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I OralMicrobiology
Michael P Dawson
Andrew J Smith
Superbugs and the Dentist: An
Update
Abstract:This paper presents an overview of three of the most commonly encountered 'superbuqs; 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.
Clinical Relevance: Many dental practitioners will treat a wide range of patients in a variety of healthcare settings ranging from general
practices to hospital in-patients. It 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
It is estimated that 80% of human antibiotic
prescribing is carried out in the community
by general practitioners.' 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 1996).' In the fields
of veterinary medicine and agriculture,
there isalso extensive use of antimicrobials,
for therapy/prophylaxis and growth
promotion, respectively.
Whether this rate of prescription
is justifiable or not is debatable, but the
exposure of patient-borne bacteria to
antibiotics on this scale is unarguably a
major selection pressure for the modern
phenomenon of drug-resistant micro-
Michael P Dawson, BDS,MFDS,Specialist
Registrar in Oral Microbiology and
Andrew J Smith, BDS,PhD, FDS,MRCPath,
ACIST,Senior Lecturer and Consultant inMicrobiology, Infection Research Group,
Glasgow Dental Hospital and School, UK.
198 DentalUpdate
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.'
When resistant bacteria are
introduced into the healthcare environment
the additional problem of spread becomes
apparent. In 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.'
As we emerge into the 'post-antibiotic era; dental practitioners should be
aware of the main nosocomial pathogens
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.
In 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-Resistant Staphylococcus
Aureus (MRSA)
• Vancomycin-Resistant Enterococci (VRE)
• Extended Spectrum I3-Lactamase
Producers (ESBLs)
MRSA
What isMRSA?
MRSAis a variant of the
bacterium Staphylococcus aureus, a gram
positive coccus that is a human commensal
organism and commonly inhabits skin andmucous membrane surfaces. Staphyloccocus
aureus is readily spread from one person
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t..e ll wa ll s tr uc tu re 10 .r M'&lhicii'lIin S : e . n s i r l l i V i e a ·lI,fJl'eJJS
1 6 a c c te < ( ia l o a n
w a U ,
in . c o r p o m , 1 i i : ~ : g
~nOmla~"B P l
a~d PBP2
Figure 1. Structural effects of the mecA gene.
Exposure to healthcare institutions (eg hospitals)
Prolonged hospitalization
Exposure to antimicrobial agents
Severe underlying medical illness
Enteral tube feeding
Insulin-receiving diabetics
HIV patients
Use of IVdrugs, in the medical setting or recreat ionally
Decubitis ulcers or pressure sores
Post-operative surgical wounds
Exposure to Intensive Care Unit (lCU)
Haemodialysis
Skin conditions (eg Eczema)
Indwelling catheters (IV or urinary)
Residing on a ward with MRSAcolonized patients
(Based on information from references-')
Table 1. Risk factors for MRSA colonization/
infection.
to another and 20-40% of the population
carry it in their nose asymptomatically,
intermittently shedding the bacteria. MRSA
is similar in many respects to 'normal'S.
aureus but is resistant to the 13-lactam,
methicillin. Used in the early 1960s to
treat staphylococcal infect ions, methic ill in
is now obsolete. It 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
May 2006
of resistance to flucloxacil lin. Flucloxacil lin
is now the empiric antibiotic of choice
for staphylococcal infections in most
institutions.
Like 'normal'S. aureus, MRSA can
affect patients of all aqes" and can cause aspectrum 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 MRSA have been found
to be higher than for methic ill in-sensi tive
S.aureus (MSSA).5
MRSA is common in hospitals,
presenting major problems for infection
control teams worldwide and incidences
continue to rise. It is resistant to almost all
I3-Lactams and often other antibiotic groups
too. Therapeut ic opt ions 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 penicil lins
(eg oxacillin, nafcillin and methicillin) were
developed owing to problems of acquired
penicil lin resistance in staphylococcal
species in the 1950s and 1960s (about 99%
of'normal' S.aureus are now resistant to
penicillin by the production of penicillinase
enzyme.)
In turn, resistance to methicil lin
(and the other 13-lactams) has evolved
in S.aureus with the acquisition of the
mecA gene. The gene is believed to have
originated from a distantly related species,
with recent studies suggesting it has
been passed between different S.aureus
lineaqes." MecA causes the bacteria to
produce a new protein, Penicillin Binding
Protein 2a (PBP2a). PBP1 and PBP2 are
responsible for the staphylococcus'
sensitivity to penicillin, but the altered form
of PBP2a allows no such susceptibility (see
Figure 1).
Predisposing factors for MRSA acquistionl
infection (Table 1)
Exposure to healthcare
institutions, such as hospitals, is in itself
a predisposing factor for developing
MRSA. Once in hospitals, the spread of
MRSA is difficult to control and its survival
is facilitated by the increasing use of
antibiotics.
In 1999, Vicca summarized some
of the main causes of MRSA acquisition
in hospitals/inadequate ward staff, staff
training, overcrowding of patients, lack
of isolat ion facil ities, frequent relocat ion
of patients and staff and poor attentionto infection control procedures increase
the risk of MRSA and other nosocomial
infectlons,"
Epidemiology of MRSA
Though there are considerable
differences in the MRSA rates reported
across Europe, the last 10 years has seen an
increase in MRSA infection, especially in the
UK where, for example, it causes 40% of all
S.aureus bacteraernias."
The two most common types
of MRSA clones in the UK are E(pidemic)-
MRSA 15 and E-MRSA 16. (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.')
EMRSA 15 and 16 have been coined 'super-
clones' as they have demonstrated great
potent ia l for national and internat ional
spread. Compared with other MRSA
variants, EMRSA 15 and 16 are more
capable of survival, colonization and
spreading themselves within the hospital
environment. Both are typically resistant to
a wide range of antibiotics.
MRSA is mostly a hospital
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Denture stomatitis
Angular cheil it is
Osteomyelitis
Oral mucositis
(Based on information from reference")
Oral mucosal lesions
Endodontic infections
Parotitis
Infection of jaw cysts
Table 2. Oral diseases caused by S.aureus (including MRSA).
pathogen in debilitated patients and so
the ICU ward represents a greater risk than
many others. Infected and colonized
patients are recognized as being the main
reservoir but colonized staff can also transmitthe bacteria to patients and can cause wider
spread," 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 MRSA (CA-MRSA),"·12.13 with
nursing homes also being affected.
Occasionally, the CA-MRSA arises from
healthcare settinqs!" and, occasionally,
from household contacts."
Interest ingly, CA-MRSA appears
to have evolved along different linesfrom hospital-acquired MRSA, since
many isolates have different genetic
components, toxins and resistance
patterns from their hospital-acquired
counterparts."
Reports of CA-MRSA invasive
skin infection have shown that there
is potential for wide and rapid spread
within community groups who have close
personal contact.":" In the US, some of
the patient groups identified in reports on
CA-MRSA are:
• Intravenous drug users;• Children in day care;
• Athletes;
• Military personnel; and
• Prison inmates.":"
In healthcare institutions, the
traditional measures for controlling an
outbreak of MRSA focus on the following:
• Reducing 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).
200 DentalUpdate
Vancomycin Intermediate S.aureus (VISA) and
Vancomycin Resistant S.aureus (VRSA)
The current antibiotics of
choice for the treatment of MRSA are
the glycopept ides, eg vancomycin.
The recent increase in MRSA 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 S.aureus strains with reduced
susceptibl l l ty '? or complete resistance" to
vancomycin. These are termed VISA and
VRSA, respectively. This is obviously of
great public health concern and represents
the continuing evolution and adaption of
micro-organisms to our standard antibiotic
treatments.
The dental significance of MRSA
Recent studies have suggested
that Staphylococcus aureus is more
commonly isolated from the mouth than
was previously thought. L ike methicil lin-
sensit ive S.aureus, MRSA 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 S.aureus were
methlcillln-reslstant," while other groups
have reported MRSA carriage rates of
10% on the dentures of denture-wearing
patients" and 19% from the mouths of an
elderly inst itutional ized qroup."
Of all the oral specimen types
collected in the three-year study, the
tongue was found to be the most common
area from which MRSA was isolated (28%).
The clinical conditions most frequently
associated with patients carrying MRSA
were erythema, swelling, pain or a burning
sensation of the oral mucosa. It was also
noted that patients with oral MRSA 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
methici ll in-sensi tive S.aureus.
When present in the
nasopharynx or colonizing dentures, MRSA
has proved difficult to eradicate from these
sites.24.25
It 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
MRSA transmission recorded in general
dental practice, with the dentist reported as
the source."
In local terms, S.aureus
(including MRSA) can cause or contribute to
the oral infections shown in Table 2.
There is a r isk 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 justification for
'special ' precautions for MRSA colonized/
infected patients in the dental surgery
- standard precautions are sufficient to
restrict cross-infection.
VRE
What isVRE?
Vancomycin-Resistant
Enterococci (VRE) are gram-posit ive cocci
that are facultatively anaerobic and can
survive in environments not tolerated by
other, less hardy bacteria.
There are 18 species in the
enterococcus genus, of which Enterococcus
faecalis and Enterococcus faecium 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 ,"
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."
Cross-infect ion occurs mainly
via the faecal-oral route, with diarrhoea
presenting a greater problem for infection
control in hospitals/nursing homes.
Enterococci are a potential cause of serious
disease, especial ly in the acute healthcare
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I OralMicrobiology
S,acte~iialCe~~ Baote:~lla!l! CeU
A , i s
t ; J 1
Bacterial Celli
A 8 . P i,asm ~ d
B,ao~er~aJi 8 ! U I
B & P lasm [d
DG o n j U g j a l l : O f J lo r 0 1 9 !1 11 8A & ! B
atriJdIDuplio a tio n o~ P la sm id
'l" ransfe lr o , tCo p ie d P la sm i d
~ro m Ce~11 to Cell B
Figure 2. Horizontal transfer of antibiotic resistancegenes in enterococci: Cell A contains the plasmid
encoding for resistanceto antibiotic(s), while Cell B is initially susceptible to the samedrug. In Cell A,
the plasmid isduplicated and,by the formation of a pilus,the two bacteria are temporarily joined. This
allows the transfer of the copied plasmid (andtherefore resistance)to CellB.Both cellsarenow resistant
to the drug.
setting. They may cause nosocomial
bacteraemia, surgical wound infection
and urinary tract infection. Enterococci
are not highly virulent organisms and
VREinfections are most often seen in
immunocompromised patients or thosewith an underlying medical illness. VRE
causes serious and sometimes fatal disease
in some patient groups, eg liver transplant
and leukaemic patients. In addition,
compared with antibiotic-susceptible
enterococci, the risk of mortality associated
with serious VREinfection, such as
bacteraemia, is several times hlqher."
The first reports ofVRE were
from Europe in 1988, with the USfollowing
shortly afterwards.
VREhas been on the increase
for over a decade, with European resistancerates stabilizing at 1.6-5.3% in 2001.31 In
the US, there was a continued rise, with
202 DentalUpdate
the proportion of resistant enterococci
about 15.8% at the same time. Enterococcus
faecium, which is less pathogenic than
E . iaecalis, accounts for more than 90% of
USVRE.
Though many cases ofVREinfection may resolve without drug
therapy, it has been reported that
enterococci account for 10-20% of all cases
of endocarditis, the treatment for which
can be difficult and lengthy. A 4-6 week
course of a 13-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."
Over time, however, the
standard drug therapies are becominginsufficient to treat VREinfection and,
for many cases, there is NO antimicrobial
option available for treatment of the
infection."
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)." Probably
the main factor responsible for resistance
developing was the large-scale use of
vancomycin in US hospitals during the
late 1980s. This increase in prescribing
was largely an attempt to combat MRSA
and pseudomembranous colitis caused byClostridium difficile.
Vancomycin resistance is
mostly due to either the VanA or the VanB
gene,36 and it is thoug ht that these genetic
elements were acquired by enterococci
once they had developed in other species.
VREare intrinsically resistant to many
antibiotics, but can also acquire resistance
via the exchange of genes between
bacteria.
Predisposing factors for VRE colonization!
infection (Table 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.
It has been shown that antibiotics, such
as the cephalosporins which reach high
concentrations in the gut but are inactive
against enterococci, favour colonization
with VREand may therefore predispose to
subsequent infection.
Epidemiology ofVRE
Most enterococcal infections
occur in hospitals, with VanA clonal strains
implicated in UKand UShospital outbreaks.
However, colonization frequently occurs in
the community," and household contact,
including food preparation, may lead to
community transrnlsslon." Inthe hospital
environment, contaminated medical devices
and hands of healthcare workers are likely
to be the cause of transmission between
patients.
It is thought that the resistantbacteria causing European outbreaks
were spread via the food chain, with the
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Prolonged hospitalization
Diabetes mellitus
Exposure to Intensive Care Unit
Organ transplant
Malignancy
Intra-abdominal surgery
Hepatobiliary disease
Renal failure
Haematologic malignancy
Enteral tube feeding
Infection/colonization with oxacillin resistant S.aureus/C. difficile within the preceding 12
monthsExposure to 3rd generation cephalosporins, eg ceftriaxone, cefotaxime
Exposure to other antibiotics, particularly clindamycin, cephalosporins, aztreonam,
ciprofloxacin, aminoglycosides and metronidazole.
(Based on information from reference")
Table 3. Riskfactors for VREcolonization/infection.
R-~ I
Extended Spectrum Beta-
Lactamases cleave the
Beta-Lactam ring
s
H N
/-·B.2
'C 'O O 'H
~\. y )
8 , e t a .Bl a c t i a m D ihyd rothlazl r r u e
FUng Ring.
Figure3. Action of ESBLenzymes on 13-lactamstructure.
May 2006
original animals being fed quantities of
glycopeptide antlbiotics." 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. Figure 2 illustrates the transfer of
transposons via bacterial plasm ids.
In hospitals, spread of
VREinvolves both person-to-person
transmission and the selective pressure
exerted by antibiotic exposure. Unidentified
patient/staff sources ofVRE continue to
playa major 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. In healthcare
institutions, enterococci may be spread
via environmental surfaces (where they
can persist for several weeks on medical
equipment if hygiene standards are
lnadequate.v-")
Thedental significanceofVRE
Enterococci have been
associated with the failure of endodontictreatment. The bacteria (especially
E . faecalis) have been isolated in 23-70%
of positive cultures obtained from the
obturated canals of teeth still giving rise to
apical periodontitis symptoms." They have
also been found in the periapical lesions of
refractory endodontic treatment cases."
but it is unclear whether VREhave a major
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." It was
noted that, in this group of hospitalized
patients, the oral cavity was colonized with
enterococci to a higher degree than healthy
patient controls," possibly reflecting their
extensive antibiotic treatment history.
Extended Spectrum B-lactamase Producers
What are extended spectrum B-Iactamase
producers?Extended Spectrum 13-lactamase
(ESBL)-producing micro-organisms are
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Prolonged hospitalization
Long-term care in Intensive Care Units
Ventilator dependence
Increasing age
Low birth weight
IVor urinary catheterization
Nasogastric tube
Gut colonization often precedes infection
Severe illness
Neonates
Exposure to long-term antibiotics
Surgical instrumentation
Gastrostomy/jejunostomy tube
Emergency abdominal surgery
(For oral infection) Xerostomia,and conditions causing it
Residence in nursing homes or institutions with widespread use of 3rd generation
cephalosporins
(Based on information from reference=)
Table 4. Riskfactors for ESBL-producer colonization/infection.
enteric gram-negative bacilli (rod-shaped
bacteria that reside most commonly in
the intestine). They are also known as
enterobacteriaceae and may produce ESBL
enzymes. ESBL-producing organisms first
became evident in Europe in the mid-
80s and the enzymes they prod uce are
mostly seen in the Klebsiella (especially K .
pneumoniae) and Esche ri ch ia co li species."
In addition to breakingdown the 13-lactam ring of the 1st and
2nd generation cephalosporins and
early penicillin antibiotics, the ESBLs
have evolved to break down the latest
generation of extended spectrum 13-
lactam antibiotics, such as ceftriaxone (3rd
generation cephalosporin) Figure 3.
As a result, infections with 13-
lactamase producers are more difficult
to treat than those due to drug-sensitive
organisms, with increased morbidity and
mortality rates.
The most effective remainingagent in these infections is the carbapenem
group of antlblotlcs," eg meropenem.
Despite its effectiveness,
it should be noted that, with the
increased use of carbapenems for ESBL-
related infections, there is scope for the
carbapenem resistance developing in
other organisms. It 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.lt has
been shown that these measures can
significantly reduce the rate of ESBL
occurrences."
204 DentalUpdate
Why have ESBL-producers evolved?
The 13-lactam group of
antimicrobials have been repeatedly
modified by biochemists in response
to evolving resistance mechanisms by
organisms producing 13-lactamases of
different types. The genes responsible for
producing ESBLenzymes are contained on
bacterial plasmids, mobile portions of DNA
that are often seen in enterobacteriaceaesuch as E.coli and K . 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 aqents.'?
Predisposing factors for ESBL-producers (Table
4)
As with other MDR 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 ESBL-producing
bacteria.
Epidemiology of ESBL-producers
ESBL-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"
and is a widespread problem. Since 2003,
new highly resistant strains of E.coli have
disseminated throughout hospitals and
the community in England and parts of
Northern Ireland. Although the first of
these was recorded as recently as 2001,
one region has reported over 300 cases of
urinary tract infection, with the new strains
in only 18 months.
The dental significance of ESBL-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."
However, persistent carriage of coliforms
(including ESBL-producers) can be an
indicator of underlying medical illness" or
immunodeficiency. For this reason, they may
be seen in patients who have resided in, orare 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."
There is insufficient evidence to
determine whether colonization/infection
of the oral cavity with ESBL-producers
affects treatment outcome. However, the
presence of multiple antibiotic-resistant
organisms will restrict treatment options
should the need arise.
Infection control procedures
are now paramount in controlling the
appearance and spread of ESBLs,therefore
dental staff need to ad here to local standard
infection control guidelines.
Conclusion
It 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
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