Gonococcal Arthritis
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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] In Western Europe, however, gonococcal arthritis is uncommon, [2] probably because of the 70% decline in gonococcal infections over the past 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 as a bacteremic infection (arthritis-dermatitis syndrome) or as a localized septic arthritis. Arthritis-dermatitis syndrome includes the classic triad of dermatitis, tenosynovitis, and migratory polyarthritis.
Patients with gonococcal arthritis usually require initial hospitalization for intravenous (IV) antibiotic therapy; upon improvement, they can be switched to oral antibiotics. Unlike Staphylococcus aureus septic arthritis, gonococcal arthritis is rarely associated with joint destruction.
Gonococcal arthritis is caused by infection with the gram-negative diplococcus N gonorrhoeae, a highly infectious organism that exclusively infects humans; it is capable of colonizing diverse mucosal surfaces. The risk of infection from a single contact with N gonorrhoeae is estimated to be 60-90% for women and 20-50% for men. [1] Common sites of infection include the urethra, cervix, pharynx, and rectum. 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 (60% of cases) or with a localized septic arthritis (40%). These presentations may represent different phases of a disease continuum.
The risk of dissemination after mucosal infection depends on both the ability of the patient’s immune system to control the infection and the virulence of the organism. Factors that correlate with an increase in this risk have been identified for both the host and the organism. Host-related risk factors for disseminated infection include the following [2] :
Female sex
Pregnancy
Menses
Low socioeconomic or educational status
IV drug use
Multiple sexual partners
Organism-related risk factors for DGI include the following [1, 2, 3, 4] :
Antigenic variation of pili
Protein Por B1A on the outer membrane – This inhibits host factor H and C4-binding protein, making host complement cascade less effective
Lack of protein Por B1B
Strains with nutritional requirements for arginine, hypoxanthine, and uracil (ie, AHU strains) – These are often associated with protein IA
Colony opacity (Opa) protein-independent invasion – Opa proteins are adhesins crucial to the process of N gonorrhoeae attachment to host cells, particularly avoidance of carcinoembryonic antigen-related cell adhesion molecule-3 (CEACAM3) [5]
According to the Centers for Disease Control and Prevention (CDC), gonorrhea is the second most commonly reported notifiable disease in the United States, with 555,608 cases reported in 2017. Sexually transmitted diseases are typically underreported, however, and the CDC estimates that approximately 820,000 cases of gonorrhea occur yearly in the US. [4]
The rate of reported gonorrhea cases in the US has been increasing since 2010, after declining from their peak of 467.7 cases per 100,000 population in 1975 to an historic low of 98.1 cases per 100,000 population in 2009. In 2016-2017, gonorrhea rates increased by 18.6%. As of 2017, the national rate of gonococcal infection was 171.9 cases per 100,000 population. [4] Within the United States, however, rates of infection vary by region (highest in the South, at 194.0 cases per 100,000 population, and lowest in the Northeast) and by demographics (see below).
International statistics
The World Health Organization (WHO) estimates that 78 million cases of gonococcal infection occur annually. [6] The incidence of gonococcal infection is lower in Europe than in North America. In Sweden in 1992, for example, it was lower than 5 per 100,000 population, whereas in the United States in 1995, it was 150 per 100,000. [2] Gonococcal infection is common in developing countries, partly because of limited public health infrastructure and limited access to health care.
A 3-year retrospective study from France of 21 cases of disseminated gonococcal infection, which included 14 cases of arthritis, found that the number of cases increased from to 2009 to 2011. Men were at higher risk than women. [7] In a study of indigenous people in central Australia, the incidence of gonococcal arthritis was 911 of 100,000 gonococcal notifications. Cases were significantly more likely to occur in young (≤29 years) indigenous women than young indigenous men; risk was almost twice as high in women than in men. [8]
In the United States, the highest rates of gonorrheal infection are in persons aged 20-24 years. However, rates are also high in those females ages 15-19 and males ages 25-29. In addition, during 2016-2017 the gonorrhea rate increased in all age groups, as follows [4] :
In 2017, the rate of reported gonorrhea cases was higher in men than in women (202.5 versus 141.8 cases per 100,000 same-sex population). Rates in women fell in 2012-2014, from 107.9 to 100.4 per 100,000, but have been rising since then; rates in men have increased steadily since 2012, when the rate was 105.0 per 100,000. [4]
Gonococcal infection is most common in African Americans. [4] Cases per 100,000 by race/ethnicity were as follows in 2017:
For patients with septic arthritis resulting from gonococcal infection, proper antibiotic treatment and joint drainage typically leads to full recovery. For patients with more severe manifestations of DGI, the prognosis varies, depending on complications or comorbidities. For example, patients with acute endocarditis may require valve surgery and can expect to undergo at least 4-6 weeks of antibiotic therapy. DGI-associated morbidity has decreased dramatically in the postantibiotic era. Complications are rare (1-3% of cases). [1]
Patient education is an integral part of proper therapy. Patients should learn about the sexual transmission of the disease and be informed regarding barrier methods of preventing it (condoms). In addition, education regarding specific risk factors or high-risk behaviors may help prevent further gonococcal infections or more severe sexually transmitted diseases (eg, HIV infection). Also important are identification, examination, and treatment of patients’ sexual partners.
For patient education resources, see the Sexual Health Center and the Arthritis Center, as well as Gonorrhea and Sexually Transmitted Diseases.
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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. 2008 Sep-Oct. 15(5):369-71. [Medline].
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Victoria Fernandes Sullivan, MD Fellow in Rheumatology, Walter Reed National Military Medical Center
Disclosure: Nothing to disclose.
Rachel Robbins, MD, FACP Assistant Professor of Medicine, Uniformed Services University of the Health Sciences; Staff Rheumatologist, Walter Reed National Military Medical Center
Rachel Robbins, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, Association of Program Directors in Internal Medicine
Disclosure: Nothing to disclose.
Michael P Keith, MD, FACP, FACR Chief of Rheumatology, Walter Reed National Military Medical Center; Associate Professor of Medicine, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine
Michael P Keith, MD, FACP, FACR is a member of the following medical societies: American College of Physicians, American College of Rheumatology, Clinical Immunology Society
Disclosure: Nothing to disclose.
Herbert S Diamond, MD Visiting Professor of Medicine, Division of Rheumatology, State University of New York Downstate Medical Center; 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, Phi Beta Kappa
Disclosure: Nothing to disclose.
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
Timothy M Straight, MD Instructor, Department of Medicine, Uniformed Services University School of Medicine
Timothy M Straight, MD is a member of the following medical societies: American College of Physicians
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
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