Lecture 4: Digestive Trac Infections Flashcards Preview

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Flashcards in Lecture 4: Digestive Trac Infections Deck (64):
1

hantavirus

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

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Ebola

hemorrhagic fever
west africa

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etiological agent

the cause of the disease

4

pathogenesis

ability to become a pathogen
concept of a bacterium, virus, organism CAUSING a disease

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ex) pathogenesis of flu

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

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virulence

measure of pathogeneisis
measure of HOW MUCH disease POTENTIAL strain has

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virulence of flue

one strain has flagellla
both can cause disase, but the one with flagella is more efficient... MORE VIRULENT

8

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

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

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Contact
Adhesion (and invasion)
Growth

the INFECTION parts

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inflammation and immune response
clearance and death

DISEASE

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Contact

going from one person to another
-direct contact (sexual, doorknob)
-airborne aerosol (sneeze)
-ingestion (fecal oral: food, water)
-arthropod vector

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adhesion and invasion

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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Growth

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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Inlammation and immune response

get immmune response through vaccination or prior infection or innate cells

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Inlammation and immune response

get immmune response through vaccination or prior infection or innate cells

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Clearance and Death: 2 options

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

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viruelence (from clicker)

ability to CAUSE DISEASE
NOT ability to infect

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what drives evolution

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

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Yersinia

GENUS for plauge

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Evolution of Yersinia species (1)

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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Type 3 secretion in Yersinia

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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what was on the plasmid Yersinia got

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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Yersinia enterolitica

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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self limiting

disease that goes away on its own doesnt usually kill host

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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

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Yersinia in rodents

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

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fleas to rodents to humans

fleas can get into pet rodents
then to humans

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bubonic plauge

jump from rodent to human
death in 2-3 weeks

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pneumonic plauge

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

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plasmid

circular piece of extra-chromosomal replicating DNA

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plasmid

circular piece of extra-chromosomal replicating DNA

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3 virulence plasmids of Yersiniae

pYV
pMT1
pPla

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pYV

immune system avoidance, toxicity
T3SS

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pMT1

transmission to fleas
antigen

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pPla

intra-dermal site disseminiation
plasminogen activator

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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

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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

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Bubonic plauge: specifics

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

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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

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where did the plauge come from

soil in a small area in CHina

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where do big outbreaks come from

weather changes
cause it to jump from soil

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most common foodborne pathogens

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

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Digestive Tract Infections

disease is based on LOCATION
tells what tissue is infected, not what microbe is causing

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iflamation of digestive tract

vimiting and/or diarrhea

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Gastritis

stomach

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Gastroenteritis

stomach and small intestine

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Enteritis

small intestine

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Enterocolitis

large and small intestine

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Colitis-large

large intestine

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Peyer's Patch

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

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Peyer's Patch

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

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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

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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

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symptoms of norwalk viruses

extremem vomiting and diarrhea
creastes aerosols that coat surfaces

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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)

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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

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lymph nodes in intestines

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

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lymph nodes in intestines

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

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Why M cells are taken advantage of

they can transport large things

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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

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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