2. CLOSTRIDIUM TETANI
Morphology and Physiology-
• long thin gram-positive organism that stains gram negative in
old cultures
• round terminal spore gives drumstick appearance
• motile by peritrichous flagella
• grow on blood agar or cooked meat medium with swarming
• beta-hemolysis exhibited by isolated colonies
• spores resist boiling for 20 minutes
3. PATHOGENICITY DETERMINANTS
• play a role in local infection only in conjunction with other bacteria that
create suitableenvironment for their invasion
• systemic-acting, plasmid-mediated A-B neurotoxin (tetanospasmin)
produced intracellularly: Mode of Action — one of most poisonous
substances
• binds gangliosides in synaptic membranes (synapses of neuronal cells) and
blocksrelease of inhibitory neurotransmitters; continuous stimulation
by excitatory transmitters
• muscle spasms (spastic paralysis) (trismus )(lockjaw), risus sardonicus,
opisthotonos),
cardiac arrhythmias, fluctuations in blood pressure
4. PATHOGENESIS AND IMMUNITY
• Tetanospasmin is responsible for clinical manifestations
of tetanus.
• An A-B toxin, released when the bacteria lyse.
• Subunit A is a zinc endopeptidase that acts on CNS:
Inhibits release of an inhibitory mediator (e.g.,
GABA or glycine) which acts on postsynaptic spinal
neurons (causing spastic paralysis).
5. DIAGNOSIS/ TREATMENT/
PREVENTION
• empirical diagnosis on basis of clinical manifestations
• treat to prevent elaboration and absorption of toxin
clean wound (debridement), control spasms
metronidazole administered to eliminate vegetative bacteria
that produce neurotoxin
• passive immunity (human tetanus immunoglobulin)
• vaccination (active) as preventative antitoxin administered to
bind free tetanospasmin
6. Clinical Diseases
Foodborne botulism
Incubation period: 18-24 hrs.
Symptoms: double vision, inability to swallow, speech diffic
ulty, bulbar paralysis, constipation, and abdominal pain. Bil
ateral descending weakness of peripheral muscle. Death o
ccurs from respiratory paralysis or cardiac arrest. No fever.
Mortality is high.
Recovery may need months to years.
Patients who recover do not develop antitoxin.
7. Clinical Diseases
Infant botulism
Occurs in the first month of life. Weakness, signs of paralysis,
C. botulinum and its toxin are found in feces. May be caused
by ingestion of the bacteria or spores which grow in the gut a
nd produce toxin.
Feeding of honey has been implicated as a possible cause.
Patients recover with supportive therapy alone.
Wound botulism
Develops from contaminated wounds.
Symptoms similar to those of food borne botulism with longer
incubation time. Less GI symptoms.
8.
9. Clostridium tetani Gram Stain
NOTE: Round terminal spores give cells a
“drumstick” or “tennis racket” appearance.
11. TREATMENT
• Stomach lavage and high enemas.
• Trivalent (A, B, E) antitoxin administered intravenously
promptly.
• Adequate ventilation by mechanical respirator.
12. PREVENTION AND CONTROL
• Spores of C. botulinum are widely distributed in soil and often
contaminate vegetables, fruits etc.
• Strict regulation of commercial canning has largely reduced
the danger of widespread outbreaks. The chief danger lies in
home-canned foods (vegetables, smoked fish or vacuum-
packed fresh fish). The cans with toxic food may swell or may
show innocuous appearance.
• The risk from home-canned food can be reduced by boiling
the food for 20 min.
• Children younger than 1 year should not eat honey.
13. SIGNS AND SYMPTOMS
• Stiffness of the neck, jaw, and other muscles, often
accompanied by a grotesque, grinning expression
• Difficulty swallowing
• Irritability
• Uncontrollable spasms of the jaw, called lockjaw, and
neck muscles
• Painful, involuntary contraction of other muscles
