Pathogen

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pathogen

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etiology or cause of disease (koch's postulates)

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pathogen source

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animate and inanimate reservoirs - food, water, soil

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transmission

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how the pathogen is transferred from host to host

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host susceptibility

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pathogen interaction with host immunity

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virulence

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ability of disease to survive and thrive

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infectious disease links

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pathogen
source of pathogen
transmission to host *
susceptibility of the host
exit from host

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successful pathogen must

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increase in #
defeat host - avoid/evade/compromise
infect host
stay in host
damage host
exit & survive long enough to infect something else

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mechanism of pathogenicity

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portals of entry
number of invading microbes
adherence
penetration or invasion of host defenses
damage to host cell
exit

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portals of entry

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mucous membranes: respiratory tract, GI tract, genital tract
skin
parenteral route

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preferred port of entry

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pathogens need to enter particular pat of the body to cause disease

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ID 50

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infectious dose for 50% of test population

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LD 50

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lethal dose for 50% of test population

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adherence

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adhesins/lignands bind specifically to complementary surface receptors on the cells of certain host tissues
glycoproteins or lipoproteins
receptors are sugars

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biofilms

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come together in mass, cling to surfaces, take in and share available nutrients
attach to living and non-living surfaces

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penetration or invasion of host defenses

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capsules
cell wall components
extracellular enzymes
antigenic variation
invasins

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capsules

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antiphagocytic factors:
phagocytosis blocked by capsule
incomplete phagocytosis where bacteria reproduce in phagocyte (engulfed but not digested)

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cell wall components

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m protein
opa protein
mycolic acid

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mprotein

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resist phagocytosis (strep pyogenes)

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opa protein

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inhibits T helper cells (gonorrhea)

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mycolic acid

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resists digestion (mycobacterium tubercul)

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extra cellular enzymes

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coagulase and kinase
hyaluronidase and collagenase
Iga protease

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coagulase & kinase

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coagulase coagulates fibrinogen
kinase digest fibrin clots
1. bacteria produce coagulase
2. clotting pro attach outside blood vessel
3. prod kinase dissolving clot and releasing bac into cell wall

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hyaluronidase and collagenase

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hyaluronidase hydrolyzes hyaluronic acid and collagenase hydrolyzes collagen
1. invasive bacteria reach epithelial surface
2. bac prod hyaluronidase and collagenase - allows bac thru epithelial
3. bac invade deeper tissues

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IgA protease

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destroy IgA antibodies

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antigenic variation

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alter surface proteins to change what virus looks like so they can survive longer

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invasins

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surface protein produced by salmonelle typhimurium and ecoli that rearranges nearby actin filaments in the cytoskeleton of a host cell

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membrane ruffling

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disruption in cytoskeleton of host cell

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damage to host cells

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siderophores
direct damage
toxins

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siderophores

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proteins secreted by some pathogens to obtain free iron
iron needed by pathogen
take iron from iron transport proteins by binding the iron even more tightly
taken up by siderophore receptors on the bacterial surface
iron brought into bacteria

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direct damage

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direct damage to host as pathogens use the host cell for nutrients and roduce waste products
cell usually ruptures
most damage done by toxins

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toxin

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substance that contributes to pathogenicity

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toxigenicity

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ability to produce a toxin

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toxemia

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presence of toxin in hosts blood

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toxoid

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inactivated toxin used in a vaccine

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antitoxin

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antibodies against a specific toxin

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exotoxin

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specific for ss and fxn in host cell
from inside cell
AB bacterium, membrane disrupting toxins, superAg
gram +
byproducts of growing cell
protein chemistry
no fever, small LD50, neutralized by antitoxin

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AB bacterium

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produce and release exotoxin
B binding component of exotoxin attaches to host cell receptor
AB exotoxin enters host cell by endocytosis
AB exotoxin enclosed in pinched off portion of plasma membrane during pinocytosis
AB components of exotoxin separate: A alters cell fxn by inhibiting pro synthesis, B released from cell

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membrane disrupting toxins

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disrupt phospholipid bilayer by making pro channels

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super Ag

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intense immune response b/c cytokines from host cells
fever nausea, vomiting, diarrhea, shock, death
toxic shock syndrome/food poisons

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naming exotoxins

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neurotoxins attack nerve cells
cardiotoxins attack heart cells
hepatotoxins attack liver cells
leukotoxins attack leukocytes
enterotoxins attack lining of GI
cytotoxins attack wide variety of cells

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Endotoxin

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gram -
outer membrane of microbe
lipid A chemistry
fever, not neutralized by antitoxin
LD50 large
pyrogenic response

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pyrogenic response

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macrophage ingests gram- bac
bac degraded releasing endotoxin
macrophage produce IL1 and TNF alpha cytokines
cytokines released in blood stream and travel to hypothalymus
cytokines induce hypo to prod prostaglandins to incr temp
fever

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lysogenic conversion

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bacteriophages incorporate dna into bacterial chromosome, b/c prophage and remain latent (lysogeny)
host change characteristics

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cytopathic effects

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visible effects of viral infection
result in cell death are called cytocidal effects
result in damage are noncytocidal

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portals of exit

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cough/sneeze
feces/saliva
urine/vaginal secretions
skin
blood