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
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
3
Q
Botulism: species sensitivity
A
- all are susceptible
- **horses»_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)
4
Q
Why are dogs the next most commonly affected species to botulism?
A
- Eat dead and gross things
5
Q
Botulism: target in the body
A
- Lower motor neurons
o Prevents release of ACh from presynaptic nerve terminal
o **flaccid paralysis
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
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
8
Q
Botulism: symptomatic and supportive care=intensive care cases
A
- Mechanical ventilation
- Enteral/parenteral feeding
- Repositioning
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
10
Q
Botulism: prognosis
A
- *Guarded to poor
- Rapid development of symptoms: POOR
- Slow development of signs: GUARDED
- Recumbent horse: grave
11
Q
Botulism: increased odds of survival
A
- Elevated rectal temperature
- Dysphagia (unsure why)
- **Antitoxin (odds ratio=120 (120x chance higher of surviving))
12
Q
Botulism: decreased odds of survival
A
- Increased respiratory effort
- Inability to stand
13
Q
What is the survival rate overall for botulism?
A
- 48%
- Higher survival rate in horses that arrived standing and stayed standing throughout
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
15
Q
Botulism: differential diagnoses for progressive LMN signs
A
- Coonhound paralysis
- Tick paralysis
- Myasthenia gravis
- Rabies
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)
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
18
Q
Tetanus: species sensitivity
A
- HORSES and small ruminants (also guinea pigs)
- Cats, dogs, cattle
- Birds
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
20
Q
Tetanus: onset
A
- Latent period!
- *days to weeks after wound infection
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
22
Q
Tetanus: cardiac and respiratory disturbances
A
- Tachycardia, bradycardia
- Hypertension, hypotension
- Sweating
- Congested MM
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
Q
Tetanus: prevention
A
- Vaccination
o Core in horses
o Risk based in cattle
26
Q
Tetanus: clinical diagnosis
A
- History and clinical signs
o SPASTIC paralysis - *no specific postmortem lesions
27
Q
Tetanus: confirmation
A
- Typically based on history and clinical presentation
o Difficult to detect tetanolysin in plasma
o PCR for C. tetani
28
Q
Tetanus: differential diagnoses
A
- *strychnine=extensor rigidity
- Tremorgenic mycotoxins
- Meningitis, polioencephalomalacia, hypomagnesia (ruminants)
- Myopathy: myositis, white muscle disease, hyperkalemic period paralysis
29
Q
Anthrax: cause
A
- 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
Q
Anthrax: onset
A
- Peracute to acute
- *Sudden death
31
Q
Anthrax: clinical features
A
- *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
Q
Anthrax: pigs
A
- Subacute to chronic
o Swelling, fever, enlarged lymph - Don’t see here=not in pasture nodes
33
Q
Anthrax: horses
A
- Acute
o Fever, depression, subcutaneous swelling, colic, signs of sepsis
34
Q
Anthrax: postmortem lesions
A
- Dark, un-clotted blood
- Enlarged spleen
- Swollen, congested, hemorrhagic lymph nodes
35
Q
Anthrax: management
A
- Often cannot intervene fast enough
- Antibiotics: penicillins
- Quarantine: separate sick animals and remove from contaminated area
- Field test kits available
- *reportable disease
36
Q
Anthrax: diagnosis
A
- DO NOT NECROPSY
o Inform lab of risk group 3 materials
o Blood and edema fluid
o Microscopy, culture, PCR - PPE
37
Q
Anthrax: differential diagnoses
A
- Water hemlock
- Urea
- Cyanide
- Nitrate
- Bracken fern
- Dicoumaraol
- Non toxic: blackleg, redwater, grass tetany, lightning strike
38
Q
Anthrax: prevention
A
- Vaccination
39
Q
Cyanobacteria/blue green algae
A
- 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
Q
**How do animals become exposed to cyanobacteria/blue green algae? What is it common in?
A
- Consumption of contaminated water
- Common in dogs and livestock
41
Q
**What are some factors that contribute to harmful algal blooms?
A
- 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
Q
Microcystins
A
- Microcystis aeruginosa
- Global distribution
- Prototypical toxin: “fast death factor”
- Stable in environment
- Extremely toxic
43
Q
Microcystins: mechanism of action
A
- Inhibition of protein phosphatases=
o Disruption of cytoskeleton
o Oxidative damage
o Inhibition of glucose metabolism
44
Q
What is the target organ of microcystins?
A
- LIVER
o Selective uptake into hepatocytes via organic anion transport polypeptides
o Acute liver failure
45
Q
Microcystins: onset
A
- Within 20mins to several hours post-ingestion
46
Q
Microcystins: clinical features
A
- 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
Q
Microcystins: clinical pathology
A
- Elevated liver enzymes
- Indicators of liver failure
- Coagulopathy
48
Q
Microcystins: prognosis
A
- Poor to grave
49
Q
Anatoxin-A
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
Q
Anatoxin-A: clinical features
A
- *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
Q
Cyanobacterial toxins: management
A
- NO antidote available
- Window for decontamination is narrow=often missed
52
Q
Microcystin: management
A
- Aggressive symptomatic and supportive care
o IVFT, colloids, vitamin K1, hepatoprotectants, plasma/blood transfusions
53
Q
Anatoxin-A: management
A
- Aggressive symptomatic and supportive care
- Seizure control
- Mechanical ventilation: can be several days to weeks
54
Q
Blue green algae: diagnosis
A
- 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
Q
Cyanobacteria: DDx
A
- 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)
