Lecture 5: Mucusal Infections Flashcards
Merkel cells
one of the first transformative viruses identified (cancer causing)
Enteric Bacterial Pathogens
E. Coli (EPEC and EHEC (enteropathogenic and enterohemorrhagic)
Shigella (dysenteriae)
Salmonella (serovar typhi and serovar typhimurium)
Yersinia (enterocolitica)
Enteric Bacterial Pathogens
E. Coli (EPEC and EHEC (enteropathogenic and enterohemorrhagic)
Shigella (dysenteriae)
Salmonella (serovar typhi and serovar typhimurium)
Yersinia (enterocolitica)
Core and Pan Genome of Enteric Bacteria: Core of EHEC, Shigella, and Salmonella
Gram Negative
Bile salt resistant
Bile start and studying enteric bacteria
streak fecal matter on plate with bile salt
things that arent enteric will die
study whats left
Shigella vs. the other species
was though to be different until recently
BUT: found that shigella is an E. Coli that lost some genes and gained a few plasmids
“subspecies of E. coli” say som
special things about EHEC
T3SS
urea gene
lactose gene
Special things about Salmonella
two T3SSs
ability to H2S
STUDY TO CORE-PAN GENOME FIGURE
STUDY TO CORE-PAN GENOME FIGURE
How E. coli causes diarrhea
1) inhibits absorptive function of intestine
2) opens tight junctions between cells (bloody)
3) causes inflammation
diarrhea
caused by excess fluid in GI tract
intestines absorb water usually, in this case they dont
feces become thinner
Caused by inflammation OR an actual function of the bacteria
how cholera causes diarrhea
causes epithelial cells to pump salt into the lumen of the gut
water rushes into gut from body
rice water diarrhea
active function of toxin
how cholera causes diarrhea
causes epithelial cells to pump salt into the lumen of the gut
water rushes into gut from body
rice water diarrhea
active function of toxin
pathotypes
groups of bacteria that cause disease in a certain way
who has E. coli
most mammals, usually doesn’t cause disease
ETEC
enterotoxin e.c.
most common
produces a toxin that produces a protein that degreulates water absoprtion of intestines
TRAVELER’s diarrhea
EIEC
enteroinvasive e.c. mild diarrhea the one that evolved into shigella can invade host cells-lives at epi layer pretty self-limiting: goes away on its own often get traveling
EPEC
enteropathogenic e.c.
major cause of infant dirrhea and death oitside US
ADHERES tightly to epi cells
serious inflammation
EHEC
enterohemorrhagic E.c. bloody diarrhea sometimes a problem in the US its EPEC plus a toxin: SHIGA TOXIN destroys epithelial cells, blood goes into lumen of the gut... pretty bad
EHEC
enterohemorrhagic E.c. bloody diarrhea sometimes a problem in the US its EPEC plus a toxin: SHIGA TOXIN destroys epithelial cells, blood goes into lumen of the gut... pretty bad
more on EHEC
lose some genes from EPEC
add a toxin
one of worst enteric infections you can get
more on EHEC : US strain
O157 H7 (these are ANTIGENS) we have the strongest response to these 2 antigens HEMORRHAGIC diarrhea has shiga toxin fecal contamination of undercooked foods
EHEC: what does O157 mean
O=LPS
157=bloody diarrhea
EHEC: what does H7 mean?
FLAGELLA
EHEC secretion
LEE type 3 secretion system
CAUSES PEDESTAL FORMATION
what is HEmorrhagic diarrhea
bright red blood
EHEC
Pedestal formation
cause actin to polymerize underneath the bacteria
this lets the bacteria move pretty well?
DECREASES SURFACE AREA of epithelial cells
EHEC transmission
mostly foodborne
because it has a requires a high infectious dose
EPEC secretion
secrete proteins into the host
bacteria stick to the bacterial protein
this causes actin to polymerize under the bacteria
other proteins secreted lead to death of host cell… bacteria eventually kills the host cell by apoptosis because thats the only way the bacteria can get off the surface
How EHEC differs from EPEC
because it also has a bacteria phage that contains the SHIGA TOXIN
shiga toxin: A-B toxin
B part of protein : sticks to cell sruface
A part of protein: has catalytic activity that kills the cell
How shiga toxin kills the cell
retrograde transport
retrograde transport
vesicle meant to go outside moves backwards
vesicle fueses with the Golig again, eventually the ER again
in the ER: the B portion forms a pore, A goes to cytosol, finds RIBOSOME
A and ribosome
a portion cleaves the ribsomal RNA
this stops protein synthesis
cell dies because it cant make proteins