Clostridium botulinum disease

Clostridium botulinum

GATHER BY BEHROUZ LATIFI

Introduction Clostridium botulinum: Gram Positive Rod , Spread everywhere

including water, earth, vegetable… Spore forming ,inactivated at higher temp

Anaerobic Spore forming ,inactivated at higher temp

Anaerobic Seven neurotoxin whose subtypes labeled

A_G ,All causes flaccid paralysis

Classification Class : Clostridia

Order : Clostridiale

Family : Clostridiaceae

Genus : Clostridium

Species: C. botulinum

History and Epidmiology Botulism = Botulus

For the first time the disease was eating sausages In U.S.A average 145 cases each year Approximately 15% food borne Approximately 65% infant form Approximately 20% wound form In IRAN : Gilan whit 79 case during 5 year the

most and Western Azerbaijan whit 4 case during 5 year least

Transmission 1) Ingestion organism spores neurotoxin

2) Wound contamination

3) Inhalation

Botulism Pathagenesis

Toxin inter blood stream from mucosal or wound bind to peripheral cholinergic nerve ending inhibits release of acetylcholine. preventing muscle from

contracting can result from airway obstruction or paralysis of respiratory

muscles

secondry complication related to prolonged ventilatory supportand intensive care

Human disease human contaminated by neurotoxin type A, B, E, F Type A is powerful toxin know in the earth type A Infection dos 0.09ng/kg So that a person weighing 90kg

with 0.9ng toxin A dies

three form disease :

Foodborne Wound Infant

Food borne botulism Second most common form caused by toxin ingested form contamination food including conserve, packing food, vegetable,

hot dog, kielbasa

Food borne botulism symptoms 12-36 h after Muscle weakness Diarrhea Blurred vision Vomiting Eventual paralysis

Wound botulism Organism and spore inter wound Develop under anaerobic conditions From ground in dirt or gravel It does not penetrate intact skin Associated whit addicts of black _ tar heroin

Infant botulism

Babies eat honey Most common form Affects babies from 1 week _ 1 year

Caused by

Ingestion contaminated food stuff Lack of breast milk House hold dust containing spores

Infant clinical signs Poor feeding Many gag Weak cry Decreased movement Appearing lethargic Flat, blunted facial expression Decreased muscle tone( hypotonia )

Adult clinical signs Nausea, vomiting, diarrhea Double vision Difficulty speaking or swallowing Descending weakness or paralysis Shoulders to arms to thighs to caw Symmetrical flaccid paralysis Respiratory muscle paralysis Causes temporary muscle paralysis that may take 3 to 6 months

Diagnosis

clinical signs Toxin in serum, stool, suspected food, gastric aspirate Culture of stool or gastric aspirate

(egg yolk agar , sxt ) Mouse neutralization test

Treatment Botulinum anti toxin Botulism immunoglobulin

Washing the stomach and the administration of antitoxin three valent( A ,B , E)

Penicillin , Metronidazole , Guanidine hydrochloride

Animal botulism Cattle and sheep (type C , D) Doge ( type C and few D )

Horses ( type B , C )

Foal ( type B )

Birds , poultry ( type C , E )

Achalasia Clinical: a primary esophageal motility disorder characterized by

the absence of esophageal peristalsis and impaired relaxation of the lower esophageal sphincter (LES) in response to swallowing

Pathophysiology: a failure of smooth muscle fibers to relax, which can cause a sphincter to remain closed and fail to open when needed

Treatment: Mechanical(pneumatic dilation) Medical(botulinum toxin) Surgery( heller myotomy )

botox Botulinum toxin A

Bioterrorism Many countries :

Botulinum toxin as a biological weapon potential bioterrorism threat

A one-liter bottle of the toxin (type A ) could kill the entire population of Earth

Thanks…