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Botulism is caused by a toxin produced by the bacterium Clostridium botulinum. There are 7 types of C. botulinum (A-G) that can produce distinct toxins. The toxins are absorbed in the small intestine and paralyze involuntary muscles, which can lead to death if not treated. Symptoms include nausea, vomiting, difficulty swallowing and breathing. The bacteria spores can survive in improperly canned foods and produce toxin when conditions allow the bacteria to grow. The toxin prevents the release of acetylcholine at neuromuscular junctions, inhibiting muscle contraction.

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G Edited

Botulism is caused by a toxin produced by the bacterium Clostridium botulinum. There are 7 types of C. botulinum (A-G) that can produce distinct toxins. The toxins are absorbed in the small intestine and paralyze involuntary muscles, which can lead to death if not treated. Symptoms include nausea, vomiting, difficulty swallowing and breathing. The bacteria spores can survive in improperly canned foods and produce toxin when conditions allow the bacteria to grow. The toxin prevents the release of acetylcholine at neuromuscular junctions, inhibiting muscle contraction.

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rishiraj.pgdm12nc
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© © All Rights Reserved
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Download as DOCX, PDF, TXT or read online on Scribd
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Botulism

Introduction: Botulism is a disease caused by the ingestion of food


containing some neurotoxin secreted by Clostridium botulinum.
This is a rod-shaped soil bacterium, which is saprophytic in nature, forms spores,
gas forming and anaerobic also. There are seven types of this bacteria found
based on their serological specificity of toxins. The different types are of
following-
1. Type A: It is the commonly causing human botulism in the western part of
United States.
2. Type B: found more often found than type A in all over the world and less
toxic for human beings.
3. Type C: Causes botulism in fowls, cattle, mink, and other animals but this
type does not harmful for human.
4. Type D: Associated with forage poisoning of cattle and basically found in
South Africa.
5. Type E: it is toxic for humans and chiefly obtained from fish and fish
products.
6. Type F: except its toxins, it is similar to type A and B, it is first isolated in
Denmark and produces human botulism.
7.Type G: Has isolated from the soil of Argentina but has not been implicated
in human botulism.

Growth and Toxin production:


Toxin production by C. botulinum depends on the ability of cells to grow in a food
and autolyze there. For type A, B, E, F toxins are synthesized as large,
comparatively inactive protein which becomes toxic after hydrolysis.
Factors that influence toxin production that are Composition of the medium, time
of storage, temperature, PH, OR potential, salt concentration etc.
Toxin production generally occurred in fish, meat, low or high acid canned foods
etc. the concentration of sodium chloride is useful to prevent the growth and
toxin production. A PH near neutrality favors the growth of c. botulinum. Ph of 4.5
or lower prevents the toxic production. Temperature is an important factor which
decides that the occurring of toxin production and the rate of toxin production.
35 degree is ideal for the toxin production of proteolytic strains and 28 degree is
for the non-proteolytic strains.

The Toxin:
The toxin of C. Botulinum is a protein that is purified and crystallized. It is
generally absorbed in the small intestine and it paralyzes the involuntary muscles
of our body. The heat treatment is necessary to destroy the toxin but it depends
on the medium it is heated. Heat treatment of 5 minutes at 80 degrees and 15
minutes at 90 degrees is sufficient for inactivating the A and B toxin. The growth
of C. Botulism in some foods results in rancid odor and also cause putrefaction.

The Disease:
People who are susceptible to botulism that if considerable amounts of toxin
present in the food they have taken and consumption of these foods may results
in illness and death also. The symptoms of this disease typically occur within 12 to
36 hr. The earliest symptoms are the acute digestive disturbance followed by
nausea, vomiting, and diarrhea along with fatigue, headache etc. later
constipation may occur also. Problems like double vision difficulty in swallowing
and speaking also have been seen. In this disease the swallowing of the tongue,
dryness of mouth and constriction of throat also noted. Involuntary muscles get
paralyzed first which will gradually spread to respiratory system and heart and
resulting in death by respiratory failure. Symptoms for A, B, E is similar but
nausea, vomiting and urinary retention is more severe in type E toxin. In fatal
cases, death usually occurs in 3-6 days after the poisonous food had been
ingested.
The following conditions are necessary for the outbreak of botulism-
 Presence of the spores of C. botulinum of type A, B, and E in foods.
 The food must allow the germination of spores and the growth of clostridia.
 Survival of the spores of the organism.
 Environmental conditions after processing.
 Insufficient cooking.
 Ingestion of toxin-bearing food.

Pathogenesis:
C. botulinum produces neurotoxins (BoNTs) which associates with other proteins
like hemagglutinin and other non-toxic neurotoxin associated proteins (NAPs) and
forms a large complex. These associated proteins protect the neurotoxin in from
harsh acidic environments and digestive proteases present in the host’s digestive
tract. These proteins also facilitate the absorption of neurotoxin in the general
circulation by disrupting the layer of cells which results in the formation of a
protective barrier. BoNT flows in the bloodstream until it reaches neuromuscular
junctions situated between endings of neurons and muscle cells. The heavy chain
of toxin binds to cell surface receptors and mediates the internalization process
via endocytosis. The heavy chain then enters the endosome, allows the light chain
to escape. The synaptic vesicles present in the nerve endings contain the
acetylcholine. SNARE proteins involve these vesicles to fuse with the cell
membrane in response to an electrical signal (Figure 2). After that Acetylcholine
is released in the synapse and binds to receptors and induces the muscle
contraction. The light chain of toxin cleaves these SNARE proteins, resulting in the
inhibition of the release of these neurotransmitters and causes muscle paralysis
(Figure 3).

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