1. The human body hosts trillions of commensal bacteria that normally coexist without harm. 2. Under certain conditions, usually involving an imbalance or compromised immune system, some commensal bacteria can potentially cause disease. 3. The relationship between human and commensal bacteria is complex and dynamic, with colonization of many sites of the body from birth onward. While generally beneficial, commensals may occasionally act as opportunistic pathogens.

1. COMMENSAL FLORA
FRIEND OR FOE ?
Dr. Anil Kumar
Associate Professor
Microbiology

2. ‘ We think we know what we are;
but little do we realize ,that the
burden of millions of living beings we
carry, to share our bodies all Our lives,
as Friend or Foe.’

3. INTRODUCTION
 “Commensal” –Latin : ‘Share a Table’
 Is a Symbiotic relationship where by symbiont
benefits but host is neither harmed or helped.
 Human commensal flora-all natural bacteria that
live on and in a healthy person.
 Skin,oral cavity,URT,Lower GI tract,Urogenital

4. Host –Parasite Relationship
 Needs Review –Beneficial Vs Harmful effects
 Interspecies association
 Symbiotic relationship- Dynamic state
 Pathogenic & non-pathogenic- factors
 “Balanced pathogenicity”-genetically determined
resistance in host is an evolutionary norm.

5. HISTORICAL
 Louis Pasteur E.metchinkoff
Helpful – Essential Harmful
 Germ free animals exist
 NASA astronauts renedered germ free –6 wks to regain flora
 Normal flora at one site – pathogen elsewhere
 Alloiococcus otitis & Corynebacteria otidis- commensal outer ear
Pathogen Middle ear

7. BIOTA
at
BIRTH
 Fetus in-utero-germ free
 Passage - birth canal “Momentous transition”
 Before first breath-microbes
 Mouth, skin & external ear canal
 Out numbered : 1013 cells to 1014 microbes

8. NORMAL BIOTA
 External : skin & conjunctiva
 Internal : mouth, nose, intestinal tract vagina, urethral tip
 Transient biota : presence for short periods
 Opportunists: Causing disease - immune system breaks down
 Abnormal to find in brain,heart,muscle,bone,lungs

9. DISTRIBUTION OF NORMAL FLORA
 SKIN- Staph epidermidis,Staph aureus,
Propionibacterium acnes
Pityrosporum, Dermodex folliculorum
 Conjunctiva : Staph epidermidis, Diptheroids
 Nasal cavity: Staph epidermidis,Staph aureus
 Mouth : >300 species,10:1 anaerobes : aerobes, CNS
Strep mutans, Corynebacterium
 Vagina : Lactobacillus,Clostridium,Bacteroides,
Candida spp.
 Urethra : Staph epidermidis,Enterococcus

13. COMMENSAL FLORA “AS FRIENDS”
 Microbial antagonism-
prevents colonisation –barrier function
highly adapted receptors- adhesins
deprive pathogen of space &nutrients
skin – fatty acids
gut –bacteriocin & colicin
vagina – acid environment
 Antigenic stimulation-develop immune system
 Production of vit B12 & K by gut bacteria
 Conversion of toxic metabolites
 Oxalobacter formigenes –breaks down oxalate
prevents kidney stone formation

14. UPSETTING THE BALANCE
“WHEN FRIENDS TURN FOES”

15. RESIDENT SKIN FLORA AS “FOES”
 Corynebacteria minutissimum- Erythrasma
 Propionibacterium acnes – Acne vulgaris
 Pityrosporum orbiculare –Saprophyte –Pathogen
high temp,humidity ,sweating
Changes – Yeast to Hyphal form :-
-Tinea Versicolor
- Seborrhic dermatitis
- Itchy folliculitis

16. STAPHYLOCOCCUS EPIDERMIDIS
BIOFILMS
 Microflora-infection of implanted material - Biofilm
 Extracellular polysaccharide Adhesin
 Encoded ica Operon-phase variable regulation
 ica a d b c –gene cluster 37.5% carriage strains
 Phase variation - reversible – insertion sequence
 Colonising indwelling medical devices

17. BIOFILM FORMATION ON
ORTHOPEDIC IMPLANT

18. Matrix formation in a Biofilm

19. EFFECTS OF ORAL FLORA
ON PLATELETS
 Streptococci viridans group encounter platelets
dental bacteremia- Streptococci sanguis
 Thrombogenic role- Strep. sanguis
 Induce human & rabbit platelets & fibrin aggregate
 Heart valve vegetations - Endocarditis
 Coronary thrombosis, Myocardial infarction

20. MENINGOCOCCAL MENINGITIS
 Humans natural reservoirs-
nasopharynx
 Attach microvillus-
non-ciliated epithelium
 Pili major adhesin-CD 46
 Opa & Opc attach CD 66
 Survival IgA Protease
 Carriage immunising
process-antibody respnse

21. ORODENTAL INFECTIONS
 Microbial plaques------ Caries
 Gingivitis & Periodonitis
 Normal gingiva-anaerobic gram positive cocci
 Caries-anaerobic gram positive bacilli
 Prevotella,Porphyromonas-periodonitis
 Strept.sanguis Vs Strept.mutans
 Bacteroides & Fusobacterium

22. STAPHYLOCCAL MUCOSITIS
 Severe form mucositis - Geriatric patients ,oral Crohns
 Panoral erythema, crusting ,bleeding, reduced salivary flow
 Colonisation by toxic shock syndrome -toxin strains
 Oral source Staphyloccal joint sepsis?
 Gingival plaques

23. BACTERIAL VAGINOSIS
 Overgrowth Gram variable coccobacilli
 Not clear why ?
 Reduction of lactobacilli pH > 4.5
 Grey white discharge-fishy odour

24. VAGINAL CANDIDIASIS
 Antibiotic therapy disturbs normal flora
 Over growth by yeast- Candida albicans
 Changes normal mucosa with age
 Curdy white discharge ph <4.5

25. THIN LINE DIVIDING
GUT COMMENSAL & PATHOGEN
 GI tract consortium - flora >500 species
 Vascularisation & development of Villi- nutrients
 Bacteroides thetaiotaomicron – largest genome
 Enterococci- nosocomial notoriety
 E.faecalis –vancomycin resistant
 Acquire –Pathogenicity islands-mobile genetic
elements,with virulence associated genes

26.  Spread of normal flora-sterile site:
- Intestine perforated – Peritonitis
- Skin broken –Burns – Septicaemia
- Dental extraction – Strep. Viridans
- E Coli perianal – urethra -UTI
BREAKING THE BARRIER

27. Dark Side of Good Bacteria
 Commensal Gut bacteria trigger redistribution of
protein – CFTR in epithelial cells of intestine
 Cystic Fibrosis Transmembrane Conductance
Regulator (CFTR) Protein
 Receptor for Salmonella enterica serovar Typhi
 Attach,invade & translocate into submucosa
 Effects host epithelium - selectively susceptible.

28. INFLAMMATORY BOWEL DISEASE
 Gut flora-immunological acceptance & no induction of
deletrious effect
 Tolerance-
-T cell never encounters Ag relevant form
-T cell encounter anergy/elimination
- Regulatory cells modify response
 Expression: pathogen associated molecules (PAM)
 Toll receptors-dendritic cells
 Dysfunction immunoregulatory cytokines

29. Bacteria with taste for Gluten Cause
Celiac Disease
 Gluten ingested by some Commensal bacteria
 Dendritic cells ingest such bacteria
 Indistinguishable from other bacterial peptides
 Immune system triggers reaction as Pathogen
 Toll like receptors,PMP,CD4 cells involved

30. ANTIBIOTIC ASSOCIATED
DIARRHOEA
 Disturbed composition & function
 Diarrhoea with antibiotic treatment
 Clindamycin,Cephalosporin,Ampicillin
 Clostridium difficile –infants & adults
 5% healthy adults --- 63% hospital set up
 Toxin A & B of Cl. difficle –faeces
 Candida spp. & Klebsiella oxytoca
 Nosocomial spread

31. Harmless Bacteria -Deadly Toxin
 E Coli 0157:H7 virulent strain –gastroenteritis
 Killed by antibiotic action releasing SHIGA toxin
 Releases Bacteriophages - genetic code for Shiga toxin
 Phage invade harmless E Coli of gut causing them to
produce more Shiga toxin and more phages.

32. DISEASE CAUSING SPECTRUM
 Yersinia pestis
 Bordetella pertusis
 Vibrio cholera
 Salmonella typhi
 Pseudomonas aeruginosa
 Clostridium difficile
 Staphylococcus epidermidis
 Candida albicans
 Lactobacillus

33. CONCLUSION
 Categorising as : pathogens / commensal ?
 Useful but rigid distinctions
 Separation blurred-hosts health critical
 Exist along disease causing potential
 Highly virulent-- opportunists in weak host
 Microbes on human host ALWAYS a potential to HARM

34. “Commensal Flora are destined to be our
life long Companions,no longer as trust
worthy as before,who can be reduced,
monitored but never Eliminated”