Gonococcal Arthritis ?>

Gonococcal Arthritis

Gonococcal Arthritis


Introduction
Background

Gonococcal arthritis is the most common acute septic arthritis in young adults. It is caused by the gram-negative diplococcus Neisseria gonorrhoeae. 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) in 60% of cases or as a localized septic arthritis in the other 40%. Arthritis-dermatitis syndrome includes the classic triad of dermatitis, tenosynovitis, and migratory polyarthritis. Patients with gonococcal arthritis who develop joint destruction (rare) usually require hospitalization for antibiotic therapy to avoid other potentially serious complications of DGI.
Pathophysiology

N gonorrhoeae is a highly infectious organism capable of colonizing diverse mucosal surfaces. The risk of infection from a single contact is estimated at 60-90% among women and 20-50% among men. Infection may not cause symptoms and often affects genitourinary, rectal, or pharyngeal mucosal surfaces. Hematogenous spread of the mucosal infection (0.5-3% of cases) is caused by a delay in antibiotic treatment, physiologic changes in the host, host immune system failures, and particularly virulent strains of N gonorrhoeaeand can occur even in the absence of symptoms. 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.
Frequency
United States

Although decreasing or stable in the 1990s, the national incidence of gonococcal infection increased in 2005 to 115 cases per 100,000 persons. However, rates vary by region. In the western United States, rates increased from 57 cases per 100,000 persons in 2000 to 81.5 cases per 100,000 persons in 2005to. Incidence rates declined in the northeast, south, and Midwest regions over the same period. Demographic risk factors include nonwhite ancestry, lower socioeconomic or educational status, urban residency, promiscuity or sexual activity at a young age, single marital status, homosexuality, previous history of gonorrhea infection, and intravenous drug abuse.

International

Two hundred million cases of N gonorrhoeae infection occur worldwide each year. The incidence appears to be lower in Europe than in North America. Developing countries, however, continue to have a high incidence of disease, 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. Pericarditis, endocarditis, meningitis, perihepatitis, pyomyositis, osteomyelitis, and glomerulonephritis have been reported but are now rare. Arthritis in more unusual joints (eg, sternoclavicular, hip) in patients with HIV may be more aggressive than typical cases in the general population. 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:
General
Extragenital infection
Promiscuity
Systemic lupus erythematosus
Low socioeconomic or educational status
Intravenous drug abuse
HIV infection
Women
Menses
Pregnancy
Puerperium
Chronic asymptomatic endocervical infection
Men: Homosexuality
Inherited: Patients with an inherited terminal complement deficiency (C5-C9) are susceptible to recurrent gonococcal infections, especially DGI with meningitis.

Characteristics of the gonococcus associated with increased virulence and, hence, bacteremia and DGI include the following:
The presence of pili
Protein IA on the outer membrane (inhibits neutrophil exocytosis and promotes organism endocytosis by epithelial cells)
Lack of protein II (transparent colonies [associated with DGI]) and protein III (blocking antibodies that reduce serum bactericidal activity)
Lipo-oligosaccharide ([LOS] endotoxic activity and possible reduced serum bactericidal activity)
Immunoglobulin A (IgA) proteases (protection from mucosal surface defenses)
Nutritional requirements such as arginine, hypoxanthine, and uracil (associated with lack of protein II)
Race

In the United States, the disease is more prevalent among African American, Hispanic, and Native American populations.
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.
Age

Persons younger than 30 years are at the greatest risk; however, older adults may be affected.
Clinical
History

The clinical presentation of disseminated gonococcal infection (DGI) is typically divided into a bacteremic form and a septic arthritis form. Approximately 60% of patients present with symptoms consistent with the bacteremic form, and the remaining 40% present with symptoms of more localized infection. Although each form presents with its own symptom complex, the overlap can be considerable. The time from initial infection to initial manifestations of DGI ranges from 1 day to 3 months.

Bacteremic form (arthritis-dermatitis syndrome)
Symptoms are present 3-5 days before diagnosis.
Migratory arthralgias are the most common presenting symptom in persons with DGI and are usually polyarticular. The arthralgias are typically asymmetric and tend to involve the upper extremities more than the lower extremities. The wrist, elbows, ankles, and knees are most commonly affected. Symptoms resolve spontaneously in 30-40% of cases or evolve into a septic arthritis in one or several joints.
Pain may also be due to tenosynovitis. The tenosynovitis of DGI is asymmetric and most commonly occurs over the dorsum of the wrist and hand, as well as over the metacarpophalangeal joints, ankles, and knees.
The rash associated with the bacteremic form of DGI may be overlooked by patients because it is painless and nonpruritic and consists of small papular, pustular, or vesicular lesions.
Nonspecific constitutional symptoms may include myalgias, fever, and malaise.
Septic arthritis form
Joint symptoms begin within days to weeks of gonococcal infection.
Patients may experience pain, redness, and swelling in usually one or sometimes multiple joints.

Physical
Bacteremic form (classic triad of migratory polyarthritis, tenosynovitis, and dermatitis)
Migratory arthritis has an asymmetric distribution, most commonly affecting wrists, ankles, and elbows. Seventy percent of patients have 1-3 joints with clear inflammatory signs after just a few days. Symmetric polyarthritis is less common but may occur in approximately 10% of patients.
Tenosynovitis is asymmetric, usually affecting the dorsum of wrists, hands, and ankles. Tenosynovitis of the fingers may result in dactylitis.
Dermatitis occurs in 40-70% of patients and typically involves the extremities. Lesions are usually tiny maculopapular, pustular, or vesicular lesions on an erythematous base. The center of the lesion may become necrotic or hemorrhagic. Despite their appearance, they are painless and nonpruritic. The lesions tend to disappear within a few days after treatment is initiated. Usually, 4-50 lesions are reported. Rarely, the lesions may resemble erythema nodosum or erythema multiforme.
Fever rarely involves a temperature of greater than 39°C.
Other presentations of DGI include the following:
Fitz-Hugh and Curtis syndrome (gonococcal perihepatitis)
Sepsis with Waterhouse-Friderichsen syndrome (rare)
Gonococcal endocarditis (rare in the antibiotic era)
Gonococcal meningitis (very rare in the antibiotic era)
Septic arthritis form
Septic arthritis is characterized by acute arthritis with signs of joint effusion, warmth, tenderness, decreased range of motion, and marked erythema.
Septic arthritis most commonly involves the wrists, hands, knees, elbows, and shoulders. Chronic arthritis with joint destruction is rare with appropriate antibiotic therapy.
Causes

Gonococcal arthritis is caused by infection with the gram-negative diplococcus N gonorrhoeae. The risk of dissemination following mucosal infection depends on both the ability of the patient’s immune system to control the infection and the virulence of the organism. See Mortality/Morbidity.

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