Septic arthritis may occur as a consequence of hematogenous seeding of the synovium in the setting of bacteremia or by direct extension from trauma, osteomyelitis, or placement of a contaminated joint prosthesis (which can harbor a biofilm of organisms). Early or delayed prosthetic joint infection (up to 24 months after surgery) results from the placement of a contaminated appliance (intraoperative risk 1% to 2%); late infection
is usually due to hematogenous seeding from dental work, skin infection, pneumonia, or urinary tract infection.

Clinically, acute septic arthritis is characterized by joint pain, effusion, erythema, warmth, and fever. Delayed prosthetic joint infection may have a more subtle presentation, characterized by persistent joint pain and signs of implant loosening without obvious manifestations of inflammation.

Among previously healthy, sexually active patients, disseminated gonorrhea is the most frequent cause of joint infection. Women account for two thirds of cases. Pregnancy and menstruation appear to increase the risk for dissemination, which occurs in about 1% to 3% of persons with gonorrhea (see Chapter 137). An initial bacteremic stage is characterized by fever, polyarthralgias, transient scattered tendonitis, minimal joint effusion, necrotic skin lesions, blood cultures positive for organisms, and sterile joint fluid. This phase of the illness may be followed in several days by a septic joint stage, with monoarticular or occasionally polyarticular pain, marked joint swelling, and effusion. During the septic joint stage, gonococci can be recovered from the joint in about 50% of patients.

More than 80% of cases are monoarticular, with gram-positive organisms, especially Staphylococcus aureus, predominating (60% of infectious cases, most of them methicillin resistant). Streptococcus species account for about 18%. Gram-negative Enterobacteriaceae also cause septic arthritis, particularly in intravenous drug abusers, immunocompromised persons, and the chronically ill. Joint sepsis is more likely in patients with altered host defenses (diabetes, cirrhosis, immunodeficiency), previously damaged joints (rheumatoid arthritis), or prosthetic joints. Fever, chills, and joint inflammation are usually prominent, but the presentation may be devoid of systemic symptoms, especially if the patient is debilitated or immunosuppressed. A larger joint, such as a knee or a hip, is most likely to be involved. Sternoclavicular joint infection is characteristic of intravenous drug abusers. Articular destruction can be rapid. Within 10 days of nongonococcal infection, radiographic evidence of cartilaginous and bony damage may appear. Joint injury from gonococcal arthritis is less precipitous, so that more time is available for treatment. Permanent damage is uncommon in patients who are treated.

An acute oligoarthritis can develop months after the initial infection in untreated persons, with about 60% experiencing the problem (see Chapter 160). Large joints are typically involved, especially the knees. Intermittent attacks of acute arthritis lasting weeks to months are sometimes seen, as is chronic erosive arthritis. Swelling may be more prominent than pain.

HIV-infected patients are at increased risk for mycobacterial joint infection, as are persons who have had repeated glucocorticoid injections into a joint. Often, periarticular bony disease develops in addition to joint inflammation. A chronic picture remains more common than acute inflammation.

An acute monoarticular or oligoarticular arthritis may be part of a syndrome accompanying the onset of HIV infection. The lower extremities are the usual site of involvement (see Chapter 13).

Gout is a common cause of acute monoarticular arthritis. Sodium urate crystals in the synovium incite a brisk inflammatory response after they are ingested by polymorphonuclear leukocytes. The condition is found most commonly among middle-aged and older men. Onset is rapid, peaking within 12 to 24 hours. The metatarsophalangeal joint of the great toe is the classic site, but the midfoot, ankles, knees, wrists, and olecranon bursae are other important locations. Sodium urate crystals are found in the joint fluid. They are needlelike and negatively birefringent under the polarizing microscope. Although the likelihood of a gouty attack increases with serum uric acid levels, uric acid levels are not diagnostically helpful unless they are extremely high. Alcoholic binges or the new use of thiazide diuretics may precipitate gouty attacks. A mild fever may even be present. Rapid response to colchicine or nonsteroidal anti-inflammatory drugs (NSAIDs) helps to differentiate crystal-induced arthritis from infection (see Chapter 158).

Pseudogout results when crystals of calcium pyrophosphate induce joint inflammation, and it resembles gout pathophysiologically, although the clinical features differ. Knees and wrists are the most commonly affected sites. Under the polarizing microscope, weakly positively birefringent rhomboid forms of calcium pyrophosphate are revealed in the synovial fluid. Chondrocalcinosis is usually present on radiography. Pseudogout tends to occur in older patients and seems to be associated with hyperparathyroidism, hemochromatosis, and severe degenerative joint disease.

Immunologically mediated conditions typically cause polyarthritis but may present initially as a monoarthritis. These include rheumatoid arthritis, Reiter syndrome, ankylosing spondylitis, psoriatic arthritis, the arthritis of inflammatory bowel disease, and the arthritis of sarcoidosis (see Chapter 146).