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Clostridium tetani

These are gram positive, spore-bearing, anaerobic rods having a characteristic drumstick appearance.
They are exotoxin producers and are the causative agents for the clinical condition of tetanus. C. tetani
is worldwide in distribution in the soil and in the feces of horses and other animals. Several types of C.
tetani can be distinguished by specific flagellar antigens. All share a common O (somatic) antigen,
which may be masked and all produce the same antigenic type of neurotoxin, tetanospasmin.

Morphology
Rod shaped with rounded ends.
Size 2 to 5 um * 0.4 to 0.5 m.
Possess spherical and terminal spores; spore is larger than the bacillary body.
Non-capsulated.
Motile with peritrichous flagella.
Gram positive and non acid-fast.

Cultural characters
Anaerobic
Optimum temperature: 37 C
Can grow on ordinary media but presence of blood or serum improves growth.
They have a spreading and feathery growth.
Produce haemolysis on blood agar.
Cooked meat medium:
a) Turbidity on medium.
b) Blackening of meat
Loeffler's serum slope: softened.

Biochemical behavior
Sugars are not fermented.
Indole is produced.
Milk is not coagulated.
Gelatin is liquefied.

Toxins & enzymes:


Cl. tetani produces a very powerful exotoxin, which consists of two factors:
1. Tetanospasmin
2. Tetanolysin

1. Tetanospasmin :
Tetanopasmin is a 150kD peptide made out of a heavy chain (B) and a light chain (A) joined by a
disulfide bond. The toxin initially binds with the receptors on the pre-synaptic membranes of motor
neurons. It then migrates by the retrograde axonal transport system to the cell bodies of these neurons to
the spinal cord and brain stem. The toxin diffuses to terminals of inhibitory cells, including both
glycinergic and aminobutyric acid secreting neurons from the brain stem. The toxin degrades
synaptobrevin, a protein required for docking of neurotransmitter vesicles on the presynaptic membranes.
Release of the inhibitory glycine and aminobutyric acid is blocked and the motor neurons are not
inhibited.
Generally it is the neurotoxin and is one of the most powerful exotoxins so far known. One attack of
tetanus does not confer immunity because the fatal dose of the toxin is less than the dose required to

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provoke immunity. It is antigenic and produces antitoxin. Toxoids are prepared which are used for
immunization.

Tetanolysin is a hemolysin with no recognized pathogenic ability while tetanospasmin is the peptide
responsible for tetanus.
Tetanospasmin is a 150kD peptide made out of a heavy chain (B) and a light chain (A) joined by a
disulfide bond. The heavy chain specifically binds to neuronal cells (disialogangliosides). The light chain
, a zinc endopeptidase, attacks the vessicle associated membrane protein and blocks the release of
inhibitory neurotransmitters (GABA & Glycine).
Inhibitory nerutransmitter produce inhibitors that bind to receptors on excited neurons. The binding of the
inhibitor blocks the neuron from releasing the acetylcholine that is responsible for muscle contraction. As
a result, the muscle relaxes. If these neurotransmitter are blocked (as the case when these toxins are
present), there is nothing stopping the release of acetycholine from the excited neuron. As a result, the
muscle will stay contracted
.

Tetanolysin
This factor causes lysis of RBcs in vitro. Its role in vivo is not yet clear. It is oxygen labile and is antigenic
when injected into animals. It is produced in abundance by the so called non toxic strains and may not be
produced at all by the extremely virulent ones.

Antigenic structure
Cl. tetani has flagellar (H) antigen and somatic (O) antigen. Flagellar antigen is specific and Cl. tetani can
be distinguished by 'H' antigen into 10 serological types. O- antigen is common and is shared by all
strains.
Tetanus/Lock jaw

Tetanus is a neurotoxic disease caused by absorption of exotoxin produced by Cl. tetani at the site of
infection. In this disease the toxin affects the nervous tissue and causes muscle spasm. Spasm of the
masseter muscle is very common giving rise to trismus and hence the name 'Lock jaw'.

Clinical findings
The incubation period may range from 4-5 days to as many weeks. In theory, the farther the injury site is
from the CNS, the longer the incubation period, and the less severe are the symptoms experienced. The

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disease is characterized by tonic contraction of voluntary muscles. Muscular spasms often involve the
first area of injury and infection and then the muscles of jaw which contract so that the mouth cannot be
opened. Gradually, other voluntary muscles become involved. The patient is fully conscious, and pain
may be intense. Other symptoms are fever, headache, trouble swallowing, high blood pressure and a fast
heart rate. Death usually occurs from interference with the mechanics of respiration.

Laboratory diagnosis
a) Materials: Swabs and other materials from the wound.
b) Microscopy: Gram staining of smears will reveal typical organisms.
c) Culture: Material may also be inoculated to Robertsons cooked meat media and heated to 800C
for 10 minutes after inoculation. It is then incubated at 370C.
d) Animal inoculation: Material from 5-10 day old culture from the cooked meat medium is
inoculated into a mouse at the right side of the tail. In a positive case, the animal develops
stiffness of the tail and paralysis of the right hind limb. Gradually, there is generalized muscular
involvement. A control animal previously inoculated with antitoxin is always included in this test

Prevention and control


Prevention of tetanus depends on:
Active immunization with toxoids
Proper care of wounds with contaminated soil
Prophylactic use of antitoxin
Administration of penicillin
Vaccinating a higher percentage of pregnant women against tetanus with vaccines containing
tetanus toxoid (TT). Toxoids are produced by detoxifying the toxin with formalin and then
concentrating it. Aluminum salt adsorbed toxoids are employed.
Vaccinating all females of childbearing age (approximately 1545 years) with TT vaccine in
high-risk areas where vaccination coverage is currently low.
Promoting clean delivery and childcare practices, through better hygiene and care of the
newborns umbilicus.
Improving surveillance and reporting of cases of neonatal tetanus. The case finding and reporting
will help to give appropriate treatment and vaccination to children.
Treatment
1. Administration of antitoxin: the intramuscular administration of human antitoxin gives
adequate protection. It neutralizes the toxin that has not been fixed to nerve tissue.
2. Wound care: Surgical debridement is vitally important because it removes the necrotic tissue
that is essential for the proliferation of organisms.
3. Penicillin administration: Penicillin strongly inhibits the growth of C. tetani and stops further
toxin production. Antibiotics may also control associated pyogenic infection.

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