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Animal Health and Disease > Final - Lecture 19 > Flashcards

Final - Lecture 19 Flashcards

1
Q

What bacteria causes anthrax?

A

Bacillus anthracis

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2
Q

Who does anthrax affect?

A
  • Warm blooded animals (livestock, humans)
  • Herbivores: susceptible to acute form
  • Carnivores and reptiles: relatively resistant, affected by less acute form
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3
Q

Bacillus anthracis

A
  • Gram +ve, non-motile spore forming
  • grows well on common median (blood culture)
  • vegetative form: multiplies and kills host
  • Spore form: survives environment
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4
Q

What is the predominate form of Bacillus anthracis in the environment?

A
  • spores; nutrient poor enviro and presence of O2 to sporulate
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5
Q

Where do spores germinate?

A

enviro rich in amino acids, nucleosides, glucose aka blood or tissue

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6
Q

Are spores resistant?

A
  • very resistant: temp extremes, pH, desiccation and chemicals, UV light
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7
Q

How long can Bacillus anthracis survive in a spore form?

A

50-250yrs

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8
Q

What are the three main forms of anthrax in humans?

A
  1. cutaneous
  2. gastrointestinal
  3. inhalational
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9
Q

Cutaneous Anthrax

A
  • 95% of cases; enters through cuts or abrasions
  • 1-12 day incubation
  • infection begins as: small papule to vesicle to eschar and sometimes secondary vesicle
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10
Q

What is the fatality rate of cutaneous anthrax?

A

-5-20% without antibiotics
-<1% with antibiotic treatment

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11
Q

Gastrointestinal Anthrax

A
  • appears in livestock ingesting spores; appears in ppl consuming contaminated meat or drink
  • 1-7 day incubation
  • oropharynx: sore throat, dysphagia, fever regional lymphadenopathy
  • Lower GIT: acute necrosis and inflammation, nausea, vomiting, dysentery, fever
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12
Q

Fatality rate of Gastrointestinal Anthrax?

A

25-65% without treatment

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13
Q

Inhalational Anthrax

A
  • ‘Woolsorter’s disease’
  • incubation 1-43 days
  • symptoms: cough, fatigue, fever
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14
Q

Fatality of inhalation anthrax

A
  • 85-97% without antibiotics
  • 75% with antibiotics
  • 45% with intensive therapy
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15
Q

Pathogenesis of anthrax

A
  1. lung
  2. macrophage engulphs spore
  3. spore germinate in macrophage in lymph nodes and release from dead macrophage
  4. vegetative bacteria divides extracellularly and releases toxins
  5. mild illness to fulminating disease and raid death
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16
Q

What two plasmids do important anthrax toxins promote disease on?

A
  1. pOX1: encodes for protective antigen, lethal factor and edema factor
  2. pOX2: encoded for proteins that synthesize polyglutamic acid capsule: helps protect dividing bacteria to evade engulfment and phagocytosis
17
Q

What are the 3 actions btw anthrax toxins and plasmids?

A
  1. Protective antigen combines with lethal factor to form lethal toxin
  2. Protective antigen combines with edema factor to form edema toxin
  3. 7x PA form heptamer: pore in cell membrane and allows lethal and edema toxin inside the cell
18
Q

What is the common affect of lethal toxin?

A

Impairment of host defense and immunity
- virtually all cells involved in immune fxns require MAPK pathways for proper fxn
- alters innate immunity and adaptive immunity

19
Q

How does lethal toxin affect neutrophils?

A
  • inhibition of chemotaxis
  • decrease production of superoxide anions
  • cripples innate immunity
20
Q

How does lethal toxin affect macrophages?

A

reduce chemotaxis and phagocytosis

21
Q

What are the stages of lethal toxin?

A
  1. macrophage death (toxin induces selling and lysis of macrophages)
  2. initially univalent cation permeability followed by ATP depletion
  3. loss of mitochondrial fxn
  4. shutdown of protein synthesis and eventual loss of membrane integrity
  5. activation of macrophage with agonists of toll-like receptors makes macrophages more susceptible to lethal toxin
22
Q

What are the cell mechanisms for macrophage death induced by lethal toxin?

A
  1. Nalp1B gene
  2. Modulation of Wnt target genes
  3. LRP6 and co-receptor Wnt target genes
  4. Lethal Toxin blocks survival pathways of activated macrophages
23
Q

How does lethal toxin affect adaptive immunity?

A
  • impairment of cognitive interactions btw dendritic cells and T lymphocytes- priming lymphocytes
  • decrease in up-regulation of co-stimulatory molecules
24
Q

What are the 2 microenvironments?

A
  1. low-lying depressions with standing water and devitalized plant material
  2. rock lands with dry courses of water
25
Q

Where does exposure to spores usually occur with grazing animals?

A

dry weather forces grazing animals to feed closer to the ground where spores are concentrated; exposure via inhalation or ingestion of dust

26
Q

How do mosquitoes and biting flies contribute to anthrax spread?

A

will transfer Bacillus anthracis by biting animals

27
Q

What are the 3 forms of anthrax in animals?

A
  1. peracute: ruminants
  2. acute: ruminants and equine
  3. subacute-chronic: swine, dogs, cats
28
Q

What does a peracute infection in ruminants look like?

A
  • sudden death
  • bloody discharge
  • incomplete rigor mortis
  • rapid bloat
29
Q

What does an acute infection in equine look like?

A

Ingestion
- colic
- fever
- weak
- death within 48-96 hours

Insect bite
- hot swelling
- spread to throat, sternum abdomen, genitalia
- death

30
Q

What is something you should NEVER do to a carcass that you know has anthrax?

A
  • NEVER OPEN CARCASS!!!!
  • no necropsies
31
Q

What are the best way to dispose of carcasses?

A
  1. incineration (best way)
  2. burial
32
Q

Is there a vaccine for Anthrax?

A

Yes!
- vaccinate in endemic areas
- immunity within 10 days following injections

33
Q

How can the spread of Anthrax be controlled?

A
  1. must report to authorities
  2. quarantine area
  3. do not open carcasses; destroy them
  4. minimize contact
  5. wear protective clothing
  6. vaccinate susceptible animals
  7. do not use high pressure cleaners
34
Q

Is Anthrax a bioterrorism pathogen?

A

Yes
- has significant public heath concerns with corresponding economic costs

Animal Health and Disease (21 decks)

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