Title: PharmaNote
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Permanent Link: http://ufdc.ufl.edu/UF00087345/00042
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Title: PharmaNote
Series Title: PharmaNote
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Creator: University of Florida College of Pharmacy
Publisher: College of Pharmacy, University of Florida
Publication Date: July 2006
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Volume ID: VID00042
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Amy Bittle, Pharm.D. Candidate

Microbial resistance to antibiotics represents
one of the most common reasons for the failure to
cure an infection. Methicillin-resistant S. aureus
(MRSA), first detected after the introduction of me-
thicillin in the early 1960's, has emerged as the most
commonly identified antibiotic resistant pathogen in
hospitals across the United States.1 According to the
Centers for Disease Control and Prevention, the
prevalence of MRSA was 57% in US intensive care
units in 2002; this represents an increase of 30-40%
from the mid-1990s.2 MRSA is not strictly a nosoco-
mial pathogen; many genetically distinct strains have
now been identified in the community among healthy
patients without predisposing factors for MRSA ac-
quisition.1 The high incidence and continuously
growing rate of hospital-acquired (HA) MRSA and
now community-acquired (CA) MRSA is a major
threat and poses a difficult challenge for health-care
MRSA is one of the leading pathogens found
in both nosocomial pneumonia and skin and soft tis-
sue infections (SSTIs).3 The prevalence of MRSA in
ventilator-associated pneumonia (VAP) constitutes
about 50% of the episodes caused by S. aureus.4
Hospital-acquired Pneumonia (HAP) is estimated to

account for almost half of infections found in the
ICU and approximately 60% of deaths from nosoco-
mial infections.5 Skin and soft tissue infections are
another significant cause of morbidity and mortality
in hospitals. Reports from the SENTRY Antimicro-
bial Surveillance Program reported a methicillin re-
sistance rate of 30% among S. aureus isolates in the
United States between 1997 and 1999 in skin and
soft tissue infections.6 Methicillin resistance in S.
aureus confers resistance to B-lactams, in addition to
macrolides, fluoroquinolones, tetracyclines, linco-
samides, and aminoglycosides. 3 Treatments effective
against MRSA include quinupristin/dalfopristin, dap-
tomycin, oritavancin, and tigecycline. Vancomcyin
has been the traditional drug used for nosocomial
pneumonia or complicated skin and soft tissue infec-
tions (cSSTIs) caused by gram-positive resistant or-
ganisms.3 Linezolid, an alternative agent, has gener-
ally been reserved for the treatment of serious infec-
tions due to its high cost and hematologic concerns.
The purpose of this paper is to compare the efficacy,
tolerability, and cost of vancomycin and linezolid in
the treatment of nosocomial pneumonia and skin and
soft tissue infections caused by MRSA.

rIa U I




Linezolid vs. Vancomycin: An Evaluation in the
Treatment of Skin and Soft Tissue Infections and
Hospital-Acquired Pneumonia Caused by
Methicillin-Resistant S. aureus (MRSA)


Volume 21, Issue 10, July 2006


Vancomycin is a glycopeptide used to treat
serious infections caused by gram-positive bacteria.
After increasing resistance rates to oxacillin and the
introduction of MRSA, the use of vancomycin in
clinical practice skyrocketed.8 Vancomycin inhibits
cell wall synthesis by binding to the D-alanlyl-D-
alanine C-terminus of the nascent murein monomer,
inhibiting peptidoglycan synthesis.9 Vancomycin is
slowly bactericidal, with the degree of killing de-
pendent upon the time that the serum concentration
is above the organism's minimum inhibitory concen-
tration (MIC). Vancomycin does not exhibit a post-
antibiotic effect. In vitro studies demonstrate that
vancomycin exhibits slower bactericidal activity
compared to B-lactams in methicillin-susceptible S.
aureus.7 The concentration of vancomycin required
to inhibit most strains of S. aureus is typically be-
tween 0.5 and 2 mg/L. According to the Clinical and
Laboratory Standards Institute (CLSI), S. aureus iso-
lates with vancomycin MICs of 4 mg/L or less
should be considered susceptible, isolates with van-
comycin MICs between 8 and 16 mg/L are vancomy-
cin-intermediate, and isolates with vancomycin
MICs > 32 mg/L are considered vancomycin-
resistant.10 The emergence of S. aureus strains inter-
mediate or resistant to vancomycin has led to many
treatment failures.
Some pharmacokinetic properties of vanco-
mycin have contributed to its relatively high inci-
dence of treatment failure in VAP and SSTIs. Table
1 shows the clinical success rates of vancomycin in
various studies.11-14 Vancomycin has poor tissue
penetration, especially into the lungs.15 Concentra-
tions of vancomycin in the epithelial lining fluid
(ELF) do not reach 20% of the plasma concentra-
tion.16 In a study by Cruciani et al., an intravenous
(IV) infusion of 1 g of vancomycin over 1 h failed to

achieve sustained lung concentrations above the MIC
for susceptible S. aureus over a 12 h dosing inter-
val.17 The difficulties in obtaining adequate local se-
rum concentrations have led to higher doses and in-
tense pharmacokinetic monitoring to improve effi-
cacy and avoid toxicity. Studies have evaluated the
potential of higher trough concentrations of 15-20
mg/L to enhance efficacy with vancomycin. A con-
tinuous IV infusion of vancomycin has also been
studied. However, there is no clear consensus in the
literature supporting elevated trough concentrations
of 15-20 mg/L or continuous IV infusion. Higher
trough concentrations of vancomycin may increase
the risk of nephrotoxocity, particularly if the patient
is also receiving aminoglycosides.18
Vancomycin's high molecular weight con-
tributes to poor oral absorption. Therefore, vancomy-
cin must be administered IV for systemic infections.
IV access typically requires hospitalization and is
associated with additional resources and increased
costs. It also enhances the risk of phlebitis, puncture
accidents, as well as catheter-related and hospital-
acquired bloodstream. 3

An emergence of staphylococci intermediate
or resistant to vancomycin has led to failures in noso-
comial pneumonia and SSTIs caused by MRSA. The
first clinical isolate of S. aureus with reduced suscep-
tibility to vancomycin was reported in 1997 from
Japan. These isolates were known as vancomycin-
intermediate S. aureus (VISA), also known as glyco-
peptide-intermediate S. aureus (GISA), since MICs
ranged from 8-16 mg/L.19 VISA strains produce an
excess amount of non-cross-linked D-alanyl-D-
alanine residues, which bind to vancomycin mole-
cules and sequester them. This prevents vancomycin
from reaching its target site, leading to treatment fail-

Table 1. Clinical success of vancomycin in MRSA nosocomial pneumonia
Trials N Dose Infection Success rate
Stevens et al 220 1 g vancomycin IV q 12 h HAP 53.8%

Fagon et a112 20 1 g vancomycin IV q 12 h HAP 40%

Wunderink et al13 54 1 g vancomycin IV q 12 h HAP 35.5%

Kollef et a114 91 1 g vancomycin IV q 12 h plus aztreonam VAP 21%

N = number of patients

PharmaNote 10 Volume 21, Issue 10, July 2006

ures. VISA strains also have a thicker cell wall with
increased amounts of peptidoglycan that further ob-
structs the movement of vancomycin molecules.19
Heteroresistant VISA (hVISA) also demonstrates
decreased susceptibility to vancomycin and is con-
sidered to be a precursor to VISA. hVISA is more
common, and now accounts for up to 26% of MRSA
isolates in Japan.8 Vancomycin MICs in hVISA are
in the susceptible range (< 4 mg/L); however sub-
populations have MICs > 4 mg/L exhibiting reduced
susceptibility. There are no standardized methods to
identify hVISA, which makes predicting treatment
failures difficult. Several published studies show
vancomycin to be ineffective for hVISA strains.8
Vancomycin-resistant S. aureus (VRSA) is rare and
is defined as an MIC > 32 mg/L. To date, there have
been 4 cases of VRSA. All cases have been in the
United States with each isolate from a single patient:
2 have been from Michigan, one from Pennsylvania,
and one from New York.10 VRSA strains obtain their
resistance by conjugal transfer of plasmids contain-
ing the vanA operon from vancomycin-resistant En-
terococcus faecalis.10 Common screening methods,
such as Vitek or Microscan, are not effective, with
about two-thirds of confirmed VRSA isolates not
reliably detected by automated testing systems.10
The development of resistance to vancomycin
in S. aureus has been associated with prolonged ex-
posure to low serum concentrations of the drug.20
Physicians tend to underdose vancomycin in patients
with renal failure.18 Moise et al. found a significant
association between decreased creatinine clearance
and vancomycin treatment failure.21 The majority of
cases of VISA have occurred in patients receiving
prolonged, suboptimal, or repeated courses of van-
comcyin or in patients receiving peritoneal or hemo-
dialysis.20 In addition, a polymorphism has been
identified among VISA and hVISA strains in the ac-
cessory gene regulator (agr). The agr operon in S.
aureus controls many virulence pathways. The agr
group II polymorphism was found to be an independ-
ent predictor of vancomycin failure in patients with
MRSA infection.21

Linezolid (Zyvox), an oxazolidinone, en-
tered the US market on April 18, 2000.22 Its ability to
target both susceptible and multi-drug resistant
strains makes it a highly effective agent to treat both
HAP and CAP, as well as SSTIs. Linezolid provides

inhibitory activity against most gram-positive cocci,
such as staphylococci, streptococci, and enterococci.
This includes resistant S. pneumoniae, staphylococci
resistant to methicillin, vancomycin, and B-lactam
antibiotics, and vancomycin-resistant enterococci
(VRE).23 In vitro studies show susceptible MICs for
staphylococci are between 0.5 and 4 mg/L.24 Line-
zolid is bacteriostatic for S. aureus. Unlike vancomy-
cin, it exhibits a post-antibiotic effect of 3-4 hours.15
Linezolid exerts its antimicrobial effects by prevent-
ing formation of the 70 S initiation complex of ri-
bosomes. Because of its mechanism of action, there
is virtually no cross-resistance between linezolid and
other classes of antibiotics (lincosamides, mac-
rolides, streptogramins, and chloramphenicol) affect-
ing ribosome mediated protein synthesis.23 Resis-
tance to linezolid is extremely rare. According to the
LEADER National Surveillance Study in 2004, all
2,872 isolated organisms of S. aureus showed sus-
ceptibility to linezolid. 25
The pharmacokinetics of linezolid give it an
advantage over vancomycin. Linezolid is 100%
bioavailable and can be administered both orally and
parentally. 3 Patients can transition to oral therapy-
with no dosage adjustments, which may facilitate
earlier discharge.23 Linezolid has excellent tissue
penetration. Protein binding with linezolid is 31%,
which provides free drug concentrations of > 40 mg/
L in the ELF.15 In Conti et al., following an IV or
oral dose, plasma concentrations were 15-20 mg/L,
while bronchoalveolar lavage concentrations (BLC)
exceeded 64 mg/L.26 Metabolism of linezolid is
through non-enzymatic oxidation of the morpholine
ring and is not dependent on hepatic enzyme action.
No dosage adjustments are necessary for patients
with hepatic or renal dysfunction.23
Linezolid appears to be safe and well toler-
ated in clinical trials. Common drug-related adverse
events include diarrhea, nausea, and headache, and
are typically of limited duration. Hematologic events
(anemia, thrombocytopenia, leukopenia, and neutro-
penia) have been reported; decreased platelet counts
are often associated with prolonged treatment
courses of more than 14 days. In phase III studies,
2.4% of patients treated with linezolid and 1.5% of
patients treated with comparator drugs developed
reversible thrombocytopenia.27 Other serious adverse
effects reported with linezolid include lactic acidosis,
pseudomembranous colitis, and peripheral and optic

PharmaNote Volume 21, Issue 10, July 2006

Volume 21, Issue 10, July 2006


Table 2: Clinical trial summaries
Trial N Study Design tion Treatment Result

544 MN, R Analysis Linezolid 600 mg IV q 12 Linezolid had higher rates of clinical
Ko tal1N, (11Analysis
Kollef et a14 (91 of 2 DB, R VAP or vancomycin 1 g IV cure (62.2 vs 21.1%), survival
MRSA studies q 12 for 7-21 days plus (84.1% vs 61.1%) and eradication
cohort) aztreonam (60.5 vs 23%)

Vancomycin 1 g q 12 IV Response to treatment was higher in
Weigelt et a28 1,180 aLCCMN, cSSTI or linezolid 600 mg q 12 linezolid group (88%) compared to
PO or IV. vancomycin group (67%).

Linezolid 600 mg q 12 IV Linezolid was equal in efficacy and
Wunderink et a'13 396 RA, DB HAP or vancomycin 1 g q 12 tolerability compared to vancomy-
IV plus aztreonam for cin. Clinical cure rates (67.9%
7-21days vs 64.9%)

1,019 MN, R Analysis Vancomycin 1 g IV q 12 Clinical cure rates were higher with
(160 in
Wunderink et a129 (16 of 2 DB, Ra HAP or 600 mg linezolid IV linezolid (59% vs 35.5 %O), survival
S studies q 12 plus aztreonam analysis was 85% vs 67%

R, OL M SST Vancomycin 1 g q 12 IV Microbiological success was 87%
Weigelt et al30 135 MC or linezolid 600 mg PO/ with linezolid vs 48% with vancom-
IV q 12 for 7-21 days cyin. (CI 16.51-60.27, p=0.002)

Ra=Randomized, DB=Double-blind, R=Retrospective, OL=Open-Label, CC-Comparator Controlled, MN=Multi-National, MC=Multi-Center

Clinical Trials adverse events in the study by Weigelt et al.28 Line-
Numerous head-to-head clinical trials have zolid and vancomycin reported similar drug-related
been conducted comparing the clinical efficacy of events. In the vancomycin arm, rash, phlebitis, ana-
linezolid and vancomycin to treat both HAP and phylaxis, and drug related allergic reactions were the
cSSTIs (table 2). Wunderink et al. evaluated 1,019 most common adverse effects, while gastrointestinal
patients with suspected nosocomial pneumonia (160 disturbances (nausea, diarrhea) and thrombocyto-
patients had documented MRSA pneumonia in the penia (3.5%) occurred more frequently in the line-
MRSA subset) and randomized them to receive ei- zolid group. No difference between the two groups
their 1 g of vancomycin every 12 h or 600 mg of line-
i-> iTable 3. Comparison of adverse events
zolid every 12 h, each with aztreonam. Clinical cure -- -------
rates with linezolid were 59% vs 35.5% treated with Linezolid Vancomycin
Adverse Events N=592 (%) N=588 (%)
vancomycin (p<0.01). Kaplan-Meier survival rates Serious Adverse 1(22.1)
were 85% for linezolid vs. 67% with vancomycin Events 131(22.1) 121(20.6)
(p=0.05).13 Weigelt et al. randomized 1,180 patients Drug-Related 2 (<) 8.4)
with suspected or proven MRSA infections to re- Events
ceive vancomycin 1 g every 12 h IV or linezolid 600 Most Common events (>1%)
mg every 12 h administered either orally or IV. The Anemia 7 (1.2) 10 (1.7)
primary outcome, defined as clinical response to Diarrhea 31(5.2) 9(1.5)
treatment, was significantly higher in the linezolid Headache 10 (1.7) 4 (0.7)
group (88.6%) compared to the vancomycin group Nausea 24 (4.1) 8 (1.4)
(66.9%) at the Test of Cure (TOC) visit for MRSA Pruritis 6 (1.0) 10 (1.7)
infections (p<0.001). 28 Rash 3 (0.5) 16 (2.7)
Thrombocyto- (3.5) 0
Adverse Effects penma
Vomiting 8 (1.4) 5 (0.9)
Table 3 lists the frequency of drug related Vomiting 8 (.4) 5(0.9)
N = number of events

PharmaNote Volume 21, Issue 10, July 2006

was observed in the frequency of adverse events
leading to drug discontinuation.28

Linezolid has been avoided due its high ex-
pense. The average retail cost of Zyvox surveyed
from three local pharmacies in Gainesville is $72.78
for one 600 mg tablet. For a 1 g vial of generic IV
vancomycin, the average retail cost from local phar-
macies is $15.39. However, clinical studies demon-
strate that linezolid is more cost effective in the long
run. The oral form of linezolid has led to decreased
costs versus the intravenous administration of vanco-
mycin. Shah et al. evaluated the direct cost of vanco-
mycin in MRSA infections. After including secon-
dary expenses (monitoring, drug administration, pro-
fessional involvement, and adverse events), each
dose of vancomycin generated an estimate increase
in cost between $23 and $43.31 Clinical trials with
oral linezolid have substantially decreased hospital
costs by reducing length of stay (LOS), reducing re-
sources associated with intravenous therapy, and fa-
cilitating earlier hospital discharges. Li et al., in a
phase III, open-label, comparator-controlled, multi-
center, multinational study, randomized 230 patients
to receive linezolid 600 mg twice a day vs 1 g vanco-
mycin IV twice a day for the treatment of cSSTIs.
LOS was shorter with linezolid than vancomycin (9
vs 14 days), and the estimated odds for hospital dis-
charge in the linezolid group was 1.87 times the esti-
mated odds of discharge in the vancomycin group.32
Sharpe et al. studied 60 patients requiring surgical
intervention for MRSA infected skin lesions. Patients
were randomized to receive oral linezolid 600 mg
every 12 h or 1 g vancomycin IV every 12 h for 7-21
days. LOS was 3 days shorter with linezolid and
saved $6,438 per patient in total hospital charges.
Outpatient charges with linezolid also resulted in a
savings of $388 per patient.33

Vancomycin has remained the drug of choice
for the treatment of MRSA, particularly in hospital-
acquired pneumonia, and skin and soft tissue infec-
tions. However, due to several parameters associated
with the pharmacokinetics of vancomycin, as well as
increasing prevalence of hVISA and VISA, treatment
failures have been observed. Linezolid, which is
available orally, is very effective in treating MRSA
intermediate or resistant to vancomycin. Clinical tri-

als show linezolid to have superior clinical out-
comes, increased cost effectiveness, and favorable
tolerability compared to vancomycin.

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cus aureus: an evolutionary, epidemiologic, and therapeu-
tic odyssey. Clinical Infectious Diseases 2005; 40:562-
2. Tenover FC, Pearson, ML, et al. Methicillin-
resistance in Staphylococcus aureus. Emerg Infect Dis
2004; 10:2052-3.
3. Li, JZ, Wilke, RJ, Rittenhouse, BE, et al. Effect of
linezolid vs vancomycin on length of hospital stay in pa-
tients with complicated skin and soft tissue infections
caused by known or suspected methicillin-resistant
staphyloccoci: results from a randomized clinical trial.
Surgical Infections 2003; 4: 57-70.
4. Chastre J, Fagon JY, et al. Ventilator-associated
pneumonia. Am J Respir Crit Care Med 2002; 165:867-
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7. Jones RN, et al. Microbial features of vancomycin in
the 21st Century: minimum inhibitory concentration creep,
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8. Levine, DP, et al. Vancomycin: A history. Clinical
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9. Kitzis MD, et al. Monitoring of vancomycin serum
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PharmaNote Volume 21, Issue 10, July 2006

Volume 21, Issue 10, July 2006


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Results from a randomized clinical trial. Surgical Infec-
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The PharmaNote is Published by:
The Department of Pharmacy
Services, UF Family Practice Medical
Group, Departments of Community
Health and Family Medicine and
Pharmacy Practice
University of Florida

John G. Gums
Pharm.D. Editor

R. Whit Curry, M.D. Associate Editor

Shawn D. Anderson, Assistant Editor

101 XWK W ^ S V ^ S W^V

PharmaNote Volume 21, Issue 10, July 2006

Volume 21, Issue 10, July 2006


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