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Y1 - Microbio Exam 2 > 10_Enterics I > Flashcards

10_Enterics I Flashcards

1
Q

microbiome:

define

A
  • all the microbes (microbiota) in and on our bodies
  • includes bacterial, viruses, and eukaryotes
  • microbiota used to be called “normal flora”
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2
Q

where is the microbiome?

A
  • vast numbers of bacteria exposed on the body sites exposed to the environment; and many thousand species of bacteria in the microbiome
  • not usually inside the tissue (blood, deep tissue, sterile)
  • > 100x more genetic material in microbes than human genome
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3
Q

What are the most abundant bacterial phyla in the gut microbiome?

A
  • FIRMICUTES
    • Staph, Strep, Bacillus, Clostridium
  • BACTERIODETES
    • Bacteroides, Prevotella, Porphyromonas
  • ACTINOBACTERIA
    • Mycobacterium, corynebacterium
  • PROTEOBACTERIA
    • Escherichia, and other gram negative enteric organisms
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4
Q

How do gut microbiomes of humans vary?

A

Humans look similar at the phylum level, but

*EACH INDIVIDUAL VARIES AT THE SPECIES LEVEL

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5
Q

Protective functions of:

Gut Microbiome

A
  1. Pathogen displacement
  2. Nutrient competition
  3. Receptor competition
  4. Production of anti-microbial factors, e.g. bacteriocins, lactic acids
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6
Q

Structural functions of:

gut microbiome

A
  1. barrier fortification
  2. induction of IgA
  3. apical tightening of tight junctions
  4. immune system development
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7
Q

Metabolic functions:

of gut microbiome

A
  • control IEC differentiation and proliferation
  • metabolize dietary carcinogens
  • synthesize vitamins (e.g. biotin, folate)
  • ferment non-digestible dietary residure and endogenous epithelial-derived mucus
  • ion absorption
  • salvage of energy
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8
Q

which characteristics of the microbiota in the gut vary amongst individuals?

A
  1. antibiotic therapy
  2. birth method - c-section vs. vaginal birth
  3. diet - vegetarian versus a non-vegetarian
  4. disease states
  5. geographical location
  6. age
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9
Q

how does the microbiota harm us?

A

due to breakdown in the balance betweem microbiota and host immune system

  1. overgrowth of pathogens (e.g. UTI, flesh-eating disease, septic shock)
  2. Inflammatory bowel disease
  3. obesity
  4. type I diabetes
  5. GI cancers - H. pylori
  6. Oral diseases - cavities and gingivitis
  7. Allergy-like (atopic) diseases
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10
Q

Process of inflammation in the Gut Mucosa

A

PAMPS activate the Pathogen recognition receptors –> leads to production of proinflammatory cytokines

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11
Q

**Organism, disease, and mechanism:

  1. shigella species
  2. non-typhoidal salmonella ssp
  3. Yersinia enterocolitica
  4. Campylobacter jejuni
  5. Escherichia coli
  6. Vibrio cholerae
  7. Vibrio vulnificus
  8. Salmonella typhi
  9. Helicobacter pylori
A
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12
Q

define a pathogen:

(4 key characteristics)

A
  1. EVADES/ OVERCOMES defense mechanisms
  2. Finds niche to multiply
  3. Causes disease
  4. Ensures transmission to susceptible host
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13
Q

Diagnosis of diarrheal diseases:

If symptoms include:

  1. Rapid onset (1-16 hours), &
  2. Short duration (<1 day)
A

Think: food intoxication

E.g. Staphylococcus aureus, Bacillus cereus, Clostridium perfringens

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14
Q

Diagnosis of diarrheal diseases:

If symptoms include:

  1. Slower onset, &
  2. Longer duration (>1 day)
A

Think: INFECTION

  • If duration is < 10 days –> likely viruses or bacteria
  • If duration is > 10 days –> likely parasites or HIV
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15
Q

Diagnosis of diarrheal diseases:

If symptoms include:

  1. No fever, or low grade fever
  2. No white blood cells in stool sample
A

Think: SECRETORY DIARRHEA

Consider: Viruses (e.g. rotavirus), or bacteria such as Enterotoxigenic E. Coli, Enteropathogenic E. Coli, Enterohemorrhagic E. coli, or vibrio cholerae.

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16
Q

Diagnosis of diarrheal diseases:

If symptoms include:

  1. fever, &
    1. white blood cells in the stool sample (neutrophils)
A

Think: INFLAMMATORY DIARRHEA

Consider: Campylobacter, Salmonella, Shigella, or EIEC (Enteroinvasive E. coli).

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17
Q

Vibrio cholerae:

causes, transmission, symptoms, conditions for growth

A
  • caused by virulence factors (cholera toxin)
  • transmission:
    • ONLY affects humans
    • human – human transmission (Fecal-oral route), usually thru contaminated water or possibly by food
  • symptoms: rice water stools, aka secretory diarrhea (no WBC or blood in stool)
  • the bacteria grows in salt and fresh water

Epidemiology: 101,000 cases annually –> 2,345 deaths. Only 54 annual cases in US, 0 deaths

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18
Q

What is characteristic of the secretory diarrhea caused by Cholera?

(and amplification)

A
  • Cholera is dease of fluid loss in the GI tract
    • Can result from as little as 25 ug of toxin
  • Rice water stool, w/ 10-20L (or 17-20L) excreted by a cholera patient
    • Filled w/ 105 - 108 bacteria/mL
    • Appearance is due to lots of mucus and bacteria in the stool –> causing it to look turbid.
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19
Q

Important names of scientists working on Cholera, just in case

A
  • Dr. John Snow mapped the cases of cholera in London to find the cause – which was a street pump
  • Robert Koch identified V. cholera bacteria as the cause of cholera outbreaks (comma bacillus) in the stools of cholera patients)
  • Von Pettenkofer and Emmerich were two researchers who challenged Dr. Koch –> determined that some individuals carry genetic mutation which is resistant to cholera
20
Q

Draw the hierarchy/branching of Vibrios

A
21
Q

process of the cholera toxin infecting a cell

A
  1. cholera toxin binds to intestinal epitheium (enterocytes), enters cell
  2. A subunit permanently ribosylates the Gs alpha subunit of heterotrimeric G protein –>
  3. constitutive cAMP production
  4. high cAMP –> activates (CFTR) cystic fibrosis transmembrane regulator
  5. results in efflux of ions and water from the infected enterocytes
  6. causing secretory diarrhea
22
Q

what is the benefit to the pathogen?

A

You only have to consume a certain amount of bacteria to get sick –>

the number of bacteria amplify in the body –>

excrete into the environment

23
Q

what is the structure of the Vibrio cholerae?

A
  • gram negative, comma shaped bacterium
  • Tcp pili (toxin co-regulated pilus) bundle located at one pole
  • has a single flagellum extending from the same space
24
Q

cholera:

diagnosis and treatment

A
  • diagnosis by dark-field microscopy
    • first, isolate organism on TCBS agar (Thiosulfate-citrate-bile-sucrose)
    • second, test serotype using antiserum to agglutinate organisms
  • treatment:
    • fluid replacement w/ oral rehydration salts or intravenous fluids
    • antibiotics is recommended for severely ill patients (e.g. doxycycline for first line tx for adults, azithromycin for children & pregnant women)
25
Q

Cholera vaccines:

what is available?

A
  • whole killed vibrios given orally plus B subunit of cholera toxin (not available in the US)
    • oral vaccines provide protection in 52% of cases the 1st year following vaccination, and in
    • 62% of cases the second year
26
Q

name the 2 non-cholera vibrios.

how do they differ?

A
  1. V. parahemolyticus
    • causes shellfish poisoning
    • Hemolysin causes Kanagawa phenomenon
  2. V. vulnificus
    • fatal bacteremias
    • opportunistic pathogen in patients w/ underlying liver disease
27
Q

Kanagawa phenomenon:

define

A

Production of beta-hemolysis on a special high-salt mannitol medium (Wagatsuma agar) by most strains of Vibrio parahaemolyticus, which produces a heat-stable hemolysin.

28
Q

quorum sensing was first discovered with which bacteria?

how?

A
  • with marine bacteria “Vibrio fischeri”
    • isolated from light-producing organ of the squid
    • V. fischeri can produce light only when large #s of bacteria were present
  • Each V. fischeri can produce a very small amount of chemical molecular called autoinducer
29
Q

Enterotoxigenic E. Coli:

transmission, symptoms, consequences

A
  • human to human transmission
  • sxs:
    • most common cause of traveler’s diarrhea
    • typical secretory diarrhea (no WBC or blood in stool)
    • causes infant mortality in developing countries
30
Q

what are the 3 types of fimbriae (= Pili) of the bacteria causing secretory diarrhea?

what bacteria is associated with each?

A
  1. Conjugative
    • e.g. E. coli, F. pili
  2. Type IV fimbriae
    • e.g. Toxin co-regulated pilus of V. cholerae
  3. Chaperone/ Usher
    • e.g. colonization factors of Enterotoxigenic E. coli
31
Q

what are the assembly/ structural proteins of the

CHAPERONE/ USHER FIMBRIAE?

A

Chaperone “CUTS” off romance

  • chaperone (200-250 aa);
    • located in periplasm
    • sequesters subunits/ adhesin
  • usher (~800-900aa)
    • located in outer membrane
    • sequesters subunits/ adhesins
  • tip adhesion (~300-400aa)
    • single copy at distal end of filament
    • N-terminus = binding specificity
  • subunits (major and minor) - (~150-200 aa)
    • major: main filament
    • minor: tip fibrillum
32
Q

what are the surface appendages

of the chaperone/usher fimbriae?

A
  1. THICK (6-8nm) - rigid fimbriae w/ tip fibrillum
    • > 3 subunits per turn
    • e.g. E. coli CFA/ fimbriae from ETEC, or E. coli P fimbriae
  2. THIN (2 nm) - flexible fibrillar structures
    • 2 subunits per turn
    • e.g. F18 fimbriae from ETEC
33
Q

what is the purpose of the chaperone/ usher fimbriae?

A

allows the bacteria to bind to carbohydrate receptors on epithelial cells –> results in disease

(if the fimbriae is destroyed or ineffective, then the bacteria can’t cause disease)

34
Q

epidemiology of chaperone/ usher fimbriae

points to a role as host range factors

A

For example, in the human isolates of Enterotoxigenic E. coli (ETEC) have the following chaperone/ usher fimbriae:

  • CFA/I, CS1, CS2, CS3, CS4, CS5, CS6
35
Q

E. coli and respective symptoms.

Which are pathogenic? Commensal?

Symptoms caused?

A
36
Q

where are the TYPE III secretion system needle structure encoded?

A
  • encoded on pathogenicity islands of pathogenic:
    • E. coli
    • Shigella
    • Yersinia
    • Salmonella
    • Pseudomonas
37
Q

Enteropathogenic E. coli (EPEC):

transmission, symptoms, mortality

A
  • human to human transmission by virulence factors/ mechanisms
  • symptoms:
    • weanling diarrhea significantly contributes to infant mortality (developing countries)
    • typical secretory diarrhea (no WBC or blood in stool)
38
Q

which bacteria has the LEE pathogenicity island? and what is it?

A
  • LEE pathogenicity island: locus of enterocyte effacement –> encodes the proteins responsible for attaching and effacing (AE) lesions in the large intestine
  • These are found on the EPEC (enteropathogenic E. coli)
39
Q

EHEC (Enterohemorrhagic E. coli)

transmission, sxs

A
  • transmission:
    • animal to human (zoonosis)
    • raw or undercooked ground meat products, raw milk and faecal contamination of vegetables
  • sxs:
    • Shiga toxin can cause blood in stool
    • Shiga toxin can cause hemolytic uremic syndrome
40
Q

how is E. coli O157:H7 differentiated?

A

differentiated by its inability to ferment sorbitol

41
Q

which types of E. coli have the LEE genetic region?

what about STX phage?

A
  • LEE gene –> found in Enteropathogenic and Enterohemorrhagic E/ coli (EPEC, and EHEC)
  • STX phage –> is found in the Enterohemorrhagic E. coli (just EHEC)
42
Q

Shiga-like toxin:

found in which E. coli? encoded by what? function?

A
  1. found in Enterohemorrhagic E. coli
  2. encoded by STX phage
  3. Function:
    • bacteria remain localized in the intestinal lumen
    • upon bacterial lysis, the toxin is released and enters the blood stream
    • –>
    • damage to the microvasculature –>
      • blood in stool and/or
      • hemolytic uremic syndrome (HUS)
43
Q

hemolytic uremic syndrome (HUS):

define

A

a group of blood disorders characterized by low red blood cells, acute kidney failure, and low platelets

sxs include: bloody diarrhea, fever, vomiting, and weakness

44
Q

what do the following pathogens have in common?

ETEC, EPEC, EHEC, and V. cholerae

A
  • Non-invasive
  • Colonization factors
  • Toxin production
  • Lead to secretory diarrhea
45
Q

What type of agar is used for detection of enteric bacterial species?

A

Sorbitol MacConkey agar:

Lactose + –> E. coli, enterobacter, klebsiella

Lactose - –> Salmonella, Shigella, Proteus

46
Q

List 3 Lactose Positive bacteria (by MacConkey agar),

List 3 Lactose Negative bacteria

A

Positive:

  1. E. coli
  2. Enterobacter
  3. Klebsiella

Negative

  1. Salmonella
  2. Shigella
  3. Proteus
47
Q

What is the EMB agar?

A

Eosin methylin blue media;

designed to discourage the growth of gram positive bacteria

Y1 - Microbio Exam 2 (18 decks)

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