Principles of Pathogenesis 2 Flashcards
describe the stages of acute infection
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
difference between acute and chronic infection
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
terminology for chronic infections
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
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
chronic - slower, slower, longer but less severe, yes, there are advantages and disadvantages
acute - faster, faster, shorter, yes, there are advantages and disadvantages
define pathogenicity and virulence
pathogenicity is the ability to cause damage and virulence is how we measure that ability
fact about virulence
virulence can be different depending on who it is or can even vary where in the body it is
key to pathogen success
it recognizes in its environment, communicates it, then responds to it
how does pathogen respond to environmental signal
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
the ability to cause damage
virulent
what is pathogenicity islands (PAIs)
cluster of genes encoding for virulence factors
what is the role of clustering genes together
you can control them with the same switch
what is the difference between exogenous and endogenous in term of exposure and entry
exogenous - externally acquired
endogenous - home grown
what does it mean by you can get a cross over between exogenous and endogenous exposure and entry
your endogenous infection can become transmitted to someone else and become a exogenous infection to the other individual
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?
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.
what is so important about the site of entry in which a microorganism gets in
same way they get in, is the same way they shed
what are some specialized adhesion structures and when do microorganisms express them
pili and fimbrae
expressed when it is beneficial for them - depending on the environmental conditions
what helps define tissue specificity
tissue tropism
specific adhesion
biofilm formation
what is streptococcus mutans’ bacterial adhesin and attachment site
bacterial adhesin - cell bound protein
attachment site - pellicle of tooth
what is Enterotoxigenic E. coli’s bacterial adhesin and attachment site
bacterial adhesin - Type I fimbriae
attachment site - Intestinal epithelium
what is Plasmodium sp.’s bacterial adhesin and attachment site
bacterial adhesin - MSP
attachment site - erythrocytes
what are some options for acquiring iron for microorganisms that need them
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
some microorganisms need a host to survive: what is the difference between facultatively intracellular and obligately intracellular
facultatively - they need to be intracellular in some of their stages
obligately - they need to be intracellular at all times to survive
examples of organisms that are facultatively intracellular and those that are obligately intracellular
facultatively - salmonella histoplasma
obligately - chlamydia and all viruses
what normally happens to a phagocytosed bacterium that is trying to resist being broken down
a. Prevent fusion of phagosome and lysosome
b. Escape from phagolysosome
c. Resist/inactivate lysosomal enzymes
d. Inactivate harmful oxygen species
what is a way in which a pathogen can try to disguise itself
antigenic variation – changing its recognizable surface antigen making it more difficult to recognize and eradicate
how effective is the immune system to antigenic variation and how does this affect the body?
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
what is the most common defense system used by bacteria
capsule
composition of capsule
low immunogenicity
mimic body’s own substances
importance of understanding composition of capsule
helpful for identification and vaccine development
in the spread and disseminate phase: what happens in the presence and absence of streptokinase
presence - barrier is broken down enabling the spread of pathogen
absence - barrier is not broken and the infection is walled off by fibrin barrier
given the enzyme IgA protease, what is its effect and target AND benefit
effect and target - cleavage of sIgA
benefit - evasion
given the enzyme hyaluronidase, what is its effect and target AND benefit
effect and target - degrade hyaluronic acid
benefit - spread
given the enzyme urease, what is its effect and target AND benefit
effect and target - inactivation of urea
benefit - survival
for exotoxin: what is the structure, site of action, mechanism of action and effects on cells
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
an example of a pore formation toxin is listeriolysin O, what is the effect and mechanism?
effect: Cell death occurs due to osmotic lysis or apoptosis.
Mechanism: Protein pores destabilize membrane
often responsible for cytolytic activity
pore formation toxin like listeriolysin O is also called
CFTs = Channel Forming Toxins
example of an endotoxin
LPS
what is LPS’s toxic effect
triggers immune response which can result in endotoxic or septic shock (if in high amounts)
what can give a similar response as LPS
peptidoglycan
fungal cell wall
if in high conc
advantage of virulence factor surface attachment
Prevention of removal; advantages of being a biofilm
advantage of virulence factor degradative enzymes
Release of nutrients; breakdown of tissue barriers
advantage of virulence factor survival at 37 oC
Adaptation to body environment
advantage of virulence factor opportunistic or true pathogen
Able to adapt to body environment
Able to evade immune defences
advantage of virulence factor dimorphism
Able to adapt to body environment
example of contact vs. no contact transmission
contact: sexual or skin contact, fomites (objects that carry infection), droplets, animal bites
no contact: food, insects, water, soil, aerosols
difference between aerosol and droplet transmission
aerosol (no contact): inhaled from the air so like measles
droplet there is contact: ebola
what do these vectors carry respectively: mosquito, tick, sand fly, fleas
mosquito - malaria
tick - lyme disease
sand fly - leishmaniasis
fleas - bubonic plague
cause of syphilis and hepatitis respectively
T. pallidum and HBV
