Page 839 - Clinical Small Animal Internal Medicine

74 Diseases of the Neuromuscular Junction 807

Other Disorders of Neuromuscular Botulism
VetBooks.ir Transmission (exotoxin) of Clostridium botulinum which is contained in
Botulism occurs by ingesting the preformed neurotoxin
carrion or spoiled food. In rare cases, botulism may occur
Presynaptic Disorders
as a result of colonization of the gastrointestinal (GI) tract
Tick Paralysis (toxico‐infectious) or wound infection. There are eight
A salivary neurotoxin secreted by certain tick species can botulinum toxins but type C1 is the most common in dogs
interfere with ACh release, resulting in impaired neuro- although there have been infrequent reports of type C2
muscular transmission and clinical weakness. The signs and D. Botulism has not been reported in the cat.
are usually that of an acute progressive lower motor neu- Botulinum neurotoxins inhibit neurotransmitter
ron (LMN) disease. The North American common wood release from the presynaptic nerve terminals by cleaving
ticks, Dermacentor variabilis and Dermacentor ander- proteins required for synaptic vesicle fusion with the
soni (Rocky Mountain wood tick), are most often respon- plasma membrane. They may affect either the synaptic
sible for the disease. In Australia, Ixodes holocyclus is the vesicles (synaptobrevin) or the plasma membrane
most important species. Less commonly associated ticks (SNAP‐25 and syntaxin), depending on the neurotoxin
are Ixodes cornuatus, I. hirsti, I. pacificus, and I. serotype. The neurotoxins enter the nerve terminal by
scapularis. specifically interacting with the luminal domain of syn-
The clinical signs are commonly seen as pelvic limb aptic vesicle proteins (synaptotagmin or SV2, depending
ataxia that then progresses to involve the thoracic limbs, on serotype) which are briefly exposed during exocytotic
leading to recumbency in 24–72 hours. Dysphonia and membrane fusion. This leads to a presynaptic blockade
dysphagia can be early signs, and masticatory muscle of ACH release and resulting muscle weakness. There
weakness and facial paresis may also be present. Death may be some disturbance in autonomic function as well.
may occur within several days from respiratory paralysis. The clinical signs may occur within hours to days and
The diagnosis is made by clinical signs and resolution of are typically an acute onset of symmetric diffuse LMN
signs following tick removal. Prognosis is usually good, dysfunction starting in the pelvic limbs and progressing
with recovery occurring in 1–3 days following complete forward. The severity of dysfunction may range from
tick removal. mild weakness to complete tetraplegia with respiratory
In Australia, the clinical signs with Ixodes spp tend to paralysis. The spinal reflexes are not intact and there is
be more severe and include autonomic disturbances often paresis associated with cranial nerve functions
that include peripheral vasoconstriction, arterial such as the facial musculature, laryngeal, pharyngeal and
hypertension, increased pulmonary capillary hydro- esophageal musculature.
static pressure, pulmonary congestion and edema, The diagnosis can be made by detection of the toxin
tachyarrhythmias, and pupillary dilation. In addition in ingested material, serum, vomit, and feces and by a
to the previously described clinical presentation, other neutralization test in small mice. Samples should be
signs may include voice change, depressed gag reflex, collected as early as possible in the course of the disease.
megaesophagus, salivation, regurgitation and/or vom- ELISA tests have been used in the detection of botuli-
iting, dyspnea, and cyanosis. Death may occur within num toxin in people but not for type C (reportedly used
1–2 days in untreated patients. In addition to tick in cattle) so obtaining a diagnosis by this method would
removal and supportive care, neutralization of circu- be difficult. Electrodiagnostic studies may be useful to
lating toxins can be attempted with tick antitoxin differentiate botulism from other acute disorders such as
serum. The antitoxin serum adverse effects are ana- polyradiculoneuritis. There may be a slight decrease in
phylaxis and autonomic disturbance. The antiserum motor nerve conduction velocity and decreased ampli-
treatment needs to be given in the early stages of the tude of the compound muscle action potential (CMAP).
disease and is expensive. Alpha‐adrenergic blocking Repetitive nerve stimulation may reveal a decremental
agents such as phenoxybenzamine hydrochloride and response at low (>5 Hz) rate or incremental response at
prazosin may help with the hypertension. Severely high (>50 Hz) rate. EMG may show some spontaneous
affected animals with respiratory compromise may activity such as fibrillation potentials and positive sharp
require ventilator support. waves but it is often normal.
The prognosis can be guarded even with appropriate Treatment of botulism consists of supportive care,
treatment. The prognosis seems to be inversely related to with mildly or moderately affected dogs recovering over
the severity of clinical signs, as dogs with mild disease a period of several days. Intensive management may be
recovered more quickly than those with severe paresis/ required for dogs needing ventilatory support or having
paralysis and respiratory compromise. megaesophagus and dysphagia as they are at high risk for