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• W2529991064 abstract "In this issue of Clinical Microbiology and Infection, Rieg et al. [[1]Rieg P. Joost I. Weiß V. Peyerl-Hoffmann G. Schneider C. Hellmich M. et al.Combination antimicrobial therapy in patients with Staphylococcus aureus bacteremia—a post hoc analysis in 964 prospectively evaluated patients.Clin Microbiol Infect. 2016; https://doi.org/10.1016/j.cmi.2016.08.026Abstract Full Text Full Text PDF PubMed Scopus (37) Google Scholar] report on the role of combination therapy in patients with Staphylococcus aureus bacteraemia. In patients with implanted devices, they observed fewer late complications related to S. aureus bacteraemia with combination therapy (4.5%; 9/202) than with monotherapy (10.6%; 15/142; p 0.03). Most of the patients in the former group were treated with a rifampin combination. These results trigger the discussion on rifampin in orthopaedic-device-related infections (ODRI). In this commentary, we discuss three frequently asked questions. First, should rifampin be added to the anti-staphylococcal treatment in patients with orthopaedic implants and S. aureus bacteraemia? Second, at which time should rifampin be started in patients with established ODRI after debridement or replacement surgery? Third, what is the optimal rifampin dose in ODRI? Because it is unlikely that randomized controlled trials investigating these questions will be performed, our viewpoints are presented here. Several studies have shown a high seeding rate to orthopaedic devices following community-acquired S. aureus bacteraemia, ranging from 30% to 40%. In contrast, the risk of ODRI is markedly lower following hospital-acquired S. aureus bacteraemia [[2]Tande A.J. Palraj B.R. Osmon D.R. Berbari E.F. Baddour L.M. Lohse C.M. et al.Clinical presentation, risk factors, and outcomes of hematogenous prosthetic joint infection in patients with Staphylococcus aureus bacteremia.Am J Med. 2016; 129 (221 e211–20)Abstract Full Text Full Text PDF PubMed Scopus (54) Google Scholar]. This points towards the importance of early anti-staphylococcal treatment, as the duration of bacteraemia before antimicrobial treatment is generally longer in community-acquired than in hospital-acquired sepsis. Asymptomatic haematogenous seeding to an implant may already have occurred when a patient with community-acquired S. aureus bacteraemia is seeking medical help. If patients with occult ODRI are treated with rifampin combinations for S. aureus bacteraemia, the clinical diagnosis may be delayed without elimination of the biofilm infection. Therefore, we do not recommend routine adjunctive rifampin treatment in patients with S. aureus bacteraemia. As rapid detection and surgical debridement are needed to cure ODRI with implant retention [[3]Zimmerli W. Widmer A.F. Blatter M. Frei R. Ochsner P.E. Role of rifampin for treatment of orthopedic implant-related staphylococcal infections: a randomized controlled trial. Foreign-body infection (FBI) study group.JAMA. 1998; 279: 1537-1541Crossref PubMed Scopus (868) Google Scholar], delayed diagnosis should be avoided. Therefore, after S. aureus bacteraemia, body sites with orthopaedic devices must be carefully and repeatedly examined for clinical signs of infection. Upon suspicion of ODRI, rapid diagnostic workup is required. The optimal time-point for starting rifampin therapy in patients with staphylococcal ODRI is still a matter of debate between physicians prescribing it early in the treatment course (i.e. immediately after surgery), and those recommending a delayed treatment start (i.e. after all drains have been removed and the wound is dry). Choosing the optimal time for starting the anti-biofilm treatment with rifampin is particularly important in patients with acute ODRI treated either with debridement and implant retention or one-stage exchange. There are several arguments for starting rifampin treatment early. After initial attachment of staphylococci to foreign body surfaces, the process of biofilm formation via cell–cell adhesion and matrix elaboration starts. In vitro studies have shown that this process is initiated within a short period of time after surface contact [[4]Peters G. Locci R. Pulverer G. Adherence and growth of coagulase-negative staphylococci on surfaces of intravenous catheters.J Infect Dis. 1982; 146: 479-482Crossref PubMed Scopus (432) Google Scholar]. Taking into account that minimal biofilm eradication concentrations (MBEC, also called biofilm MBC) of bacteria are considerably higher than their corresponding MICs, and that rifampin has good activity on susceptible biofilm staphylococci [[5]Saginur R. Stdenis M. Ferris W. Aaron S.D. Chan F. Lee C. et al.Multiple combination bactericidal testing of staphylococcal biofilms from implant-associated infections.Antimicrob Agents Chemother. 2006; 50: 55-61Crossref PubMed Scopus (257) Google Scholar], early start of rifampin after bacterial adhesion to the implant may be advantageous. Nonetheless, we prefer not to start rifampin in the early course of infection, for the following reasons. First, the use of rifampin is endangered by the emergence of rifampin resistance. The risk is highest when administering rifampin either as monotherapy or to an infectious focus containing a high bacterial load [[6]Svensson E. Hanberger H. Nilsson M. Nilsson L.E. Factors affecting development of rifampicin resistance in biofilm-producing Staphylococcus epidermidis.J Antimicrob Chemother. 1997; 39: 817-820Crossref PubMed Scopus (26) Google Scholar]. In the same line of reasoning, the newly published guidelines for staphylococcal prosthetic valve endocarditis recommend the delay of rifampin treatment until blood cultures have turned negative [[7]Habib G. Lancellotti P. Antunes M.J. Bongiorni M.G. Casalta J.P. Del Zotti F. et al.2015 ESC guidelines for the management of infective endocarditis: The task force for the management of infective endocarditis of the European Society of Cardiology (ESC). Endorsed by: European Association for Cardio-Thoracic Surgery (EACTS), the European Association of Nuclear Medicine (EANM).Eur Heart J. 2015; 36: 3075-3128Crossref PubMed Scopus (2749) Google Scholar]. Similarly, in orthopaedic surgery, the upcoming course of additional interventions (e.g. removal of haematoma, second-look surgery because of persistent wound secretion) is difficult to estimate shortly after the first surgery. In the early postoperative period, the bacterial load is unpredictable, but probably still high in the case of debridement and implant retention. Second, rifampin penetrates well into all body fluids. Therefore, the skin microbiome is rapidly modified by antimicrobial therapy, and it is conceivable that patients treated with rifampin will select rifampin-resistant staphylococci [[8]Valentin T. Leitner E. Rohn A. Zollner-Schwetz I. Hoenigl M. Salzer H.J. et al.Rifaximin intake leads to emergence of rifampin-resistant staphylococci.J Infect. 2011; 62: 34-38Abstract Full Text Full Text PDF PubMed Scopus (53) Google Scholar]. Drainages in close proximity to the device and oozing wounds may therefore facilitate exogenous super-infection by rifampin-resistant staphylococci from the skin microbiome. For these reasons, in patients with staphylococcal ODRI, we do not administer rifampin before all the drains have been removed, the wound is dry, and the bacterial load is lowered by debridement surgery and initial antimicrobial therapy with a standard intravenous regimen (e.g. 3–5 days after surgery). A retrospective multicentre search for rifampin-resistant staphylococci causing periprosthetic joint infection revealed that 44 of 48 cases had a previous episode of prosthetic joint infection, and 93% of these had been treated with rifampin. This case–control study demonstrates that starting rifampin therapy when bacterial load is still high, and multiple previous surgical revisions, are independent risk factors for developing a secondary prosthetic joint infection with rifampin-resistant staphylococci [[9]Achermann Y. Eigenmann K. Ledergerber B. Derksen L. Rafeiner P. Clauss M. et al.Factors associated with rifampin resistance in staphylococcal periprosthetic joint infections (PJI): a matched case–control study.Infection. 2013; 41: 431-437Crossref PubMed Scopus (84) Google Scholar]. These observations suggest that the previously raised concern of early rifampin treatment regarding the possible emergence of resistance is justified. In different clinical studies, various doses and/or intervals of rifampin have been used, namely 900 mg once daily, 450 mg twice daily, 600 mg once daily, or 300 mg twice daily. In a neutropenic murine infection model with S. aureus isolates, the pharmacokinetic/pharmacodynamic indexes that best predict rifampin efficacy are concentration-dependent killing (Cmax/MIC) and the area under the curve (AUC)/MIC [[10]Hirai J. Hagihara M. Kato H. Sakanashi D. Nishiyama N. Koizumi Y. et al.Investigation on rifampicin administration from the standpoint of pharmacokinetics/pharmacodynamics in a neutropenic murine thigh infection model.J Infect Chemother. 2016; 22: 387-394Abstract Full Text Full Text PDF PubMed Scopus (11) Google Scholar]. Furthermore, rifampin has a long post-antibiotic effect in an S. aureus biofilm infection mouse model [[11]Kadurugamuwa J.L. Sin L.V. Yu J. Francis K.P. Purchio T.F. Contag P.R. Noninvasive optical imaging method to evaluate postantibiotic effects on biofilm infection in vivo.Antimicrob Agents Chemother. 2004; 48: 2283-2287Crossref PubMed Scopus (51) Google Scholar]. The AUC0–24h between 900 mg once daily and 450 mg twice daily probably does not significantly influence the AUC/MIC ratio. Though, in our experience, 450 mg twice daily is better tolerated than 900 mg once daily. This is particularly important when considering that in ODRI the compound is commonly administered for 6–12 weeks or even longer. It is uncertain whether once-daily or twice-daily dosing matters after a steady state has been reached, as all of the above mentioned regimens have shown clinical efficacy. In our view, it is clinically useful to start treatment at a high dose (e.g. 450 mg twice daily), and reduce the dose in case of intolerance. Severe nausea, frequently occurring in the elderly, does not respond to anti-emetic drugs. In a trial on the role of rifampin in staphylococcal ODRI, severe nausea was observed in 17% of the patients treated with 450 mg twice daily [[3]Zimmerli W. Widmer A.F. Blatter M. Frei R. Ochsner P.E. Role of rifampin for treatment of orthopedic implant-related staphylococcal infections: a randomized controlled trial. Foreign-body infection (FBI) study group.JAMA. 1998; 279: 1537-1541Crossref PubMed Scopus (868) Google Scholar]. In these patients, rifampin therapy could be continued after a temporary cessation with a reduced dose of 300 mg twice daily, indicating that these adverse events are—as observed in patients with anti-tuberculous treatment—dose dependent. In contrast to the AUC0–24h, Cmax probably differs between once and twice daily regimens. However, even when considering Cmax/MIC or Cmax/MBEC as efficacy variable, there are in vitro arguments and mathematical extrapolations supporting that 300 mg twice daily may be as efficient as 600 mg once daily. Cmax in adults with tuberculosis treated with 300 mg rifampin once daily is approximately 6.6 mg/L (range 2.9–14 mg/L) [[12]Bhatt N.B. Barau C. Amin A. Baudin E. Meggi B. Silva C. et al.Pharmacokinetics of rifampin and isoniazid in tuberculosis-HIV-coinfected patients receiving nevirapine- or efavirenz-based antiretroviral treatment.Antimicrob Agents Chemother. 2014; 58: 3182-3190Crossref PubMed Scopus (27) Google Scholar]. In six elderly male nursing home residents who received 300 mg rifampin orally every 12 hours for 14 days (in addition to ciprofloxacin), Cmax after doses 12 and 27 were 9.4±3.1 and 7.3±2.3 mg/L, respectively [[13]Chandler M.H. Toler S.M. Rapp R.P. Muder R.R. Korvick J.A. Multiple-dose pharmacokinetics of concurrent oral ciprofloxacin and rifampin therapy in elderly patients.Antimicrob Agents Chemother. 1990; 34: 442-447Crossref PubMed Scopus (28) Google Scholar]. Rifampin bone/serum concentration ratios of 0.2–0.5 are found in humans (reviewed in ref. [[14]Landersdorfer C.B. Bulitta J.B. Kinzig M. Holzgrabe U. Sorgel F. Penetration of antibacterials into bone: pharmacokinetic, pharmacodynamic and bioanalytical considerations.Clin Pharmacokinet. 2009; 48 (89–24)Crossref PubMed Scopus (230) Google Scholar]). Hence, calculated Cmax in bone are 1.3–4.5 mg/L (range of medians, total range 0.6–6 mg/L). However, this calculation does not take into account the accumulation in bone, as distribution in and elimination from various comportments is not linear [[15]Mouton J.W. Theuretzbacher U. Craig W.A. Tulkens P.M. Derendorf H. Cars O. Tissue concentrations: do we ever learn?.J Antimicrob Chemother. 2008; 61: 235-237Crossref PubMed Scopus (291) Google Scholar]. Nonetheless, most staphylococci have a MIC for rifampin of ≤0.064 mg/L. There is no uniformly accepted microbiological method for determining MBEC. Many ‘biofilm’ staphylococci have a minimal bactericidal concentration of ≤2 mg/L, and in combination with another compound, rifampin is active against the majority of these isolates [[5]Saginur R. Stdenis M. Ferris W. Aaron S.D. Chan F. Lee C. et al.Multiple combination bactericidal testing of staphylococcal biofilms from implant-associated infections.Antimicrob Agents Chemother. 2006; 50: 55-61Crossref PubMed Scopus (257) Google Scholar]. Hence, it is likely that bone levels of rifampin with 300 mg twice daily are high enough to potentially cure the infection. Therefore, we recommend a delayed treatment start of adjunctive rifampin in staphylococcal ODRI with 450 mg twice daily; in case of intolerance, we recommend reducing the dose to 300 mg twice daily. Both authors have no conflicts of interest. No external funding was received for this manuscript." @default.
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• W2529991064 title "The use of rifampin in staphylococcal orthopaedic-device-related infections" @default.
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