades.[1]

Although the pathogenesis of articular involvement is controversial, it is ultimately a consequence of disseminated gonococcal infection (DGI). Gonococcal arthritis manifests as either a bacteremic infection (arthritis-dermatitis syndrome; 60% of cases) or as a localized septic arthritis (remaining 40%). Arthritis-dermatitis syndrome includes the classic triad of dermatitis, tenosynovitis, and migratory polyarthritis.

Patients with gonococcal arthritis usually require initial hospitalization for intravenous antibiotic therapy; upon improvement, they can be transitioned to oral antibiotics. Unlike in Staphylococcus aureus septic arthritis, joint destruction is rare in gonococcal arthritis.

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Pathophysiology

N gonorrhoeae is a highly infectious organism capable of colonizing diverse mucosal surfaces. The risk of infection from a single contact with the organism is estimated at 60%-90% among women and 20%-50% among men.[1] Common sites of infection include the urethra, cervix, pharynx, and rectum; however, infection may be asymptomatic in some patients. Hematogenous spread of the mucosal infection occurs in 0.5%-3% of cases,[3] and disseminated infection is thought to play a major role in the pathogenesis of gonococcal arthritis. Patients with DGI may present with dermatitis-arthritis syndrome or with a localized septic arthritis. These presentations may represent different phases of a disease continuum.

Factors that correlate with increased risk of a disseminated infection have been identified for both the host and the organism.

Host factors for disseminated infection include the following:[2]

Characteristics of the gonococcus associated with DGI include the following:[1, 2, 3]

  • Antigenic variation of pili
  • Protein IA on the outer membrane (inhibits host factor H and C4-binding protein, making host complement cascade less effective)
  • Lack of protein II
  • AHU strains with nutritional requirements for arginine, hypoxanthine, and uracil (often associated with protein IA)
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Epidemiology

Frequency

United States

In 2005, 339,593 cases of gonococcal infection were reported in the United States, making it the second most commonly reported communicable disease.[4] Although rates of gonococcal infection declined from 1975-1997, the national rate of gonococcal infection increased in 2005 to 115 cases per 100,000 persons.[4] However, rates vary by region and demographics, as described below.

International

  • According to the World Health Organization, gonococcal infection is among the curable sexually transmitted infections, of which 340 million cases occur annually.[5]
  • The incidence of gonococcal infection is lower in Europe than in North America. For example, the incidence of gonococcal infection in Sweden in 1992 was less than 5 per 100,000 population, while the incidence in the United States in 1995 was 150 per 100,000.[2]
  • Gonococcal infection is high in developing countries, partly because of limited public health infrastructure and limited access to health care.

Mortality/Morbidity

Morbidity associated with DGI has decreased dramatically in the postantibiotic era. Complications of DGI including pericarditis, endocarditis, meningitis, perihepatitis, pyomyositis, osteomyelitis, and glomerulonephritis are now rare and occur in only 1%-3% of cases.[1]

Race

In the United States, gonococcal infection is most common in African Americans.[4] The prevalences in with, Hispanic, Native American, and Asian populations are similar and dramatically lower than in African Americans.[4]

Sex

The disease is 3-4 times more common in females than in males, possibly because of the increased risk of asymptomatic infection in females.[2]

Age

The highest rates of infection in the United States are among persons aged 15-29 years; however, older adults may be affected.[4]

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Contributor Information and Disclosures
Author

Michael P Keith, MD, FACP, FACR  Chief of Rheumatology, National Naval Medical Center and Walter Reed Army Medical Center; Assistant Professor of Medicine, Uniformed Services University of the Health Sciences

Michael P Keith, MD, FACP, FACR is a member of the following medical societies: American College of Physicians, American College of Rheumatology, and Clinical Immunology Society

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Lawrence H Brent, MD  Associate Professor of Medicine, Jefferson Medical College of Thomas Jefferson University; Chair, Program Director, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center

Lawrence H Brent, MD is a member of the following medical societies: American Association for the Advancement of Science, American Association of Immunologists, American College of Physicians, and American College of Rheumatology

Disclosure: Genentech Honoraria Speaking and teaching; Genentech Grant/research funds Other; Amgen Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; Abbott Immunology Honoraria Speaking and teaching; Takeda Honoraria Speaking and teaching; UCB Speaking and teaching; Omnicare Consulting fee Consulting; Centocor Consulting fee Consulting

Alex J Mechaber, MD, FACP  Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine

Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD  Adjunct Professor of Medicine, Division of Rheumatology, University of Pittsburgh School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa

Disclosure: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Timothy M Straight, MD, to the development and writing of this article.

References
  1. Dalla Vestra M, Rettore C, Sartore P, Velo E, Sasset L, Chiesa G, et al. Acute septic arthritis: remember gonorrhea. Rheumatol Int. Nov 2008;29(1):81-5. [Medline].

  2. Bardin T. Gonococcal arthritis. Best Pract Res Clin Rheumatol. Apr 2003;17(2):201-8. [Medline].

  3. Rice PA. Gonococcal arthritis (disseminated gonococcal infection). Infect Dis Clin North Am. Dec 2005;19(4):853-61. [Medline].

  4. Centers for Disease Control and Prevention. Sexually transmitted disease surveillance 2005 supplement, gonococcal isolate surveillance project (GISP) Annual Report 2005. Atlanta, GA. US Department of Health and Human Services, Centers for Disease Control and Prevention, January 2007. Available at http://www.cdc.gov.std.gisp2005/. Accessed May 12, 2009.

  5. World Health Organization Fact Sheet Number 110. Available at http://www.who.int/mediacentre/factsheets/fs110/en/index.html. Accessed May 12, 2009.

  6. Marker-Hermann E. Septic arthritis, osteomyelitis, gonococcal and syphilitic arthritis. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatology. 4th ed. Philadelphia, PA: Mosby Elsevier; 2008:1013-28.

  7. Davis BT, Pasternack MS. Case records of the Massachusetts General Hospital. Case 19-2007 - a 19-year-old college student with fever and joint pain. N Engl J Med. Jun 21 2007;356(25):2631-7. [Medline].

  8. Liebling MR, Arkfeld DG, Michelini GA, Nishio MJ, Eng BJ, Jin T, et al. Identification of Neisseria gonorrhoeae in synovial fluid using the polymerase chain reaction. Arthritis Rheum. May 1994;37(5):702-9. [Medline].

  9. Read P, Abbott R, Pantelidis P, Peters BS, White JA. Disseminated gonococcal infection in a homosexual man diagnosed by nucleic acid amplification testing from a skin lesion swab. Sex Transm Infect. Oct 2008;84(5):348-9. [Medline].

  10. Kimmitt PT, Kirby A, Perera N, Nicholson KG, Schober PC, Rajakumar K, et al. Identification of Neisseria gonorrhoeae as the causative agent in a case of culture-negative dermatitis-arthritis syndrome using real-time PCR. J Travel Med. Sep-Oct 2008;15(5):369-71. [Medline].

  11. Update to CDC's Sexually Transmitted Diseases Treatment Guidelines 2006: Fluoroquinolones no longer recommended for treatment of gonococcal infections. Available at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5614a3.htm. Accessed May 1, 2009.

  12. [Guideline] Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2006. MMWR. 2006;55(No. RR-11):42-49.

  13. [Guideline] Centers for Disease Control and Prevention. Sexually Transmitted Diseases Treatment Guidelines, 2010. MMWR. RR-12;59:49-55. [Medline].

  14. MMWR. Availability of Cefixime 400 mg tablets---United States, April 2008. Available at http://www.cdc.gov.mmwr/preview/mmwrhtml/mm5716a5.htm. Accessed May 1, 2009.

  15. Centers for Disease Control and Prevention. Notice to readers: discontinuation of spectinomycin. MMWR. 2006;55:370.

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