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45 Cards in this Set
- Front
- Back
What does Enterobacteriaceae suggest about their location?
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Entero=gut
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What are the antigens involved with enterobacteriaceae?
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O Antigen: LPS (lipopolysach.)
K Antigen: Capsule H Antigen: Peritrichous flagella Pilli are not part of formal typing scheme |
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What are the genera of enterobacteriaceae that are the most virulent for humans?
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1. Escherichia
2. Shigella 3. Salmonella 4. Klebsiella 5. Yersinia |
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What is the habitat of enterobacteriaceae?
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Lower GI tract and female genital tract.
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These two enterobacteriaceae are strict human pathogens?
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Shigella & Salmonella.
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What toxins are present with enterobacteriaceae?
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Endotoxin (LPS): Not secreted.
Enterotoxin: Secreted. Exotoxin |
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Pathogenicity Island?
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Microorganisms living close together may conjugate and exchange genetic material which may lead to the transfer of resistance/virulence factors.
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Type III secretion?
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Unique 'needle-like' secretion into host cells w/o having to contact host cell.
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E. coli: What types of pili are there?
What types of cells do each type of pili bind to? |
Type 1 pili-bind to D-mannose...common on epithelial cells.
P pili-bind to uroepithelial cells (urinary tract infections) and erythrocytes |
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What are 4 types of toxins coming from E. coli?
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1. alpha-hemonlysin: cytotoxin, causing cell death
2. Shiga & Shiga-like toxin: AB toxin prevents protein elongation 3. Labile toxin (LT): AB toxin, causing secretion of fluid and electrolytes into the bowel lumen 4. Stable toxin (ST): same as LT |
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What do E.coli toxins cause in the host?
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Diarrhea. Caused by the toxin and not the bacterium itself.
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What are the two main types of E.coli infections a host might contract (sites)?
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1. Urinary tract (UTI) or (UPEC-Uropathegenic E.coli)
2. Intestinal infection |
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E.coli urinary tract infection (UPEC):
What percentage of people have one in their life span? What is greater danger? What type of pili? |
40% have one in lifetime (more common in women)
Infections in upper UT may lead to sepsis and septic shock. P pili. Pyelonephritis-spreading to pelvis and kidneys. |
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What are 5 types of E.coli intestinal infections?
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1. ETEC (enterotoxigenic)
2. EPEC (enteropathogenic) 3. EIEC (enteroinvasive) 4. EHEC (enterohemorrhagic) 5. EAEC (enteroaggregative) |
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ETEC (enterotoxigenic):
1. What type of diarrhea? 2. What types of toxins cause the fluid outpouring into small intestine? 3. Where is it most prevalent? 4. Invasive? |
1. Watery diarrhea. (Traveler's diarrhea)
2. Cytotoxins/Stable Toxins 3. Leading cause of morbidity and mortality in developing countries. (greater than 2 yrs old) 4. No invasion or inflammation. |
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EPEC (enteropathegenic):
1. What type of diarrhea? 2. Where is it most prevalent? 3. Invasive? |
1. Watery diarrhea
2. Accounts for about 20% of diarrhea among infants in developing countries 3. Non-invasive |
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EIEC (enteroinvasive):
1. Similar to what? 2. What type of diarrhea? 3. Invasive? |
1. Shigella
2. Bloody diarrhea 3. Yes. Enter into host cell. |
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EHEC (enterohemorrhagic):
1. What type of diarrhea? 2. Invasive? 3. What antigenic marker? |
1. Bloody diarrhea
2. Not invasive 3. O157:H7 |
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EAEC (enteroaggregative):
1. What type of diarrhea? 2. Invasive? 3. How long does it take symptoms to appear after ingestion? |
1. Watery diarrhea
2. Not invasive, but forms a biofilm on the intestinal surfaces 3. Starts 2-4 days after infectious dose |
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What are the common species (3) of the Shigella genus?
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1. S.flexneri
2. S.dysenteriae 3. S.sonni |
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Do Shigella have flagella?
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No, therefore no H antigen.
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Shigellosis:
1. What is it? 2. How is it spread? 3. What type of diarrhea? 4. What type of dose is necessary? |
1. Dysentary (diarrhea + WBC + RBC)
2. Spread fecal-oral route (poor sanitation) 3. Bloody diarrhea (begins with a watery diarrhea, followed by presence of blood and pus) 4. Low infectious dose (< 200 organisms) |
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Shigellosis:
1. Why is it so potent (low infectious dose)? 2. Invasive? |
1. Acid resistant (can pass through stomach into intestine)
2. Yes. Transcytose through M cells. Unlike EPEC & EHEC: no A/E lesion |
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Salmonella:
How many species? |
One species (S.enterica) with many serotypes
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Salmonella:
1. Flagella? 2. Opportunists or Strict pathogens? 3. What are 2 types of Salmonellosis (Infections)? |
1. Yes
2. Strict pathogens 3. Gastroenterities (S.enterica) & Typhoid fever (serotype typhi) |
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Salmonella-Gastroenteritis:
1. Onset? 2. How long does it last? 3. Recent years? |
1. 1-2 days after eating
2. Lasts 3-4 days (self-limiting in healthy individuals) 3. Outbreaks have increased with large scale food production |
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Salmonella-Typhoid fever:
1. What is special about it? 2. Transmission? 3. Where is it prevalent? 4. How is it different than S.enterica? |
1. Strictly human, no animal model.
2. Fecal-oral transmission. 3. Areas with poor sanitation. 4. Similar to S.enterica, but persist in macrophage longer, can spread to other sites, causing bacteremia. |
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Yersinia:
What are the important species for us to know? |
1. Y.pestis* (bubonic plague)
2. Y.pseudotuberculosis 3. Y.enterocolitica 2&3 cause gastroenteritis |
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Shigella vs. Salmonella:
What is different about how they spread? |
Shigella: Type III secretion system. Spreads horizontally along small intestine cells.
Salmonella: Spreads more 'vertically' into lymph nodes. More systemic spread. |
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Vibrio:
1. General characteristics? 2. What is most virulent species? 3. What type of toxin? 4. Important serotypes? |
1. Curved rods with single polar flagellum
2. V.cholerae 3. Cytotoxin (AB) 4. 150 O antigen serotypes: O1 & O139 cause cholera |
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V.cholerae:
1. Toxin? 2. Type of diarrhea? 3. Source? 4. Incubation time? 5. Dosage? |
1. AB toxin (2 As & 5 Bs)
2. Most dramatic watery diarrhea known 3. Contaminated water, under cooked seafood 4. About 2 days 5. High dosage required |
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Campylobacter:
1. General characteristics? 2. Common human pathogens? 3. Where is it prevalent? 4. Incubation time? 5. What may it mimic? 6. What type of diarrhea? 7. Duration? 8. Reservoir? |
1. Curved rod with polar flagellum
2. C.jejuni, C.coli 3. Most common cause of GI infection in developed countries 4. 1-7 days after ingestion 5. Acute appendicitis 6. Watery or dysenteric with blood and pus 7. Self limiting-up to 1 week 8. Animal reservoir |
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Helicobacter pylori:
1. Associated with what condition? 2. Nobel prize winners? 3. General characteristics? 4. Site? 5. Virulence factors? 6. Diagnosis? |
1. Stomach ulcers
2. Barry Marshall & Robin Warren 3. Slender, curved rod with polar flaggela 4. Limited to the mucosa of the stomach 5. Urease-generates ammonia (rasies pH to allow for growth) Vacuolating toxin (VacA-causes cell death) & Cag stimulate inflammation 6. Measure the CO2 levels (biproduct of Urease), ingestion of Carbon 13 or 14 labeled urea |
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Pseudomonas aeruginosa:
1. Aerobic? 2. Flaggela? |
1. Aerobic but can grow slowly under anaerobic conditions.
2. Single polar flaggelum. Produce colorful water soluble pigments. |
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Pseudomonas aeruginosa:
1. Where can it grow outside a host? 2. Antimicrobic resistance? 3. What do they produce?*** |
1. Sinks and faucet aerators
2. Most resistance b/c it grows in biofilm and makes a lot of polysaccharides that aren't penetrated. 3. Alginate forming a mucoid exopolysaccharide slime layer*** |
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Pseudomonas aeruginosa:
1. What types of toxin? 2. What else do they produce? 3. Range of infection? 4. Who is most susceptible?*** |
1. Exotoxin A, similar to Diphtheria toxin
2. Exoenzyme S & elastase (breaks down elastin in lungs & vessels-hemmorrhagic destruction) 3. Very wide. Difficult to treat (biofilm) 4. ***Burn victims, leukemia, Cystic Fibrosis patients |
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Haemophilus:
1. Haemo- means what? 2. General characteristics? 3. What type of agar? |
1. Blood
2. Smallest bacteria, grow in blood 3. Chocolate agar |
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Haemophilus influenzae:
1. # of serotypes? 2. Most virulent serotype? 3. Most virulent serotype's capsule?*** 4. Causes what condition? 5. Mechanism of invasion?*** 6. Vaccine? |
1. Six
2. Type b (Hib) 3. Capsule contains ribose, ribitol & phosphate, called polyribitol phosphate (PRP)* 4. Major cause of meningitis in children under 2 (also epiglottitis & pneumonia) 5. ***Invades between epithelial cells (smallest bacteria) 6. Vaccine has drastically reduced prevalence |
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Bordetella pertusis:
1. What does it cause? 2. What toxin? 3. What is the 2 component system?*** |
1. Whooping cough
2. Pertusis toxin (an AB toxin) 3. Sensor domain & Modular domain: Environmental factor is sensed to change production *** BvgS regulatory (sensory) protein of membrane BvgA regulatory protein of cytoplasm Act is 2nd regulator that allows for transcription of Pertusis toxin. |
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Legionella pneumonia:
1. Name? 2. Transfer? 3. Intracellular or extracellular? 4. Opportunist or strict pathogen? 5. Site? (Macro & micro) |
1. 1976 American Legion convention (first discovered)
2. Aerosol 3. Intracellular 4. High mortality rate in immunocompromised 5. Lung, multiplies in macrophages. |
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Campylobacter:
1. Motile? 2. Aerobic? 3. Use of actin? |
1. Yes
2. Micro-aerophillic 3. Manipulates cellular microtubules as opposed to using actin |
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How does H.pylori survive in the stomach?
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Urease metabolizes urea into ammonia to raise the local pH.
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Psudomonas aeruginosa:
1. Growth requirement? 2. Large production of what? 3. Susceptible populations? |
1. Minimal: ammonia and CO2
2. Mucoid exopolysaccharide slime layer 3. Burn patients, Cystic Fibrosis patients, Leukemia patients |
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Haemophilus influenzae:
1. What is most virulent serotype? 2. Vaccine contains what? |
1. Type b (Hib)
2. Contains purified PRP. |
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Bordetella pertusis:
1. Toxin? 2. Virulence factors? |
1. Pertussis toxin (PT): an AB toxin
2. PT is major virulence factor, also adenylate cyclase |