BIO3 - Chapter 15

Mechanisms of Pathogenicity

pathogenicity

the ability to cause disease by overcoming the defenses of a host

virulence

the degree or extent of pathogenicity

what are the portals of entry

mucous membranes

skin

peternal route (induced route)

what are the different mucous membranes

respiratory tract

gastrointestinal tract

genitourary tract

conjuctiva

how microbes enter the respiratory tract

through nose, mouth - ex. common cold, influenza, covid, measles

how microbes enter the gastrointestinal tract

through food, water, dirty fingers - food poisinging, chloera, shigellosis

how microbes enter the genitourary tract

through sex intercourse - UTI, gonorrhea, syphilis

what is conjunctiva

delicate membrane that covers the eyeballs & lines of eyelids - conjunctivitis (pink eye)

skin as a portal of entry

unbroken skin is impenetrable by most microbes (ex. ring worm, athlete’s foot), but some gain access through openings in the skin (sweat gland ducts, hair follicles; ex. acne)

paternal route (induced route) as a portal of entry

microbes are deposited directly into tissues when barriers are penetrated - cuts, wounds, injections, surgery, punctures, bites, etc. (HIV/AIDS [through injection], rabies)

significance of a preffered portal of entry

some pathogens have a preferred portal of entry that is a prerequisite to thier being able to cause disease

ID₅₀

Infectious Dose for 50% of the test population - the virulence of a microbe

LD₅₀

Lethal Dose (of a toxin) for 50% of the test population - potency of toxin

adhesins/ligands

surface molecules on pathogens that bind to receptors on host cells; form biofilms

biofilms

communities that share nutrients

how pathogens penetrate host; factors that contribute to ability to invade a host

capsules

cell wall components

enzyme

antigenic variation

invasins

intracellular growth

significance of capsules

made of glycocalyx, prevent phagocytosis

significance of cell wall components

cell walls of certain bacteria contain chemical substances that contribute to virulence

M protien

cell wall component; mediates the attachment & resists phagocytosis

opa

cell wall component; protein that allows attachment to host cells

waxy lipid

cell wall component; (mycolic acid) resists digestion

significance of enzymes in penetration

production of extracellular enzymes & related substances can aid in bacterial virulence

significant enzymes

coagulases, kinases, hylarunoidases, collagenases, IgA proteases

coagulases

cause clots in blood

kinases

digest fibrin clots

hyaluronidases

hydrolyzes hyaluronic acid

collagenases

hydrolyzes collagen

IgA proteases

destroy IgA antibodies

antigenic variation in penetration

alter surface anitgens, unaffected by the antibodies

methods of penetration into the host cell cytoskeleton

invasins & recruitment of host actin

how invasins work

alter host actin to enter a host cell

how recruitment of host actin works

use of actin to move from one cell to the next

actin

a cellular protein active in muscular contraction & cellular movement

ways bacterial pathogens damage host cells

siderophores

direct damage

toxins

inducing hypersensitivity reactions

how pathogens damge host cells using the host’s nutrients

siderophores - use host’s iron

how pathogens damge host cells with direct damage

disrupt host cell function (cell division, protein synthesis), prod. waste products, prod. toxins

toxin

poisonous substance that contributes to pathogenicity

toxigenicity

ability to produce a toxin

toxemia

presence of toxin in the host’s blood

intoxications

presence of toxin without microbial growth

what are the 2 types of toxins

exo- & endo- toxins

exotoxin

protein, prod. & secreted by bact., many are enzymes, soluble in bodily fluids, destroy host cells & inhibit metabolic functions

specific for a structure of function in host cell

toxoid

inactivated toxin used in a vaccine

antitoxin

antibodies against a specific toxin

3 major types of exotoxins

A-B toxins, membrane-disrupting toxins, superantigens

action of an A-B toxin

B (binding) component of exotoxin attaches to host cell receptor

A-B exotoxin enters host cell by endocytosis

A-B exotoxin enclosed in pinched-off portion of plasma membrane during pinocytosis

A-B components of exotoxin separate. The A component alters cell function by inhibiting protein synthesis. B component is released from the host cell

how membrane-disrupting toxins works

lyse host’s cells by making protein channels in the plasma membrane & disrupting phospholipid bilayer

Leukocidins

kill white blood cells

hemolysins

kill red blood cells

how superanitgens work

stimulate an intense immune response from host cells, which release large amount of cytokines

cytokines

small proteins regulate immune responses & mediate cell-to-cell communication

consequence of high level of cytokines in bloodstream

fever, nausea, vomiting, diarrhea, shock, & death

what kind of bact prod exotoxins

mostly gram +

exotoxin relation to microbe

by-products of growing cell

exotoxin chemistry

protein

are exotoxins neutralized by antitoxin

yes

exotoxin LD₅₀ size

small

how do endotoxins differ from exotoxins

• part of the outside portion of the cell wall or gram (-) bact

• are lipopolysaccharides

• are released when gream (-) bact. die, & their cell wall undergo lysis

how are endotoxins similar to exotoxins

prod. same signs & symptoms (not to the same degree though): chill, fever, weaknesss, aches, shock, or even death

what kind of bact prod endotoxins

gram -

endotoxin relation to microbe

outer membrane

endotoxin chemistry

Lipid A

are endotoxins neutralized by antitoxin

no

endotoxin LD₅₀ size

relatively large

what does a limullus amebocyte lysate (LAL) assay test for

endotoxins

significance of plasmids

may carry genes for toxins, production of antibiotics, & enzymes

significance of lysogenic conversion

changes characteristics of a microbe due to incorporation of a prophage

cytopathic effects (CPE)

visible effects of viral infection on a cell

CPE examples

• stopping cell synthesis

• causing cell lysosomes to release enzymes

• creating inclusion bodies in the cell cytoplasm

• fusing cells to create a syncytium

• changing host cell function or induing chromosomal changes

• inducing antigenic changes on the cell surface

  • loss of contact inhibition in the cell, leading to cancer

significance of alpha & beta interferons

produced by virally-infected cells & protect neighboring cells from viral infection

action of alpha & beta interferons

inhibit synthesis of viral proteins & host cell proteins & kill virus-infected host cells by apoptosis

significance of fungi

• toxic metabolic products

• provoke an allergic response

• trichothecene toxins inhibit protein synthesis

• proteases modify host cell membranes

  • capsules prevent phagocytosis

ergot

fungi; alkaloid toxins that cause hallucinations

aflatoxin

fungi; carcinogenic toxin prod. by aspergillus

mycotoxins

prod. by mushrooms & are neurotoxic (phalloidin & amanitin)

significance of protozoa

presence of protozoa & their waste products causes symptoms

ways protozoa avoid host defenses

• digesting cells & tissue fluids

• growing in phagocytes

• antigenic variation

significance of helminths

• use host tissue for growth

• prod. large masses; cause cellular damage

• prod. waste products

• prod. waste products that cause symptoms

significance of algae

some prod. a neurotoxin called saxitoxin

portals of exit

• respiratory tract

• gastrointestinal tract

• genitourinary tract

• skin

• blood

*first 3 = mucous membrane

ex of exiting via respiratory tract

coughing & sneezing

ex of exiting via gastrointestinal tract

feces & saliva

ex of exiting via genitourinary tract

urine & vaginal secretions

ex of exiting via blood

biting arthropods & needles or syringes

effects of exotoxins on body

specific to cells or functions in host (functional cells, nerves, GI tract)

effect of endotoxins on body

fever, weakness, aches, shock

can exotoxins be denatured by heat

yes

can endotoxins be denatured by heat

no

is a high or low LD₅₀ more potent

low

most often used portal of entry

mucous membrane

food infection v. food intoxication

food infection is the ingestion of live microbes, while food intoxication is the ingestion of toxins produced by bacteria