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Botulism 127
PEARLS & CONSIDERATIONS • Vaccination Technician Tips
○ Injectable, intranasal (IN), and oral vac- Caution is warranted when preparing a vaccine:
VetBooks.ir • Shedding of organisms may continue for > cats. Comparative efficacy of vaccine types in dogs has caused severe acute hepatic injury. Diseases and Disorders
Comments
cines are available for dogs; intranasal for
erroneous SQ injection of intranasal vaccine
3 months after resolution of clinical signs.
is not well defined, but IN vaccination
Client Education
Transmission of infection to other animals
and immunocompromised people may has some advantages (rapid onset of Highly contagious disease. Care should be taken
protection, mimics natural route of
continue during that time, warranting suit- exposure at mucosal surface). Mild cough to avoid coughing dogs at dog parks, pet stores,
able precautions. and/or nasal discharge can occur after IN and other areas where dogs may congregate.
• B. bronchiseptica is the evolutionary progeni- vaccination.
tor of B. pertussis, a human-specific pathogen ○ Effective in reducing infection rate and SUGGESTED READING
that is the causative agent of whooping severity of clinical signs Ford RB: Canine infectious respiratory disease. In
cough. ○ Vaccinate at least 5 days before anticipated Greene CE, editor: Infectious diseases of the dog
exposure (boarding) if possible. and cat, ed 4, Philadelphia, 2012, Saunders, pp
Prevention ○ Some IN vaccines may be used as early 55-65.
• Limit transmission by quarantine of new as 2 weeks of age. AUTHOR: Marcella D. Ridgway, VMD, MS, DACVIM
animals and isolation of infected animals. ○ Animals receiving modified live vaccines EDITOR: Joseph Taboada, DVM, DACVIM
• Decrease stress, overcrowding, and provide shed bacteria that may cause infection ±
adequate hygiene and care. disease in susceptible animals and humans.
• Disinfect cages and other surfaces (1 : 32 • Natural immunity lasts at least 6 months
dilute bleach solution). after infection.
Botulism Client Education
Sheet
BASIC INFORMATION PHYSICAL EXAM FINDINGS DIAGNOSIS
• Decreased LMN reflexes (patellar, others)
Definition and muscle tone in all limbs Diagnostic Overview
An acute, rapidly progressive generalized • Cranial nerve abnormalities (decreased/absent The diagnosis is based on a history suggestive
lower motor neuron (LMN) paralytic disorder palpebral and menace, decreased jaw tone of toxin ingestion and the resultant clinical
caused by ingestion of Clostridium botulinum and gag, mydriasis, voice change) signs. Toxin identification may be undertaken
exotoxin • Level of consciousness maintained, pain to confirm the diagnosis, but treatment, which
perception preserved is supportive and may be urgently required, is
Epidemiology • In severely affected animals, decreased initiated based on neurologic deficits and history.
SPECIES, AGE, SEX abdominal and intercostal muscle tone can
Any breed dog, either sex. Cats appear highly require ventilation or lead to death from Differential Diagnosis
resistant to botulism (no natural cases reported). ventilatory failure. • Early tick paralysis
• Tail wag is maintained. • Early polyradiculoneuritis
RISK FACTORS • Parasympathetic dysfunction can also be • Rabies
Contaminated food/carrion ingestion observed (heart rate changes, regurgitation
due to megaesophagus). Initial Database
ASSOCIATED DISORDERS • CBC, serum biochemical analysis, and
Aspiration pneumonia, ventilatory failure Etiology and Pathophysiology urinalysis: usually normal
(respiratory arrest) • C. botulinum is a gram-positive, saprophytic, • Assess oxygenation: pulse oximetry or arterial
spore-forming bacterial rod in soil. blood gas analysis (p. 1058)
Clinical Presentation • Clinical signs develop after ingestion of • Neurologic examination (p. 1136) consistent
DISEASE FORMS/SUBTYPES preformed toxin; it enters the gastrointestinal with diffuse LMN dysfunction
There are seven antigenically identified types (GI) lymphatics and is transported to the • Thoracic and abdominal radiographs may
of botulinum neurotoxins, all with similar neuromuscular junction (NMJ) of cholin- occasionally reveal megaesophagus (with or
neurotoxic effects. Dogs: type C; large animals: ergic nerves. without signs of aspiration pneumonia) and
type B; humans: types A, B, F. • A metalloprotease (botulinal toxin) prevents carrion skeletal remains in the GI tract, but
the presynaptic release of acetylcholine at radiographic abnormalities are not required
HISTORY, CHIEF COMPLAINT the NMJ. Toxin binding is quick, irreversible, to make the diagnosis of botulism.
• LMN paresis/paralysis that is often ascending and independent of temperature and neural
○ Begins as weakness in the pelvic limbs activity. Advanced or Confirmatory Testing
and can progress to quadriplegia • The severity of signs varies with the • Confirmatory diagnosis is based on finding
• History of ingestion of carrion or other amount of toxin ingested and individual the toxin in serum, feces, vomitus, or food
source of anaerobic bacterial contamination susceptibility. samples.
○ The incubation period after ingestion • Blocked release of acetylcholine from the • Preferred method of toxin identification is
ranges from hours to 6 days. presynaptic membrane causes symmetrical, the mouse neutralization test.
○ Botulism is especially likely if multiple ascending LMN paresis/paralysis. • Other in vitro tests (radioimmunoassay,
animals are affected. • Duration of illness in dogs: 14-24 days passive hemagglutination, enzyme-linked
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