TETANUS

HASHMI FURQAN
 Epidemiology
– Reservoirs. C. tetanus is found in feces and soil.
– Incidence
• Tetanus is prevalent in third-world countries.
• Each year, 50-150 cases are reported in the United States;
however, the actual number of cases may be twice as high
because there is poor compliance with mandatory notification.

– Fatality rates More than 50% of the infected individuals

are over 60 years of age. On average, the fatality rate is
15%-30%, but infants and the elderly have greater
fatality rates.
Causative Agent
• Clostridium tetani (spore producing bacterium) G +ve
bacilli
Determinants of Pathogenicity
• C. tetani produces a potent neurotoxin tetanospasmin,
at the site of infection.
• The toxin inhibits the release of inhibitory transmitter
causing spastic paralysis.
 Pathogenesis

• The usual mode of infection is by penetrating trauma, which

provides an anaerobic environment for growth of the organism.
• The organism begins to elaborate toxin, which binds to peripheral
nerve endings, is internalized, and travels via retrograde intra-
axonal transport to the spinal cord, where it interferes with the
activity of the inhibitory neuron.

• Incubation period  few days to as long as 3 weeks, depending

on the site of injury and the dosage.
– A longer incubation time is usually related to injury sites
farther from the CNS.
– Shorter incubation times are associated with more
serious disease and with increased mortality rates.
 Clinical Disease

• Local tetanus is characterized by persistent spasm around the

injury site. This is a mild form with a low mortality rate.

• Cephalic tetanus is associated with dysfunction of one or more

of the cranial nerves, most commonly cranial nerve VII.

• Generalized tetanus is the most common from of tetanus. The

spasm of potent muscles predominates over that of weak
muscles, leading to the typical symptoms of Trismus (lockjaw),
Risus Sardonicus, and Opisthotonos.

• Other symptoms include seizures, tachycardia, arrhythmias,

bacterial meningitis, hypocalcaemia, and respiratory arrest.
•
 Treatment
• Treatment must be initiated based on a clinical
diagnosis, because C. tetani is difficult to isolate and
there is no time to wait for the results of bacteriological
examinations.
– Debridement. Wounds should be debrided.
– Tetanus Immunologlonbulin (TIG) and Tetanus
Toxin should be administered to provide passive
and long-lasting immunity, respectively.
– Penicillin G & Metronidazole are particularly.
– Supportive care
• Respiratory support may be necessary
• The patient should be placed in a dark, quiet
room because sudden noise can trigger
spasmodic crises.
• Valium (benzodiazepine)  prevents the spasm
 Control and Prevention

• Tetanus is a fully preventable disease. Prevention

involves immunization with Tetanus Toxoid
(chemically detoxified toxin)
– In infants, tetanus toxoid is administered in
association with diphtheria toxoid killed Bordetella
pertussis, beginning at 6-8 weeks of age.
– Boosters should be administered at 6—12 months
of age, pre school age, and every 10 years
thereafter. (In adults, it is recommended to continue
boosting with diphtheria and tetanus toxoids only)
RABIES
• Preventable viral disease.
• Transmitted through rabid animal bite (cat, bat, dog,
rodents, horse, donkey, raccoons, skunks, fox etc).
• Rabies virus  Mononegavirales, viruses with a
nonsegmented, negative-stranded RNA genomes. Bullet
shaped virus (Rhabdoviridae). Genus [Lyssavirus,
Ephemerovirus & Vesiculovirus].
• The genus Lyssavirus includes rabies virus, Lagos bat,
Mokola virus, Duvenhage virus, European Virus1 & 2
and Australian bat virus.

• Replication fusion of rabies virus envelope to the host

cell membrane (adsorption)  infection (interaction of
the G protein and specific cell surface receptors.

• After adsorption it penetrates the host cell and enters the

cytoplasm
• The early symptoms of rabies in people are similar to
that of many other illnesses, including fever, headache,
and general weakness or discomfort.

• Progression of disease  more specific symptoms

appear including insomnia, anxiety, confusion, slight or
partial paralysis, excitation, hallucinations, agitation,
hypersalivation (increase in saliva), difficulty swallowing,
and hydrophobia (fear of water).

• Death usually occurs within days of the onset of these

symptoms.
• Diagnosis:
– direct fluorescent antibody (DFA) test, which looks for
the presence of rabies virus antigens in brain tissue.
In humans, several tests are required.
 Prevention and treatment
Rabies vaccine (inactivated rabies virus)
•Pre- and post-exposure prophylaxis
Pre-exposure prophylaxis
•Immunization should be to high risk exposure as in lab
staff (handling rabies virus).
•Animal handlers
•Travellers (where rabies id enzootic).
•3 doses of Rabies vaccine.
Post-exposure management
•Cleansing of wound by soap and water.
•Disinfectant.
•Dressing the wound (covering)
• Fully immunized individuals
– 2 doses of cell-derived vaccine (I.M)
– Day 0 and day 3.

• Unimmunized individuals
– 5 doses (over 1 month) (I.M).
– Day 0, 3, 7, 14 and 30.

Vaccine available in Pakistan

– Verorab (GSK).