Genus Clostridium

Botulinum
 Physiology and Structure
Further subdivision are based
on phenotypic and genetic
•heterogeneous collection
properties represent 4
• Large
separate species. Seven
•fastidious,
antigenically distinct
• sporeforming
botulinum toxins (A to G)
•anaerobic rods.
have been described; human
disease is associated with
types A, B, E, and F.
Other species of clostridia produce botulinum toxins,
including C. butyricum (type E toxin), C. baratii (type F
toxin), and Clostridium argentinense (type G toxin).
Human disease has only rarely been associated with C.
butyricum and C. baratii and not definitively demonstrated
with C. argentinense.
 Pathogenesis and Immunity
c. botulinum toxin progenitor protein consisting of a small subunit
with zinc-endopeptidase activity and a large, nontoxic subunit.

The c. botulinum toxin is complexed with nontoxic proteins that

protect the neurotoxin during passage through the digestive tract
(this is unnecessary for tetanus neurotoxin). The carboxyl-terminal
portion of the botulinum heavy chain binds specific sialic acid
receptors and glycoproteins on the surface of motor neurons and
stimulates endocytosis of the toxin molecule.

Also the botulinum neurotoxin remains at the neuromuscular

junction where endopeptidase inactivates the proteins that
regulate release of acH. Because acH is necessary for muscle
contraction, the resulting clinical presentation of botulism is a
flaccid paralysis.
 Epidemiology
commonly found in soil and water throughout the world.
Four forms of botulism have been identified:
1. classic or foodborne botulism
2. infant botulism
3. wound botulism
4. inhalation botulism
In the US, fewer than 25 cases of foodborne botulism are seen
annually;
Most are associated with consumption of home-canned foods
(types A and B toxins) and occasionally with consumption of
preserved fish (type E toxin). The food may not appear spoiled,
but even a small taste can cause full-blown clinical disease.
 Epidemiology
Infant botulism is more common and has been
associated with consumption of foods (e.g., honey,
infant milk powder) contaminated with botulinum
spores and ingestion of spore-contaminated soil
and dust (most common source).
Wound botulism is the rarest with low incidence
Inhalation botulism is the concentrated toxin for
purposes of aerosolization as a biological weapon.
When administered in this manner, inhalation
disease has a rapid onset and potentially high
mortality
 Clinical disease
Patient with foodborne botulism typically become weak and dizzy 1 to 3 days
after being contaminated.
Initial signs include
• blurred vision with fixed dilated pupils
• dry mouth (anticholinergic effects of the toxin),
• Constipation
• abdominal pain
• No fever is associated
• Bilateral descending weakness of the peripheral muscles develops in
patients with progressive disease (flaccid paralysis), and death is most
commonly attributed to respiratory paralysis
• From Clinical course patients maintain a clear sensorium throughout the
disease which may continue to progress because the neurotoxin is
irreversibly bound and inhibits the release of excitatory neurotransmitters
for a prolonged period. Recovery is possibile and often requires many
months to years, or until the affected nerve endings regrow.
 Clinical disease
Infant botulism is caused by neurotoxin produced in vivo
by C. botulinum colonizing the GI tracts of infants due
to the absence of competitive bowel microbes, the
organism can become established in the GI tracts of
infants. The disease typically affects infants younger
than 1 year and the symptoms are initially nonspecific
(constipation, weak cry). Progressive disease with
flaccid paralysis and respiratory arrest can develop;
however, mortality in documented cases of infant
botulism is very low (1% to 2%). Some infant deaths
attributed to other conditions (e.g., sudden infant
death syndrome) may actually be caused by botulism
 Clinical disease
Wound botulism develops from toxin production by C.
botulinum in contaminated wounds. Although the
symptoms of disease are identical to those of
foodborne disease, the incubation period is generally
longer (4 days or more), and the GI tract symptoms
are less prominent.
 Laboratory Diagnosis
• Clinical diagnosis of foodborne botulism is
confirmed if toxin activity is find in suspected food
or in the patient’s serum, feces, or gastric fluid.
• Infant botulism is confirmed if toxin is detected in
the infant’s feces or serum, or the organism
cultured from feces.
•Wound botulism is confirmed if toxin is detected in
the patient’s serum or wound, or if the organism is
cultured from the wound. Toxin activity is most
likely to be found early in the disease.
.
 Laboratory Diagnosis
No single test for foodborne botulism has
sensitivity greater than 60%; in contrast, toxin is
detected in the serum of more than 90% of infants
with botulism
By heating 10 min at 80° C to kill all non–spore-
forming bacteria. Culture of the heated specimen
on nutritionally enriched anaerobic media allows
the heatresistant C. botulinum spores to
germinate.
 Treatment, Prevention, and Control
Patients with botulism require
• adequate ventilatory support (to muscle flaccidity)
• elimination of the organism from the GI tract through the judicious use of
gastric lavage and metronidazole or penicillin therapy
• use of trivalent botulinum antitoxin versus toxins A, B, and E

Protective levels of antibodies do not develop after disease, so patients remain

susceptible to botulism.

Disease is prevented by destroying the spores in food (virtually impossible for

practical reasons), preventing spore germination (by maintaining the food in an
acid pH or storage at 4° C or colder), or destroying the preformed toxin (all
botulinum toxins are inactivated by heating at 60° C to 100° C for 10 minutes).
Infant botulism has been associated with consumption of honey contaminated
with C. botulinum spores, so children younger than 1 year should not eat honey.
( in the past incidence was much higher because baby bottle top was sprinkled
with honey to make infant eat easily)