Botulism

Syn: Limber neck, Lion disease

• It is highly fatal motor paralysis intoxications in animals and man caused by powerful neurotoxin of Clostridium botulinum.
• It is characterized by partial or complete paralysis of muscles of locomotion, head and neck.
• In case of human being, it is responsible for food poisoning.

Etiology:

• Clostridium botulinum
• Gram +ve rod, spore forming anerobes and produces neurotoxins.
• Organism is seen singly or in pairs as short chain
• Organism are saprophytic; i.e. they proliferate on decaying animal matter.
• 7 different neurotoxins are produced; A-G
• C &E; botulism in animals
• A, B &E; botulism in human beings

Epidemiology:

• Horse, cattle, sheep, goat, duck, goose, turkey, pheasants, water fowls and man are susceptible.
• Bacteria is common inhabitant of alimentary tract of herbivorous animals.
• Pasture gets contaminated with excreta of such animals.
• Organism multiplies in decaying animal and decomposed plant materials.
• Usual source of toxin is decaying carcass or vegetable materials such as decaying grass, hay, grain or spoiled silage.
• Disease is worldwide in distribution; but more common in tropical and subtropical region; areas where improper feed storage or carcass contamination occurs.
• Disease is more frequent during warm seasons; especially in summer and early autumn

Transmission:

• Ingestion of contaminated feed and water by decaying carcass, spoiled silage, poultry litter.
• Ingestion of preformed toxin
• Organism may gain entry through wound, cuts or bruises.
• Horse may become affected by ingestion of contaminated hay and silage by toxic fluid exudating from decomposed rat or cat carcass.

Pathogenesis:

Clinical Signs:

• Disease appears as acute, sub-acute, or chronic form.
• IP varies from 2-6 days depending on the amount of toxin ingested.
• Partial or complete paralysis of muscles of locomotion.
• Stiff gait, marked inclination to lie down and difficult to raise its body
• Animals fails to hold its head in normal positions and head is turned/rested towards flank.
• Profuse salivation/paralysis of muscles of throat
• Paralysis initially occur in hind quarter and progress toward fore quarter, head and neck.
• Tongue protrudes from mouth and paralyzed.
• Disease ends fatally.

PM lesion:

• No characteristics macroscopic or microscopic lesion.

Diagnosis:

• Based on clinical signs and negative PM findings
• Testing of suspected food for toxin; suspected food is macerated with equal volume of physiological saline. Mixture is then centrifuged and clear supernatant fluid is injected into guinea pig.
• Isolation and identification of organism in fresh meat broth.
• FAT

Differential diagnosis

1. Milk fever:

• Subnormal temperature
• Occurs after parturition
• Hypocalcemia/ respond to Ca therapy

2. Rabies (paralytic form):

• Dropped jaw
• Furious form is preceded before paralysis
• Excessive salivation, death within 7-10 days

Treatment:

• No reliable treatment is available.
• Administration of botulinum anti-toxin if available; 20 ml IV infusion diluted with 0.9% NaCl before administration
• Magnesium sulphate @50-300 gm, PO, BID, for 2-3 days for removing toxins from GI tract.
• Nikethamide @5ml IM for 1 week.
• Guanidine HCl @11mg/kg, b.wt., IM for 1 week
• Neurobion @3-5 ampoule, IM, OD, 1 week

Control:

• Access to contaminated feed and carcass should be avoided as far as practicable.
• Cattle and sheep grazing phosphorus deficient pasture should be provided with adequate phosphorus.
• Vaccination in endemic areas; combined bivalent toxoid can be used.
• Proper disposal of carcass; either by burying or burning.
• Avoidance of feeding poultry litter to ruminants.
• Proper storage and handling of feed should be ensured.