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Raphael Adolfo MEB31

1. Explain the consequence of TETANUS and BOTULISM in skeletal muscle contraction.

Tetanus is a noncommunicable disease, meaning that it cannot be passed directly from one
person to another. Tetanus causes convulsive muscle spasms and rigidity that can lead to respiratory
paralysis and death. It is sometimes called "lockjaw" because one of the most common symptoms is a
stiff jaw that cannot be opened. Sometimes tetanus is localized, that is; it affects only the part of the
body where the infection began. However, in almost all reported cases, tetanus spreads to the entire
body.
Tetanus is caused by a bacterium called Clostridium tetani, whose spores (the dormant form)
are found in soil, street dust, and animal feces. The bacteria enter the body through cuts and abrasions
but will multiply only in an environment that is anaerobic, or oxygen-free. Deep puncture wounds and
wounds with a lot of dead tissue provide an oxygen-free environment for the bacteria to grow. As C.
tetani grows, it excretes a highly poisonous toxin called tetanospasmin into the bloodstream, spreading
it throughout the nervous system. The infection is usually transmitted through deep puncture wounds
or through cuts or scratches that are not cleaned well. Tetanus toxin affects the nerve endings, causing
a continuous stimulation of the muscles. Initial symptoms may include restlessness, irritability, a stiff
neck, and difficulty swallowing.

Botulism is an acute, progressive condition caused by botulinum toxin, a natural poison


produced by the spore-forming bacteria Clostridium botulinum. Exposure to the botulinum toxin
usually occurs from eating contaminated food although, in infants, it may be caused by specific types
of clostridia obtained from soil or inhaled spores, causing growth of the bacteria in the infant's
intestine. Breathing may be severely compromised in progressive botulism because of failure of the
muscles that control the airway and breathing. Three types of botulism have been identified: food-
borne, wound, and infant botulism.
In humans, botulinum toxin latches onto specific proteins in nerve endings and irreversibly
destroys them. These proteins control the release of acetylcholine, a neurotransmitter that stimulates
muscle cells. With acetylcholine release blocked, nerves are not able to stimulate muscles. Ironically,
this action of the botulinum toxin has given it a beneficial niche in the world of medicine. Certain
medical disorders are characterized by involuntary and uncontrollable muscle contractions. Medical
researchers have discovered that injecting a strictly controlled dose of botulinum toxin into affected
muscles inhibits excessive muscle contractions. The muscle is partially paralyzed and normal
movement is retained.
2. Describe MYASTHENIA GRAVIS and give its consequence to the process of muscular contraction.

Myasthenia gravis (MG) is a chronic autoimmune disease characterized by fatigue and muscular
weakness, especially in the face and neck that results from a breakdown in the normal communication
between nerves and muscles caused by the deficiency of acetylcholine at the neuromuscular (nerve-
muscle) junctions. MG is the most common primary disorder of neuromuscular transmission. MG is a
chronic autoimmune neuromuscular disease characterized by varying degrees of weakness of the
skeletal (voluntary) muscles of the body. The hallmark of this disease is muscle weakness that increases
during periods of activity and improves after periods of rest. Muscles that control eye and eyelid
movements, facial expression, chewing, talking, and swallowing are often, but not always, involved.
The muscles that control breathing and neck and limb movements may also be affected.

Myasthenia gravis is an autoimmune disease caused by abnormal antibodies carried in the


blood stream. Nerves release a chemical called acetylcholine (ACh) that activates receptors on muscles
to trigger contraction. The normal neuromuscular junction releases ACh from the motor nerve terminal
in discrete packages (quanta). The ACh quanta diffuse across the synaptic cleft and bind to receptors
on the folded muscle end-plate membrane. Stimulation of the motor nerve releases many ACh quanta
that depolarize the muscle end-plate region and then the muscle membrane, causing muscle
contraction. The myasthenia antibodies interfere with this process by binding to specific sites on the
surface of the muscles, the post-synaptic muscle membrane is distorted and simplified, having lost its
normal folded shape. The most common antibodies are directed against the muscle acetylcholine
receptor (AChR). ACh is released normally, but its effect on the post-synaptic membrane is reduced.
The post-junctional membrane is less sensitive to applied ACh, and the probability that any nerve
impulse will cause a muscle action potential is reduced.

References:
http://www.tox.si/novice/zadnja-novice/92-tetanus-toxin-vs-botulinum-toxin-neurotoxins-produced-by-
bacterias-clostridium-tetani-and-clostrid
http://www.ninds.nih.gov/disorders/myasthenia_gravis/detail_myasthenia_gravis.htm
http://iai.asm.org/content/80/5/1662.full
http://www.mda.org.nz/media/1244/Myasthenia%20Gravis%20April10.pdf
http://www.encyclopedia.com/medicine/diseases-and-conditions/pathology/botulism
http://www.encyclopedia.com/medicine/diseases-and-conditions/pathology/tetanus
http://www.encyclopedia.com/medicine/diseases-and-conditions/pathology/myasthenia-gravis

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