Clostridium botulinum (Botulism)

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Clostridium botulinum (Botulism)

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Clostridium botulinum (Botulism)

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The antitoxin used for botulism is (a passive/an active) vaccine.

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A 1-year-old infant boy is brought to the emergency department because of a 2-day history of poor feeding and constipation. His medical history is noncontributory. Upon further interrogation, the mother claims that she recently started sweetening his meals with honey. Physical exam shows generalized muscle weakness. His temperature is 36.5°C (97.6°F), pulse is 70/min, respirations are 16/min, blood pressure is 120/80 mmHg.  Which of the following mechanisms best explains the pathogen that is affecting this child? 

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Clostridia, as a family, are obligate anaerobes, meaning that oxygen is toxic to them.

In nature, they thrive in deep, compact soil, and when they feel the stress of fresh oxygenated air, they often produce spores, which are metabolically inert and extremely resilient to the environment.

Then, when environmental conditions improve, the spores are able to sprout into fully fledged Clostridia.

When doing a Gram stain, Clostridium botulinum stains purple, or Gram positive, and it’s a bacillus, meaning that it looks like a big cylinder or rod under the microscope.

Clostridium botulinum is notorious for producing a toxin, called botulinum toxin, which causes botulism.

Historically, to preserve foods, processes like sausage making and canning became popular.

Unfortunately, since these environments block out air, if a Clostridium botulinum spore gets in during the food preparation process, it can grow and produce botulinum toxin, contaminating the food.

In fact, this is how Clostridium botulinum gets its name, since botulus means sausage in Latin.

When it infects a can, the can begins to bulge with air because the bacteria metabolized sugars into short chain fatty acids that form a gas.

And although the short chain fatty acids are mostly made up of carbon dioxide and hydrogen, the gas is particularly foul smelling.

Now, nerves that use the neurotransmitter acetylcholine are those we use for muscle control.

Upon ingesting a contaminated food product, botulinum toxin works by binding specifically to these nerves, inhibiting muscle contraction.

The toxin comes in eight distinct types, named type A, B, C, D, E, F, G, and H, and they vary in their toxicity.

The neuron takes in the botulinum toxin by endocytosis, creating a small vesicle that floats within the neuron’s cytoplasm.

The toxin then activates and slips out of the vesicle, and starts to cleave SNARE proteins.

SNARE proteins tug vesicles containing acetylcholine to the plasma membrane, where they get released into the synapse, and transmit a signal to the muscle.

Without SNARE proteins, acetylcholine doesn’t get released, and no signal is sent out by the affected nerves.

The result is that muscles get completely relaxed and flaccid.

Muscle weakness usually starts in the muscles supplied by the twelve cranial nerves - so, the muscles that control the face, eye movements, chewing and swallowing.

In addition, nerves of the autonomic nervous system that rely on acetylcholine are also affected.

Early on, botulism can cause a bulbar palsy, or impairment of cranial nerves IX, X, XI and XII, and over time there may be a descending paralysis.