biofilm in chronic wound and its implication.ppt

PPT about biofilm in chronic wounds

1. WOUNDINFECTION AND
BIOFILMS
Dr.Jithin eldo paul
Junior resident
Dept of general surgery

2. HISTORY
HIPPOCRATES
JOSEPH LISTER
LOUIS PASTEUR
WILLIAM HALSTED

3. PATHOGENS
-Bacteria, Fungi, Protozoa
MRSA
Staph aureus
Coagulase negative staph bacteroids
Pseudomonas aeroginosa peptostreptococcus
prevotella
E.coli,kliebsiella,
enterococcus,proteus
Chronic wounds –change in bacterial flora over time

4. PATHOGENESIS
Modes of spread
direct contact
airborne
self contamination
Ulcer and bacteria-interaction
Contamination
Colonization
Critical colonization
infection

5. VIRULENCE
Exotoxin production
Endotoxin release
Bacterial synergy
BIOFILM PRODUCTION
microbial colony encased ina matrix
adhered to wound surface

6. INFECTIONINCHRONICWOUND
Purulent secretions
Signs of inflammations
Fever
Pain and erythema
Increase in ulcer size
Discolouration of granulation tissue
Foul odour
critical bacterial load > 100000/gm of tissue

7. Pathogens
planktonic
sessile
Sessile state –in response to stress like
nutrient limitation
immune attack-
adaptive mutation and phase variation
genotype changes
Geneticalychanged subpopulation of cells that survive
environmental stress

8. BIOFILM
Population of microbes attached irreversably on
a biotic or abiotic surface and encased in a
hydrated matrix of exopolymeric
substances,protiens,polysaccharides and nucliec
acids.

9. Attachment phase
attachment
immobilization
Accumulation phase
cell to cell interaction
microcolony formation
confluent 3D structure

10. Moist surface or water abundant substrate
Reverasble to irreversable attachment
Final stage –production of EPS
EPS and bacteria trap particulate materials
Focus for further attachment and growth of other
organisms –biological diversity

11. Contributors
fibrinogen
fibronectin binding protiens
MSCRAMM family adhesins
capsular polysachride adhesion factors
bacterial DNA
autolysins
overall downshift in metabolic activities
perseverance mode

12. BACTERIAINBIOFILM
Behave differently
QUAROM SENSING
communication between bacterias
autoinducers
regulates bacterial gene expression
Poly or monomicrobial
Bacterial synergism
Nutrition
Phagocytic resistant

13. ANTIMICROBIAL TOLERANCE
Trapping of antimicrobials in EPS
Evade immune detection by repressing ligands
Elevated expression of reflux pumps
Altered metabolic activity within biofilm

14. EVIDENCEOFBIOFILMINCHRONICWOUND
Invadindg organism associated with a surface.
Examination showing bacteria in microcolonies.
Infection confined to a particular location.
Difficult to eradicate with sensitive antibiotics.

15. Clinical observations
Acute wound with chronic wound
Host factor for devolopment of wound is cured or
normalized
Repeated use of biocides fail to heal wound

16. DIOGNOSIS
Wound swabs
Tissue culture and biopsy
PCR
Denaturing Gradient Gel Electrophoresis

17. THERAPEUTIC STRATEGIES
quarom sensing inhibitors-jams communication
brominated furanones -pseudomonas
RNA111 inhibiting peptides –MRSA
Iron binding compounds –lactoferrin
Targeting EPS
DISPERSIN B –staph epidermis

18. Bioelectric effect
Biofilm penetrating drugs
rifampicin,quinolones,fusidic acid
silver-hydrogel dressings
liposomes containing amikacin
Surgical debridement
slough,sequestrum
implant,mesh

19. NEWERDRUGS
Lipoglycopeptides –dalbavancin,telavancin
Lipopeptides –daptomycin
Streptogramins –quiniprstin,dalfopristin
Glycylcycline –tigecycline
linezolid

20. TOCONCLUDE
Biofilm –important cause for chronic wound
Habitat of its own
Difficult in
identfying
diognosing
treatment

21. THANKYOU