Tetanus

F de Assis Aquino Gondim, Faculdade de Medicina Christus, Fortaleza, Brazil

r 2014 Elsevier Inc. All rights reserved.
This article is a revision of the previous edition article by Bradley A Cole, volume 4, pp 498–499, r 2003, Elsevier Inc.

Tetanus occurs when spores from the anaerobic gram-positive those older than 60 years of age. Nonimmunized, partially
bacteria Clostridium tetani release the neurotoxin tetano immunized, and heroin intravenous drug users are also at
spasmin. Clostridium tetani is ubiquitous on soil, dust, and higher risk in the USA. Worldwide, neonatal (umbilical stump
10–25% of human gastrointestinal tract (GI) tracts, but spores infection), childhood, and maternal tetanus are much more
require anaerobic conditions to germinate, such as with wound common. Mortality is also especially high in the elderly.
infection and tissue necrosis. Inoculation of C. tetani spores can
occur after any trauma causing skin or mucosal breakdown
although its exact source/localization is not always evident.
Diagnosis
Released tetanospasmin (heavy chain, C-fragment) binds to the
axons of a motor and autonomical neurons (ganglioside con-
The diagnosis is primarily a clinical one since wound cultures
taining receptors) and gain access to the central nervous system
are positive for C. tetani in only one-third of cases and there is
by retrograde axonal transport within 2–14 days (75–250 mm/
no other serological test to identify the toxin. Cerebrospinal
day), finally reaching the central inhibitory interneurons in the
fluid studies are normal, and other laboratory studies may
spinal cord and brainstem. The release of inhibitory neuro-
reveal nonspecific findings such as a mildly elevated white
transmitters glycine (spinal cord) and GABA (brainstem) is
blood cell count. Other conditions that can produce severe
impaired, resulting in excessive muscle activity, rigidity, and
sustained muscle rigidity should be considered, including
autonomical hyperactivity.
strychnine intoxication (no trismus), stiff-person syndrome
(slower onset and no trismus or facial involvement), neuro-
leptic malignant syndrome due to dopamine-blocking agents,
Signs and Symptoms hypocalcemic tetany, and meningoencephalitis (encephalo
pathy and seizures).
Symptoms typically develop within days to 3 weeks after in-
oculation (usually 8 days). Three major subtypes are described:
generalized, cephalic, and localized. Local tetanus may result
Treatment
only in muscle rigidity in the involved extremity and lasts for
months, spontaneously subsiding. When tetanospasmin
Prevention of tetanus by appropriate wound care (cleaning
reaches the blood stream and other nerve terminals, there is a
and antibiotics) and immunization is the key. Tetanus is given
sequential involvement of short and long nerves: head, trunk,
with the diphtheria and pertussis vaccinations in five doses
axial trunk, and then extremities. Early symptoms may include
from age 2 months to age 4–6 years. Booster tetanus–diph-
restlessness, headaches, and low-grade fever, followed by ri-
theria vaccinations should be given every 10 years thereafter.
gidity of the masseter (trismus or lockjaw) and other facial
This is especially important in the elderly, less than half of
muscles (cephalic forms), including the upper lip (risus sardo-
whom have received a tetanus booster within the past 10 years.
nicus). Eventually, stiffness and reflex spasms of axial muscles
Patients with tetanus-prone wounds and an incomplete or an
(opisthotonus) and abdominal muscles occur, followed by ri-
uncertain vaccination history should receive three vaccinations
gidity of proximal muscles in the arms and legs. Muscle spasms
(at 1, 2, and 6–12 months) as well as an injection of the
may be severe and are triggered by sensory stimuli such as
human tetanus immune antitoxin (there are different proto-
anxiety or attempts to move the muscles. Touching the pos-
cols with intramuscular, subcutaneous, and intravenous ad-
terior pharynx may trigger masseter spasms (positive spatular
ministration). Patients with wound injuries do not need to
test). Patients may eventually become unable to speak or
receive tetanus boosters if these were given within the past
swallow, and laryngospasm may result in respiratory failure
5 years.
and asphyxia. Autonomical hyperactivity with blood pressure
Patients with tetanus need to be carefully searched for the
and heart rate fluctuations, arrhythmias, diaphoresis, fever, and
wound. If tetanus is suspected clinically, human tetanus im-
hypersalivation are also common in generalized tetanus.
mune globulin should be given intramuscular, preferably near
the wound site. Combined intramuscular and intrathecal im-
mune globulin is more effective than intramuscular injection.
Epidemiology This will remove the circulating toxin but not remove the toxin
that is already present in the central nervous system. Wound
Tetanus is much more common in developing countries. There care, including washing and dressing, removal of a foreign
are approximately 300 000 reported cases worldwide/year. body, and antibiotic treatment is vital. Intravenous metroni-
From 1995 to 1997, only 124 cases were reported in the USA. dazole for 7–10 days is the drug of choice. Clindamycin, ery-
More than one-third of tetanus cases in the USA occurred in thromycin, and penicillin are alternatives.

Encyclopedia of the Neurological Sciences, Volume 4 doi:10.1016/B978-0-12-385157-4.00647-3 417

418 Tetanus
Intubation may be required early in the course, and
nasogastric tube feeding is also frequently necessary. Recovery
of respiratory function typically takes more than 4 weeks, and
tracheostomy should be considered. Muscle spasms are treated
with diazepam or lorazepam, frequently in very high doses.
Severe cases may require neuromuscular blockade with pan-
curonium or vecuronium. Monitoring and treatment of
autonomical instability are also important. High blood pres-
sure should be treated with b-blockers such as labetalol. The
acute phase of tetanus lasts approximately 1 week, and it is
during this time that there is the greatest risk of respiratory
failure and arrhythmias. Usually, there is stabilization during
the next 2 or 3 weeks, with the total course of the illness for
most patients lasting between 1 and 2 weeks. After the course
of the disease, patients should receive a booster immunization
treatment.
See also: Rigidity. Spasms. Tetany. Tropical Neurology
Further Reading
Centers for Disease Control and Prevention (2011) Updated recommendations for
use of tetanus toxoid, reduced diphtheria toxoid and acellular pertussis (Tdap)
vaccine from the advisory committee on immunization practices, 2010. Morbidity
and Mortality Weekly Report 60: 13–15.
Farrar JJ, Yen LM, Cook T, et al. (2000) Tetanus. Journal of Neurology,
Neurosurgery, and Psychiatry 69: 292–301.
Pearce JM (1996) Notes on tetanus (lockjaw). Journal of Neurology, Neurosurgery,
and Psychiatry 60: 332.
Reddy P and Bleck TP (2010) Clostridium tetani (Tetanus). In: Mandell GL, et al.
(eds.) Mandell, Douglas, and Bennett’s Principles and Practice of Infectious
Diseases, 7th edn., vol. 2, pp. 3091–3096. Philadelphia: Churchill Livingstone
Elsevier.
Srinavasan J and Sabin TD (2002) Tetanus. In: Katirkl B, Kaminski HJ, Preston DC,
Ruff RL, and Shapiro BE (eds.) Neuromuscular Disorders in Clinical Practice,
1st edn., pp. 1257–1263. Massachusetts: Butterworth-Heinemann.
Zimmerman RK (2000) Adult vaccination, part 1: Vaccines indicated by age.
Teaching immunization for medical education (TIME) Project. Journal of Family
Practice 49(9 Suppl): S41–S50.
Relevant Websites
http://www.emedicinehealth.com/tetanus/article_em.htm
Medscape.
http://www.nlm.nih.gov/medlineplus/tetanus.html
NIH.
http://www.who.int/topics/tetanus/en/
World Health Organization.