Host-Microbe Interactions and Pathogenesis Part 2

pathogenicity vs virulence

pathogenicity is the ability of a microorganism to cause disease, virulence is how nasty the microorganisms can get, aka their severity.

explain how virulence depends on host factors (example of 1918 flu pandemic)

pathogens are often more virulent in those with immature or suppressed immunity (elderly, children)

cytokine storm: in healthy people, a severe, overactive immune reaction can cause damage in the host’s own organs

the 1918 flu was most deadly in healthy young adults because of this overreaction

explain how virulence depends on microbial factors (example of 1918 flu pandemic)

Virulence depends on specific microbial factors such as toxin production, ability to invade tissues, replication rate, and evasion of the immune system.

In the 1918 influenza pandemic, the Influenza A virus subtype H1N1 had unusually high virulence due to:

• Rapid replication in host cells

• Strong immune system overreaction (cytokine storm)

• Efficient transmission between people

These microbial traits made the virus far more severe and deadly than typical flu strains.

what is infectious dose?

the number of cells or viruses needed to infect half of the people who are exposed to them

what is lethal dose?

the amount of a toxin required to kill half of hosts exposed to it if not treated

what aspects of pathogenicity (infection vs toxin severity) do infectious dose and lethal dose apply to?

• Infectious dose (ID): relates to infection — the number of organisms needed to establish infection in a host.

• Lethal dose (LD): relates to toxin severity (virulence) — the amount of pathogen or toxin required to kill the host.

endotoxin

part of the cells structure and released only when the cell dies (Specifically Lipid A in the LPS of gram-negative bacteria)

exotoxin

made in the microbial cell and secreted into environment, toxin proteins made in both gram - and gram +

where does endotoxin come from?

found in the outer membrane of gram - bacteria as part of the LPS molecule

how is endotoxin released in the body? what are the potential effects?

it is released when the bacteria dies and this is often due to antibiotic treatment or the host’s immune response.

can trigger a body wide inflammatory reaction (low levels: fever, chills, hypotension high levels: sepsis, organ failure, death.

3 major types of exotoxins

type 1, type 2, type 3

how does E. coli enterotoxin act as a toxin?

when consumed, the toxin binds to the intestinal cells, and causes them to leak salt and water.

this results in diarrhea, abdominal pain, cramping.

e. coli bacteria that produce this enterotoxin cause food poisoning.

why are adhesion structures needed for virulence?

they keep bacteria from being washed away

how do fimbriae contribute to the ability of a microbe to cause disease?

made of protein, have adhesions on the very end (little proteins), which allow bacteria to attach to specific proteins on specific kinds of cells

how do adhesion structures help cells stick to other cells and tissues?

fimbriae, capsules, and slime layers

how do pathogens enter cells?

the lower the ID₅₀…

the more virulent the pathogen

type 1 toxins

-bind to receptors on the cells of their hosts

-generates signal inside of the cell, can alter cell physiology or lead to cell death

-toxin does not enter the cell

how does S. aureus enterotoxin act as a toxin?

it works differently, it is a T-cell superantigen, which over activates T-cells and this results in food poisoning by killing the cells that line the digestive tract

type 2 toxins

break open holes in the membrane of host cells

cause cells cytoplasm to leak into tissue

causes an inflammatory reaction

can cause death of cells

how does hemolysis act as a toxin?

hemolysin destroys the RBC membrane, they punch holes in host cells membrane

causes water to rush in the cell by osmosis, bursts cell like a popped balloon

type 3 toxins

use a cell receptor,

aka A-B toxins,

Binding “B” part binds to receptor and Active “A” puts a toxic effect inside the cytoplasm

how does Pertussis act as a toxin?

produces a pertussis toxin that destroys the ciliated epithelial cells of the lung. mucus builds up, and causes severe lung irritation.

whooping cough

irritation and mucus combination

how does Botulinum toxin (BOTOX) act as a toxin?

affects the nerve cells that cause muscle contraction, called alpha motor neurons

in the neuron, it blocks the response of acetylcholine (so now, muscles can not contract)

muscles are now paralyzed because they cant contract (flaccid paralysis)

how does tetanus toxin act as a toxin?

also produces paralysis but differently.

blocks the release of the neurotransmitter glycine (which usually causes muscles to relax)

causes spastic paralysis, where muscles cant relax

(often called lockjaw because spastic paralysis often affects the muscles of the face and jaw first)

how do capsules contribute to the ability of a microbe to cause disease?

they are made of densely packed and organized sugars with chemical stickiness ( sharp on microscope)

how do slime layers contribute to the ability of a microbe to cause disease?

mafe of loosely packed and disorganized sugars (fuzzy on microscope)