203 L15 Flashcards
Mechanism of infection
What are the 4 steps required to get an infection?
- Colonise the host
- Evade host defences
- Proliferate
- Cause damage
Colonise the host
Bacteria —– to prevent being washed away and anchor to their preferred niche
They do this via specific ——– molecules (often reversible) for example staphlyococcus ——– use —— acid and pseudomonas ———– use ——- capsule.
They do this via non specific ———.
In gram negative bacteria this is the —–, —— and —— membrane ——-.
In gram positive bacteria this is ——— in the cell wall and ———-.
Examples
Neisseria ————
- ——— attach to the receptor on ————— cell surface
- —– retract allowing adhesion of ———- ——— adhesin to receptor on cell surface.
Staphylococcus ———-
- ———- acids mediate initial ———– to the cell surface
- ———– mediate stronger interaction with ——- proteins - e.g. fibrinogen, fibronectin, collagen.
It’s more dangerous because it can bind to ——- proteins as well as ——-. Therefore can grow on medical devices when they get covered by the host’s cells and proteins.
Bacteria stick to prevent being washed away and anchor to their preferred niche
They do this via specific adhesion molecules (often reversible) for example staphlyococcus aureus use techoic acid and pseudomonas aeruginosa use alginate capsule.
They do this via non specific adhesins.
In gram negative bacteria this is the pili, fimbrae and outer membrane adhesins.
In gram positive bacteria this is proteins in the cell wall and MSCRAMMS.
Examples
Neisseria Meningitidis
Pili attach to the receptor on nasopharengeal cell surface
Pili retract allowing adhesion of outer membrane adhesin to receptor on cell surface.
Staphylococcus aureus
Techoic acids mediate initial attachment to the cell surface
MSCRAMMS mediate stronger interaction with matrix proteins - e.g. fibrinogen, fibronectin, collagen.
It’s more dangerous because it can bind to matrix proteins as well as cells. Therefore can grow on medical devices when they get covered by the host’s cells and proteins.
Colonise the host
Bacteria —– to prevent being washed away and anchor to their preferred niche
They do this via specific ——– molecules (often reversible) for example staphlyococcus ——– use —— acid and pseudomonas ———– use ——- capsule.
They do this via non specific ———.
In gram negative bacteria this is the —–, —— and —— membrane ——-.
In gram positive bacteria this is ——— in the cell wall and ———-.
Examples
Neisseria ————
- ——— attach to the receptor on ————— cell surface
- —– retract allowing adhesion of ———- ——— adhesin to receptor on cell surface.
Staphylococcus ———-
- ———- acids mediate initial ———– to the cell surface
- ———– mediate stronger interaction with ——- proteins - e.g. fibrinogen, fibronectin, collagen.
It’s more dangerous because it can bind to ——- proteins as well as ——-. Therefore can grow on medical devices when they get covered by the host’s cells and proteins.
Bacteria stick to prevent being washed away and anchor to their preferred niche
They do this via specific adhesion molecules (often reversible) for example staphlyococcus aureus use techoic acid and pseudomonas aeruginosa use alginate capsule.
They do this via non specific adhesins.
In gram negative bacteria this is the pili, fimbrae and outer membrane adhesins.
In gram positive bacteria this is proteins in the cell wall and MSCRAMMS.
Examples
Neisseria Meningitidis
Pili attach to the receptor on nasopharengeal cell surface
Pili retract allowing adhesion of outer membrane adhesin to receptor on cell surface.
Staphylococcus aureus
Techoic acids mediate initial attachment to the cell surface
MSCRAMMS mediate stronger interaction with matrix proteins - e.g. fibrinogen, fibronectin, collagen.
It’s more dangerous because it can bind to matrix proteins as well as cells. Therefore can grow on medical devices when they get covered by the host’s cells and proteins.
Evade host defences
Hosts defences
——-, ———- barriers have ———- secretions, ——– restriction (—— is important for ———, host keeps it tightly bound to its proteins so the bacteria have to work to get through it),
Evading these defences
————–, ———– cells, ——-.
Crossing the skin/mucous barrier
Surgery, biting insects
Invasion by Listeria
Listeria gets ——— by cells, —— it. Ends up in the ——– of the cell and rearranges the hosts ——– ———- to form a – of —— that it uses to move from one cell to the other.
Resisting antimicrobial fluids
Alter the surface ——- to —– peptides
Produce ——— to chop up proteins
Produce a ——— barrier (capsule, S-layer, outer membrane)
Evading the immune system
——— the cells so the immune defences do not ——- the invader as —— ——.
Capsule
The capsule protects any —— on the surface of the ——– that would be recognised by the ——– response. It stops ———- being deposited on the ——— of bacteria which is needed for cells to be able to —— the bacteria. E.g. Streptococcus ————- capsule - India Ink doesn’t penetrate the area around the bacteria
Invading the immune system Bacteria attaches to —– cell and ——– the cell preventing the ——– system from recognising it. E.g ———– ———- which causes TB hides inside the ———-.
Mimicking the host to appear as self
The bacteria binds the ——– the other way at the —- region not the ——— region so it looks like ——–. E.g. staphylococcus ——– - ——— binds to the —- region of the ——- inhibiting the activation of complement, phagocytosis and ADCC.
———- bind to ——– —– proteins. As well as being involved in ———–, the cell is covered in a layer of ——- proteins and so is recognised as ——–.
Bacteria bind to ——- – and evade ———– killing. If —– forms on a cell it can target complement -mediated damage. ——– — binds to our cells and degrades —– forming on the surface to protect us from ——. E.g. —— acid capsule of Neisseria ————- & —– protein capsule of streptococcus —— bind —— — and evade ——— killing.
Destroying the immune system Normally complement (C3) becomes ------ which attracts the ---------- cells to come and help kill the bacteria. Bacteria is recognised and taken up by ---------- cells. They fuse with --------- which kills the bacteria and are then presented on the surface for the immune response
Kill the phagocyte
Bacillus ——— produces a —— that is pumped out and kills the ———- cell releasing the bacteria
Detoxify the phagocyte
———— ————- detoxify the phagocyte by detoxifying —— or preventing the fusion of ———– with the endocytosed bacteria so the —— doesn’t change and bacteria can ——-.
Complement factor proteolysis
C5 is deposited on the bacterial cell and is changed to —– and —–. —– is a ———— for the ———- cells. Streptococcus ———- forms a —— ———— that destroys the —— signal so the ——— cells don’t come.
Complement disruption - Staphylococcus —— secretes ——– which bind to the ——- cells stopping them from seeing —–.
Confuse the immune system
——– disruption - secretion of ———-
Mimicking - binding ——- —
Outer membrane blebs - blebs of bacteria outer membrane containing ———– and outer membrane ——— released as immune ——– so the host tries to kill those instead of the bacteria
Antigenic variation
Bacteria that ———- the immune system response have a ——– antigen that is no longer ———- by the immune system
Bacteria produce really long ——- stopping the host from depositing things like —– on the surface which is needed for ——— to work and lyse the bacteria.
Evade host defences
Hosts defences
Skin, mucus barriers have antimicrobial secretions, iron restriction (iron is important for enzyme, host keeps it tightly bound to its proteins so the bacteria have to work to get through it),
Evading these defences
Complement, phagocytic cells, antibodies.
Crossing the skin/mucous barrier
Surgery, biting insects
Invasion by Listeria
Listeria gets internalised by cells, invading it. Ends up in the cytoplasm of the cell and rearranges the hosts actin cytoskeleton to form a tail of ActA that it uses to move from one cell to the other.
Resisting antimicrobial fluids
Alter the surface charge to repel peptides
Produce proteases to chop up proteins
Produce a physical barrier (capsule, S-layer, outer membrane)
Evading the immune system
Hide the cells so the immune defences do not recognise the invader as non-self.
Capsule
The capsule protects any proteins on the surface of the bacteria that would be recognised by the immune response. It stops complement being deposited on the surface of bacteria which is needed for cells to be able to lyse the bacteria. E.g. Streptococcus pneumoniae capsule - India Ink doesn’t penetrate the area around the bacteria
Invading the immune system Bacteria attaches to host cell and enters the cell preventing the immune system from recognising it. E.g Myobacterium tuberculosis which causes TB hides inside the macrophages.
Mimicking the host to appear as self
The bacteria binds the ——– the other way at the —- region not the ——— region so it looks like ——–. E.g. staphylococcus ——– - ——— binds to the —- region of the ——- inhibiting the activation of complement, phagocytosis and ADCC.
———- bind to ——– —– proteins. As well as being involved in ———–, the cell is covered in a layer of ——- proteins and so is recognised as ——–.
Bacteria bind to ——- – and evade ———– killing. If —– forms on a cell it can target complement -mediated damage. ——– — binds to our cells and degrades —– forming on the surface to protect us from ——. E.g. —— acid capsule of Neisseria ————- & —– protein capsule of streptococcus —— bind —— — and evade ——— killing.
Destroying the immune system Normally complement (C3) becomes ------ which attracts the ---------- cells to come and help kill the bacteria. Bacteria is recognised and taken up by ---------- cells. They fuse with --------- which kills the bacteria and are then presented on the surface for the immune response
Kill the phagocyte
Bacillus ——— produces a —— that is pumped out and kills the ———- cell releasing the bacteria
Detoxify the phagocyte
———— ————- detoxify the phagocyte by detoxifying —— or preventing the fusion of ———– with the endocytosed bacteria so the —— doesn’t change and bacteria can ——-.
Complement factor proteolysis
C5 is deposited on the bacterial cell and is changed to —– and —–. —– is a ———— for the ———- cells. Streptococcus ———- forms a —— ———— that destroys the —— signal so the ——— cells don’t come.
Complement disruption - Staphylococcus —— secretes ——– which bind to the ——- cells stopping them from seeing —–.
Confuse the immune system
——– disruption - secretion of ———-
Mimicking - binding ——- —
Outer membrane blebs - blebs of bacteria outer membrane containing ———– and outer membrane ——— released as immune ——– so the host tries to kill those instead of the bacteria
Antigenic variation
Bacteria that ———- the immune system response have a ——– antigen that is no longer ———- by the immune system
Bacteria produce really long ——- stopping the host from depositing things like —– on the surface which is needed for ——— to work and lyse the bacteria.
Evade host defences
Hosts defences
——-, ———- barriers have ———- secretions, ——– restriction (—— is important for ———, host keeps it tightly bound to its proteins so the bacteria have to work to get through it),
Evading these defences
————–, ———– cells, ——-.
Crossing the skin/mucous barrier
Surgery, biting insects
Invasion by Listeria
Listeria gets ——— by cells, —— it. Ends up in the ——– of the cell and rearranges the hosts ——– ———- to form a – of —— that it uses to move from one cell to the other.
Resisting antimicrobial fluids
Alter the surface ——- to —– peptides
Produce ——— to chop up proteins
Produce a ——— barrier (capsule, S-layer, outer membrane)
Evading the immune system
——— the cells so the immune defences do not ——- the invader as —— ——.
Capsule
The capsule protects any —— on the surface of the ——– that would be recognised by the ——– response. It stops ———- being deposited on the ——— of bacteria which is needed for cells to be able to —— the bacteria. E.g. Streptococcus ————- capsule - India Ink doesn’t penetrate the area around the bacteria
Invading the immune system Bacteria attaches to —– cell and ——– the cell preventing the ——– system from recognising it. E.g ———– ———- which causes TB hides inside the ———-.
Mimicking the host to appear as self
The bacteria binds the ——– the other way at the —- region not the ——— region so it looks like ——–. E.g. staphylococcus ——– - ——— binds to the —- region of the ——- inhibiting the activation of complement, phagocytosis and ADCC.
———- bind to ——– —– proteins. As well as being involved in ———–, the cell is covered in a layer of ——- proteins and so is recognised as ——–.
Bacteria bind to ——- – and evade ———– killing. If —– forms on a cell it can target complement -mediated damage. ——– — binds to our cells and degrades —– forming on the surface to protect us from ——. E.g. —— acid capsule of Neisseria ————- & —– protein capsule of streptococcus —— bind —— — and evade ——— killing.
Destroying the immune system Normally complement (C3) becomes ------ which attracts the ---------- cells to come and help kill the bacteria. Bacteria is recognised and taken up by ---------- cells. They fuse with --------- which kills the bacteria and are then presented on the surface for the immune response
Kill the phagocyte
Bacillus ——— produces a —— that is pumped out and kills the ———- cell releasing the bacteria
Detoxify the phagocyte
Mycobacterium ————- detoxify the phagocyte by detoxifying —— or preventing the fusion of ———– with the endocytosed bacteria so the —— doesn’t change and bacteria can ——-.
Complement factor proteolysis
C5 is deposited on the bacterial cell and is changed to —– and —–. —– is a ———— for the ———- cells. Streptococcus ———- forms a —— ———— that destroys the —— signal so the ——— cells don’t come.
Complement disruption - Staphylococcus —— secretes ——– which bind to the ——- cells stopping them from seeing —–.
Confuse the immune system
——– disruption - secretion of ———-
Mimicking - binding ——- —
Outer membrane blebs - blebs of bacteria outer membrane containing ———– and outer membrane ——— released as immune ——– so the host tries to kill those instead of the bacteria
Antigenic variation
Bacteria that ———- the immune system response have a ——– antigen that is no longer ———- by the immune system
Bacteria produce really long ——- stopping the host from depositing things like —– on the surface which is needed for ——— to work and lyse the bacteria.
Evade host defences
Hosts defences
Skin, mucus barriers have antimicrobial secretions, iron restriction (iron is important for enzyme, host keeps it tightly bound to its proteins so the bacteria have to work to get through it),
Evading these defences
Complement, phagocytic cells, antibodies.
Crossing the skin/mucous barrier
Surgery, biting insects
Invasion by Listeria
Listeria gets internalised by cells, invading it. Ends up in the cytoplasm of the cell and rearranges the hosts actin cytoskeleton to form a tail of ActA that it uses to move from one cell to the other.
Resisting antimicrobial fluids
Alter the surface charge to repel peptides
Produce proteases to chop up proteins
Produce a physical barrier (capsule, S-layer, outer membrane)
Evading the immune system
Hide the cells so the immune defences do not recognise the invader as non-self.
Capsule
The capsule protects any proteins on the surface of the bacteria that would be recognised by the immune response. It stops complement being deposited on the surface of bacteria which is needed for cells to be able to lyse the bacteria. E.g. Streptococcus pneumoniae capsule - India Ink doesn’t penetrate the area around the bacteria
Invading the immune system Bacteria attaches to host cell and enters the cell preventing the immune system from recognising it. E.g Myobacterium tuberculosis which causes TB hides inside the macrophages.
Mimicking the host to appear as self
The bacteria binds the antibody the other way at the Fc region not the Fab region so it looks like self. E.g. staphylococcus auoreus
Protein A binds to the Fc region of the antibody inhibiting the activation of complement, phagocytosis and ADCC.
MSCRAMMS bind to extracellular matrix proteins. As well as being involved in attachment, the cell is covered in a layer of host proteins and so is recognised as self.
Bacteria bind to factor H and evade complement killing. If C3b forms on a cell it can target complement -mediated damage. Factor H binds to our cells and degrades C3b forming on the surface to protect us from damage. E.g. sialic acid capsule of Neisseria meningitidis & M protein capsule of streptococcus pyogenes bind factor H and evade complement killing.
Destroying the immune system Normally complement (C3) becomes C3b which attracts the phagocytic cells to come and help kill the bacteria. Bacteria is recognised and taken up by phagocytic cells. They fuse with lysosomes which kills the bacteria and are then presented on the surface for the immune response
Kill the phagocyte
Bacillus anthracis produces a toxin that is pumped out and kills the phagocytic cell releasing the bacteria
Detoxify the phagocyte
Myobacterium tuberculosis detoxify the phagocyte by detoxifying ROS or preventing the fusion of lysosomes with the endocytosed bacteria so the pH doesn’t change and bacteria can surivive.
Complement factor proteolysis
C5 is deposited on the bacterial cell and is changed to C5b and C5a. C5a is a chemoatrractant for the phagocytic cells. Streptococcus pyogenes forms a C5a peptidase that destroys the C5a signal so the phagocytic cells don’t come.
Complement disruption - Staphylococcus aureus secretes CHIPS which bind to the immune cells stopping them from seeing C5a.
Confuse the immune system
complement disruption - secretion of CHIPS
Mimicking - binding factor H
Outer membrane blebs - blebs of bacteria outer membrane containing lipopolysaccarides and outer membrane proteins released as immune decoys so the host tries to kill those instead of the bacteria
Antigenic variation
Bacteria that survive the immune system response have a mutated antigen that is no longer recognised by the immune system
Bacteria produce really long antigen stopping the host from depositing things like C3b on the surface which is needed for complement to work and lyse the bacteria.
Evade host defences
Hosts defences
——-, ———- barriers have ———- secretions, ——– restriction (—— is important for ———, host keeps it tightly bound to its proteins so the bacteria have to work to get through it),
Evading these defences
————–, ———– cells, ——-.
Crossing the skin/mucous barrier
Surgery, biting insects
Invasion by Listeria
Listeria gets ——— by cells, —— it. Ends up in the ——– of the cell and rearranges the hosts ——– ———- to form a – of —— that it uses to move from one cell to the other.
Resisting antimicrobial fluids
Alter the surface ——- to —– peptides
Produce ——— to chop up proteins
Produce a ——— barrier (capsule, S-layer, outer membrane)
Evading the immune system
——— the cells so the immune defences do not ——- the invader as —— ——.
Capsule
The capsule protects any —— on the surface of the ——– that would be recognised by the ——– response. It stops ———- being deposited on the ——— of bacteria which is needed for cells to be able to —— the bacteria. E.g. Streptococcus ————- capsule - India Ink doesn’t penetrate the area around the bacteria
Invading the immune system Bacteria attaches to —– cell and ——– the cell preventing the ——– system from recognising it. E.g ———– ———- which causes TB hides inside the ———-.
Mimicking the host to appear as self
The bacteria binds the ——– the other way at the —- region not the ——— region so it looks like ——–. E.g. staphylococcus ——– - ——— binds to the —- region of the ——- inhibiting the activation of complement, phagocytosis and ADCC.
———- bind to ——– —– proteins. As well as being involved in ———–, the cell is covered in a layer of ——- proteins and so is recognised as ——–.
Bacteria bind to ——- – and evade ———– killing. If —– forms on a cell it can target complement -mediated damage. ——– — binds to our cells and degrades —– forming on the surface to protect us from ——. E.g. —— acid capsule of Neisseria ————- & —– protein capsule of streptococcus —— bind —— — and evade ——— killing.
Destroying the immune system Normally complement (C3) becomes ------ which attracts the ---------- cells to come and help kill the bacteria. Bacteria is recognised and taken up by ---------- cells. They fuse with --------- which kills the bacteria and are then presented on the surface for the immune response
Kill the phagocyte
Bacillus ——— produces a —— that is pumped out and kills the ———- cell releasing the bacteria
Detoxify the phagocyte
Mycobacterium ————- detoxify the phagocyte by detoxifying —— or preventing the fusion of ———– with the endocytosed bacteria so the —— doesn’t change and bacteria can ——-.
Complement factor proteolysis
C5 is deposited on the bacterial cell and is changed to —– and —–. —– is a ———— for the ———- cells. Streptococcus ———- forms a —— ———— that destroys the —— signal so the ——— cells don’t come.
Complement disruption - Staphylococcus —— secretes ——– which bind to the ——- cells stopping them from seeing —–.
Confuse the immune system
——– disruption - secretion of ———-
Mimicking - binding ——- —
Outer membrane blebs - blebs of bacteria outer membrane containing ———– and outer membrane ——— released as immune ——– so the host tries to kill those instead of the bacteria
Antigenic variation
Bacteria that ———- the immune system response have a ——– antigen that is no longer ———- by the immune system
Bacteria produce really long ——- stopping the host from depositing things like —– on the surface which is needed for ——— to work and lyse the bacteria.
Evade host defences
Hosts defences
Skin, mucus barriers have antimicrobial secretions, iron restriction (iron is important for enzyme, host keeps it tightly bound to its proteins so the bacteria have to work to get through it),
Evading these defences
Complement, phagocytic cells, antibodies.
Crossing the skin/mucous barrier
Surgery, biting insects
Invasion by Listeria
Listeria gets internalised by cells, invading it. Ends up in the cytoplasm of the cell and rearranges the hosts actin cytoskeleton to form a tail of ActA that it uses to move from one cell to the other.
Resisting antimicrobial fluids
Alter the surface charge to repel peptides
Produce proteases to chop up proteins
Produce a physical barrier (capsule, S-layer, outer membrane)
Evading the immune system
Hide the cells so the immune defences do not recognise the invader as non-self.
Capsule
The capsule protects any proteins on the surface of the bacteria that would be recognised by the immune response. It stops complement being deposited on the surface of bacteria which is needed for cells to be able to lyse the bacteria. E.g. Streptococcus pneumoniae capsule - India Ink doesn’t penetrate the area around the bacteria
Invading the immune system Bacteria attaches to host cell and enters the cell preventing the immune system from recognising it. E.g Myobacterium tuberculosis which causes TB hides inside the macrophages.
Mimicking the host to appear as self
The bacteria binds the antibody the other way at the Fc region not the Fab region so it looks like self. E.g. staphylococcus auoreus
Protein A binds to the Fc region of the antibody inhibiting the activation of complement, phagocytosis and ADCC.
MSCRAMMS bind to extracellular matrix proteins. As well as being involved in attachment, the cell is covered in a layer of host proteins and so is recognised as self.
Bacteria bind to factor H and evade complement killing. If C3b forms on a cell it can target complement -mediated damage. Factor H binds to our cells and degrades C3b forming on the surface to protect us from damage. E.g. sialic acid capsule of Neisseria meningitidis & M protein capsule of streptococcus pyogenes bind factor H and evade complement killing.
Destroying the immune system Normally complement (C3) becomes C3b which attracts the phagocytic cells to come and help kill the bacteria. Bacteria is recognised and taken up by phagocytic cells. They fuse with lysosomes which kills the bacteria and are then presented on the surface for the immune response
Kill the phagocyte
Bacillus anthracis produces a toxin that is pumped out and kills the phagocytic cell releasing the bacteria
Detoxify the phagocyte
Myobacterium tuberculosis detoxify the phagocyte by detoxifying ROS or preventing the fusion of lysosomes with the endocytosed bacteria so the pH doesn’t change and bacteria can surivive.
Complement factor proteolysis
C5 is deposited on the bacterial cell and is changed to C5b and C5a. C5a is a chemoatrractant for the phagocytic cells. Streptococcus pyogenes forms a C5a peptidase that destroys the C5a signal so the phagocytic cells don’t come.
Complement disruption - Staphylococcus aureus secretes CHIPS which bind to the immune cells stopping them from seeing C5a.
Confuse the immune system
complement disruption - secretion of CHIPS
Mimicking - binding factor H
Outer membrane blebs - blebs of bacteria outer membrane containing lipopolysaccarides and outer membrane proteins released as immune decoys so the host tries to kill those instead of the bacteria
Antigenic variation
Bacteria that survive the immune system response have a mutated antigen that is no longer recognised by the immune system
Bacteria produce really long antigen stopping the host from depositing things like C3b on the surface which is needed for complement to work and lyse the bacteria.
Proliferate
Bacteria need ———
All nutrients are freely available except —– which is needed by bacteria as a ——- for essential ———.
In the host there is ——– restriction - Lactoferrin in secretions, Transferrin in blood, functional in enzymes, stored as ferritin in cells
Bacteria get the iron by:
Produce siderophores (small iron chelators) - proteins that try and bind to iron
Specific binding proteins - transferrin
Increasing available iron - haemolysin (breaking RBC), protease activity
Adapting to high iron niche of phagosome
Evolving enzymes that use other cofactors e.g. Manganese
Bacteria need nutrients
All nutrients are freely available except iron which is needed by bacteria as a cofactor for essential enzymes.
In the host there is iron restriction - Lactoferrin in secretions, Transferrin in blood, functional in enzymes, stored as ferritin in cells
What is a peptic ulcer?
Break in the lining of the stomach or duodenum, where hydrochloric acid and pepsin are present
What causes peptic ulcer disease?
Helicobacter pylori
Helicobacter pylori
Is a ——- coloniser
About —-% of the world’s population is infected by H.pylori
Transmission - primarily person to person via —– oral or —— oral contact, contaminated —– and —–, contaminated ——-, H. pylori can be present in ——- so can be transmitted sexually
Is a gastric coloniser
About 50% of the world’s population is infected by H.pylori
Transmission - primarily person to person via fecal oral or gastro oral contact, contaminated food and water, contaminated animals, H. pylori can be present in saliva so can be transmitted sexually
Helicobacter pylori
Is a ——- coloniser
About —-% of the world’s population is infected by H.pylori
Transmission - primarily person to person via —– oral or —— oral contact, contaminated —– and —–, contaminated ——-, H. pylori can be present in ——- so can be transmitted sexually
Is a gastric coloniser
About 50% of the world’s population is infected by H.pylori
Transmission - primarily person to person via fecal oral or gastro oral contact, contaminated food and water, contaminated animals, H. pylori can be present in saliva so can be transmitted sexually
How does the H. pylori lead to disease.
It has to first get to the cells in the ———.
Once it’s in the ——— the —— allows it to swim really fast to the ——- layer coating the cells. Its ——– shape gives a screw like movement that allows it to penetrate the ——-. They use ——– to produce a cloud of ——– on their outside to neutralise the —– acid.
Once they have penetrated the mucus layer they attach to the ——– epithelium —– - carbohydrate receptor with their ——- adhesin.
They can now set up a ——— infection. The immune response is not effective because the ————- of the bacteria is poorly recognised by ——– and the —— is poorly recognised by ——-, so there is low levels of ——– production. This allows the bacteria to ——— the immune response.
The bacteria also produces vacuolating toxin A (VacA) which inhibits ———- maturation, proliferation of — and — cells and generation of ——–.
The bacteria coat themselves with ——— and ——— so can mimic the host and appear as ——–.
All these factors allow the bacteria to cause ——– infection and ———-. This results in the loss of function of cells in the ——– area. Depending on where the cells are there are different outcomes of the ———.
How does the H. pylori lead to disease.
It has to first get to the cells in the stomach.
Once it’s in the stomach the flagellum allows it to swim really fast to the mucus layer coating the cells. Its helical shape gives a screw like movement that allows it to penetrate the mucus. They use urease to produce a cloud of ammonia on their outside to neutralise the stomach acid.
Once they have penetrated the mucus layer they attach to the stomach epithelium lewis b carbohydrate receptor with their BabA adhesin.
They can now set up a chronic infection. The immune response is not effective because the LPS of the bacteria is poorly recognised by TLR4 and the flagellum is poorly recognised by TLR5, so there is low levels of cytokine production. This allows the bacteria to evade the immune response.
The bacteria also produces vacuolating toxin A (VacA) which inhibits phagosomal maturation, proliferation of B and T cells and generation of NOS.
The bacteria coat themselves with plasminogen and cholesterol so can mimic the host and appear as self.
All these factors allow the bacteria to cause chronic infection and inflammation. This results in the loss of function of cells in the inflamed area. Depending on where the cells are there are different outcomes of the infection.
How does the H. pylori lead to disease.
It has to first get to the cells in the ———.
Once it’s in the ——— the —— allows it to swim really fast to the ——- layer coating the cells. Its ——– shape gives a screw like movement that allows it to penetrate the ——-. They use ——– to produce a cloud of ——– on their outside to neutralise the —– acid.
Once they have penetrated the mucus layer they attach to the ——– epithelium —– - carbohydrate receptor with their ——- adhesin.
They can now set up a ——— infection. The immune response is not effective because the ————- of the bacteria is poorly recognised by ——– and the —— is poorly recognised by ——-, so there is low levels of ——– production. This allows the bacteria to ——— the immune response.
The bacteria also produces vacuolating toxin A (VacA) which inhibits ———- maturation, proliferation of — and — cells and generation of ——–.
The bacteria coat themselves with ——— and ——— so can mimic the host and appear as ——–.
All these factors allow the bacteria to cause ——– infection and ———-. This results in the loss of function of cells in the ——– area. Depending on where the cells are there are different outcomes of the ———.
How does the H. pylori lead to disease.
It has to first get to the cells in the stomach.
Once it’s in the stomach the flagellum allows it to swim really fast to the mucus layer coating the cells. Its helical shape gives a screw like movement that allows it to penetrate the mucus. They use urease to produce a cloud of ammonia on their outside to neutralise the stomach acid.
Once they have penetrated the mucus layer they attach to the stomach epithelium lewis b carbohydrate receptor with their BabA adhesin.
They can now set up a chronic infection. The immune response is not effective because the LPS of the bacteria is poorly recognised by TLR4 and the flagellum is poorly recognised by TLR5, so there is low levels of cytokine production. This allows the bacteria to evade the immune response.
The bacteria also produces vacuolating toxin A (VacA) which inhibits phagosomal maturation, proliferation of B and T cells and generation of NOS.
The bacteria coat themselves with plasminogen and cholesterol so can mimic the host and appear as self.
All these factors allow the bacteria to cause chronic infection and inflammation. This results in the loss of function of cells in the inflamed area. Depending on where the cells are there are different outcomes of the infection.
What is an ulcer?
A lesion found on the mucous membrane
What is a gastric ulcer?
A lesion found on the mucous membrane of the stomach
