TETANUS

By Abhijeet manna

Sem IV
 INTRODUCTION TO TETANUS

A. Defination : Tetanus, also known as lockjaw, is a serious bacterial infection

caused by Clostridium tetani. It affects the nervous system, leading to muscle
stiffness and spasms, often starting in the jaw and neck and spreading throughout
the body. Tetanus can be prevented by vaccination and is typically contracted
through a wound contaminated with tetanus spores.

B. Key points about tetanus include:

 Transmission
 Symptoms
 Treatment
 Prevention
 Global impact.

Microscopic view of C.tetani

B. Historical background : The historical background of tetanus dates back to
ancient times, although the understanding of the disease and its causes has
evolved significantly over the centuries.
• 19th Century: In the 19th
century, scientists began to
make significant strides in
understanding tetanus. In
1884, the German • Late 19th to Early 20th
bacteriologist Arthur Century: Further research
• Ancient Times: Nicolaier discovered the by other scientists,
Tetanus has likely been bacterium Clostridium tetani, including Emil von Behring
recognized since which is responsible for and Kitasato Shibasaburō,
ancient times, with causing tetanus. He led to the development of
descriptions of demonstrated that the tetanus antitoxin, which
symptoms resembling bacterium produced a toxin could neutralize the toxin
the disease found in that caused the characteristic produced by Clostridium
historical texts. symptoms of the disease. tetani. This was a significant
However, the specific advancement in the
cause and mechanisms treatment of tetanus and
of tetanus were not marked the beginning of
understood at this immunotherapy for the
time. disease.
 ETIOLOGY AND PATHOGENESIS
A. Cause :
Tetanus is caused by the bacterium clostridium tetani, which is commonly
found in soil, dust and manure. There are different types of tetanus
(differentiate by age):
• Neonatal tetanus.
• Adult Tetanus

(differentiate by • Generalized tetanus(most common),

infected area) • Cephalic tetanus
• Localized tetanus,

B. Transmission :
• Spores of C. tetani usually enter the body through an open wound, leading to spores
germination under anaerobic conditions.

• Once spore germination has occurred, toxins are released ,then it travels through the
bloodstream and lymphatic system to nerve endings
 PATHOGENESIS
• Neurons (also called neurones or nerve cells) are the fundamental units of the brain
and nervous system, the cells responsible for receiving sensory input from the external
world, for sending motor commands to our muscles, and for transforming and relaying
the electrical signals at every step in between.
• An action potential is a brief electrical
impulse that travels down the axon of a neuron,
allowing it to communicate with other neurons
or cells.
• Depolarization.
• Repolarization.
• Hyperpolarization.
• Resting state.
• Failed initiations.
• Neurotransmitters are body’s chemical
messengers.
• Examples of excitatory neurotransmitters
include glutamate, epinephrine and
norepinephrine.
• Gamma-aminobutyric acid (GABA),
glycine and serotonin are examples of
inhibitory neurotransmitters.
• VAMP
• Synaptobrevin
• Syntaxin1
• SNAP25
Tetanolysin is capable of locally
damaging otherwise viable tissue surrounding the infection and
optimizing the conditions for bacterial multiplication.
Tetanospasmin is composed of a heavy chain and light chain,
which are attached by a disulphide bond.
Tetanus toxin
1. Heavy chain : that contains the ganglioside -
binding domain, attaches to gangliosides on the
peripheral nerves, and the toxin is internalized.
Through trans-synaptic spread, the toxin can spread
to the central nervous system.

2. Light chain : contains a zinc metallo-protease

domain, cleave proteins synaptobrevin (SV2)
 Mechanism of Action of Tetanospasmin
• binds to gangliosides GD1b and GT1b on the
membranes of local nerve terminals

• transported intra-axonally and retrogradely to the

cell body and into the spinal cord

• then the toxin deposite outside the cell where

bind to receptor GT1b on inhibitory neurons

• take up the toxin by endocytosis creating an

internal vesicle with the toxin inside

• inside the cell the vesicle becomes acidified

and low ph the disulfied bond brakes

• part of the toxin behaves as

a pore that allows the other
to enter to the cytoplasm

• tetanus toxin is a protease

that cleave vamp

• inhibiting release of
inhibitory neurotransmitter.
Symptoms : Symptoms can include:
• jaw cramping or the inability to open the mouth
• muscle spasms often in the back, abdomen and extremities
• sudden painful muscle spasms often triggered by sudden
noises
• trouble swallowing
• seizures
• headache
• fever and sweating
• changes in blood pressure or fast heart rate.

In neonatal tetanus, symptoms include muscle spasms,

which are often preceded by the newborn’s inability to
suck or breastfeed, and excessive crying.

Complications: Tetanus can lead to serious

complications, including respiratory failure, aspiration
pneumonia, fractures, and cardiovascular problems.
Mortality rates are highest in individuals who develop
severe forms of tetanus with respiratory involvement.
 TREATMENT AND DIAGNOSIS
A. Diagnosis by laboratory tests: Several laboratory tests can help diagnose tetanus:
• Toxin Detection: Testing for the presence of tetanus toxin in
the blood, serum, or wound can confirm tetanus infection.
• Cultural Tests: Culturing the bacteria Clostridium tetani from a
wound or other infected tissue can confirm the presence of the
bacterium.
• Serology: Serological tests can detect antibodies to tetanus
toxin in the blood, indicating exposure to the bacterium or
vaccination against tetanus.
• Complete Blood Count (CBC): A CBC may show elevated
white blood cell count, which can indicate infection and
inflammation, but it is not specific to tetanus.
B. Treatment :
Tetanus is a medical emergency requiring:
Formaldehyde-induced modification on tyrosine residues: cross-
link bridge formation. Groups R1, R2, R3 and R4 represent N and
•care in the hospital C-terminal functions.
•immediate treatment with medicine called human tetanus immune globulin (TIG)
•aggressive wound care( cleaning and disinfection )
•drugs to control muscle spasms( diazepam or valium or baclofen )
•antibiotics( metronidazole or penicillin )
•tetanus vaccination ( diphtheria and tetanus (DT) vaccines ; diphtheria, tetanus, and pertussis
(whooping cough) (DTaP) vaccines ; tetanus and diphtheria (Td) vaccines tetanus,
diphtheria, and pertussis (Tdap) vaccines.)

People who recover from tetanus do not have natural immunity and can be infected again, and
therefore need to be immunized.
 PREVENTION AND CONTROL
A. Prevention : •Primary series: consist of three doses given during
infancy and early childhood, at ages 2 months, 4 months and 6 months. Sometimes an
additional booster dose is given at 15-18 months.
•Booster doses: given around age 4-6 years, another
doses between ages 11-12. After that, booster doses are recommended every 10 years to
maintain immunity.
• Neonatal tetanus can be prevented by immunizing
women of reproductive age with TTCV

B. Control: Public health measures to control tetanus involve:

• Vaccination Campaigns
• Routine Immunization Programs
• Education and Awareness
• Surveillance and Monitoring
• Access to Healthcare
 EPIDEMIOLOGY AND GLOBAL BURDEN:
A. Number of new tetanus infection :
 EPIDEMIOLOGY AND GLOBAL BURDEN:
B. Deaths from tetanus :
C. High risk population & geographic regions :
D. Progress in tetanus control and elimination efforts :
 Conclusion

In conclusion, significant progress has been made in controlling and eliminating tetanus through
widespread vaccination, improved healthcare infrastructure, and targeted public health
interventions. Vaccination campaigns, booster doses for adolescents and adults, and efforts to
eliminate maternal and neonatal tetanus have reduced the burden of tetanus world wide.
However, challenges persist, including reaching underserved populations, addressing vaccine
hesitancy, and responding to outbreaks in high-risk regions.

THANK YOU