Clostridium tetani is a gram-positive, obligate anaerobic, spore-forming rod-shaped bacterium found in soil, intestines, feces and contaminated wounds. It produces an exotoxin called tetanospasmin that causes the acute disease tetanus, resulting in painful muscle rigidity and spasms. Tetanus spores can survive for years until entering the body through a wound, where they germinate and release the toxin that is carried through the bloodstream to nerve cells.
3. • Heat resistant spores and usual
antiseptics.
• survive autoclaving at 121 C for 10-15
minutes.
• resistant to phenol and other chemical
agents.
RESISTANCE
5. • Organism is sensitive to heat.
• Sensitive to oxygen.
SENSITIVITY
6. Tetanus
• acute, often fatal, disease caused by an
exotoxin produced by Clostridium tetani.
• rigidity and convulsive spasms of skeletal
muscles.
• involves the jaw (lockjaw) and neck and then
becomes generalized.
EPIDEMIOLOGY
7. • Enters through the wound.
• Spores germinate in the presence of anaerobic
condition.
• Tetanospasmin spread in through blood and
lymphatic.
• Interferes with release of neurotransmitters,
blocking inhibitor impulses.
PATHOGENESIS
8. • 3 to 21 days
• Neonatal tetanus, symptoms usually appear
from 4 to 14 days after birth
INCUBATION PERIOD
11. • persistent contraction of muscles in
the same anatomic area as the injury.
• Precede the onset of generalized
tetanus, but is generally milder.
• 1% of cases are fatal.
LOCAL
12. • Occurs with otitis media (ear infections)
• Head injuries.
• Involvement of the cranial nerves,
especially in the facial area.
CEPHALIC
13. • Trismus
• stiffness of the neck and difficulty in
swallowing
• rigidity of abdominal muscles.
• rise of 2°-4°C above normal temp.
• sweating and elevated blood pressure
• episodic rapid heart rate
• Spasms
GENERALIZED
14. • Occurs in infant
• infection of the unhealed umbilical
• estimated >270,000 deaths worldwide per
year.
NEONATAL TETANUS
A Neurotransmission is controlled by the balance between excitatory and inhibitory neurotransmitters. B. The inhibitory neurotransmitters (e.g., GABA, glycine) prevent depolarization of the postsynaptic membrane and conduction of the electrical signal. C. Tetanospasmin does not interfere with production or storage of GABA or glycine, but rather their release (presynaptic activity). D. In the absence of inhibitory neurotransmitters, excitation of the neuroaxon is unrestrained.