Lecture 4 Flashcards
What is the GI tract? What is it prone to?
Tube running from mouth to anus
Has lots of normal floura, but is prone to pathogens
What does dental plaque consist of? What kind of bacteria? What leads to tartar?
Bacteria encased in biolfilm —> attach to both the tooth and eachother
—anaerobes + aerobes
Salt, crusty substance
What is s. Mutans?
What does it cause?
What does sugar fermentation result in?
How does flouride work?
Biofilm on teeth!
Cavities and tooth decay
Sugar fermentation results in acid production —> drop in the pH causes calcium phosphate of the teeth to dissolve
-Hardens tooth enamel so increases acid resistance and less tooth decay
What causes red gums?
What is the bacteria that lives in plaque and what toxins does it produce??
Bacterial products released from plaque trigger inflammation
—gram neg anaerobic bacteria—> P. Gingivalis
-produces proteases + toxins that can result in periodontitis
What are the toxins associated with diarrhea?
What causes inflammation?
What is associated with infections of SI and colon?
Enterotoxin— causes electrolyte water flow from intestinal cells
Cytotoxins— cell death
Intestinal cell alterations + invasions
SI: watery diarrhea
Colon: mucus, pus, blood
How are diarrheal diseases transmitted?
What are the infecting doses required of acid sensitive and resistant pathogens?
Oral-fecal route —> contaminated by human OR animal feces
Acid sensitive pathogens require high infecting dose
Acid resistant pathogens have low infecting does
What is the treatment for diarrhea + how is it prevention ?
Oral rehydration therapy—ORT, antibiotics not helpful
- chlorinate water + avoid unclean water
What is the bacteria that causes cholera + what is its virulence factor ?
When does it occur? And what are treatment?
Gram negative pathogen— vibrio cholerae, spreads very easily, BUT we need a large dose of it to cause the disease because it is sensitive to acid
Cholera toxin
Poverty, natural diseasters, poor sanitation — most fatal disease
ORT
How does the cholera AB toxin work?
How does the vaccines work?
B contacts the membrane
-A subunit will bind to G protein on adenylate cyclase complex, keeping it on—> making cAMP levels high
-cAMP binds ion pumps that pump out electrolytes constantly + water follows —->rice water stool
Short lived protection, can reduce outbreak
What are virulent E. coli and what toxin do they produce? ?
Enterohemorrahic Ecoli—> EHEC
Shiva toxin producing E. coli—-> STEC
What kind of secreting system do shiga producing E. coli use?
What does intimin bind to?
What does it produce and what does this toxin cause?
Where does it come from?
Secretion T3SS—> injections the proteins,
It makes the Tir receptor and places it on the host
Intimin binds to Tir on host cell surfaces—> inducing intestinal cell alterations, and
Shiga Toxin (stx)—> causes dysentery (blood)
Undercooked beef and un cleaned stuff —> cattle is the main reservoir but does infect them bc they don’t support the receptor
What kind of toxin is shiga and what does it target?
What happens when its life threatening?
AB toxin
Targets epithelial and endothelial cells
The A subunit binds the ribosome, which cleaves RNA—> preventing protein synthesis
HUS—-> if the toxin gets into the blood stream which can damage small vessels + clotting, which leads to kidney damage
What are the symptoms of shigellosis?
What is the pathogen that causes it ?
What does it do that’s special?
What are the 2 common types?
Inflammation, dysenteric from some shiga toxin
Shigella, pathogens are the only reservoir in humans
Avoids detection by immune system, resistant to acid, so only need a small dose to be infected
S sdysenteriae is most virulent bc has shiga toxin Shigella
S. Sonnei is most common
How does shigella enter ??
What happens when inside ( think M cels and T3SS)?
1) Enter via antigen sampling M cells
2) Multiple inside macrophages —> escape
3) Induce uptake by epithelial cells using T3SS
4) Multiply causing actin polymerization to move around
5) Inflammation + cell death—> makes epithelium come off
**if produces shiga, can abuse HUS ***
what are symptoms of C. difficile???
Mild diarrhea—- leading cause of hospital acquired diarrhea, can develop writhing 5/10 days and can occur a lot
Can cause colitis and
toxic megacolon— can not pass gas or stool
Why does C diff cause infection after antibiotic treatment?
C diff is a poreforming bacterium
Surrounded by a tough + highly impermeable coating
Are resistant to antibiotics
How is c diffuse present in the Intestine?
How to treat?
When are antibiotics not used and why?
-As spores and usually do not grow unless the onditions are ideal, then will leave the spores + grow in high numbers
Grow in 2 toxins
Antibtiocs when they r out of the spores, but reoccurs often
Fecal microbiota transplant from health person
STEC infections because it may result in getting HUS
How does rehydration therapy, blood transfusion, antitoxin therapy, debridement, fecal microbiota transplant + antibiotics work?
Rehydration: electrolytes in the mouth or via IV that treat cholera
Blood: only if STEC or shigellpois lead to HUS
Antitoxin: neutralize toxins in the body
Debridement:
Surgical removal of dead/ infected tissue
Necrosis
Fecal transplant: recurrent C diffile
Antibiotics: prevent growth of bacterial but resistant occurs
What is the new paradigm for antibiotic development ?
Target virulence properties
Adhesion
Gene regulation, quorum sensing
Invasion
Toxins
Why is the phage therapy a promising alternative to antibiotics ?
If the agent is known and specific phage that target the isolate are available, can be used to infect + lyse the bacteria at the site of infection
What is hemolytic uremic syndrome (HUS)? Infections with which microbes may have HUS as a post infection outcome?
Blood clot formation + damage to kidneys that filters blood, leads to urine + kidney failure
Shiga producing toxins like E. coli + Shigella Dysenteriae
