2. Clostridium tetani
Causative agent of Tetanus
Tetanus: an acute ds manifested by skeletal muscle spasm
and autonomic nervous system disturbance.
Known since ancient time; isolated by Kitasato (1889).
Widely distributed in soil and intestine of man and animals.
Ubiquitous
3. Morphology
Gram positive
Slender bacillus with
spherical, terminal spores
drumstick appearance
Non-capsulated & motile
(peritrichate flagella)
Young cultures strongly
Gram positive
Old cultures even be
Gram negative
4. Resistance
Resistance of Cl. Tetani spores to heat vary in different strains.
Most of the stains are killed by boiling for 10-15mins.
Some resist boiling for 3 hrs.
Autoclaving at 1210C for 20mins kills the spores of most strains.
Spores are killed with Iodine (1% aqueous solution), H2O2 and
Glutaraldehyde(2%) within few hours.
Spores may survive in soil for years.
7. Tetanospasmin
Proteinous in nature.
Heat labile and oxygen stable.
Powerful neurotoxin.
Rapidly destroyed by proteolytic enzymes.
Plasmid coded.
Responsible for clinical manifestation of tetanus.
8. Tetanospasmin
Lethal to mice and pigs in minute doses (0.0000001mg for
mouse).
Good Ag and is specifically neutralized by the antitoxin.
Is plasmid coded.
Can be toxoided by formaldehyde retains Ag property
looses virulence property used for vaccine preparation.
9.
10. Mechanism of Action of Tetanus
Toxin
Toxin binds to receptors (polysialogangliosides) present on motor nerve
terminals which results in toxin internalization.
After internalization, tetanus toxin gets transported in retrograde way to
the gamma-aminobutyric acid (GABA) and glycine producing inhibitory
neuron terminals
Toxin prevents presynaptic release of inhibitory neurotransmitters
glycine and GABA, which leads to spastic muscle contractions.
11.
12.
13.
14.
15. Pathogenesis
Mode of transmission
Injury (superficial abrasions, punctured wounds, RTA)
Surgery done without proper asepsis.
Neonates: Following abortion/delivery, due to unhygenic
practices
16. Cl. Tetani has litte invasive power
Tetanus develops following contamination of wounds with Cl. Tetani
spores
Source of infection may be soil, dust, faeces etc
Infection remains localized in the wound
Germination of spores and toxin production occur only if favorable
condition exist
17. Pathogenic effects are due to tetanospasmin (neurotoxin)
Acts presynaptically, Specifically blocks synaptic inhibition in the spinal
cord
Abolition of spinal inhibition leads to uncontrolled spread of impulses
initiated anywhere in the central nervous system.
Results in muscle rigidity and spasms due to the simultaneous
contraction of agonists and antagonists.
18. Clinical Manifestations
I.P. 6-10 days.
Muscles of the face and Jaw are
affected first (due to shorter
distances for the toxin to reach
the pre-synaptic terminals).
First symptoms
Increase in the masseter tone
leading to trismus or lockjaw,
followed by muscle pain and
stiffness, back pain and difficulty in
21. Opistotonos position
Abnormal posture of body (due to generalized spastic contraction of
the extensor muscles)
Respiratory muscles spasm airway obstruction.
24. Laboratory Diagnosis
Specimen
Wound swab
Exudate or tissue from the wound.
Gram Staining
GPB with terminal and round spores (drum stick appearance).
But indistinguishable C. tetani from morphologically similar to C.
tetanomorphum and C. sphenoides.
27. Active immunisation
Most effective method
Tetanus toxoid (formal toxoid)
Dose:- 0.5ml I.M.
TT(Tetanus toxoid) is given with DPT in
children
DPT:- 6,10,14 weeks of birth.
DPT:-Booster dose 16-24 weeks and 5years.
TT:- Additional 2 doses of TT at 10 and 16
years.
For prevention of Neonatal tetanus, all
pregnant women are given 2 doses of TT at
28. Passive Immunisation
Antitetanus serum (ATS) prepared by immunising horse with
toxoid for preventing tetanus.
Human antitetanus immunoglobulins (HTIG).