Community-acquired septic arthritis due to methicillin-resistant Staphylococcus aureus

G. Kallarackal, T. M. Lawson and B. D. Williams

Department of Rheumatology, University Hospital of Wales, Heath Park, Cardiff CF14 4XW, UK

SIR, We report a case of septic arthritis due to methicillin-resistant Staphylococcus aureus (MRSA) acquired in the community.

A 75-yr-old retired bank clerk was admitted to the University Hospital of Wales (UHW) with a 2-day history of pain and swelling of the left knee associated with fever and rigors. There was no history of trauma, inflammatory joint disease or diabetes mellitus. His only medical history was ulcerative colitis, which was diagnosed 2 yr earlier and was well controlled by prednisolone 5 mg daily, mesalazine 800 mg three times daily and azathioprine 100 mg daily. He had never previously been admitted to hospital and had been seen last in the gastroenterology outpatient clinic 6 months earlier.

On examination he had a temperature of 37.5°C with a pulse rate of 100/min and blood pressure of 145/90 mmHg. He had a tender, warm, left knee joint with a moderate effusion and restricted active and passive movements. Systemic examination was otherwise normal. Investigations were as follows: haemoglobin 10 g/dl; white cell count 7.1 x 109/l (normal differential count); platelets 384 x 109/l; normal urea, creatinine and electrolytes, and liver function tests; C-reactive protein (CRP) 206 mg/l; erythrocyte sedimentation rate (ESR) 127 mm/h. Turbid fluid (75 ml) was aspirated from the left knee and, although microscopy showed numerous polymorphs, no organisms or crystals were identified. Septic arthritis was suspected clinically and, as the patient was allergic to penicillin, treatment with i.v. teicoplanin (200 mg daily) was commenced and the azathioprine discontinued. After 24 h in culture, Gram-positive cocci were detected in the joint aspirate and were subsequently identified as MRSA. The organism was sensitive to teicoplanin, which was therefore continued. Over the next 5 days the knee effusion did not settle despite daily aspiration and MRSA was consistently identified in the joint fluid culture. Serum levels of teicoplanin were found to be subtherapeutic. As teicoplanin levels are not routinely measured in our hospital, the patient was commenced on i.v. vancomycin (750 mg twice daily) to facilitate drug level monitoring. However, after 4 days of treatment with vancomycin he became leukopenic (white cell count 2.29 x 109, neutrophils 1.53 x 109, lymphocytes 0.35 x 109). The vancomycin was stopped and he was recommenced on high-dose i.v. teicoplanin (800 mg once daily). The knee effusion resolved and intravenous teicoplanin was continued for 4 weeks. The CRP and ESR returned to normal and he regained full mobility of the joint prior to discharge.

Methicillin resistance results from the development of an altered penicillin-binding protein which interferes with the binding of ß-lactam antibiotics [1]. MRSA was first reported in 1961 [2] and the burden of MRSA colonization and infection has increased considerably since then, particularly in hospitals [3]. In addition to the increase in hospital-acquired MRSA infections, MRSA infection in the community in England and Wales has increased substantially since 1993 [4]. In 1997 the Public Health Laboratory in Wales reported that MRSA accounted for 15% of all cases of S. aureus infection in the community, and 70% of these were inpatients who had been admitted to hospital on at least one occasion during the previous year [5]. Between 1995 and 1996, 56 cases of community-acquired S. aureus bacteraemia/septicaemia were admitted to UHW. In 12 (21%) of these cases the organism was MRSA [6]. Although this represents a high incidence of community-acquired MRSA infection, the authors did not identify risk factors such as age, site of residence and previous carrier state.

Coello et al. [7] prospectively studied a cohort of 479 patients who were initially asymptomatic carriers of MRSA and assessed the risk factors for progression to clinical infection. Admission to an intensive care setting, administration of three or more antibiotics, skin ulceration, surgical wounds, nasogastric or endotracheal intubation and urinary or intravenous catheterization were all identified as independent risk factors predisposing to progression to clinical infection.

Data from 1158 cases of septic arthritis reported to the Public Health Laboratory Service Communicable Disease Control Centre from England and Wales between 1989 and 1993 revealed that over a third of the isolates were due to S. aureus but no cases of MRSA septic arthritis were reported [8]. Although community-acquired MRSA septic arthritis has not been reported previously in the UK, cases of MRSA septic arthritis in immunocompromised hospital inpatients have been described [9]. In the USA several cases of community-acquired MRSA septic arthritis have been reported in intravenous drug abusers [10].

The patient described above was not known to be a carrier of MRSA and had never been admitted to hospital previously. Although he was elderly and on immunosuppressive therapy, the development of septic arthritis due to MRSA in the community setting is unusual. The empirical treatment of community-acquired septic arthritis does not generally include antibiotics that cover MRSA. However, the increasing incidence of MRSA infection in the community may soon necessitate the use of glycopeptide antibiotics in cases of septic arthritis until the antibiotic sensitivities of the causative organism are determined.

Notes

Correspondence to: Dr G. Kallarackal. Back

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Accepted 2 May 2000