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Micro Exam 4 > Lecture 4: Digestive Trac Infections > Flashcards

Lecture 4: Digestive Trac Infections Flashcards

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1
Q

hantavirus

A 
kangraroo rate urine
can be inhaled
you get really sick
NE AZ
cleaning cabins
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2
Q

Ebola

A

hemorrhagic fever

west africa

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3
Q

etiological agent

A

the cause of the disease

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4
Q

pathogenesis

A

ability to become a pathogen

concept of a bacterium, virus, organism CAUSING a disease

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5
Q

ex) pathogenesis of flu

A

hand to mouth to mucus membranes
how it is spread
proteins N, H

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6
Q

virulence

A

measure of pathogeneisis

measure of HOW MUCH disease POTENTIAL strain has

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7
Q

virulence of flue

A

one strain has flagellla

both can cause disase, but the one with flagella is more efficient… MORE VIRULENT

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8
Q

Stages of infection (every organism is a little different though)

A 
Contact 
Adhesion (and invasion)
Growth 
Inflammation and immune response
clearance and death
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9
Q

Contact
Adhesion (and invasion)
Growth

A

the INFECTION parts

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10
Q

inflammation and immune response

clearance and death

A

DISEASE

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11
Q

Contact

A

going from one person to another

  • direct contact (sexual, doorknob)
  • airborne aerosol (sneeze)
  • ingestion (fecal oral: food, water)
  • arthropod vector
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12
Q

adhesion and invasion

A

protein protein interactions

these factors are great for vaccines! purify proteins and inject just the proteins (H and N for flu)

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13
Q

Growth

A

can also interfer with infection by inhibiting growth

HIV: HAART: targets reverse transcriptase, integrase, and protease to keep virus from replicating

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14
Q

Inlammation and immune response

A

get immmune response through vaccination or prior infection or innate cells

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15
Q

Inlammation and immune response

A

get immmune response through vaccination or prior infection or innate cells

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16
Q

Clearance and Death: 2 options

A

-clear the pathogen
-we die
it is a WAR that must be won
OTHER OPTION: persistant and latent infections

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17
Q

viruelence (from clicker)

A

ability to CAUSE DISEASE

NOT ability to infect

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18
Q

what drives evolution

A

SURVIVAL
not usually to cause death of host
if host is dying… this probably isnt what it evolved to do

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19
Q

Yersinia

A

GENUS for plauge

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20
Q

Evolution of Yersinia species (1)

A

first was in soil… there was lots of competition
evolved: got a plasmid with type 3 secretion (needle complex)
So that it could kill amebae (phagocytic cells) with were eating it
THIS IS NOT THE PATHOGENIC ONE

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21
Q

Type 3 secretion in Yersinia

A

intended to kill its predator after Yersinia was infected
side effect: kills phagocytic cells in humans
the goal was to survive in the soil

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22
Q

what was on the plasmid Yersinia got

A

Type 3 secretion system
manipulates host cell signaling and protein expression
makes host think its not infected
allows bacteria to grow within immune cells of lymph node

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23
Q

Yersinia enterolitica

A

human pathogen, get it form soil, fecal oral
gets into digetstive tract and causes severe diarrhea
usually localized
causes inflammation of digestive tract
self limiting
can’t persis, human not ideal host

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24
Q

self limiting

A

disease that goes away on its own doesnt usually kill host

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25
Evolution of Yersinia species (2)
acquires a few more plasmids, insect toxin, factor X can now inhabit FLEAS (new host) can grow in flea, then can get to rodents
26
Yersinia in rodents
usualy not lethal in AZ, Colorado, US SW endemic in rodent populations
27
fleas to rodents to humans
fleas can get into pet rodents | then to humans
28
bubonic plauge
jump from rodent to human | death in 2-3 weeks
29
pneumonic plauge
infection of lungs jump from human to human death in 2-3 days
30
plasmid
circular piece of extra-chromosomal replicating DNA
31
plasmid
circular piece of extra-chromosomal replicating DNA
32
3 virulence plasmids of Yersiniae
pYV pMT1 pPla
33
pYV
immune system avoidance, toxicity | T3SS
34
pMT1
transmission to fleas | antigen
35
pPla
intra-dermal site disseminiation | plasminogen activator
36
what the plasmid does in flea
bacteria forms a biofilm flea has 2 compartnments: saliva storage and stomach biofilm won't let bloodmeal get to stomach so flea keeps biting, trying to get food to its stomach THIS SPREADS THE BACTERIA
37
how Yersinia changes the flea
causes flea to feed over and over and over may cause them to bite abnormal hosts (fleas are usually specific to just one host type) starve to death eventually
38
Bubonic plauge: specifics
blood bacteria picked up by macrophages...and kills macs goes to lymph nodes necrosis and large black swelling at lymph nodes
39
pneumoni plage: specifics
drowning due to inflammation of lungs
40
Yersinia Pestis
gram negative acquisition of 3 plasmids makes it a killer (as opposed to orginal soil one) 1-3 cases in AZ a year... mortality rate of 15% rodents resivoir: no disease here
41
Yersinia Pestis
gram negative acquisition of 3 plasmids makes it a killer (as opposed to orginal soil one) 1-3 cases in AZ a year... mortality rate of 15% rodents resivoir: no disease here
42
where did the plauge come from
soil in a small area in CHina
43
where do big outbreaks come from
weather changes | cause it to jump from soil
44
most common foodborne pathogens
``` Norwalk-like viruses (67%) Campylobacter (14%) Salmonella (10%) Clostribdium perfringens (1.8%) Shiga-toxin producing E. (0.7%) ```
45
Digestive Tract Infections
disease is based on LOCATION | tells what tissue is infected, not what microbe is causing
46
iflamation of digestive tract
vimiting and/or diarrhea
47
Gastritis
stomach
48
Gastroenteritis
stomach and small intestine
49
Enteritis
small intestine
50
Enterocolitis
large and small intestine
51
Colitis-large
large intestine
52
Peyer's Patch
lymph nodes along digestive tract/intestines specailized region M-cells
53
Peyer's Patch
lymph nodes along digestive tract/intestines specailized region M-cells
54
M-cells
transport things from lumen of intestines and exposing them to adaptive and innate immunity toxins enter body through M cells... because M cells transport large things exploited by pathogens
55
Norovirus
(+)ssRNA virus, non-enveloped 20 million cases just in the US very low infectious dose (approx 10 virions) creaes a TON of virions can be shedding virus after no more symptoms
56
symptoms of norwalk viruses
extremem vomiting and diarrhea | creastes aerosols that coat surfaces
57
Best clean up for Norovirus
10% bleach | resistant to alocohol and detergent
58
More on noroviruses
not culturalble in lab, little know about pathogenesis symptoms 18-36 hrs after exposure infects stomach and intestines where it replicates in hige numbers gastroenteritis loasts for 24-60 hrs treatment: oral rehydration (pedialite)
59
important features of the small intestines
high surface area for transport of molecules into the body | only a thin layer of mucus is protecting you from bacteria in the lumen of the gut
60
lymph nodes in intestines
Peyers pathces | Have M cells on surface to transport things from lumen and exposing them to immunity
61
lymph nodes in intestines
Peyers pathces | Have M cells on surface to transport things from lumen and exposing them to immunity
62
Why M cells are taken advantage of
they can transport large things
63
Why M cells are taken advantage of
they can transport large things they are involved in determining tolereance a good place for pathogens to invade
64
Why M cells are taken advantage of
they can transport large things they are involved in determining tolereance (T-reg cells!) a good place for pathogens to invade

Micro Exam 4 (8 decks)

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