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Microbial mechanisms of pathogenicity
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Pathogenicity
the ability to cause disease
more pathogenic = more dangerous
Virulence
the degree of pathogenicity
Portals of entry
most pathogens have a preferred portal of entry/invasion
mucous membranes(most bacteria)
skin
parenteral route
Parenteral route
deposited directly into tissues when barriers are penetrated (punctures, injections, bites, cuts, wounds and surgery)
ID 50
infectious dose for 50% of a sample population
What does ID 50 measure
virulence of a microbe
LD 50
lethal dose for 50% of a sample population
what does LD 50 measure
potency of a toxin
Which does a lower LD 50 or ID 50 mean?
microbe is more virulent/toxic, might not detect the bug in a sample, so give whole population vaccines
Ex. Bacillus anthracis- skin is easier to acquire bc only 10-50 ID
Adherence(Adhesion)
process where pathogens attach to host tissues
higher adherence = bugs will stay, not get coughed out and be more virulent
Adhesins (ligands)
bind to receptors on the host cells
Glycocalyx
type of adhesins, capsules and slime layer (IN SUGARS)
Fimbriae
hair like adhesins,
Pilli
bigger hair like structure
Biofilms
communities that share nutrients
happens more in nature (community of obligate aerobes on top, anaerobes most deep, etc. sharing nutrients based on oxygen)
Capsules
help cell penetrate host defenses
glycocalyx around the cell wall
help bug survive, bc they impair phagocytosis
Ex. streptococcus pneumoniae
M protein
resists phagocytosis
not only in bacteria → can go to heart. makes our immune system confused and causes autoimmune disorders
Famous m protein bug?
Streptococcus pyogenes!!!!!!!
Another name for streptococcus pyogenes?
Group A strep, GAS
Opa protein
allows attachment to host cells
Ex. neisseria gonorrhoeae
Waxy lipid(mycolic acid)
resists digestion, acid fast staining
Waxy lipid bug?
Mycobacterium tuberculosis!! KNOW THIS!
Different enzymes
coagulates, kinases, hyaluronidase, collagen's, IgA proteases
What bacteria produces enzymes
strepto and stapho bacteria
Coagulases
isolates the bug
coagulate fibrinogen
Kinases
digest fibrin clots, once bug is built they can now spread
Hyaluronidase
digest polysaccharides that hold cells together, so cells fall apart
Collagenase
breaks down collagen, skin gets fragile
Hyaluronidase and collagenase are?
very big vigilance factors, because it helps bacteria swim deeper into tissue
IgA proteases
destroys IgA antibodies
IgA antibodies
present in mucus, to help protect us
Antigenic variation
pathogens alter their surface antigens (and antibodies are rendered ineffective)
change shape to prevent antibodies from blocking their receptor
Invasins
helps them get into the host cell cytoskeleton
surface proteins produced by bacteria that rearrange actin filaments of the cytoskeleton, causes membrane ruffling
Actin and Invasins
use actin to move from one cell to the next (shigella and listeria)
cells can never reach bacteria, because they jump to another cell before lysosomes comes
Siderophores
uses host nutrients (they need iron- part of chemical formula)
proteins secreted by pathogens that bind iron more tightly than host cells
used if RBCS are ruptured
Direct damage
disrupts host cell function
uses host cell nutrients
produces waste products
multiples in host cells and causes ruptures
Toxins
poisonous substances produced by microorganisms
produce fever, cardiovascular problems, diarrhea, and shock
Toxigenicity
ability of a microorganism to produce a toxin
Toxemia
emia= in the blood
presence of toxin in the host’s blood
Intoxications
presence of toxin without microbial growth
bacteria died, but produced toxins during its time, making someone sick
Exotoxins
made in cytoplasm and then released OUTSIDE of the cell
proteins produced and secreted by bacteria
grow fast by ribosomes = more toxins grow
Solubility and exotoxins
its soluble in bodily fluids, destroy host cells and inhibit metabolic functions
Antitoxins
antibodies against specific exotoxins
Toxoids
inactivated exotoxins used in vaccines/chemical treatment
they look similar to toxin, but through heat they are inactive
What type of bacteria have exotoxins?
mostly gram positive, but both gram negative and positive produce them!
A-B toxins
contain an enzyme component (A PART)
and binding component (B PART)
Ex. T dap
A-B Toxin action
bacterium produces and releases the A-B toxin
B (binding) component of exotoxin attaches to host cell receptor
3. the plasm membrane of the host cell invaginates (FOLDS INWARD), and the exotoxin enters the cell
A-B receptor are enclosed in pinched of portion of plasma membrane during PINOCYTOSIS
A-B components separate, and B component is released
A component
alters host cell function by inhibiting protein synthesis
it kills the host
B component
finds the host, blocks the receptor and then is released
How does endotoxin enter the cell
receptor-mediated endocytosis
Membrane-disrupting toxins
lyse host cells by disrupting plasma membranes
MD exotoxin- Leukocidins
kill phagocytic leukocytes
MD exotoxin- Hemolysins
kill erythrocytes by forming protein channels
MD exotoxin- streptolysins
hemolysis produced by streptococci (kills RBCS by GAS)
Superantigens
causes an intense immune response due to release of cytokines from host cells (T cells)
Superantigens symptoms
fever, nausea, vomiting, diarrhea, shock, and death
Genotoxins
damage DNA
Genotoxins symptoms
causes mutations, disrupting cell division, and leading to cancer
Endotoxins
intracellular, don’t get from gram positive (bc no LPS)
What does gram negative have?
endotoxins and exotoxins
Endotoxins in bacteria?
lipid A portion of lipopolysaccharides of gram negative bacteria
released during bacterial multiplication and when g negative bacteria die
Endotoxins causes?
causes disseminated intravascular coagulation
Macrophage endotoxin steps?
a macrophage ingests a gram-negative bacterium
the bacterium is degraded in a vacuole, releasing endotoxins, that induce the macrophage to produce cytokines