Clostriduim tetani Infection TETANUS
Direct cause
Cardiovascular instability spasms cause respiratory failure, fractures, tendon rupture.
affected organs/organ system: Neuro-muscular junction, peripheral motor end plates spinal cord, brain, sympathetic nervous system
Abdominal and limb muscle stiffness opisthotonus (spine arch backwards) seizures, tachycardia headache, fever, diarrhea, high blood pressure, powerful and painful muscle contractions (tetany)
Recent wound punctures lock jaw, neck and chest stiffness, difficulty in swallowing, muscle rigidity spasms of face and arm
induces long term potentiation (LTP) of GABA receptor mediated fast inhibitory post synaptic potential
steps of internalization
Endocytosis mediated bye the heavy chain
Retrograde transport across alpha motor neuron
binds to receptors and acidic lipids
Release of toxins to presynaptic space. Ganglioside-recognition domain in the heavy chain C terminal, binds neuronal gangliosides and allowa toxin internalization
Toxins adsorb to the negatively charged presynaptic membrane of the peripheral nerve terminals
Binding to inhibitory neuron membrane and Re-internalization
Endocytosis, traslocation of toxininto the cytosol, Light, chain cleaves the SNARE complex
Inhibition of VAMP complex
Treatment: Anticonvulsanta (diazepam),skeletal muscle relaxants (baclofen), Drugs including antibiotics such as erythromycin, penicillin, chloramphenicol, tetracycline is most effective. Tetanus vaccine/toxoid (tetanospasmin inactivated in formaldehyde) protects host from the effets of toxin
Tatanospasmin: contain heavy chain that helps binding to neuronal gangliosides and a light chain that exerta biological effet of the toxin
Positive with acridine orange stain, terminal spore with drumstick like appearance, Bacteria sensitive to heat, spores are resistant to heat, cannot survive in oxygen, mainly found in soil, intestinal tracts of animals and humains, mode of transmission by contaminated wounds and during tissue injury
Blocking of inhibitory neurotransmitters
Neurons fire continuously and cause muscle contraction and movement becomes jerky due to absence of counteracting inhibitory signals
Muscle spasms, spastic paralysis, convulsive contractions of voluntary muscles
in the absence of inhibitory postsynaptic potential, GABA and glycine do not reach synaptic cleft, action potentials accumulate more frequently
Binding of GABA to receptors increase of chloride ions in the postsynaptic cells. Biding of GABA to its receptors activates secondary messengers and opens potassium channels. This causes increasesing membrane potential called inhibitory postsynaptic potential IPSP and inhibiting it
Excitatory postsynaptic potential combined effet of neurous depolorization of neurons at the presynaptic terminals evoke action potential. Acetylcholine neurotransmitter binds to receptors, opens sodium channels, causes influx of sodium ions and reduce membrane potential. when the polarization of postsynaptic membrane reaches threshold, action potential is generated
Ach acts on nicotinic receptors at the neuromuscular junctions, skeletal muscles, brain and parasympathetic nervous system
serve muscle spasms, stiffness, breathing
Toxin clock the release oh inhibitory neurotrans GABA and glycine at the motor nerve endings. this leads to uncontrolled activation of neurons
toxins lyse cells and spread via lymphatic system and blood vascular system and is taken up by the axon terminals through endocytosis at peripheral neuromuscular junction and each motor neurons spinal cord and brain stem by retrograde transport
infection occurs by contaminated wounds. Bacterial spores release tetanospasmin and tetanolysin toxin
Infection clostridium tetani anaerobic, gram positive soil bacillus
complication pulmonary embolism, fractures, hypertension, laryngospam, nosocominal infections, pneumonia, death
clinical types: generalized: most mommon type Localized: muscle rigidity close to the site of injury, very uncommon, 1 % fatality rate. Cephalitic localized, affects cranial nerves, may occur after ear head injuries, muscle of face, eyelids tongue, lips are affected. Neonatal occurs in newborns 90% fatality, spread through non sterile environment during umbilical cord cut
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pathophysiology
toxin block inhibitory motor neurons in the spinal cord
toxins inhibitory autonomic neurons in the spinalcord
incubation period is 3-21 days with an average of 7 days