A man with fever and joint pain

A Norwegian man in his sixties was admitted to the Department of Medicine owing to severe pain in the right ankle. The pain was accompanied by intermittent fever above 39 °C. Apart from hospitalisation for malaria in 2011, he had otherwise been mostly in good health. The patient took Albyl-E 75 mg 1 × 1 as primary prophylaxis against heart disease. He had returned to Norway five days earlier from a stay abroad. During the journey and for two weeks prior to admission, he had noticed transient nasal congestion and a sore throat. Upon admission he had increasing pain in the right ankle. He had sprained the ankle a month earlier, but there was no major trauma in his case history. He also reported general pain in the shoulders, back and left hip. Upon arrival at the hospital, the patient had a high fever with temperature 39 °C, normal blood pressure (119/65), and a steady pulse of 86. Auscultation of the heart and lungs was normal. He had diffuse rubor on both the medial and the lateral side of the right ankle, as well as warmth and a petechial rash over the ankle joint (Fig. 1).

Blood tests on admission revealed CRP 248 (< 5 mg/l), leukocytes 21.5 (3.5 – 11.0 × 10⁹/l) with neutrophil granulocytes 19.4 (1.7 – 8.2 × 10⁹/l), thrombocytes 186 (145 – 348 × 10⁹/l), INR 1.3 (< 1.1), sedimentation rate 15 ((1) – 20), creatinine 92 (60 – 105), bilirubin 26 (< 19), LD 244 (105 – 205) and CK 79 (40 – 280).

The orthopaedic surgeon was consulted in the emergency ward. By this stage the blood test results were also available. Diagnostic puncture of the ankle joint was indicated, but not X-ray examination of the ankle. A total of 2 – 3 ml of opaque synovial fluid was drained from the right ankle around midnight on the day of admission, but drainage of all of the synovial fluid was not possible due to pain. The synovial fluid was sent for cultivation and microscopy, but not for cell counting.

The following morning, the patient was still febrile and his CRP level had risen to 317. The preliminary results from the Department of Microbiology arrived at about the same time: synovial fluid microscopy showed gram negative cocci in pairs and abundant leukocytes. The microbes could be seen intracellularly (Fig. 2).

Samples were taken from the urethra and tonsillar region to test for gonococci and chlamydia, in addition to serology to test for syphilis, HIV and hepatitis viruses. It eventually came to light from the case history that the patient had had unprotected sex in countries outside Europe on a couple of occasions in the past year.

Two days after admission, the ankle was swollen and red but with a good range of movement. We punctured the ankle again and aspirated 1 ml of clear fluid. Two days later, we repeated the puncture and aspirated 3 ml of purulent fluid. A total of 5 ml of straw-coloured fluid was also aspirated from the patient’s right knee because of increased swelling. The final microbiology results now revealed growth of Neisseria gonorrhoeae from the synovial fluid aspirated from the right ankle upon admission, on both blood agar and chocolate agar. The microbe was catalase-positive and showed agglutination in serogroup WI. The identity of the bacteria was confirmed using both the Vitek II system and MaldiTof (bioMérieux) mass spectrometry technology. The microbe was resistant to penicillin G, ampicillin and ciprofloxacin, but sensitive to ceftriaxone, azithromycin and spectinomycin.

After ten days of antibiotic treatment, the patient was still experiencing fever and pain, and CRP remained elevated at 145. We therefore chose to administer prednisolone, initially 40 mg 1 × 1 for four days, followed by gradual tapering over three weeks. Two days after initiation of prednisolone, the patient became afebrile and his CRP level decreased rapidly. Seven days later, the patient was discharged with oral azithromycin, and prednisolone in decreasing doses. His CRP level was at that point 6. He was told that he could use the ankle to pain threshold and received instructions from a physiotherapist regarding exercises.

Secretions from the urethra and throat tested negative for gonococci, and blood cultures were negative. A urine sample tested negative for Chlamydia trachomatis DNA, and serological tests for syphilis (Treponema pallidum-specific antibody) and HIV antigen/antibody were also negative. The patient was monitored weekly in the outpatient clinic. The swelling gradually improved, CRP remained normal and the patient reported less pain. Prednisolone and antibiotics were discontinued after 3 and 4.5 weeks of treatment respectively (18 days intravenous ceftriaxone, azithromycin × 3/week for 2.5 weeks).

After discontinuation of treatment, the patient experienced increasing oedema and pain in the right knee, accompanied by an increase in his CRP level to 43. He was readmitted, and 15 ml of yellowish fluid was aspirated from the knee joint. This was analysed with cell counting (leukocytes 5.7 × 10⁹/l), but microscopy and cultures were negative. The rheumatologist injected 2 ml of Lederspan (a corticosteroid preparation) as we now considered the patient to have post-infectious reactive arthritis. At a check-up one week later, his CRP level had fallen to 1. The CRP level subsequently increased slightly to 17, and he was treated with diclofenac 50 mg 1 × 3 for one week. At the final check-up, his CRP level was < 1, SR level was 2, and he had mild oedema in the knee, but no pain.