23 year old patient is demonstrating severe face and muscle spasms. Patient has fresh tattoo obtained from a "sketchy" tattoo parlor. Blood results show he is infected with Clostridium Tetani, a bacterium that is transmitted by dirty needles. Patient was never vaccinated against this bacterium.

Upstream Causes

Direct Cause - The direct cause is due to the tattoo parlors dirty needles used when given the tattoo, which was contaminated with Clostridium Tetani.

Indirect Cause - Possible indirect cause is lack of choosing a sterile tattoo parlor and not being vaccinated against the bacterium.

Background Information

Systems Involved in this case map

Nervous system

Lymphatic system

Muscular system

Immune systen

The Nervous system receives, integrates, and responds to information.

Sensory Input - Nervous system uses sensory receptors to monitor changes occurring both inside and outside the body. Gathered information is called sensory input.

Integration - processes and interpets sensory input and make decisions

Motor output - the nervous system activates effector organs, the muscles and glands, to cause a response.

CNS PNS SNS ANS

CNS - includes brain and spinal cord, integrative and control centers.

PNS - Cranial nerves and spinal nerves, communication lines between the CNS and the rest of the body.

SNS - Somatic (voluntary) motor nerve fibers, Conducts impulses from CNS to skeletal muscles

ANS - visceral (involuntary) motor nerve fibers, Conducts impulses from the CNS to effectors (muscles and glands)

Events at the Neuromuscular Junction

  1. Action potential arrives at axon terminal of motor neuron.
  1. Voltage gated Ca2+ channels open. Ca2+ enters the axon terminal, moving down its electrochemical gradient.
  1. Ca2+ entry causes ACh (a neurotransmitter) to be released by exocytosis.
  1. ACh diffuses across the synaptic cleft and binds ACh receptors on the sarcolemma
  1. ACh binding opens chemically gated ion channels that allow simultaneous passage of Na+into the muscle fiber and K+ out of the muscle fiber. More Na+ ions enter than K+ ions exit , which produces a local change In the membrane potential called the end plate potential.
  1. ACh effects are terminated by its breakdown in the synaptic cleft by acetylcholinesterase and diffusion away from the junction

Skeletal muscle contraction

Events at Neuromuscular Junction

A motor neuron fires an action potential down its axon

the motor neurons axon terminal releases ACh into the synaptic cleft.

ACh binds receptors on the junctional folds of the sarcolemma.

ACh binding causes a local deporlization called an end plate potential

muscle fiber excitation

The local depolarization triggers an AP in the Adjacent sarcolemma

Excitation contraction coupling

AP in sarcolemma travels down T tubules

Sarcoplasmic reticulum releases Ca2+

Ca2+ binds to troponin which shifts tropomyosin to uncover the myosin binding sites on actin. myosin heads bind actin

Cross bridge cycle

Contraction occurs via cross bridge cycling

Muscle Twitch

The response of a muscle to a single simulation. The muscle fibers contract quickly and then relax.

Latent period - first milliseconds following stimulation when excitation contraction coupling is occurring.

period of Contraction - cross bridge is active

period of relaxation - pumping of Ca2+ back into SR

Temporal or wave, summation

two identical stimuli are delivered to a muscle in rapid succession, the second twitch will be stronger

contributes to contractile force, creates smooth muscle, and continuous muscle contractions by rapidly stimulating specific number of muscle cells

Incomplete tetanus

the degree of wave summation becoming greater and greater , progressing to sustain a quivering contraction

complete tetanus

Evidence of muscle relaxation disappears and contractions fuse into smooth, sustained contraction plateau

Clostridum Tetani

is an obligate anaerobic bacteria whose spores produce two distinct toxins, tetanolysin, which causes local tissue destruction, and tetanospasmin, which causes clinical tetanus.

Tetanus neurotoxin binds to the presynaptic membrane of the neuromuscular junction, is internalized and transported to the spinal cord.

The spastic paralysis induced by the toxin is due to the blockade of neurotransmitter release from spinal inhibitory interneurons.

Widespread intoxication through the systemic circulation results in continuous involuntary muscle contraction of clinical generalized tetanus, whereas local internalization and transport of toxin can result in a localized state of muscle hyperexcitability.

Graded Muscle Contractions

An in increase in the frequency of stimulation causes TEMPORAL SUMMATION.

The higher the frequency, the greater the strength of contraction of a given motor unit.

An increase in the strength of stimulation causes RECRUITMENT

The stronger the stimulation, the more motor units are activated, and the stronger the contraction.

Motor or efferent neuron

carry impulses away from the CNS to the effector organs ( muscles or glands) of the body.

Motor neurons are Multipolar.

Sensory or afferent neurons

transmits impulses from sensory receptors in the skin or internal organs toward or into the central nervous system.

Theses neurons are unipolar

cell bodies are located outside in sensory ganglia outside the CNS

Downstream effects

Effect 1

Effect 2

Effect 3

Effect 4

tetanus toxin is transferred to inhibitory presynaptic terminals surrounding motor neurons. The toxin then destroys a vesicular synaptic membrane protein

This will result in inactivation of inhibitory neurotransmission that normally suppresses motor neuron and muscle activity

Because inhibitory neurotransmission is inactivated. suppression of motor neuron and muscle activity will not occur

This will cause the patients muscles to experience enhanced excitability and activation of the affected motor neurons.

Patient is now experiencing a widespread of the toxin. Leading to enhanced excitability and activation of the affected motor neurons

Patient possibly received the bacterium via needle onto is arm, the toxin is considered to be in a localized state which has resulted in muscle hyperexcitabillity.

Because the toxin is starting to cause muscle spasms in the arm this will result to a widespread intoxication through the circulatory system.

Patient will then begin to experience continuous involuntary muscle contractions such as muscle spasms of the face leading to inability to speak.