Nongonococcal Infectious Arthritis

Nongonococcal Infectious Arthritis

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Nongonococcal infectious arthritis is an acute or subacute illness with potentially significant morbidity and mortality. It can be caused by bacteria, mycobacteria, or fungi. Both healthy individuals and individuals with predisposing conditions can be infected. [1] Nongonococcal infectious arthritis is typically a monoarticular disease, but in approximately 10% of patients, it affects multiple joints. [2, 3]  Without treatment, the condition results in joint destruction.

For patient education resources, see the Arthritis Center and the Infections Center, as well as Knee Pain.

Infectious arthritis ensues when foreign organisms invade the synovium or joint space. These organisms invade the joint via the following 3 pathways:

Hematogenous dissemination from a distant site

Periarticular infection, such as osteomyelitis or adjacent soft-tissue infection

Direct introduction through penetrating trauma or procedural intervention, such as arthrocentesis or surgical repair

Bacteria

Gram-positive cocci, especially Staphylococcus aureus, are the predominant etiologic agents. Streptococcal species are also common, especially group A streptococci. [4] If a prosthetic joint was implanted within the preceding 6 months, S epidermidis and S aureus are major pathogens.

The Gram-negative coccobacillus Kingella kingae has emerged as a prime etiology of septic arthritis and osteomyelitis in children aged 6-48 months. [5, 6]  Kingella kingae is unlikely to be a novel human pathogen; rather, its increased recognition appears to be the result of improved methods of detection. [5]

Gram-negative bacilli are also more common in elderly patients with chronic medical conditions. Pseudomonas aeruginosa and methicillin-resistant S aureus (MRSA) are more prevalent in the infectious arthritis that affects individuals who abuse intravenous (IV) drugs. Salmonella species exhibit a predilection for individuals with systemic lupus erythematosus.

Pasteurella multocida should be considered after a cat bite, Eikenella corrodens after a human bite. In endemic areas, Brucella species can be a cause of monoarticular arthritis. [7]

Dubost and colleagues examined changes in the distribution and antibiotic susceptibility profiles of organisms responsible for septic arthritis in a single-center retrospective study of 374 patients treated between 1979 and 2008 at a French hospital. Over the three decades studied, no significant time trends in the proportions of staphylococci (67%, 65%, and 64%), streptococci (14%, 21%, and 17%), or Gram-negative rods (7%, 10%, and 14%) were detected. Tuberculosis was significantly more common between 1979 and 1988 (10%, 4%, and 2% over the three decades studied). There were no significant changes in the proportions of methicillin-resistant staphylococci over time (13%, 11%, 15%). [8]

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, may cause infectious arthritis 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.

The presence of a preexisting, chronic, inflammatory, destructive arthritis, especially rheumatoid arthritis, is correlated with infectious arthritis. The introduction of anti–tumor necrosis factor (TNF) agents into the treatment of inflammatory arthritis may further 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 at particular risk for infectious arthritis. Comorbid nonarticular conditions, such as diabetes mellitus, immunodeficiency diseases, cancer, or IV drug abuse, also increase the risk of infectious arthritis.

The yearly incidence of bacterial arthritis ranges from 2-5 cases per 100,000 persons in the general population to 28-38 cases per 100,000 persons in patients with rheumatoid arthritis (RA). [2]

Age older than 80 years has been shown in some studies to be an independent risk factor for susceptibility to bacterial arthritis. Sex is not an independent risk factor for infectious arthritis. No inherent racial predilections for infectious arthritis are recognized.

Nongonococcal infectious arthritis carries a mortality of 11%. [9] Irreversible loss of joint function may result if the condition is not treated immediately and for an appropriate duration. Joint destruction occurs in 25%-50% of cases. [10] Morbidity and mortality are higher in elderly individuals and individuals with preexisting medical conditions.

Wang DA, Tambyah PA. Septic arthritis in immunocompetent and immunosuppressed hosts. Best Pract Res Clin Rheumatol. 2015 Apr. 29 (2):275-89. [Medline].

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

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

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

Yagupsky P. Diagnosing Kingella kingae infections in infants and young children. Expert Rev Anti Infect Ther. 2017 Oct. 15 (10):925-934. [Medline].

Hernández-Rupérez MB, Suárez-Arrabal MDC, Villa-García Á, et al. Kingella kingae as the Main Cause of Septic Arthritis: Importance of Molecular Diagnosis. Pediatr Infect Dis J. 2018 Mar 31. [Medline].

Bosilkovski M, Zezoski M, Siskova D, Miskova S, Kotevska V, Labacevski N. Clinical characteristics of human brucellosis in patients with various monoarticular involvements. Clin Rheumatol. 2016 Feb 9. [Medline].

Dubost JJ, Couderc M, Tatar Z, Tournadre A, Lopez J, Mathieu S, et al. Three-decade trends in the distribution of organisms causing septic arthritis in native joints: Single-center study of 374 cases. Joint Bone Spine. 2014 Oct. 81(5):438-40. [Medline].

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

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

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

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].

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

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

Edward Dwyer, MD Associate Professor of Medicine, Columbia University Medical Center

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

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.

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.

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

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.

Nongonococcal Infectious Arthritis

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