TETANUS (CLOSTRIDIUM

TETANI)
Gizeshwork ,MD
ETIOLOGY

 Tetanus is an acute, spastic paralytic illness historically

called lockjaw that is caused by the neurotoxin produced
by Clostridium tetani
 C.tetani a motile, gram-positive, spore-forming obligate
anaerobe whose natural habitat worldwide is soil, dust,
and the alimentary tracts of various animals.
o It forms spores terminally, producing a drumstick or
tennis racket appearance microscopically.
 Tetanus spores can survive boiling but not autoclaving,
whereas the vegetative cells are killed by antibiotics,
heat, and standard disinfectants.
 Unlike many clostridia, C. tetani is not a tissue-invasive
organism and instead causes illness through the effects of
a single toxin, tetanospasmin, more commonly referred
to as tetanus toxin.
 Tetanospasmin is the 2nd most poisonous substance
known, surpassed in potency only by botulinum toxin.
 The human lethal dose of tetanus toxin is estimated to
be 10−5 mg/kg.
EPIDEMIOLOGY
 Tetanus occurs worldwide and is endemic in
approximately 90 developing countries, although its
incidence varies considerably.
 The most common form, neonatal (or umbilical)
tetanus, kills approximately 500,000 infants each year,
with about 80% of deaths in just 12 tropical Asian and
African countries.
 It occurs in infants whose mothers are not immunized.
EPID…
 Most non-neonatal cases of tetanus are associated with a
traumatic injury, often a penetrating wound inflicted by a
dirty objects.
 Tetanus also occurring after illicit drug injection,use of
contaminated suture material and after intramuscular
injection of medicines, most notably quinine ,animal
bites, abscesses (including dental abscesses), ear and
other body piercing, chronic skin ulceration, burns,
compound fractures, frostbite, gangrene, intestinal
surgery, ritual scarification, infected insect bites, and
female circumcision.
 Rare cases have no history of trauma.
PATHOGENESIS
 Tetanus occurs after introduced spores germinate,
multiply, and produce tetanus toxin in the low oxidation-
reduction potential (Eh) of an infected injury site.
 A plasmid carries the toxin gene.
 Toxin is released after vegetative bacterial cell death and
lysis.
 Tetanus toxin (and the botulinum toxins) are 150 kd
simple proteins consisting of a heavy (100 kd) and a light
(50 kd) chain joined by a single disulfide bond.
 Tetanus toxin binds at the neuromuscular junction and
enters the motor nerve by endocytosis, after which it
undergoes retrograde axonal transport to the cytoplasm
of the α-motoneuron.
 In the sciatic nerve, the transport rate was found to
be 3.4 mm/hr.
 The toxin exits the motoneuron in the spinal cord and
next enters adjacent spinal inhibitory interneurons,
where it prevents release of the neurotransmitters
glycine γ-aminobutyric acid (GABA).
 Tetanus toxin thus blocks the normal inhibition of
antagonistic muscles on which voluntary coordinated
movement depends; in consequence,
 affected muscles sustain maximal contraction and
cannot relax.
 The ANS is also rendered unstable in tetanus.
CLINICAL MANIFESTATIONS
 Tetanus is most often generalized but may also be
localized.
 The incubation period typically is 2-14 days but may be
as long as months after the injury.
 In generalized tetanus,

trismus (masseter muscle spasm, or lockjaw)

Headache, restlessness, and irritability are early
symptoms, often followed by stiffness, difficulty
chewing, dysphagia, and neck muscle spasm.
sardonic smile of tetanus (risus sardonicus) results
from intractable spasms of facial and buccal muscles.
opisthotonos positioning
 Laryngeal and respiratory muscle spasm can lead to airway
obstruction and asphyxiation.
 Because tetanus toxin does not affect sensory nerves or
cortical function, the patient unfortunately remains conscious,
in extreme pain, and in fearful anticipation of the next tetanic
seizure.
C/F….
 seizure
 The smallest disturbance by sight, sound, or touch may trigger
a tetanic spasm.
 Dysuria and urinary retention result from bladder sphincter
spasm; forced defecation may occur.
 Fever, occasionally as high as 40 oC, is common because of
the substantial metabolic energy consumed by spastic muscles.
 Notable autonomic effects include tachycardia, dysrhythmias,
labile hypertension, diaphoresis, and cutaneous
vasoconstriction.
 The tetanic paralysis usually becomes more severe in the 1st
wk after onset, stabilizes in the 2nd wk, and ameliorates
gradually over the ensuing 1-4 wk.
C/F…
 Neonatal tetanus, the infantile form of generalized
tetanus, typically manifests within 3-12 days of birth as
progressive difficulty in feeding (sucking and
swallowing), associated hunger, and crying.
 Paralysis or diminished movement, stiffness and rigidity
to the touch, and spasms, with or without opisthotonos,
are characteristic.
 The umbilical stump may hold remnants of dirt, dung,
clotted blood, or serum, or it may appear relatively
benign.
C/F….
 Localized tetanus results in painful spasms of the
muscles adjacent to the wound site and may precede
generalized tetanus.
 Cephalic tetanus is a rare form of localized tetanus
involving the bulbar musculature that occurs with
wounds or foreign bodies in the head, nostrils, or face. It
also occurs in association with chronic otitis media.
 Cephalic tetanus is characterized by retracted eyelids,
deviated gaze, trismus, risus sardonicus, and spastic
paralysis of the tongue and pharyngeal musculature.
DIAGNOSIS

 Clinically
 The typical setting is an unimmunized patient (and/or mother)
who was injured or born within the preceding 2 wk, who presents
with trismus, other rigid muscles, and a clear sensorium.
 Results of routine laboratory studies are usually normal.

 A peripheral leukocytosis may result from a secondary bacterial

infection of the wound or may be stress induced from the
sustained tetanic spasms.
 The cerebrospinal fluid is normal, although the intense muscle
contractions may raise intracranial pressure.
 C. tetani is not always visible on Gram stain of wound material
and is isolated in only about 30% of cases.
DIFFERENTIAL DIAGNOSIS

 parapharyngeal, retropharyngeal, or dental abscesses or,

rarely, from acute encephalitis involving the brainstem.
 Rabies

 strychnine poisoning.

 Hypocalcemia

 Epileptic seizures(occasionally)

 narcotic withdrawal, or other drug reactions may

suggest tetanus.
TREATMENT
 Eradication of C. tetani and the wound environment
conducive to its anaerobic multiplication, neutralization
of all accessible tetanus toxin, control of seizures and
respiration, palliation, provision of meticulous
supportive care, and, finally, prevention of recurrences.
TREATMENT…
 Surgical wound excision and debridement
 human tetanus immunoglobulin (TIG)

 TAT - the usual dose of is 50,000-100,000 U, with half given

intramuscularly and half intravenously, but as little as 10,000 U
may be sufficient
 Penicillin G (100,000 U/kg/day divided every 4-6 hr IV for 10-14
days) remains the antibiotic of choice because of its effective
clostridiocidal action and its diffusibility, which is an important
consideration because blood flow to injured tissue may be
compromised.
 Metronidazole (500 mg every 8hr IV for adults) appears to be
equally effective.
 Erythromycin and tetracycline (for persons >8 yr of age) are
alternatives for penicillin-allergic patients.
TREATMENT …
 muscle relaxants.
 Diazepam provides both relaxation and seizure control.
Alternate with CPZ every 4-6hrs
 The initial dose of diazepam 0.1-0.2 mg/kg every 3-6 hr
given intravenously is subsequently titrated to control the
tetanic spasms, after which the effective dose is sustained for
2-6 wk before a tapered withdrawal.
 The highest survival rates in generalized tetanus are achieved
with neuromuscular blocking agents such as vecuronium and
pancuronium, which produce a general flaccid paralysis that
is then managed by mechanical ventilation.
 Autonomic instability is regulated with standard α- or β- (or
both) blocking agents; morphine has also proved useful.
TREATMENT…
 Supportive Care
 Meticulous supportive care in a quiet, dark, secluded
setting is most desirable. Because tetanic spasms may be
triggered by minor stimuli, the patient should be sedated
and protected from all unnecessary sounds, sights, and
touch, and all therapeutic and other manipulations must
be carefully scheduled and coordinated.
 tracheostomy

 Cardiorespiratory monitoring

 Prophylactic subcutaneous heparin may be of value but

must be balanced with the risk for hemorrhage.
COMPLICATIONS

 Aspiration of secretions and pneumonia

 pneumothorax and mediastinal emphysema(after mechanical
ventilation).
 The seizures may result in lacerations of the mouth or tongue, in
intramuscular hematomas or rhabdomyolysis with myoglobinuria and
renal failure, or in long bone or spinal fractures.
 Venous thrombosis, pulmonary embolism, gastric ulceration with or
without hemorrhage, paralytic ileus, and decubitus ulceration are
constant hazards.
 Excessive use of muscle relaxants, which are an integral part of care,
may produce iatrogenic apnea.
 Cardiac arrhythmias, including asystole, unstable blood pressure, and
labile temperature regulation reflect disordered autonomic nervous
system control that may be aggravated by inattention to maintenance
of intravascular volume needs.
PROGNOSIS

 Recovery in tetanus occurs through regeneration of

synapses within the spinal cord and thereby the
restoration of muscle relaxation.
 However, because an episode of tetanus does not result
in the production of toxin-neutralizing antibodies, active
immunization with tetanus toxoid at discharge with
provision for completion of the primary series is
mandatory.
 The most important factor that influences outcome is the
quality of supportive care.
 Mortality is highest in the very young and the very old.

 Most fatalities occur within the 1st wk of illness

PROGNOSIS..
 A favorable prognosis is associated -with a long incubation period,
-absence of fever, and
localized disease.

 An unfavorable prognosis

- onset of trismus <7 days after injury and

- with onset of generalized tetanic spasms <3 days after onset of trismus.
-Age neonates , old age
-fever
- cephalic tetanus(because of breathing and feeding difficulties)

.
Reported case fatality rates
for generalized tetanus are 5-35%, and
for neonatal tetanus they extend from <10%
with intensive care treatment to >75% without it.
PREVENTION
 Tetanus is an entirely preventable disease.
 A serum antibody titer of ≥0.01 U/mL is considered
protective.
 Active immunization should begin in early infancy with
combined diphtheria toxoid–tetanus toxoid–acellular pertussis
(DTaP) vaccine at 2, 4, and 6 mo of age, with a booster at 4-6
yr of age and at 10-yr intervals thereafter throughout adult life
(tetanus and reduced diphtheria toxoid [Td] or tetanus, and
reduced diphtheria and pertussis toxoids [Tdap]).
 For unimmunized persons >7 yr of age, the primary
immunization series consists of 3 doses of Td toxoid given
intramuscularly, with the 2nd given 4-6 wk after the 1st and
the 3rd given 6-12 mo after the 2nd.
PREVENTION…
 Immunization of women with tetanus toxoid prevents
neonatal tetanus, and the World Health Organization is
currently engaged in a global campaign for elimination
of neonatal tetanus through maternal immunization with
at least 2 doses of tetanus toxoid.
 Clean delivery and proper care practice
WOUND MANAGEMENT

 Tetanus prevention measures after trauma consist of

inducing active immunity to tetanus toxin and of
passively providing antitoxic antibody
 Tetanus prophylaxis is an essential part of all wound
management, but specific measures depend on the nature
of the injury and the immunization status of the patient.
 A tetanus toxoid booster (preferably Td or Tdap) is
administered to all persons with any wound if the tetanus
immunization status is unknown or incomplete.
 A booster is administered to injured persons who have
completed the primary immunization series if
 (1) the wound is clean and minor but ≥10 yr have passed
since the last booster or
 (2) the wound is more serious and ≥5 yr have passed
since the last booster.

 Persons who experienced an Arthus reaction after a dose
of tetanus toxoid–containing vaccine should not receive
Td more frequently than every 10 yr, even for tetanus
prophylaxis as part of wound management.
 In a situation of delayed wound care, active
immunization should be started at once.