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54 Cards in this Set
- Front
- Back
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Define the following:
Enteritis Enterocolitis Gastroenteritis Diarrhea Dysentery |
Enteritis: inflammation of the mucosa of the intestines
Entercolitis: inflammation of the small + large intestines Gastroenteritis: inflammation of stomach and intestinal lining Diarrhea:fluid stools from disease of the small intestine Dysentery: inflammation of the GI tract with blood & pus in the feces (usually a disease of the large intestine). |
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What are the 2 families of enteric bacilli?
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Enterobacteriaceae & Vibrionaece
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Where is Enterobac. family found? What types of infections do they cause?
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-Found in normal flora of the gut
-found in diarrhea, UTI, & opportunistic infections |
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What are the major divisions of the Enterobac. family? Give examples of each.
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Lactose fermenters: E. Coli, Klebsiella, Enterobactor
Non-lactose fermenters: Salmonella + Shigella |
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What agar is best for detecting Lactose vs. Non-lactose fermenters?
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McConkey Agar
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Compare and contrast the flagella of enterobacteri. fam vs. the Vibrio fam.
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Bacterio fam: peritrichous flagella
Vibrio: polar flagella (i.e. Vibrio Cholera) |
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What type of laboratory testing could you do to identify a member of the Vibrio family?
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-blood/fecal sample on McConkey agar or EMB Agar contains dyes that inhibit the growth of gram +'s...since we're looking for gram negatives)
-Biochemical tests: assess if bacteria can ferment lactose, gas formation, enzyme detection -cell surface antigen testing (using antiserum serotypes |
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What types of cell surface antigens can be tested for?
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O antigen - polysaccharide portion of LPS
H antigen - flagella protein found on motile cells K antigen - capsular polysaccharide |
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What does ETEC pathogen cause? What are the virulence factors?
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Adult/Travelers diarrhea from uncooked foods/unpeeled fruit/salads.
Virulence factors: Heat stable toxin (ST): not destroyed at high temps; plasmid encoded Heat labile toxin (LT): destroyed at lower temps; causes non-inflammatory diarrhea; plasmid encoded |
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What is the mechanism of action for the LT and ST toxins associated with ETEC?
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LT: works just like cholera; Increase in cAMP, increase in Cl- across the membrane; increase in fluids across the membrane.
ST: guanylate cyclase stimulated, GTP formed, increase in cGMP, no NaCl transport into the intestinal wall --> fluids not being absorbed |
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What population does EPEC affect most? What is the typical treatment? What are the virulence factors?
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-Predominant cause of infant diarrhea
-No known toxins, but virulence factors include the ADHESINS: bundle forming pilus that allows the bacteria to adhere to intestinal cells Signal transduction: EPEC proteins are secreted into the epithelial cells causing actin/cytoskeletal rearrangement (pedestals) Intimin: allows for very tight adherence of bacteria to cells causing loss of microvilli (effacement) --> KNOWN AS ADHERENCE AND EFFACEMENT LESIONS -Typical treatment: self-resolving, but can become chronic. |
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What does an EHEC infection cause? What is the reservoir? What is the route of transmission?
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-Causes: severe abdominal cramping and copius, bloody diarrhea
Reservoir: Cattle Route of transmission: zoonosis (undercooked meat, raw milk, unpasturized juice) Secondary method of transmission: person to person |
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What will a culture of someone with EHEC show? Serological tests will show?
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-It will be negative for sorbitol fermenting
Serological tests would show: O polysaccharide (from LPS) and H flagella proteins (most predominant types found in E. Coli)- only 10 bacterial cells needed for the presence of an infection |
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What are the EHEC virulence factors? What do they cause?
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-Shiga-like toxin: stop protein synthesis + destroyes epithelial lining and dead cells slough off and cause the bloody diarrhea.
A/E Lesion: Like EPEC: Intimin allows for tight adherence; Type 3 secretion of bacteria into the cell causing cytoskeletal rearrangement and pedestal formation, actin polymerization) Acid Tolerance: Allows the bacteria to move through the stomach without being killed. |
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What other diseases can be associated with a small percentage of EHEC cases?
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Hemolytic Uremic Syndrome: causes kidney failure; usually in small children. May be due to the Shiga toxin getting into blood and traveling to the kidney. Most common has of acute renal failure in children in the US.
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What are the manifestations of EIEC? What population does this occur in most frequently? What are the virulence factors for EIEC?
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EIEC causes dysntery of the intestinal epithelium (blood & pus in the urine)
Mostly occurs in children Virulence factors: plasmid encoded invasion factors via Type 3 mechanism causing actin rearrangement & intracellular motion & cell to cell spread. |
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What occurs in EAggEC?
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Fimbrial adheshion to cell walls without causing any obvious histological changes.
Causes persistent diarrhea |
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What type of E. Coli causes UTI's? Who are the likely patients?
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-Uropathogenic E. coli
-likely to affect young sexually active women, urinary catheters, enlarged prostate (can obstruct the urine outflow). |
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What is the virulence factors associated with Uropathogenic E. Coli?
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P fimbriae: adherence factor; binds sugars on human uroepithelial cells
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What is the difference betweeen cystitis and pyelonephritis?
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Cystitis= UTI of the bladder
Pyelonephritis = infection of the kidney |
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What is the most common cause of nosocomial gram (-) bacteremia?
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E. Coli Systemic-Opportunistic Infections
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How does E. Coli meningitis occur? Why is this infection significant? What other condition does this type of infection occur?
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-Infant colonized with vaginal E. Coli via ruptured amniotic membrane during childbirth; caused by strains carrying the K-1 capsule which is also found in the Strep B.
MOST COMMON CAUSE OF NEONATAL MENINGITIS |
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What distinguishes Salmonella from E. Coli?
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E. Coli = lactose fermenter
Salmonella = non-lactose fermenter (forms H2S gas) |
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How is Salmonella transmitted? What are the antigens present with Salmonella?
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Fecal-oral route; ingesting food that has been contaminated with animal feces.
Antigens: -H toxin - from flagella -O - from LPS -K - from the capsule ANTIGENIC VARIATION IS COMMON IN SALMONELLA |
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What are the 3 main species of Salmonella? What is remarkable about the resevoirs of the different strains of Salmonella?
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-Typhi (HUMAN is the ONLY RESERVOIR; not zoonotic)
-Enteriditis -Typhimurium |
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Which of the strains of Salmonella are likely to cause gastroenteritis?
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Typhimurium
Enteritidis |
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What is the infectious dose for gastroenteritis, and how could it be compromised?
What is the treatement for gastroenteritis? |
Large dose is required unless patient is taking antacids and has low stomach acid.
Infection is self-limiting |
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What are the virulence factors for gastroenteritis?
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Enterotoxin: cholera-like (increases cAMP and Cl- is released & water follows)
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What strain of Salmonella causes Typhoid fever? What is the reservoir? What is the route of transmission?
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Typi
HUMANS are the reservoirs Fecal/Oral: Human feces contaminates food due to poor sanitation. |
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What is a key difference in symptoms between Typhoid fever & Gastroenteritis? What are typhoid fever carriers?
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There usually isn't diarrhea with Typhoid fever
Carriers are people that have had the symptoms of TF resolve, but the organism persists in their bile. |
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What is the mechanism of invasion of Salmonella typhi?
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organisms in the stomach progress to the small intestine & invade intestinal cells via the "M cells" & cause membrane ruffling which indicates actin rearrangement.
Bacteria remain in lysosomes which they are resistant to) and move to the lamina propria. They then enter the blood stream/lymph system (primary bacteremia) where they are ingested by macrophages and then carried to the liver, spleen, & mesenteric lymph nodes. Continuous bacteremia occurs if the organism persists |
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What are the major virulence factors of S. typhi?
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Cell invasion system: which allows the bug to enter cells and them later become taken up by monocytes where they can evade the immune system & persist
Proteins secreted by Type 3 secretion and cause cytoskeletal rearrangements. Acid resistant Capsule can evade complement mediated lysis |
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What are the other infections that can occur as a result of Salmonella?
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Pneumonia
Osteomyelitis Menegitis Endocarditis |
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What you think of ETEC, what mechanisms of action should you think of?
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G-protein type regulatory mechanisms altered...BY ACTION OF PLASMIDS
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What are the 2 toxins associated with ETEC? What does each one do?
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Heat stable: (ST); this acts just like CHOLERA; increased cAMP levels cause the Cl- levels crossing into the lumen of the gut to INCREASE and water will follow = DIARRHEA
Heat labile: Causes an increase in cGMP, NaCl transport across the cell is inhibited; water stays with the NaCl + causes diarrhea. |
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When you see EPEC, what should pop into your head about the overall actions of this molecule?
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STICKY INVASION!!! + NO TOXINS
Adhesins: bundle-forming pili for close adherence A/E lesions: attachement + effeacement causing loss of microvilli Cytoskeletal rearrangement: pedestal formation Type 3 secretion of proteins |
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When you see EHEC what should pop into your head?
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Bloody + pus-filled diarrhea...why does this occur?
There is a Shiga-like toxin that prevents protein synthesis, damages the intestinal lining, causes cell death, then sloughing off of the cells which makes the diarrhea bloody. LOW DOSE INFECTION |
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Other than the Shiga toxin, what other virulence factors assist EHEC?
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A/E lesion: close adherence of the protein; Type 3 secretion; actin rearrangement
Acid resistance: can move through the stomach without being killed. |
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What syndrome should you think about with EHEC?
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Hemolytic Uremic syndrome: kindey failure in children possibly due to the Shiga toxin being carried to the kidneys.
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What should immediately pop into you head when you see EIEC?
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I= Intracellular MOVEMENT! This occurs via the invasion plasmid antigens.
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What 2 EC infections could present with similar symptoms? How can you distinguish among them?
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EHEC & EIEC have similar symptoms: BLOODY diarrhea but EIEC is less severe.
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Which form of E. Coli can bind to intestinal cells, but cause NO histological damage?
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EAggEC; can bind to intestinal cells without causing any histological changes
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What is the virulence factor of uropathogenic E. Coli?
What population is this most found in? |
the P-fimbriae which allows the sticking of the E. Coli to the urogenital cells in the upper urinary tract.
Youn sexually active women |
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Which population is most vulnerable to E. Coli menengitis? Why?
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Neonates; it may be transmitted to the baby via a vaginal delivery where the mother has colonized vaginal E. Coli (similar process to Strep B)
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What is the major virulence factor for the development of menengitis from Strep B and E. coli?
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K-1 capsule found in both organisms.
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What other infections (outside the ones that are affected by typhi) are caused by Salmonella?
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Osteomyelitis
Menengitis Endocarditis Pneumonia |
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What type of dose infection does Salmonella require to become infected?
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HIGH doses to become infected
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Salmonella gastroenteritis is common for which strains of salmonella? Which other infection does it act like?
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S. typhium + S. enteridis
Works like cholera |
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Why is Salmonella typhi considered a facultative intracellular organism
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After moving into intestinal epithelial cells, it moves into lymphyoid tissue where it can go to MANY tissues after it lives inside a macrophage
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What is the treatment for S. gastroenteris?
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Self-limiting
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Which 3 infections all involve the Shiga toxin? How does the Shiga toxin work?
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EIEC
EHEC Shigella THEY ALL INVADE INTESTINAL MUCOSA, inhibit protein synthesis, & cause the death and sloughing off of cells --> No surprise that all of these conditions present with BLOODY diarrhea. |
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What type of infection dose does Shigella require?
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High infectivity -- Low infectious dose
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How can you distinguish between Shigella, Salmonella, & E. Coli
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E. Coli - lactose fermenter
Salmonella - non-lactose fermenter, H2S gas + Shigella: non-lactose fermenter; no H2S gas |
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What is the mechanism of Shigella pathogenesis?
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Enters host cell intestinal cells via invasion plasmid through M cells, go through the lamina propria and pass thru lamina propria: some are injested by macrophages and kills their host
If they remain inside the epithelial cell, then they evade phagocytosis |
