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
How is typhoid fever prevented? Are there any vaccines?
Control of water supplies and sewage disposal Pasteurization of milk Two vaccines: 1. Ty21a - oral attenuated 2. ViCPS - Vi capsule antigen vaccine
26
What does S. choleraesuis cause?
Bacteremic syndrome - high fever, bacteremia after onset of gastroenteritis, microabscesses
27
Sources/hosts of S. choleraesuis?
Swine | Contaminated food
28
Infectious dose of S. choleraesuis?
1000 organisms
29
Incubation period of S. choleraesuis?
6-72 hours
30
What pathogenicity islands, etc. does S. choleraesuis have?
SPI-1 and SPI-2 | Virulence/antibiotic resistance plasmid
31
Who is most susceptible to S. choleraesuis?
Young Pts with sickle cell anemia Cancer patients
32
How is S. choleraesuis treated?
Appropriate antibiotics
33
What do S. enteriditis and S. typhimurium cause? How many serotypes?
Acute gastroenteritis (1-4 days) with diarrhea, confined to GI tract Low fever Rare bacterimia, more likely in young or old >2200 serotypes
34
Sources/hosts of S. enteriditis and S. typhimurium?
Reptiles and poultry (contact with droppings) | Raw and undercooked eggs, other foods
35
Incubation period of S. enteriditis and S. typhimurium?
8-48 hours
36
How is S. choleraesuis diagnosed?
Blood culture
37
How are S. enteriditis and S. typhimurium disagnosed?
Stool culture
38
How are S. enteriditis and S. typhimurium treated?
Self limiting -> fluid replacement Vulnerable patients treated with antibiotics (ampicillin, trimethoprim, ceftriaxone, cipro) to prevent/control bloodstream infections
39
List the general components in the infectious process of S. enteriditis and S. typhimurium. (3)
T3SS-mediated invasion of epithelial cells LPS Toxins and host-damaging proteins
40
How is Shigella spread?
4Fs: Food, Fingers, Feces, Flies
41
Who is most susceptible to Shigella?
Children under 10
42
Sources/hosts of Shigella?
No animal reservoir
43
Infectious dose of Shigella?
100 bugs (LOW)
44
Incubation period of Shigella?
1-4 days
45
Symptoms of Shigella (and their causes)? (3)
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
How is Shigella diagnosed?
Stool sample (up to 1-4 weeks after recovery)
47
List the steps of pathogenesis of Shigella infections. (7)
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
How does Shigella promote its own cell to cell spread?
T3SS toxins -> actin polymerization -> zooms across, into, and out of cells
49
How exactly does Shiga toxin in S. dysenteriae work?
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
How is Shigella treated?
Fluid and electrolyte replacement Cipro, trimethoprim if severe Antibiotic susceptibility testing should be considered
51
How is Shigella prevented? Are there any vaccines?
Improve sanitation No vaccines - but one with O-Ag conjugated to Shiga toxin has promise
52
Shigella and salmonella: glucose fermentation test
Positive for both
53
Shigella and salmonella: color on MacConkey agar
Colorless for both (neither ferments lactose)
54
Shigella and salmonella: ACID production with glucose
Positive for both
55
Shigella and salmonella: GAS production with glucose
Salmonella positive, shigella negative
56
Shigella and salmonella: motility
Salmonella positive, Shigella negative
57
Shigella and salmonella: H2S production
Salmonella positive, Shigella negative
58
How is an oxidase test performed? What does it test for?
1% tetramethyl-p-phenylnediamine HCl (TMPD reagent) reacts with cytochrome oxidase -> turns PURPLE Tests for presence of cytochrome oxidase
59
Shigella and salmonella: oxidase test
Negative for both (NOT purple)
60
How can indole or urease tests distinguish Salmonella from other Gm- bacteria?
Salmonella is both indole negative and urease negative
61
What is the Klinger Iron Agar test? What is it used for
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
How are immunochromatographic assays used for diagnosis of Shigella?
Detects Shiga toxin 1 and 2
63
Does Shigella have H antigen? Salmonella?
``` Shigella = NO Salmonella = yes ```