Principles of Pathogenesis 2 Flashcards

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1
Q

describe the stages of acute infection

A

exposure
incubation phase: period from exposure till first symptom
prodrome: having symptoms but cannot pinpoint what the problem is – low level symptom
peak of acute phase symptoms: most severe symptom
convalescence: immune system kicks in and severity of symptom goes down

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2
Q

difference between acute and chronic infection

A

chronic has longer incubation phase and prodrome and also severity of symptoms stay at a constant low level because for some reason immune system cannot clear it out

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3
Q

terminology for chronic infections

A

chronic
latent - microorganisms is present and not replicating at a high level or not replicating at all
persistent - not being cleared, not being eradicated from the body
carrier - individual’s is persistently shedding microorganism and can be harmful to someone else

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4
Q

compare the two infection types chronic and acute for the following: growth rates of pathogen, symptom onset speed, duration of symptoms, risk to others of infection, advantages to pathogen

A

chronic - slower, slower, longer but less severe, yes, there are advantages and disadvantages

acute - faster, faster, shorter, yes, there are advantages and disadvantages

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5
Q

define pathogenicity and virulence

A

pathogenicity is the ability to cause damage and virulence is how we measure that ability

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6
Q

fact about virulence

A

virulence can be different depending on who it is or can even vary where in the body it is

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7
Q

key to pathogen success

A

it recognizes in its environment, communicates it, then responds to it

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8
Q

how does pathogen respond to environmental signal

A

it has a receptor (membrane protein) on itself that receives signal from environmental changes then sends signal to response regulator –> genes –> mRNA –> protein and enzyme released which helps with appropriate adaptation to the environment

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9
Q

the ability to cause damage

A

virulent

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10
Q

what is pathogenicity islands (PAIs)

A

cluster of genes encoding for virulence factors

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11
Q

what is the role of clustering genes together

A

you can control them with the same switch

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12
Q

what is the difference between exogenous and endogenous in term of exposure and entry

A

exogenous - externally acquired

endogenous - home grown

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13
Q

what does it mean by you can get a cross over between exogenous and endogenous exposure and entry

A

your endogenous infection can become transmitted to someone else and become a exogenous infection to the other individual

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14
Q

vibrio cholerae in water has 10^4 - 10^6 infectious dose while vibrio cholerae in food has 10^2 - 10^4 infectious dose. Why is the infectious dose lower for V. cholerae when it is in food compared to in water?

A

probably because of heat from cooking but the levels in the water can be brought down to the levels in food if sodium bicarbonate is added to the water

Food and Sodium Bicarb help protect the virus from stomach acid.

If the virus was in just water, then many of the virions would be destroyed prior to getting to their site of infection.

But taken with food, a greater percentage of virions reach the site of infection so you need fewer in the infectious dose.

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15
Q

what is so important about the site of entry in which a microorganism gets in

A

same way they get in, is the same way they shed

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16
Q

what are some specialized adhesion structures and when do microorganisms express them

A

pili and fimbrae

expressed when it is beneficial for them - depending on the environmental conditions

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17
Q

what helps define tissue specificity

A

tissue tropism
specific adhesion
biofilm formation

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18
Q

what is streptococcus mutans’ bacterial adhesin and attachment site

A

bacterial adhesin - cell bound protein

attachment site - pellicle of tooth

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19
Q

what is Enterotoxigenic E. coli’s bacterial adhesin and attachment site

A

bacterial adhesin - Type I fimbriae

attachment site - Intestinal epithelium

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20
Q

what is Plasmodium sp.’s bacterial adhesin and attachment site

A

bacterial adhesin - MSP

attachment site - erythrocytes

21
Q

what are some options for acquiring iron for microorganisms that need them

A

forming siderophores to chelate iron (this way the have a higher affinity for iron than the compound in which iron is attached to)

bind iron containing compounds

breakdown of iron containing compounds

22
Q

some microorganisms need a host to survive: what is the difference between facultatively intracellular and obligately intracellular

A

facultatively - they need to be intracellular in some of their stages

obligately - they need to be intracellular at all times to survive

23
Q

examples of organisms that are facultatively intracellular and those that are obligately intracellular

A

facultatively - salmonella histoplasma

obligately - chlamydia and all viruses

24
Q

what normally happens to a phagocytosed bacterium that is trying to resist being broken down

A

a. Prevent fusion of phagosome and lysosome
b. Escape from phagolysosome
c. Resist/inactivate lysosomal enzymes
d. Inactivate harmful oxygen species

25
Q

what is a way in which a pathogen can try to disguise itself

A

antigenic variation – changing its recognizable surface antigen making it more difficult to recognize and eradicate

26
Q

how effective is the immune system to antigenic variation and how does this affect the body?

A

it is hard for it to recognize since pathogen can repeatedly change its surface antigen

hence one can have multiple infections from the same pathogen due to its constant change in surface antigen

27
Q

what is the most common defense system used by bacteria

A

capsule

28
Q

composition of capsule

A

low immunogenicity

mimic body’s own substances

29
Q

importance of understanding composition of capsule

A

helpful for identification and vaccine development

30
Q

in the spread and disseminate phase: what happens in the presence and absence of streptokinase

A

presence - barrier is broken down enabling the spread of pathogen

absence - barrier is not broken and the infection is walled off by fibrin barrier

31
Q

given the enzyme IgA protease, what is its effect and target AND benefit

A

effect and target - cleavage of sIgA

benefit - evasion

32
Q

given the enzyme hyaluronidase, what is its effect and target AND benefit

A

effect and target - degrade hyaluronic acid

benefit - spread

33
Q

given the enzyme urease, what is its effect and target AND benefit

A

effect and target - inactivation of urea

benefit - survival

34
Q

for exotoxin: what is the structure, site of action, mechanism of action and effects on cells

A
Class (cellular target)
• Structure: A‐B, A‐5B (a is active enzymatic part and b is binding)
• Site of action
– Neurotoxins
• Mechanism of action – ADP‐ribosylation
• Effect on cells: Haemolysin, Cytolysin
35
Q

an example of a pore formation toxin is listeriolysin O, what is the effect and mechanism?

A

effect: Cell death occurs due to osmotic lysis or apoptosis.

Mechanism: Protein pores destabilize membrane

often responsible for cytolytic activity

36
Q

pore formation toxin like listeriolysin O is also called

A

CFTs = Channel Forming Toxins

37
Q

example of an endotoxin

A

LPS

38
Q

what is LPS’s toxic effect

A

triggers immune response which can result in endotoxic or septic shock (if in high amounts)

39
Q

what can give a similar response as LPS

A

peptidoglycan
fungal cell wall
if in high conc

40
Q

advantage of virulence factor surface attachment

A

Prevention of removal; advantages of being a biofilm

41
Q

advantage of virulence factor degradative enzymes

A

Release of nutrients; breakdown of tissue barriers

42
Q

advantage of virulence factor survival at 37 oC

A

Adaptation to body environment

43
Q

advantage of virulence factor opportunistic or true pathogen

A

Able to adapt to body environment

Able to evade immune defences

44
Q

advantage of virulence factor dimorphism

A

Able to adapt to body environment

45
Q

example of contact vs. no contact transmission

A

contact: sexual or skin contact, fomites (objects that carry infection), droplets, animal bites

no contact: food, insects, water, soil, aerosols

46
Q

difference between aerosol and droplet transmission

A

aerosol (no contact): inhaled from the air so like measles

droplet there is contact: ebola

47
Q

what do these vectors carry respectively: mosquito, tick, sand fly, fleas

A

mosquito - malaria
tick - lyme disease
sand fly - leishmaniasis
fleas - bubonic plague

48
Q

cause of syphilis and hepatitis respectively

A

T. pallidum and HBV