Bacterial toxins Flashcards
Clostridium botulinum
-anaerobic, gram positive, spore forming rod
-very resistant spores
-lowest LD50 of any toxin… only need a very small amount
-Type C and Type D exotoxins… likely carrion associated
How do animals get exposed to C. botulinum?
Ingestion in feed, water, carrion. Or wound botulism, toxicoinfectious botulism
- Livestock=improperly ensiled feed and poultry litter, dead animals in feed/water, poultry manure on pasture
-Dogs= ingestion of garbage, dead animals, water
-contamination of equipment
Describe species sensitivity for botulism
All susceptible!
-Horses much greater sensitivity than ruminants, pigs, cats, dogs
-dogs 2nd most common but not because they are sensitive
-issue for migratory birds and waterfowl
What are dogs commonly affected by botulism?
Because they are often in contact with dead carcasses= rolling, eating
What does C. botulinum target?
Target the lower motor neurons and prevent release of acetylcholine from presynaptic nerve terminal
RESULTS IN FLACCID PARALYSIS
What is the onset of botulism?
12 hours to multiple days post exposure
What are the signs of botulism?
Early:
hindlimb weakness= decreased LMN reflexes and muscle tone
Later:
quadriplegia and then death from resp failure and aspiration
PM: none
Neuro exam for botulism
Will see decreased reflexes and muscle tone
-tongue, eyelids, tail
-later= cranial nerve deficits
-conscious
Shaker foal syndrome
-2wks to 8mths
-from soil
Signs:
-tremors that progress to recumbency, dysphagia, constipation, reduced tongue tone, mydriasis
Managing botulism
-Symptomatic and supportive care
-antitoxin
What sorts of symptomatic and supportive care?
-mechanical ventilation
-enteral/parenteral feeding
-repositioning
Botulism antitoxin
Botulism neurotoxin antibodies
-used to reduce the circulating toxin prior to binding to neurons
-does not reverse clinical signs
Botulism prognosis
Guarded to poor
-recumbent= grave
-slow development= guarded
-rapid development= poor
What are factors that indicate an increased odds of survival to botulism?
-elevated rectal temp
-dysphagia
-antitoxin
What are factors that indicated a decreased odds of survival for botulism?
-increased resp effort
-inability to stand (highest survival in horses that could stand)
Botulism diagnosis
-history in ingestion of spoiled food or carrion
-progressive LMN signs
-Toxin/bacterial ID= ELISA, PCR, mass spectrometry
-stomach contents, feces, suspect food/carrion
**hard to detect in serum because low LD50 so likely wont see in serum
What was old way to detect botulism?
Mouse bioassay
Differential diagnoses to botulism
-coonhood paralysis (polyradiculoneuritis)
-tick paralysis
-myasthenia gravis
-rabies
Prevention of botulism
-avoid round bales- inside might be rotten
-avoid feeding wet hay
-avoid feeding spoiled silage and haylage
-vaccination in horses
Tetanus
-Cause= Clostridium tetani (gram pos)
-spores are resistant; enter wounds creating anaerobic environment
Common exposures for tetanus
Wounds
-recent field surgery
-shearing
-retained placenta
-docking
-castration
-floating teeth
Species sensitivity for tetanus
Horses and small ruminants greater than cats, dogs, cattle
All greater than birds
What two exotoxins are produced by clostridium tetani?
- Tetanospasm
- Tetanolysin
Tetanospasm
-prevents release of GABA and glycine leading to uncontrolled muscular contractions
Tetanolysin
Causes local tissue necrosis and lysis of RBCs
Onset/timing of tetanus
-Long latent period; days to weeks after wound infection
Clinical signs of tetanus
-generalized musculoskeletal stiffness (sawhorse stance)= extensors more than flexors and muscle tremors (tetany)
-prolapsed third eyelid/abnormal blinking
-sardonic grin/lock jaw in dogs
-flared nostrils, fixed gaze, erect ears and tail
-opisthotonus
-death due to respiratory failure
-reflex spasms
-cardiac and resp disturbances
-still conscious
What cardiac and resp signs are seen with tetanus?
-tachycardia, bradycardia
-hypertension, hypotension
-sweating
-congested MM
Management of tetanus
-penicillin, antitoxin, toxoid
-wound management & supportive care
Prognosis of tetanus
Guarded to poor in symptomatic animals
-recovery can take several weeks to mths
-fatality rate in horses= 50-80%
Tetanus prevention
Vaccination
-core vaccine in horses
-risk based vaccine in cattle
Diagnosis of tetanus
-spastic paralysis
-no PM lesions
-difficult to detect in plasma
-PCR for C. tetani
Differential diagnoses for tetanus
-strychnine or tremorgenic mycotoxinx
-Ruminants: meningitis, polioencephalomalacia, hypomagnesemia
-Myopathy (myositis, white muscle disease, hyperkalemic period paralysis
Anthrax
-caused by Bacillus anthracis
-spores in soil and extremely resistant
-outbreaks linked with flooding, excavation, contaminated feed
-all species (most common in cattle and sheep)
Clinical signs of anthrax in cattle
Peracute/acute
-sudden death
-septicemia (febrile, tremors, resp issues, collapse, death)
-edema
-terminal hemorrhage from orifices (nostrils, mouth, anus, vulva)
-bleeding from breakdown of lymphatic tissues and blood vessels
-incomplete rigor mortis
Clinical signs of anthrax in pigs
Subacute to chronic (rare because not on pasture)
-swelling
-fever
-enlarged lymph nodes
Clinical signs of horses
Acute
-fever
-depression
-SQ swelling
-colic
-signs of sepsis
Postmortem lesions of anthrax
-dark, unclotted blood
-enlarged spleen
-swollen, congested, hemorrhagic lymph nodes
Management of anthrax
-often cannot intervene fast enough
-penicillin
-quarantine sick animals and remove from contaminated area
-REPORTABLE DISEASE
-field tests available
Diagnosis of anthrax
-PPE, do not necropsy
-inform lab of risk group 3 materials
-samples: edema fluid, blood
-microscopy, culture, PCR
Differential diagnosis for anthrax
Toxins:
-water hemlock
-urea
-cyanide
-nitrate
-bracken fern
-dicoumarol
Non-toxins:
-blackleg
-redwater
-grass tetany
-lightening strike
Cyanobacteria/blue green algae
-not true bacteria or algae = Photosynthetic prokaryotic organisms
-numerous species (multiple toxins; not all toxic)
How do animals become exposed to blue green algae/cyanobacteria?
Harmful algae blooms
-consumption of contaminated water
*dogs and livestock
Factors contributing to cyanobacteria/blue green algae
-warm, sunny weather (15-30C) for multiple days
-mid summer to autumn
-shallow water bodies
-nutrient input/eutrophication (nitrogen, phosphorous; agricutural run off, manure)
Microcystins
Microcystis aeruginosa (and others)
-clumped colonies
-global distribution
-stable in environment
-extremely toxic (LD 0.5 mg/kg)
What toxin is produced by mycrocystins?
Microcystin-LR
-fast death factor
-many toxin congeners
Mycocystins mechanism of action
Inhibition of protein phosphatases
-disruption of cytoskeleton
-oxidative damage
-inhibition of glucose metabolism
What does mycrocystins target?
Liver
-selective uptake into hepatocytes via organic anion transport polypeptides causing acute liver failure
Onset of microcystins
Within 20mins to several hours post ingestion
Prognosis of microcystins
poor to grave
Clinical signs of mycrocystins
- Acute liver failure
(vomiting, diarrhea with blood, weakness, shock, pale/icteric MM, hepatic encephalopathy, seizures) - Death within several hours (hypovolemic shock secondary to intrahepatic hemorrhage or liver failure)
- photosensitization if animals do survive
Clinical pathology of microcystins
-elevated liver enzymes
-indicators of liver failure
-coagulopathy
Anatoxin-A
Dolichospermum spp
-filamentous appearance
-less stable in environment
-very fast death factor; extremely toxic
What is the target organ for Anatoxin-A?
CNS
-cholinergic toxidrome: post synaptic aAChR agonist and inhibitor of acetylcholinesterase
Clinical signs of Anatoxin-A
Peracute and neuroexcitation syndrome
-rigidity and tremours leading to seizures
-collapse
-abdominal breathing and dyspenia, cyanosis
-urination
-death within mins to hrs due to resp failure
-dead near water
-no specific PM or histological lesions
Management for microcystins
Aggressive symptomatic and supportive care (dextrose, vit K1, hepatoprotectants, blood transfusions
Management for Anatoxin-a
Aggressive symptomatic and supportive care
-seizure control
-mechanical ventilation (several days to weeks)
Diagnosis of blue green algae
-History of access to water where algae bloom present
-quick death; often near water
-sample water or stomach contents
-hepatic necrosis and hemorrhage of microcystins
Differential diagnoses for cyanobacteria
- acute neurotoxicity (water hemlock, strychnine, insecticides, stimulants; anthrax, cyanide, nitrate if found dead)
- Acute liver failure (Sago palm in dogs, acetaminophen, aflatoxin, Amanita mushrooms, copper, xylitol in dogs)
