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Microbiology - Quiz 2 > Salmonella and Shigella > Flashcards

Salmonella and Shigella Flashcards

1
Q

Explain the relationship between species, strain, and serotypes.

A

Species: E. coli, etc

Strain: subpopulation within a species that descended from the SAME PARENT

Serotype: a subset of strains within species that are bound by COMMON ANTIBODIES
—Distinguished by specific antisera that recognize bacterial surface elements

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2
Q

Explain the use of flagellar and LPS antigens as the basis for strain identification. What is the K antigen?

A

O antigen = polysaccharide component of LPS
—Only in Gm- bacteria

H antigen = flagellar antigen

K antigen = polysaccharide capsule component

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3
Q

Briefly, list the syndromes caused by Salmonella (5) and Shigella (4) species.

A

SALMONELLA

  1. S. typhi - typhoid fever (rarely S. paratyphi)
  2. S. choleraesuis - sepsis syndrome
  3. S. enteriditis and S. typhimurium - gastroenteritis with diarrhea

SHIGELLA

  1. S. dysenteriae - most severe; dysentery in developing world
  2. S. flexneri - some dysentery in US, developing world
  3. S. sonnei - dysentery in US
  4. S. boydii - dysentery in India
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4
Q

Explain the basic elements of the Type III secretion system.

A

NEEDLE COMPLEX: similar to a flagellum; provides passage for molecule through membrane

BASE connects needle with bacterial membranes

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5
Q

Explain the role of endotoxin (Lipid A) in disease. What happens when there is too much?

A

Lipid A: the part of LPS buried in bacterial outer membrane

Host innate immune system + low [LPS] -> rapid response:

  1. Macrophages -> TNFalpha in tissue
  2. Increased phagocyte/lymphocyte migration into tissue -> phagocytosis
  3. Increased platelet adhesion to blood vessel wall -> occlusion -> drainage to local lymph node
  4. Removal of infection

Too much Lipid A in blood -> endotoxic shock -> highly lethal

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6
Q

Describe the properties of enterics. (6)

A 
Live in the gut
Gm- rods
Ferment glucose
Oxidase negative
Facultative anaerobes
Reduce nitrate

Include Salmonella, Shigella, E. coli, Campylobacter, Vibrio, others

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7
Q

What does S. typhi cause? How many serotypes? What else can cause this?

A

Typhoid (enteric) fever - 1 serotype

Rarely caused by Salmonella paratyphi

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8
Q

What does S. choleraesuis cause? How many serotypes?

A

Septicemia (bacteremic syndrome) - 1 serotype

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9
Q

What do S. enteritidis and S. typhimurium cause? How many serotypes?

A

Acute gastroenteritis with diarrhea

- >1500 serotypes

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10
Q

What are the three phases of typhoid fever?

A

Early GI phase (week 1)
Bacteremic phase (weeks 2-3)
Late GI phase (week 3+)

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11
Q

What characterizes the early phase of typhoid fever? (4)

A

SUBCLINICAL
Episodic fever
Abdominal pain
Constipation

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12
Q

List the steps in the pathogenesis of typhoid fever. (7)

A
  1. Invasion of intestinal Peyers patches
  2. T3SS-mediated ingestion by macrophages
  3. Survival/proliferation inside phagocytic vacuoles of macrophages -> spread
  4. T3SS-mediated killing of macrophage
  5. Dissemination via thoracic duct to blood, bone marrow, liver, gall bladder
  6. LPS in blood causes fever/shock
  7. Re-invasion of GI tract
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13
Q

How does S. typhi infect humans? List non-human vectors and infectious dose.

A

Contaminated food or water
NO non-human vectors
ID = 1,000-100,000 bacteria (high)

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14
Q

How is S. typhi well suited to colonize the gut? (2)

A

Resistant to killing by stomach acid

Adhesins promote attachment to intestinal epithelium

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15
Q

What is the incubation period of S. typhi?

A

7-14 days

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16
Q

What are pathogenicity islands? How are they acquired?

A

Encode genes for virulence

Acquired through horizontal gene transfer

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17
Q

What characterizes the bacteremic phase of typhoid fever? (5)

A 
Bradycardia
Skin rash (rose spots = bacterial emboli)
Leukopenia
Hepato/splenomegaly
Confusion
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18
Q

What characterizes the late GI phase of typhoid fever? (2)

A 
Intestinal hemorrhage (common)
Intestinal perforation (rare)
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19
Q

Where does S. typhi hide in its chronic phase? Why is this phase important?

A

Gallbladder
Presents in 3% of patients

Important source for spreading infections under poor hygienic conditions

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20
Q

What pathogenicity islands does S. typhi have? What do they do?

A

SPI-1: encodes T3SS genes for INVASION of macrophages

SPI-2: encodes T3SS genes for INTRACELLULAR SURVIVAL

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21
Q

What is a T3SS?

A

Type III secretion system: protein appendage found in Gm- bacteria that allows bacterium to deliver proteins to host cytoplasm

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22
Q

True/false: Diarrhea is a major feature of typhoid fever.

A

False. Diarrhea is NOT a major feature of typhoid fever

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23
Q

How is typhoid fever diagnosed?

A 
Stool culture (week 1 or after 3rd week)
Blood culture (between 2nd and 3rd week)
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24
Q

How is typhoid fever treated?

A

Antibiotics (need to access INTRACELLULAR bacteria)
–Fluoroquinolones or ceftriaxone

Chronic carrier state: ampicillin, cipro, cholecystectomy

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25
Q

How is typhoid fever prevented? Are there any vaccines?

A

Control of water supplies and sewage disposal
Pasteurization of milk

Two vaccines:

  1. Ty21a - oral attenuated
  2. ViCPS - Vi capsule antigen vaccine
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26
Q

What does S. choleraesuis cause?

A

Bacteremic syndrome - high fever, bacteremia after onset of gastroenteritis, microabscesses

27
Q

Sources/hosts of S. choleraesuis?

A

Swine

Contaminated food

28
Q

Infectious dose of S. choleraesuis?

A

1000 organisms

29
Q

Incubation period of S. choleraesuis?

A

6-72 hours

30
Q

What pathogenicity islands, etc. does S. choleraesuis have?

A

SPI-1 and SPI-2

Virulence/antibiotic resistance plasmid

31
Q

Who is most susceptible to S. choleraesuis?

A

Young
Pts with sickle cell anemia
Cancer patients

32
Q

How is S. choleraesuis treated?

A

Appropriate antibiotics

33
Q

What do S. enteriditis and S. typhimurium cause? How many serotypes?

A

Acute gastroenteritis (1-4 days) with diarrhea, confined to GI tract
Low fever
Rare bacterimia, more likely in young or old

> 2200 serotypes

34
Q

Sources/hosts of S. enteriditis and S. typhimurium?

A

Reptiles and poultry (contact with droppings)

Raw and undercooked eggs, other foods

35
Q

Incubation period of S. enteriditis and S. typhimurium?

A

8-48 hours

36
Q

How is S. choleraesuis diagnosed?

A

Blood culture

37
Q

How are S. enteriditis and S. typhimurium disagnosed?

A

Stool culture

38
Q

How are S. enteriditis and S. typhimurium treated?

A

Self limiting -> fluid replacement

Vulnerable patients treated with antibiotics (ampicillin, trimethoprim, ceftriaxone, cipro) to prevent/control bloodstream infections

39
Q

List the general components in the infectious process of S. enteriditis and S. typhimurium. (3)

A

T3SS-mediated invasion of epithelial cells

LPS

Toxins and host-damaging proteins

40
Q

How is Shigella spread?

A

4Fs: Food, Fingers, Feces, Flies

41
Q

Who is most susceptible to Shigella?

A

Children under 10

42
Q

Sources/hosts of Shigella?

A

No animal reservoir

43
Q

Infectious dose of Shigella?

A

100 bugs (LOW)

44
Q

Incubation period of Shigella?

A

1-4 days

45
Q

Symptoms of Shigella (and their causes)? (3)

A

Fever - LPS
Diarrhea and abdominal cramps - Shiga toxin
Bloody diarrhea with mucus - T3SS effectors

Self-limiting
Rare hemolytic uremic syndrome
Intestinal ulceration with S dysenteriae

46
Q

How is Shigella diagnosed?

A

Stool sample (up to 1-4 weeks after recovery)

47
Q

List the steps of pathogenesis of Shigella infections. (7)

A
  1. Oral ingestion
  2. Invade intestinal cells in terminal ileum/colon
  3. T3SS-induced uptake by macrophages into phagocytic vacuoles
  4. T3SS-dependent escape from phagocytic vacuole -> cytoplasm of macrophages
  5. Apoptosis of macrophages
  6. Infection of new cells
  7. IL-1/TNF secretion from monocytic cells -> fever, systemic symptoms
48
Q

How does Shigella promote its own cell to cell spread?

A

T3SS toxins -> actin polymerization -> zooms across, into, and out of cells

49
Q

How exactly does Shiga toxin in S. dysenteriae work?

A
  1. Subunit B binds receptor on intestinal cells
  2. A subunit interferes with 60S rRNA -> inhibits protein synthesis
  3. Fluid malabsorption -> diarrhea
  4. Apoptosis of mucosal cells -> ulceration
50
Q

How is Shigella treated?

A

Fluid and electrolyte replacement
Cipro, trimethoprim if severe
Antibiotic susceptibility testing should be considered

51
Q

How is Shigella prevented? Are there any vaccines?

A

Improve sanitation

No vaccines - but one with O-Ag conjugated to Shiga toxin has promise

52
Q

Shigella and salmonella: glucose fermentation test

A

Positive for both

53
Q

Shigella and salmonella: color on MacConkey agar

A

Colorless for both (neither ferments lactose)

54
Q

Shigella and salmonella: ACID production with glucose

A

Positive for both

55
Q

Shigella and salmonella: GAS production with glucose

A

Salmonella positive, shigella negative

56
Q

Shigella and salmonella: motility

A

Salmonella positive, Shigella negative

57
Q

Shigella and salmonella: H2S production

A

Salmonella positive, Shigella negative

58
Q

How is an oxidase test performed? What does it test for?

A

1% tetramethyl-p-phenylnediamine HCl (TMPD reagent) reacts with cytochrome oxidase -> turns PURPLE

Tests for presence of cytochrome oxidase

59
Q

Shigella and salmonella: oxidase test

A

Negative for both (NOT purple)

60
Q

How can indole or urease tests distinguish Salmonella from other Gm- bacteria?

A

Salmonella is both indole negative and urease negative

61
Q

What is the Klinger Iron Agar test? What is it used for

A

Has lactose, glucose, and iron, plus pH indicator

  • Acid = yellow (fermentation)
  • Alkaline = red (NO fermentation, or top of glucose fermentation)
  • Gas production = bubble at bottom of tube
  • H2S production = BLACK

Distinguish between Salmonella and Shigella:

  • Salmonella = black with a bubble
  • Shigella = red with yellow bottom
62
Q

How are immunochromatographic assays used for diagnosis of Shigella?

A

Detects Shiga toxin 1 and 2

63
Q

Does Shigella have H antigen? Salmonella?

A 
Shigella = NO
Salmonella = yes

Microbiology - Quiz 2 (10 decks)

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