Host-Microbe Interactions and Pathogenesis Part 3

what are the 4 things a pathogen must do to be successful?

1. adhere to the hosts tissues (adherence structures)

2. invade tissues and take nutrients (make enzymes and binding proteins)

3. evade the immune system long enough to replicate/reproduce (confuse and suppress)

4. find a new host, they must spread if they want to persist in a population

invasins

proteins that assist in tissue invasion

the effects of toxins can…

kill cells and release their nutrients into the surrounding environment

in many cases, clotting at the site of injury can…

trap bacteria so that phagocytes can destroy them more easily

coagulase

an invasin that is produced by staphylococcus aureus and it enhances coagulation (clotting)

streptokinase

an invasin produced by some strands of streptococcus that destroys clotting proteins

hyaluronidase

destroys sugars that hold cells together in epithelial tissue

collagenase

destroys the collagen proteins that hold cells together in connective tissue

how can some pathogens accomplish both tissue invasion and nutrient aquisition?

they can use toxins, toxins allow invasion by destroying the actual cells of a tissue

what is it called when toxins or infections kill cells?

cytopathic effect

what are the 2 general pathways for immune system evasion?

hiding from host defenses (pathogens prevent their immune cells from identifying antigens)

and undermining host defenses (even if identified, pathogens can prevent activation of immune cells or block immune cell function)

antigenic masking

a way of hiding from the immune system, pathogens have receptors that bind to host self-antigens

these antigens coat the surface of the cell, so pathogens are much harder to recognize using adaptive immune cells

anthrax

makes an A-B toxin called lethal toxin, it is released after bacterial cells are brought in by phagocytosis, and once lethal toxin gets into the cytoplasm of the macrophage, causes the cell to die by apoptosis. After the cell dies, bacteria can escape from the dying macrophage

q-fever (coxiella burnetii)

a flu-like infection acquired from livestock, rare in the US, causes intracellular infections inside of lysosomes.

it is mostly immune to phagocytosis, and will live and grow inside of phagocytic cells

how do microbes do tissue invasion and nutrient acquisition using coagulase?

enhances blood clotting to trap bacteria in a thick clot, hiding them from phagocytes

how do microbes do tissue invasion and nutrient acquisition using streptokinase?

dissolves blood clots, allowing bacteria to escape and invade other tissues

how do microbes do tissue invasion and nutrient acquisition using hyaluronidase?

destroys the sugars (extracellular matrix) holding epithelial cells together

how do microbes do tissue invasion and nutrient acquisition using collagenase?

breaks down collagen proteins in CT and destroys physical barriers like the skin

how do microbes do tissue invasion and nutrient acquisition using cytopathic effect?

the killing of host cells by toxins (C. diff binary toxin), which release nutrients like sugars and amino acids for the microbe to use

2 ways pathogens use to survive host defenses

hiding or undermining

antigen masking

pathogen coats itself in host self-antigens, so adaptive immune cells cant recognize it as foreign

antigenic mimicry

using capsules or slime layers made of sugar similar to those found on human cells to “blend in”

antigenic variation

rapidly mutating or switching surface antigens so that memory cells from previous infections can no longer work

what are the methods that pathogens can prevent destruction by neutrophils and macrophages

killing phagocytes, blocking fusion, escape, adaptation

staphylococcus aureus

produces coagulase to hide in clots, uses binding proteins to coat itself in host antigens

streptococcus

produces streptokinase to dissolve clots and escape

neisseria meningitis

builds capsule out of sialic acid, to avoid detection (mimincry)

trypanosoma brucei

causes sleeping sickness by constantly swapping surface antigens, making immune responses start over repeatedly (antigenic variation)

bacillus anthracis (anthrax)

makes lethal toxin, which causes macrophages to die by apoptosis

coxiella burnetii

adapted to live and grow in the lysosomes of phagocytic cells