Page 1120 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Nervous system 1095

VetBooks.ir carcasses or decaying vegetable matter, such Table 10.7 Clinical signs of botulism in horses
as big-bale preserved forage or grass clippings.
This syndrome is sometimes known as ‘forage
poisoning’. ALIMENTARY
• Foal botulism: ingestion of spores. A syndrome Mild colic due to non-strangulating obstructions
known as toxico-infectious botulism or ‘shaker- Reduced prehension of food and ability to swallow
foal syndrome’ occurs in foals from a few days to Reduced tongue tone (see Table 10.8)
several months of age. The spores are ingested, Reduced borborygmi and ileus
proliferate in the GI tract and produce BoNT,
which is absorbed from the intestinal lumen. MUSCULOSKELETAL
The intestinal flora of adult horses’ intestinal Weak tail tone
tracts appears to have a protective effect against Poor anal sphincter tone
the proliferation of C. botulinum spores. Low head carriage (with associated head oedema and
• Wound botulism: wound contamination by respiratory stridor in some cases)
spores. Contamination of open wounds with Muscle fasciculations
C. botulinum leads to BoNT production in vivo. Stumbling and tripping (due to weakness not
An anaerobic environment (such as an umbilical proprioceptive deficits)
abscess, castration site, injection abscess) is Increased recumbency
required for the germination of spores and
production of BoNT within the host. OCULAR
Mydriasis
Foal botulism and wound botulism are very rare, Ptosis
in comparison to adult botulism. Slow pupillary light response
BoNT acts pre-synaptically at peripheral cholin- RESPIRATORY
ergic neuromuscular junctions. BoNT is a protease
that inactivates SNARE (soluble N-ethylmaleimide- Dysphonation
sensitive factor attachment protein receptor) pro- Respiratory stridor (related to head oedema)
teins, preventing release of acetylcholine at the Reduced respiratory rate (6–12 breaths per minute)
neuromuscular junction, and causing flaccid paraly- Altered respiratory movement (prominent abdominal
sis. The effect of BoNT at the neuromuscular junc- muscular effort)
tion is irreversible and so an improvement in clinical Respiratory muscle paralysis
signs is only achieved by the regeneration of new URINARY
motor end plates. This explains why there is a few
days’ delay in noticeable clinical improvement even Bladder distension
after treatment of a botulism patient with antitoxin, Urinary incontinence
which has no effect on neurons already affected by
internalised BoNT.

Clinical presentation respiratory effort and reduced respiratory rate may
In general, the severity and rate of progression of be observed. Urine dribbling (from bladder disten-
clinical signs may be associated with the amount of sion and sphincter paralysis) may be noted. Sensory
BoNT ingested. Clinical signs develop within hours nerve function remains unaffected. GI impactions
or days (1–16 days) of intoxication (summarised in may result from the dual effects of ileus and dehy-
Table 10.7). Over time, affected horses demonstrate dration. Recumbent patients can suffer from severe
symmetrical muscle fasciculations starting at the decubital ulcers. Dysphagic patients may develop
triceps, progressing to larger muscle groups and aspiration pneumonia, and become dehydrated and
ultimately resulting in recumbency. Exaggerated malnourished (Figs. 10.53, 10.54).