Nongonococcal Infectious Arthritis Clinical Presentation

  • Author: Edward Dwyer, MD; Chief Editor: Herbert S Diamond, MD   more...
 
Updated: Jan 19, 2012
 

History

  • The clinical course of bacterial arthritis is typically acute in onset.
    • Patients with joint prostheses are the exception. These patients' symptoms may persist for weeks or months before a diagnosis is made.
    • Individuals with mycobacterial or fungal arthritis also tend to have a much more indolent or subacute prodrome before the diagnosis is considered.
    • The sternoclavicular and sacroiliac joints are preferentially involved in patients who use illicit parenteral drugs.
  • Joint pain, swelling, erythema, and loss of motion are common presenting symptoms.
    • The most commonly affected joint in persons with bacterial arthritis is the knee.
    • The shoulder, hip, elbow, and wrist joints are infected less frequently.
  • Approximately 10% of individuals with bacterial arthritis have infection in multiple joints, particularly in the presence of a preexisting destructive joint disease (eg, rheumatoid arthritis) or compromising medical conditions (eg, diabetes, those that require glucocorticoid therapy).[5]
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Physical

  • During the first 24 hours of hospitalization, 78% of patients with nongonococcal bacterial arthritis exhibit fever; however, the fever rarely exceeds 39°C (102.2°F).[1]
  • The patient may have decreased range of motion in the joint.
  • Swelling, tenderness to palpation, erythema, warmth to touch, and pain upon movement of the affected joint are common physical examination findings.
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Causes

  • Risk factors
    • The presence of a preexisting, chronic, inflammatory, destructive arthritis, especially rheumatoid arthritis, is correlated with infectious arthritis. The recent introduction of anti–tumor necrosis factor (TNF) agents in the treatment of inflammatory arthritis may additionally predispose this population to infectious arthritis.
    • A person undergoing immunosuppressive therapy, such as with corticosteroids or cytotoxic agents, is more likely to become infected.
    • A person who has a prosthetic joint has greater risk of infection.
    • Elderly individuals are particularly at risk for infectious arthritis.
    • Comorbid nonarticular conditions, such as diabetes mellitus, immunodeficiency diseases, cancer, or intravenous drug abuse, also increase the risk of infectious arthritis.
  • Bacteria
    • Gram-positive cocci, especially Staphylococcus aureus, are the predominant etiologic agents. Streptococcal species are also common, especially group A streptococci.[6]
    • If a prosthetic joint was implanted within the preceding 6 months, Staphylococcus epidermidis and S aureus are major pathogens.
    • Gram-negative bacilli are more common in elderly patients with chronic medical conditions.
    • Pseudomonas aeruginosa and methicillin-resistant S aureus are more prevalent in the infectious arthritis that affects individuals who abuse intravenous drugs.
    • Salmonella species exhibit a predilection for individuals with systemic lupus erythematosus.
    • Consider Pasteurella multocida subsequent to a cat bite or Eikenella corrodens after a human bite.
  • Mycobacteria
    • In addition to the common pathogen Mycobacterium tuberculosis, nontuberculous species, such as Mycobacterium kansasii, may spread from a pulmonary focus and infect a joint.
    • Mycobacterium marinum should be considered in individuals exposed to aquatic or marine environments.
  • Fungi
    • Candida organisms, including Candida albicans and Candida parapsilosis, are causative in debilitated hospitalized patients or in patients on long-term antibacterial therapy.
    • Sporothrix schenckii may infect the hand or wrist joints of a person frequently exposed to moist soil, rose thorns, or the outdoors.
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Contributor Information and Disclosures
Author

Edward Dwyer, MD  Assistant Professor, Department of Medicine, Columbia University College of Physicians and Surgeons

Edward Dwyer, MD is a member of the following medical societies: Alpha Omega Alpha and American College of Rheumatology

Disclosure: Nothing to disclose.

Specialty Editor Board

Robert E Wolf, MD, PhD  Professor Emeritus, Department of Medicine, Louisiana State University School of Medicine in Shreveport; Chief, Rheumatology Section, Medical Service, Overton Brooks Veterans Affairs Medical Center

Robert E Wolf, MD, PhD is a member of the following medical societies: American College of Rheumatology, Arthritis Foundation, and Society for Leukocyte Biology

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

Elliot Goldberg, MD  Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University School of Medicine

Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and American College of Rheumatology

Disclosure: Nothing to disclose.

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

References

  1. Smith JW, Chalupa P, Shabaz Hasan M. Infectious arthritis: clinical features, laboratory findings and treatment. Clin Microbiol Infect. Apr 2006;12(4):309-14. [Medline].

  2. García-De La Torre I, Nava-Zavala A. Gonococcal and nongonococcal arthritis. Rheum Dis Clin North Am. Feb 2009;35(1):63-73. [Medline].

  3. Gupta MN, Sturrock RD, Field M. A prospective 2-year study of 75 patients with adult-onset septic arthritis. Rheumatology (Oxford). Jan 2001;40(1):24-30. [Medline].

  4. Kaandorp CJ, Krijnen P, Moens HJ, Habbema JD, van Schaardenburg D. The outcome of bacterial arthritis: a prospective community-based study. Arthritis Rheum. May 1997;40(5):884-92. [Medline].

  5. Goldenberg DL, Reed JI. Bacterial arthritis. N Engl J Med. Mar 21 1985;312(12):764-71. [Medline].

  6. Shirtliff ME, Mader JT. Acute septic arthritis. Clin Microbiol Rev. Oct 2002;15(4):527-44. [Medline].

  7. von Essen R. Culture of joint specimens in bacterial arthritis. Impact of blood culture bottle utilization. Scand J Rheumatol. 1997;26(4):293-300. [Medline].

  8. Chambers HF. Community-associated MRSA--resistance and virulence converge. N Engl J Med. Apr 7 2005;352(14):1485-7. [Medline].

  9. Harrington JT. Mycobacterial and fungal arthritis. Curr Opin Rheumatol. Jul 1998;10(4):335-8. [Medline].

  10. [Best Evidence] Mathews CJ, Kingsley G, Field M, Jones A, Weston VC, Phillips M, et al. Management of septic arthritis: a systematic review. Ann Rheum Dis. Apr 2007;66(4):440-5. [Medline].

 
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