Botulism is caused by a potent neurotoxin produced by Clostridium botulinum bacteria. It causes descending flaccid paralysis beginning with cranial nerves. There are several forms of transmission including foodborne (from contaminated foods), wound, and intestinal (from spore ingestion). Clinical manifestations include nausea, blurred vision, weakness, and respiratory failure. Diagnosis involves detecting toxin in samples or through electromyography. Treatment requires intensive care including ventilator support and administration of botulism antitoxin to prevent progression of paralysis.

1. BOTULISM
BY,
ROUFABDUR
GROUP NO 7
9TH SEMESTER

2. INTRODUCTION
 Botulism is a paralytic disease caused by potent
protein neurotoxins elaborated by Clostridium
botulinum.
 Botulism is characterized by symmetrical,
descending, flaccid paralysis of motorand
autonomic nerves usually beginning with cranial
nerves.

3. ETIOLOGY
Clostridium botulinum
• Gram positive rods
• Spore forming
• Anaerobic bacteria
• Found in soil and marine
environment throughout the world.
• Produces toxin that causes botulism
• Seven neurotoxic subtypes, labeled
A-G
• First recognized and isolated in
1896 by Van Ermengem

4. Neurotoxins
Seven different types : A through G
 Different types affect different species
 All cause flaccid paralysis
 Only a few nanograms can cause illness
 Binds neuromuscular junctions
Toxin: Destroyed by boiling
Spores: Higher temperatures to be inactivated
 toxins A, B, E and F cause illness in humans
 toxins C and D cause illness in birds and mammals
 toxin G has been associated with sudden death, but not with
neuroparalytic illness.
 Toxin type A produces the most severe syndrome, with the
greatest proportion of patients requiring mechanical ventilation.
Toxin type B appears to cause milder disease than type A.

5. PATHOGENESIS
• Toxin enters bloodstream from mucosal surface or
wound
• Binds to peripheral cholinergic nerve endings
• Inhibits release of acetylcholine, preventing muscles
from contracting
• Symmetrical, descending paralysis occurs beginning
with cranial nerves and progressing downward
• Can result from airway obstruction or paralysis of
respiratory muscles
• Secondary complications related to prolonged
ventilatory support and intensive care

6. TRANSMISSION
 Ingestion
 Organism
 Spores
 Neurotoxin
 Wound contamination
 Inhalation
 Foodborne botulism
 caused by eating foods that contain
botulism toxin
 Intestinal botulism(infant and child/adult)
 caused by ingesting spores of the bacteria which
germinate and produce toxin in the intestines.
 Wound botulism
 C. botulinum spores germinate in the
wound.

7. Clinical Manifestations
Food-borne botulism
 Incubation period - 18-36 h (depending on toxin dose can range from
a few hours to several days).
 Home-canned goods (foodborne)
• particularly low-acid foods such as asparagus, beets, and corn
 Nausea, vomiting, diarrhea
 Diplopia, dysarthria, dysphonia, dysphagia
 Descending weakness or paralysis
• Shoulders to arms to thighs to calves
 Symmetrical flaccid paralysis
 No fever
 Respiratory muscle paralysis

8. Wound botulism
• Incubation period – 10 days.
• Gastrointestinal symptoms are lacking
• Wound botulism has been documented:
• After traumatic injury involving contamination with soil
• After cesarean delivery
• After antibiotics have been given to prevent wound infection
• When present, fever is probably attributable to concurrent infection with other bacteria).
Intestinal(infant) botulism
 May be one cause of sudden infant death.
 Honey can contain C. botulinum spores
 not recommended for infants <12 months old
 Constipation
 Lethargy
 Poor feeding
 Weak cry
 Bulbar palsies
 Failure to thrive

9. Diagnosis
A diagnosis of botulism must be considered in patients with
symmetric descending paralysis who are a febrile and mentally
intact.
A 14-year-old with botulism. Note the weakness
of his eye muscles and the drooping eyelids in
the image to the left, and the large and non
moving pupils in the right image.
Laboratory diagnosis
 Toxin in serum, stool, gastric
aspirate, suspected food
 Culture of stool or gastric aspirate
o Takes 5-7 days
 Electromyography also
diagnostic
 Mouse neutralization test
o Results in 48 hours
Botulinum toxin can be detected by a variety of techniques,including:
 Enzyme-linked immunosorbent assays (ELISAs);
 Electrochemiluminescent(ECL)tests

10. Treatment
 Persons of all ages (including infants)
in whom botulism is suspected should
be hospitalized immediately in an
intensive care setting, with frequent
monitoring of vital capacity and
mechanical ventilation if required.
 In adults, botulism can be treated by
passive immunization with a horse-
derived antitoxin, which blocks the
action of the toxin circulating in the
blood
 Intensive care immediately
o Ventilator for respiratory
failure
 Botulinum antitoxin
o Derived from equine source
o CDC distributes
o Used on a case-by-case basis
 Botulism immune globulin
o Infant cases of types A and G
 Equine antitoxin
o Trivalent and bivalent
antitoxins available
through the CDC
o Licensed trivalent
antitoxin neutralizes type
A, B, and E botulism
toxins
o Effective in the
treatment of
foodborne, intestinal,
and wound botulism
o Effectiveness for inhalation
botulism has not been proven
o Does not reverse current paralysis,
but may limit progression and
prevent nerve damage if
administered early
 Hypersensitivity to equine antitoxin
o 9% of people experience some
hypersensitivity.

11. Botulism Vaccine
 A toxoid vaccine (antigen types A, B, C, D, and E) is
available for laboratory workers at high risk of
exposure
 Limited supplies of this vaccine available