We are talking native joints here. See PJI for prosthetic joints. Tap the joint. And do not forget to look for crystals. Gout and pseudo-gout can fool you; at least they can fool me. About 1.5% of the time infection will coexist with crystal disease, the hint is a WBC more than 50,000 in the joint (PubMed).
Bacteremia or direct extension. Bacteria like to go to joints with the most prior trauma; knees (and ex-jocks) therefore predominate; the organisms from percutaneous injury can be variable, be sure to include fungal and AFB cultures.
And the occasional case that occurs after a therapeutic injection; it is like as not due to breakdown in infection control practice (PubMed).
And acupuncture; increasing number of reported cases; I guess they do not know how deep to put the damn needle (PubMed). And aseptic technique, like reality based medicine, is not an acupuncturists strong point (PubMed).
Any organism can involve a joint. Common causes include
Immune complex: Acute Hepatitis B where every single joint can become inflamed from immune complex deposition. Also acute Tuberculosis can lead to an inflammatory reactive arthritis called Poncets (PubMed). Acute Rheumatic Fever, post streptococcal arthritis, post Campylobacter and post C. difficile reactive arthritis (PubMed) probably falls in this category.
Parvovirus B19: adults can get a polyarticular small joint arthritis. Usually have an exposure to a child with parvovirus. Treatment is supportive.
Chikungunya virus, found in Africa, the Indian Ocean and now Europe and the Caribbean can cause severe polyarthritis that can persist for months.
Lyme. Usually a monoarticular arthritis.
Neisseria gonorrhoeae: acute, usually mono-articular, arthritis that follows a migratory tenosynovitis. Patients are sexually active and can grow the organisms out of the usual important orifices: cervical = urethral > rectal > oral. Remember:all three.
Streptococci: Group B tends to occur in diabetics, Pneumococcus and Group A streptococci love to go to joints as well.
Staphylococcus aureus: the most common organism in community acquired septic arthritis.
Coagulase negative staphylococcus: post operative, especially prosthetic joints.
Pseudomonas aeruginosa: IVDA, one of few who get sternoclavicular joint infections. Rheumatoid arthritis and IVDA are the main risks for getting the SC infected.
Debridement, either with daily percutaneous taps or take them to OR for arthroscopic debridement (probably preferred), but you gotta wash it out. Even the SI joint (PubMed). Cefazolin or vancomycin is typical pending cultures and no history to suggest an unusual organism.
Normal joints are treated for two weeks iv for streptococcal infections and three weeks iv if infected with staphylococcus aureus or gram negative rods.
And how long to treat as native joint septic arthritis? I was taught 2 weeks IV for streptococci and 3 weeks iv for S. aureus and gram negative rods. Up to Date says 2 weeks iv then two week po. There is no data whatsoever I can find to support that. Given all the data in other infections to suggest a week at most is sufficient if there is good source control, I suspect that long courses of iv are steer manure. Three studies suggest a week of IV then po is more than fine. It all depends on the host, the bug, chronicity of infections and the adequacy of source control (PubMed)(PubMed)(PubMed). I suspect that low risk patients need IV for a couple of days after washout then home on po for a total of 14 days.
Here is a curious study (although they do caution that "due to study limitations, the data cannot be used directly for antibiotic therapy recommendations for septic arthritis" (PubMed):
"A total of 169 episodes of septic arthritis in 157 adult patients (median age 63 years; 65 females) were included. In 21 episodes (21/169, 12%), arthritis recurred after the end of antibiotic treatment. Multivariate analysis showed that Gram-negative infection (odds ratio (OR) 5.9, 95% confidence interval (CI) 1.4-25.3), immune suppression (OR 5.3, 95% CI 1.3-22.0), and lack of surgical intervention were associated with recurrence. The size of the infected joint, the number of surgical drainages (OR 1.3, 95% CI 1.0-1.7), arthrotomy vs. arthroscopic drainage (OR 0.5, 95% CI 0.2-1.8), duration of antibiotic therapy (OR 1.0, 95% CI 0.95-1.05), and duration of intravenous antibiotic therapy (OR 1.0, 95% CI 1.0-1.0) were not. Seven days of intravenous therapy had the same success rate as 8-21 days (OR 0.4, 95% CI 0.1-1.7) and >21 days (OR 1.1, 95% CI 0.4-3.1). Fourteen days or less of total antibiotic treatment had the same outcome as 15-28 days (OR 0.4, 95% CI 0.1-2.3) or >28 days (OR 0.4, 95% CI 0.1-1.6)."
Small joint infections of the hands and wrist can, after debridement, be treated with 14 days, much of it with oral, with excellent results PubMed
Antibiotic impregnated spacers do increase cure rates (PubMed).
And steroids? In children dexamethasone leads to more rapid improvement (PubMed). Should we do the same for adults? Probably, but for me giving steroids for infection is the definition of an un-natural act.
Is the joint infected? Or the bursa? Or is in cellulitis? Best way to find out is to put pressure across the joint. When the joint is infected the patient will scream and try to hit you. Infected joints cannot be moved.
Should you give prophylactic antibiotics with dental work to prevent joint infections? People do based on no data. The two studies I have found had no benefit (Prosthetic Joint Infection (PJI) Due to Dental Procedures" ICAAC-IDSA 2008; Abstract K-551). There is a study (PubMed), and I quote, "Dental procedures were not risk factors for subsequent total hip or knee infection. The use of antibiotic prophylaxis prior to dental procedures did not decrease the risk of subsequent total hip or knee infection." Ha!
Relevant links to my Medscape blog
Last Update: 05/08/18.