Exam 4: Intestinal Bacteria Flashcards
- lives in stomach
- wants to live in neutral area
- live in epithelia because mucus makes it less acidic
hylobacter pylori
what are koch’s postulates?
- infectious agent must be found in the diseased individuals and not in healthy individuals
- grow infectious agent in pure culture
- recapitulate disease in model host with pure culture
- needed to recapture pathogen
- if you can remove infectious agent, you should be able to get rid of disease
does H. pylori follow Koch’s first postulate?
no because it is found in both sick and healthy individuals
what are non-invasive ways to look for H. pylori?
- serology test
- ELISA (enzyme linked immunosorbent assay)
- urea breath test
- looks for antibody that responds to pathogens in patients
- if antibodies are there, pathogen must be there
serology test
- type of serology test
- if there are more antibodies present, there is greater color intensity of the assay
ELISA
- breaks down urea into CO2 and NH3
- H. pylori has it
urease
how does the urea breath tes work?
give 13C-urea or 14C-urea to patient and look for 13C-CO2 or 14C-CO2 in breath
what are invasive methods of looking for H. pylori?
- biopsy
- microscopy
- gram staining (H. pylori Gram -, spiral shape, motile)
how can H. pylori be grown in pure culture?
- it is microaerophilic
- prefers 2-5% oxygen and 5-10% CO2
- takes 5-10% of blood (sheep, horse)
how do you recapitulate a disease in a model host with pure culture?
- multiple cell lines
- primary cells
-usually immortalized by viruses or derived from cancer cells
~in gastric epithelium
multiple cells lines
have a limited life span
primary cells
what poses a threat for H. pylori?
- acid
- peristalsis
- muscosal barrier
- immune detection
how does H. pylori deal with acid?
- urease
- proton driven pump that transports urea into cells to neutralize acid
how does H. pylori deal with peristalsis?
- gets to epithelium with chemotaxis (flagella)
- rotates, corkscrew motion to penetrate mucus
during chemotaxis, what does H. pylori move toward and away from?
- moves away from acid (H+)
- moves toward amino acids
when is H.pylori able to penetrate the mucus the fastest?
when the environment is viscous
how does H. pylori deal with the mucosal barrier?
- BabA
- SabA
- attach to our blood group antigens
- binds to fucose
BabA
- attach to our blood group antigens
- binds to things with sialic acid
SabA
what is the gene protein of non-secretor people?
Le
what is the gene protein of secretor poeple?/
Le + Se
what is the antigen of non-secretor people?
substrate + fucrose
what is the antigen of secretor people?
Le^a + fucrose
- gram -
- microaerophilic
- spiral and polar flagella
- H+ gated urea channel and urease
- chemotaxis + swimming
- BabA and SabA bind to blood group antigens
- upper intestinal tract
H. pylori
how does H. pylori evade our immune system?
- LPS
- flagella
what does H. pylori add to its LPS so its not recognized by the host receptor TLR4?
sialic acid
how does H. pylori prevent its flagella from being recognized by TLR5?
-flagella is sheathed/covered by outer membrane
how does H. pylori compete with gastric epithelium for nutrients?
- H. pylori neutrophil activating protein (HP-NAP)
- vacuolating cytotoxin A (VacA)
- cytotoxin associated gene A (CagA)
-recruit and activate neutrophils–>secrete ROS–> damage epithelium and release nutrients
HP-NAP
- a secreted protein
- insert itself into epithelial membrane
VacA
what does VacA cause once its inserted into the epithelial membrane?
-cause endocytosis
~disruption of endosomal membrane
-no antigen presentation
-release nutrients
- oncogene
- changes the transcription activity of host
- de-differentiation–> proliferation & move & anti-apoptotic
cytotoxin associated gene A (CagA)
- aquatic organism (wide range of salinity)
- does not want to be in human body
- causes watery diarrhea
- not much inflammation
- gram -
- comma shaped
- single polar flagella (sheathed), motile
- 3 types of pili that are all type 4
vibrio cholerae
what are the 3 types of pili of vibrio cholerae?
- mannose sensitive hemagglutinin pili (MSHA)
- toxin co-regulated pili (TCP)
- chitin regulated pili
eukaryotic microbe and macrobe attachments
chitin regulated pili
what are the 2 chromosomes of vibrio choleae?
-chromosome 1 (3mbp)
-chromosome 2 (1mbp)
~both have essential genes
the box on chromosome 1 is a….?
prophage
what does the box on chromosome 1 contain?
- toxin co-regulated pili (TCP)
- cholera toxin (CTX)~ makes it human pathogen
can infect other cholera pathogen that dont have TCP or CTX
-lysogenic conversion
filamentous phage
what is the environment of vibrio cholerae (outside of human)?
-biofilm (biotic or abiotic surface)
-viable but not culturable state (VBNC)
~alive, active
how does vibrio cholerae resist stomach acid?
- acid tolerance responses (get rid of H+)
- infectious dose
how does Vibrio cholerae penetrate mucosa in GI tract and then infect the small intestine?
- protease and mucinases (degrade mucus)
- flagella and MSHA (attach to epithleium)
- closely related
- 16s sequence ~ 96% similarity
- gram - rods
- peritrichous flagella
- metabolic and serotype differences
shigella, e. coli, salmonella
what are types of shigella?
-flexneri
-dysentariae (bloody)
~both cause diarrhea
what is a type of salmonella enterica?
serovar Typhi Typhimurium
intracellular pathogen
shigella
secretes shiga toxin and AB toxin
dysentariae
host receptor for AB toxin of dysentariae?
Gb3 (globotriaosylceramide)
when is E. coli bad?
when it has virulence factors
-infections in intestine, extraintestinal, urinary tract
what are the pathovars of bad E.coli?
- EPEC (enteropathogenic E.coli)
- ETEC (enterotoxigenic E.coli)
- EHEC (enterohemorrhagic E. coli)
-locus of enterocyte effacement pathogenicity island (LEE)
~more than 1 gene
-long range attachment by type 3 secretion system
-secretes its own receptor (Tir)
~intimin binds to it (short range)
EPEC
what happens when Tir and intimin bind?
- actin pedestal formation
- actin polymerization
- causes effacement ~ cells slough off
-has heat labile toxin
-heat stable toxin
~both AB toxin
-plasmid encoded
ETEC
-LEE +—> attachment/effacement lesion
-shiga like toxin –> bloody diarhhea
- O157: H7
~O antigen on LPS
~H antigen on flagella
EHEC
foodborne illnesses
S. enterica
- serovar
- dependent on H antigen
- local gastroenteritis
- strong inflammation in intestines
Typhimurium
- serovar
- systemic infection (typhoid fever)
- good at hiding~polysaccharide capsule
- no inflammation
- evade immune system
- invasive ~ cross epithelium and spread to peripheral organs
- bactermia —> fever
typhi
host receptor is GM1
cholera toxin
causes watery diarrhea
cholera
host receptor is GB3 (endothelium)
shiga toxin
- inhibits protein synthesis
- cellular apoptosis
shiga toxin
- causes hemolytic uremic syndrome (HUS)
- lysis of RBC
- lysis of platelets
- renal failure
shiga toxin
-ETEC
-increase camp
increase Cl- eflux
-watery diarrhea (travellers)
heat labile toxin
- ETEC
- increase cGMP
- increase Cl- efflux
- watery diarrhea (travellers)
heat stable toxin
shigella dysenteriae and EHEC
shiga toxin
