Title: PharmaNote
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Permanent Link: http://ufdc.ufl.edu/UF00087345/00038
 Material Information
Title: PharmaNote
Series Title: PharmaNote
Physical Description: Serial
Creator: University of Florida College of Pharmacy
Publisher: College of Pharmacy, University of Florida
Publication Date: February 2006
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Bibliographic ID: UF00087345
Volume ID: VID00038
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Kevin Scharfman, Pharm.D. Candidate

In the early 1940s, the discovery of penicillin
was seen as the beginning of a new era in the treat-
ment of infectious diseases. One year after its intro-
duction, the first isolates of penicillin resistant
Staphylococcus aureus were reported by Rammel-
kamp.1 In 1944, the first description of penicillinase-
producing strains of S. aureus was published. Peni-
cillin-resistance was a rapidly growing problem and
by the 1950s, penicillinase-resistant strains were
common in hospitals throughout the world. Commu-
nity strains were still largely susceptible to penicil-
lin.2 By the 1960s, penicillinase-resistant S. aureus
was as equally prevalent in the community as it was
in hospitals.3
In 1961, a new penicillinase-resistant semi-
synthetic penicillin, methicillin, was introduced. Not
surprisingly, less than a year later, methicillin-
resistant S. aureus (MRSA) was reported.3 MRSA
was a hospital-based problem, especially in intensive
care units (ICU) until the early 1980s. Like penicillin
resistant strains of S. aureus, MRSA eventually
emerged in the community. In 1982, the first case of
MRSA was reported outside of the hospital among

intravenous drug abusers.3 Over the past decade, the
emergence of community-associated MRSA (CA-
MRSA) has become a topic of much concern. The
initial belief that CA-MRSA originated from MRSA
that left the hospital has been challenged by the dis-
covery of novel strains of MRSA, genetically differ-
ent from hospital-acquired strains.1 9
Currently, more than 50% of S. aureus isolates in
hospitals (even higher in intensive care units) are
methicillin-resistant and prevalence in the commu-
nity is rising.2'9'10 Failure to appreciate CA-MRSA
as an evolving problem can lead to suboptimal pa-
tient care and contribute to the rapidly growing an-
timicrobial resistance problem. Fluoroquinolone use
has been attributed to the increase in MRSA isolates.
The growing problem of resistance is compounded
by the fact that there are very few new antibiotics in
the approval process. Spellberg et al noted that new
antibacterial agents constitute 6 of 506 drugs in the
developmental process.21 With few new drugs and
growing resistance problems, physicians are running
out of options. Some old and nearly obsolete antibi-
otics are re-emerging and proving beneficial when
used synergistically in the treatment of certain infec-
tions like CA-MRSA. In this article, pertinent litera-
rIa U I






Volume 21, Issue 5, February 2006


Table 1: Clinical Trial Summaries.
Author Design Infection (n) Treatment Outcome

Markowitz et al.2


S. aureus bacteremia

TMP 320mg/SMX 1600mg IV
101 2h or Vancomycin g q
q12h or Vancomycin 1g q12h

Overall cure rate= 86%
with TMP/SMX and 98%
with vancomycin (p<0.02)

Skin/soft tissue, arthri-
tis, meningitis, pros-
P/O thetic valve endocardi-
tis, spondylodiskitis
with abscess.


Skin and soft tissue

TMP 320-480mg/SMX 1600-
2 2400mg/day (divided) +/- Ri-
fampin (8) or PenG or Metroni-
dazole (5)

TMP/SMX, Rifampin, Clinda-
39 mycin, Vancomycin, Linezolid,

Overall cure rate= 96%

Complete response
with TMP/SMX + Ri-
fampin (6/6), Clindamycin
(1/1), Vancomycin (5/5),
Linezolid (11/11), Mupi-
rocin (3/3), Moxifloxacin
(9/16), TMP/SMX (6/12).

Aguilar et al.26

Bacteremia, osteomye-
R/R litis, septic arthritis,
pneumonia, lymphade-
nitis, and others

Clindamycin 30-40mg/kg/
day divided q8h (46)
46 [Clindamycin only (20), Vanco-
mycin initially (18), beta-
lactam initially (8)] Vancomy-
cin only (6)

Cure or clinical improve-
ment in 45 of 46 patients
treated with clindamycin.

Skin and soft tissue

Ruhe et al.15

Clumeck et al.20

Pneumonia, osteomye-
LR litis, skin and soft tis-
sue, and endocarditis.

Severe S. aureus infec-

Doxycycline or Minocycline
100mg PO bid

S Long acting tetracyclines +/-

Rifampicin 600mg/day + mino-
25 cycline 200 or 400mg/
day administered IV or PO bid.

Overall clinical success
rate= 83%

Overall cure rate= 85%

Mean duration tx = 22
days. Overall cure rate=
76%, clinical improve-
ment= 4%, failure= 20%

Ra=randomized; R=retrospective; P=prospective; LR=literature review; CS=case series; O=observational; CR=chart review; C=comparative; DB=double blind

ture is reviewed with respect to the prevalence, iden- generally linked to hospital contact.3 Recently, re-
tification, and proper treatment of CA-MRSA as it searchers have identified novel strains of CA-MRSA
differs from hospital-acquired strains, that are genetically unique and exhibit characteristic
traits. These new strains differ in their epidemiology,
The New Isolate and Resistance resistance phenotype, and clinical virulence.
MRSA was once believed to only be a hospital-
acquired pathogen and cases in the community were

PharmaNote 45 Volume 21, Issue 5, February 2006

Jemni L.13

Iyer et al.22

Figure 1. Example of Positive D-Test.


C= clindamycin-impregnated disk. E= erythromycin-impregnated disk.
Blunting of the zone of inhibition (shaded area in figure) denotes presence of
inducible erm gene. Though isolate may be reported as susceptible, induction of
erm can result in MLSBi phenotype and in vivo clindamycin resistance.

Methicillin-resistance is carried chromosomally by
the mecA gene. The mecA gene enters a cassette
called the staphylococcal chromosomal cassette
(SCC) that is incorporated into chromosomes. To
date there are five SCCmec types.8 Types I-III are
common in hospital-acquired strains. Type IV and
the more recently discovered type V strains have a
community-based origin. Unlike multi-drug resistant
hospital-acquired methicillin-resistant staphylococ-
cus aureus (HA-MRSA) strains, CA-MRSA resis-
tance is usually limited to p-lactam antimicrobials.3
Another distinguishing feature of CA-MRSA is the
presence of numerous exotoxin virulence factors, most
notably the Panton-Valentine leukocidin (PVL)
toxin. The PVL toxin is lethal to neutrophils and is
associated with skin necrosis.3'6 These virulence fac-
tors are believed to be the cause of the increasing
number of CA-MRSA skin and soft tissue infections,
and less commonly necrotizing pneumonia. Also, the
presence of toxins appears to increase the likelihood
that colonized patients will progress to infection
(compared with HA-MRSA). Fluoroquinolone use
has been identified as a reason for the increase in
MRSA infections. A case control study of 121 pa-
tients with MRSA found that levofloxacin use was
independently associated with MRSA infections (OR
8.01).14 Fluoroquinolones are more active against
MSSA than MRSA, thus fluoroquinolone exposure
exerts a selective pressure for MRSA. As methicil-
lin-susceptible S. aureus (MSSA) isolates are sup-

pressed, MRSA persists and may colonize or infect
the 'space' once occupied by MSSA.4'14

Clinical Presentation
CA-MRSA cases generally lack traditional risk
factors associated with MRSA infections. However,
increased outbreaks and persistent transmission have
been documented in various groups including Alas-
kan natives, Native Americans, Pacific Islanders,
correctional facility inmates, competitive sports par-
ticipants, children in day care centers, homeless per-
sons, IV drug users, men who have sex with men,
and military personnel.3'7 Community-associated
strains are less frequently associated with endocardi-
tis, bacteremia, sinusitis, and brain abscesses when
compared to hospital-acquired strains. CA-MRSA
primarily causes skin and soft tissue infections
(abscesses, cellulitis, furunculosis, impetigo, infected
wounds), but has been associated with severe ne-
crotizing pneumonia, fascitis, myositis, osteomye-
litis, and prosthetic joint infections.3'5 Insect and spi-
der bites can also be mistaken for CA-MRSA infec-
tions due to the presence of a central necrotic region
associated with skin lesions.

Treatment Considerations
The selection of initial antibiotic regimens should
be guided by the prevalence of CA-MRSA in the
community, presence or absence of health-care asso-
ciated risk factors, severity and type of clinical pres-
entation, and patient specific factors. When consider-
ing probable pathogens, it is important to consider if
the patient has an abscess, diabetes mellitus, recent
use of antibiotics, a recent hospital stay, close con-
tact with hospitalized patient or day care, or is im-
munocompromised. Patient allergies and renal/
hepatic function should be evaluated as well.
When CA-MRSA is suspected, it is important to
obtain culture and sensitivity reports. The sensitivity
of community and hospital strains differ greatly.
Unlike multi-drug resistant hospital-acquired strains,
CA-MRSA is generally susceptible to non-p-lactam
antibiotics. There are several treatment options avail-
able; however, many have not been clinically tested
and efficacy data is often not available.8 TMP/SMX
(Bactrim, Septra), clindamycin (Cleocin), doxy-
cycline (Adoxa, Doryx), minocycline (Dinacin,
Minocin), and rifampin (Rifadin) have in vitro ac-
Incision and drainage should be performed and

PharmaNote Volume 21, Issue 5, February 2006

Volume 21, Issue 5, February 2006


Table 2. Summary of Treatment Options for CA-MRSA.




Inhibits bacterial
folic acid synthesis

PO: TMP 320mg
SMX 1600mg ql2h
(divided ql2h)

Inhibits bacterial
protein synthesis

PO: 150-450mg
IV/IM: 300mg q6,
q8, or ql2h


Inhibit bacterial
protein synthesis

PO: 100mg ql2h

Inhibit bacterial
protein synthesis

PO: 100mg ql2h


Inhibits bacterial
RNA synthesis

PO: 300-600mg
(never as mono-

Adverse Drug

GI distress, photo-
(avoid if sulfa-

GI distress,

GI distress, photo- GI distress, photo-
sensitivitGI distress, photo-ivity

Reddish orange/
brown urine, sa-
liva, sweat, tear
(bodily fluid),
flu-like syndrome

*dosing based on Trimethoprim component.

cultures analyzed when appropriate.3 There has been
controversy about whether incision and drainage of
cutaneous abscesses without antibiotic therapy is suf-
ficient. A recent review noted small (<5cm) cutane-
ous abscesses without cellulitis or systemic symp-
toms can be treated with incision and drainage alone
with close follow up.3 However, this strategy has
been challenged.
A handful of small, nonrandomized studies have
reported results of CA-MRSA treatment strategies.
(Table 1) Lee et al conducted a prospective observa-
tional study to determine if incision and drainage of
abscesses, without antibiotic use, is adequate therapy
in CA-MRSA skin and soft tissue infections.24 Sixty-
nine children were identified with positive MRSA
cultures. All abscesses were drained and initial anti-
biotics were started before culture results were
known. Fifty-two patients received cephalexin, 7 re-
ceived amoxicillin/clavulanate, 5 received clindamy-
cin, and 1 patient received TMP/SMX with rifampin.
Two patients never filled their prescriptions. Thirty-
seven patients were on an ineffective antibiotic based
on culture results and never had their antibiotic
changed. Of these 37 patients, 31 improved, 1 dete-
riorated, and 5 had no follow-up. The study con-
cluded that incision and drainage without adjunctive
antibiotic therapy was effective management of CA-
MRSA skin and soft tissue abscesses with a diameter
of <5 cm in immunocompetent children. Abscesses
with a diameter of>5 cm were identified as a signifi-

cant predictor of hospitalization (p=0.004). It is not
clear from these results whether incision and drain-
age alone was sufficient or if the antibiotics were ef-
fective despite in vitro susceptibility results suggest-
ing resistance.
Severe or life threatening infections should be
treated with empiric vancomycin (Vancocin), line-
zolid (Zyvox), quinipristin-dalfopristin (Synercid),
or daptomycin (Cubicin) when C/S reports are
pending.8'9 Daptomycin should be limited to resistant
skin and soft tissue infections because it is inacti-
vated by surfactant and has no indication in the treat-
ment of pneumonia. In areas with a low prevalence
of CA-MRSA or if suspicion for CA-MRSA is low,
patients with less severe infections can be initially
treated with a penicillinase-resistant penicillin like
oxacillin, nafcillin (Nallpen, Unipen), dicloxacillin
(Dycill", Pathocil) or a first generation cepha-
losporin like cefazolin (Ancef') or cephalexin
The Infectious Diseases Society of Washington
and the Washington State Health Department pub-
lished interim guidelines for evaluation and manage-
ment of CA-MRSA skin and soft tissue infections in
the outpatient setting.23 They recommend empiric
therapy be guided by local S. aureus susceptibility
and be modified based on culture and sensitivity re-
sults. For susceptible CA-MRSA infections, recom-
mended treatment includes TMP/SMX 160 mg/800

PharmaNote Volume 21, Issue 5, February 2006

Volume 21, Issue 5, February 2006


mg by mouth twice daily, minocycline or doxycy-
cline 100 mg by mouth twice daily, or clindamycin
300-450 mg by mouth four times daily. Duration of
treatment for most infections is 7-10 days, but varies
depending on severity of infection and clinical re-
sponse. The use of fluoroquinolones is not recom-
mended for treatment of MRSA in most areas due to
high resistance rates and their role in MRSA selec-
TMP/SMX has become a viable option for the
treatment of CA-MRSA. The combination drug in-
hibits two steps in the biosynthesis of folic acid,
which render it bactericidal against most pathogens.
TMP/SMX has excellent oral bioavailability, is inex-
pensive, has been used for decades, and carries an
abundance of safety data.5 Many physicians are fa-
miliar with TMP/SMX in the treatment of urinary
tract infections and often under-dose the medication
when treating CA-MRSA. Although strong double-
blinded, randomized controlled trials are lacking,
there are many published articles supporting its use
in this setting. 10,12
Markowitz et al performed a randomized, dou-
ble-blind comparative trial evaluating 101 intrave-
nous drug abusers hospitalized for S. aureus infec-
tions.12 Forty-three patients received TMP 320 mg/
SMX 1600 mg IV every 12 hours (10 mg/kg/day
based on trimethoprim component) and 58 patients
received vancomycin Ig IV every 12 hours. The
overall cure rate was 86% in the TMP/SMX group
and 98% in vancomycin group (P < 0.02). Treatment
failure occurred in 4 patients with tricuspid valve
endocarditis and in 2 patients with infections caused
by MSSA (1 developed septic arthritis, 1 had a pseu-
doaneurysm relapse). This study concluded that
TMP-SMX may be considered as an alternative to
vancomycin in non-life threatening MRSA infec-
Iyer and Jones conducted a retrospective chart
review of 39 patients who were evaluated and treated
for a positive MRSA skin infection.2 Twenty pa-
tients were HIV positive and 19 were previously
healthy with no comorbidities. All patients were
treated with antimicrobial therapy and patients who
presented with abscesses were also treated with inci-
sion and drainage. Twelve of the 39 patients were
treated with TMP/SMX and 6 achieved prompt reso-
lution. Rifampin was added to TMP/SMX in the
other 6 patients and produced successful eradication
of the MRSA infection. Patients treated with vanco-

mycin, linezolid, mupirocin, and clindamycin all
achieved complete responses. Only 9 of 16 patients
treated with moxifloxacin (Avelox) received com-
plete responses. The author concluded that treatment
with TMP/SMX in combination with rifampin led to
a lower recurrence and better response rates when
compared to TMP/SMX alone.
In another study, 27 patients with MRSA infec-
tions were treated with TMP/SMX.13 The infections
consisted of 15 soft tissue infections, 4 bacteremias,
2 arthritis, 1 meningitis, 1 prosthetic valve endocar-
ditis, and 1 spondylodiskitis with abscess. The daily
doses of TMP/SMX ranged from TMP 320-480mg
and SMX 1600-2400mg. TMP/SMX plus rifampin
was used in 8 patients and TMP/SMX plus penicillin
G and/or metronidazole was used in 5 patients with
polymicrobial soft tissue infections. Overall cure rate
was 96%. The study concluded that TMP/SMX con-
stitutes an effective alternative for treatment of
MRSA infections.
Clindamycin is an option for CA-MRSA infec-
tions. It is a bacteriostatic agent that inhibits protein
synthesis by binding to the bacterial ribosomal 50S
subunit. It has good penetration into skin and soft
tissue. It has activity against gram-positive bacteria
as well as anaerobes. Clindamycin is a reasonable
option for treatment of diabetic patients as well as
patients with abscesses due to the increased likeli-
hood of anaerobic organisms. It is a good option for
patients with a sulfa-allergy who are unable to take
TMP/SMX. Clindamycin is relatively inexpensive,
available in intravenous and oral formulations, and
may be able to inhibit production of toxins and viru-
lence factors associated with CA-MRSA.11 One po-
tential disadvantage of clindamycin use is its associa-
tion with Clostridium difficile colitis, though this
complication can occur with any antibiotic.
There are reported treatment failures with clinda-
mycin from an inducible resistance mechanism. Clin-
damycin resistance is attributed to modification of
the drug-binding site (the ribosome) caused by me-
thylation. This mode of inducible resistance is
termed MLSBi. Its presence renders macrolides, lin-
cosamides, and group B streptogrammins ineffective.
MLSBi genes encode methylation of the 23S ribo-
somal subunit, which is a binding site for the three
drug classes previously mentioned. MLSBi resis-
tance is not often detected by standard laboratory
testing methods. When culture and sensitivity reports
show erythromycin resistance, but clindamycin sus-

PharmaNote Volume 21, Issue 5, February 2006

Volume 21, Issue 5, February 2006


ceptibility, further analysis is warranted. A double-
disk diffusion test (D-test) can be used to differenti-
ate between clindamycin susceptibility and inducible
resistance via the MLSBi mechanism. A positive D-
test is indicated when MLSBi gene is present and the
clindamycin zone of inhibition is blunted on the side
nearest the erythromycin disk.1 The zone of inhibi-
tion of clindamycin will be shaped like a D. (See
Figure 1) The presence MLSBi indicates a signifi-
cant risk for clinical failure and clindamycin should
not be used.
Martinez-Aguilar et al conducted a retrospective
chart review to compare clindamycin efficacy in
MRSA and MSSA isolates in children.26 Thirty-nine
of 46 patients with MRSA received clindamycin plus
incision and drainage. Twenty patients received clin-
damycin only, 18 received vancomycin initially, and
8 received a beta-lactam initially. Cure or clinical
improvement was seen in 45 of 46 patients with
MRSA, which was not a statistically significant dif-
ference when compared to MSSA isolates. The study
concluded that clindamycin was effective in treating
infections caused by susceptible CA-MRSA isolates
in children.
Long-acting tetracyclines, minocycline and doxy-
cycline, have been used in the management of
MRSA infections. Minocycline and doxycycline
bind to the 30S and possibly the 50S ribosomal sub-
units and inhibit bacterial protein synthesis. They
may also cause alterations in the cytoplasmic mem-
branes. These drugs are bacteriostatic, have good ab-
sorption, and excellent tissue penetration. They have
superior anti-staphylococcal activity when compared
to tetracycline.15
The SENTRY Antimicrobial Surveillance Pro-
gram evaluated the frequency of occurrence and an-
timicrobial susceptibility of isolates collected in the
US, Canada, Latin America, Europe, and the West-
ern Pacific Region.16 In the US, the following MRSA
resistance rates were reported for nosocomial iso-
lates: 89% to ciprofloxacin, 93% to erythromycin,
79% to clindamycin, and 26% to TMP/SMX. Resis-
tance to tetracycline was only 16%. Double-blinded
randomized controlled trials are lacking, but a recent
case series and review reported that long-acting tetra-
cyclines may be a reasonable treatment alternative
for patients with certain types of MRSA infections. 15
The case series reviewed medical records of adult
patients treated with doxycycline or minocycline for
tetracycline susceptible MRSA infections. Medical


records were reviewed over a 5.5-year period and
3739 MRSA specimens were isolated. A total of 45
patients were treated with doxycycline or mino-
cycline 100 mg BID, but only 24 patients were in-
cluded in the study. The overall clinical success rate
was 83%. In a literature review, a total of 85 patients
from 9 studies were identified as being treated for
MRSA infections with long-acting tetracyclines with
or without rifampin.15 The infections included pneu-
monia, osteomyelitis, skin and soft tissue infections,
and endocarditis. The overall cure rate was 85% (72
of 85 patients). The majority of clinical failures oc-
curred in more severe infections including endocar-
ditis and osteomyelitis.
Rifampin has been used synergistically in the
treatment of MRSA infections. Rifampin should
never be used as a single agent due to the rapid de-
velopment of resistance.17 Rifampin inhibits bacterial
RNA synthesis by binding to the DNA-dependent
RNA polymerase and blocking RNA transcription.
Rifampin is dosed 300-600mg PO ql2h when used
as synergy with other antibiotics.25 The SENTRY
Antimicrobial Surveillance Program showed an 8%
resistance rate to MRSA.16 Rifampin has activity
against staphylococci in the stationary-phase and the
ability to eliminate intracellular staphylococcus.5
There is very little data supporting the use of ri-
fampin in the treatment of CA-MRSA. This treat-
ment option was adapted from the use of rifampin
with ciprofloxacin in staphylococcal orthopedic de-
vice infections and prosthetic valve endocarditis.5 In
a randomized controlled trial by Zimmereli et al,
ciprofloxacin plus rifampin was compared to cipro-
floxacin alone.18 Of the 24 patients that completed
the trial, 100% of patient in the ciprofloxacin plus
rifampin group and 58% of patients in ciprofloxacin
monotherapy group achieved clinical cure.
Iyer and Jones, in a retrospective chart review,
concluded that TMP/SMX in combination with ri-
fampin was a viable first-line agent in the treatment
of MRSA infections.22 The regimen was given to pa-
tients who did not respond to TMP/SMX monother-
apy and it resulted in complete responses in all 6 pa-
tients. Treatment options for CA-MRSA are summa-
rized in Table 2.

Prevention and Decolonization
Data regarding prevention of CA-MRSA is lim-
ited, but basic infection-control principles should al-
ways be used. Personal hygiene should be stressed,

Volume 21, Issue 5, February 2006

including daily showers, use of antibacterial soap,
hand sanitizer, and coverage of any open or draining
lesions.3 Limiting inappropriate antimicrobial use
may be beneficial in preventing MRSA outbreaks.
MRSA decolonization has been attempted to
eradicate and prevent outbreaks. Universal decoloni-
zation of CA-MRSA is not recommended due to lack
of compelling outcomes data; however, it may be
beneficial in patients with recurrent disease, within
families, or among discrete patient populations. Vari-
ous methods of decolonization have been attempted
using combinations of systemic and topical antibiot-
ics including TMP/SMX, tetracyclines, or clindamy-
cin each with or without rifampin, mupirocin, and
chlorhexidine body washes.3 Currently, no one regi-
men is preferred.
The Infectious Diseases Society of Washington
and the Washington State Health Department state
the efficacy of decolonization in the outpatient set-
ting is not routinely recommended.23 They recom-
mend consultation with an infectious disease special-
ist before attempting. The interim guidelines state it
is reasonable to consider decolonization for patients
with recurrent MRSA infections despite appropriate
therapy and MRSA infections with ongoing trans-
mission in a well-defined cohort with close contact.
Decolonization regimens listed include rifampin
300mg bid for 5 days in combination with TMP/
SMX, doxycycline, or minocycline. Another regimen
includes topical intranasal mupirocin used bid for 5
days with or without systemic antimicrobial therapy.
Skin antisepsis with chlorhexidine or other agents
may also be used in addition to one or both of the
above regimens.
Parras et al evaluated MRSA decolonization
from the nasal and extranasal carriage using mupiro-
cin vs. oral co-trimoxazole plus fusidic acid.19 These
regimens were administered during a 5-day period
and were combined with daily or twice daily chlor-
hexidine soap baths. The efficacy and safety of both
regimens were similar and at the end of treatment,
100% of patients had complete eradication of nasal
MRSA. Mupirocin proved to be very effective in this
study. Resistance to mupirocin has been demon-
strated in MRSA, but its effect on CA-MRSA is un-

The emergence of CA-MRSA in the community
leaves practitioners with fewer viable treatment op-

tions in the community. Luckily, CA-MRSA strains
are currently not multi-drug resistant and can be ef-
fectively treated with several oral antibiotic regi-
mens, including TMP/SMX +/- rifampin, clindamy-
cin, minocycline, or doxycycline. Vancomycin, line-
zolid, and other similar drugs should be reserved for
severe or life threatening infections. Abscesses
should be routinely drained and cultured. Decoloni-
zation should not be routinely performed, but may be
valuable in select instances. The incidence of CA-
MRSA is increasing and it is imperative for practitio-
ners to identify these infections and treat them appro-

1. Deresinski S. Methicillin-resistant Staphylococ-
cus aureus: An Evolutionary, Epidemiologic,
and Therapeutic Odyssey. Clin Infect Dis
2. Chambers, Henry F. The Changing Epidemiol-
ogy of Staphylococcus aureus? Emerg Infect Dis
3. Kowalski, Todd J. Epidemiology, Treatment,
and Prevention of Community-Acquired Methi-
cillin-Resistant Staphylococcus aureus Infec-
tions. Mayo Clin Proc 2005;80:1201-8.
4. MacDougall et al. Pseudomonas aeruginosa,
Staphylococcus aureus, and Fluoroquinolone
Use. Emerg Infect Dis 2005; 11:1197-1204.
5. Ellis, Michael W. and Lewis II, James S. Treat-
ment approaches for community-acquired me-
thicillin-resistant Staphylococcus aureus infec-
tions. Curr Opin Infect Dis 18:496-501.
6. Francis et al. Severe Community-Onset Pneu-
monia in Healthy Adults Caused by Methicillin-
Resistant Staphylococcus aureus Carrying the
Panton-Valentine Leukocidin Genes. Clin Infect
Dis 2005;40:100-7.
7. Weber, Todd J. Community-Associated Methi-

cillin-Resistant Staphylococcus aureus. Clin In-
fect Dis 2005;41:S269-72.
8. Rybak, Michael J. and LaPlante, Kerry L. Com-
munity-Associated Methicillin-Resistant
Staphylococus aureus: A Review. Pharmaco-
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9. Zetola et al. Community-acquired methicillin-
resistant Staphylococcus aureus: an emerging
threat. Lancet Infect Dis 2005;5:275-86.
10. Grim et al. Trimethoprim-Sulfamethoxazole as a
Viable Treatment Option for Infections Caused

Phrm~oe olme21 Isu 5 Fbrar 20

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by Methicillin-Resistant Staphylococcus aureus.
Pharmacotherapy 2005;25:253-64.
11. Lewis II, James S. and Jorgensen, James H.
Inducible Clindamycin Resistance in Staphylo-
cocci: Should Clinicians and Microbiologists
be Concerned? Clin Infect Dis 2005;40:280-5.
12. Markowitz et al. Trimethoprim-
Sulfamethoxazole Compared with Vancomycin
for the Treatment of Staphylococcus aureus
Infection. Ann Intern Med 1992; 117:390-98.
13. Jemni, L. Efficacy of trimethoprim-
sulfamethoxazole against clinical isolates of
methicillin-resistant Staphylococcus aureus: a
report from Tunisia. Clin Infect Dis
14. Graffunder, Eileen M. and Venezia, Richard A.
Risk factors associated with nosocomial methi-
cillin-resistant Staphylococcus aureus (MRSA)
infection including previous use of antimicrobi-
als. Journal of Antimicrobial Chemotherapy
15. Ruhe et al. Use of Long-Acting Tetracyclines
for Methicillin-Resistant Staphylococcus
aureus Infections: Case Series and Review of
the Literature. Clin Infect Dis 2005;40:1429-
16. Diekema et al. Survey of Infections Due to
Staphylococcus Species: Frequency of Occur-
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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

Benjamin J. Epstein Assistant Editor
Pharm.D., BCPS

IPharLm Volume 21r Issue5,WFebrar1200

Volume 21, Issue 5, February 2006


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