botulism dr/ mona m. awny assistant lecturer of forensic medicine & clinical toxicology
TRANSCRIPT
Botulism
Dr/ Mona M. AwnyAssistant lecturer of forensic
medicine & clinical toxicology
Food poisoning
Most common bacterial food-borne pathogens:
Clostridium botulinum Clostridium perfringens Escherichia coli Staphylococcus aureus Bacillus cereus Vibrio cholera
Clostridium botulinum ?
Gram +ve anaerobic bacillus that release neurotoxin “Botulin”.
Clostridium botulinum: Toxin types: A / B / C alpha / C beta D / E / F / G
Physical properties:
- Spores withstand 100 c for hours.
- Toxins are heat-labile and destroyed by boiling for 10 min. or heating at 80 c for 30 min.
Food sources
Mainly not exposed to heat:
1. Salted fish “Fesikh”
2. Honey
3. Uncooked cold meat “Beef”
4. Home canned food
Botulism
Fatal condition caused by ingestion of improperly preserved or canned food
Types of Botulism Food related botulism: Classic
botulism and Infant botulism Wound botulism
Dissemination of toxins
Toxins are distributed to target sites via hematogenous dissemination
Toxins act on the presynaptic part of neuromuscular junctions leading to decreasing the amount of ACH release
Mechanism of action “Neurotoxicity”
Clinical presentation Symptoms & signs develop within 12 –
36 hrs after ingestion Severity of disease depends on type of
toxin (type A gives most severe picture)
1. GIT symptoms
2. Anticholinergic symptoms
3. Neurological symptoms
1. Initial vague & GIT symptoms:
Malaise, weakness, dizziness, diplopia & blurred vision
Nausea, vomiting, diarrhea or constipation
2. Anticholinergic manifestations:
Dry mucous membranes Markedly dilated pupils & blurred vision Urinary retention (palpable urinary
bladder) Absent bowel sounds & abdominal
distention No hyperthermia or tachycardia
3. Neurological manifestations:
Cranial nerve palsy Bilateral symmetrical descending flaccid
paralysis of:
1. Bulbar musculature
2. Limbs
3. Resp. muscles & diaphragm No sensory loss Normal mental status
Cranial nerve palsy
Motor cortex
Bulb/brainstem
Bulbar musculature
Bulbar musculature
Eye movement
M. of facial expression
Speaking & swallowing
Symmetrical descending flaccid paralysis
Diaphragm
No sensory lossNormal mental statusDeath from respiratory
failure
Investigations
1. General tests:
ECG Abdominal U/S CSF Pulmonary function tests ABG
Investigations
2. Toxin-specific tests: C. botulinum toxin or spores in serum,
stool, gastric contents or wound specimens
Electromyography (EMG): Shows a defect in transmission at the
neuromuscular junction
Differential diagnosis
Guillian-Barre syndrome: Ascending paralysis, ↑CSF protein, normal
EMG Cerebrovascular stroke: Asymmetric Poliomyelitis: Fever & meningeal signs Anticholinergic poisoning: Fever & altered mental status
Management
1. General: ABC’s (early elective tracheostomy &
mechanical ventilation) Emesis & gastric lavage Nasogastric suction (ileus) Foley catheterization (urine retention)
Management
2. Toxin-specific measures:
Trivalent ABE antiserum Sensitivity test Dose: 1 vial IM & 1 vial IV A dose/ 4hrs if serum toxin persists
Follow-up & disposition
Admission to ICU Monitoring of vital capacity & vital signs Prolonged hospitalization Slow recovery Rehabilitation program Complete recovery of paralysis takes up to
6 months
Wound botulism
Soil Symptoms Wound swab Antitoxin,
debridement, high-dose IV penicillin
Prevention