2. DefinitionDefinition
Botulism is a paralytic disease
caused by potent protein neurotoxins
elaborated by clostridium botulinum.
Botulism is characterized by
symmetrical, descending, flaccid
paralysis of motor and autonomic
nerves usually beginning with cranial
nerves
3. Etiologic AgentEtiologic Agent
C. botulinum is an anaerobic gram-
positive organism that form spors;
C. botulinumC. botulinum is in soil and marine
environments throughout the world.
C. botulinumC. botulinum elaborates the most
potent bacterial toxin.
4. – SporesSpores
UbiquitousUbiquitous
Resistant to heat, light, drying and radiationResistant to heat, light, drying and radiation
Spores may survive boiling for several hoursSpores may survive boiling for several hours
at 100at 100 oo
CC
Specific conditions for germinationSpecific conditions for germination
– Anaerobic conditionsAnaerobic conditions
– Warmth (10-50Warmth (10-50oo
C)C)
– Mild alkalinityMild alkalinity
5. NeurotoxinsNeurotoxins
Seven different types: A through GSeven different types: A through G
– Different types affect different speciesDifferent types affect different species
– All cause flaccid paralysisAll cause flaccid paralysis
– Only a few nanograms can cause illnessOnly a few nanograms can cause illness
– Binds neuromuscular junctionsBinds neuromuscular junctions
Toxin: Destroyed by boilingToxin: Destroyed by boiling
Spores: Higher temperatures to beSpores: Higher temperatures to be
inactivatedinactivated
6. NeurotoxinsNeurotoxins
– toxins A, B, E and F cause illness in humanstoxins A, B, E and F cause illness in humans
– toxins C and D cause illness in birds andtoxins C and D cause illness in birds and
mammalsmammals
– toxin G has been associated with sudden death,toxin G has been associated with sudden death,
but not with neuroparalytic illness, in a fewbut not with neuroparalytic illness, in a few
patients in Switzerland.patients in Switzerland.
– Toxin type A produces the most severeToxin type A produces the most severe
syndrome, with the greatest proportion ofsyndrome, with the greatest proportion of
patients requiring mechanical ventilation. Toxinpatients requiring mechanical ventilation. Toxin
type B appears to cause milder disease thantype B appears to cause milder disease than
type A.type A.
10. Food-borne botulismFood-borne botulism
– Caused by eating foods thatCaused by eating foods that
contain botulism toxincontain botulism toxin
– Outbreaks have been associatedOutbreaks have been associated
with a variety of foods such aswith a variety of foods such as
garlic packed in oil, bakedgarlic packed in oil, baked
potatoes wrapped in aluminum foil,potatoes wrapped in aluminum foil,
home-canned vegetables, jerky,home-canned vegetables, jerky,
and fermented fish.and fermented fish.
11. Food-borne botulismFood-borne botulism
Food-born botulism can occur when:Food-born botulism can occur when:
1. Food to be preserved is contaminated1. Food to be preserved is contaminated
with spores;with spores;
2. Preservation does not inactivate the2. Preservation does not inactivate the
spores but kills other putrefactive bacteria thatspores but kills other putrefactive bacteria that
might inhibit growth of C. botulinum and providesmight inhibit growth of C. botulinum and provides
anaerobic conditions, that allows germination andanaerobic conditions, that allows germination and
toxin production;toxin production;
3. Food is not heated to a temperature that3. Food is not heated to a temperature that
destroys toxin before being eaten.destroys toxin before being eaten.
12. Intestinal botulismIntestinal botulism (infant and(infant and
child/adult)child/adult)
Caused by ingesting spores of theCaused by ingesting spores of the
bacteria which germinate andbacteria which germinate and
produce toxin in the intestines.produce toxin in the intestines.
13. Intestinal botulismIntestinal botulism (infant and(infant and
child/adult)child/adult)
Infants <12 months of age are particularlyInfants <12 months of age are particularly
susceptible tosusceptible to C. botulinumC. botulinum spores becausespores because
their digestive tracts are not fully developed andtheir digestive tracts are not fully developed and
therefore not able to prevent the germinationtherefore not able to prevent the germination
and subsequent toxin production in theand subsequent toxin production in the
intestines.intestines.
Adults or children >12 months rarely developAdults or children >12 months rarely develop
intestinal botulism, but may be more susceptibleintestinal botulism, but may be more susceptible
if they have pre-existing intestinal conditions.if they have pre-existing intestinal conditions.
14. Wound botulismWound botulism
– Wound botulism occurs whenWound botulism occurs when
C. botulinumC. botulinum spores infect andspores infect and
germinate in the wound, producinggerminate in the wound, producing
toxin which is absorbed into thetoxin which is absorbed into the
bloodstream.bloodstream.
– Typically, there are very few casesTypically, there are very few cases
of wound botulism reported eachof wound botulism reported each
year.year.
15. EpidemiologyEpidemiology
The highest incidence rate is reported from the Republic ofThe highest incidence rate is reported from the Republic of
Georgia and Armenia, where illness is associated withGeorgia and Armenia, where illness is associated with
home-canning practices.home-canning practices.
Number of botulism cases and cases per 100,000 persons
in Georgia, 1980–2002.
16. EpidemiologyEpidemiology
In the United States during 1990–2000,In the United States during 1990–2000,
the median number of foodborne cases ofthe median number of foodborne cases of
botulism per year was 23 (range, 17–43).botulism per year was 23 (range, 17–43).
Since the early 1990s, cases in the UnitedSince the early 1990s, cases in the United
States have occurred almost exclusively inStates have occurred almost exclusively in
injection drug users.injection drug users.
17. PathogenesisPathogenesis
Toxin enters bloodstream from mucosal surface orToxin enters bloodstream from mucosal surface or
woundwound
Binds to peripheral cholinergic nerve endingsBinds to peripheral cholinergic nerve endings
Inhibits release of acetylcholine, preventingInhibits release of acetylcholine, preventing
muscles from contractingmuscles from contracting
Symmetrical, descending paralysis occursSymmetrical, descending paralysis occurs
beginning with cranial nerves and progressingbeginning with cranial nerves and progressing
downwarddownward
Can result from airway obstruction or paralysis ofCan result from airway obstruction or paralysis of
respiratory musclesrespiratory muscles
Secondary complications related to prolongedSecondary complications related to prolonged
ventilatory support and intensive careventilatory support and intensive care
19. Food-borne botulismFood-borne botulism
Incubation periodIncubation period -- 18-36 h (depending18-36 h (depending
on toxin dose can range from a few hours toon toxin dose can range from a few hours to
several days).several days).
Home-canned goods (foodborne)Home-canned goods (foodborne)
20. Nausea, vomiting, diarrheaNausea, vomiting, diarrhea
Diplopia, dysarthria, dysphonia,Diplopia, dysarthria, dysphonia,
dysphagiadysphagia
Descending weakness or paralysisDescending weakness or paralysis
– Shoulders to arms to thighs to calvesShoulders to arms to thighs to calves
Symmetrical flaccid paralysisSymmetrical flaccid paralysis
No feverNo fever
Respiratory muscle paralysisRespiratory muscle paralysis
21. Wound botulismWound botulism
Incubation period –Incubation period – 10 days.10 days.
Gastrointestinal symptoms are lackingGastrointestinal symptoms are lacking
Wound botulism has been documented:Wound botulism has been documented:
– After traumatic injury involving contamination withAfter traumatic injury involving contamination with
soil;soil;
– After cesarean deliveryAfter cesarean delivery
– After antibiotics have been given to prevent woundAfter antibiotics have been given to prevent wound
infection.infection.
When present, fever is probablyWhen present, fever is probably
attributable to concurrent infection withattributable to concurrent infection with
other bacteria.other bacteria.
22. Intestinal (infant)Intestinal (infant)
botulismbotulism
May be one cause of sudden infantMay be one cause of sudden infant
death.death.
Honey can containHoney can contain C. botulinumC. botulinum
sporesspores
– not recommended for infants <12not recommended for infants <12
months oldmonths old
24. DiagnosisDiagnosis
A diagnosis of botulism must beA diagnosis of botulism must be
considered in patients with symmetricconsidered in patients with symmetric
descending paralysis who are afebriledescending paralysis who are afebrile
and mentally intact.and mentally intact.
25. A 14-year-old with botulism. Note the weakness of hisA 14-year-old with botulism. Note the weakness of his
eye muscles and the drooping eyelids in the image toeye muscles and the drooping eyelids in the image to
the left, and the large and non moving pupils in thethe left, and the large and non moving pupils in the
right image.right image.
26. Laboratory diagnosisLaboratory diagnosis
Toxin in serum, stool, gastric aspirate,Toxin in serum, stool, gastric aspirate,
suspected foodsuspected food
Culture of stool or gastric aspirateCulture of stool or gastric aspirate
– Takes 5-7 daysTakes 5-7 days
Electromyography also diagnosticElectromyography also diagnostic
Mouse neutralization testMouse neutralization test
– Results in 48 hoursResults in 48 hours
27. Laboratory diagnosisLaboratory diagnosis
Botulinum toxin can be detected by aBotulinum toxin can be detected by a
variety of techniques, including: variety of techniques, including:
Enzyme-linked immunosorbent assaysEnzyme-linked immunosorbent assays
(ELISAs);(ELISAs);
Electrochemiluminescent (ECL) testsElectrochemiluminescent (ECL) tests
29. TreatmentTreatment
Persons of all ages (including infants) in whomPersons of all ages (including infants) in whom
botulism is suspected should be hospitalizedbotulism is suspected should be hospitalized
immediately in an intensive care setting, withimmediately in an intensive care setting, with
frequent monitoring of vital capacity andfrequent monitoring of vital capacity and
mechanical ventilation if required.mechanical ventilation if required.
In adults, botulism can be treated by passiveIn adults, botulism can be treated by passive
immunization with a horse-derived antitoxin,immunization with a horse-derived antitoxin,
which blocks the action of the toxin circulatingwhich blocks the action of the toxin circulating
in the bloodin the blood
30. TreatmentTreatment
The decision to administer botulinum AntitoxinThe decision to administer botulinum Antitoxin
must be based on a clinical diagnosis andmust be based on a clinical diagnosis and
cannot be postponed while laboratorycannot be postponed while laboratory
confirmation is awaited.confirmation is awaited.
Botulinum antitoxin neutralizes only toxinBotulinum antitoxin neutralizes only toxin
molecules that have not yet bound to nervemolecules that have not yet bound to nerve
endings; it cannot reverse existing paralysis.endings; it cannot reverse existing paralysis.
Thus antitoxin should be given early in theThus antitoxin should be given early in the
course of illness, ideally <24 h after symptomcourse of illness, ideally <24 h after symptom
onset.onset.
31. TreatmentTreatment
Infant botulism is treated with a licensed human-originInfant botulism is treated with a licensed human-origin
antitoxin;antitoxin; Botulism immune globulin was approved forBotulism immune globulin was approved for
use on October 23, 2003 for the treatment of infantuse on October 23, 2003 for the treatment of infant
botulism caused by types A and G.botulism caused by types A and G.
Other forms of botulism are treated with equine-sourceOther forms of botulism are treated with equine-source
antitoxin.antitoxin.
Treatment with equine-origin antitoxins long used in theTreatment with equine-origin antitoxins long used in the
United States is associated with anaphylaxis, otherUnited States is associated with anaphylaxis, other
hypersensitivity reactions and serum sickness.hypersensitivity reactions and serum sickness.
32. Equine antitoxinEquine antitoxin
A new heptavalent despeciated equine antitoxin hasA new heptavalent despeciated equine antitoxin has
replaced the previously used non-despeciated equinereplaced the previously used non-despeciated equine
antitoxin in the United States.antitoxin in the United States.
Effective in the treatment of foodborne, intestinal, andEffective in the treatment of foodborne, intestinal, and
wound botulismwound botulism
Effectiveness for inhalation botulism has not beenEffectiveness for inhalation botulism has not been
proven.proven.
33. PreventionPrevention
No prophylaxis or licensed vaccine forNo prophylaxis or licensed vaccine for
botulism is available.botulism is available.
An experimental vaccine for administrationAn experimental vaccine for administration
to laboratory workers is available from theto laboratory workers is available from the
CDC.CDC.