Page 788 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Botulinum Neurotoxins Chapter | 55 747

VetBooks.ir 1991). Birds may act as vectors, transporting toxin or bac- that ingest low doses of toxin may show only mild dys-
phagia and recover with minimal treatment. Ingestion of
terial spores from a rotting carcass to nearby horse farms
large doses is more likely to induce peracute disease with
(Schoenbaum et al., 2000).
Wound botulism occurs from the contamination of an a poor prognosis. In peracute illness, muscle paralysis
anaerobic wound with the Clostridium bacteria and is progresses rapidly and the animal is recumbent within
most commonly associated with botulinum toxin B. Distal 8 12 h; ultimately, paralysis of the respiratory muscles
limb wounds, castration sites, umbilical hernias, and results in death.
injection site abscesses are the usual suspects. With the exception of EGS, the clinical presentation is
Shaker foal syndrome is a form of toxicoinfectious not related to the botulinum toxin serotype involved
botulism occurring in foals of around 2 5 weeks of age (Whitlock, 1996; Whitlock and Buckley, 1997; Johnson
(Rooney and Prickett, 1967; Vaala, 1991; Whitlock, et al., 2010). Early signs are typically progressive and
2002). The syndrome is most common in fast-growing include depression, exercise intolerance, difficulty with
foals on high planes of nutrition and is most commonly grain consumption, myasthenia, dysphagia, ataxia, gait
associated with botulinum toxin serotype B with occa- stiffness, muscle tremors (particularly in the triceps and
sional cases involving serotype C1 (MacKay and quadriceps muscle groups), decreased tail tone, mydriasis,
Berkhoff, 1982). Gastrointestinal ulceration and liver ptosis, decreased pupillary light responses, and decreased
abscesses have been documented postmortem in foals that palpebral reflexes. Exercise typically worsens the paresis.
succumbed to botulism (Swerczek, 1980). Exposures to Dysphagia and pharyngeal weakness are often associated
stress, high nutrient diets, or corticosteriod use are reputed with secondary aspiration pneumonia. Horses often have
to play a role in susceptibility by promoting gastric ulcers difficulty in drinking. Stridor may develop due to pharyn-
that act as an anaerobic nidus for colonization. geal/laryngeal paresis/paralysis. Low head carriage is
Furthermore, as in human neonatal toxicoinfection, the noted in some cases. During the initial stages of the dis-
immature GI tract of foals may be more permissible to ease vital signs typically remain normal. However evi-
overgrowth by C. botulinum. Sand colitis or other causes dence of progressively worsening gut stasis (decreased
of gastrointestinal irritation may be risk factors. borborygmi, ileus, colic, and constipation) is common
Equine grass sickness (EGS) is a polyneuronopathy with disease progression. Diarrhea is often associated
affecting both the central and the peripheral nervous sys- with serotype C, possibly in association with C2 toxin.
tems of grazing (mostly) horses (Pirie et al., 2014). The Urine retention with resultant bladder distention often
etiology of the disease remains uncertain although toxi- occurs, thereby increasing the risk of urinary tract
coinfectious exposure to botulinum toxin C1 was pro- infection.
posed as a cause in the 1920s. Critically, EGS is not As the disease progresses, horses spend more time in
associated with classical botulinum toxin induced overt sternal recumbency and ultimately become laterally
flaccid paresis/paralysis. There is limited evidence of: (1) recumbent. Heart and respiratory rates may increase as
a greater frequency of detection of botulinum toxin C1 in recumbent horses struggle to stand. In late stages, dyspnea
the ileal contents and/or feces of horses with EGS cf and other signs of respiratory distress may be observed.
healthy horses; (2) low antibody status to C. botulinum With serotype C intoxication, an exaggerated expiration
type C as a risk factor; (3) survivors of chronic EGS have and “prolonged abdominal lift” may be noted. In the final
higher levels of antibodies against C. botulinum serotype stages of botulism, horses are laterally recumbent, demon-
C cf nonsurvivors; (4) the specific action of C. botulinum strate significant respiratory difficulty, and develop
type C1 neurotoxin on nerve terminal syntaxin at cholin- anoxia. As the anoxia progresses, horses may exhibit ago-
ergic synapses may account for the neuroanatomical dis- nal paddling. At this point, the patient either dies due to
tribution of some EGS-associated neuronal dysfunctions; respiratory failure or is euthanized.
(5) C. botulinum type C can produce C2 and C3 ADP- In shaker foal syndrome, the first clinical signs are
ribosylating toxins capable of inducing ultrastructural cel- typically increased periods of recumbency and muscle
lular disarray; and (6) two successful vaccine trials using tremors. Soon after the foal rises, muscle tremors are
partly neutralized C. botulinum toxin, were conducted in evident, and after brief periods of standing, the foal col-
the 1920s. However, the disease has not been experimen- lapses from weakness. Recumbent foals appear to be
tally reproduced with C. botulinum type C. bright and alert. Foals may dribble milk from their muz-
zles soon after nursing due to dysphagia and pharyngeal
muscle paresis and aspiration pneumonia is common.
Clinical Signs, Diagnosis, and Treatment Constipation and ileus are also frequently observed. Other
The onset of classical equine botulism is variable with clinical signs are similar to those observed in the
signs starting between 12 h and 10 days postexposure adult horse.
(i.e., gradual, acute, or peracute depending on exposure The characteristic spectrum of EGS clinical signs are
dose, duration and individual sensitivity). Adult horses due to neuronal degeneration in the autonomic nervous