3.
5 HOURS
Continuing Education
Overview: The author describes
the all-too-common phenomenon of
inappropriate antimicrobial prescrib-
ing and the role it played in her sis-
ter’s illness and death. The author
details the ways in which bacteria
become resistant to antimicrobials,
discusses the prevalence and costs of
health care–associated infections
resulting from antimicrobial resist-
ance, and provides practical tips on
using culture-and-sensitivity reports to
ensure that patients are receiving the
appropriate antimicrobial treatments.
ajn@wolterskluwer.com
By Mary C. Vrtis, PhD, RN
Her sister’s death informs the author’s examination of
nosocomial infection, antibiotic resistance, and the impor-
tance of culture-and-sensitivity reports.
n February 24, 1997, my youngest sister, Catherine Vrtis, died
O from severe complications of infection and its treatment. Cathy
had been on peritoneal dialysis for chronic renal failure. In the
months before she died, she had been hospitalized three times
with high fevers and severe abdominal pain. She was 31 years old.
Cathy had developed renal failure at age 19 because of an unspecified
autoimmune process. The youngest of nine siblings, she was the second to
have developed renal failure: our sister Rosie had done so at age 13. By the
time we found our paternal grandfather’s autopsy report and discovered that
he too had died of autoimmune kidney disease, Rosie had already received
two transplanted kidneys—the first from our sister Donna and the second
from our sister Jeanne after the autoimmune disorder had damaged the first
transplanted kidney. (Our brother Tony also donated a kidney to Rosie at a
later date.) Even though it was clear that this was a familial disease, I donated
a kidney to Cathy when she was 22. She was 11 years younger than me, and
I loved her as if she were my own child. It was not a difficult decision: the
disease would likely recur, but my kidney could buy her some time.
Could Cathy’s death have been prevented if her clinicians had been pay-
ing more careful attention? Perhaps. Despite recurrence of the disease seven
years after the transplantation, Cathy’s overall health was very good until
October 1996. She suddenly developed severe abdominal pain and was hos-
pitalized. A culture grown from a sample of peritoneal fluid on October 18,
during Cathy’s first hospitalization, showed the presence of Escherichia coli.
The infection was attributed to contamination during peritoneal dialysis,
even though Cathy was meticulous in performing it. She was placed on iv
ciprofloxacin and released three days later to continue the antimicrobial
therapy at home, through an implanted central venous catheter. Her
abdominal pain was attributed to peritonitis, so peritoneal dialysis was
stopped and hemodialysis—through a subclavian dialysis catheter, three
times a week—was begun.
AJN ▼ June 2008 ▼ Vol. 108, No. 6 49
 On November 12 severe abdominal pain recurred,
and her fever was 103.8°F. She was hospitalized
again and continued receiving iv ciprofloxacin until
December 22, when she went home for a Christmas
celebration.
After dialysis on December 26, Cathy ran a fever
of 103.5°F and was hospitalized a third time, with
a diagnosis of sepsis. Extreme abdominal pain radi-
ated to her left shoulder. Ciprofloxacin therapy was
resumed. She had gone through several courses of
ciprofloxacin (a fluoroquinolone) over a two-month
period, and she was still ill. This should have sug-
gested to her clinicians one of two possibilities: that
the infecting organism (or organisms) had become
resistant to fluoroquinolones or that she had a con-
current infection with anaerobic bacteria, against
which fluoroquinolones have “marginal” activity.1, 2
(Intraabdominal abscesses are typically caused by a
mixture of both aerobic and anaerobic bacteria.2)
Additional cultures of peritoneal fluid, although
indicated, were not taken. A computed tomographic
(CT) scan of Cathy’s abdomen found nothing abnor-
mal. Because long-term use of intravascular catheters
and dependence on hemodialysis are two major risk
factors for catheter-related sepsis,3 her hemodialysis
catheter was replaced.
On January 20 or soon after, Cathy’s condition
deteriorated rapidly. She became hypotensive and
experienced acute respiratory distress, requiring
mechanical ventilation. According to the physician
who intubated her, the cause was an overwhelming
Gram-negative sepsis. For the third time since
November, the nephrologist refused our requests for
an infectious disease consultation because he didn’t
see the need. Therefore, additional laboratory testing
was not performed at that time. A second abdominal
CT scan was also negative. No cause for her abdom-
inal pain was identified. About two weeks later,
when Cathy’s abdominal pain was intractable
despite high doses of morphine and hydromorphone,
an exploratory laparotomy with lysis of adhesions
was performed. The surgeon said the abdominal
adhesions were so severe that the bowel was “com-
pletely glued together.” A second laparotomy was
later performed to remove recurrent adhesions; the
transplanted kidney, assumed to be infected by then,
was also removed.
Infectious disease consultation. After the first op-
eration in early February, the high fever returned and
Cathy continued to deteriorate. Finally, on February
21, at my insistence, the hospital’s infectious disease
physician was called in. (In retrospect, it’s remark-
able how difficult it was for us, Cathy’s family, to get
the nephrologist to take this obvious step. I had spo-
ken to the nephrologist on previous visits and by
phone from my home, 600 miles away. But it wasn’t
until I had come to stay with Cathy in the ICU and
made it clear that I would go in person to the hospi-
50 AJN ▼ June 2008 ▼ Vol. 108, No. 6
tal’s medical director if our demands weren’t met,
that the nephrologist consented to an infectious dis-
ease consultation.)
The consulting physician reviewed Cathy’s records
from all three hospitalizations and, within an hour,
noticed that the final culture report from October 18
showed not only E. coli but also the anaerobic organ-
ism Bacteroides fragilis. The culture-and-sensitivity
report had been sent to the nephrologist, who had
apparently overlooked or ignored this crucial piece of
information. The physician then met with Cathy
and us and reported her findings. In addition to the
chart review, she had conducted an extensive litera-
ture review and had spoken with other infection con-
trol physicians to determine whether infection with
this organism had ever been associated with peri-
toneal dialysis. Her findings suggested that peritonitis
caused by B. fragilis was always secondary to a bowel
rupture, and she concluded that Cathy’s severe pain in
October had been caused by a ruptured bowel. The
primary diagnosis had been incorrect since the first
hospitalization.
First-generation fluoroquinolones such as cipro-
floxacin, which Cathy had been given, are ineffec-
tive against most anaerobic bacteria, such as Bacter-
oides.4, 5 Metronidazole, to which B. fragilis is sus-
ceptible, was initiated by iv infusion. (Note that in
2005 Hermsen and colleagues recommended the use
of the newer broad-spectrum quinolones, levofloxacin
or moxifloxacin, in addition to metronidazole to treat
abdominal anaerobic infection.2)
The final months. Cathy spent the last two months
of her life in the hospital. Although she had an occa-
sional good day, her overall condition continued to
deteriorate because of complications of infection,
including
• systemic sepsis, caused by an unknown organism,
possibly B. fragilis.
• methicillin-resistant Staphylococcus aureus (MRSA)
bacteremia, for which she was treated with iv van-
comycin.
• systemic candidiasis, for which she needed iv
amphotericin B. (Antibiotics suppress protective
flora, allowing for an overgrowth of Candida albi-
cans, which produces hydrolytic enzymes and pro-
teinases that damage and digest human cells.)
• Stevens–Johnson syndrome, a life-threatening re-
action to antimicrobials, featuring massive skin
loss and huge, weeping wounds. This adverse
drug reaction is associated with a 5% to 15%
mortality rate.6, 7
• respiratoryfailure, secondary to acute respiratory dis-
tress syndrome, for which she required continuous
mechanical ventilation for more than one month.
• disseminated intravascular coagulopathy (DIC),
which caused bleeding at iv puncture sites and the
gums, lips, and gastrointestinal tract. (DIC occurs
when the clotting sequence is activated within the
http://www.nursingcenter.com
 blood vessels because endotoxins are released
from the cell walls of dead Gram-negative bacte-
ria.8 Because circulating clotting factors are re-
duced, bleeding from damaged tissues such as iv
insertion sites cannot be stopped.)
Two months and four operations after Cathy’s
third admission, she had massive gastrointestinal
bleeding. She bled to death, despite many transfusions.
SCOPE OF THE PROBLEM
I have no way to know whether Cathy’s life could
have been saved if a clinician had noticed the report
indicating the presence of B. fragilis. Would Cathy
have experienced the secondary Candida and MRSA
infections? Would the skin sloughing of Stevens–
Johnson syndrome have occurred if she hadn’t needed
additional antimicrobials to treat the MRSA? Would
she have spent the last month of her life on a ventila-
tor if these complications hadn’t occurred? I will never
know. Still, I can’t help but think that maybe I would
still have my sister in my life if someone had noticed
the culture report and intervened sooner.
Health care–associated infections. Data from the
National Nosocomial Infections Surveillance system
and other sources suggest that about 1.7 million
hospitalized patients in the United States developed
a health care–associated infection in 2002; those
infections caused or were associated with about
99,000 deaths.9 Urinary tract infections topped the
list, followed by surgical-site infections, pneumonia,
and bloodstream infections. Urinary tract infections
occurred in an estimated 561,667 cases (33% of the
total), and the mortality rate was 2.3% (approxi-
mately 13,088 deaths). Surgical-site infections
occurred in an estimated 290,485 cases (almost
17% of the total), and the mortality rate was 2.8%
(8,205 deaths). While there were fewer cases of
pneumonia and bloodstream infections, these condi-
tions are associated with much higher mortality
rates: an estimated 250,205 hospitalized patients
acquired health care–associated pneumonia, and
14.4% (35,967 patients) died as a direct result;
bloodstream infections, identified in 248,678 hospi-
talized patients, resulted in 30,665 deaths, a mortal-
ity rate of 12.3%.
The geriatric population is particularly at risk for
health care–acquired infections for a variety of rea-
sons (as noted by several commentators in a special
issue Emerging Infectious Diseases from the Centers
for Disease Control and Prevention; go to www.cdc.
gov/ncidod/eid/vol7no2/contents.htm). For example,
the immune response may be diminished as a result of
factors such as chronic diseases, medications, malnu-
trition, functional impairments, diminished cough
reflex, dysphagia, thinning skin, incontinence, an
enlarged prostate, or invasive devices (such as uri-
nary catheters and feeding tubes).10 Also, older adults
with diminished functional status are especially at
ajn@wolterskluwer.com
risk for infections related to complications of limited
mobility, including respiratory infections, pneumo-
nia, and infected pressure ulcers.11 As health care
delivery moves out of acute care into community-
based settings, the challenges in addressing infection
control issues are rapidly changing.12
Antimicrobial resistance. With more microor-
ganisms developing greater resistance to antimicrobial
agents, the number of deaths resulting from infection
is expected to rise. Of particular concern are those
organisms with resistance to multiple antimicrobial
medications, such as MRSA, vancomycin-resistant
enterococci (VRE), and vancomycin-resistant Staphy-
lococcus aureus (VRSA), as well as organisms that
produce extended spectrum β-lactamases (ESBLs),
such as E. coli, Klebsiella pneumoniae, and Enter-
obacter species.13-16 (ESBLs produced by these bacteria
can inactivate multiple classes of antibiotics, includ-
ing penicillins, cephalosporins, and aztreonam [Azac-
tam], by breaking down the β-lactam that interferes
with the formation of bacterial cell walls.15, 17, 18)
Costs. The numerous costs associated with antimi-
crobial resistance are borne not only by patients but
by health care organizations, insurers, the pharma-
ceutical industry, employers, and the government.
They include the costs of treatment, prevention,
research, and development of new therapeutic agents,
as well as those related to lost productivity and dimin-
ished marketability of existing medicines. The annual
cost of infection in the United States because of drug-
resistant bacteria has been estimated at $4 billion to
$5 billion.19
In terms of its effects on patients and the costs
associated with it, antimicrobial resistance is an enor-
mous problem. (For an interesting discussion of how
resistance-related costs are calculated and why better
methods are needed, see www.journals.uchicago.edu/
doi/pdf/10.1086/323758.) But how does antimicro-
bial resistance develop and how does it work?
CAUSES AND MECHANISMS OF RESISTANCE
Antimicrobials target particular microorganisms or
groups of organisms; no single antimicrobial targets
every type of infectious agent. A patient may be
receiving one or more antimicrobials, but that doesn’t
ensure that the patient’s infection is being treated.
When a microorganism is not sensitive to a particular
drug, no amount of the drug—not even a toxic
amount—will have the desired effect on the infection.
If the antimicrobial isn’t appropriate for the specific
type of infectious organism, the microorganisms will
continue to multiply, and the infection will worsen.
Whenever an antimicrobial medication is admin-
istered to treat an infectious organism, the patient’s
normal bacterial flora—which produce substances
that may inhibit or kill pathogens and which com-
pete with them for nutrients and binding sites—are
also exposed to the drug. If the normal flora are sen-
AJN ▼ June 2008 ▼ Vol. 108, No. 6 51
 Figure 1. Acquired Antimicrobial Resistance:
Three Methods of Horizontal Gene Transfer
Bacterial
plasmid donor
Resistance Dead
gene on bacterium
plasmid
(B) TRANSFORMATION
Resistance
gene
(A) CONJUGATION
(C) TRANSDUCTION
Bacteriophage
Chromosome
Bacterium
infected by Bacterium receiving
a virus resistance genes
Figure 1. Bacteria often develop resistance as a result of
mutations, but they can also acquire resistance genes from other
bacteria in a variety of ways that are known collectively as
“horizontal gene transfer.” Clockwise from upper left: (A) in con-
jugation, a resistant bacterium can directly transfer a plasmid
containing a resistance gene to an antibiotic-sensitive bacterium
through a protruding structure called a sex pilus. This process
has recently been captured on video for the first time (see
www.sciencemag.org/cgi/content/full/319/5869/1533/DC1).
(B) In transformation, a bacterium can absorb genetic material—
chromosome fragments or plasmids—from dead bacteria and
incorporate that material into its own chromosome or plasmid. If
the absorbed genetic material contains a resistance gene, the
receiving bacterium acquires resistance. (C) In transduction, a
virus known as a bacteriophage can transfer genetic material
that may include resistance genes from one bacterium to another.
The bacterium that receives this material can incorporate it into its
own chromosome or plasmid and acquire resistance.
sitive to the medication and are killed, pathogens
that are not sensitive to that medication or that have
developed mechanisms for countering its effects
then thrive.15, 20 Life-threatening superinfections—
new infections that are caused by a virus, bacterium,
or fungus different from the one that caused the ini-
tial infection—can result. For example, systemic
candidiasis—which Cathy developed—is often a
superinfection. Clostridium difficile, which thrives
as normal bowel flora are eliminated, causes severe
diarrhea and may result in pseudomembranous coli-
tis and other life-threatening complications. The
Society for Healthcare Epidemiology of America
52 AJN ▼ June 2008 ▼ Vol. 108, No. 6
has named C. difficile as the number-one cause of
nosocomial infectious diarrhea.12
How resistance develops. Bacteria that are unaf-
fected by one or more antimicrobials are said to be
resistant. Some bacteria are inherently resistant, hav-
ing evolved this trait over time by spontaneous muta-
tion and natural selection, in response to harmful
substances produced by other bacteria and fungi—in
effect, naturally occurring antibiotics. In recent
decades, many kinds of bacteria that were previously
susceptible to antimicrobials have developed resist-
ance as an adaptation to increasing amounts of
antimicrobials in their environment (human bodies
and the animals we eat). Sometimes this is caused by
spontaneous gene mutation, but at other times it
results from the transfer of genetic material from a
resistant organism to a susceptible one, which is of
special concern to clinicians. Either way, once resist-
ance develops, bacteria pass on the trait to subse-
quent generations.
In the case of mutation, more than one gene may
have to mutate for resistance to develop. According
to Tenover,
Although a single mutation in a key bacterial
gene may only slightly reduce the susceptibility
of the host bacteria to [a specific] antibacterial
agent, it may be just enough to allow its initial
survival until it acquires additional mutations
or additional genetic information resulting
in full-fledged resistance to the antibacterial
agent. However, in rare cases, a single muta-
tion may be sufficient to confer high-level, clin-
ically significant resistance upon an organism.15
As examples of those rare instances, Tenover points
to rifampin resistance in S. aureus and fluoroquino-
lone resistance in Campylobacter jejuni.
When several different bacteria or strains of bacte-
ria infect a single host, they can exchange genetic mate-
rial—and antimicrobial resistance—in several ways.
This sharing, also known as horizontal gene transfer,
occurs in at least three ways: conjugation, transfor-
mation, and transduction (see Figure 1, at left).
Conjugation. In cell-to-cell conjugation, genetic
material in the form of plasmids is transferred from
one bacterium to another. A plasmid is a circular
piece of genetic material that often carries a resist-
ance gene and is independent of the chromosomes of
the host bacterial cell. Plasmids often carry only a
few genes and can replicate themselves. A single bac-
terial cell might have one plasmid or many, and may
even have many copies of the same plasmid. When
bacterial cells conjugate, one bacterium extends a
tube called a sex pilus toward another bacterium and
penetrates it. After the plasmid copies itself, one copy
goes through the pilus to the other cell, transferring
resistance to the formerly susceptible bacterium.
In the laboratory, for example, antimicrobial re-
sistance to the fluoroquinolones has been shown to
http://www.nursingcenter.com

transfer via plasmids from K. pneumoniae to previ-
ously sensitive strains of E. coli.21 VRE also become
resistant by acquiring vanA and vanB resistance genes
from other bacteria in this manner. 22 The vanA gene
is also easily transferred through conjugal plasmid
transfer to other organisms, such as VRSA.23 The
development of the ability to produce ESBLs can also
result from the transfer of bacterial genetic material
from one kind of bacteria to another. For example,
Heritage and colleagues were able to demonstrate
the transfer of an ESBL plasmid from K. pneumoniae
to a laboratory strain of E. coli by cultivating both
organisms on the same agar plate overnight. The
plasmid conferred resistance to cephalosporins in
subsequent E. coli clones.24 All of these organisms are
becoming serious problems in health care facilities
because of cross contamination among patients, pri-
marily as a result of poor hand hygiene.16, 25
Transformation is another way for susceptible
bacteria to acquire resistance. In this case, bacteria
incorporate into their own chromosomes or plas-
mids genetic material that’s been released into their
environment by dead bacteria.15
Transduction. Even bacteria can become infected
with viruses. When a virus called a bacteriophage
infects a bacterial cell, it takes over the reproductive
mechanism of the bacterium in order to replicate its
own DNA or RNA, producing more virus particles.
If the bacterium is resistant, its resistance gene may
be incorporated into the viral genetic material in
such a way that it becomes transferable to other
bacteria that the virus may subsequently infect.
According to Tenover, however, “this is now thought
to be a relatively rare event.”15
Mechanisms of resistance. Not all antimicrobials
act in the same way to kill bacteria (see Figure 2, at
right). In response, bacteria have developed different
ways to protect themselves from the specific antimi-
crobials used to treat them (see Figure 3, page 54),
including15, 26
• inactivation or destruction of the antimicrobial
agent, usually by enzymes such as β-lactamases.
• active removal (efflux) of the antimicrobial from
the microorganism.
• changes in the cell-wall binding site that prevent
the antimicrobial from attaching to the bacterium.
• changes in the cell wall, such as thickening, that
prevent the organism from absorbing the med-
ication.
• changes in the drug target sites within the bacter-
ial cell, such as ribosomes, that prevent the antimi-
crobial from binding to them, thus interrupting
microbial metabolism.
• development of an alternative metabolic pathway
so that internal processes critical to organism sur-
vival, such as folate synthesis, are no longer affected
by the drug.
When bacteria acquire resistance through expo-
ajn@wolterskluwer.com
Figure 2. Mechanisms of Action of Antimicrobial Medications
(A) Interference with
cell wall synthesis
Antibiotic
Antibiotic
Ribosome
synthesizing
(E) Disruption protein
of membrane
structure
Antibiotic
(B) Inhibition
of protein
synthesis
Antibiotic
(D) Interference
with nucleic
acid synthesis
Antibiotic
(C) Disruption
of metabolic
pathway
Figure 2. Antimicrobial medications act on different bacteria in a variety
of ways. Clockwise from the top: (A) Some antimicrobials (including
cephalosporins, daptomycin, penicillins, and vancomycin) interfere with
cell wall synthesis; (B) others (including aminoglycosides, chloramphenicol,
clindamycin, erythromycin, and tetracyclines) inhibit protein synthesis by
bacterial ribosomes; (C) sulfonamides and trimethoprim disrupt meta-
bolic pathways; (D) fluoroquinolones and rifampin interfere with nucleic
acid synthesis; and (E) polymyxins disrupt cell membrane structure.
sure to a single antimicrobial, the organism also fre-
quently becomes resistant to other similar drugs. For
example, a microorganism that produces β-lactamase
enzymes can deactivate many antimicrobials, includ-
ing almost all cephalosporins, penicillins, and az-
treonam. Even though they may have only one
mechanism of resistance, β-lactamase producers are
multidrug resistant. Similarly, organisms that pro-
duce carbapenem-hydrolyzing enzymes will inacti-
vate both imipenem (Primaxin) and meropenem
(Merrem). Such widespread resistance creates major
obstacles to treating active infection.
REVIEWING CULTURE-AND-SENSITIVITY REPORTS
When culture-and-sensitivity testing is ordered, the
nurse or physician obtains a sample of body fluid
(such as blood, sputum, urine, or wound drainage)
from the patient and sends it to the hospital’s labora-
tory. There, the sample is incubated to see whether
any organisms present in the sample will “culture
out,” or grow. If growth occurs, tests are then per-
formed to determine which microorganisms are pres-
ent and whether the organisms will grow in the
presence of specific antimicrobials. With automated
equipment, it’s possible to have results within one
AJN ▼ June 2008 ▼ Vol. 108, No. 6 53
 Figure 3. Mechanisms of Resistance to Antimicrobial
Medications
be obtained on different dates. Make sure you
check both aerobic and anaerobic results, if both
Antibiotic
(A) Active removal were ordered.
(efflux) • When a culture is positive for a pathogen, verify
Antibiotic
(B) Changes that the physician or NP has a copy of the report—
in antibiotic
target site don’t simply fax it to the provider’s office. Call to
make sure that the report arrived and point out
(F) Antibiotic your concerns to the office staff.
altering
enzyme • If you’re sure that the physician or NP has seen
the results and you have expressed your concerns
about insensitivity or resistance but the physician
Antibiotic or NP fails to act, get further help. If you are in a
(E) Changes Plasmid Ribosome hospital, contact the infection control practitioner
in cell wall carrying (ICP). Even the smallest hospitals have ICPs. The
binding site resistance
genes ICP usually has the knowledge and the clout nec-
Antibiotic essary to address inappropriate care.
Antibiotic • If you don’t feel comfortable going to the ICP,
notify your supervisor. Your supervisor can noti-
fy the organization’s infection control department,
(D) Changes in cell
(C) Alternative the infectious disease director, or the facility’s med-
metabolic
wall permeability pathway ical director. Make sure to clearly document the
actions that have been taken.
Antibiotic • Review information on the microorganism caus-
ing the infection. If drug-resistant pathogenic bac-
teria such as MRSA, VRE, or VRSA are involved,
Figure 3. Resistance genes have developed to defend the bacterium
against the different mechanisms of antimicrobial action. For example, follow your facility’s isolation guidelines. You
they may instruct the bacterium to (A) pump out molecules of the may want to contact the ICP at your facility for
antimicrobial from the bacterial cell through a process known as efflux, more advice. Hospital ICPs typically review all
(B) change the structure of a target site such as a ribosome so that the positive culture reports, but early intervention can
antimicrobial can no longer attach to it, (C) create an alternative chem- decrease the risk of cross contamination.
ical pathway to make necessary metabolites, (D) change the perme- • Review the sensitivity data. Laboratories use sim-
ability of the bacterial cell wall so that the antimicrobial can no longer
enter the bacterium, (E) change binding sites on the cell wall so that ilar techniques and methods of reporting when
the antimicrobial can no longer attach to them, or (F) make an enzyme performing culture-and-sensitivity testing. If the
that can break down the antimicrobial. medication’s name has an “R” next to it, that
means the organism is resistant; if an “I,” an inter-
mediate response is indicated (the organism is
day. Sometimes further tests must be conducted inhibited; some, but not all, of the bacteria will be
manually, in which case it may take up to three days killed); if an “S,” the organism is sensitive to it
to receive the culture report. and the medication is likely to cure the infection.
Most nurses are not legally responsible for pre- The numbers under the heading “MIC [minimum
scribing the correct medications but are obligated inhibitory concentration] sensitivity” refer to the
to ensure the appropriateness of the medications “lowest concentration of an antimicrobial drug
patients receive. Nurses should review culture-and- that will inhibit the visible growth of microorgan-
sensitivity results as soon as they are available and isms after overnight incubation.”27
act when a medication needs to be changed. Be • Determine whether the medication prescribed to
proactive: make looking at laboratory results a part the patient is appropriate, based on the sensitivity
of your practice when reviewing a chart for the first data. If a particular bacterium shows an interme-
time, then ensure that the culture-and-sensitivity diate response to the antimicrobial, continued
results are back whenever a new order is written. exposure to it increases the risk that the infectious
You can make the difference between a short- organism (and others in the body) will adapt
term infection and a long, life-threatening illness by to the hostile environment and become resistant to
taking the following steps: that type of drug.
• Depending on the system your facility uses, look • If the patient is not taking a medication to which
in the computer system or in the patient’s chart the bacteria are sensitive, an appropriate antimi-
for the results after cultures are obtained. Most crobial must be identified. The NP or physician
hospital laboratories will provide a preliminary must be made aware of the problem as soon as
result as well as a final report. Look for both. it becomes apparent. Finding the right medica-
• If multiple tests were performed, final results may tion is sometimes difficult because the costs of
54 AJN ▼ June 2008 ▼ Vol. 108, No. 6 http://www.nursingcenter.com
 testing are far too high for microbiology labora-
tories to test every antimicrobial available. The
sensitivity test uses drugs representing various
classes of antibiotic medication. Antibiotics of a
given type tend to cause a similar response in the
same bacteria. For example, organisms that are
resistant to cefazolin (Ancef, Zolicef) will proba-
bly be resistant to all cephalosporins.
• If the antibiotic that the patient takes is not on
the report list, sensitivity to that particular drug
was not tested.
• If the culture shows that multiple types of bacte-
ria are present, the process becomes even more
complicated. Ideally, finding a single antimicro-
bial medication to which all the organisms are
sensitive is the best option. More likely, the patient
will need more than one medication.
• When yeast (most often C. albicans) is also de-
tected, antibacterial medications will not affect it.
(Candida species often appear in routine cultures
while other fungi, such as Histoplasma capsula-
tum, do not; special fungal cultures are needed to
detect them.) The first line of defense will have
to be antifungal agents, such as fluconazole
(Diflucan, Trican) or amphotericin B. Patients
with serious, life-threatening bacterial infections
often develop secondary systemic fungal infec-
tions because of the suppression of normal flora.
• If the infection is viral, the culture report will be
negative unless special viral cultures were ob-
tained. The antimicrobials discussed here will not
kill viruses. If the patient’s immune response is inad-
equate, it may be necessary to prescribe an appro-
priate antiviral (assuming that one is available).
• If the patient is taking the wrong medication, make
certain that the physician or NP knows this. Point
out the medications that the microorganism is sen-
sitive to. You may save a life! ▼
Mary C. Vrtis is a legal nurse consultant with Aperio Medical Legal
Consulting in Front Royal, VA. Contact author: marycvrtis@
yahoo.com. The author of this article has disclosed no signifi-
cant ties, financial or otherwise, to any company that might
have an interest in the publication of this educational activity.
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