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
E. Focal
Bacilus anthraxis or Clostriudium Bascilium
Systeminc infection
P spreads throughout body of organism
-E: Yersinia pestis
Secondary infection
Primary infection can lead to secondary by another P
eg. influenza and pneomonia
Mechanisms of viral spread
-V may remain localised to body surface through which they entered (skin, respiratory tract, intestine, etc)
-Or they can cause generalised infections associated with viremia (V in blood)
-papilloma V cause warts and repliacte in skin epithelia and spread through neighboring cells
-Cells that infect mucosal layer, like coronaviruses, spread in similar way. Infection is limited to mucosa probably due to limited cell tropism in other tissues
Lymphatic system
Complex network of tissues, organs and vessels in vertebrates that is part of immune system and complementary to circulatory system
-Lymph nodes, lymphoid organs and lymphoid tissues such as bone marrow make up this system
-excess fluid from blood is carried in lymph to heart
V and Lymph
Many V will move from a localised site and disseminate within host, firstly through lymphatic system and then into blood stream and to other organs
-Polio goes from gut to nervous system
-rabies
-smallpox
