Botulism poisoning

     Botulism is a life threatening paralytic disease caused by the Clostridium botulinum neurotoxin. It can be caused by botulism poisoning with food which contains botulinum toxin or by botulism poisoning through an open wound. The toxin is produced by CB which contaminates traumatic wounds or causes infant botulism. Cb can be get in the gastrointestinal tract and start developing botulism.

Etiology

• Clostridium botulinum, anaerobic Gram-positive;
• There are 6 types to F, the most common cause of human disease are types A, B and E;
• Exotoxina contained by the virus which leads to botulism poisoning is very powerful and it is destroyed by boiling for 10 minutes or by autoclaving in 3 minutes;
• Spores are very resistant, being destroyed by boiling in 5-6 hours and by autoclaving in 30 minutes.

Epidemiology process events

     The disease has a sporadic evolution, or family or community outbreaks.

     The incidence per 100,000 persons in 1998 was 0.18 in UK and 0.28 in the west of the country.

Diagnosis

     Clinical diagnosis

     Incubation: 12-48-hour, rarely up to 6-8 days, the diagnosis for botulism poisoning is as difficult as short as the incubation is.

     Onset: 24-48 hours, loss of appetite, nausea, abdominal pain, diarrhea, constipation, flatulence.

State of the patient suffering from botulism poisoning is characterized by:

• paresis, eye paralysis - intrinsic - accommodation disturbances, mydriasis, fotomotor reflex disappearance, and extrinsic - external strabismus and ptosis for nerve III, VI, internal strabismus, diplopia for IV
• deglutition disorders: dysphagia with esophageal muscle paresis and reduced saliva, wave palate paresis;
• parasympathetic disorder: reducing saliva, nasal, eye dryness, sweat, constipation, bladder paresis;
• other paralysis: the legs - flaccid, symmetrical, with ROT abolished.

     The mood is sometimes altered with insomnia, but consciousness is preserved.

Evolution, clinical forms resulting from botulism poisoning

• super acute form;
• mild forms.

     Healing is slow, paresis and paralysis are healed in months and the accommodation disorders may require correction by glasses.

Prognosis

• serious signs are tachycardia, dyspnea;
• respiratory paralysis can occur with cyanosis.

     Laboratory diagnosis confirms clinical suspicion of botulism poisoning by highlighting the presence of botulinum toxin in serum, stool, stomach content, vomiting and very rarely the bacillus toxin is found in faeces.

     Pathological products: blood, suspect food and feces. Harvested products are sent to reference laboratories.

Bacteriological diagnosis

1. The isolation consist of Clostridium botulinum cultivation from food, liquid vomiting (gastric aspirate) or faeces, in special conditions of anaerobiosis.
2. Identification

     The biological sample on laboratory mice allows the identification and even titration of botulinum toxin in patient's serum. The method consists of injecting the patient's serum (collected sterile) in equal doses, intraperitoneally, in several pairs of mice, one partner from each pair being previously protected with a known dose of botulinum antitoxin (7 antigenic types denoted A to F ). Within 24 hours a single mouse will survive, namely the one protected with antitoxin serum corresponding to the patient's toxin.

     The faster this identification is being made, the greater the chances therapeutic. The patient will be given monovalent serum toxin exactly matching the type of the toxin, even if he was initially given polyvalent antitoxin serum.

Epidemiological data

• Reservoir of infection - intestine of animals, fish, where you can remove and contaminate soil, water and other environmental elements
• Botulism poisoning by eating contaminated fruit, vegetables, canned or smoked food
  Not always does the retainer looks different from other good, healthy cans. The same goes for food which might look healthy but isn't in fact.
  Conditions that favor the production of botulinum toxin are: temperature 22-370C, pH> 4.6 and alkaline environment, direct contact of a wound with soil or contaminated objects.
• General Responsiveness
• Short-term immunity

Prevention and control

     Measures against the source of infection

     Screening: epidemiological, clinical and laboratory

     Declaring: nominal monthly

     Isolation: immediate internment, isolation is not necessary.