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

Lecture 4: Digestive Trac Infections Flashcards

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
Q

Evolution of Yersinia species (2)

A

acquires a few more plasmids, insect toxin, factor X
can now inhabit FLEAS (new host)
can grow in flea, then can get to rodents

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26
Q

Yersinia in rodents

A

usualy not lethal
in AZ, Colorado, US SW
endemic in rodent populations

27
Q

fleas to rodents to humans

A

fleas can get into pet rodents

then to humans

28
Q

bubonic plauge

A

jump from rodent to human

death in 2-3 weeks

29
Q

pneumonic plauge

A

infection of lungs
jump from human to human
death in 2-3 days

30
Q

plasmid

A

circular piece of extra-chromosomal replicating DNA

31
Q

plasmid

A

circular piece of extra-chromosomal replicating DNA

32
Q

3 virulence plasmids of Yersiniae

A

pYV
pMT1
pPla

33
Q

pYV

A

immune system avoidance, toxicity

T3SS

34
Q

pMT1

A

transmission to fleas

antigen

35
Q

pPla

A

intra-dermal site disseminiation

plasminogen activator

36
Q

what the plasmid does in flea

A

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
Q

how Yersinia changes the flea

A

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
Q

Bubonic plauge: specifics

A

blood
bacteria picked up by macrophages…and kills macs
goes to lymph nodes
necrosis and large black swelling at lymph nodes

39
Q

pneumoni plage: specifics

A

drowning due to inflammation of lungs

40
Q

Yersinia Pestis

A

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
Q

Yersinia Pestis

A

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
Q

where did the plauge come from

A

soil in a small area in CHina

43
Q

where do big outbreaks come from

A

weather changes

cause it to jump from soil

44
Q

most common foodborne pathogens

A 
Norwalk-like viruses (67%) 
Campylobacter (14%)
Salmonella (10%)
Clostribdium perfringens (1.8%)
Shiga-toxin producing E. (0.7%)
45
Q

Digestive Tract Infections

A

disease is based on LOCATION

tells what tissue is infected, not what microbe is causing

46
Q

iflamation of digestive tract

A

vimiting and/or diarrhea

47
Q

Gastritis

A

stomach

48
Q

Gastroenteritis

A

stomach and small intestine

49
Q

Enteritis

A

small intestine

50
Q

Enterocolitis

A

large and small intestine

51
Q

Colitis-large

A

large intestine

52
Q

Peyer’s Patch

A

lymph nodes along digestive tract/intestines
specailized region
M-cells

53
Q

Peyer’s Patch

A

lymph nodes along digestive tract/intestines
specailized region
M-cells

54
Q

M-cells

A

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
Q

Norovirus

A

(+)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
Q

symptoms of norwalk viruses

A

extremem vomiting and diarrhea

creastes aerosols that coat surfaces

57
Q

Best clean up for Norovirus

A

10% bleach

resistant to alocohol and detergent

58
Q

More on noroviruses

A

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
Q

important features of the small intestines

A

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
Q

lymph nodes in intestines

A

Peyers pathces

Have M cells on surface to transport things from lumen and exposing them to immunity

61
Q

lymph nodes in intestines

A

Peyers pathces

Have M cells on surface to transport things from lumen and exposing them to immunity

62
Q

Why M cells are taken advantage of

A

they can transport large things

63
Q

Why M cells are taken advantage of

A

they can transport large things
they are involved in determining tolereance
a good place for pathogens to invade

64
Q

Why M cells are taken advantage of

A

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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