Micro Ch 15--Methods of Pathogenicity

Portals of entry

Skin, mucous membranes, parenteral route

Skin entry

must be broken to be penetrable

or get through pores, ex. hair follicles

Mucous membranes entry

inhale, ingest

respiratory tract, digestive tract

Parenteral route

deposited directly into tissue

injections, bites

ID50—Infectious dose

number of pathogens that infect 50% of the group

LD50—Lethal dose 50

the dose that kills 50% of group

How do pathogens attach to host tissue?

through adherence to host tissue

Adhesins

on pathogen bind to host cell’s receptors on glycocalyx, fimbrae, flagella

Ways that pathogens can defend

capsules, cell wall components, enzymes, antigenic variation, biofilms

Phagocytosis

ingestion of a pathogen by a host cell so it can destroy it with lysozomes

Capsules for overcoming host cell’s defenses

on outside of cell wall to resist phagocytosis

Phagocytotic cell

type of cell within the body capable of engulfing and absorbing bacteria and other small cells and particles

Phagocytosis

when a phagocyte engulfs a bacteria

Components of a cell wall

M & Opa protein, waxy lipid

What do M, Opa, & waxy lipid do?

M & waxy lipid—resists phagocytosis

Opa—allows attachment to host cells

Waxy lipid cell component for overcoming host cell’s defenses

defense system that resists digestion by phagocytes

Enzymes for overcoming host cell’s defenses

coagulases, kinases, collagenases, hyaluronidase, IgA protease

Antigenic variation for overcoming host cell’s defenses

pathogens alter surface antigens—different genes

old antibodies host made are no longer effective against pathogen because they don’t know its the same pathogen

biofilms for overcoming host cell’s defenses

shields for antibiotics and disinfectants from host cell

help evade phagocytosis

What are invasins?

a surface protein on a pathogen that allows it to survive inside a phagosome

What do invasins do

they either

1. escape from phagosome before the lysosome gets to it

2. prevent the lysosome from fusing

How do bacterial cells damage host cells

1. Steal host’s nutrients

2. Cause direct damage

3. Produce toxins

Stealing the host’s nutrients

Siderophores steal iron, a necesary nutrient

Direct damage in immediate viscinity

Disrupt host cell functions

Produces waste products

Causes ruptures

Produce toxins

endotoxins- within

and

exotoxins- outside

Toxins

poisonous substances produced by micros causing fever, shock, etc due to being overwhelmed from toxic waste

Exotoxins

bodily fluids

destroy host cells and inhibit metabolic function

highly specific targets

some lethal

Endotoxins

lipid A portion in Gram - bacteria

released during death or multiplication

fever, chills, inflammation

What role could plasmids play in pathogenicity

Plasmids may carry genes for toxins, enzymes, antibiotics

Lysogenic conversion

changed characteristics of a microbe due to incorporation of a prophage

Types of plasmids

R plasmids

Virulence plasmids

R plasmids

resistance factors to antibiotics

Virulence plasmids

carry genes effecting micropathogenicity

CPEs

visible effects of virus infections

Name 5 CPE effects

1. Disrupting cell junctions

2. Inducing a cytokine storm

3. Stopping macromolecule synthesis within cells

4. Create inclusion bodies in cell cytoplasm

5. Syncytium, the fusion of adjacent cells together

Ergot

fungal toxin causing hallucinations, found on rye

Aflatoxin

fungal toxin that is carcogenic, found in aspergillus (peanut butter)

Mycotoxins

fungal mushroom toxins

Portals of exit

Respiratory tract, GI tract, geniurinary tract, skin, blood