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Micro Exam 2 > Neely: Intra-Abdominal Infections I > Flashcards

Neely: Intra-Abdominal Infections I Flashcards

1
Q

NORMAL FLORA OF INTESTINAL TRACT

Mouth:

Stomach:

A

Mouth: thousands of bacteria in the mouth; many more anaerobes (100:1); main reservoir for introduction into intestinal tract

Stomach: acidic environment where most oral bacteria killed; similar bacteria to those in mouth and throat.

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2
Q

NORMAL FLORA OF INTESTINAL TRACT

Stomach to Small Intestine:
What type of bacteria?

Colon:
What type of bacteria?

A

Stomach to Small Intestine: mostly Gram positive
- Enterococcus: can live in the presence of bile salts (highest concentration in duodenum).

Colon: beneficial bacteria; mostly anaerobes (1000:1)

  • 400-500 different species (mainly strict anaerobes; therefore cannot be cultured)
  • Do not cause disease in the environment (only if they get into normally sterile parts of the body)
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3
Q

PROTECTION OF THE INTESTINAL TRACT
Mucous Membranes

Goblet Cells Produce?
Lubricant does what?
Physical barrier:

A

Goblet Cells: produce mucus

Lubricant to protect mucous membrane

Physical barrier to trap bacteria that is expelled by peristalsis

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4
Q

PROTECTION OF THE INTESTINAL TRACT
Mucous Membranes

M Cells Aid in:

What do M cells phagocytose?

A

M Cells: aid in presentation of antigens to underlying cells of the immune system (in Peyer’s patches)

Phagocytose bacteria and other Ags and pass to macrophages under the M cell

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5
Q

PROTECTION OF THE INTESTINAL TRACT
Mucous Membranes

Absorptive Cells (Enterocytes):
What do Bacteria that reach mucosal cells have to deal with?
Mucosal cells formed in? Move up what? Are released into:
A

Absorptive Cells (Enterocytes): some of the most rapidly dividing cells in the body

Bacteria that reach mucosal cells have to deal with rapid turnover

Mucosal cells formed in crypts, move up the villous surface, and are released into the lumen as new cells replace them

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6
Q

PROTECTION OF THE INTESTINAL TRACT

Other Protective Mechanisms: (5)

A
  • sIgA
  • Stomach acid
  • Bile salts
  • Rapid flow of material through small intestine (washes bacteria out of SI)
  • Slow rate of material through colon with dense bacterial population (protective normal flora)
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7
Q

PROTECTION OF THE INTESTINAL TRACT

When does infection occur?

A

Infection occurs when organisms with virulence mechanisms overcome the protective mechanism of the GI tract

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8
Q

What tests identify gram negative bacteria?

A

Oxidase Reaction

Growth on MacConkey agar

Metabolism - Oxidative or fermentative

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9
Q

What does the oxidase reaction detect?

What is Mac agar selective for?

3 types of metabolism:

A

Oxidase Reaction: detects presence of cytochrome oxidase (transfers electrons to O2)

Growth on MacConkey agar: selective for Gram negative

Metabolism: oxidative, fermentive or inert

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10
Q

Enterobacteriaceae

Oxidase:
MacConkey Growth/Color:
Metabolism:

A

Oxidase: Negative
MacConkey Growth/Color: Yes/Varies by species
Metabolism: Fermentation

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11
Q

Vibrionacea

Oxidase:
MacConkey Growth/Color:
Metabolism:

A

Oxidase: Positive
MacConkey Growth/Color: Yes/Colorless to light pink
Metabolism: Fermentation

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12
Q

Campylobacteriaceae

Oxidase:
MacConkey Growth/Color:
Metabolism:

A

Oxidase: Positive
MacConkey Growth/Color: No growth
Metabolism: Inert

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13
Q

Pseudomonadaceae

Oxidase:
MacConkey Growth/Color:
Metabolism:

A

Oxidase: Positive
MacConkey Growth/Color: Yes/Colorless
Metabolism: Oxidative

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14
Q

Enterobacteriaceae family includes: (6)

A

Enterobacteriaceae family includes

E.coli 
Klebsiella 
Salmonella
Shigella
Yersinia
Proteus

(YEP KiSS)

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15
Q

Enterobacteriaceae

G+/-:
Shape:
Aerobe or anaerobe?

A

All are Gram negative rods and facultative anaerobes

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16
Q

Is Campylobacteriaceae G+ or -?

A

G-, but does not grow on MacConkey; Requires a specialized media to grow.

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17
Q

BACTERIAL AND PARASITIC GI INFECTIONS:
Terms

Secretory:
Non-inflammatory:
Inflammatory:
*Invasive:

A

Secretory: watery, non-inflammatory

Non-inflammatory: no leukocytes in the stool

Inflammatory: presence of leukocytes in the stool

Invasive: organism can invade into the epithelial cells

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18
Q

BACTERIAL AND PARASITIC GI INFECTIONS:
Terms

*Non-Invasive:
Enterotoxin:
Neurotoxin:
Cytotoxin:

A

Non-Invasive: bacteria stay in the lumen, but may cause disease by secreting toxins

Enterotoxin: toxin released by a microorganism in the intestine

Neurotoxin: toxin that acts directly on neurons

Cytotoxin: toxin having a specific toxic action on cells of special organs

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19
Q

Secretory Diarrhea (Non-Invasive and Non-Inflammatory) caused by:

A

Secretory Diarrhea (Non-Invasive and Non-Inflammatory): caused by toxogenic bacteria, noninvasive parasites, or virus

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20
Q

Secretory Diarrhea (Non-Invasive and Non-Inflammatory)

Bacterial Enterotoxigenic Diarrhea: (2)

A

Enterobacteriaceae and Vibrionaceae

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21
Q

Secretory Diarrhea (Non-Invasive and Non-Inflammatory)

Bacterial Neurotoxin Group: (3)

A

Bacterial Neurotoxin Group: ingested organisms produce a neurotoxin (usually the preformed toxin is ingested)

C.botulinum, B.cereus, S.aureus

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22
Q

Secretory Diarrhea (Non-Invasive and Non-Inflammatory)

Non-Inflammatory Parasitic: (2)

A

Non-Inflammatory Parasitic: G.lamblia, C.parvum

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23
Q

Invasive/Tissue Damaging Diarrhea (Inflammatory)

Bacterial Cytotoxin Caused Inflammation: (2)

A

C.difficile, EHEC

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24
Q

Invasive/Tissue Damaging Diarrhea (Inflammatory)

Bacterial Invasive Infection: (3)

A

Shigella, Salmonella, EIEC

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25
Q

Invasive/Tissue Damaging Diarrhea (Inflammatory)

Parasitic Invasive: (1)

A

E.histolytica

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26
Q

Miscellaneous Intestinal Infections:

Gastric and duodenal ulcers:

Food-borne bacteremia and meningoencephalitis:

Parasitic GI Helminths

A

Gastric and duodenal ulcers: H.pylori

Food-borne bacteremia and meningoencephalitis: L.monocytogenes

Parasitic GI Helminths

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27
Q

Vibrio Cholerae (O1 and O139)

G+/-?

Ox +/-?

Shape:

Grows in:

A

Vibrio Cholerae (O1 and O139)

Gram negative

Oxidase positive

Comma shaped motile rod

Grows in freshwater ponds and brackish water (can colonize shellfish)

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28
Q 
Vibrio Cholerae (O1 and O139)
Virulence Factors
A

Motility
Adherence
Cholera Toxin (Choleagen)

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29
Q 
Vibrio Cholerae (O1 and O139)
Motility via:
A

Motility: single polar flagellum

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30
Q

What is Cholera Toxin aka?

A subunit:
B subunit:

A

Cholera Toxin (Choleagen): A-B type ADP-ribosylating toxin

A subunit: enzymatic; only 1 subunit

B subunit: binding; 5 identical subunits

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31
Q

Vibrio Cholerae (O1 and O139)

Adherence via: (2)

What does this allow the bacteria to do?

What is Tcp pili?

A

Adherence: pili and other adhesins (most important VF)

Allow bacteria to adhere tightly to the epithelium of the SI

Tcp pili= toxin co-regulated pili (long, filamentous pili)

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32
Q

Vibrio Cholerae (O1 and O139)

What does the toxin attach to?
What does it bind?

A

Toxin attaches to the surface of a mucosal cell (binds GM1 gangliosides)

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33
Q

Vibrio Cholerae (O1 and O139)

What is released from the toxin? What does it enter?

What does A1 subunit do to Gs?

A

A1 subunit is released from the toxin (choleagen) and enters the host cell

A1 subunit ADP-ribosylates membrane protein Gs (turns on adenylate cyclase constitutively)

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34
Q

Vibrio Cholerae (O1 and O139)

What causes an increase in cAMP?

Increase in cAMP causes ion imbalance that results in: (3)

A

Adenylate cyclase causes an increase in cAMP

Increase in cAMP causes ion imbalance that results in:

Water loss (the major effect of cholera)
Hypersecretion of fluids and chloride ions
Inhibition of sodium absorption.

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35
Q

Vibrio Cholerae (O1 and O139)

Onset time:
Sensitivity to stomach acid:
Replication:

A

Rapid onset 2-3 days after inoculation

Need to ingest a lot because of sensitivity to gastric acids (~108 cfu)

Replicates to very high numbers

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36
Q

Vibrio Cholerae (O1 and O139)

Attaches to:
Produces and secretes:

A

Attachment to epithelial cells in the small intestine (flagella and pili help).

Produces and secretes CTX toxin.

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37
Q

Vibrio Cholerae (O1 and O139)

Initial Clinical Manifestations: (3)

Net result:

A

Initial Clinical Manifestations:

  • Vomiting
  • Massive watery diarrhea with mucous flecks (rice-water stools)
  • No PMNs in stool

Rapid dehydration and electrolyte loss

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38
Q

Vibrio Cholerae (O1 and O139)

Transmission:
Carriers:

A

Fecal-Oral: via water, fish, and shellfish

Carriers: recovered patients can still shed the organism (important in endemic regions)

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39
Q

Vibrio Cholerae (O1 and O139)

Clinical Identification:
Lab Tests:
Ox +/-?
Special Medium:

A

Clinical Identification: Stool specimen only

Lab Tests: oxidase positive, curved Gram negative rod

Special Medium: thiosulfate citrate bile sucrose (TCBS)

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40
Q

Vibrio Cholerae (O1 and O139)

Two biotypes of O1 V. cholerae:

A

Antigens: O1 and O139 are markers for strains that produce cholera toxin (the others do not, and therefore only produce non-epidemic diarrhea and extra-intestinal infections)

Epidemic Cholera via O1 and O139:

  • Classic: More virulent
  • El Tor (worse): Survives better
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41
Q

GDP + Gs =
GTP + Gs =
Gs + CTX =

A

GDP + Gs = no activation
GTP + Gs = transient activation
Gs + CTX = continuously activates Adenylate cyclase

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42
Q

What is the most common cause of traveler’s diarrhea?

Where is the highest incidence?

A

Enterotoxigenic E.Coli (ETEC): Most common cause of Traveler’s diarrhea

Highest incidence in the tropics and in the young

Similar to Vibrio cholera.

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43
Q

Types of pathogenic E.coli (5):

A

Enterotoxogenic (ETEC)

Enteroadherent (EAEC) or Enteroaggregative (EAggEC)

Enteropathogenic (EPEC)

Enteroinvasive (EIEC)

Enterohemmorrhagic (EHEC)

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44
Q

Enterotoxigenic E.Coli (ETEC)

Virulence Factors: (2)

A

Adherence

Endotoxins

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45
Q

Enterotoxigenic E.Coli (ETEC)

Adherence:
Where are adhesins? What do they bind?
What is the bundle-forming pilus similar to?

A

Adherence:

Adhesins: colonization factors on pili (bind epithelial cells in SI)

Bundle-forming pilus: similar to Tcp pili in V.cholerae

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46
Q

Enterotoxigenic E.Coli (ETEC)

Exotoxins (2):

A

Heat Labile Toxin (LT)

Heat Stable Toxin (ST)

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47
Q

Enterotoxigenic E.Coli (ETEC)

Heat Labile Toxin (LT)

Inactivated at what temp?
How similar is it to cholera toxin?
Binds what receptor?
Secreted by what mechanism?

A

Heat Labile Toxin (LT): inactivated at 100 degrees C for 30 minutes

Shares ~75% aa sequence with cholera toxin
5B:1A subunit (same structure as cholera toxin)

Binds same receptor (GM1 ganglioside) and has the same MOA as cholera toxin

Heat stable ST toxin is secreted by type II secretion

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48
Q

Enterotoxigenic E.Coli (ETEC)

Heat Stable Toxin (ST)

What happens at 100 degrees C?
Family of small molecules or a single toxin?
MOA:
Result:

A

Heat Stable Toxin (ST): not inactivated at 100 degrees C for 30 minutes

Family of small molecules (not a single toxin)

MOA: binds a guanylate cyclase in the membrane of the host cell, resulting in activate and increase in cGMP

Result: fluid and electrolyte loss

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49
Q

Enterotoxigenic E.Coli (ETEC)

Colonizes:
What leads to diarrhea?

A

Etiology/Pathogenesis:

Colonizes the SI with adhesins

Production of LT and ST leads to diarrhea

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50
Q

Enterotoxigenic E.Coli (ETEC)

Incubation period:
Starts as:
Progresses to:

A

Clinical Manifestations: incubation period of 1-2 days

Starts as: nausea, vomiting, weakness, dizziness and abdominal pain; also a low grade fever

Progresses to: watery diarrhea (mild to severe)

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51
Q

Enterotoxigenic E.Coli (ETEC)

Transmission:

A

Contaminated food and beverages are the major vehicles of transmission

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52
Q

Enterotoxigenic E.Coli (ETEC)

Identification of Organism:

A

ELISA or agglutination tests for presence of toxins

DNA probes for LT or ST genes

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53
Q

Enteropathogenic E.Coli (EPEC)

Causes:
Previously associated with:
Can cause:

A

o Causes severe (often fatal) watery diarrhea in infants and children in developing countries
o Previously associated with outbreaks in nurseries in developed countries
o Can cause Traveler’s diarrhea in adults

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54
Q

Enteropathogenic E.Coli (EPEC)
Virulence Factors

Attaching and Effacing Lesion

Non-intimate binding:
- occurs via:
Intimate binding:
- mediated by:
Effacement of the cell membrane:
A

Non-intimate binding: occurs via the bundle-forming pilus

Intimate binding: mediated by bacterial proteins (Tir and intimin)

Effacement of the cell membrane: loss of microvilli and the formation of a pedestal-like structure beneath the organism

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55
Q

Enteropathogenic E.Coli (EPEC)
Virulence Factors

What type of secretion?

A

Type III Secretion: proteins injected right into the cell so that Abs to the proteins never see them

Injects a receptor for itself into the cell (allows it to bind any cell)

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56
Q

Enteropathogenic E.Coli (EPEC)

Etiology/Pathogenesis:
What can cause death?
What is malabsorptive diarrhea caused by?

A

Dehydration and electrolyte balance can cause death

Malabsorptive Diarrhea: most likely caused by a loss of absorptive capacity of mucosal cells due to damage of the host cell surface

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57
Q

Enteropathogenic E.Coli (EPEC)

Symptoms: (3)

A

Watery diarrhea (non-bloody, mucous-filled)
Fever
N/V

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58
Q

Enteropathogenic E.Coli (EPEC)

Transmission:
Identification:

A

Transmission: Fecal-oral route

Identification: ELISA and multiplex PCR

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59
Q

Clostridium botulinum

Botulinal Toxin
What type of toxin?
What is death usually due to?
What type of toxin? what does it bind?

A

Botulinal Toxin: neurotoxin; usually ingested as a preformed toxin and travels in the bloodstream to neurons, resulting in flaccid paralysis (death usually due to respiratory collapse)

AB Toxin: B portion binds ganglioside receptors on nerve cells.

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60
Q

Clostridium botulinum

What does Botulinal Toxin block?
How can you inactivate it?

A

Toxin internalized and blocks presynaptic release of ACh at the NMJ (prevents muscle contraction).

Can be inactivated by boiling for 10-15 minutes.

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61
Q

Clostridium botulinum

Spores
Heat resistance:
Locations:

A

Spores are heat resistant: can withstand 100 degrees Celsius for 3-5 hours

Spore Locations: found in animal feces, soil and lake sediment

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62
Q

Types of Botulism: (3)

A

Food Botulism
Infant Botulism
Wound Botulism

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63
Q

Food Botulism

What is the result?
How long does it take for side effects to occur?

A

Spore germinates in foods, resulting in bacterial growth and toxin production (food needs to be anaerobic, like canned goods)

Ingestion of preformed toxin, which is absorbed in the stomach and enters the bloodstream; Sx occur 12-36 hours later

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64
Q

Infant Botulism

What can happen to the infant’s colon?
Rare cause of:

A

C.botulinum can colonize the infant colon (ie. spores in honey), and since they are without complete colonic microflora, it can grow and produce toxin

Rare cause of Sudden Infant Death Syndrome

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65
Q

Wound Botulism:

A

Spores colonize deep wounds (anaerobic), grow and produce toxin that enters the bloodstream

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66
Q

Clostridium botulinum

Associated with diarrhea?
Recovery period:

A

Not associated with diarrhea

Recovery period is long: affected nerve endings need to regenerate

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67
Q

Clostridium botulinum

Identification of Organism:
Anaerobic?
G +/-?
Lab confirmation by:

A

Anaerobic, Gram negative, spore-forming bacillus
Organism can be grown in oxygen free lab environment

Laboratory confirmation by immunoassay for toxin in food, gastric contents or blood

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68
Q

What is the most common bacterial form of food poisoning?

A

Staphylococcus aureus

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69
Q

Staphylococcus aureus

Virulence Factors:

A

Pre-formed toxin (enterotoxin)

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70
Q

Staphylococcus aureus

Pre-formed toxin (enterotoxin)

A

Pre-formed toxin (enterotoxin): ingested and absorbed into the gut, stimulating neural receptors
- Stimulus transferred to the vomiting center in the CNS

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71
Q

Staphylococcus aureus

Symptoms (2):

A

Symptoms:
o Vomitting (projectile) within hours
o Diarrhea less frequently

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72
Q

Staphylococcus aureus

Transmission:

A

Transmission:
o Can multiply/make toxins in foods that are unrefrigerated for extended periods of time
o Re-heating the food does not destroy the heat-stable enterotoxins

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73
Q

Bacillus cereus

2 Forms:

A

Emetic (Vomiting) Form

Diarrheal Form

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74
Q

Bacillus cereus
Emetic (Vomiting) Form

Cause:
Associated with:
Incubation period:
Symptoms:
Duration:
A

Cause: ingestion of pre-formed heat stable enterotoxin ingested in reheated foods

Often associated with Chinese restaurants (fried rice)

Short incubation period: 1-6 hours (rapid onset)

Symptoms: N/V and abdominal cramps (similar to S.aureus food poisoning)

Duration: usually 24 hours or less

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75
Q

Bacillus cereus
Diarrheal Form

Cause:
Associated with:
Incubation period:
Symptoms:
Duration:
A

Cause: heat-labile toxin formed in vivo, which activates adenylate cyclase and causes intestinal fluid secretion

Associated with meat or vegetable containing foods after cooking (food held above room temperature for a prolonged period)

Long incubation period: 8-16 hours

Symptoms: severe abdominal cramps and diarrhea (may be a small volume or profuse and watery)

Duration: usually 24 hours or less

76
Q

C.perfringens

Similar to:
Cause:
- Where is C.perfringens type A produced?

A

Very similar to B.cereus diarrheal form

Cause:
o Temperature abuse of prepared foods (meat, meat products, gravy)
o Contaminated with enterotoxin producing C.perfrigens type A (toxin produced in GI tract)

77
Q

C.perfringens

Onset:
Symptoms:

A

Onset: 8-24 hours after ingestion of contaminated meat

Symptoms: abdominal cramps and watery diarrhea
o Without fever, nausea or vomiting

78
Q

Giardia lamblia
Basics:

Virulence Factors
Life Cycle:
Adhesion:
Flagella:

A

Basics: flagellated, enteric protozoan

Virulence Factors:
Life Cycle: two stages- trophozoite (free living) and cyst (infective)

Adhesion: via sucking/adhesive disk on the trophozoite; adheres to upper SI mucosal surface

Flagella: motility and attachment

79
Q

Giardia lamblia
Etiology/Pathogenesis

Infection due to:
Associated with:
Incubation:

A

Infection: due to oral ingestion of cysts (trophozoites destroyed by gastric activity)

Often associated with drinking contaminated water (cysts can survive in water up to 3 months)

Incubation: 7-10 days

80
Q

Giardia lamblia
Etiology/Pathogenesis

Symptoms: (3)

A

Symptoms:

  • Acute onset of watery diarrhea
  • Abdominal cramps, bloating and flatulence
  • Some patients progress to chronic diarrhea with malabsorption (weight loss common)
81
Q

Giardia lamblia

Identification of Organism: (3)

A

Microscoping examination of stool, duodenal aspiration or duodenal biopsy

Antigen testing for G.lamblia in the stool

String test (swallowing a string to obtain a sample from the upper part of the small intestine)

82
Q

Cryptosporidium parvum

Basics:
Symptoms: Immunocompromised vs Immunocompetent

A

Basics: small coccidian protozoan parasite

Symptoms:
o Immunocompromised: severe, watery, prolonged diarrhea
o Immunocompetent: mild diarrhea

83
Q

Cryptosporidium parvum

Life Cycle:

  • What is ingested?
  • What is released in intestine?
  • What is shed in feces?
A

o Oocyst ingested in contaminated water
o Sporozoite released in intestine
o Sporozoite enters intestinal epithelial cells (infects the microvilli)
o Undergoes sexual and asexual replication
o Oocysts produced (infective stage) which are then shed in the feces

84
Q

Microsporidia (Microspora):

A

Group of obligate intracellular, spore forming protists

85
Q

Cyclospora cayetanesis:
How long does diarrhea last?
More severe in what type of patient?

A

Cyclospora cayetanesis: have cyanobacterium-like bodies
o Cause prolonged diarrhea (up to 7 weeks)
o More severe in AIDs patients

86
Q

Isospora belli:
Clinically indistinguishable from:

Description of diarrhea:
Infects what part of intestine?
More severe in what type of patient?

A

Isospora belli: clinically indistinguishable from giardiasis, cryptosporidiosis and microsporodiosis

o Diarrhea without blood or leukocytes
o Infects entire intestine
o More severe in AIDS patients

87
Q

Clostridium difficile is normal flora in what percent of people?

A

Normal flora in ~5% of healthy adults; can cause acute inflammation of the colonic mucosa in some cases

88
Q

Clostridium difficile

2 Exotoxins produced:

A

Toxin-A Enterotoxin

Toxin-B Cytotoxin

89
Q

Clostridium difficile
Toxin-A Enterotoxin

Causes accumulation of:
Chemotactic for:
What does cell lysis cause the release of?

A

Toxin-A Enterotoxin: causes accumulation of viscous, bloody fluid

Chemotactic for PMNs, resulting in cell lysis

Cell lysis causes release of inflammatory mediatiors, which causes:

  • Fluid secretion
  • Altered membrane permeability
  • Hemorrhagic necrosis of mucosa
90
Q

Clostridium difficile
Toxin B Cytotoxin

Disrupts:
Decreases:
What is it similar to?

A

Disrupts the actin polymerization and cytoskeletal architecture

Decreases cellular protein synthesis (similar to diphtheria toxin)

91
Q

Clostridium difficile

Source:
Cause of Diarrhea:

A

Source: endogenous or from the environment (nosocomial infections)

Cause of Diarrhea: altered intestinal flora from a course of antibiotics (antibiotic associated colitis)

Symptoms: variable
 Asymptomatic carrier
 Mild diarrhea

92
Q

Pseudomembranous colitis:

A

Pseudomembranes/plaques consist of fibrin, mucus, necrotic epithelial cells, and leukocytes adherent to the underlying inflamed mucosa

93
Q

Clostridium difficile
Identification

Characteristics:
Selective Media:
Tests:

A

Characteristics: spore forming, anaerobic, Gram positive rod

Selective Media: CCFA (cycloserine, cefoxitin, fructorse agar); culturing organism not helpful

Tests: toxin tests in stool are the most useful clinically (EIA test)

94
Q

Enterohemorrhagic E.Coli (EHEC)

AKA:
Causes:

A

Also called Shiga-toxin E.coli (STEC) or Verocytotoxin E.Coli (VTEC)

Causes: diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome (HUS)

95
Q

Enterohemorrhagic E.Coli (EHEC)
Adhesins

Bind to:
Mediated by: (2)

A

Tight binding to mucosal cells

Mediated by Tir and intimin

96
Q

Enterohemorrhagic E.Coli (EHEC)

Virulence Factors: (3)

A

Adhesins
Shiga Toxins
Type III Secretion

97
Q

Enterohemorrhagic E.Coli (EHEC)

Shiga Toxin 
aka:
Type of toxin:
What does B subunit bind?
What does A modify? Block?
A

Shiga Toxin: AB type toxin (aka Shiga-like or Vero toxin)
B subunit binds Gb3 ganglioside on host cell

A subunit enzymatically modifies 28S ribosomal RNA of the 60S-ribosomal subunit

  • Blocks proteins synthesis
  • Eventually leads to cell death
98
Q

Enterohemorrhagic E.Coli (EHEC)

Shiga Toxin causes:
Leads to:

A

Capillary thrombosis and associated inflammation of the colonic mucosa (leads to hemorrhagic colitis)

99
Q

Enterohemorrhagic E.Coli (EHEC)

Shiga Toxin types:
Encoded by:

A

Types: strains may carry one or both; encoded by bacteriophages

Shiga Toxin I (StxI)
Shiga Toxin II (StxII)

100
Q

Enterohemorrhagic E.Coli (EHEC)

Type III Secretion:

A

Inserts toxin and its own receptor into the host cell; causes attaching and effacing lesions like EPEC

101
Q

Enterohemorrhagic E.Coli (EHEC)

Cause:
Outbreaks occur from what?
How many organisms are needed for infection?
Incubation period:

A

Shiga-toxin producing strains colonize the intestinal tract of cattle and other farm animals

Outbreaks occur from contaminated meat (hamburger), milk and apple cider

Only a small number of organisms required for infection

Incubation Period: 3-4 days

102
Q

Enterohemorrhagic E.Coli (EHEC)

Symptoms (4):

A

Symptoms:
Severe, crampy abdominal pain

Copious watery diarrhea that develops into grossly bloody diarrhea

Little to no fever*

Hemolytic Uremic Syndrome

103
Q

Enterohemorrhagic E.Coli (EHEC)
Hemolytic Uremic Syndrome

What percent of patients?
Results in:
Caused by:

A

Hemolytic Uremic Syndrome: develops in 5-10% of patients (esp. young kids)

Acute renal failure, thrombocytopenia and hemolytic anemia

Caused by Shiga toxin damage to endothelial cells of renal glomeruli

104
Q

Enterohemorrhagic E.Coli (EHEC)

Serotyping (3):

A

O Antigens: outer region 1 of LPS (endotoxin) polysaccharide Ag

H Antigens: flagella proteins

K Antigens: extracellular polysaccharide Ags

105
Q

What causes 50-80% of EHEC infections?

What does it not ferment?

A

Serotype O157:H7: causes 50-80% of infections

Does not ferment sorbitol (almost all other strains do), therefore can be identified with MacConkey agar.

However, sorbitol positive strains may also produce Shiga toxins

106
Q

Enterohemorrhagic E.Coli (EHEC)

Other Methods of identification: (3)

A

Anti-O157:H7 serum

Demonstrate cytotoxicity with Vero Cells

DNA probe for detection of Shiga toxin genes

107
Q

What produces bacillary dysentery?

A

Shigella

Basics: produces bacillary dysentery (blood and mucus in stool)

108
Q

Shigella

Virulence Factors: (5)

A 
Invasion
Type III Secreation
Actin-Based Motility
Bacillary Dysentery
Shiga Toxin
109
Q

Shigella
Invasion

Enters through:
Deep or superficial?

A

Invasion: enters through M cells only

Superficial: very rare penetration beyond mucosa

110
Q

What is the primary virulence characteristic of Shigella?

A

Invasiveness

111
Q

Shigella
Type III Secretion

What does actin rearrangement cause?

A

Used to induce actin rearrangements causing pseudopods at the basolateral surface of epithelial cells in order to take up bacteria

112
Q

Shigella
Actin-Based Motility

What happens once the bacterium is in the cell?

A

Actin-Based Motility: once in the cell, causes rapid polymerization and depolymerization of actin at one pole, causing the bacteria to be propelled through the cell to invade adjacent ones

113
Q

Shigella

What happens to invaded cells?
What is the result?

A

Invaded cells die and slough off (surface erosion of gut wall)

Results in the formation of shallow ulcers (ulcerative colitis)

114
Q

Shigella

Bacillary Dysentery definition:
What causes damage to the epithelium, allowing more invasion by bacteria?

A

Bacillary Dysentery: local inflammation with abundant neutrophils, RBCs and mucus in the stool

Shigellae promotes cytokine release and an inflammatory response to cause damage to the epithelium, allowing more invasion by bacteria

115
Q

What species of shigella produces shiga toxin?

What does it play a role in?

A

Shiga Toxin: one species (S.dysenteriae type 1) produces Shiga toxin; plays a role in local destruction of the mucosa in this case

116
Q

Shigella

Spread:
How infectious?

A

Spread: only human to human (by food, fingers, feces, and flies)

Highly Infectious: only need <1000 organisms for infection

117
Q

Shigella
Four Serotypes:

Group A:
Group B:
Group C:
Group D:

A

Group A: S.dysenteriae (Shiga bacillus- largest producer of toxin)

Group B: S.flexneri* (causes the rest of US cases)

Group C: S.boydii

Group D: S. sonnei* (causes 60-80% of US cases)

118
Q

Shigella

Disease:

A

Organisms multiply in the lumen of the small intestine, with higher numbers occurring in the lower intestine

119
Q

Shigella

First 12 Hours:
12-72 Hours:

A

First 12 Hours: abdominal pain, cramping, and fever (while bacteria localized in SI)

12-72 Hours:

  • Organism no longer detectable in upper intestine
  • Fever decreases
  • Pain becomes more severe (localizes to lower quadrants)
  • Dysentery develops (cramps, tenesmus and lethargy)
  • Bloody, low volume diarrhea with large number of PMNs in mucoid stool
120
Q

Shigella

Identification of Organism
Motile?
G +/-? 
Lac +/-? 
Ox +/-?
Serological identification
A

o Basics: non-motile, Gram negative bacillus
o Lab Tests: lactose negative, oxidase negative
o Serological identification of serogroups

121
Q

Enteroinvasive E.Coli (EIEC)

Basics:

Virulence Factors

  • Behaves like:
  • Infects and spreads similar to:
A

Basics: relatively rare

Virulence Factors
o Behaves like Shigella (no Shiga toxin)
o Infects and spreads cell-to-cell similar to Shigella

122
Q

Salmonella

Found in what species?
Exceptions:

A

Found in almost all animal species

Exceptions: some found in only humans (S.typhi)

123
Q

Salmonella

Virulence Factors: (3)

A

Adherence and Invasion
Type III Secretion
Endotoxin

124
Q

Salmonella
Adherence and Invasion

Binds and invades what?
What happens inside the cell?

A

Organism binds microvilli and can invade M cells or epithethial cells

Bacteria engulfed in a vesicle (remain inside the phagosome and replicate)

125
Q

Salmonella
Type III Secretion

What leads to ruffling and bacterial-mediated endocytosis?

A

Extensive actin rearrangement where the bacteria attaches leads to ruffling and “bacterial-mediated endocytosis”

126
Q

Salmonella
Endotoxin

What is released upon lysis?
What happens because of this?

A

Lipid A of LPS released upon lysis

Induces inflammatory response that contributes to mucosal damage

127
Q

Salmonella

Transmission:
How many Serotypes?
Not as infectious as:

A

Transmission: usually by contaminated food (poultry meat or eggs)

Many Serotypes: over 2400 based on O and H Ags

Not as infectious as Shigella: requires a large inoculum for infection

128
Q

Salmonella

Causes 3 main clinical syndromes

A

Gastroenteritis (Enterocolitis)
Bacteremia
Enteric (Typhoid) Fever

129
Q

Salmonella
Gastroenteritis (Enterocolitis)

Incubation Period:
Onset:
Fever:

A

Incubation Period: 8-48 hours
Onset: abrupt
Fever: usually low

130
Q

Salmonella
Gastroenteritis (Enterocolitis)

Duration:
GI Symptoms:
Blood Culture:
Stool Culture:

A

Duration: 2-5 days
GI Symptoms: N/V/D at onset
Blood Culture: negative
Stool Culture: positive for several weeks

131
Q

What is the most common form of Salmonella infection?

A

Gastroenteritis (Enterocolitis)

132
Q

Salmonella

Bacteremia

A

Rare event that sometimes develops after gastroenteritis; secondary infection can occur

133
Q

Salmonella
Bacteremia

Incubation Period:
Onset:
Fever:

A

Incubation Period: variable
Onset: abrupt
Fever: rapid rise and spike (septic)

134
Q

Salmonella
Bacteremia

Duration:
GI Symptoms:
Blood Culture:
Stool Culture:

A

Duration: variable
GI Symptoms: often absent
Blood Culture: positive during fever
Stool Culture: infrequently positive

135
Q

Salmonella
Enteric (Typhoid) Fever

Classically associated with:

A

Classically associated with S.typhi or S.paratyphi (others may also cause)

136
Q

Salmonella
Enteric (Typhoid) Fever

Incubation Period:
Onset:
Fever:

A

Incubation Period: 7-20 days
Onset: insidious (gradual)
Fever: gradual, and then high plateau

137
Q

Salmonella
Enteric (Typhoid) Fever

Duration:
GI Symptoms:
Blood Culture:
Stool Culture:

A

Duration: several weeks
GI Symptoms: constipation early; bloody diarrhea late
Blood Culture: positive in 1-2 weeks of disease
Stool Culture: negative early; positive after 2 weeks

138
Q

Salmonella
Other Symptoms

Early:
Late:
Maculopapular Rash:

A

Early: chills, headache, anorexia, weakness and muscle aches

Late: fever, swollen LNs, enlargement of the liver and spleen

Maculopapular Rash (Rose Spots): 1/3 of patients get this on lower trunk

139
Q 
Campylobacter
Virulence Factors (3):
A

Flagella
Toxins
Protein S

140
Q

Campylobacter

Flagella:

A

Flagella: motility through mucus layer of SI (multiplies in the mucus layer)

141
Q

Campylobacter
Toxins (3):
Effects on intestinal cells:

A

Toxins: enterotoxin, endotoxin (LPS) and cytotoxin destroys intestinal cells (bloody diarrhea)

142
Q

Campylobacter
Protein S:
Blocks:
Causes what?

A

Protein S: surface protein functioning as a capsule

Blocks complement binding
Causes serum resistance to phagocytosis

143
Q

Campylobacter

Infective Dose:
Transmission:
Incubation Period:

A

Infective Dose: 500-1,000,000

Transmission: most commonly associated with eating chicken (milk, water and other meats have also been implicated)

Incubation Period: 1-7 days

144
Q

Campylobacter

Symptoms: (4)

A

Fever and malaise

Abdominal pain and cramps

Profuse watery or bloody diarrhea (due to mucosal inflammation)

PMNs in the stool

145
Q

Guillan-Barre Syndrome

How long after infection?
Why does demyelination occur?
How long does it take to recover?

A

Guillan-Barre Syndrome: auto-immune mediated attack on nerve tissue 1-3 weeks following infection

Demyelination occurs due to similarities between host myelin and the surface of Campylobacter organism

Takes months to recover

146
Q

Campylobacter

Motile or non-motile?
Spore forming?
Ox +/-?
What is characteristic in the stool sample?

A

Basics: motile, non-spore forming, comma-shaped Gram negative bacillus

Lab Tests: oxidase positive

Stool Sample: characteristic darting motility of organism

147
Q

Campylobacter

MacConkey Agar:
Incubation temp?
O2 and CO2 for incubation

A

Culture: selective media (will not grown on MacConkey even though it is Gram negative)

  • Incubate at 42 degrees C
  • Microaerophilic and capnophilic
148
Q

Vibrio parahemolyticus

Basics:
Where is it a major problem?
Invades what?
Produces what?

A

Basics: halophilic (grows in brackish water) and contaminates seafood; major problem in Japan

Invasion: invades intestinal cells

Virulence: produces heat stable cytotoxin

149
Q

Yersinia enterocolitica

Carriage:
Transmission:

A

Carriage: carried by livestock (mainly pigs), rabbits and rodents

Transmission: contaminated food, water or blood products

150
Q

Yersinia enterocolitica

Enterocolitis (Most Common)

Effects:

What happens after invasion of terminal ileum?
What can it mimic?

A

Enterocolitis (Most Common):

Bloody diarrhea, fever and abdominal pain (1-2 weeks; due to necrosis of Peyer’s patches)

Mesenteric lymphadenitis (after invasion of terminal ileum; can cause abscesses and can mimic acute appendicitis; most common in young kids)

151
Q

Yersinia enterocolitica

Transfusion Related Septicemia:

A

Grows at lower temperatures and can multiply to toxic levels in refrigerated blood stored for several weeks

152
Q

Entamoeba histolytica (Amebic Dysentery)

Virulence Factors: (4)

What is the infectious stage of the life cycle?

How does it adhere to the luminal surface?

What are proteolytic enzymes involved in the dissolution of?

A

Life cycle: cyst stage (infectious stage; environmentally resistant) and trophozoite stage (invasive in the tissue)

Galactose-Specific Adhesion: adheres to luminal surface by galactose-inhibitable surface protein

Proteolytic Enzymes: involved in the dissolution of extracellular matrix that anchors cells in tissue structure

Cytolytic Enzymes

153
Q 
Entamoeba histolytica (Amebic Dysentery)
Transmission:
A

Cyst is ingested, and its wall breaks down in the SI; trophozoites form from the nuclei and cytoplasm of the cyst (colonize the colon)

154
Q 
Entamoeba histolytica (Amebic Dysentery)
Disease process

When does it begin?
Where does erotion of mucosa begin?
What can happen to ulcers?
How are amebic liver abscesses formed?

A

Disease Process: begins upon invasion of mucosal surface

Erosion of mucosa begins at base of the crypts and progresses to ulceration

Ulcers can extend into the submucosa to produce flask shaped lesions

Although rare, trophozoites can also enter the venules in the colon wall to be carried to extraintestinal sites (most commonly the liver- causing amebic liver abscess)

155
Q 
Entamoeba histolytica (Amebic Dysentery)
Identification:
A

Microscopic examination of stool or colonoscopic sample

  • Irregular shedding of organisms in stool
  • Identification based on characteristic ultra-structure of cyst and/or trophozoite
156
Q

What is the major etiological agent of chronic gastritis and peptic ulcers?

A

Helicobacter pylori:

Basics: major etiological agent of chronic gastritis and peptic ulcers; major risk factor for gastric cancer

90% of duodenal and 70-80% of gastric ulcers

157
Q

Helicobacter pylori

Virulence Factors:

A

Urease
Flagella
Cytotoxin and Mucinase

158
Q

Helicobacter pylori
Urease

Converts what to what?
What does this do for H.pylori?

A

Converts urea to ammonia and CO2; protects it from stomach acid (allows bacteria to establish in the mucin layer in the stomach)

159
Q

Helicobacter pylori

Flagella:

A

Allow rapid penetration of the gastric mucus

160
Q

Helicobacter pylori

Cytotoxin and Mucinase

A

Localized destruction of tissue; stimulate infiltration of inflammatory cells

161
Q

Helicobacter pylori
Pathogenesis

What type of gastritis?
Penetrates?
Adheres to?

A

Chronic type B gastritis (superficial and atrophic) with possible progression to adenocarcinoma

Penetrates the mucus layer of the host and adheres to the gastric mucosa

162
Q

Helicobacter pylori
Identification

G+/-?
Shape:
Gastric biopsy:
Special media:

A

Basics: Small Gram negative curved bacillus

Gastric Biospy: culture or urease test (CLO test)

Special Media: enriched in 6-8% O2 (microaerophilic); incubate at 37 degrees C for 3-7 days

163
Q

Helicobacter pylori
Pathogenesis

How does it produce ammonia?
How does it form an ulcer?
What could happen if allowed to perpetuate?

A

Produces ammonia using urease to neutralize gastric acid

Proliferate, migrate and finally form infectious focus; Results in development an ulcer by destruction of mucosa, inflammation and cell death

Increase secretion of gastrin and gastric acid stimulated by infection promotes gastric metaplasia

164
Q

Listeria monocytogenes

Basics:

A

Basics: usually only cause infections in immunocompromised

165
Q 
Listeria monocytogenes
Virulence Factors (4):
A

Internalin
Listeriolysin O (LLO)
Actin Mediated Motility
Lipoteichoic Acid (LTA)

166
Q

Listeria monocytogenes
Virulence Factors

Internalin
What type of protein?
Induces what process?
What does this help the intracellular pathogen avoid?

A

Internalin: bacterial surface protein that induces phagocytosis (intracellular pathogen can then avoid Ab-mediated defenses)

167
Q

Listeria monocytogenes
Virulence Factors

What does LLO enable bacteria to do?

A

Listeriolysin O (LLO): enables bacteria to escape from phagosome and avoid intracellular killing

168
Q

Listeria monocytogenes
Virulence Factors

Actin Mediated Motility
What does it allow the organism to do? Avoid?

A

Actin Mediated Motility: enables the organism to spread from cell to cell (avoid Abs, complement and neutrophils)

169
Q

Listeria monocytogenes
Virulence Factors

LTA causes:

A

Lipotechoic Acid (LTA): causes septic shock

170
Q

Listeria monocytogenes

Where is it found?
What is notable about it?
Where is it found?
What are the highest rates found?
Incubation period:
A

Ubiquitous: found in soil, decaying vegetation and fecal flora of many animals

Only pathogenic Listeria species in humans

Cause: most human infection is from food (raw vegetables, raw milk, soft cheeses, fish, poultry, and meats)

Immunocompromised: highest infection rates seen in infants, pregnant women (~30% of all cases) and other immunocompromised individuals

Incubation Period: 11-70 days (mean ~1 month)

171
Q

Listeria monocytogenes
Disease Process

Where does it cross the mucosal barrier?
What happens in healthy people?
Immunocompromised?
What can it cause?

A

Crosses the mucosal barrier through M cells in the intestine and enters the bloodstream

Healthy People: cleared by macrophages

Immunocompromised: hematogenous dissemination can occur to any site (particularly the CNS and placenta)

Can cause meningitis and still births/birth defects

172
Q

Listeria monocytogenes
Identification

G +/-?
Anaerobic?
Spore-forming?
Motility:
Ox +/-?
Cat +/-?
What type of hemolysis?
A

Basics: Gram positive, facultative anaerobe, non-spore forming, tumbling motility at room-temperature, non-motile at 37 degrees C

Lab Tests: oxidase negative, catalase positive, beta-hemolytic

173
Q

What organisms cause disease with preformed toxins? (3)

A

C.botulinum, S.aureus, B.cereus

174
Q

What organisms cause disease with toxin formed in the intestine? (5)

A

V.cholerae, E.coli (ETEC, EHEC), B.cereus, C.perfringens

175
Q

What organisms cause disease by invasion? (6)

A

Salmonella, Shigella, Yersinia enterocolitica, Campylobacter, Listeria, V.parahemolytica

176
Q

Nematodes (Round Worms): (3)

A
  • Ascaris lumbricoides
  • Enterobius vermicularis (pinworm)
  • Ancylostoma duodenale and Necator americanus (hookworms)
177
Q

Ancylostoma duodenale and Necator americanus (hookworms)

Infects what percent of the world population?
What type is found in the tropics and North America?
Temperate zones?

A

Infects 24% of the world’s population

Necator: worldwide tropics and North America

Ancylostoma: temperate zones

178
Q

Ascaris lumbricoides

How common worldwide?
Transmission:

Where do adults live?
What organ do the larvae pass through?

A

Very common: found world wide

Transmission: eating viable eggs from feces-contaminated soil or food

Disease Process:
o Adults live in lumen of SI
o Larvae pass through lungs

179
Q

Ascaris lumbricoides
Symptoms

Low Infestation:
High Infestation:

A

Low Infestation: asymptomatic in most; can also cause GI upset, colic and loss of appetite

Heavy Infection: adult worms ball up in SI and result in physical obstruction

180
Q

What is the most common helminth?

A

Enterobius vermicularis (pinworm)

  • Found worldwide
  • Mainly in children
181
Q

Enterobius vermicularis (pinworm)

Transmission:
Where does the adult live?
When does the female deposit eggs? Where? What does this lead to?

A

Transmission: fecal-oral route (most common in children)

Disease Process:
o Adult lives in cecum
o Female deposits eggs at night in the perianal area, leading to perianal pruritis (severe itching)

182
Q

Ancylostoma duodenale and Necator americanus (hookworms)

Transmission:
Where does the adult live?
What organ do the larvae pass through?
How much blood can each worm withdraw

A

Transmission: through the skin from infected soil or from drinking contaminated water

Disease Process:
o Adult lives in small intestines
o Larvae pass through the lungs
o Each worm can withdraw up to 0.2ml of blood/day

183
Q

Cestodes (Tapeworms): (2)

A 
Taenia saginata (Beef Tapeworm)
Taenia solium (Pork Tapeworm)
184
Q

Taenia saginata (Beef Tapeworm)

Distribution:
What organ does it inhabit?
Adult length:
Transmission:

A

Worldwide distribution

Basics: inhabits the small intestine; adult is 3-10 meters in length

Transmission: occurs by eating uncooked beef

185
Q

Taenia solium (Pork Tapeworm)

Distribution:
What organ does it inhabit?
What is cysticeorocosis? What causes it?
Transmission:

A

Worldwide distribution

Basics: inhabits small intestine; can invade gut wall and migrate to various tissues (such as muscles or brain, causing cysticeorocosis)

Transmission: occurs by eating uncooked pork

Micro Exam 2 (18 decks)

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