Botulism - Clostridium infection

1. BOTULISM
 YUZBASHEVA NIHAL 221B
 AZERBAIJAN MEDICAL
UNIVERSITY
 INFECTIOUS DISEASES
DEPARTMENT

2. botulism(n.)
 "poisoning caused by eating imperfectly
preserved food," 1878, from German
Botulismus (1878), coined in German
from Medieval Latin botulus "sausage"
(see bowel) + -ismus suffix of action or
state (see -ism). The sickness first was
traced to eating tainted sausage
(sausage poisoning was an old name for
it).

3. Etiology

4. Characteristics
 Gram-positive obligate anaerobic
motile baccilus
 Spore-forming
 Toxin-forming
 Heat sensitive
 Prefers low acid environment
 Causes Botulism disease

5. Toxins
 8 types of toxins (A, B, C1, C2, D, E, F,
and G), all except C2 are neurotoxins;
C2 is a cytotoxin of unknown clinical
significance
 Toxins A, B, E and F cause illness in
humans
 Type G (from C. argentinense) has been
associated with sudden death, but not
with neuroparalytic illness
 In our country more prominent: A, B
and E

6. Botulinum
neurotoxin

7. Epidemiology

8. Epidemiology
 Food-borne botulism is associated
primarily with home-canned food
(particularly vegetables, fruit, and
condiments) and less commonly with
meat and fish
 Foodborne botulism can occur when :
 (1) food to be preserved is
contaminated with spores
 (2) preservation does not inactivate
the spores but kills other putrefactive
bacteria that might inhibit growth of C.
botulinum and provides anaerobic
conditions at a pH and temperature
that allow germination and toxin
production,
 (3) food is not heated to a temperature
that destroys toxin before being eaten.

9. Epidemiology
 Other types of Botulism disease:
- Wound Botulism
- Drug Abuser’s Botulism
- Newborn’s Botulism
- Intestinal Botulism
- Bioterrorism and Biologic Warfare

10. Pathogenesis

11. Pathogenesis

12. Pathogenesis
 Main targets of botulinum toxin:
- Motor neurons of medulla oblongata
- Motor neurons of spinal cord
- Mostly specific for cholinergic neurons

13. Pathogenesis
- Decreased function of respiratory
muscles
- Paresis of intercostal nerves,
diaphragm
- Functional dysfunctions in upper
respiratory airways
- Formation of mucus in respiratory
airways
- Hypoxia

14. Pathogenesis
- Decreased secretion of saliva, gastric
acid
- Secondary infections due to previous
notion
- Dysfunctions in the innervation of the
esophagus
- Continuous paresis of the
gastrointestinal tract
- Increased fragility of blood vessels’
walls, and their paresis
- Decreased phagocytic function of
leukocytes
- Abnormalities in the erythrocyte
metabolism

15. Pathogenesis
 Types of hypoxia that develops:
- Hypoxic
- Histotoxic
- Hemic
- Circulator

16. Pathological
Anatomy
 Non-specific and mainly related to the
development of hypoxia
 Hyperemia of internal organs
 Destructive and degenerative changes
of the nervous system
 Small hemorrhages of the mucous and
serous layers of the GI
 Grayish presentation of the muscles
 Dilated vessels, congestion in the
capillaries
 Swelling of muscle fibers

17. ClinicalFindings
 Incubation period: 2-12hours up to
7days but can be as long as 12days
 Incubation period and severity of the
disease is inversely proportional mostly
 Develops independently from alcohol
intake
 Acute start

18. ClinicalFindings
 Starts mostly with 3 symptoms:
- Dyspeptic disturbances
- Visual disturbances
- Respiratory insufficiency

19. Dyspeptic
Disturbances
 Gastroenteritis and general
intoxication
 Nausea and vomiting
 Abdominal pain
 Diarrhea
 Fullness in the stomach and belching
 Subfebrile temperature
 The feeling of “something stuck” in the
esophagus

20. Dyspeptic
Disturbances

21. Visual
Disturbances
 Begins to appear at the end of the first
day
 Decreased vision, blurry vision, web in
front of the visual area
 Disturbances of accommodation
 Diplopia
 Ptosis (in severe cases non-ability to
open the eyes)
 Decreased reaction to the light
 Mydriasis, anisocoria, horizontal
nystagmus, strabismus
 Decreased mobility of the eye balls

22. Visual
Disturbances

23. Visual
Disturbances

24. Bulbar
Symptoms
 Arises due to damage of the IX and XII
nerves
 Painful swallowing and chewing act
 Pharyngeal paresis (causes food to
stuck in the respiratory airways)
 Paresis of the soft palate (causes
liquids to come out of the nose)
 Hoarseness of the voice
 Absence of sensory involvement and
intact deep tendon reflexes

25. Muscle
Weakness
(Hypotonia)
 First symptoms in occipital muscles
 Non-ability to keep head straight
 Paresis of skeletal muscles
 Weakness of intercostal and phrenic
muscles
 Shortness of breath
 Non-ability to cough or to release
sputum
 Hypercapnia, respiratory acidosis

26. Muscle
Weakness
(Hypotonia)

27. Muscle
Weakness
(Hypotonia)

28. Mask
Face

29. Terminal
Period
 Worsening of the neuroplegia
 Severe respiratory insufficiency which
is mostly one of the leading causes of
the deat

30. OtherClinical
Findings
 No significant changes in peripheral
blood
 Can be mild and latent form of the
disease as well
 Moderate-severe form accompanied by
different degree of development related
symptoms
 Slow healing process accompanied by
diminishing of hyposalivation as one of
the first indications

31. Wound Botulism
and
Neonatal
botulism
 Absence of GI and intoxication
symptoms
 Longer incubation period (4-14days)
 Nervous system symptoms are
characteristic
 More common in neonates using
artificial food
 Can be accompanied by weakness,
constipation, rejection of food in
neonates

32. Complications
 Aspiration pneumonia
 Inflammatory parotitis
 Secondary bacterial infections
 Botulism Myositis
 Infectious myocarditis and myopia
 Prognosis is bad and causes death in ¼
of cases

33. Diagnosis
 Anamnesis and clinical symptoms
 Demonstration of toxin by bioassay of
mice (may have negative result in case
of wound and neonatal botulism)
 Wound cultures yielding the organism

35. Treatment
 Patients should be hospitalized and
monitored closely, both clinically and
by spirometry, pulse oximetry, and
measurement of arterial blood gases for
incipient respiratory failure.
 Intubation and mechanical ventilation
should be strongly considered when the
vital capacity is <30% of predicted,
especially when paralysis is
progressing rapidly and hypoxemia
with absolute or relative hypercarbia is
documented

36. Treatment
 Treatment should not await laboratory
analyses, which may take days.
 Bivalent preparation containing toxin
types A and B and an investigational
monovalent type E preparation can be
obtained.
 The bivalent preparation is
administered routinely; monovalent
type E antitoxin is given in addition
when exposure to type E toxin is
suspected (after seafood ingestion, for
example).
 Neither the use of antibiotics to
eliminate an intestinal source of
possible continued toxin production nor
the administration of guanidine
hydrochloride and other drugs to
reverse paralysis is of proven value.

37. Treatment

38. <3