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TOXICOLOGY > 6 – Bacterial Toxins > Flashcards

6 – Bacterial Toxins Flashcards

1
Q

Botulism: causative agent

A
  • C. botulinum: anaerobic, gram-positive, spore forming
    o Multiple exotoxins
    o Lowest LD50 of any known toxin
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2
Q

Botulism: exposure

A
  • ingestion of preformed toxin in FEED, WATER, OR CARRION (carcass)
    o livestock: improper feed, poultry litter, dead animals, poultry manure on pasture
    o dogs: ingestion of garbage, dead animals, water
    o other forms: wound botulism, toxicoinfectious botulism
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3
Q

Botulism: species sensitivity

A
  • all are susceptible
  • **horses&raquo_space;»> ruminants, pigs, cats, dogs
    o Very small amounts of carrion-contamination can kill horses
    o Dogs next most commonly affected, but not due to sensitivity
  • *major problem in migratory birds and waterfowl (ex. mass die off) (NOT vultures=stomach pH just above 0)
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4
Q

Why are dogs the next most commonly affected species to botulism?

A
  • Eat dead and gross things
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5
Q

Botulism: target in the body

A
  • Lower motor neurons
    o Prevents release of ACh from presynaptic nerve terminal
    o **flaccid paralysis
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6
Q

Botulism: clinical features

A
  • Ascending LMN paralysis
  • Onset: 12 hors to multiple days post-exposure
  • Earliest: hindlimb weakness
  • Neuro exam: decreased reflexes and muscle tone, but are conscious
  • Progresses to quadriplegia
  • Death due to respiratory failure, aspiration
  • NO PM LESTIONS
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7
Q

Botulism: shaker foal syndrome clinical features

A
  • 2 weeks to 8 months
  • Source: soil
  • Tremors that progress to recumbency
  • Dysphagia
  • Constipation
  • Reduced tongue tone
  • Mydriasis
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8
Q

Botulism: symptomatic and supportive care=intensive care cases

A
  • Mechanical ventilation
  • Enteral/parenteral feeding
  • Repositioning
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9
Q

Botulism: antitoxin

A
  • Botulism neurotoxin antibodies
  • Purpose: REDUCE circulating toxin prior to binding to neurons
    o Does NOT reverse existing clinical signs
  • Side effects possible
  • *if available, but expensive
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10
Q

Botulism: prognosis

A
  • *Guarded to poor
  • Rapid development of symptoms: POOR
  • Slow development of signs: GUARDED
  • Recumbent horse: grave
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11
Q

Botulism: increased odds of survival

A
  • Elevated rectal temperature
  • Dysphagia (unsure why)
  • **Antitoxin (odds ratio=120 (120x chance higher of surviving))
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12
Q

Botulism: decreased odds of survival

A
  • Increased respiratory effort
  • Inability to stand
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13
Q

What is the survival rate overall for botulism?

A
  • 48%
  • Higher survival rate in horses that arrived standing and stayed standing throughout
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14
Q

Botulism: diagnosis

A
  • History of ingestion of spoiled food or carrion
  • Progressive LMN signs
  • Toxin ID or bacterial ID
  • Serum, stomach contents, feces, suspect food/carrion
  • Used to: mouse bioassay
  • CSF=normal
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15
Q

Botulism: differential diagnoses for progressive LMN signs

A
  • Coonhound paralysis
  • Tick paralysis
  • Myasthenia gravis
  • Rabies
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16
Q

Botulism prevention

A
  • Round bales are risky
    o Interior: may be rotten
    o Exterior: visual inspection, feel for warmth
  • Avoid feeding wet hay
  • Avoid feeding spoiled silage and haylage
  • Horses: vaccination (not a core vaccine)
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17
Q

Tetanus: cause

A
  • Clostridium tetani (gram negative, spore-forming anaerobe)
    o Ubiquitous
    o Commensal of GIT
  • Spores=very resistant
  • Exposure scenario: SPORES ENTER A WOUND
    o Creates anaerobic environment
    o Recent field surgery, shearing, retained placenta, docking, castration
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18
Q

Tetanus: species sensitivity

A
  • HORSES and small ruminants (also guinea pigs)
  • Cats, dogs, cattle
  • Birds
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19
Q

C. tetani produces 2 exotoxins

A
  • *tetanospasmin: prevents release of GABA and glycine=uncontrolled muscular contractions (CLINICAL SIGNS we see)
  • Tetanolysin: local tissue necrosis and lysis of RBCs
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20
Q

Tetanus: onset

A
  • Latent period!
  • *days to weeks after wound infection
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21
Q

Tetanus: clinical features

A
  • Generalized musculoskeletal stiffness=SAWHORES STANCE
    o Extensors>flexors
    o Progresses to muscle tremors (“tetany”)
  • *start at face and go down (descending)
  • *prolapsed 3rd eyelid, abnormal blinking
  • ‘sardonic grin’ in dogs, lock jaw
  • Flared nostrils, fixed gaze, erect ears and tail
  • Opisthotonus
  • Death due to respiratory failure
  • Reflex spasms
  • *cardiac and respiratory disturbances
  • **consciousness is UNAFFECTED
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22
Q

Tetanus: cardiac and respiratory disturbances

A
  • Tachycardia, bradycardia
  • Hypertension, hypotension
  • Sweating
  • Congested MM
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23
Q

Tetanus: management

A
  • Penicillin, antitoxin, toxoid
  • Wound management and supportive care
24
Q

Tetanus: prognosis

A
  • Guarded to poor in symptomatic animals
  • Recovery can teak several weeks to months
  • Fatality rate in horses: 50-80%
25
Tetanus: prevention
- Vaccination o Core in horses o Risk based in cattle
26
Tetanus: clinical diagnosis
- History and clinical signs o SPASTIC paralysis - *no specific postmortem lesions
27
Tetanus: confirmation
- Typically based on history and clinical presentation o Difficult to detect tetanolysin in plasma o PCR for C. tetani
28
Tetanus: differential diagnoses
- *strychnine=extensor rigidity - Tremorgenic mycotoxins - Meningitis, polioencephalomalacia, hypomagnesia (ruminants) - Myopathy: myositis, white muscle disease, hyperkalemic period paralysis
29
Anthrax: cause
- Bacillus antracis - Anthrax toxin complex: 3 proteins - Spores extremely environmentally resistant=SOIL - *outbreaks associated with liberation of spores in environment (flooding, excavation) - **all species susceptible (outbreaks most common in cattle and sheep)
30
Anthrax: onset
- Peracute to acute - *Sudden death
31
Anthrax: clinical features
- *sudden death - Septicemia: febrile, tremors, respiratory difficulty, collapse, death - Edema - **terminal hemorrhage from orifices - Bleeding due to breakdown of lymphatic tissues and blood vessels - Incomplete rigor mortis
32
Anthrax: pigs
- Subacute to chronic o Swelling, fever, enlarged lymph - Don’t see here=not in pasture nodes
33
Anthrax: horses
- Acute o Fever, depression, subcutaneous swelling, colic, signs of sepsis
34
Anthrax: postmortem lesions
- Dark, un-clotted blood - Enlarged spleen - Swollen, congested, hemorrhagic lymph nodes
35
Anthrax: management
- Often cannot intervene fast enough - Antibiotics: penicillins - Quarantine: separate sick animals and remove from contaminated area - Field test kits available - *reportable disease
36
Anthrax: diagnosis
- DO NOT NECROPSY o Inform lab of risk group 3 materials o Blood and edema fluid o Microscopy, culture, PCR - PPE
37
Anthrax: differential diagnoses
- Water hemlock - Urea - Cyanide - Nitrate - Bracken fern - Dicoumaraol - Non toxic: blackleg, redwater, grass tetany, lightning strike
38
Anthrax: prevention
- Vaccination
39
Cyanobacteria/blue green algae
- Not true bacteria or true algae o Photosynthetic prokaryotic organisms - “harmful algal blooms” o Major public health and environmental health problem - Numerous species of blue green algae=multiple toxins (not all are toxic)
40
**How do animals become exposed to cyanobacteria/blue green algae? What is it common in?
- Consumption of contaminated water - Common in dogs and livestock
41
**What are some factors that contribute to harmful algal blooms?
- Warm, sunny weather: multiple consecutive days - Time of year: mid-summer to autumn - Shallow water bodies - Nutrient input/eutophication o Nitrogen, phosphorous o Agricultural run-off, manure, etc.
42
Microcystins
- Microcystis aeruginosa - Global distribution - Prototypical toxin: “fast death factor” - Stable in environment - Extremely toxic
43
Microcystins: mechanism of action
- Inhibition of protein phosphatases= o Disruption of cytoskeleton o Oxidative damage o Inhibition of glucose metabolism
44
What is the target organ of microcystins?
- LIVER o Selective uptake into hepatocytes via organic anion transport polypeptides o Acute liver failure
45
Microcystins: onset
- Within 20mins to several hours post-ingestion
46
Microcystins: clinical features
- Acute liver failure o Vomiting, diarrhea with blood o Weakness, shock o Pale and/or icteric MM o Hepatic encephalopathy, seizures - *death within several hours o Hypovolemic shock secondary to intrahepatic hemorrhage or liver failure - If survive=photosensitization
47
Microcystins: clinical pathology
- Elevated liver enzymes - Indicators of liver failure - Coagulopathy
48
Microcystins: prognosis
- Poor to grave
49
Anatoxin-A
- Dolichospermum spp. - Less stable in environment - “very fast death factor” - Extremely toxic - Target organ CNS o Cholinergic toxidrome: post-synaptic AChR agonist and inhibitor of acetylocholinesterase
50
Anatoxin-A: clinical features
- *peracute neuroexcitation symptoms - Rigidity and tremors that progess to seizures - Collapse - Abdominal breathing and dyspnea - Urination - Death within minutes to hours due to respiratory FAILURE - Often found dead near water - No specific PM or histological lesions
51
Cyanobacterial toxins: management
- NO antidote available - Window for decontamination is narrow=often missed
52
Microcystin: management
- Aggressive symptomatic and supportive care o IVFT, colloids, vitamin K1, hepatoprotectants, plasma/blood transfusions
53
Anatoxin-A: management
- Aggressive symptomatic and supportive care - Seizure control - Mechanical ventilation: can be several days to weeks
54
Blue green algae: diagnosis
- History: access to river or pond, algal bloom present - Clinical signs: *found dead in proximity to a contaminated water source - Diagnostic samples: water and stomach contents - Histology: microcystins, but none for anatoxin-a
55
Cyanobacteria: DDx
- Acute neurotoxicity o Water hemlock, strychnine, 1080, organophosphate insecticides o Found dead: anthrax, cyanide, nitrate - Acute liver failure o Sago palm (dogs), acetaminophen, aflatoxin, copper, xylitol (dogs)

TOXICOLOGY (20 decks)

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