Septic Arthritis
The United States sees roughly 20,000 cases of septic arthritis each year.1 It’s a serious illness in native joints that can lead to cartilage damage, reduced mobility, and even death. Timely diagnosis and prompt treatment are key to minimizing joint damage. However, diagnosing septic arthritis can be challenging and time consuming, often leaving physicians to make treatment decisions without knowing the cause of the infection.
What is septic arthritis?
Also known as infectious arthritis, septic arthritis is an infection in a native joint—usually a large joint like the knee, hip, or shoulder.1 The septic joint infection is often the result of pathogens that travel through the bloodstream from another part of the body. Septic arthritis can also be a result of an infection in a penetrating injury, open wound, or a surgical procedure. Older adults, those with compromised immune systems, infants, and people with artificial joints are most likely to develop septic arthritis.
Septic arthritis can be very painful. Symptoms, which usually develop rapidly, include pain and swelling in the joint. Other symptoms include fever, chills, fatigue, and warmth at the site of infection. Sometimes the pain and swelling are so severe that the joint becomes immobile.
Septic arthritis can be serious.
Septic arthritis can very quickly begin damaging joint cartilage and bone—cartilage destruction can start quickly.2 This destruction can be irreversible, with up to 32% of septic arthritis patients experiencing long-term decreased mobility.3
In most cases, septic arthritis requires hospitalization.3 And even with antibiotic therapy, the mortality rate for in-hospital septic arthritis ranges from 7% to 15%.6
Challenges in diagnosing septic arthritis.
Because septic arthritis can quickly lead to permanent cartilage damage and even death, rapid and appropriate therapy is essential. However, diagnosing septic arthritis isn’t necessarily straightforward because the symptoms are similar to those of other joint diseases like rheumatoid arthritis, osteoarthritis, and gout.3
In order to test for the presence of pathogens, a sample of joint fluid is extracted with a needle in a procedure called arthrocentesis. This fluid, called synovial fluid, acts as a lubricant within a joint. A lab will try to culture pathogens from the sample to help pinpoint what is causing the infection. This usually takes 48–72 hours, but sometimes even longer depending on the pathogen.
Because it can take so long to get culture results—and joint damage can occur rapidly—clinicians generally prescribe broad-spectrum antibiotics while awaiting lab results. Unfortunately, overuse of antibiotics exacerbates the problem of antimicrobial resistance and may cause unpleasant side effects for patients.
Changing the game with the syndromic approach.
Newly granted an FDA De Novo authorization, the BIOFIRE® Joint Infection (JI) Panel takes a syndromic testing approach to joint infection diagnostics. Instead of lengthy and laborious—and often inconclusive—send-out serial testing, the BIOFIRE JI Panel identifies 39 clinically relevant targets, including 31 causative pathogens and 8 antimicrobial resistance markers. The test requires only 0.2 mL of synovial fluid and returns results in about an hour.
The BIOFIRE JI Panel uses multiplex PCR technology to identify pathogens and antimicrobial resistance genes at the molecular level. The BIOFIRE JI Panel can detect difficult-to-grow anaerobes and fastidious pathogens. Compared to traditional testing, it may help facilitate increased diagnostic yield and improved polymicrobial detection.7
Fast, accurate, and comprehensive testing with the BIOFIRE JI Panel may offer several benefits. For example, it may help determine whether the joint is infected and may help reduce time to effective therapy by identifying pathogens faster.
References
- Brusch J. Medscape. Accessed on Apr. 19, 2021. Retrieved from: https://emedicine.medscape.com/article/236299-overview#:~:text=Approximately%2020%2C000%20cases%20of%20septic,cases%20per%20100%2C000%20person%2Dyears.
- Smith R.L, et al. J Bone Jt Surg. 1987; 69(7):1063-8
- Costales C and Buter-Wu S. Journal of Clinical Microbiology. Jan 2018, 56 (2) e01358-17.
- Peter W, et al. J PediatrOrthop. 1992;12 (6):806–810.
- Aronson J, et al. Z Kinderheilk1992;12(1):38–44.
- Margaretten ME, et al. 2007 Apr 04;297(13):1478-88.
- Graue C, et al. ID Week 2020. Poster 322.
