Lecture 4: Digestive Trac Infections Flashcards
hantavirus
kangraroo rate urine can be inhaled you get really sick NE AZ cleaning cabins
Ebola
hemorrhagic fever
west africa
etiological agent
the cause of the disease
pathogenesis
ability to become a pathogen
concept of a bacterium, virus, organism CAUSING a disease
ex) pathogenesis of flu
hand to mouth to mucus membranes
how it is spread
proteins N, H
virulence
measure of pathogeneisis
measure of HOW MUCH disease POTENTIAL strain has
virulence of flue
one strain has flagellla
both can cause disase, but the one with flagella is more efficient… MORE VIRULENT
Stages of infection (every organism is a little different though)
Contact Adhesion (and invasion) Growth Inflammation and immune response clearance and death
Contact
Adhesion (and invasion)
Growth
the INFECTION parts
inflammation and immune response
clearance and death
DISEASE
Contact
going from one person to another
- direct contact (sexual, doorknob)
- airborne aerosol (sneeze)
- ingestion (fecal oral: food, water)
- arthropod vector
adhesion and invasion
protein protein interactions
these factors are great for vaccines! purify proteins and inject just the proteins (H and N for flu)
Growth
can also interfer with infection by inhibiting growth
HIV: HAART: targets reverse transcriptase, integrase, and protease to keep virus from replicating
Inlammation and immune response
get immmune response through vaccination or prior infection or innate cells
Inlammation and immune response
get immmune response through vaccination or prior infection or innate cells
Clearance and Death: 2 options
-clear the pathogen
-we die
it is a WAR that must be won
OTHER OPTION: persistant and latent infections
viruelence (from clicker)
ability to CAUSE DISEASE
NOT ability to infect
what drives evolution
SURVIVAL
not usually to cause death of host
if host is dying… this probably isnt what it evolved to do
Yersinia
GENUS for plauge
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
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
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
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
self limiting
disease that goes away on its own doesnt usually kill host
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
Yersinia in rodents
usualy not lethal
in AZ, Colorado, US SW
endemic in rodent populations
fleas to rodents to humans
fleas can get into pet rodents
then to humans
bubonic plauge
jump from rodent to human
death in 2-3 weeks
pneumonic plauge
infection of lungs
jump from human to human
death in 2-3 days
plasmid
circular piece of extra-chromosomal replicating DNA
plasmid
circular piece of extra-chromosomal replicating DNA
3 virulence plasmids of Yersiniae
pYV
pMT1
pPla
pYV
immune system avoidance, toxicity
T3SS
pMT1
transmission to fleas
antigen
pPla
intra-dermal site disseminiation
plasminogen activator
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
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
Bubonic plauge: specifics
blood
bacteria picked up by macrophages…and kills macs
goes to lymph nodes
necrosis and large black swelling at lymph nodes
pneumoni plage: specifics
drowning due to inflammation of lungs
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
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
where did the plauge come from
soil in a small area in CHina
where do big outbreaks come from
weather changes
cause it to jump from soil
most common foodborne pathogens
Norwalk-like viruses (67%) Campylobacter (14%) Salmonella (10%) Clostribdium perfringens (1.8%) Shiga-toxin producing E. (0.7%)
Digestive Tract Infections
disease is based on LOCATION
tells what tissue is infected, not what microbe is causing
iflamation of digestive tract
vimiting and/or diarrhea
Gastritis
stomach
Gastroenteritis
stomach and small intestine
Enteritis
small intestine
Enterocolitis
large and small intestine
Colitis-large
large intestine
Peyer’s Patch
lymph nodes along digestive tract/intestines
specailized region
M-cells
Peyer’s Patch
lymph nodes along digestive tract/intestines
specailized region
M-cells
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
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
symptoms of norwalk viruses
extremem vomiting and diarrhea
creastes aerosols that coat surfaces
Best clean up for Norovirus
10% bleach
resistant to alocohol and detergent
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)
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
lymph nodes in intestines
Peyers pathces
Have M cells on surface to transport things from lumen and exposing them to immunity
lymph nodes in intestines
Peyers pathces
Have M cells on surface to transport things from lumen and exposing them to immunity
Why M cells are taken advantage of
they can transport large things
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
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
