BOTULISM

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This is a word most of us have not used in the past few decades, it is rare in humans in today’s world, 145 documented cases in the USA last year, and only sporadic (less than rare) in dogs, negligible numbers was the answer I found.

WHAT IS BOTULISM?

Botulism is a rare, serious, and potentially fatal illness caused by a toxin produced by the bacterium Clostridium Botulinum. The toxin can be found in food, soil, and marine sediments, world wide.

C. Botulinum is an intoxication not an infection.

Clostridium Botulinum is a Gram-positive, rod-shaped, anaerobic, spore-forming, motile bacterium with the ability to produce the neurotoxin botulinum. The botulinum toxin can cause a severe flaccid paralytic disease in humans and other animals and is the most potent toxin known to mankind, natural or synthetic, with a lethal dose of 1.3–2.1 ng/kg in humans.

HOW IS THE C. BOTULINUM TOXIN PRODUCED?

C. Botulinum is found in soil, vegetation, water, food, and does not pose a threat until it begins to produce a toxin, and this happens when C. Botulinum is exposed to low oxygen levels (anaerobic environment), and optimum temperatures for growth and toxin production which is 82-95 degrees Fahrenheit..

7 TYPES OF BOTULISM

A, B, E and F are the main causes of human botulism.

C (C1 – neurotoxin, C2 – not a neurotoxin, but affects vascular permeability), and D are found in cases of animal botulism –

  • wild waterfowl are the most susceptible (Limber Neck Disease)
  • commercial poultry (large pheasant and chicken farms)
  • cattle (mostly South Africa and South America where phosphorous in the soil is low)
  • horses (Shaker Foal Syndrome)
  • ruminants (goats, sheep, llama, alpaca)
  • some species of fish
  • cats are NOT affected by botulism
  • dogs and pigs are generally not affected (rare), maybe sporadically

TOXICOINFECTIOUS BOTULISM / WOUND BOTULISM

This is the name given to the disease in which C. BOTULINUM grows in tissues of a living animal and produces toxins there. The toxins are liberated from the lesions and cause typical botulism. Gastric ulcers, foci of necrosis in the liver, abscesses in the navel and lungs, wounds of the skin and muscle, and necrotic lesions of the GI tract are predisposing sites for development of toxicoinfectious botulism.

Rapidly closing wounds such as punctures, that were in contact with contaminated soil, are at increased risk for developing the neurotoxin, as it is the perfect anaerobic environment with the optimal temperatures to grow the toxin.

HISTORICALLY

HUMANS – C. BOTULINUM was linked primarily to home-canned foods, and improperly smoked summer sausages. In recent decades however, botulism illnesses have been linked to foods such as un-refrigerated homemade salsa, baked potatoes sealed in aluminum foil, honey (the primary cause of botulism in infants), garlic in oil, and traditionally prepared salted or fermented fish.

ANIMALS – Botulinum intoxication was/is linked to spoiled foods, rotting carcasses, anaerobic vegetation, low nutrients in soil, stagnant water, and wounds. Kentucky is considered an endemic state for C. Botulinum in range animals.

SIGNS OF INTOXICATION IN DOGS

For human / animal the time frame is 3 hours to 8 days, the earlier the symptoms appear, the more serious the intoxication. Dogs generally present 12- 36 hours after exposure.

  • nausea , vomiting
  • weakness
  • visual blurring / facial paralysis
  • low to no rectal tone
  • ascending paralysis (rear legs forward)
  • difficulty swallowing / chewing / gagging / hyper salivation
  • bladder / stomach paralysis
  • complications with paralysis of diaphragm / lungs/ can occur 1-3 days after onset of symptoms
  • death is usually caused by respiratory failure when the diaphragm and lungs become fully involved, breathing is affected and results in death from asphyxia.

TREATMENT

If botulism is caught in the early stages, an injection of an antitoxin (every veterinary clinic has an antitoxin on-site) can lessen the severity of the intoxication by neutralizing any toxin that has not yet bound to nerve endings. The antitoxin has been used with variable success. This is generally only given if paralysis has not yet set in or is minimal.

The only real treatment for C. Botulinum intoxication is supportive care, however if the diaphragm and/or respiratory system is involved, death from asphyxia or euthanasia (humane care) is certain.

HOW RARE IS C. BOTULINUM IN DOGS?

In my state not one person involved with RHUMB had seen a clinical case of C. Botulinum intoxication.

  • 4 Veterinarians – never
  • 1 Pathologist – never
  • 2 Livestock extensions in our state – never in any animal species
  • AG extension – never
  • State Veterinarian – never
  • 5 working ranches with working dogs – never

In a multiple dog household, if the food has been spoiled or contaminated with C. Botulinum C1 toxin, all household dogs succumb. LINK

In multiple dog households where the dogs are free to scavenge and eat carrion that has C. Botulinum C1 toxin, all household dogs succumb.

Duck and Goose hunting dogs can become intoxicated with C. Botulinum C1 if the water is stagnant or has anaerobic vegetation with the toxin present.

DID RHUMB DIE FROM BOTULISM?

C. Botulinum was on our list of LOWER MOTOR NEURON EVENTS. Her signs and symptoms were very close to this type of lethal intoxication.

Rhumb was not a scavenger, and we had no carrion on the property, we had no anaerobic vegetation present, and the winter temperatures just don’t support that being viable. Could it have been en vivo toxicoinfectious botulism, there is that possibility as she had little dings and scrapes from time to time just from daily work. In my life with my dogs, over 26 years, I have had dogs with lots of little dings and scrapes, and never this. But it is a possibility.

And then there is the glaring observation – we still have 4 optimally healthy dogs in our home, who worked along side of her, ate with her, and slept with her. We have 20 living ducks (water fowl who are HIGHLY susceptible to C. Botulinum), 2 living goats, and 36 very healthy and alive quail.

However, in talking with the Chief Toxicologist at Michigan State University, who did her initial tox-screen, he had reseverations about –

  • time frame
  • the rapid paralysis (happening in hours instead of days, her respiratory system was involved almost at the same time as her limbs. The respiratory system is generally not involved for 1-3 days after the initial onset of paralysis)
  • lacrimation (excessive tearing)
  • if we had a lethal neurotoxin in our environment, we would have many dead animals, not just one

But more on all of that in the next post – I hope you all find this helpful.

Nancy

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