1 by- himanshu r pardeshi. to study morphology, pathogenesis, clinical features, treatment &...
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By- Himanshu R Pardeshi 1
Created by : Himanshu R Pardeshi S.Y. B-pharm
By- Himanshu R Pardeshi 2
Learning objectives ; To Study Morphology, pathogenesis,
clinical features , treatment & prevention of :
Clostridium tetani Clostridium bolutinum
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CLOSTRIDIUM TITANI
Tetanus
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MORPHOLOGY Distributed in soil, & grows in intestine
of humans and horses. Size : 5µm x 0.5 µm Shape : slender rods with parallel sides
& rounded ends with spherical terminal spores (drumstick)
Non-Specific, gram positive, Motile, forms spore.
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GROWTH OF CL.TETANI Obligate anaerobe ,
at 37°C Grows on ordinary
media, and improved when blood or serum is included in agar media.
On Blood agar it has tendency to swarm over the surface.
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Identification tests: Forms indole &
liquefies gelatin slowly.
Do not ferment sugars
MR & VP tests are negative.
H₂S not formed. Nitrates are not
reduced to nitrites.
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MECHANISM It grows in the wounds in anaerobic
condition as a consequence, toxin is liberated there. The toxin travels along the nerves to reach the nervous system and produces tetanus by two ways :
By Blocking acetylcholine at myoneural junc. Countering inhibitory influences on muscle
reflex.
Thus lowers the lower motor activity leads to muscle rigidity & spasm
Once toxin reaches the spinal cord the toxin can no longer be neutralised by antitoxin.
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Removal of inhibitory influences on ANS causes increased autonomic activity such as tachycardia sweating & hypotension
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Clinical significance: Incubation period :5-15 days/ longer Stage of rigidity: Stiff jaws. Further
spreads to neck within 24 hrs. Stage of spasm :Painfull contractions
devlop within muscles due to rigidity of spasm. Period is called as ‘period of onset’.
The spasms causes the grimacing of the face and arching of neck and back, & even causes respiratory failure.
In mild cases only spasm over localised area become rigid.
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TREATMENT Immunoglobin
20,000 IU. Sedation: Diazapam
used to control mild spasm
Fluid and electrolyte balance is imp.
Neonatal-Unique problem in developing countries.
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Prevention : Immunisation with tetanus toxoid
provides protection for atleast ten years/ longer.
Universal childhood immunisation with 3 primary dose followed by boosters at school entry and leaving in developing counteries.
Wounds should be thoroughly cleaned and foreign bodies or dead bodies must removed.
Penicillin for contaminated wounds may reduce likelihood of tetanus.
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CLOSTRIDIUM BOTULINUM
Botulism
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MORPHOLOGY; Occurs in soil,
veges, hay & silage Gram positive of
5µm x 1µm in size. Non-capsulated &
motile by peritrichate flagelle.
Produces buldging spores.
Obligate anaerobe at 35°C
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Identification Liquefies
coagulated serum and produces a saccharolytic or proteolytic reactions.
Resistance: Resistant to heat
survives for several hours at 100°C.
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PATHOGENESIS Produces powerful exotoxin responsible
for its pathogenicity. This toxin is pure crystalline protien & probably is the most toxic substance known to humans.
Normally occurs in inactive form and is probably converted to active toxins by action of proteolytic enzyme.
Its toxin acts as neurotoxin, blocking the action of acetylcholine at synapses & neuromuscular junctions & leads to paralysis.
Death occurs due to respiratory paralysis.
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CLINICAL FEATURES
•In food poisoning botulism, after incubation period there is onset of vomiting, tiredness, thirst & bulbar & ocular muscle paralysis.•Followed by flacid paralysis of limb & trunk muscles & Death due to respiratory failure .
•In Infants: Severe with occurrence of difficulty in feeding.
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TREATMENT & PREVENTION Its activity can be neutralised by specific
antitoxin. Standard Canning to prevent occurrence
of botulism; most of the out breaks are due to inadequate home preservation of food.
In home preservation it should be pressure cooked or should be boiled for 20 minutes.
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THANK you!!!
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