pathogenicity
the ability to cause disease by overcoming host defenses and immune system
virulence
the degree of pathogenicity/how sick pathogenic microbes make you depends on the virulence
virulent factors: microbe properties
portals of entry
- mucous membrane
i. respiratory tract - easiest entry.
ex. common cold.
ii. gastrointestinal tract - undercooked food, water, contaminated fingers.
iii. genitourinary tract - sexually transmitted.
ex. HIV
iv. conjunctiva - membrane that lines the eyelids. - skin
i. hair follicles
ii. sweat glands
ex. hookworm larvae - parenteral
punctures, wounds, bites, cuts, injections
ex. tettanus
ID50
infectious dose.
the dose that will cause an infection to 50% of the population.
measures the virulence.
high ID50: means you need to encounter more microbes in order to get sick. therefore, it is less potent.
low ID50: means you need to encounter less microbes in order to get sick. therefore, it is very potent.
LD50
lethal dose.
the lethal dose for 50% of the population.
measures the amount of toxins released by the microbe that harm the host.
a high LD50 = low virulence. you need a larger volume/dose of the toxin for it to be lethal.
low LD50 = high virulence. you need a smaller volume/dose of the toxin for it to be lethal, very potent!
adherence
process where pathogens attach to host tissues: adherence.
adhesions/ligands: proteins on the pathogen that bind to host receptors found on host cells. how firmly they attach affects their ability to cause disease.
glycocalyx, fimbriae, and biofilms increase adherence.
how do pathogens penetrate the hosts defenses?
capsules
cell wall
enzymes
antigenic variation
capsules
glycocalyx (slime or capsule)
helps avoid phagpcytes.
cell wall
M protein - phagocyte resistence
Opa protein - allows attachment to host cells.
waxy lipid - mycolic acid (virulence factor) resists digestion from phagocytes.
enzymes
- coagulases
- kinases - digest fibrin clots
- hyaluronidase - digest polysaccharides/break bonds
- colagenase - breaks down collagen layr to get into deeper tissue
- Iga protease
antigenic variation
when antigens are altered by pathogens making antibodies ineffective
penetration to the host
- invasins - surface proteins made by bacteria that rearrange actin filaments of the cytoskeleton, causing the host cells plasma membrane to RUFFLE>
- actin - give the microbe the ability to move SIDEWAYS.
ex. Shigella and Listeria. can survive within phagocytes and live within their cytoplasm.
biofilms
helps evade phagocytes
microbes are shielded by the extracellular polymeric substance
pathogens damage the hosts cells by
- using the hosts nutrients
*SIDEROPHORES - bind iron more tightly that host cells do. iron is required for RBCS. steal iron from the host - cause direct damage by
disrupting host cell function
using the hosts cell nutrients
producing waste product
multiplying in host cells causing cells to rupture - producing toxins.
transported by blood and lymph causing damage to other sites.
toxins are poisonous substances produced by the microbe.
toxigenicity
the ABILITY of a microbe to produce a toxin.
toxemia
the presence of toxins in the blood
intoxications
the presence of lingering of a toxin WITHOUT microbial growth or after lysis.
2 types of toxins:
- exotoxins: PROTEINS. affect cell function.
come from DNA and are hydrophilic.
mostly in gm (+)
part of normal growth and metabolism
harm over and over due to enzymatic nature.
rapidly transmitted throughout the body. - endotoxins: LIPIDS. only gm (-)
part of the cell wall in GM (-), not part of normal metabolism.
the LIPID A portion (lipopolysaccharide): hydrophobic.
these toxins are released during lysis and multiplication.
!! stimulate macrophages to release cytokines which are chemicals that will initiate an immune response by inducing the hypothalamus to produce prostaglandins which cause a fever by resetting body temperature.
cause coagulation.
