Superbug n Update

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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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OralMicrobiology I

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

DentalUpdate 199



I OralMicrobiology

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

May 2006



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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OralMicrobiology I


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

DentalUpdate 203



I OralMicrobiology


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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OralMicrobiology I

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