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Infection of an orthopedic prosthesis was ..

Prevention of prosthetic joint and other types of orthopedic hardware infection

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Diagnosis of Periprosthetic Infection - Orthopedic Clinics

1. Widmer AF. New developments in diagnosis and treatment of infection in orthopedic implants. Clin Infect Dis. 2001 Sept; 33(2): 94-106.
2. Berbari EF, Hanssen AD, Duffy MC et al. Risk factors for prosthetic joint infection: case-control study. Clin Infect Dis. 1998;27(5):1247-54.
3. Buttaro M, Gonzalez Della Valle A, Piccaluga F. Psoas abscess associated with infected total hip arthroplasty. J Arthroplasty 2002;17(2):230-4.
4. Ricci MA, Rose FB, Meyer KK: Pyogenic psoas abscess: worldwide variations in etiology. World J Surg. 1986;10(5):834-43.
5. Dauchy FA, Dupon M, Dutronc H, De Barbeyrac B, Lawson-Ayayi S, Dubuisson V, et al. Association between psoas abscess and prothetic hip infection: a case control study. Acta Orthopaedica 2009; 80:198-200.
6. Qureshi N, O’Brien D, Allcutt D: Psoas abscess secondary to discitis: a case report of conservative management. J Spinal Disord. 2000;13(1):73-6.
7. Mallick IH, Thoufeeq MH, Rajendran TP. Iliopsoas abscesses. Postgrad Med J. 2004;80(946):459-62.
8. Sadat-Ali M, Al-Habdan I, Ahlberg A: Retrofascialnontuberculous psoas abscess. Int Orthop. 1995;19:323-26.
9. Simons GW, Sty JR, Starshak RJ: Retroperitoneal and retrofascial abscesses: a review. J Bone Joint Surg Am. 1983;65(8):1041-58.
10. Yang SS, Bronson MJ: Cystic enlargement of the iliopsoas bursa causing venous obstruction as a complication of total hip arthroplasty: a case report. J Arthoplasty 1993;8(6):657-61.
11. Chandler S B. The iliopsoas bursa in man. Anatomical Record. 1934;58(3):235 – 240.
12. Steinbach L S, Schneider R, Goldman A B, et al. Bursae and abscess cavities communicating with the hip: diagnosis using arthrography and CT. Radiology 1985;156:302-3.
13. Zimmerli W, Trampuz A, Ochsner PE. Prosthetic-joint infections. N Engl J Med. 2004;351(16):1645-54.
14. Lentino JR. Prosthetic joint infections: bane of orthopedists, challenge for infectious disease specialists. Clin Infect Dis. 2003;36(9):1157-61.
15. Berbari E, Baddour LM, Sexton DJ et al: Treatment of prosthetic joint infections. Up to date Sep 19, 2013.

Prosthesis infections after orthopedic joint replacement: the possible role of bacterial biofilms

These guidelines are intended for use by infectious disease specialists, orthopedists, and other healthcare professionals who care for patients with prosthetic joint infection (PJI). They include evidence-based and opinion-based recommendations for the diagnosis and management of patients with PJI treated with debridement and retention of the prosthesis, resection arthroplasty with or without subsequent staged reimplantation, 1-stage reimplantation, and amputation. Full text*Every 12 to 18 months following publication, IDSA reviews its guidelines to determine whether an update is required. This guideline was published in January of 2013 and is the most current version.

Prosthesis infections after orthopedic joint ..

Role of sonication in the microbiological diagnosis of implant-associated infections: Beyond the orthopedic prosthesis



Fredrik Lindberg, co-founder and current CEO will remain in the company as Chief Scientific Officer being responsible for key customer relations, driving the clinical publication program as well as the product development pipeline for “the first of its kind” products for the treatment and prophylaxis of deep bone and orthopedic prosthesis infections.

AB - Staphylococcus epidermidis is a frequent pathogen in infections associated with orthopedic implants. We studied 123 S. epidermidis strains from infections related to orthopedic implants, as regards their ability to express a factor of virulence, namely the slime, an extracellular polysaccharide, which mediates adherence to implants and bacterial colonization. The slime-producing ability was determined by PCR detection of icaA and icaD genes responsible for slime synthesis, and by culture on Congo red agar plates in which slime-producing strains form black colonies, while nonslime-forming ones develop red colonies. 56% of the S. epidermidis isolates were icaA- icaD-positive and grew to become black colonies. In the evaluation of the distribution of slime-forming strains in different sites and types of implants, we found a slight, but not statistically significant, increase in slime-forming strains in total joint prostheses, where tissue compression near the articular faces can form niches in which bacteria crowd, sheltered by the slime. Our findings confirm the role of ica genes as a virulence marker in the pathogenesis of implant-associated orthopedic infections. However, they do not show the existence of a higher frequency of slime-positive strains in a specific type of implant.

Prosthetic joint infection: Treatment

Occurrence of ica genes for slime synthesis in a collection of Staphylococcus epidermidis strains from orthopedic prosthesis infections

Prostheses-related infections are now thought to be biofilm-associated infections,,, which are highly resistant to antibiotic treatment. The mechanisms for the biofilm bacterial cells to become resistant to antibiotics are not fully understood. It is believed that in addition to conventional resistance mechanisms such as beta-lactamase and efflux pumps,, poor antibiotic penetration, nutrient limitation, slow growth, adaptive stress responses and formation of persister cells are involved. In addition, in vitro and in vivo studies of antibiotic pharmacokinetics/pharmacodynamics in bacterial biofilms have indicated that, biofilm bacteria are significantly more resistant than their planktonic counterparts, and antibiotic treatment, therefore, requires a higher dose and combination., It is, therefore, not recommended to treat implant infections with antibiotics only. On the basis of appropriate surgical intervention, if the clinical signs and symptoms of implant infection have been observed for less than three weeks, the implant is stable and the surrounding tissue is in a good condition, antibiotic treatment becomes crucial. Due to the integrated resistance of bacterial biofilm, it is important to choose highly active, better penetrating and combined antibiotic treatment. For the infections caused by staphylococci, Zimmerli et al. performed a randomized, placebo-controlled, double-blind clinical trial on 33 patients with proven staphylococcal infection and stable orthopedic implants from 1992 through 1997. They found that patients treated with initial debridement and 2-week intravenous flucloxacillin (2 g q.i.d. for methicillin- sensitive) or vancomycin (1 g b.i.d. for methicillin-resistant) together with rifampin (450 mg p.o., b.i.d.), followed by three (hip implants) or six (knee implants) months of ciprofloxacin (750 mg p.o., b.i.d.) and rifampin treatment had a 100% cure rate compared with the ciprofloxacin-placebo group (58% cure rate). It is, therefore, recommended to treat staphylococcal implant infections with 2-4 weeks intravenous beta (β)-lactam (for methicillin- sensitive) or glycopeptide (for methicillin- resistant) in combination with rifampicin to minimize the bacterial burden and risk of antibiotic resistance, followed by long-term rifampicin (450 mg p.o. b.i.d.) and levofloxacin (750 mg p.o., q.d. to 500 mg b.i.d.) or other fluoroquinolones.,, For details, please refer to the new protocol of antibiotic treatment up-dated in 2012 by Zimmerli et al. Application of the combination with rifampicin (20 mg/kg) and fluoroquinolone showed good results in a French clinical study. Fusidic acid was recently recommended as an efficient antibiotic for the treatment of bone and joint infections caused by S. aureus and MRSA. In our clinical practice, cefuroxim 1.5 g i.v., t.i.d. and fusidic acid (Fucidin) 500 mg p.o., t.i.d. are used as initial treatment followed by dicloxacillin 1g p.o., q.i.d. together with fucidin 500 mg p.o., t.i.d. or rifamicin 600 mg p.o., b.i.d. for the treatment of Staphylococcus aureus infection. For methicillin-resistant staphylococal infections, vancomycin 1g i.v., b.i.d and fucidin or rifampicin p.o. are applied initially followed by rifampicin and fucidin or moxifloxacin 400 mg p.o., q.d. or linezolid 600 mg p.o. b.i.d. according to the sensitivity results. Spanish colleagues recently reported that combination treatment with rifampicin and linezolid showed a 69.4% success rate (34 of 49 patients) for prosthetic joint infection with retention of the implant after two years. Recently, daptomycin has also been recommended as a new option for the treatment of implant infections, due to its good effect systemically and locally against methicillin-resistant staphylococci and enterococci in patients with implant-associated infections., By using such antibiotic treatment, prosthetic knee-associated infections in many patients could be well controlled. Soriano et al., in a study of 85 patients with orthopedic implant infections, reported that 47- and 60-day treatment with linezolid showed a 72.2% and a 42.8% success rate in acute and chronic infections, respectively, when the implant was not removed. However, in a clinical study of 112 patients with prosthetic joint infection carried out in the UK, arthroscopic debridement and empirical treatment with vancomycin 1g i.v. every 12 h, plus meropenem 500 mg i.v. t.i.d. for inpatients and ceftriaxone 1 g i.v. q.d. plus teicoplanin 400 mg i.v. q.d. for outpatients, followed by oral rifampicin and quinolones could not avoid failure (18% recurred infection over 2.3 years). The authors concluded that antibiotic therapy may simply postpone, rather than prevent failure. But arthroscopic debridement might not be sufficient to remove the infected tissue, and, in our opinion, the doses of meropenem and ceftriaxone used in the study were too low.

In recent years, new techniques have been developed to increase the detection rate of infection, especially biofilm infections. In many countries, as well as in our own laboratory, synovial fluid and 5 samples from periimplant tissues are recommended for microbiological diagnosis of orthopedic implant-associated infections. In addition, the orthopedic implants removed from patients can be placed in sterile saline, vortexed and sonicated in an ultrasonic bath. The fluid from sonication is then cultured and sent to 16s or 18s polymerase chain reaction (PCR) detection.,, It is reported that sonication cultures improved the microbiological detection of the implant infection., PCR detection is a more sensitive molecule tool, which is also applied in diagnosis of orthopedic implant infection. ,,, Furthermore, detection of serum IgM against Staphylococcal slime polysaccharide antigens was used recently for diagnosis of staphylococcal periprosthetic joint infections with 89.7% sensitivity and 95.1% specificity. , Sometimes blood leukocyte count, Creactive protein, interleukin-6 and procalcitonin also give indications. The combination of microbiological routine and new methods, together with clinical symptoms and blood inflammatory markers, will give us a better picture of orthopedic implant infections.

Prosthesis-related infection is a serious complication for patients after orthopedic joint replacement, which is currently difficult to treat with antibiotic therapy.
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Biofilm layer on the prosthesis, ..

These guidelines are intended for use by infectious disease specialists, orthopedists, and other healthcare professionals who care for patients with prosthetic joint infection (PJI). They include evidence-based and opinion-based recommendations

Infections associated with orthopedic implants ..

Staphylococcus epidermidis is a frequent pathogen in infections associated with orthopedic implants. We studied 123 S. epidermidis strains from infections related to orthopedic implants, as regards their ability to express a factor of virulence, namely the slime, an extracellular polysaccharide, which mediates adherence to implants and bacterial colonization. The slime-producing ability was determined by PCR detection of icaA and icaD genes responsible for slime synthesis, and by culture on Congo red agar plates in which slime-producing strains form black colonies, while nonslime-forming ones develop red colonies. 56% of the S. epidermidis isolates were icaA- icaD-positive and grew to become black colonies. In the evaluation of the distribution of slime-forming strains in different sites and types of implants, we found a slight, but not statistically significant, increase in slime-forming strains in total joint prostheses, where tissue compression near the articular faces can form niches in which bacteria crowd, sheltered by the slime. Our findings confirm the role of ica genes as a virulence marker in the pathogenesis of implant-associated orthopedic infections. However, they do not show the existence of a higher frequency of slime-positive strains in a specific type of implant.

Order now
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