Gonococcal arthritis is a type of bacterial arthritis that results from the bacteremic spread of Neisseria gonorrhoeae, a sexually transmitted pathogen. It is a clinical manifestation of disseminated gonococcal infection. It consists of two major clinical forms: localized septic arthritis and arthritis-dermatitis syndrome.
Neisseria gonorrhoeae, a gram-negative diplococcus, is the etiologic pathogen in gonococcal arthritis. It is usually transmitted sexually and is an important cause of bacterial arthritis in sexually active adolescents. However, it may also be acquired perinatally during childbirth and may cause gonococcal infection in newborns.
Approximately 0.5% to 3% of patients who are infected with N. gonorrhoeae develop disseminated gonococcal infection (DGI). There is a paucity of recent epidemiologic data that looks into the incidence of DGI in patients with arthritis, but historical data in the 1980s show that N. gonorrhoeae were associated with up to 14% of patients who have arthritis. Gonococcal arthritis is more commonly seen in young healthy individuals although it may occur in any age group.
Host risk factors that are associated with disseminated gonococcal infection (DGI) include complement deficiencies, menstruation, pregnancy, history of pelvic surgery, and intrauterine devices (IUD). Specific strains of N. gonorrhoeae have virulence factors that have been associated with dissemination. These include strains containing a specific outer membrane called the porin 1A serotype that promotes resistance, diminished host inflammatory response, and host cell invasion and strains that require specific substrates for growth. It is also hypothesized that the pathogenesis of DGI may be partly immune-mediated. This is supported by the fact that the pathogen is frequently not isolated from both the synovial fluid and blood of patients with clinical manifestations of dissemination.
Disseminated gonococcal infection (DGI) usually consists of two major clinical syndromes: the arthritis-dermatitis syndrome and localized purulent arthritis without associated skin lesions. There are, however, patients who present with symptoms that overlap between these two classic presentations. Although localized infection of the genitourinary tract, rectum, or pharynx by N. gonorrhoeae is a prerequisite for dissemination, patients with clinical manifestations of DGI often do not manifest symptoms of localized gonococcal infection.
A high clinical suspicion is necessary for patients who present with joint pain or swelling that is concerning for septic arthritis especially in those who are sexually active and younger than 40 years old and in certain at-risk populations such as in men who have sex with men (MSM). A thorough history and physical examination including an emphasis on sexual history are needed in patients with suspected gonococcal arthritis. Menstrual history and pregnancy need to be assessed in premenopausal patients. Skin and joint examination may provide information that heightens clinical suspicion especially in patients who present with the typical triad of tenosynovitis, arthralgia, and skin lesions.
Definitive diagnosis of disseminated gonococcal infection (DGI) or gonococcal arthritis is made through the identification of the etiologic pathogen in a specimen taken from a non-mucosal site (such as blood, synovial fluid, or skin lesions). Microbiologic tests, however, are not always positive and in such cases, diagnosis is made clinically. A clinical diagnosis may be supported by evidence of N. gonorrhoeae infection from specimens obtained from mucosal sites. Screening for other sexually transmitted illnesses such as HIV, syphilis, and chlamydia is often recommended since these frequently co-exist with gonococcal infection.
Two sets of blood cultures should be obtained, and a positive result helps distinguish gonococcal arthritis from other pathogens that cause septic arthritis. Positive blood cultures, however, are only positive in less than 1/3 of cases and is more frequently seen in patients who present with arthritis-dermatitis syndrome. Specimens from mucosal sites should also be obtained and are frequently helpful in patients who have a high clinical suspicion of DGI but who have sterile synovial fluid or blood specimens. Nucleic acid amplification testing (NAAT) of either urine specimens in both men and women or vaginal swabs in women is preferred, if available. The culture of a urogenital specimen is an alternative.
In patients who demonstrate joint swelling and effusion, arthrocentesis and synovial fluid analysis should be performed. Typically, a synovial fluid analysis will show white blood cell (WBC) count of 50,000 cells/mm3 or more; although, a cell count below 10,000 cells/mm3 is not uncommon. This may be associated with reduced glucose concentration and elevated LDH level but these findings are non-diagnostic and of limited value. In patients who present with localized purulent arthritis, N. gonorrhoeae will be isolated in only about 50% (range of 25% to 75%) of synovial fluid specimens. This is even less in patients who present with the arthritis-dermatitis syndrome. NAAT of synovial fluid is more sensitive (greater than 75%) than culture and should be performed if available.
Obtaining skin lesion specimens is usually not done because of the difficulty of sampling and its very poor yield. The culture of skin lesions is often negative. NAAT of skin specimens may be slightly more sensitive, but this is not widely available.
Initial management in the inpatient setting is recommended for patients with a presumptive diagnosis of disseminated gonococcal infection (DGI) or gonococcal arthritis. Ceftriaxone as a parenteral therapy, either given intravenously or intramuscularly, is the preferred initial antibiotic of choice. Intravenous administration of 1 gm every 24 hours is usually preferred in patients presenting with purulent arthritis. A single dose of 1 gram of azithromycin by mouth is usually added to cover potential coinfection with C. trachomatis. Alternative antimicrobial agents include third-generation cephalosporin such as cefotaxime and ceftizoxime, which are given as 1 gm every 8 hours. A dose of 100 mg of doxycycline twice a day for 7 days is an alternative to azithromycin.
Widespread resistance to oral cephalosporins such as cefixime has been documented. Oral cephalosporins are therefore not recommended as initial therapy. Although not always possible, the microbiologic diagnosis should be attempted, and antimicrobial susceptibility testing should be performed to guide antibiotic therapy. After 1 to 2 days of clinical improvement with ceftriaxone as parenteral therapy, a seven-day course of antibiotics may be completed with daily intramuscular ceftriaxone given at 250 mg daily. Patients with septic arthritis or those who are immunocompromised or slower to respond to treatment may require a longer course of therapy (7 to 14 days). De-escalation to oral antibiotic therapy (such as cefixime, fluoroquinolones, or penicillin) may be done only in patients who do not have septic arthritis and only if culture and susceptibility results are available. However, not all laboratories are capable of performing N. gonorrhoeae culture and sensitivity testing. In cases wherein the microbiologic diagnosis is not established, the course of therapy should be completed with a parenteral cephalosporin.
Partners of patients diagnosed with DGI within 2 months should be contacted and treated whenever possible. Patients with recurrent DGI or gonococcal arthritis will require further evaluation for complement deficiency.
Patients with a history of beta-lactam allergy are often able to tolerate ceftriaxone. Due to the absence of effective alternative parenteral agents, patients who have a history of IgE mediated hypersensitivity reaction to beta-lactams may undergo either skin testing or graded challenge testing. Patients who test positive for these tests should undergo desensitization. Those with a history of severe, non-IgE mediated reaction will require consultation with an Infectious Disease specialist.
Patients presenting with localized purulent arthritis should undergo joint drainage, either arthroscopically or through repeated joint aspirations until there is evidence of response such as the resolution of fever, leukocytosis, joint pain, and effusions. Open surgical drainage may be necessary if aspiration is not adequate.
Disseminated gonococcal arthritis has an excellent prognosis if appropriate therapy is given. Rare complications such as meningitis, perihepatitis, osteomyelitis, and endocarditis may occur if treatment is delayed or inadequate.
After the patient has completed treatment, re-evaluation is necessary. Patients also need to be screened for other sexually transmitted infections in 3-6 months. More important, the partners need to be contacted and treated.
Gonococcal arthritis is ideally managed with a multidisciplinary team of healthcare professionals. While the acute joint problem is managed by a physician, many patients may require a short program in physical therapy to regain their joint mobility and muscle strength. The nurse should educate the patient on sexually transmitted infections and how to practice safe sex. Once a patient has been diagnosed with one STD, the nurse should inform the patient on getting tested for other STDs. The pharmacist should ensure compliance with antibiotics to ensure that full healing occurs. Finally, the social worker should recommend that the partner be examined and treated, otherwise the cycle of infection transmission will continue. (Level V)
When patients with gonococcal arthritis are treated with antibiotics, there is usually full recovery without any sequelae. For those who have other manifestations besides the arthritis, the prognosis may depend on the severity of the infection. For example, if a patient has gonococcal endocarditis, antibiotics may be required for 4-6 weeks and if the valve is damaged, valve replacement may be required. In general, complications following gonococcal arthritis are rare. (Level V)