Resistance to antibiotics and other antimicrobial agents

112 Pages·1998·10.9 MB·English

by  Great Britain. Parliament. House of Lords. Science and Technology Committee

HOU/L
HOUSE OF LORDS SESSION 1997-98
7th REPORT
SELECT COMMITTEE ON
SCIENCE AND TECHNOLOGY
“se
RESISTANCE TO ANTIBIOTICS
AND OTHER ANTIMICROBIAL AGENTS
REPORT
Ordered to be printed 17 March 1998
LONDON: THE STATIONERY OFFICE
£13.30
HL Paper 81-I
PCA
mm
I
HOUSE OF LORDS SESSION 1997-98
7th REPORT
SELECT COMMITTEE ON
SCIENCE AND TECHNOLOGY
RESISTANCE TO ANTIBIOTICS
AND OTHER ANTIMICROBIAL AGENTS
REPORT EaXZetloom > Centre for Medical
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CONTENTS
Paragraph
CHAPTERGUINIRODUCTION... .wrsrtavtsccsserveerer. erpovlornteio s 1.1
WAU IS FOSISGANGE Dans d6 s brew ka ben eda ye oe OOM AAO ons. dogdbws 1.7
PET We en ak uel wii ola ere een ea oo 0g oR te dig eln Mu RR: 1.10
GEPOKS-1TEGOMION Fh ns 6 sue na chetines nie sea esky) eROtOMOIINE Simishev 429 1.14
The intetiauonal dimension” ....-2.25....--......,-.,. Soanionngiet vacis 1.15
emer OE er See eran fee si Oe cok ses ee eae ee aay > es 1.16
Pees anubrotic resistance matter oSEO P CE 1.19
@nn tesishurce.p]e controlled? «0 h.aia dew ico eee. bees sy Dardve-edaule bal
meknowledtementsopmmy.:.- sce ww ds WOeeNh Sgeih ansezs”: bas widowy-ts 1.42
CHAPTER 2 PRUDENT USE INHUMAN MEDICINE............8.0..0... pe |
Bresent. use wn the United Kingdomigc tn AS E.OUL Oe PRT.eo e ee xs 23
Rewards more prudent use... ~.. MPLA AN CIE A, ATS oe oe 2.8
Sr aries, DOMCICS ANU PUIUCHNGS: open bhe es ode Kyideke eer rere rertes | 2.10
Parad testing. <n une we ome sou won 3 (ONIORUOTG SENG? BslnOMmiusnd % 2.16
Prescription checking and.control . AiO GW. ee ee oe eee pe oy BOE AAD
Rnarmaceuticablicensinpisevé savedcoaiet ook MVS wie teasioewal toe celsteesiine 223
PRasmachotcal salesmanship obial chesiuco ius. bhO Meosto rieaas, 2w tagyt cae! 2.24
Bere Ounictd GU AnDIOUGE J .aaahuKn dt al drier rnmiicibeeincc e 2.26
Medical education: undergraduate, postgraduate and vocational ............... 2.31
Pontinuinerotessional development ono. po nesep eceyer sp > SEDI MAL sb Ad de fe 2.32
(pA PLEETILL cite alta gn Meth iain, ohne ad niet at pheiiinnn ini etna tebn RN 11 Teer “Fs * 2.34
Tissot2 ) cavitievsan p ie pie Madet ab Told carl athe Regen iegeip-olt leeraA ta dCp ict ira ailisa a aie I oI bs
Nt iah NC ted Ma aete h IM eh ca id IE el acta i ec apc ck Sk ok 2.36
ATE aNGDIOTCS bdd TOryouns Desai os FAME 0G 1G PSEA SOL ee 2.40
PRI ENTI ta gi errr N aew = beginc uesi ponnseas eara rbrer oFd or ata sty EROS ELSES | PSL 2.46
BHAPTERUSPRUDENEUSEINANIMALS 1. wha. 8.c ouiowhe sii) fain. ana ah 3.1
PaVitgaTedicilionine news 4eitebadiuridl-a clits have rds dewule ans iaa acto end epee
PECL D UT ECE iene teeth ie aya desl heyy gin« in op eis te peer etieses biee RR ua)
PILE RRAET a ALEC ICETTIS ei aio css ch cached nance uths pPhe~' eienar, TOPRIM Aaah ¢ apt [ia Aye]
SR aATT IAN Seg i a dortc as J casas heno cS ng hoo nLd ,* hg gens aakeae JAD
MATGLaE] )in Female cepa tire eee alee Meri wine) tae aaa aCe Re EEE ICI fe 3.18
eT Oe ee id. Me ictal dota s anols tatin wena ve » Hbee ales 3.20
Pi coli,t.01..... MOTOS LINO: ALAG CA HFA ESS HOd 28 SG 8) 3.25
BPVECISIY GAPCTICTICE istcrsepserecaue«n1+e MaeDRaVOy GsMsEs rBtENg aatsr Heses VsaYsr.o Psaelalnsi sel y¢ 32d
US experience 0... cectne eeee ee e eee 3.30
PACERSINE FEE ANGI. FGUROLES . WUE Re, od 08 aa edn 3:4A
Pquacnitivel i lass is. was ae Ae. Sse cult Les gare ay oo) Gem foots 3.33
Uses of antimicrobial agents on plants...) oe ss eae eee nail) cele ee 3.34
Sheep Wormnstand:scabw? waist irl ides, menos 0 aalbioetea des halen tl. sthiarinsart 3.36
Antibiotic-resistance marker genes in genetically-modified organisms .......... 3.42
64 EM WEN Ee: USE RsS fO B CO Ly Gale TFT A C1) I I A A Pa 4.1
iifection'control.in. hospitals . .2-OUALi/, INS Ate i> OHA CSA. SASTRY.) 4.2
Site COMICIMMEAIISn TR Oe omits re es tia ets che sel Fed be ding 4.3
Contracting for infection control ....0 2. ee eleSb eee eee 4.7
EOoET Tati Naeger agireeiae re Gren gman we tA ayia achee rage al ste Piea aa gee 4.9
TeOLATION Pee Poe teres Coe aoe etme cate n oad OP USNhAHE DCs «> 4.12
Overcrowding and “hot-bedding” ......... 6. ccc cece eee eee e ees 4.13
Keency staffs. flee sopes 0.08 en a ae, Lies sikh ok 4.16
Screenings: (60 Aubotaulass) 16.0 ong ees ao QL A idl votiall « ob 4.17
Training sus of ities and the Thin Pay: deny ep ogaline se are Ah Het ct 4.19
fafection. control usthe. COMMUDIY 05 oy >a chicas sae snes acs ARE GhHEO «> 4.20
Power to enforce treatment... ..,........ebibpa-Iniddaervna)i nwienndw.. 4.26
Sirveitlancess-eesverrtr er cay trecwerr rier gece Comers casper bea 4.27
PAEEOTICOUINOL TS DUISONS i. ck hoc tien cs weiner g 113k AWOL: & 4.29
EE ENON TIES Be OOP ee oh ee ee ee 4.30
A national MRSA strategy? .... =. 2oablts as Zoetistind ... ee ee 4.35
CHAPTER 5 SURVEILLANCE:...).\.\.). eRors 2o k ee 5.1
DEY to TEPOCRIIOY. sa. ee SN) Sayan aee’w aitin cobra a na a ote Ja
Scoatnd ‘lNorathérnn Idrel and | 203. < s een pete eet oe oc oe en a
Information! technology~. «vs a s-.\45 054s sees eee ieee sos. «eee akan Soe 5.10
Einkingsand feedback: the IGARE modelii in. murpe-S see blaeces sbeo ee 5.11
Resources for the: PHIGS 's:s0 Sneek s a ees Rete: wpe MS ec c,s re paneer eed, SOO
Erisis inclinical academic microbiologys cc tee sac Ves |. oe > a ble ee ae Dakd
A national strategy for surveillance .~ 2. s6h6 «6565 <0 6 50 6 ohn eee EOD 5.18
CHAPTER 6 NEW DRUG.DEVELOPMENT ......J.A0R.RL. S.omm.ieb.es 3: 6.1
How hard-is industry trying?-... sea <a 146 56ecn sen wd me oe > abs RR RInOS ee 6.2
Licensing: fast-tracking and “orphan drug” designation ....................4. 6.5
CHAPTER-/7 VACCINES. «.. 55.05. SUL, WRI AL ie oe 7A
HEV. oc FAR os ou i ee EMR ASA EAR ls whee eh pie eee a en a! J3
Meningocoecus | «45-6 2%! ayer Sik 6 hm ot ee ere er tet 7.4
(See re oer ee ee eee err mC (e)
Streptocéccus pneumoniae (pneumococcus) ks i... anes ee eee ee 7.6
Hospital“infections °.~ «2+... se one ssh enka on nee klnin @ oO Ren he keegan la
Barriers‘and bottlenecks y4 .). 2a atin ey ome. 6 4a nln ee ae a 7.8
Surveillance for-antigQemic VAriatwOm oes. esos occi e oso males ob et oo oa onto toe tne SEONG 1G 7.10
Researchtys sss .4 i)einettens Kk Gs pan lene hile e eared Citas ss< ap sA leo pe p dS
CHAPTER'S ANTIVIRAL DRUGS 4.4.2.0: 6. dino 10 EO eRe Tecoigesion 8.1
Prudent tse of antivirals t)2.45. 65-25 ody soders ie ener ete ena eat 8.4
Sturvei lance 6: 3.1h54 4v em APN AN sealed, 4 ole Znt eed see inte ices aed 8.6
ReSearcky’, & 26.5, aa Fae nee papel desec ateb etting ©t e fao ed sph rx eAa ik fg 8.8
CHAPTER>9 INTERN ATIONAS 5. schbs oontaes ini te cote en eh ee a 9.1
World Health Organization? 2.0.23 9. 5 31. 2.4. 2 pec eee ee ee 93
Malaria .'0% oe. antsegestabe apd ethang cdsa nclade oc cenate queda s Meade meta PSO eee Pa pw Ra eiea oD
New drugs .:.+.:.9.- rte. hehiaecahan saida tero tieatorcha pede lbp ea ROR al ellc l Cotya ie a 9.9
Prudent. usé. of rugs oho resets ceesiciste chants s eo ete Pear at ANAL olg c ys pp 9.12
Infection control and Vaccination s.6,.)<.:...1 gn beebdees ove desto tu ed oanaps sind 1d an) RE 9,13
Survet lane» 2-.'...5.0: xaeaeehat etv ersc ablualee oho hd eh chk keo me ca ea ai hs 9.14
RESCATCHE 2 5: shore ater Tete hse boatt ee bce otsi tgC onky Jha RCC Pae ew i Rani aa hee 948
CHAPTER 10 RESOURCES FOR RESEARCH AND DATA-COLLECTION .. 10.1
Research into different ways of using antibiotics .............0c0 c.ec.e 0ne e 10.2
Research into strategies of professional and public education ................ 10.3
Collection of: prescribing data): s3 453-2 Abie ae ee eee ade 10.4
Research into infection. control yo. 10. gae tgs aan ae eee ea ae 10.8
Collection of denominator data for disease surveillance ...............0.0.0.. 10.9
surveillance beyond:the-hospital «+2... 244-1 a a-olean oe al a Re 10.11
Research into systems of surverllancebst thant: yueI2nas 81 (enue tebe Sonn 10.14
Ay funding gap? ioif. b cutie gcdiw bd deli) Se ARRREE se te ee ae ee ate an 10.15
CHAPTER 11 CONCLUSIONS AND RECOMMENDATIONS .............. 11.1
CHAPTER 12 SUMMARY OF RECOMMENDATIONS .......... 000000005 12.1
APPENDIX | Sub-Committee I
oP OT EC PH SS et mh alt Mid in Wt ee | é 6a) & Rw le 6's, me ee
APPENDIX 2. «W ithesseS:) cee 0 la ns dncsrbucul ooe cRUcE-vONe.n D ap
APPENDIA 3: +P arsi aisitie PALS: HO s bea aay oa ackas ae oe es
ee PEN LLA 442 SECONG VISILIO. PHLS HQ) i431 a beet tau aoe eee
APPENDIX 5 Visit to King’s College Hospital
FeO Pe Pe wey mh hw eel my @e e ee ee
APPENDIX 6 ~ Visit-to-'USA «2.4 2a ei ea ta des oc ene on ob YOURS oat bs de
APPENDIX 7 Some important antimicrobial agents
See 8 a 2 @ @ 8 © Oh9 BI) BD eS Bee
APPENDS 6 Glossary; 29"s'7 fae 4 oe 4 ae ee Bee i. ee
APPENDIX 9 Acronyms
PS Se EP a ES Oe FO ONE BW OL Te ee, 6 fe 6) s. ae 6.2 Seka teen ae eee
References to evidence
Q refers to a question in oral evidence; p refers to a page of written evidence. All the evidence is
printed in a separate volume, HL Paper 81-II, Session 1997-98.
SEVENTH REPORT
17 March 1998
By the Select Committee appointed to consider Science and Technology.
ORDERED TO REPORT
RESISTANCE TO ANTIBIOTICS
AND OTHER ANTIMICROBIAL AGENTS
CHAPTER | INTRODUCTION )
1.1 Antibiotics have saved countless lives and transformed the practice of medicine since the
first flowering of antimicrobial chemotherapy in the 1930s and ’40s.' Many people are old enough
to remember when these and other antimicrobial drugs were not available. Their memories include
patients with pulmonary tuberculosis isolated in sanatoria until either they died or their disease
healed itself; frequent postoperative wound infections; bone infections (osteomyelitis) followed by
discharging sinuses requiring drainage for year after year; syphilis advancing to its late stages and
ending in insanity despite the use of arsenical drugs; cases of tuberculous meningitis, invariably
fatal; and simple cuts and scratches giving rise to fatal septicaemia.
1.2 LP Garrod wrote in 1968, “No one recently qualified, even with the liveliest imagination,
can picture the ravages of bacterial infection which continued until little more than 30 years ago”.
Since then, many new antibacterial agents have been developed and antiviral chemotherapy, then
in its infancy, has become possible for an increasing range of viral diseases. As well as its uses in
the direct treatment of infection, antimicrobial chemotherapy has also helped to make possible
medical advances such as transplantation and the treatment of many forms of cancer which carry
a special risk of infection.
1.3. But the worm in the bud emerged early when, during the development of penicillin, the
enzyme which destroys it was isolated and it was presciently predicted (by Abraham and Chain)
that penicillin resistance would become a problem. So it has, and so also, at greatly varying
intervals following its introduction, has resistance to each new antibiotic.
1.4 “Resistance” means that an organism ceases to be killed or inhibited by a drug. While
antibiotics can cause, as can all active therapies, a wide range of adverse effects ranging from trivial
to fatal, resistance is a special problem, since the agent loses its former efficacy and the future
treatment of other patients is therefore jeopardised.” The problem of antibiotic resistance has now
become a major concern in medicine throughout the world.
1.5 The fact of antibiotic resistance is widely known, though not so widely understood. In the
United Kingdom, the aspect most talked about among the public at large is probably MRSA
(methicillin-resistant Staphylococcus aureus), an infection associated principally with hospitals and
nursing homes. Other aspects of the problem are familiar to the people affected: for instance,
resistant TB (tuberculosis) is a major threat to people with AIDS, while resistant malaria is the
scourge of Africa and the Far East. Both Houses of Parliament have debated MRSA and other
For terminology, see Box 1, and the glossary in Appendix 8.
Resistance should be distinguished from tolerance. When a patient develops tolerance to a drug, no other patient
is affected; but a resistant organism can infect others.
6 SEVENTH REPORT FROM THE
Box |
HISTORY AND TERMINOLOGY
Historically the concept of attacking invading organisms without harming the host was
introduced at the turn of the century by the German Paul Ehrlich. This concept he called
chemotherapy. The invading organisms he first studied were not bacteria but rather the
protozoa that cause malaria and sleeping sickness; but in 1910 he made his great discovery
of salvarsan (the 606th synthetic chemical he had tried) which was effective in treating the
spirochaete (a type of bacterium) which causes syphilis. He called it a “magic bullet”. In
the 1930s the sulphonamide drugs were introduced: they were the first effective drugs that
attacked the common bacteria such as streptococci and could cure pneumonia and
meningitis, although they caused serious problems and side effects. They were not called
antibiotics; they were known as “chemotherapeutic agents”.
“Antibiotic” was the term originally applied to naturally occurring compounds such as
penicillin which attacked infecting bacteria without harming the host. “Antibiotic” is now
regularly used to refer to synthetic compounds as well as natural compounds, and to refer
to antiviral as well as antibacterial drugs. In the public mind, however, “antibiotics” are still
largely equated with penicillin.
Penicillin, the first antibiotic, was identified in a mould by Alexander Fleming in 1928; but
it was not available for use until Florey and Chain and their colleagues purified it in 1940
and showed how effective it could be. Unlike the sulphonamides it seemed completely
harmless to the host and very effective against many bacteria. As it was a naturally
occurring product, not a synthetic chemical, it was not called a chemotherapeutic drug,
although that would have been a perfectly correct description. It would also have been a
correct general description to include not only all antibacterial agents but also agents against
viruses, protozoa, worms and other parasites, with all of which our report is concerned.
However, the word “chemotherapy” is now used and recognised by the public as the term
to describe the drug treatment of cancer.
“Cancer chemotherapy” is a legitimate term if we regard cancerous cells as invasive, being
therefore, like infecting organisms, foreign to the host. Cancer chemotherapy thus seeks to
attack the invader without damaging the host. Chemotherapy against microbial infection is
referred to as antimicrobial chemotherapy.
This report is concerned with various forms of antimicrobial chemotherapy, and mainly with
antibacterial antibiotics, or antibacterials. It deals also with antiviral antibiotics, or
antivirals; and with antimalarial and anthelmintic drugs.
For an historical account of the development of resistance to antibiotics, see the evidence
of Professors Phillips and Roberts of the Royal College of Pathologists, p 453.
resistant infections in the past year or two (the Commons on 19 March 1997, the Lords on
4 November 1996). The Government are seized of the issue: it features in the Chief Medical
Officer’s annual reports for 1995 and 1996, and Ministers are awaiting advice on different aspects
of it from the Standing Medical Advisory Committee and the Advisory Committee on the
Microbiological Safety of Food (p 373). So we bring the matter before the House confident that
it deserves Parliamentary time and attention. This enquiry has been an alarming experience, which
leaves us convinced that resistance to antibiotics and other anti-infective agents constitutes a major
threat to public health, and ought to be recognised as such more widely than it is at present.
SELECT COMMITTEE ON SCIENCE AND TECHNOLOGY 7
1.6 We begin our report with a brief account of what resistance is and why it matters; for more
on these questions, we refer the reader to arecent report by the Parliamentary Office of Science and
Technology, Diseases Fighting Back (October 1994). We consider how far resistance can be
controlled, and how. We then proceed to consider the evidence we have received on the various
means of control: prudent use of antimicrobial agents in human medicine (Chapter 2) and in
animals (Chapter 3); infection control (Chapter 4) and disease surveillance (Chapter 5); and
development of new drugs (Chapter 6) and vaccines (Chapter 7). Chapter 8 considers the special
problems of resistance in viruses, and Chapter 9 considers international issues including malaria.
Chapter 10 considers the sources of support for research and data-collection. Our recommendations
are set out in Chapter 11, and summarised in Chapter 12. Appendix 7 contains notes on some
important antimicrobial agents, Appendix 8 a glossary of other terms, and Appendix 9 a list of
acronyms.
What is resistance?
1.7 All antibiotic resistance has a genetic basis. Some organisms are inherently resistant to
many antibiotics (“innate resistance’’). This resistance probably evolved as a response to exposure
to antibiotics present in the natural environment. Many such organisms pose no threat to healthy
people, but may become important pathogens in vulnerable patients in hospital. Examples include
the Pseudomonas species and some Enterococci.
1.8 Acquired resistance can arise by a number of diverse mechanisms:
(1) Mutational resistance. These mutations have occurred randomly in a small proportion of
the particular bacterial population. The most familiar example is seen in the bacterium
causing tuberculosis, where a few organisms are naturally resistant to, for example,
streptomycin. In the presence of streptomycin as a single antibiotic these resistant
organisms soon become the dominant population.
(ii) By horizontal transfer of genes determining resistance from one organism to another.
This can occur by the direct transfer (conjugation) between bacteria of genetic material
carried on small pieces of DNA (plasmids) situated within the bacterial cell but outside
the bacterial chromosome, or by similar pieces of DNA carried on a bacterial virus, a
bacteriophage (transduction), or by direct transfer of naked DNA (transformation).
1.9 | While these mechanisms have been known for many years, what has emerged more
recently is knowledge of the great frequency and flexibility with which bacteria are able to
exchange genetic material. and the crucial importance of these mechanisms in bacterial evolution.
It is now known, for example, that genetic interchange can take place between a much more diverse
variety of organisms than was formerly thought. and is probably a common event in the natural
world. There is a global pool of resistance genes which can spread between different bacterial
populations occupying different habitats, e.g. between man, animals and the environment. Genes
carrying antibiotic resistance factors are easily able to spread if the host organism gains an
evolutionary advantage in acquiring them. The importance of these processes for antibiotic
resistance in man and animals is that, by whichever process genes for resistance have been acquired,
the presence of an antibiotic in the environment oft he bacterium imposes “selection pressure” and
encourages resistance to spread. The antibiotic kills all susceptible bacteria, thereby “selecting out”
the resistant strain; in this way a previously minor population of antibiotic-resistant organisms
rapidly becomes dominant. Although there are enormous variations in the speed with which
resistance to any antibiotic emerges, and in its geographical spread once it has emerged, it 1s
indisputable that resistance has developed to many new agents after their introduction, with
consequent diminution or actual loss of their former value to medicine. Thus has appeared the
vicious circle repeatedly witnessed during the last half century, in which the value of each new
antibiotic has been progressively eroded by resistance, leading to the introduction of a new and
usually more expensive agent, only for this in its turn to suffer the same fate.
8 SEVENTH REPORT FROM THE
Clinical resistance
1.10 Bacterial species differ greatly in their inherent susceptibility or resistance to various
antibiotics. There is also a range of susceptibility within any species, so that some organisms are
more susceptible than others. Clinical resistance, 1.e. whether the antibiotic will or will not work
in a patient or animal, is a more complex concept in which many other factors are involved such
as the precise location of the infection, the distribution of the drug in body fluids and the state of
the patient’s immune system.
1.11. Resistance is measured in the clinical microbiology laboratory by qualitative or
quantitative methods which attempt to relate the test results to the expected effect in clinical
practice, taking into account such factors as the range of serum concentrations achieved when the
antibiotic is administered. Most laboratories use an agar disc susceptibility test in which isolates
(i.e. samples) are categorised as susceptible, resistant or intermediate.
1.12 There is much continued discussion about the best methods of antibiotic testing, about
quality control and about international agreement on methods. In practice, the results of these
pragmatic tests often relate well to clinical success or failure, for example in tuberculosis and in
gonorrhoea.
1.13. Atamore basic level, the biochemical mechanisms responsible for antibiotic resistance
have been analysed in great detail. Resistance arises (1) if the bacteria can inactivate the drug before
it reaches its target within the bacterial cell; (11) if the outer layers of the cell are impermeable, and
prevent the drug from entering; (iii) if the drug enters but is then pumped back out again (“efflux”’);
(iv) if the target is altered so that it is no longer recognised by the antibiotic, or (v) if the bacteria
acquire an alternative metabolic pathway that renders the antibiotic’s target redundant (“by-pass”).
Although some hundreds of resistances are known, virtually all can be ascribed to one of these five
broad types of mechanism. See Figure 1, which represents the antibiotic as a bullet and the target
as a roundel.*
Cross-infection
1.14 Bacteria inhabit a global environmental pool in which resistant bacteria, and genes
transferring antibiotic resistance between bacteria, can and do spread easily between people and
animals. A continuous process of exchange of genes takes place within the microbial world. The
two variable factors affecting the spread of antibiotic resistance are the selection pressure exerted
by antibiotic use, and the ease with which resistant organisms are able to spread between people
by “cross-infection”.
The international dimension
1.15. Because the amount of interaction between human populations, and with them their
commensal* microbes, varies greatly, the type and frequency of antibiotic resistance in any
particular organism differs greatly between geographical locations. In the longer term, however,
once antibiotic resistance is established in an organism, it spreads with lesser or greater speed
throughout the world. Modern methods of molecular epidemiology have enabled the spread of
bacteria to be tracked and it is clear that bacteria, some of them carrying antibiotic resistance
factors, can spread between countries and continents with phenomenal speed in this era of mass
travel.
—_—_—_—_——— nw ee a
We are indebted for this simple account of a complex matter, and for the Figure, to Dr David Livermore, Head
of the PHLS Antibiotic Reference Unit. See also Diseases Fighting Back, Parliamentary Office of Science and
Technology, October 1994; and the memoranda of the Association of Medical Microbiologists (p 2) and the
Society for General Microbiology (p 485). ;
Commensal microbes, or “flora”, are the numerous and diverse micro-organisms which inhabit the skin. nose.
mouth and gut. They do not normally cause disease in healthy people.