Lecture 5 Flashcards
(16 cards)
What is a bioflim
A biofilm is a structured community of bacteria attached to a surface, embedded within a self-produced extracellular matrix. Biofilms:
Provide protection from immune responses and antibiotics.
Require multiple coordinated steps to form.
Biofilm Formation - Summary
*Conditioning film
-Organic and inorganic particles
*Arrival of bacteria to a surface
*Attachment of bacteria to a surface
-Reversible binding
-Irreversible binding
*Biosynthesis of the biofilm matrix
Biofilm formation: Step 1: conditioning film formation
Surfaces (abiotic or biotic) become coated with a conditioning film before bacterial colonisation begins.
This film consists of organic (e.g. proteins, glycoproteins) and inorganic (e.g. ions, minerals) particles.
It alters surface properties (like charge and hydrophobicity), allowing initial bacterial interactions.
STEP 2: Bacteria Reach the Surface
Mechanisms of approach:
Diffusion – passive movement
Chemotaxis – directed movement toward chemical signals
Turbulence impaction – physical contact via flowing fluids
Flow matters:
Laminar flow → thicker boundary layer, fewer bacteria attach
Turbulent flow → better mixing, more bacteria contact surface
Rough surfaces decrease boundary layer → more attachment
STEP 3: Initial (Reversible) Attachment
Bacteria hover 30–100 nm above the surface due to electrostatic repulsion.
Reversible binding via:
Generic adhesins:
Surface structures: pili, fimbriae, flagella, teichoic acids
Functions: bind to abiotic surfaces or host cell glycoproteins
Encoded on: nucleoid (not plasmids)
🧠 Note: Heat or drying can convert reversible to irreversible attachment.
STEP 4: Specific Binding by Specfic Adhesins
Some specific adhesins bind specifically to host cell receptors (glycoproteins).
E.g. E. coli -> Mannose via fimbriae
Teichoic acids bind to fibronectin
Flagella interact with Toll-like receptor 5 (TLR5)
STEP 5: Attachment Proteins (Pathogen-Specific Adhesins)
▸ After initial attachment, pathogens use specialised attachment proteins (encoded on plasmids) to dock firmly to host adhesion proteins.
▸ These sugar-binding proteins lock into specific glycans on host glycoproteins/glycolipids.
Step 6: QS controlled irreversible binding
As more bacteria accumulate, they release signalling molecules (autoinducers):
Gram-negative: AHLs (acyl-homoserine lactones)
Gram-positive: oligopeptides
Once the signal threshold is reached - They activate genes (like the alg gene) that trigger alginate production (a sticky polysaccharide) - forms a slime-like matrix
This cements them to the surface — making attachment permanent.
The bacteria also:
Stop expressing planktonic (free-swimming) genes like flagella
Start expressing biofilm-supporting genes (EPS, stress response, virulence, etc.)
Step 7: Biofilm maturation
Bacteria divide and build a 3D matrix
▸ Biofilm grows by in-place cell division.
▸ Cells are embedded in EPS (exopolymeric substances).
Step 7: Biofilm maturation - Mature composition
Cells 2–5% of volume
Water ~98%
Matrix (EPS) Polysaccharides, DNA, proteins, glycoproteins, phospholipids, absorbed nutrients and waste
Function of EPS in mature biofilms
Structural framework (“cellular cement”)
Protects from dehydration, starvation, waste buildup
Limits antibiotic diffusion
Shields from immune cells (e.g., macrophages)
Prevents colonisation by other bacteria
Biofilm Architecture & Dynamics
Growth is layered (outer layers grow faster)
Flow effect:
Low flow → compact, slow biofilms (e.g. in humans)
High flow → fast-growing, less stable → sloughing
STEP 8: Sloughing & Programmed Detachment
Sloughing:
Caused by turbulence, immune attack, or surface abrasion
Fragments may spread infection
Programmed detachment:
Cells synchronously leave the biofilm
Become:
More hydrophilic
Lower in LPS
Able to divide 2–3 times before reattaching
Biofilm Protection Advantages
Biofilms protect bacteria against:
Desiccation
Starvation
Toxic waste
Immune responses (except amoebae)
Other bacteria (invasion resistance)
Colonisation of Biofilm-Coated Surfaces by Pathogens: Step 1: Pathogen docking
In healthy tissue:
Adhesion proteins (receptors) are hidden under host biofilms
In compromised tissue:
Some receptors may be exposed
To access receptors, pathogens:
Secrete enzymes to degrade the biofilm:
Glycosidases
Proteases
DNases
Colonisation of Biofilm-Coated Surfaces by Pathogens: Step 2: QS-Dependent Pathogenic Behaviour After Docking
They attach using:
Generic adhesins to biofilm matrix (non-specific)
Specific adhesins to host receptors
▸ They then “pause” and use QS to count their own density
Only when a quorum is reached
▸ Pathogens upregulate additional virulence genes
▸ These new genes are QS-controlled
▸ This is when they become truly infectious and cause disease
