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Septic Arthritis

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  • Septic Arthritis

    Septic Arthritis is also known as infectious arthritis, bacterial, or fungal arthritis. It is the purulent invasion of a joint by an infectious agent which produces arthritis. The condition is an inflammation of a joint that's caused by infection. Typically, septic arthritis affects one large joint in the body, such as the knee or hip. Less frequently, septic arthritis can affect multiple joints. Septic arthritis is considered a medical emergency. If untreated, it may destroy the joint in a period of days. The infection may also spread to other parts of the body.

  • Septic Arthritis

    Pathophysiology: The major consequence of bacterial invasion is damage to articular cartilage. This may be due to the particular organism's pathologic properties, such as the chondrocyte proteases of S aureus, as well as to the host's polymorphonuclear leukocytes response. The cells stimulate synthesis of cytokines and other inflammatory products, resulting in the hydrolysis of essential collagen and proteoglycans. Infection with N gonorrhoeae induces a relatively mild influx of white blood cells (WBCs) into the joint, explaining, in part, the minimal joint destruction observed with infection with this organism relative to destruction associated with S aureus infection.

  • Septic Arthritis

    Statistics: A 19-year-old first-year college student attended the accident and emergency department after three days of pain in the left knee. There was no history of joint trauma, headache or photophobia and she was not sexually active. There had been no recent febrile illness in her family or flatmates. On examination her temperature was 38 °C and she had an erythematous rash on the extensor surfaces of her legs. The left knee was tender and swollen with a moderate effusion and reduced range of motion. The peripheral blood white cell count was 15.8×109/μL and C-reactive protein was 27 mg/L. About 75 mL of purulent fluid was aspirated from her left knee. Treatment was started with intravenous flucloxacillin and benzylpenicillin and an arthroscopic knee washout was performed. She responded well clinically and was afebrile within 24 hours.
    Microscopic examination of the Gram-stained smear revealed numerous polymorphonuclear neutrophils with intracellular Gram-negative diplococci. Blood culture and knee aspirate taken before antibiotic therapy were sterile. Infection with Neisseria meningitidis serogroup C was established by polymerase chain reaction performed on the knee aspirate by the National Meningococcal Reference Laboratory.
    Intravenous benzylpenicillin was continued for two weeks and the patient received oral rifampicin 600 mg twice daily for two days to clear any potential nasal carriage. Close college contacts were given rifampicin and immunized against N. meningitidis serogroup C.

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