BASICS
Gradually progressive, symmetric muscular weakness in horses characterized by flaccid paralysis and dysphagia.
- Systemic absorption of the Clostridium botulinum neurotoxin inhibits acetylcholine release at the neuromuscular junction, leading to flaccid paralysis
- After toxin absorption from the digestive tract or infected wounds, botulinum toxin circulates in the bloodstream and, subsequently, is bound by specific endopeptidase receptors on motor end plates. Once attached to the receptor, the toxin is translocated within the cell and bound to acetylcholine vesicles, preventing electrical signals from reaching the myoneural junctions
- With relatively small doses of toxin, clinical signs may not become apparent for ≥10 days after ingestion. However, horses may become recumbent and die within 8 h with massive doses
- Botulism spores are relatively ubiquitous in the environment. Ingestion rarely leads to clinical botulism, however, because the spores do not elaborate toxin unless present in an anaerobic environment with a high pH and appropriate nutrients
- Botulism spores are pH sensitive and do not form toxin at pH < 4.5
- Three forms of the disease are recognized in horses. The most common in adult horses is ingestion of the preformed toxin. Young foals develop toxicoinfectious botulism through ingestion of spores and subsequent sporulation with toxin formation in the gut. Toxin elaboration can also occur in wounds such as castration sites and deep penetrating wounds, including deep IM injections (wound botulism)
- Progressive muscular weakness over several hours to days frequently manifests as trembling of the larger muscle groups, especially triceps and gluteals
- As clinical signs progress, affected horses lie down more frequently than normal and may become unable to stand. They may struggle to stand, get up and stand for several minutes, then lie down, at first in sternal recumbency, then later lateral recumbency
- Slow chewing and dysphagia may be seen in adult horses. Drooling and feed at the nostrils may also be noted due to difficulty swallowing
- Affected foals attempt to suckle the mare, but milk drools from the foal's mouth
Respiratory distress during the terminal phases of botulism. Secondary aspiration pneumonia possible.
- Horses that remain standing can void the bladder, which helps to differentiate botulism from herpesvirus infections
- Down horses will retain urine in the bladder, requiring periodic catheterization
- More than 85% of equine botulism cases in the USA
- Most frequently occurs in the mid-Atlantic region in North America
- May occurs as an individual or multiple cases
- Several cases occurring over a few days suggests a point source of toxin such as silage (haylage) or spoiled hay from large hay bales
- Generalized muscle weakness or dysphagia typically is the first clinical sign detected
- Astute owners also may detect mild depression, decreased exercise tolerance, and reluctance to eat hay or grain
- Generalized muscle weakness, with early signs being toe-dragging, decreased tail tone, eyelid tone, and tongue tone
- A “grain test” can be used to assess for early dysphagia. Most normal horses should be able to consume 225 mL (8 oz) of grain within 2 min
- As the disease progresses, dysphagia becomes more obvious, and muscular weakness may progress to the point of recumbency and respiratory paralysis
- Vital signs are normal during the early stages of disease. Once the horse is recumbent, however, both the heart and respiratory rate increase in proportion to the intensity of the struggle to rise
- Borborygmus sounds are typically reduced
- The source of toxin in most cases of individual equine botulism is rarely determined but most likely is ingestion of a small amount of preformed toxin in roughage (typically hay). It is often impossible to subsequently identify toxin in roughage samples, because the offending material has been consumed
- In herd outbreaks, the point source is most often hay in plastic bags or round bales
- Rarely has commercial grain been associated with equine botulism
- Roughage contaminated with a carcass typically results in type C botulism
- Wound botulism may develop secondary to infected castration sites, clamped umbilical hernias, and deep IM injections with counterirritants—iodine preparations
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS