Adherence, Colonisation and Invasion Flashcards
Virulence steps
contact
adhesion
Invasion
infection
adherence
It is the enhanced ability of M to attach to host tissues
-it is neccessary but not suffficient to start a disease
-There are many different receptors coating the P and the tissue where it binds
Adhesions
Glycoproteins or lipoproteins found on P surface that enable it to bind to host cells
Virus adhesion
Viruses attach to receptor molecules on cell surface, these can be proteins, carbs or lipids
-they have a single primary receptor as well as co-receptor ( HIV-1: CD4 and CCR5, CXCR4)
Attachment factors
Low affinity receptors that are involved and facilitate an initial low affinity binding which is initial step
Heparan sulfate
-Found in ECM
-Serves as an attachment factor for many viruses, therefore these receptors have low specificity
Binding NB
serves to overcome repulsive electrostatic forces
Viral receptors
-diverse
-Have own cellular function ( cytomegalovirus binds to epidermal growth factor, EGF is a powerful mitogen)
-Viruses (V) subvert cell receptors/proteins to utilise them to gain entry
-dictate cell tropism
E. B binding
S.aureus binding is facilitated via fibrinogen using the N2 and N3 domains of its SDrG adhesion protein
-Opa adhesion proteins of Neisseria species attach to carcinoembryonic antigen related adhesion molecules (CEACAM) on epithelial surface
Capsules
It is a thick hydrated polysaccharide-based( or peptide based) coating outside the plasma membrane and celll wall
Capsule function
-Sticky and contains specific receptors to facilitate attachment on host tissues
-Capsules found in encapsulated strains of Streptococcus pneumonia protect from phagocytosis
Fimbriae, Flagella and Pili
surface protein structures that function in attachment
-pili are longer and fewer in number than fimbriae
-pili used in horizontal gene transfer (conjugation)
Fimrbia and flagella adhesion
-Flagella facillitate adherence to host cells
-Fimbriae possess adhesins which alow for attachment to cells or ECM
-E.coli use them to attach to mannose receptors
Colonization
Growth of micro-organisms after they’ve gained access to host tissue
Biofilms
A hydrogel composed of polysaccharides, proteins, lipids and DNA that comprises a consortium of bacteria/M that adhere to one another within the gel matrix
Biofilm phenotype effect
-B within biofilm are physiologically distinct from planktonic cells
-They are more protected, exhibit communal behaviour
-undergo a phenotypic shift and express/regulate different protein sets
-antibiotic resistance
E. biofilms
Pseudomonas aeruginosa are opportunistic P that form biofilms on hospital equipment and on damaged tissue surfaces (burns)
Invasion
-Dissemination of a P throughout local tissues or body
-P may produce exoenzymes or toxins which allow them to colonise and damage host tissue as they spread deeper
-P may also produce virulence factors (mainly enzymes) to protect them against immune system defences
-A P’s specific virulence factors determine degree of tissue damage
E. specialised enzymes
H.pylori
-Contact with stomach acid keeps the mucin lining the epithelial cell layer in spongy-like state that is impermeable to H.pylori
-B releases urease which neutralises stomach acid by forming ammonia from urea hydrolysis
-This causes mucin to liquify which allows B to swim through it
exoenzymes
-Virulence factors that facilitate invasiveness
-Invasiveness requires P to break down host tissues to gain access to deeper or distal tissues
-includes: Hyaluronidase, Coagulase and streptokinase
Hyaluronidase
-catalyses the hydrolysis of hyaluronan, a constituent of the ECM which increases tissue permeability
-Other enzymes that degreade ECM include collagenase, chondroitin sulfatase, neuramidase
-streptococcus pyogenes
Coagulase and streptokinase
-When staphylococus aureus enter cut, they produce coagulase
-Clot walls off pathogen, blocking access to immune cells
-When P has produced enzymes to fight immune system, streptokinase dissolves clot which release P to bloodstream and deeper tissues
Streptococcus pyogenes
Local infection
-Confined to small area of body, typically near point of entry (like boil with staphylococcus)
-P is largely contained to location
-Include urinary tract infections confined to bladder or pneumonia to lungs
Focal infection
Localised P and toxins it produces goes to secondary location
