Rifampin aureus

Intranasal S. aureus increases the risk of S. aureus exit-site infections, tunnel infections, peritonitis, and subsequent catheter loss.49 Several measures have been used to decrease the risk of peritonitis caused by S. aureus, including mupirocin cream applied daily around the exit site, intranasal mupirocin cream twice daily for 5 days each month, or rifampin 300 mg orally twice daily for 5 days, repeated every 3 months.49 Mupirocin use is preferred over rifampin to prevent the development of resistance to rifampin, although mupirocin resistance has also been reported.49 Other measures that have been used to decrease both S. aureus and P. aeruginosa infections include gentamicin cream applied twice daily and ciprofloxacin otic solution applied daily to the exit site.49... 

For methidllin-resistant staphylococci (both methiciUin-resistant S. aureus and CNST), vancomycin is used with rifampin for 6 weeks or more (Table 37-7). An aminoglycoside is added for the first 2 weeks if the organism is susceptible. 

In addition to M. tuberculosis, rifampin is active against Staphylococcus aureus, Neisseria meningitidis, Haemophilus influenzae, Chlamydiae, and certain viruses. Rifampin resistance results from a point mutation or deletion in rpoB, the gene for the p-subunit of RNA polymerase, thereby preventing the binding of RNA polymerase. 

Staphylococcus aureus Abscesses bacteremia cellulitis endocarditis osteomyelitis pneumonia others If methicillin-sensitive nafcillin or oxacillin If methicillin-resistant vancomycin gentamicin or rifampin 1 st-generation cephalosporin clindamycin erythromycin trimethoprim-sulfamethoxazole a penicillin + a penicillinase inhibitor... 

Antistaphylococcal penicillins Methicillin [meth i SILL in], naf-cillin [naf SILL in], oxacillin [ox a SILL in], cloxacillin [klox a SILL in], and dicloxacillin [dye klox a SILL in] are penicillinase-resistant penicillins. Their use is restricted to the treatment of infections caused by penicillinase-producing staphylococci. Because of its toxicity, methicillin is rarely used. Methicillin-resistarft strains of Staphylococcus aureus (MRSA), currently a serious source of nosocomial (hospital-acquired) infections, are usually susceptible to vancomycin, and rarely to ciprofloxacin or rifampin. 

Rifampin is effective against Staph, aureus, Haemophilus spp., R. equi and a variety of mycobacteria. At very high concentrations, it has activity against poxviruses and adenoviruses. Rifampin also has antifungal activity when combined with other antifungal agents. Resistance develops rapidly therefore, it is usually administered concurrently with another antimicrobial agent. In equine practice, is most commonly used in combination with erythromycin for the treatment of R. equi infections in foals. It may also be used in the treatment of refractory osteomyelitis and endocarditis caused by Staph, aureus. 

Other, nonlabeled uses of rifampin include the treatment of serious infections such as endocarditis and osteomyelitis caused by methicillin-resistant 5. aureus or 5. epidermidis. Legionnaires disease when resistant to eiythromycin, and prophylaxis of H. injluenaie-induced meningitis. 

The presence of S. aureus warrants the use of either cefazolin or vancomycin. If the strain of S. aureus is methicillin resistant, then vancomycin should be used. Oral rifampin can be added if there is an inadequate clinical response, defined as continued cloudy dialysate, abdominal pain, and elevated dialysate white blood cells. 

Bernardini J, Piraino B, Holley J, et al. A randomized trial of Staphylococcus aureus prophylaxis in peritoneal dialysis patients mupirocin calcium ointment 2% applied to the exit site versus cyclic oral rifampin. Am J Kidney Dis 1996 27 695-700. 

For treatment of endocarditis due to penicillin-susceptible staphylococci (minimum inhibitory concentration <0.1 mcg/mL), aqueous crystalline penicillin C sodium (Table 109-4, first regimen) can be used for 4 to 6 wk instead of nafcillin or oxacillin. Shorter antibiotic courses have been effective in some drug addicts with right-sided endocarditis due to Staphylococcus aureus (see text). See text for comments on use of rifampin. 

In a patient with a positive skin test or a history of immediate hypersensitivity to penicillin, vancomycin is the agent of choice. Vancomycin, however, kills S. aureus slowly and is regarded as inferior to penicillinase-resistant penicillins for MSSA. Rifampin as an adjunctive therapy is controversial however, this agent, added to vancomycin in refractory or complicated infections in patients with left-sided IE may result in dramatic patient improvement. Generally, antibiotic therapy should be continued for 4 to 6 weeks. Unfortunately, left-sided IE caused by S. aureus continues to have a poor prognosis, with a mortality rate of 25% to 47%. Eor reasons discussed in the following section, those with IE associated with TVDA have a more favorable response to therapy. 

Dworkin RJ, Lee BL, Sande MA, Chambers HF. Treatment of rightsided Staphylococcus aureus endocarditis in intravenous drag abusers with ciprofloxacin and rifampin. Lancet 1989 2 1071-1073. 

The role of the penicillinase-resistant penicillins for most staphylococcal disease is decreasing with the increasing frequency of so-called methicilhn-resistant microorganisms. Both S. aureus and S. epidermidis increasingly are resistant. Vancomycin is the drug of choice for serious infection caused by methicillin-resistant variants of these strains rifampin is given concurrently when a foreign body is present. 

Fig. 2. Real-time in vivo bioluminescence monitoring of S. aureus Xen-29 in the mouse model of soft-tissue biofilm infection during treatment with rifampin. Effect of 4 days of rifampin treatment (twice a day with 30 mg/kg) on a 3-week-old biofilm. A representative animal from the group receiving antibiotic or the untreated infected group is shown. Note the response to treatment including relapse that can be monitored non-invasively within the same animal throughout the study period. See Color Plate 7, following p. 46.)...

To provide protection against P. aeruginosa, Raad et P developed novel antimicrobial-coated PU CVCs based on a combination of chloihexidine and minocycline-rifampin (CH-MR). CH-MR coating was shown to provide better protection against methicillin-resistant S. aureus, P. aeruginosa, and Candida spp. and a prolonged antimicrobial durability than CH/SS and MR coatings. ... 

Riedel DJ, Weekes E, Forrest GN. Addition of rifampin to standard therapy for treatment of native valve infective endocarditis caused by Staphylococcus aureus. Antimicrob Agents Chemother 2008 52(7) 2463-7. 

Exit site infections are common and are recognized by redness, exudation and crusting. Topical agents applied to catheter exit site, such as povidone iodine, mupirocin, bacitracin zinc and polymixin B sulphate ointments have been proven effective [20, 21]. Oral rifampin or nasal mupirocin ointment reduced the incidence of S. aureus bacteremia [22]. 

A potential case of an interaction between quinidine and flucloxacillin was demonstrated in a 63-year-old patient with recently diagnosed dilated cardiomyopathy who was admitted to the hospital with polymorphic ventricular tachycardia and ventricular fibrillation episodes induced by bradycardia. The patient was on a heart failure regimen of furosemide, spironolactone and perindopril, and was initiated on oral quinidine in the hospital for the prevention of ventricular arrhythmias. The patient s temporary pacemaker lead was removed and an implantable cardioverter-defibrillator was placed due to continued ventricular fibrillation. The next day, the patient became febrile. Culture of pacemaker lead tip and blood cultures were positive for S. aureus. Flucloxacillin and rifampin were initiated, but rifampin was discontinued due to the development of renal insufficiency and liver test abnormalities. These were normalised after rifampin was discontinued. The patient required continuous pacing to prevent ventricular tachycardia episodes, and quinidine was increased to 2800 mg per day (maximum daily dose). Quinidine plasma levels were subtherapeutic at 1.1 mg/L. The authors speculate that this interaction was due to quinidine being a substrate of Pgp and CYP3A4, and flucloxacillin s ability to induce these enzymes. While this may be a potential mechanism, the authors do not comment on how long the patient received rifampin. Rifampin is also a CYP3A4 inducer and could have been parf of fhe reason for fhe decrease in quinidine level [46 ]. 

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