new update 2019 for botulism ,for training of rural health care physician on early detection of the disease.

2. botulismBY
Dr, WLAA SALAH MANAA
SPECIALEST OF PEDIATRIC
‫الشيخ‬ ‫كفر‬ ‫حميات‬ ‫مستشفى‬

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.

14. Etiology

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

16. Its natural habitat:
soil ,dust,
marin sediment

19. Cbotulinum

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

21. 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.

22. • Action: block
neuromuscular
junction
transmission

23. • 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.

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

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

26. Epidemiology

27. Infant botulism
• Reported from all coutries except Africa.
• Notably, 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,

28. 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.

30. 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)

31. 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. ،‫جاالبينو‬ ‫الفلفل‬
‫والفاصوليا‬ ،‫والزيتون‬ ،‫والهليون‬

32. 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.)

33. 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).

35. A heroin user with a wobbly head

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

38. Pathogenesis

39. 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.

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

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

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

43. 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)

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

45. Clinical Picture

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

48. 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

49. 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).

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

51. drymouth
slurred
double
breathing
swallowingdrooping
blurry muscle

56. 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.

57. 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.

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

59. 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

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

61. Diagnosis

62. • 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

63. • 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)

65. • 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.

67. 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).

69. Guillain-Barre syndrome (GBS)
particularly Miller Fisher variant)
• ascending paralysis
• Miller Fisher variant may be descending
• Abnormal CSF protein 1-6 wk after illness
onset
• Paresthesias commonly occur.
• EMG shows abnormal nerve conduction
velocity;
• Outbreaks of GBS do not occur (unlike
botulism)

71. 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

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

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

75. polioresp

76. 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).

77. Complication
• Due to:
1- prolonged hospitalization( ws- ms)
2- pt is under ventilator.
3- nosocomial infections.
4- iatrogenic.

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

79. Sequels
1- chronic fatigue.
2- > incidence of strabismus.

80. 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