Synonyms: Equine grass tetany, Equine dysautonomia, Limber neck, and Shaker foal syndrome.
Clostridium botulinum produces potent neurotoxins during their vegetative transformation.
The vegetative cells multiply rapidly and elaborate stable and highly lethal toxins types such as B, C, and D which when ingested or absorbed by tissues develop botulism.
The preformed toxin is the main source of intoxication.
Botulism causes toxemia and flaccid paralysis in humans, animals, and birds.
Clostridium botulinum is a spore (oval, subterminal endospores) forming, a gram-positive organism that appears as a single/paired/short chain.
It does not grow up in animals but on decaying organic matters
Spores survive for a long time in the environment. It remains in the intestine as a normal inhabitant in cattle and sheep.
Seven Antigenically distinct toxin types (A-G) are identified.
In farm animals, the disease is produced primarily by types B, C, and D.
Type-A- is present in neutral or alkaline soil.
Type–B– and E – in damp soil.
Type–C- in acidic soil – subtypes Ca, Cb.
Type–D– alkaline soil.
Clostridial multiplication is inhibited at >pH 4.5.
A-E-type toxins are pathogenic for mammals.
Prevalence of infection
Spores survive in the environment for long period.
The disease is distributed worldwide.
Heat and moisture favor the germination of spores.
Source of infection
The proliferation of organisms occurs in decaying vegetable or animal matters.
The toxin is stable, particularly in bones.
In sheep, due to dietary deficiency of protein or net energy.
Phosphorous deficient cattle or sheep chew and ingest dead carcasses, bones, debris and get the highest possible infection.
Meat and milk containing toxins cause a public health hazard.
The spread of infection by ingestion of contaminated material or birds or blowflies is possible.
Spread of infection through injury.
Cattle and sheep are susceptible to type C and D while horses are susceptible to type B toxins.
Pigs, dogs, and cats were found to be resistant.
Human is also susceptible for botulinum toxins.
Botulism toxins are neurotoxins absorbed by the intestinal tract or the wound and traverse through the bloodstream to peripheral cholinergic nerve terminals and neuromuscular junction, postganglionic parasympathetic nerve endings, and peripheral ganglia.
The toxin has a heavy chain that binds to the receptors and is translocated into the cells and the light chain of the toxin blocks the release of acetylcholine at the neuromuscular junction/motor nerve endings.
Toxins produce functional flaccid paralysis.
The animal dies due to respiratory paralysis.
Cattle and horses
The incubation period is 3-17 days.
After exposure to toxic material even within a day, the clinical signs may appear.
It may depend on the amount of toxin released and ingested.
Toxico-infectious botulism can also be a cause for “equine grass tetany” (equine dysautonomia).
No rise in temperature or clinical signs is seen.
Animals die immediately.
One of the most important signs is the development of progressive symmetric, muscular paralysis of the limb muscles and the muscles of jaw, tongue, throat, and muscle weakness.
Paralysis starts in the mid quarters and proceeds to the forequarters, followed by head and neck.
Muscle weakness, an obvious muscle tremor, and fasciculation may be enough to cause limb tremor.
Colic in horses is an important sign.
Partial or complete paralysis of muscles of locomotion.
Restlessness, respiratory distress, disinclination to rising, pronounced roaring sound and persists up to 3 months in some animals.
In-coordination, stumbling, knuckling, ataxia, inability to raise or to lift the head, mydriasis, and ptosis occur early.
Difficulty to make hay for 3 weeks.
Mydriasis is prominent in type-C botulism in horses.
Sternal recumbency, turning of head on the ground or into the flank.
Reduced tongue tone, paralysis, tongue hangs out from the mouth, difficulty in chewing, or swallow and drooling of saliva is prominent.
Depression of rumen motility and constipation present.
Paralysis of chest muscles results in terminal abdominal type respiration.
Animals are alert and conscious until the end of death.
Toxico-infectious botulism in foals by the type-B toxin.
In young foals of up to 8 months highest prevalence occurs.
The multiplication of organisms in the intestine and production of toxins causes the disease called “shaker foal syndrome”.
Type–B toxin has been isolated from the feces of naturally infected animals.
Muscle tremor is a prominent early sign.
If the foal walks, show stiff gait, stilted gait, dragging of toes, and drooling of saliva from the mouth.
Attempts to eat hay but regurgitate it through nostrils.
Constipation occurs consistently.
Rapid progression to severe muscular weakness, prostration, loss of condition, and unable to rise.
Prostrate foals are bright and alert has normal sense, pain perception, dilation of pupils with a sluggish pupillary light reflex, and in the later period, complete cessation of peristaltic movement.
Temperature varies from slightly elevated to depressed.
Death occurs 72 hours after the onset of signs due to respiratory failure.
Affected sheep do not show typical flaccid paralysis.
Stiffness while walking, in-coordination, and excitability in the early stages are noticed.
Head held on one side or bobbed up and down while walking (Limber neck).
Lateral switching of tail, salivation, and serous, nasal discharge are common.
Terminal abdominal respiration, limb paralysis followed by rapid death.
Affected pigs show staggering, recumbency, vomiting, pupillary dilatation, flaccid paralysis of the muscle, anorexia, and adypsia.
In dogs, symptoms develop more quickly, within 12-36 hours after exposure to the toxin.
There is generalized weakness, the paralysis which spread from the hind limbs to the forelimbs.
In addition, increased respiratory effort, facial nerve paralysis, and difficulty in swallowing.
The disease progresses to fatal respiratory failure.
Botulism toxin is an agent of bioterrorism.
Meat and milk containing toxins should not be used for human consumption.
Humans get infections by eating improperly cooked meat, its products, and milk.
Non-specific subendocardial, subepicardial hemorrhages and congestion of intestines are found.
Non-specific perivascular hemorrhages in the corpus striatum, cerebellum, and cerebrum are present.
Based on clinical signs and necropsy findings.
Demonstration of toxin in serum, feed, intestinal contents, and wounds.
In foals arterial blood analysis show acidemia, hypercapnia, hypoxemia, and desaturation of Haemoglobin.
Repeated arterial blood gas analysis should be conducted during the first 48 hours of treatment.
Demonstration of spores of Cl.botulinum in feed.
Mice: Injected with toxin and neutralized with polyvalent antitoxin.
But the sensitivity is low in mice as compared to ruminants and horses to botulism toxin.
In chronic/sub-acute conditions, ELISA is used for the detection of types C and D in cattle.
Suspected contaminated feed material, liver, rumen contents, and serum, etc.
o Parturient paresis in cattle.
o Hypocalcaemia in sheep.
o Tick paralysis.
o Organophosphate or carbamate poisoning.
o Louping ill.
o Equine protozoan myelitis.
o Equine encephalomyelitis.
o Hepatic encephalopathy.
Early administration of antitoxin before complete recumbency.
Supportive therapy includes fluid therapy, parenteral feeding, nasal in-sufflation with oxygen, and mechanical ventilation.
Although it is expensive, a single dose of specific or polyvalent antiserum administrated early in course with 30,000IU for a foal and 70,000IU for adult horses may increase the survival rate.
Antimicrobials for treating secondary complications such as aspiration pneumonia.
Avoid the use of drugs that may deplete the neuromuscular junction of acetylcholine such as neostigmine and that procaine penicillin, tetracyclines, aminoglycosides potentiate neuromuscular weakness.
Muzzling is essential to prevent aspiration pneumonia.
Frequent turning to prevent the development of muscle necrosis and decubital ulcers.
In the enzootic area, animals are vaccinated with type-specific combined C and D toxoids for occasions at bi-weekly intervals.
Stocks should be rigorously vaccinated with a toxoid on 3 occasions at 2 weeks intervals.
Carrion versus non-carrion-associated botulism is an important factor when considering a prophylactic vaccination program.
Hygienic disposal of carcasses.
In horses as the disease is sporadic caused by accidental contamination of food and water must be curtailed.
Range animals – supplementation of feeds with phosphorous and/or protein.