Salmonella and Shigella Flashcards

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1
Q

Relationship between species, strains and serotypes.

A

A strain is a population of organisms within a species that descends from a single organism - surface components often vary among strains within a species

A serotype is a strain that is differentiated by serological means, based on their surface elements:

  • O antigens (polysaccharide component of LPS, attached to lipid A in mebrane)
  • H antigens (the flagellar antigen)
  • K antigen (polysaccharide capsule component)
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2
Q

Serological tests

A
  1. agglutination
  2. ELISA
  3. western blot
  4. flow cytometry
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3
Q

List the three members of the Enterobacteriaciae (“enterics”). How do they gram stain?

A

Salmonella, Shigella, E. coli

Gram (-)

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4
Q

What are the three clinically distinguishable syndromes related to Salmonellosis in man?

A
  1. typhoid or enteric fever
    - S. Typhi (1 main and 1 rare serotype)
  2. septicemia
    - S. cholerasuis (1 serotype)
  3. acute gastroenteritis
    - S. enteriditis or S. typhimurium (>1500 serotypes)
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5
Q

Compare the epidemiology of the Salmonella species.

A

A: 16 million cases a year and >600K related deaths, common in developing world and rare in NA, Europe and Australia
- HUMANS ONLY (via food or water)

B: rare disease, rarely seen in healthy individuals; inc susc with young age, malaria, AIDS, steroid use, immune suppressive therapy, SS
- SOURCE: swine

C: 30K cases in US per year, 1.4m cases per year with 600 deaths
- SOURCE: poultry, pork, dog food, eggs; fruits and veg. can be contaminated; reptile pets; sandbox

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6
Q

Compare their clinical presentations.

A

A: typhoid fever, incubation 7-14 days (early GI phase - may be subclinical with positive stool culture)

  • wk 1: episodic fever, brachycardia, skin rash (Rose spot) diagnostic, leukopenia, enlarged liver and spleen (Bacteremic phase)
  • wk 2-3: intestinal hemorrhage or perforation (late GI phase)
  • may hide in GB (chronic phase - 3% of patients)

B: INFECTIOUS DOSE - 1000 organisms, short incubation (6-72 hours), high fever and bacteremia after onset of gastroenteritis, microabscesses can develop in any body tissue

C: symptoms begin within 8-48 hours, sudden onset of headache, chills, abdominal pain, vomiting then diarrhea with fever, lasts 1-4 days

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7
Q

Discuss the pathogenesis of A.

A

A: low pH resistant, adhesins, endocytosis into intestinal epithelieum, ingestion by macs (survive within phagocytic vacuoles enabled by Vi antigen, a polys capsule), survives acidicity of lysosome, kills mac and diss via thoracic duct to blood (fever and shock), liver, spleen and GB; reinvasion of GI tract via GB, GI bleed and sometimes diarrhea

C:

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8
Q

Discuss the virulence determinants of A

A
  1. pathogenicity islands, acquired through horizontal gene transfer, unexpected G+C content
    - SPI-1: encodes genes for invasion (T3SS)
    - SPI-2: encodes genes for IC survival
  2. endotoxin (lipid A component of LPS)
    - at low levels, pathogen clearance
    - at high levels, endotoxic shock
    fever
    inflammation
    hypotension
    disseminated intravascular coagulation
    (DIC) and bleeding
    organ failure due to lack of oxygen
    - many gram(-) induce local inflam due to LPS, and shock when they grow in bloodstream (sepsis)
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9
Q

What are the pathogenesis and virulence determinants of C?

A
  • LPS release during invasion of epithelial cells o fthe small and large intestines are responssible for many symptoms
  • T3SS mediates invasion of epithelial cells
  • EC cells produce toxins (including a pertussis-like toxin) that promote inflammation and secretion
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10
Q

Describe prevention and vaccines for A.

A

PREVENTION:

  • control of water supplies and sewage disposal
  • food safety
  • pasteurize milk
  • screen for carries among food handlers

VACCINES

  • oral attenuated vaccine (Ty21a)
  • ViCPS capsular polysaccharide vaccine (injected)
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11
Q

Steps in diagnosis of Salmonella infections.

A
  1. feces (all) or blood culture (S. typhi only)
  2. glucose fermentation, oxidase negative, reduces nitrate
  3. non-lactose fermentation
  4. motile (unlike SHIGELLA) and produce H2S
  5. urease negative (unlike PROTEUS)
  6. indole negative (unlike E. COLI)
  7. serotyping and PCR tests with O and H antigens allow species identification to trace outbreaks
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12
Q

How is A treated?

A
  • fluoroquinolines (e.g. ciproflaxin) or third generation cephalosporin (e.g. ceftriaxone)
  • chronic carrier states: 1) ampicillin or ciproflaxin 2) cholecystectomy
  • relapse can occur in 10% of patients in endemic areas
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13
Q

How is C treated?

A
  • self-limiting, death uncommon
  • fluid and electrolyte replacement
  • treat patients with predisposing conditions with appropriate antibiotics:
    • Ampicillin
    • Trimethoprim sulfa
    • third generation cepholosporin
    • fluoroquinolone (ciprofloxacin)
  • antibiotic resistance testing can be useful
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14
Q

Discuss the 1984 outbreak

A

US bioterrorism event using C

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15
Q

Shigella - epidemiology

A

Spread by 4Fs: food, fingers, feces, flies
Children , 18% of US cases
S. sonnei - 75% of US cases
S. boydii - common in India

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16
Q

Shigella - clinical presentation

A

fever (LPS)
diarrhea and abdominal cramps (Shiga toxin)
bloody diarrhea with mucus (T3SS)
self-limiting, rarely fatal
bacteremia rare
can detect in feces up to 1-4 weeks after recovery (DISSEMINATION)

17
Q

Shigella - virulence and pathogenesis

A

low inoculum (100 bugs) - acid tolerance
incubation period of 1-4 days
invade intestinal cells in terminal ileum and colon
uptake by macs via T3SS
T3SS dep cell-to-cell spread
induces apoptosis, reinfect new cells
IL-1 and TNF from monocytic cells (fever and systemic symptoms)

SHIGA TOXIN (from S. dysenteriae):
- intestinal ulceration
- exotoxin with subunits A and B:
A interferes with 60S ribosomal RNA
B binds to receptor on intestinal cells
- diarrhea ensues due to fluid malabsorption
- may lead to apoptosis of mucosal cells and ulceration

18
Q

Shigella - diagnosis

A

clinical symptoms not diagnostic

feces sample
detection of PMNs
diagnostic traits
- gluc ferm with NO gas
- lactose nonfermenters (like SALMONELLA)
- no H2S (unlike SALMONELLA)
- nonmotile, no flagella (unlike SALMONEL)
contains O antigen, not H
indole and urease negative (like SALMONELLA)

19
Q

Shigella - prevention and treatment

A

PREVENTION
- improve sanitation (human is only host)
Food preparation
Prevent spread among young children
diaper hygiene
hand washing
Avoid swallowing water from ponds, lakes, or untreated pools

  • no effective vaccine (live atten not effective)
  • recombinant O-antigen conjugated to an inactivated Shiga toxin (distinct from T3SS) is a promising candidate vaccine

TREATMENT

  • fluid and electrolyte replacement, esp in young children
  • antibiotics in severe cases (sulfa drugs such as ciprofloxin and trimethropin)
  • antibiotic susceptibility testing impt