updater material for botulsm 2023 for all pediatrician and infectious disease doctors.

2. botulism
BY:
Dr, WALAA SALAH MANAA
CONSULTANT OF PEDIATRIC & INFECTION.
‫الشـيخ‬ ‫كـفر‬ ‫حمـيات‬ ‫مـستشفى‬

4. Definition:
• Is acute flaccid
paralytic illness caused
by the neurotoxins
produced by:
clostridium botiolinium or
rarely neurotoxines of
c.butyricum & c.bratii.

5. • It is Greek word
(botulus)=sausage.
• where the Disease go
its name from out
break in Germany in
1793 by infected
sausage.

6. Types:
• 3 form of human botulism:
1)infant botulism, (common in USA)
2)food borne botulism, (classic type)
3)wound botulism, (rare type).
• Other non human types:
Avian botulism., Animal botulism.

9. Clostridium botulinum:
It is :  gram +ve .
Spore forming.
Obligate anaerobe.
need high pH.
Etiology

10. Its natural habitat:
soil ,dust,
marine sediment

11. C.botulinum

12. In 1895, Emile Van
Ermengem
first isolated the
bacterium Clostridium
botulinum

13. Toxins of botulism:
• The most poisonous substances known.
(parental lethal dose is 10-7 mgkg. )
(Just a teaspoon of pure botulism poison could kill
millions of people.)
Action: block neuromuscular junction transmission
Types: A, B, C, D, E, F, G.
C.butyricum E.
C. baratii F.

14. • Action:
block neuromuscular
junction
transmission

15. • Spores 
*Survive 2 hr at 100 °C.
*Inactivated at 120 °C .
( Boiling food before canning at
high elevations may not
inactivate the spores.)
*Factors favoring spore
germination:
Low acidity (pH > 6.0)
Low O2
High water content
• Toxins 
is heat labile=easily destroyed
at 80 c or higher for 10 min.
Inactivated after 1 minute at
85 °C, or 5 minutes at 80 °C.

16. Toxins of botulism:
• Effect :
-A B C E F  human botulism.
-C D  animal botulism.
-G  not known if human or animal.

17. Toxins
is simple di_chain
protein consisting of:
*100 kd heavy bond 
neuronal attachment
*50 kd light bond 
go inside the cell after
binding

18. Epidemiology

19. Infant botulism
• Reported from all countries except Africa.
• The infant is the only ill member in the Family.
• Age: (3 w-6 m)
(peak 2-4m)
(extreme 3day—382days).
• Sex: equal.
• It is uncommon to diagnose
(in USA 1,448)were reported from 1976:1996).
It is estimated that more than 250 cases of infant botulism occur in the United
States each year,

21. Infant botulism
• Risk factor:
1-ingestion of contaminated honey.
(10% of honey in USA may be contaminated with
spores.
so not used before (6m-1yr)
2- slow intestinal transit time (<1 stool / day).
• Sources of spores ,
home dust,vacuum cleaner dust, contaminated
honey and may corn syrup?.
• Breast feeding
protect against fulmination and sudden death.

23. Food borne botulism
Occur dt ingestion of food in
which C. bot. had multiplied &
produce its toxins.
In USA outbreak was occur
either from canned food or
other food
(e.g. sauté onion , baked
potato, chopped garlic,
peyote tea, hazelnut flavoring
added to yogurt, sweet cream
cheese, sauté onion in patty
melt sandwiches)

24. Food borne botulism
-In USA in the Last 10 yrs 150 outbreak from canned or uncooked food.
-Food with low acid (pH > 6.0) = Home canned food as, jalapeno peppers,
asparagus, olives, beans. ‫والفاصولي‬ ،‫والزيتون‬ ،‫والهليون‬ ،‫جاالبينو‬ ‫الفلفل‬
‫ا‬

25. Food borne botulism
• Type A & B
produce strong putrefactive odor.
• Type E
-appeared in native foods e.g.
fermented salmon egg ,seal flippers
(that not produce sign of spoilage) .
-another hazard of type E is
abilities to grow below 5 c (refrig.)

26. Wound botulism
• Rare disease.
• Occur with traumatic injuries.
• Occur even if no skin breakdown
(crush inj.).
• In the last yrs from injection
abusers (heroin)
(even if no abscess).

27. A heroin user with a wobbly head

30. Global cases of outbreak of human botulism caused by
Clostridium botulinum type A strains.

31. Pathogenesis

32. Pathogenesis
• All 3 form of Disease have
the same path.
Food Contaminated with Clostridium
spores Clostridium grows in
Anaerobic conditions: Produces toxin
Alkaline pH of intestine dissociates
toxin from associated proteins 
toxin is absorbed into circulation
bl. Stream 
preph. Cholinergic synapses 
Irreversible binding 
block Ach. Release 
so impair :
1-neuromusc. transmission.
2-autonomic transmission.

33. Infant botulism
• Ingestion of spores 
spores germination &
multiplication
•  production of toxins in
the large intestine.
• ( So it is infection with
spores)

34. Food borne botulism
• It is intoxication
not infection .
(i.e. ingestion of toxins
in uncooked or improper
preserved food.

35. Wound botulism
• Spores germination and colonization
Of traumatic tissue by C. butilinium.

36. Pathology
• Toxins is not cytotoxin so there is no
microscopic or macroscopic pathology
(autopsy).
• Healing occur by formation of new motor
end plat and re innervations.
(which take about 4w in experimental
animals)

37. Terminal axons at
Neuromuscular junctions
(Rat)
Botulinum toxin induces
enlargement of NMJs
(middle)
& sprouting of nerve
terminals (middle & top)

38. Clinical Picture

39. Clinical Picture
• General role:
it is not possible to have
botulism with out having
multiple bulbar palsies,,
,,,,,,,,,WHY?
As the Toxin is carried by the Blood  &
because bulbar musculature have
(relative high blood Supply + high densities
of innervations).
So  all 3 form of botulism having
symmetric descending flaccid paralysis of
Cr. Nerve musculatures.

42. Infant botulism:
• Very early cases & mild cases
may be missed.
• Early: dec. N. of defecation
constipation or even loss
of defecation.
• Then : inabilities to feed –
week cry- dec. spontaneous
movement.
• Finally : Cr. Nerve palsies

44. Cr. Nerve palsies
• Dys phagia-------- drooling of mouth secretion.
• Diplopia.
• Dry tongue.
• Dropped eye lid (ptosis).
• Dysphonia.
• Dysarthria.
• Dec. gag & corneal reflexes.
• Dilated pupils.
• Occulomotor palsy appear with frequent O/E
(pup. Light reflex).

45. • Loss of head control.
• Respiratory distress -- resp. arrest.
(Descending pattern:
facial  cervical  trunk  limb 
illius  atonic bladder.)

46. drymouth
slurred
double
breathing
swallowing
drooping
blurry muscle

51. N.B.
Fever :
Only present in wound type or in food born
type except if complication.
Par aesthesia :
is not seen in botulism as toxins act only on
motor nerves.
only seen dt , anxiety & hyperventilation.
Sensorium:
pt., remain conscious but its evaluation is
difficult dt., slurred speech.

52. Food born botulism
• Start as GIT symptom:
-nausea ,vomiting.
-diarrhea occur in 1/3 of cases
(it is dt associated organism, metabolic
byproduct of the growth of bacteria).
• Constipation occur once paralysis occur.
• Then Cr. Nerves palsies manifestations.

53. Foodborne botulism in eastern Poland: a hospital-based
retrospective study and epidemiological data review

54. wound botulism
• Clinical Picture,
like food born but
milder.

55. Incubation Period
food borne botulism wound botulism.
( 18-36 hours )
Extremes ( 2 hr—8days )
( 4—14days (
depending on how much poison is in the food

56. Degree of botulism:
• Very mild form:
-minimal ptosis ,
-flattened flaccid expression ,
-minor dysphagia, dysphonia.
• Fulminant form :
-rapid onset extensive paralysis
-RD, apnea.

57. Diagnosis

58. • Clinical picture
is enough for diagnosis
-acute onset of flaccid paralysis
-clear sensorium ,
-no fever , no par aesthesia.
• Laboratory :
- CSF,CBC,CT, MRI ,are normal sometime,
evidence of dehydration or starvation ketosis.
-Plasma nor epinephrine : Reduced

59. • Specific lab: (+ve in 46%)
1) Presence of toxins in serum.
2) Presence of toxins ± organism
in wound + stool.
3)Presence of toxins ± organism in
food ( but large amount is needed)

61. • EMG:
* show defect in N.M. transmission.
• Food born & wound :
potentiation of ! Evoked m. action potential at
higher frequency of stimulation(50Hz).
• Infant type : BSAP
(Brief, Small ,Abundant ,motor unit action Potential)
*Nerve conduction velocities & sensory
nerve function are normal.

63. Differential Diagnosis
 Guillain-Barre syndrome (GBS)
 Myasthenia gravis .
 Tick paralysis.
 Stroke or CNS mass lesion.
 Poliomyelitis.
 Encephalitis.
 Meningitis.
 Organo phosphorus pois.
 Viral polyneuritis.
 Aminoglycosids paralysis.
 Psycatric illness.
 Metabolic coma (DM).

66. Myasthenia gravis
• Dramatic improvement with edrophonium chloride (ie,
a positive Tensilon test)
• although some botulism patients may exhibit partial
improvement following administration of edrophonium
chloride (ie, a borderline Tensilon test)
• EMG shows decrease in muscle action potentials
with repetitive nerve stimulation

68. Aminoglycoside toxicity
—History of recent exposure to
aminoglycoside antibiotics
—More likely to occur in the
setting of renal insufficiency
—Most commonly seen with
neomycin

69. Poliomyelitis
 Febrile illness.
 CSF shows pleocytosis and
increased protein.
 Altered mental status may be
present.
 Paralysis often asymmetric.

70. polioresp

71. Differential Diagnosis
 Guillain-Barre syndrome (GBS)
 Myasthenia gravis .
 Tick paralysis.
 Stroke or CNS mass lesion.
 Poliomyelitis.
 Encephalitis.
 Meningitis.
 Organo phosphorus pois.
 Viral polyneuritis.
 Aminoglycosids paralysis.
 Psycatric illness.
 Metabolic coma (DM).

72. Complication
• Due to:
1- Prolonged hospitalization( ws-ms)
2- Pt is under mech. ventilator.
3- Nnosocomial infections.
4- Iatrogenic.

73. Complication
 ARDS.
 Aspiration.
 OM.
 Pneumonia.
 Tension pneumothorax.
 Recurrent atelactsis.
 Trachiitis.
 Subglotis stenosis.
 UTI , convulsion(<Na) , sepsis , transfution
reaction.,,,,,,

74. Sequels
1- chronic fatigue.
2- incidence of strabismus.

75. Prognosis
 Ventilator dependence frequency:
Type A > B > E .
 Slow improvement in strength over weeks to months
.
 1 year: Most near normal ± fatigue .
 Autonomic function may improve later than weakness
 Mortality: 5% to 10% .
 ~10% of sudden unexpected death in infancy is
caused by botulism