colonizing and invasion virulence factors

colonizing and invasion virulence factors

3. •Formation of niche (colonies) in the host (includes adhesion to cells)
•Resist Physical Removal
•Establishment of the pathogen at the appropriate portal of entry

4. •Virulence factors for colonization:
•Pili (fimbriae)
•Adhesins
•Biofilms

5. •Appendages on the cell wall of the
pathogen
•Protein tubes originate from the
cytoplasmic membrane
•Protrudes out after it penetrates the
peptidoglycan layer of the cell wall
•Fimbriae - bristle-like short fibers on the
bacterial surface
•Pili - long hair-like tubular microfibers on
the surface of bacteria

6. •Pili - long hair-like tubular microfibers on the surface of bacteria
•The pili are found in some gram negative bacteria only
•The fimbriae are found in both the gram negative and gram positive
bacteria
•Fimbriae – Attachment & agglutination of blood cells (leukocytes,
epithelial cells, erythrocytes, etc.)
•Pili – Attachment alone

7. ADHESINS
•Cell-surface components or appendages of bacteria that facilitate adhesion or
adherence to other cells or to surfaces
•Most fimbria of gram-negative bacteria function as adhesins, but in many cases it is a minor
subunit protein at the tip of the fimbriae that is the actual adhesin.
•In gram-positive bacteria, a protein or polysaccharide surface layer serves as the specific
adhesin.
•To effectively achieve adherence to host surfaces, many bacteria produce multiple
adherence factors called adhesins.

13. •Community of one or more types of microorganisms that can grow on many
different surfaces
•Bacteria, fungi and protists
•Protects the pathogen from immune system & antibiotics
•Severe diseases
•Steps:
•Attachment to a surface
•Microcolony formation
•Biofilm maturation
•Detachment (also termed dispersal) of bacteria which may then colonize
new areas

16. •Ability to invade tissues
•Aided by the production of bacterial extracellular substance which
breaks down primary and secondary defenses of the body.
•These extracellular substances are called invasins.
•Most invasins are proteins (enzymes) which damages the host cells
and/or facilitate the growth and spread of pathogens.

17. •Confused with exotoxins
•Act at a short range and may not actually kill cells as part of their range
of activity
•Exotoxins are often cytotoxic and may act at remote sites (removed
from the site of bacterial growth)
•Exotoxins typically are more specific and more potent in their activity
than invasins
•Even so, some classic exotoxins (e.g. diphtheria toxin, anthrax toxin)
may play some role in colonization or invasion in the early stages of an
infection

18. •Some invasins (e.g. staphylococcal leukocidin) have a relatively
specific cytopathic effect.
•Encompasses
•Mechanisms for colonization (adherence and initial multiplication)
•Production of extracellular substances ("invasins"), that promote the
immediate invasion of tissues
•Ability to bypass or overcome host defense mechanisms which
facilitate the actual invasive process.

19. •Spreading factors:
•Hyaluronidase:
•Attacks the interstitial cement ("ground
substance") of connective tissue by
depolymerizing hyaluronic acid.
•Collagenase:
•Breaks down collagen, the framework of muscles,
which facilitates gas gangrene due to these
organisms.
•Neuraminidase:
•Neuraminic acid (also called sialic acid), an
intercellular cement of the epithelial cells of the
intestinal mucosa.

20. •Spreading factors:
•Streptokinase & staphylokinase:
•Convert inactive plasminogen to plasmin which digests fibrin
and prevents clotting of the blood.
•The relative absence of fibrin in spreading bacterial lesions
allows more rapid diffusion of the infectious bacteria.
•Coagulase:
•Fibrinogen to fibrin
•Clotting

22. •Phospholipases:
•Hydrolyze (polar groups) phospholipids in
cell membranes
•Lecithinases:
•destroy lecithin (phosphatidylcholine) in cell
membranes.
•Hemolysins:
•Lyse RBCs and other cells
•Eg - Streptolysin

23. THANK YOU