botulism dr/ mona m. awny assistant lecturer of forensic medicine & clinical toxicology

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