Enterococcal joint prosthesis infection

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HD, Shadomy HJ, eds. Manual of clinical microbiology. Washington: American Society for Microbiology 1991: 659-73. 3. Denning DW, Follansbee SE, Scolaro M , Norris S, Edelstein H , Stevens DA. Pulmonary aspergillosis in the acquired immunodeficiency syndrome. N Engl J Med 1991; 324: 654-62. 4 Miller W T Jr, Sais GJ, Frank I, Gefter WB, Aronchick JM, Mder WT. Pulmonary aspergillosis in patients with AIDS: clinical and radiographic correlations. Chest 1994; 105: 37-44. 5 Wallace M R , Kanak RJ, Newton JA, Kennedy CA. Invasive aspergillosis in patients with AIDS. Clin Infect Dis 1994; 19: 222. 6 Staples CA, Kang E-Y, Wright JL, Phihps P, Muller NL. Invasive pulmonary aspergillosis in AIDS: radiographic, CT, and pathologic findings. Radiology 1995; 196: 409-14. 7 Kennedy MJ, Sigler L. Aspergillus, Fusarium, and other opportunistic moniliaceous hngi. In Murray PK, Baron EJ, Pfaller MA, Tenover FC, Yolken RH, eds. Manual of clinical microbiology, 6th edn. Washington, DC: American Society for Microbiology Press, 1995: 765-90. 8. Piehl M R , Kaplan RL, Haber MH. Disseminated penicdliosis in a patient with acquired immunodeficiency syndrome. Arch Pathol Lab Med 1988; 112: 1262-4. 9. Alvarez S. Systemic infection caused by Penicillium decuinbens in a patient with acquired immunodeficiency syndrome. J Infect Dis 1990; 162: 283. 10. Tsang DNC, Li PCK, Tsui MS, Lau YT, Ma KF, Yeoh EK. Penicillium marfie&: another pathogen to consider in patients infected with human immunodeficiency virus. Rev Infect Dis 1991; 13: 766-7. 11. Supparatpinyo K, Chiewchanvit S, Hirunsri P, Uthammachai C, Nelson KE, Sirisanthana T. Prnicillium marneffpi infection in patients infected with human immunodeficiency virus. Clin Infect Dis 1992;14: 871-4. 12. Jones PD, See J. Penicillium marrzefii infection in patients infected with human immunodeficiency virus: late presentation in an area of nonendemicity Clin Infect Dis 1992; 15: 744. 13. Gallagher RT, Latch GCM, Keogh RG. The Janthitrems: fluorescent tremorgenic toxins produced by Penicillium janthinellum isolates from ryegrass pastures. Appl Environ Microbiol 1980; 39: 272-3. 14. Lanigan GW, Payne AL, Cockrum PA. Production of tremorgenic toxins by Penicillium janthinellum biourgr: a possible aetiological factor in ryegrass. AJEBAK 1979; 57: 31-7. 15. Wang ZG. Identification of toxigenic mould in soft drink causing food poisoning. Chung-Hau Yu Fang i Hsueh Tsa Chih 1992; 26: 8-10.

Enterococcal joint prosthesis infection

Clin Microbiol Infect 1997; 3: 264-265

biologist. Extensive efforts are made to minimize the incidence of infection. It is common practice to identify risk factors and to avoid procedures such as urethral catheterization, in an attempt to guard against the most common infecting organisms. We report two cases of prosthesis infection which highlight the problems of identification and treatment of infection with enterococci.

Case 1 A 75-year-old man underwent right total knee replacement with cefuroxime prophylaxis (three doses). Preoperatively he had no symptoms of prostatism, and a urine sample showed no significant bacterial growth. Postoperatively he developed urinary retention, requiring multiple urethral catheterizations, each with gentamicin cover followed by oral trimethoprim. He underwent transurethral resection of the prostate 3 weeks after his arthroplasty surgery. Eight months later he presented with swelling of the right knee and an abscess on the suture line. This discharged to reveal a sinus, from which Staphylococcus aureus was cultured. In contrast, culture of joint fluid obtained by arthrocentesis grew Enterococcus faecalis. At revision arthroplasty, there was established joint infection. The prosthesis and cement were removed and a cement spacer, incorporating gentamicin, ampicillin and flucloxacillin, was inserted. At operation, superficial and sinus tract swabs grew S. aureus, E. faecalis and Proteus sp., but cultures ofjoint fluid, bone, cement and joint tissue yielded pure growths of E. faecalis. The patient was treated with intravenous flucloxacillin, ampicillin and gentamicin for 2 weeks, followed by oral flucloxacillin and amoxycillin for 4 weeks, and the infection cleared. He is awaiting the second stage of revision surgery. Case 2 A 49-year-old woman with severe rheumatoid arthritis on long-term steroid therapy and azathioprine had multiple orthopedic procedures over 20 years. These included bilateral ankle arthrodeses, an osteotomy of her right tibia and subsequent knee arthroplasty, fusion of the left knee and bilateral total hip replacements. Replacement of the right hip was complicated by recurrent dislocations, requiring open reduction on two occasions and early revision of the acetabular component. Eighteen months later she presented with severe pain in the right hip and was unable to bear weight on that joint. Radiologic changes were consistent with infection. Joint fluid obtained by arthrocentesis grew E. faecalis and skin flora. A two-stage revision was planned. At surgery the joint was seen to be grossly infected. Multiple operative cultures grew I

Infection in a joint replacement is a disaster for the patient and a challenge for both surgeon and micro-

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Letters t o t h e Editors

E. fiecalis, sensitive to ampicillin and glycopeptides (vancomycin and teicoplanin), but expressing highlevel gentamicin resistance. The patient was treated with a combination of intravenous ampicillin and teicoplanin (for which in vitro synergy was demonstrated) for 2 weeks followed by oral amoxycillin plus intramuscular teicoplanin for 4 weeks. She awaits assessment for the second stage of her surgery. These patients demonstrate several of the etiologic factors which predispose to prosthetic joint infection: urologic trauma (case l ) , rheumatoid arthritis and postoperative trauma (case 2). Both cases highlight the need to collect multiple specimens for culture in order to make the diagnosis and guide antimicrobial therapy. Enterococci may cause up to 10% of prosthetic joint infections and are associated with urologic or gastrointestinal procedures [l].Enterococci are inherently resistant to the usual orthopedic perioperative antibiotic prophylaxis regimens. Until recently enterococci were predictably sensitive in vitro to combinations of ampicillin or a glycopeptide antibiotic (vancomycin, teicoplanin) with an aminoglycoside. However, the presence of high-level gentamicin resistance abolishes the potential for synergistic use of aminoglycosides [2]. More recently, both acquired ampicillin resistance and resistance to glycopeptide drugs have emerged in enterococci, leading to hospital outbreaks of multiplyresistant organisms [3]. There is currently a need for novel therapeutic approaches in order to achieve cidal antimicrobial activity against enterococci. As nosocomial infections due to these organisms, notably multiply-resistant E . jiecicrm, increase, we can expect to encounter more enterococcal joint infections. The prevention of such infections requires a reconsideration of antibiotics for prophylaxis and in cement, as highlighted in recent correspondence [4], together with aggressive management of predisposing perioperative factors. Paul R. Chadwick' Naomi Davisz Anthony D. Clayson' Hari Panigvahi' 'Department of Microbiology, North Manchester General Hospital, Manchester, UK *Department of Orthopaedics, North Manchester General Hospital, Manchester, UK;

References 1. Brause BD. Infections associated with prosthetic joints. Clin Rheumatic Dis 1986; 12: 523-36.

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2. Leclercq R , Dutka-Malen S , Brisson-Noel A, et al. Resistance of enterococci to aminoglycosides and glycopeptides. Clin Infect Dis 1992; 15: 495-5081. 3. Woodford N, Johnson AP, Morrison D, Speller DCE. Current perspectives on glycopeptide resistance. Clin Microbiol Rev 1995; 8: 585-615. 4. Leblebicioglu H, Sanic A, Gunaydin M, Sencan I, Dabak N, Nas Y. In-vitro release of vanconnycin and netilmicin from bone cement. Clin Microbiol Infect 1996; 1: 211-13.

Treatment of disseminated Mycobacferium simiae infection in AIDS

Clin Micvobiol Infect 1997; 3: 2651-267 Mycobacteriurn simiae is a rare cause of human infection. It is usually considered to be a commensal in the sputum of patients with underlying pulmonary diseases [l]. Only a small percentage of immunocompetent patients have had proven clinical disease [2]. In recent years, M. simiae has been reported as a cause of disseminated infection in five patients with AIDS [3-61. Two patients were co-infecte'd with the M . avinm (MAI) complex [4,5]. In three cases, M. sirniae was the only microorganism isolated (from blood culture, sputum and bone marrow), clearly demonstrating the pathogenic role of A4.simiase [3,6].The choice of optimal therapy is unclear, and the outcome was poor in the five cases previously reported [3-61. We report a case of disseminated M . sirniae infection in a patient with AIDS, who was successfully treated with a combination regimen that comprised clarithromycin, sparfloxacin and cycloserine. A 52-year-old Caucasian lheterosexual man was found to be HIV positive in 1989. H e had a history of sexual contacts with prostitutes in Burkina Faso. He had been treated with zidovudine since October 1990 and was asymptomatic. In Septtmber 1994, after travel to Burkina Faso, he presented with fever, diarrhea and weight loss of 6 kg. His C D 4 cell count was 45/mm3. CT scans of the thorax and abdomen showed three right pulmonary parenchymal nodular opacities and retroperitoneal lymphadenopathy (1 x 2 cm). All other investigations were negative and no infective agent was detected in initial tests. H e was treated empirically, for suspected disseminated MA1 infection, with clarithromycin (2000 mg/day), rifabutin (600 mg/day) and ethambutol (1200 mg/day). Staining of several sputum specimens revealed acid-fast bacilli. The patient responded to this therapy within 2 weeks. Culture from blood, sputum induction and bronchoalveolar lavage yielded M . sirniae (identified by the National Mycobacterium Reference Laboratory). Rifabutin was