Tetanus

Reşat ÖZARAS, MD., Prof. Infectious Dept.

Definition

Tetanus is a toxin-mediated

infectious disease characterized by

increased muscle tone and spasms

It is caused by tetanospasmin, a powerful

protein toxin elaborated by Clostridium tetani.

Etiology-1

C. tetani anaerobic, motile gram-positive rod forms a terminal spore: resembles a tennis

racket. The organism is found worldwide

in soil in animal feces, occasionally in human feces.

Spores may survive for years in environments and are resistant to boiling for 20 min.

Vegetative cells, however, are easily inactivated and are susceptible to several antibiotics (metronidazole, penicillin, and others).

Etiology

Tetanospasmin is formed in vegetative bacteria under plasmid control.

It has a heavy chain, which mediates binding to nerve-cell receptors and entry into these cells, and a light chain, which acts to block neurotransmitter release.

Epidemiology

Tetanus occurs sporadically

and always affects nonimmunized persons Tetanus is entirely preventable by immunization In countries without a comprehensive

immunization program, tetanus occurs predominantly in neonates and young children; an estimated ~500.000 neonates died

of tetanus worldwide in 1993.

Wound classification

Clinical features Tetanus prone Non-tetanus prone

Age of wound >6 hours 6 hoursConfiguration Stellate Linear Depth >1 cm 1 cmMechanism of injury Missile, crush Sharp surface burn, frostbite (glass, knife)Devitalized tissue Present Absent Contaminants Present Absent

Pathogenesis-1

The injury may be major but often is trivial and, in some instances no injury can be identified.

Tetanus is also associated with burns, frostbite, surgery, abortion, and drug abuse

In some patients no portal of entry for the organism can be identified.

Pathogenesis-2

Contamination of wounds with spores of C. tetani.

Germination and toxin production take place only in wounds with devitalized tissue

Toxin released in the wound binds to peripheral motor neuron terminals, enters the axon, and is transported to spinal cord by retrograde intraneuronal transport.

Pathogenesis-3

The toxin then migrates across the synapse to presynaptic terminals, where it blocks release of the inhibitory neurotransmitters glycine and gamma-aminobutyric acid (GABA).

Clinical forms of tetanus

1-Generalized tetanus 2-Neonatal tetanus 3-Local tetanus 4-Cephalic tetanus

Generalized tetanus

The most common clinical form of the disease Characterized by increased muscle tone and

generalized spasms. The median time of onset after injury is 7 days;

15 percent of cases occur within 3 days and 10 percent after 14 days.

Typically, the patient first notices increased tone in the masseter muscles (trismus, or lockjaw).

Generalized tetanus

Dysphagia, stiffness or pain in the neck, shoulder, and back muscles appears concurrently or soon thereafter.

The subsequent involvement of other muscles produces a rigid abdomen and stiff proximal limb muscles

The hands and feet are relatively spared. Sustained contraction of the facial muscles results in a

risus sardonicus These spasms occur repetitively and may be

spontaneous or provoked by even the slightest stimulation.

Contraction of the back muscles produces opisthotonos

Generalized tetanus

A constant threat during generalized spasms is reduced ventilation or apnea or laryngospasm.

The severity of illness may be mild (few or no spasms), moderate (trismus and dysphagia), or severe (frequent explosive paroxysms).

Patients have no fever Mentation is unimpaired. Deep tendon reflexes may be increased. Dysphagia or ileus may preclude oral feeding.

Generalized tetanus

Autonomic dysfunction commonly complicates severe cases and is characterized by

labile or sustained hypertension, tachycardia, arrhythmia, hyperpyrexia, profuse sweating, peripheral vasoconstriction, and increased plasma and urinary catecholamine levels.

Other complications include pneumonia, fractures, muscle rupture, deep vein thrombophlebitis, pulmonary emboli, decubitus ulcer, and rhabdomyolysis.

Neonatal tetanus

It usually occurs as the generalized form It is usually fatal if left untreated. It develops in children born to inadequately

immunized mothers, frequently after unsterile treatment of the umbilical cord stump.

Its onset generally comes during the first 2 weeks of life.

Poor feeding, rigidity, and spasms are typical features of neonatal tetanus.

Local tetanus

It is an uncommon form in which manifestations are restricted to muscles near the wound.

The prognosis is excellent.

Cephalic tetanus

A rare form of local tetanus, follows head injury Trismus and dysfunction of one or more cranial

nerves, often the seventh nerve, are found The incubation period is a few days and the

mortality is high.

Diagnosis

The diagnosis of tetanus is based entirely on clinical findings.

CSF fluid examination yields normal results Muscle enzyme levels may be raised.

The differential diagnosis-1

The differential diagnosis includes local conditions also producing trismus, such as

1-Abscess,

2- strychnine poisoning,

3-dystonic drug reactions (such as

phenothiazines and metoclopramide),

4-tetany.

The differential diagnosis-2

Other conditions sometimes confused with tetanus include;

1-meningitis

2-rabies, and

3-an acute intraabdominal process

(because of the rigid abdomen).

The differential diagnosis-3

Markedly increased tone in central muscles

(face, neck, chest, back, and abdomen) with

superimposed generalized spasms and relative

sparing of the hands and feet strongly suggests

tetanus.

Treatment; the goals of therapy

1-To eliminate the source of toxin,2-Neutralize unbound toxin,3-Prevent muscle spasms, 4-Provide supportespecially respiratory supportuntil

recovery. 5-Patients should be admitted to a quiet room in an intensive

care unit6-Cardiopulmonary monitoring can be maintained continuously7-Stimulation can be minimized8-Protection of the airway is vital.9- Wounds should be cleansed, and thoroughly debrided.

Antibiotic therapy

Penicillin; 12 million units iv/day-10 days Metronidazole; 500 mgx4 or 1 gx2/day and the

absence of the GABA antagonistic activity seen with penicillin.

Clindamycin is alternative for the treatment of penicillin-allergic patients.

Antitoxin

Human tetanus immune globulin (TIG);

~5000 U IM, usually in divided doses because the volume is large.

The value of infiltrating the wound is unclear. Antibody does not penetrate the blood-brain

barrier.

Control of muscle spasms

Diazepam, a benzodiazepine and GABA agonist, is in wide use.

Barbiturates and chlorpromazine are considered second-line agents.

Mechanical ventilation and therapeutic paralysis with a neuromuscular blocking agent may be required for the treatment of spasms unresponsive to medication or spasms that threaten ventilation.

Prevention; immunization

1-Passive immunization with TIG

2-Active immunization with vaccine, preferably

Td in persons over age 7

Prevention; active immunization All partially immunized and unimmunized adults should

receive vaccine, The primary series for adults consists of three doses:

the first and second doses are given 4 to 8 weeks apart, the third dose is given 6 to 12 months after the second.

A booster dose is required every 10 years Combined tetanus and diphtheria toxoid (Td) adsorbed

(for adult use), rather than single-antigen tetanus toxoid, is preferred for persons over 7 years of age.

For clean minor wounds

Td is administered to persons who have

1-unknown tetanus immunization histories

2-received fewer than three doses of adsorbed

tetanus toxoid

3-received three or more doses of adsorbed

vaccine, with the last dose given more than 10

years previously

4-Passive immunization with TIG is not recommended for clean minor wounds

Contaminated or severe wounds

Vaccine should be given to those; if more than 5 years have elapsed since the last dose.

It is given for all other wounds if the patient's vaccination history indicates unknown or partial immunization.

The dose of TIG for passive immunization is 250 U IM , which produces a protective antibody level in the serum for at least 4 to 6 weeks

Vaccine and tetanus antitoxin should be administered at separate sites in separate syringes.

Preventing neonatal tetanus

1-Maternal vaccination even during pregnancy

2-Efforts to increase the proportion of births

that take place in the hospital

Prognosis

The application of methods to support respiration has markedly improved the prognosis in tetanus; mortality rates as low as 10 % have been reported

The outcome is poor; 1-in neonates and the elderly 2-in patients with a short incubation period, 3-a short interval from the onset of symptoms to admission, 4-or a short period from onset of symptoms to the first spasm (period of onset).