S taphylococcus lugdunensis was first described as a human pathogen by Fleurette et al1 in 1989. Since that time, S. lugdunensis has been described to cause a wide variety of infections ranging from superficial skin infections2 to life-threatening bacteremia and infective endocarditis.3 We describe the case histories of 2 patients with bone and joint infections caused by S. lugdunensis and review the literature on this topic.
PubMed and Cochrane Database searches using the search terms Staphylococcus lugdunensis and infection were performed, and all matching articles were reviewed. The references in each of the pertinent articles were also reviewed for reported patients with S. lugdunensis bone and joint infections. All cases of bone and joint infection found on these searches were assembled and reviewed.
An 81-year-old white woman with a 1-year history of low back pain due to radiographically documented grade 1 spondylolisthesis presented to the emergency department (ED) with a 2-week history of worsening low back pain. Six weeks previously, she had undergone a series of epidural injections for her chronic low back pain with little improvement. Medical history was significant for endometrial carcinoma, 18 years previously, treated with total abdominal hysterectomy and bilateral oophorectomy and radiation therapy. On admission to the hospital, the vital signs showed a temperature of 98.3°F, a pulse of 73/min, respiratory rate of 18/min, and a blood pressure of 123/64. The physical examination was completely normal except for diffuse paraspinal tenderness to palpation over the lower lumbar spine and significant pain with lower back flexion and extension. There were no focal neurological abnormalities. White blood cell count was 7200/μL. Erythrocyte sedimentation rate was 96 (normal, <20). Lumbar spine radiographs showed L4-5 spondylolisthesis and multilevel disk degenerative changes. Magnetic resonance imaging of the lumbar spine showed L2-3 disk and vertebral body signal changes suggestive of infection (discitis and contiguous vertebral osteomyelitis). There was no epidural fluid collection. L4-5 images showed severe spinal stenosis with grade 1 spondylolisthesis. Two blood cultures and a culture computed tomography-guided needle biopsy material from the L2-3 disk space were positive for S. lugdunensis as identified by the API STAPH-IDENT system. The organism was sensitive to oxacillin, vancomycin, penicillin G, clindamycin, ciprofloxacin, trimethoprim-sulfamethoxazole, moxifloxacin, rifampin, and doxycycline by Kirby-Bauer methodology. Two-dimensional transthoracic echocardiography showed no evidence of infective endocarditis. The diagnosis of S. lugdunensis discitis and contiguous L2-3 vertebral osteomyelitis was made, and the patient was treated with 8 weeks of intravenous vancomycin and oral rifampin. Vancomycin was used because of the convenience of once daily intravenous dosing done at an outpatient infusion facility after the patient's discharge from the hospital. One week after completion of antimicrobial therapy, the patient underwent uncomplicated posterior lumbar decompression of L2, L3, L4, and L5 with fusion of L4-5 with right posterior iliac crest bone graft, at which time, cultures of deep tissue showed no growth. She remained pain-free at her 3-month follow-up visit.
A 63-year-old white man with hypertension, hyperlipidemia, and osteoarthritis of the right knee underwent an outpatient partiallateral meniscectomy and chondroplasty for a lateral menisceal tear. On the second postoperative day, the patient noted increasingly severe pain, followed on the fourth postoperative day by worsening pain and swelling of the knee joint. On the sixth postoperative day, he was admitted to the hospital after ED evaluation that revealed a swollen, erythematous, and tender knee joint accompanied by fever of 101.3°F, chills, and diaphoresis. White blood cell count was 9200/mm3, and the erythrocyte sedimentation rate was 45 mm/hr. Arthrocentesis in the ED showed cloudy fluid with 16,000/mm3 WBC, and a Gram-stained smear of the fluid was negative for organisms. Cultures revealed S. lugdunensis by the API STAPH-IDENT system. The organism was sensitive to oxacillin, vancomycin, penicillin G, clindamycin, doxycycline, rifampin, and clindamycin. The patient was treated with intravenous vancomycin and intravenous rifampin. Four days after the initial arthrocentesis, when the patient failed to improve with the initial arthrocentesis and intravenous antimicrobial therapy, the patient was taken to the operating suite, and an arthroscopic lavage was performed. Cultures from the lavage were again positive for S. lugdunensis. The patient then rapidly improved and was treated with 3 more weeks of vancomycin and rifampin, followed by 3 weeks of oral trimethoprim-sulfamethoxazole. Six weeks after lavage, the patient's knee had returned to near normal condition with minimal pain and swelling and full range of motion. He remained normal on follow-up examination 3 months later.
Staphylococcus lugdunensis is an unusual cause of bone and joint infections. The total number of patients with infection due to this organism, however, may be underestimated because some clinical laboratories do not speciate all isolates of coagulase-negative staphylococci isolated in laboratory cultures and therefore may not fully identify isolates of S. lugdunensis. Physicians expecting the usual Staphylococcus epidermidis as a pathogen may not ask for further identification of a particular isolate of a coagulase-negative Staphylococcus and may therefore be unaware of S. lugdunensis as the true pathogen in a clinical infection. Staphylococcus lugdunensis generally causes infections with the same virulence as that seen with Staphylococcus aureus and tends to be much more aggressive infections than the infections seen with most coagulase-negative staphylococci.3,4 Staphylococcus lugdunensis often produces a glycocalyx that plays a role in preventing phagocytosis and in colonization, especially in helping isolates adhere to periprosthetic material. The glycocalyx is a potent stimulator of prostaglandin E2 that impedes T-cell proliferation. Staphylococcus lugdunensis also has the ability to bind fibrinogen and fibronectin and soluble extracellular matrix proteins. Other virulence factors include production of esterase, protease, fatty-acid modifying enzymes, lipase, and hemolysins.5 When S. lugdunensis is isolated from a clinical culture specimen, there is significant variance in the published literature regarding its likelihood of being a pathogen or a contaminant, varying from 91%6 to 30%7 of clinical S. lugdunensis isolates considered pathogenic.
All references obtained by the database searches described previously were reviewed for patients with bone or joint infections due to S. lugdunensis. Only patients with septic arthritis, osteomyelitis, or an infected joint prosthesis or an infected osteosynthesis device were considered to have a bone or joint infection. Deep soft tissue infections such as abscesses or bursal infections were not included in this review unless bone and/or joint infection coexisted.
With our 2 patients included in the database, 56 patients with 58 separate bone and joint infections were documented.1,8-29 One patient had 3 separate orthopedic S. lugdunensis infections documented over a 3-year period including right native knee joint infection, a left prosthetic knee joint infection, and spondylodiscitis with coexistent contiguous vertebral osteomyelitis.17 Our patient with postarthroscopy septic arthritis was the fourth such patient described, and our patient with spondylodiscitis and vertebral osteomyelitis was the 10th such patient reported. All patients are listed in Table 1. The most common type of infection was prosthetic joint infection, followed by almost equal numbers of native joint infections and spondylodiscitiswith contiguous vertebral osteomyelitis. Male subjectsoutnumbered female subjects by 3:1, and the average age was 58 years, with a range of 10 to 87 years. About onehalf of the patients on whom information was available were receiving some type of immunosuppressive therapy. Eighty percent of the patients had eventual resolution of the infection. Almost all patients except those with spondylodiscitis and vertebral osteomyelitis required surgical treatment including hardware removal for adequate treatment together with parenteral antibiotic therapy, usuallyfollowed by variable periods of oral antimicrobial therapy. Those patientswith spondylodiscitis and contiguous vertebral osteomyelitis responded well to protracted intravenous antibiotic therapy without surgical intervention. Clinically, these S. lugdunensis infections mimicked those seen with S. aureus more so than those seen with S. epidermidis and other coagulase-negative staphylococci. The characteristics of the S. lugdunensis infections often included rapid onset of symptoms and aggressive destruction of tissue with copious amounts of purulent material. This would be consistent with the aggressive infectious characteristics seen in patients with infective endocarditis due to S. lugdunensis.3 Another important characteristic of many strains of S. lugdunensis is the organism's common sensitivity to penicillin G, oxacillin, cefazolin, clindamycin, vancomycin, rifampin, trimethoprim-sulfamethoxazole, and other relatively simple-to-use antimicrobial agents.7,12 However, clinicians should be aware that antimicrobial resistance may develop during treatment with some of the antimicrobial agents.17
Staphylococcus lugdunensis is an increasingly recognized pathogen in bone and joint infections. Staphylococcus lugdunensis, unlike many other coagulase-negative staphylococcal species, causes infections of rapid onset with the presence of a great deal of purulent material and tissue destruction. Infections complicating prosthetic joints and osteosynthesis devices usually require aggressive surgical debridement and device removal for cure. Antimicrobial therapy should be guided by sensitivity testing, but almost all strains of S. lugdunensis are sensitive to nafcillin and oxacillin and often sensitive to penicillin G. When a strain of coagulase-negative Staphylococcus is isolated from 2 or more blood cultures or from a normally sterile deep wound site (bone, joint, abscess cavity, etc), the microbiology laboratory should be asked to fully identify the Staphylococcus species and perform detailed antimicrobial susceptibility testing to provide the best antimicrobial treatment options.
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