MEDICINE (COMMUNICABLE DISEASE): TETANUS

DR. EDWIN M. FORTUNO

HISTORY OF TETANUS
 Egypt over 3000 years ago.
 It was again described by Hippocrates (tension)
 1884, Carle and Rattone first noticed tetanus in animals by injecting
them with pus from a fatal human tetanus case.
 Nicolaier produced tetanus in animals by injecting them with samples of
soil.
 1889, Kitasato isolated the organism from a human victim and showed
that it produced disease when injected into animals. He reported that the
toxin could be neutralized by specific antibodies.
 World War I: only passive immunization was used for treatment and
prophylaxis.
 1924: Tetanus Toxoid was developed by Descombey and it was then
widely used during World War II.
DEFINITION OF TETANUS
 Acute disease manifested by skeletal muscle spasm and dysautonomia
 Caused by a powerful neurotoxin produced by the bacterium Clostridium
tetani  The higher coverage rate for vaccination there are now less tetanus
 Completely preventable by vaccination infection reported in our country
CAUSASTIVE ORGANISM: CLOSTRIDIUM TETANI  Philippines – 80-89% of the population is vaccinated
 It is a slender gram-positive,
anaerobic rod that may develop a
terminal spore – drumstick
 It is highly resilient, resistant to heat,
but cannot survive in the presence of
oxygen.
 Terminal spore is very resistant to
heat and the usual anti-septic.
 Autoclaving at 121 °C for 20
minutes and is relatively resistant to
phenol & other chemical agents.
 It is widely distributed in soil and it
remains nonpathogenic until
conditions are favorable for
transformation into vegetative form.
 It produces two exotoxins:
o Tetanolysin - its function is not
known with certainty.
o Tetanospasmin - a neurotoxin
that causes the clinical manifestations of tetanus. More lethal.
 Tetanospasmin: estimated human lethal dose – 2.5 ng/kg
OCCURENCE
COMMON ROUTES
 Tetanus occurs worldwide but is most frequently encountered in densely
 Clean superficial wounds populated regions in hot, damp climates with soil rich in organic matter.
 Surgical procedures o Organic matter are feces contaminated by Clostridium tetani.
 Insect bites
INCUBATION PERIOD
 Dental infections
 Time from exposure to illness – is usually between 3 and 21 days
 Compound fractures
(average 10 days). However, it may range from one day to several
 Chronic sores and infections
months, depending on the kind of wound. Most cases occur within 14
 Intravenous (IV) drug use
days or less if:
 Intramuscular injections
o More heavily contaminated wounds
EPIDEMIOLOLGY
o More serious disease
 Tetanus remains a major Public Health problem in the developing world o Worse prognosis
and is still encountered in the developed world.
PATHOGENESIS
 In 1998, 215,000 deaths occurred with more than 50% of these on the
C. tetani enters the body thru a wound
Africa continent and also asia. WHO estimated there were 213,000
↓
tetanus deaths in 2002 with 198,000 occurring in children < 5 years. As
In anaerobic conditions spore germinate
of the present, the disease is also prevalent among persons aged 40 and
↓
older.
Toxins are produced
 Reservoir: Organisms are found primarily in the soil (may reside in soul
↓
in an aerobic condition) and intestinal tracts of animals and humans.
Disseminate via blood and lymphatics
o Once it resides in an environment that is highly anaerobic they
↓
transform into their vegetative forms, that has the capacity to form the
The toxins reach the CNS
2 toxins (tetanospasmin)
↓
 Mode of Transmission: is primarily by: (there must be a breach in the
Toxins act on several site within the CNS
integrity of epithelium.
o Contaminated wounds
 The typical The typical clinical manifestations of tetanus are caused when
o Tissue injury
the toxin interferes with release of neurotransmitters, thus blocking
 To become potent, it will reside in the body with less oxygen
inhibitory impulses
concentration (necrotic tissue & GI tract)
 This leads to unopposed muscle contraction and spasm. This can also
 Communicability: Tetanus is not contagious from person to person. It is a
potentially lead to death.
vaccine-preventable disease that is infectious but not contagious.
 The toxins travel via intra-axonal transport at a rate of 75 – 250 mm/day;
 Age: It is the disease of active age (5-40 years), Neonates, female during
a process which takes 2 – 14 days to reach the CNS
delivery or abortion
 Males > females
 Occupation: Agricultural workers are at higher risk
 Setting: Rural > Urban areas
 Immunity: Herd immunity (community immunity) does not protect the
individual.
 Environmental and social factors: Unhygienic custom habits, Unhygienic
delivery practices.

 In the diagram above, the C. tetani, producing the tetanospasmin. A toxin

that has two parts, the light chain and the heavy chain, that are connected
by each other by covalent bonds. Once the tetanospasmin enters the
junction between the pre- and post-exposure neuron, you now have a
blockage of the inhibitory neuron. That is the reason why the muscle is
always in a state of excitation. That result to skeletal muscle spasm.

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 CLINICAL FEATURES
 Incubation period: 3 to 21 days, usually about 8 days.
 The further the injury site is from the CNS, the longer the incubation
period.
 Four types of Tetanus described:
o Local – slight tingling sensation on the site of the wound
o Cephalic – patient may manifest with seizure
o General – patient manifest generalized seizure
o Neonatal – baby that has been delivered normally then after 2-4 weeks
the baby now acts differently

Lock jaw (Trismus)

↓
Stiff neck
↓
Difficulty in swallowing
↓
Muscle rigidity
↓
Muscle spasm

 Picture on the left: Risus sardonicus (constant grin)

 Picture on the right: Opisthotonos (spastic paralysis of the back)
DIAGNOSIS
 No laboratory findings are characteristic of tetanus. Therefore, the
diagnosis is entirely clinical and does not depend upon bacteriologic
confirmation.
 C. tetani is recovered from the wound in only 30% of cases and can be
isolated from asymptomatic patients.
 Laboratory identification of the organism depends most importantly on the
demonstration of toxin production in mice.
 Clinically it is confirmed by noticing the following features:
o Risus sardonicus
o Lock jaw
o Opisthotonus
o Neck Rigidity
 REMEMBER: there is also dysautonomia. Which affects the autonomic
system.
COMPLICATIONS
 Tetanus complication includes:
o Laryngospasm
o Fracture
o Hypertension
o Nosocomial infections
o Pulmonary Embolism
o Aspiration Pneumonia
o Death
TREATMENT
 Three goals of management:
o Neutralize the toxin:
 administer Human tetanus immune globulin (TIG)
o Eradicate C. tetani
 local wound care and administration of antibiotic (metronidazole)
o Provide supportive care and maintain adequate nutrition
(antispasmodic drugs should be used and respiration maintained
by a breathing apparatus if necessary)
 Patient with decubitus ulcer – remove every necrotic tissue
PREVENTION
 Tetanus carries a 35% mortality rate, making prevention very important!
 The best course is childhood immunizations, with consistent booster
doses, and prompt cleaning of wounds.
 Elderly – most important population because are at risk of sustaining
wounds. The mandatory vaccine for elderly are COVID-19, anti-
pneumonia, anti-flu vaccine, vaccine for HZV and vaccine against
tetanus.
 TETANUS TOXOID (TT)
o Formalin-inactivated tetanus toxin
o Schedule -Three or four doses + booster
Booster every 10 years
o Efficacy - Approximately 100%
o Duration - Approximately 10 years
o Should be administered with diphtheria toxoid as DTaP, DT, Td, or
Tdap
Routine Td Schedule for Unvaccinated Persons 7 Years of Age and
Older
Dose Interval
Primary 1
Primary 2 4 weeks
Primary 3 6 to 12 months
 Booster dose every 10 years

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