Botulism

BOTULISM

Synonyms:  Equine grass tetany, Equine dysautonomia, Limber neck, and Shaker foal syndrome.

INTRODUCTION AND ETIOLOGY

Introduction

• 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 of intoxication.
• Botulism causes toxemia and flaccid paralysis in humans, animals, and birds.

Etiology

• Clostridium botulinum is a spore (oval, subterminal endospores) forming, gram the 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 the intestine as 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 or wet 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.

EPIDEMIOLOGY

Prevalence of infection

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

Predisposing factors

• Heat and moisture favors the germination of spores.

Source of infection

• The proliferation of the 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 the highest possible infection.
• Meat and milk containing toxin causes public health hazards.

TRANSMISSION

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 to type C and D while horses are susceptible to type B toxin.
• Pigs, dogs and cats found to be resistant.  
• Human is also susceptible for bolutinum toxins.

PATHOGENESIS

Pathogenesis

• 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 heavy chain binds 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

• 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. 
• Toxico-infectious botulism: The organism grows and produces a toxin in the alimentary tract. 

Forage botulism: Most cases of botulism is associated with the ingestion of preformed toxin in forages.

CLINICAL SIGNS

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 maybe depends on the amount of toxin released and ingested.
• Toxico-infectious botulism can also be a cause for “equine grass tetany” (equine dysautonomia).

Peracute

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

Acute

• One of the most important signs is the development of progressive symmetric, muscular paralysis of the limb muscles and the muscles of the 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 the horse is an important sign.
• Partial or complete paralysis of muscles of locomotion.

Subacute

• Restlessness, respiratory distress, disinclination to rise, 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 take 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 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 sign.
• If the foal walks, show stiff gait, a 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, recumbency, 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 improperly cooked meat, its products, and milk.

                                                       NECROPSY FINDING

Necropsy findings

• Non-specific sub endocardial, sub epicardial hemorrhages 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 the first 48 hours of treatment.
• Demonstration of spores of Cl.botulinum in the 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.
• Formalin-fixed brain.

Differential diagnosis

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

                                TREATMENT

• 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 the 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.

                                         PREVENTION AND CONTROL

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 program.

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.