Botulism Disease in Animals

Botulism disease in animals also known as Equine grass tetany, Equine dysantonomia, Limber neck and Shaker foal syndrome.

Clostridium botulinum produces potent neurotoxins during their vegetative transformation. The vegetative cells multiply rapidly and elaborate a stable and highly lethal toxins types such as B, C and D which when ingested or absorbed by tissues develops botulism. Preformed toxin is the main source for intoxication. Botulism causes toxaemia and flaccid paralysis in human, animals and birds.

Etiology

Clostridium botulinum is a spore (oval, sub terminal endospores) forming, gram positive organism, appears as single/paired/short chain. It does not grow up in animal but on decaying organic matters.

Spores survive for a long time in the environment. It remains in intestine as normal inhabitant in cattle and sheep. Seven Antigenically distinct toxin types (A-G) are identified.

In farm animals, 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 or wet soil
• Type–C: in acidic soil – subtypes Ca, Cb
• Type–D: alkaline soil

Epidemiology

Prevalence of infection

Spores survive in the environment for long period. The disease is distributed worldwide, including India.

Predisposing factors

Heat and moisture favours the germination of spores.

Source of infection

The proliferation of organism 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 carcass, bones, debris and get highest possible infection. Meat and milk containing toxin causes public health hazard.

Transmission

• The spread of infection by ingestion of contaminated material or birds or blow flies are possible.
• Spread of infection through injury.

Host Affected

• Cattle and sheep are susceptible for type C and D while horses are susceptible for type B toxin.
• Pigs and dogs also.

Pathogenesis

Botulism toxins are neurotoxins absorbed by the intestinal tract or the wound and traverse through the blood stream to peripheral cholinergic nerve terminals and neuromuscular junction, post ganglionic parasympathetic nerve endings and peripheral ganglia.

The toxin has heavy chain bind to the receptors and 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. Animal dies due to respiratory paralysis.

Types of Botulism disease in animals

• Carrion associated botulism: Multiplication of the organism in the feed produce toxin and is mostly consumed by phosphorous deficient and protein deprived animals.
• Wound botulism: The organisms produce toxins directly in the wounds.

Clinical Signs

Cattle and Horses

Incubation period is 3-17 days. After exposure to toxic material even within a day the clincal signs may appear. It may be depends on the amount of toxin released and ingested.

The toxico-infectious botulism can also be a cause for “equine grass tetany” (equine dysantonomia).

Peracute

• No rise of temperature or clinical signs seen.
• Animals dies immediately.

Acute

• 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 proceed 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 horse is an important sign. Partial or complete paralysis of muscles of locomotion.

Sub acute

• Restlessness, respiratory distress, discinlination to rise, pronounced roaring sound and persists up to 3 months in some animals.
•  In-coordination, stumbling, knuckling, ataxia, inability to rise or to lift the head, mydriasis and ptosis occur early.
•  Difficulty to take hay for 3 weeks.Mydriasis is prominent in type-C botulism in horses Sternal recumbancy, turning of head on the ground or into the flank. Reduced tongue tone, paralysis, tongue hangs out from 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.
• Animal is alert and consciousness until at the end or death.
• Foals Toxico-infectious botulism in foals by type-B toxin.In young foals of up to 8 months highest prevalence occur.The multiplication of organism in the intestine and production of toxins causes the disease called “shaker foal syndrome”.
• Type–B toxin has been isolated from feces of naturally infected animals. Muscle tremor is a prominent early signs. If the foal walks, show stiff gait, stilted gait, dragging of toes and drooling of saliva from 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 have normal sense, pain perception, dilation of pupils with a sluggish pupillary light reflex and in later period, complete cessation of peristaltic movement.Temperature varies from slightly elevated to depressed. Death occurs in 72 hours after the onset of signs due to respiratory failure.

Sheep

• Affected sheep do not show typical flaccid paralysis.
• Stiffness while walking, in-coordination and excitability in the early stages 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.

Pigs

Affected pigs show staggering, recumbancy, vomiting, pupillary dilatation, flaccid paralysis of the muscle, anorexia and adypsia.

Dogs

In dogs, symptoms develop  more quickly, within 12-36 hours after exposure to the toxin. There is generalized weakness, 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.

Zoonosis

Botulism toxin is an agent of bio-terrorism. Meat and milk containing toxins should not be used for human consumption. Human get infections by eating.

Necropsy Findings

Non specific sub endocardial, sub epicardial haemorrhages and congestion of intestines found.

Non specific perivascular haemorrhages in the corpus stratum, cerebellum and cerebrum present.

Diagnosis

• Based on clinical signs and necropsy findings.
• Demonstration of toxin in serum, feed, intestinal contents and from wounds.
•  In foals arterial blood analysis show acidemia, hypercapnia, hypoxemia and desaturation of Haemoglobin.
•  Repeated arterial blood gas analysis should be conducted during 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 condition, ELISA  is used for the detection of type C and D in cattle.

Samples collection

Suspected contaminated feed material, liver, rumen contents  and  serum etc. and formalin fixed brain.

Differential Diagnosis

• Ruminants Parturient paresis in cattle
• Hypocalcaemia in sheep
• Tick paralysis
• Rabies
• Organophosphate or carbomate poisoning
• Louping ill
• Equine protozoan myelitis
• Equine encephalomyelitis
• Hepatic encephalopathy

Treatment

Early administration of antitoxin before complete recumbancy. 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 those 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.

Prevention

In enzootic area animals vaccinated with type specific combined C and D toxoid for occasions at bi-weekly intervals.

Stocks should be rigorously vaccinated with a toxoid on 3 occasions at 2 weeks intervals. Carrion verses non-carrion associated botulism is an important factor when considering prophylactic vaccination programme.

Control

• 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.