শনিবার, ১৮ ডিসেম্বর, ২০১০

Gonococcal arthritis


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.

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
  • Female sex
  • Pregnancy
  • Menses
  • Systemic lupus erythematosus
  • Complement deficiency
  • Low socioeconomic or educational status
  • Intravenous drug use
  • HIV infection
  • Multiple sexual partners
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)

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

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.1

  • Bacteremic form (arthritis-dermatitis syndrome)6
    • Symptoms are typically 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. Diffuse involvement of fingers can result in dactylitis.1
    • 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 form6
    • Joint symptoms begin within days to weeks of gonococcal infection.
    • Patients may experience pain, redness, and swelling in usually one or sometimes multiple joints, most commonly the knees, wrists, ankles, and elbows.1

Physical

  • Bacteremic form (classic triad of migratory polyarthritis, tenosynovitis, and dermatitis)6
    • 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, which now occur in only 1%-3% of cases:1
      • Fitz-Hugh-Curtis syndrome (gonococcal perihepatitis)
      • Sepsis with Waterhouse-Friderichsen syndrome
      • Gonococcal endocarditis (rare in the antibiotic era)
      • Gonococcal meningitis (very rare in the antibiotic era)
  • Septic arthritis form6
    • 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, and elbows. 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 Pathophysiology.

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