Tetanus in Infant/Neonate
This bacterium is spore-forming, and spores are widely distributed throughout the world. Disease occurs after the spores are inoculated into a deep puncture wound. The portal of entry may also be a burn wound, infection of the skin or middle ear, or septic abortion. It also might be minor and not readily apparent. Germination leads to the production of an exotoxin, tetanospasmin. This metalloprotease destroys the protein essential for the release from the presynaptic vesicles of the neurotransmitters that prevent the firing of the neurons from the motor and autonomous systems. The retrograde neuronal transport of tetanospasmin and entry in the central nervous system accounts for the clinical manifestations of the disease that are different from those of botulism. Another toxin, tetanolysin, is also produced. The role of this toxin in infection is not known with certainty, but it is suspected that it may cause local tissue damage and thereby optimize the local conditions for bacterial replication.
In developed countries such as the United States, tetanus is rare due to the near-universal vaccination of children. Surveillance of patients who develop the disease reveals that many were inadequately vaccinated or did not receive proper prophylaxis following an injury. In the developing world, tetanus is more common, and outbreaks can be seen following natural disasters. Neonatal tetanus is also much more common in the developing world.
The period from the time of wound inoculation to the onset of symptoms can vary. It is generally about 1 week (range 1-60 days). The incubation period may be somewhat shorter in neonates.
Patients with generalized tetanus (the most common clinical presentation) present with excruciatingly painful muscle spasms, trismus (lockjaw, the common name of tetanus), risus sardonicus (sardonic smile), opisthotonus (spasms and arching of the back), a rigid abdomen, apnea, and dysphagia. Other presentations of tetanus include local tetanus (muscle contractions at the site of spore inoculation) and cephalic tetanus (involving only the cranial nerves and usually manifesting as diplopia or facial paralysis). Both of these presentations can progress to generalized tetanus.
The symptoms of generalized tetanus may last 2-4 weeks, during which time the patient will typically require intensive care. During this time, the patient might experience autonomic dysfunction (especially labile blood pressure and heart rate), which can be life-threatening. After the acute illness, symptoms continue to improve over the following weeks.
An additional clinical pattern is neonatal tetanus. This is caused by contamination of the umbilical stump when a mother has been inadequately vaccinated against tetanus. This severe form of illness has symptoms similar to generalized tetanus and usually presents within the first 2 weeks of life. Mortality is high, and survivors may suffer developmental delay.
In the United States, tetanus is more common in patients with diabetes mellitus and a history of injection drug use.
A35 – Other tetanus
76902006 – Tetanus
- Strychnine poisoning – Symptoms may mimic tetanus, and serum and urine testing for strychnine should always be performed when tetanus is suspected.
- Dystonic reactions – Lateral head turning seen in dystonic reactions is rare in tetanus. Benztropine may be administered to rule out a dystonic reaction.
- Dental infection – Dental infection may cause trismus but no other symptoms of tetanus.