Case Presentation: A 49-year-old Caucasian male presented with a two-week history of progressive asymmetrical arthralgias. He denied trauma, fevers or rashes. He endorsed night sweats. Symptoms progressed such that he was unable to walk due to pain. Exam revealed normal vital signs, pain and effusions over bilateral ankles and tenosynovitis in bilateral wrists. Chemistry and liver function tests were normal. Complete blood count was notable for leukocytosis to 18 K/uL. Antinuclear antibody, rheumatoid factor and cyclic citrullinated peptide antibody were negative. Uric acid was normal. Erythrocyte sedimentation rate and C-reactive protein were elevated to 79 mm/hr (normal <15 mm/hr) and 295 mg/L (normal <10 mg/L), respectively.  Urine gonorrhea and chlamydia amplification tests were negative. RPR, HIV, lyme, rickettsia, parvovirus B19, histoplasma antibodies were also negative. Hepatitis panel was positive for acute hepatitis B infection with positive hepatitis B surface antigen, core IgM, BE antigen, and hepatitis B DNA over 230 million copies. Hepatology was consulted and deferred treatment for hepatitis B due to patient’s normal liver function and high rates of spontaneous recovery. The patient was nearing discharge when he developed new right knee pain and effusion. He underwent bedside arthrocentesis on hospital day 7, which revealed 58 K/uL WBC with 94% polymorphonuclear leukocytes, and no crystals. With concern for septic arthritis, orthopedics was consulted and performed emergent irrigation and debridement. Culture grew Neisseria gonorrhea. The patient later revealed that he had been sexually active with an intravenous drug user about four months prior to presentation. He was treated with one dose of azithromycin and two weeks of IV ceftriaxone with improvement in his oligoarthritis.

Discussion: There is a very wide differential for patients presenting with acute oligoarthritis, including many rheumatologic and infectious diseases. This patient was found to have both acute hepatitis B and disseminated gonococcal infection (DGI). Hepatitis B associated arthritis is usually a symmetric polyarthritis that most commonly affects the proximal interphalangeal joints, knees, and ankles. It can have an additive or migratory pattern and is self-limited. It usually develops during the pre-icteric phase of acute hepatitis B. The polyarthritis in DGI is usually asymmetric and can develop a purulent arthritis usually in the knees, wrists, or ankles. Tenosynovitis is a unique finding in gonococcal arthritis and unusual in other infectious arthritis. Risk factors include systemic lupus erythematosus, recent menstruation/pregnancy, and complement deficiency. Individuals with recurrent Neisserial infections should be screened for complement deficiency. Infection likely has an immune component as many times cultures are negative.

Conclusions: This case highlights the broad differential and workup of a patient with acute oligoarthritis and the importance of avoiding premature closure and anchoring bias. This patient was found to have acute hepatitis B infection, and because the initial urine amplification test for gonorrhea was negative, the hepatitis was thought to be the cause of the patient’s symptoms, despite overall clinical picture being more consistent with DGI. Fortunately, he was still hospitalized when his knee developed septic arthritis and the causative organism was found and he was treated appropriately.