DraIMicrobioIogy

l98 DentaIUpdate May 2006

MichaeI P Dawson
Superbugs and the Dentist: An
Update
Abstract: This paper presents an overview of three of the most commonly encountered 'superbugs', with a comment on the implications of
each for the dental practitioner. The origins of antibiotic resistant micro-organisms lie in the acquisition of resistance genes and selection
pressures, with their spread facilitated by inappropriate prescribing and inadequate infection control. Dentists should attempt to rationalize
their antibiotic prescribing and ensure that they and other dental staff adhere to standard infection control procedures.
CIinicaI ReIevance: Many dental practitioners will treat a wide range of patients in a variety of healthcare settings ranging from general
practices to hospital in-patients. |t is increasingly likely that they will either knowingly or unknowingly come into contact with people
colonized or infected with drug-resistant micro-organisms. This article explains the background to some commonly occurring antibiotic-
resistant bacteria.
Dent Update 2006, 33: 198-208
|t is estimated that 80% of human antibiotic
prescribing is carried out in the community
by general practitioners.
l
The remaining
20% takes place in hospitals, where almost
50% of all patients will receive antibiotic
therapy. Though dental prescriptions
account for a relatively small proportion
of antibiotic use in primary care (7%), it is
still considerable in absolute terms (eg 3.5
million prescriptions in l996).
l
|n the fields
of veterinary medicine and agriculture,
there is also extensive use of antimicrobials,
for therapy/prophylaxis and growth
promotion, respectively.
whether this rate of prescription
is |ustifiable or not is debatable, but the
exposure of patient-borne bacteria to
antibiotics on this scale is unarguably a
ma|or selection pressure for the modern
phenomenon of drug-resistant micro-
organisms. These so-called 'superbugs' have
received significant media attention and
have been brought into the public eye by a
number of newsworthy events - outbreaks,
serious illness and fatalities caused by
nosocomial acquisition of infection.
An antibiotic-resistant organism
may exhibit resistance to one or two drugs,
or sometimes almost every agent that is
normally effective against it. whatever
the degree of resistance, it has been
well recorded that infections caused by
these bacteria are associated with higher
morbidity, mortality and hospital care costs
than their drug-susceptible counterparts.
2
when resistant bacteria are
introduced into the healthcare environment
the additional problem of spread becomes
apparent. |n their efforts to provide care,
healthcare workers will often inadvertently
facilitate the transmission of bacteria from
infected/colonized patients to those as yet
unaffected. This may be via hands, clothing,
medical equipment or by unknowingly
coming into contact with contaminated
environmental surfaces.
3
As we emerge into the 'post-
antibiotic era', dental practitioners should be
aware of the main nosocomial pathogens
MichaeI P Dawson, 8DS, MPDS, Specialist
Pegistrar in Oral Microbiology and
Andrew 1 Smith, 8DS, PhD, PDS, MPCPath,
AC|ST, Senior Lecturer and Consultant in
Microbiology, |nfection Pesearch Group,
Glasgow Dental Hospital and School, UK.
and the challenges they pose for other
medical staff. whether they are employed
in general dental practice, community or
hospital settings, dental staff may make
contact with patients who are colonized or
infected with antibiotic-resistant organisms
and have an equally important part to play
in infection control.
|n the course of this article,
three of the main drug-resistant micro-
organisms will be looked at, providing basic
information on the bacteria, their causes,
risk factors and relevance to the dental
practitioner:
Methicillin-Pesistant Staphylococcus
Aureus (MPSA)
vancomycin-Pesistant Lnterococci (vPL)
Lxtended Spectrum -Lactamase
Producers (LS8Ls)
MRSA
What is MRSA!
MPSA is a variant of the
bacterium 3TAPHYLOCOCCUSAUREUS, a gram
positive coccus that is a human commensal
organism and commonly inhabits skin and
mucous membrane surfaces. 3TAPHYLOCCOCUS
AUREUS is readily spread from one person
Andrew 1 Smith
May 2006 DentaIUpdate l99
DraIMicrobioIogy
of resistance to flucloxacillin. Plucloxacillin
is now the empiric antibiotic of choice
for staphylococcal infections in most
institutions.
Like 'normal' 3AUREUS, MPSA can
affect patients of all ages
4
and can cause a
spectrum of diseases

from relatively mild
soft tissue infections to fatal syndromes
such as septic shock and necrotizing
pneumonia. However, in some studies,
mortality rates for MPSA have been found
to be higher than for methicillin-sensitive
3AUREUS (MSSA).
5
MPSA is common in hospitals,
presenting ma|or problems for infection
control teams worldwide and incidences
continue to rise. |t is resistant to almost all
-Lactams and often other antibiotic groups
too. Therapeutic options are therefore
limited and inappropriate drug regimes will
only contribute to the mortality rate and
increased time/cost of stay in hospital.
How has MRSA arisen!
The semisynthetic penicillins
(eg oxacillin, nafcillin and methicillin) were
developed owing to problems of acquired
penicillin resistance in staphylococcal
species in the l950s and l960s (about 99%
of 'normal' 3AUREUS are now resistant to
penicillin by the production of penicillinase
enzyme.)
|n turn, resistance to methicillin
(and the other -lactams) has evolved
in 3AUREUS with the acquisition of the
MEC! gene. The gene is believed to have
originated from a distantly related species,
with recent studies suggesting it has
been passed between different 3AUREUS
lineages.
6
-EC! causes the bacteria to
produce a new protein, Penicillin 8inding
Protein 2a (P8P2a). P8Pl and P8P2 are
responsible for the staphylococcus'
sensitivity to penicillin, but the altered form
of P8P2a allows no such susceptibility (see
Pigure l).
Predisposing factors for MRSA acquistion/
infection (7abIe 1)
Lxposure to healthcare
institutions, such as hospitals, is in itself
a predisposing factor for developing
MPSA. Once in hospitals, the spread of
MPSA is difficult to control and its survival
is facilitated by the increasing use of
antibiotics.
|n l999, vicca summarized some
of the main causes of MPSA acquisition
in hospitals, 'inadequate ward staff, staff
training, overcrowding of patients, lack
of isolation facilities, frequent relocation
of patients and staff and poor attention
to infection control procedures increase
the risk of MPSA and other nosocomial
infections.'
8
pidemioIogy of MRSA
Though there are considerable
differences in the MPSA rates reported
across Lurope, the last l0 years has seen an
increase in MPSA infection, especially in the
UK where, for example, it causes 40% of all
3AUREUS bacteraemias.
9
The two most common types
of MPSA clones in the UK are L(pidemic)-
MPSA l5 and L-MPSA l6. (Clones in
microbiological terms refers to 'a group
of bacteria or cells that have multiplied
asexually from a selected mutant, thereby
possessing identical genetic endowment.')
LMPSA l5 and l6 have been coined 'super-
clones' as they have demonstrated great
potential for national and international
spread. Compared with other MPSA
variants, LMPSA l5 and l6 are more
capable of survival, colonization and
spreading themselves within the hospital
environment. 8oth are typically resistant to
a wide range of antibiotics.
MPSA is mostly a hospital
Figure 1. Structural effects of the MEC! gene.
Lxposure to healthcare institutions (eg hospitals)
Prolonged hospitalization
Lxposure to antimicrobial agents
Severe underlying medical illness
Lnteral tube feeding
|nsulin-receiving diabetics
H|v patients
Use of |v drugs, in the medical setting or recreationally
Decubitis ulcers or pressure sores
Post-operative surgical wounds
Lxposure to |ntensive Care Unit (|CU)
Haemodialysis
Skin conditions (eg Lczema)
|ndwelling catheters (|v or urinary)
Pesiding on a ward with MPSA colonized patients
(8ased on information from references
6,7
)
7abIe 1. Pisk factors for MPSA colonization/
infection.
to another and 20-40% of the population
carry it in their nose asymptomatically,
intermittently shedding the bacteria. MPSA
is similar in many respects to 'normal' 3
AUREUS but is resistant to the -lactam,
methicillin. Used in the early l960s to
treat staphylococcal infections, methicillin
is now obsolete. |t has been superceded
by flucloxacillin, which is a less toxic drug
with fewer adverse effects. Though not
in clinical use, methicillin may be used
in the laboratory testing of bacteria, and
resistance to it can be taken as a reflection
DraIMicrobioIogy
200 DentaIUpdate May 2006
pathogen in debilitated patients and so
the |CU ward represents a greater risk than
many others. |nfected and colonized
patients are recognized as being the main
reservoir but colonized staff can also transmit
the bacteria to patients and can cause wider
spread,
l0
therefore, in some units, attempts
are made to decolonize both groups.
Despite its origins as a
nosocomial pathogen, there are
increasing reports of Community-
Acquired MPSA (CA-MPSA),
ll,l2,l3
with
nursing homes

also being affected.
Occasionally, the CA-MPSA arises from
healthcare settings
l4
and, occasionally,
from household contacts.
l5
|nterestingly, CA-MPSA appears
to have evolved along different lines
from hospital-acquired MPSA, since
many isolates have different genetic
components, toxins and resistance
patterns from their hospital-acquired
counterparts.
l6
Peports of CA-MPSA invasive
skin infection have shown that there
is potential for wide and rapid spread
within community groups who have close
personal contact.
l7,l8
|n the US, some of
the patient groups identified in reports on
CA-MPSA are:
|ntravenous drug users,
Children in day care,
Athletes,
Military personnel, and
Prison inmates.
l7,l8

|n healthcare institutions, the
traditional measures for controlling an
outbreak of MPSA focus on the following:
Peducing transmission of the organism
(hand hygiene),
Screening for carriage,
Decolonization, and
General infection control measures
(eg use of barrier precautions,
patient isolation and environmental
decontamination).
6ANCOMYCIN)NTERMEDIATES. aureus6)3!AND
6ANCOMYCIN2ESISTANTS. aureus623!
The current antibiotics of
choice for the treatment of MPSA are
the glycopeptides, eg vancomycin.
The recent increase in MPSA incidence
has in turn led to greater reliance on
vancomycin as empiric therapy. Not only
is this drug expensive and potentially
toxic but, in recent times, there have been
reports of 3AUREUS strains with reduced
susceptibility
l9
or complete resistance
20
to
vancomycin. These are termed v|SA and
vPSA, respectively. This is obviously of
great public health concern and represents
the continuing evolution and adaption of
micro-organisms to our standard antibiotic
treatments.
7he dentaI significance of MRSA
Pecent studies have suggested
that 3TAPHYLOCOCCUSAUREUS is more
commonly isolated from the mouth than
was previously thought. Like methicillin-
sensitive 3AUREUS, MPSA may colonize
oral tissues and its prevalence may also
have been underestimated. One study,
over a three-year period, found 5% of
oral specimens containing 3AUREUS were
methicillin-resistant,
2l
while other groups
have reported MPSA carriage rates of
l0% on the dentures of denture-wearing
patients
22
and l9% from the mouths of an
elderly institutionalized group.
23
Of all the oral specimen types
collected in the three-year study, the
tongue was found to be the most common
area from which MPSA was isolated (28%).
The clinical conditions most frequently
associated with patients carrying MPSA
were erythema, swelling, pain or a burning
sensation of the oral mucosa. |t was also
noted that patients with oral MPSA were
more likely to be found in primary care
settings such as general dental practice,
rather than secondary care environments
which were more associated with
methicillin-sensitive 3AUREUS
when present in the
nasopharynx or colonizing dentures, MPSA
has proved difficult to eradicate from these
sites.
24,25
|t has been recognized as
forming a reservoir with potential for
causing local or systemic infection, while
presenting a continuing risk for cross-
infection. There have been two cases of
MPSA transmission recorded in general
dental practice, with the dentist reported as
the source.
26
|n local terms, 3AUREUS
(including MPSA) can cause or contribute to
the oral infections shown in Table 2.
There is a risk of cross-infection
to and from dental staff in any setting,
and so adherence to local infection
control policies, in particular the standard
(universal) infection control procedures,
is imperative. There is no |ustification for
'special' precautions for MPSA colonized/
infected patients in the dental surgery
- standard precautions are sufficient to
restrict cross-infection.
VR
What is VR!
vancomycin-Pesistant
Lnterococci (vPL) are gram-positive cocci
that are facultatively anaerobic and can
survive in environments not tolerated by
other, less hardy bacteria.
There are l8 species in the
enterococcus genus, of which %NTEROCOCCUS
FAECALIS and %NTEROCOCCUSFAECIUM are the
most commonly encountered in human
infections. They are part of the normal flora
of the human gastrointestinal and urinary
tract and are acquired from other people or
contaminated food/water.
Oral carriage rates as high as 60-
75% have been detected for enterococci,
28

with a recent study suggesting that patients
undergoing endodontic therapy were more
likely to carry the bacterium than those with
no experience of endodontic treatment.
29
Cross-infection occurs mainly
via the faecal-oral route, with diarrhoea
presenting a greater problem for infection
control in hospitals/nursing homes.
Lnterococci are a potential cause of serious
disease, especially in the acute healthcare
Denture stomatitis Oral mucosal lesions
Angular cheilitis Lndodontic infections
Osteomyelitis Parotitis
Oral mucositis |nfection of |aw cysts
(8ased on information from reference
27
)
7abIe 2. Oral diseases caused by 3 AUREUS(including MPSA).
DraIMicrobioIogy
202 DentaIUpdate May 2006
setting. They may cause nosocomial
bacteraemia, surgical wound infection
and urinary tract infection. Lnterococci
are not highly virulent organisms and
vPL infections are most often seen in
immunocompromised patients or those
with an underlying medical illness. vPL
causes serious and sometimes fatal disease
in some patient groups, eg liver transplant
and leukaemic patients. |n addition,
compared with antibiotic-susceptible
enterococci, the risk of mortality associated
with serious vPL infection, such as
bacteraemia, is several times higher.
30
The first reports of vPL were
from Lurope in l988, with the US following
shortly afterwards.
vPL has been on the increase
for over a decade, with Luropean resistance
rates stabilizing at l.6-5.3% in 200l.
3l
|n
the US, there was a continued rise, with
the proportion of resistant enterococci
about l5.8% at the same time. %NTEROCOCCUS
FAECIUM, which is less pathogenic than
%FAECALISaccounts for more than 90% of
US vPL.
Though many cases of vPL
infection may resolve without drug
therapy, it has been reported that
enterococci account for l0-20% of all cases
of endocarditis, the treatment for which
can be difficult and lengthy. A 4-6 week
course of a -lactam and aminoglycoside
(eg gentamicin) antibiotic combination
is the recommended treatment regime,
under international guidelines.
32,33
Despite
satisfactory prescribing practices and
monitoring, toxicity can occur.
34
Over time, however, the
standard drug therapies are becoming
insufficient to treat vPL infection and,
for many cases, there is NO antimicrobial
option available for treatment of the
infection.
35
Mechanisms of resistance in enterococci
Antibiotic resistance in
enterococci arises owing to alterations in
bacterial cell wall synthesis, rendering the
strain impervious to the glycopeptides
(which include vancomycin).
36
Probably
the main factor responsible for resistance
developing was the large-scale use of
vancomycin in US hospitals during the
late l980s. This increase in prescribing
was largely an attempt to combat MPSA
and pseudomembranous colitis caused by
#LOSTRIDIUMDIFFICILE
vancomycin resistance is
mostly due to either the vanA or the van8
gene,
36
and it is thought that these genetic
elements were acquired by enterococci
once they had developed in other species.
vPL are intrinsically resistant to many
antibiotics, but can also acquire resistance
via the exchange of genes between
bacteria.
Predisposing factors for VR coIonization/
infection (7abIe 3)
when undergoing antibiotic
treatment with many antibiotics, the
protective effect of the normal gut flora
is lost, leaving the host open to resistant
bacteria, especially nosocomial enterococci.
|t has been shown that antibiotics, such
as the cephalosporins which reach high
concentrations in the gut but are inactive
against enterococci, favour colonization
with vPL and may therefore predispose to
subsequent infection.
pidemioIogy of VR
Most enterococcal infections
occur in hospitals, with vanA clonal strains
implicated in UK and US hospital outbreaks.
However, colonization frequently occurs in
the community,
38
and household contact,
including food preparation, may lead to
community transmission.
39
|n the hospital
environment, contaminated medical devices
and hands of healthcare workers are likely
to be the cause of transmission between
patients.
|t is thought that the resistant
bacteria causing Luropean outbreaks
were spread via the food chain, with the
Figure 2. Horizontal transfer of antibiotic resistance genes in enterococci: Cell A contains the plasmid
encoding for resistance to antibiotic(s), while Cell 8 is initially susceptible to the same drug. |n Cell A,
the plasmid is duplicated and, by the formation of a pilus, the two bacteria are temporarily |oined. This
allows the transfer of the copied plasmid (and therefore resistance) to Cell 8. 8oth cells are now resistant
to the drug.
May 2006 DentaIUpdate 203
DraIMicrobioIogy
original animals being fed quantities of
glycopeptide antibiotics.
40
The horizontal
transfer of antiobiotic resistance genes
in enterococci is mediated by DNA
transposons. Transposons are relatively
small transposable genetic elements that
can move from one chromosomal position
to another. Pigure 2 illustrates the transfer of
transposons via bacterial plasmids.
|n hospitals, spread of
vPL involves both person-to-person
transmission

and the selective pressure
exerted by antibiotic exposure. Unidentified
patient/staff sources of vPL continue to
play a ma|or role in the spread within a
hospital, with more people colonized

than
displaying symptoms of overt infection and
intestinal colonization taking place over
extended periods of time. |n healthcare
institutions, enterococci may be spread
via environmental surfaces (where they
can persist for several weeks on

medical
equipment if hygiene standards are
inadequate.
4l,42
)
7he dentaI significance of VR
Lnterococci have been
associated with the failure of endodontic
treatment. The bacteria (especially
l. loecol|s} have been isolated in 23-70%
of positive cultures obtained from the
obturated canals of teeth still giving rise to
apical periodontitis symptoms.
43
They have
also been found in the periapical lesions of
refractory endodontic treatment cases,
44

but it is unclear whether vPL have a ma|or
impact on the outcome of endodontic
infections.
There have also been reports
of enterococcal infective endocarditis
occurring in patients receiving long-term
haemodialysis, after having received an
episode of dental treatment.
45
|t was
noted that, in this group of hospitalized
patients, the oral cavity was colonized with
enterococci to a higher degree than healthy
patient controls,
45
possibly reflecting their
extensive antibiotic treatment history.
xtended Spectrum -
Iactamase Producers
What are extended spectrum -Iactamase
producers!
Lxtended Spectrum -lactamase
(LS8L)-producing micro-organisms are
Prolonged hospitalization
Diabetes mellitus
Lxposure to |ntensive Care Unit
Organ transplant
Malignancy
|ntra-abdominal surgery
Hepatobiliary disease
Penal failure
Haematologic malignancy
Lnteral tube feeding
|nfection/colonization with oxacillin resistant 5. outeus/C. J|ll|c|le within the preceding l2
months
Lxposure to 3rd generation cephalosporins, eg ceftriaxone, cefotaxime
Lxposure to other antibiotics, particularly clindamycin, cephalosporins, aztreonam,
ciprofloxacin, aminoglycosides and metronidazole.
(8ased on information from reference
37
)
7abIe 3. Pisk factors for vPL colonization/infection.
Figure 3. Action of LS8L enzymes on -lactam structure.
Lxtended Spectrum 8eta-
Lactamases cleave the
8eta-Lactam ring
DraIMicrobioIogy
204 DentaIUpdate May 2006
enteric gram-negative bacilli (rod-shaped
bacteria that reside most commonly in
the intestine). They are also known as
enterobacteriaceae and may produce LS8L
enzymes. LS8L-producing organisms first
became evident in Lurope in the mid-
80s

and the enzymes they produce are
mostly seen in the +LEBSIELLA (especially +
PNEUMONIAE) and %SCHERICHIACOLI species.
46
|n addition to breaking
down the -lactam ring of the lst and
2nd generation cephalosporins and
early penicillin antibiotics, the LS8Ls
have evolved to break down the latest
generation of extended spectrum -
lactam antibiotics, such as ceftriaxone (3rd
generation cephalosporin) Pigure 3.
As a result, infections with -
lactamase producers are more difficult
to treat than those due to drug-sensitive
organisms, with increased morbidity and
mortality rates.
The most effective remaining
agent in these infections is the carbapenem
group of antibiotics,
47
eg meropenem.
Despite its effectiveness,
it should be noted that, with the
increased use of carbapenems for LS8L-
related infections, there is scope for the
carbapenem resistance developing in
other organisms. |t is therefore advisable
for emphasis to be placed on strict
infection control measures and on a wider
scale attempting to curb prescription
of 3rd generation cephalosporins. |t has
been shown that these measures can
significantly reduce the rate of LS8L
occurrences.
48
Why have SL-producers evoIved!
The -lactam group of
antimicrobials have been repeatedly
modified by biochemists in response
to evolving resistance mechanisms by
organisms producing -lactamases of
different types. The genes responsible for
producing LS8L enzymes are contained on
bacterial plasmids, mobile portions of DNA
that are often seen in enterobacteriaceae
such as %COLI and +PNEUMONIAE The
plasmids are genetic elements, easily
transmissible between different bacteria,
on which antibiotic-resistance genes often
arise through genetic mutations. These
mutations can be induced by the extensive
use of 3rd generation cephalosporins,
with the antibiotic pressures selecting out
resistant organisms and allowing them
to flourish. Unfortunately, many of the
plasmids also contain genetic information
that codes for resistance to other, unrelated
antimicrobial agents.
49
Predisposing factors for SL-producers (7abIe
4)
As with other MDP micro-
organisms, the likelihood of outbreaks in
healthcare institutions can be minimized
by strict infection control procedures.
Additionally, limiting the prescription of
3rd generation cephalosporins will reduce
the chance of developing LS8L-producing
bacteria.
pidemioIogy of SL-producers
LS8L-producing organisms have
been responsible for outbreaks in both
hospitals

and in nursing homes. The spread
within hospitals has been noted within
departments and between departments.
The problem of drug resistance in gram
negative organisms has risen rapidly
5l

and is a widespread problem. Since 2003,
new highly resistant strains of %COLI have
disseminated throughout hospitals and
the community in Lngland and parts of
Northern |reland. Although the first of
these was recorded as recently as 200l,
one region has reported over 300 cases of
urinary tract infection, with the new strains
in only l8 months.
7he dentaI significance of SL-producers
The enterobacteriaceae may
be present in the oral cavity transiently
or persistently. Transient acquisition is
frequently seen in healthy individuals
and the host will normally clear the
organism within a short period of time.
52

However, persistent carriage of coliforms
(including LS8L-producers) can be an
indicator of underlying medical illness
53
or
immunodeficiency. Por this reason, they may
be seen in patients who have resided in, or
are being treated in, long-stay healthcare
institutions/hospices. They are likely to
persist in the medically compromised
patient, indicating a decline in health.
The carriage of coliforms in the mouth
is also associated with increasing age,
hospitalization and xerostomia-inducing
conditions.
54
There is insufficient evidence to
determine whether colonization/infection
of the oral cavity with LS8L-producers
affects treatment outcome. However, the
presence of multiple antibiotic-resistant
organisms will restrict treatment options
should the need arise.
|nfection control procedures
are now paramount in controlling the
appearance and spread of LS8Ls, therefore
dental staff need to adhere to local standard
infection control guidelines.
ConcIusion
|t is apparent that dental
practitioners have an active role to play in
limiting the prevalence of drug-resistant
micro-organisms. Over-prescribing in
dentistry affects human populations in
Prolonged hospitalization Gut colonization often precedes infection
Long-term care in |ntensive Care Units Severe illness
ventilator dependence Neonates
|ncreasing age Lxposure to long-term antibiotics
Low birth weight Surgical instrumentation
|v or urinary catheterization Gastrostomy/|e|unostomy tube
Nasogastric tube Lmergency abdominal surgery
(Por oral infection) Xerostomia, and conditions causing it
Pesidence in nursing homes or institutions with widespread use of 3rd generation
cephalosporins
(8ased on information from reference
50
)
7abIe 4. Pisk factors for LS8L-producer colonization/infection.
May 2006 DentaIUpdate 207
DraIMicrobioIogy
the same manner as it does in general
medical practice, hospitals or veterinary
practice. Prescriptions for dental infections
impact on the rest of the body's microflora.
Practitioners should be encouraged to
develop and adhere to local prescribing
protocols, where these are designed to
rationalize drug treatment, restricting
prescriptions to cases where there is a
definite clinical indication for antibiotic
therapy.
The importance of effective
infection control within the dental surgery
should not be underestimated. Many
studies, albeit in the acute healthcare
setting, have highlighted the potential
for environmental cross-contamination.
The increasing incidence of antibiotic-
resistant micro-organisms in the community
demonstrates the need for continuing
vigilance.
|t is essential that, in the face of
the continuing evolution of antimicrobial-
resistant bacteria, both the healthcare
profession and pharmaceutical companies
work to meet the challenge. |t is only with
continuing research and development that
new agents will be discovered, and only
with continuing education of healthcare
staff and the maintenance of adequate
infection control procedures that the
existing problems of bacterial spread and
resistance can be resolved.
References
l. SMAC Peport - The path of least
resistance. Standing Medical
Advisory Committee - Subgroup on
Antimicrobial Pesistance. London:
Department of Health, l998.
2. Abramson MA, Sexton D1. Nosocomial
methicillin-resistant and methicillin-
susceptible 3TAPHYLOCOCCUSAUREUS
primary bacteremia: at what costsI
)NFECT#ONTROL(OSP%PIDEMIOL l999, 20:
408-4ll.
3. Zachary KC, 8ayne PS, Morrison v, ET
AL. Contamination of gowns, gloves,
and stethoscopes with vancomycin-
resistant enterococci. )NFECT#ONTROL
(OSP%PIDEMIOL 200l, 22: 560-564.
4. Chambers HP. The changing
epidemiology of 3TAPHYLOCOCCUS
AUREUSI %MERG)NFECT$IS 200l, 7: l78-
l82.
5. Pomero-vivas 1, Pubio M, Pernandez C,
Picazo 11. Mortality associated with
nosocomial bacteraemia due to
methicillin-resistant 3TAPHYLOCOCCUS
AUREUS. #LIN)NFECT$IS l995, 21: l4l7-
l423.
6. Pitzgerald PP, Sturdevant DL,
Mackie SM, Gill SP, Musser
1M. Lvolutionary genomics of
3TAPHYLOCOCCUSAUREUS: |nsights into
the origin of methicillin-resistant
strains and the toxic shock syndrome
epidemic. 0ROC.ATL!CAD3CI53! 200l,
98: 882l-8826.
7. Graffunder LM, venezia PA. Pisk
factors associated with nosocomial
methicillin-resistant 3TAPHYLOCOCCUS
AUREUS (MPSA) infection including
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