Clostridium Tetani

Article Author:
Elizabeth George
Article Author:
Orlando De Jesus
Article Editor:
Renuga Vivekanandan
Updated:
6/2/2020 6:45:04 PM
PubMed Link:
Clostridium Tetani

Introduction

Clostridium tetani is the causative organism for the disease process known as tetanus. Clostridia are anaerobic organisms with at least 209 species and five subspecies. Clostridium tetani is one of the 4 most well-known exotoxin producing pathogens within this category. Although widespread vaccination efforts have reduced the public health threat, tetanus is a potentially fatal condition. Thus, it is important to recognize the typical clinical presentation, immediate management, and treatment of C. tetani infection.[1][2] The key to tetanus infection is to prevent it with vaccination.

Tetanus is a serious life-threatening disorder that presents with painful muscular spasms and hypertonia. Despite widespread vaccination in the US, the disorder still occurs. Tetanus is classified into four categories; localized, generalized, neonatal, and cephalic. The severity of the illness is dependent on the amount of toxin that reaches the central nervous system.

Etiology

C. tetani is part of a genus of obligate anaerobic, saprophytic, gram-positive organisms well known for its toxin-producing ability making it one of the most dangerous of its genus. It is a spore-forming organism that cannot be eliminated from the environment and can withstand extreme temperature conditions in both indoor and outdoor environments. It is well known that tetanus spores can survive in the environment for many years and are often resistant to heat and disinfectants. The source of infection in most people is a wound. In others, tetanus may develop from a burn injury, abscess following a surgical procedure, intravenous drug abuse, or gangrene. In many cases, the patients have incomplete immunization or have not been vaccinated. In most people, the immunity from tetanus vaccine declines with advancing age. Thus, vaccination or booster shots are required for prevention.[3]

Neonatal tetanus is often the result of home delivery with the unsanitary cutting of the umbilical cord.

Epidemiology

Most cases of tetanus take place in developing countries where immunity is lacking, and particularly in areas where natural disasters have occurred. The spores of C. tetani are present in the environment irrespective of geographical location. The spores reside in the soil and can enter through an opening in the skin. All ages are susceptible to infection, and the case-fatality rate can approach 100% if immediate medical intervention is not available. Neonates are at increased risk in under-developed areas of the world when non-sterilized medical equipment is used to cut the umbilical cord. The World Health Organization (WHO) estimates that in 2015, approximately 34,000 neonates died from neonatal tetanus. Tetanus is a vaccine-preventable disease for which tetanus toxoid-containing vaccines (TTCV) are included in the routine childhood immunization schedule. The average annual incidence in the United States from 2001 to 2008 was 0.01 per 100,000 population per WHO. The age groups at highest risk are children and the elderly secondary to reduced immunity. Tetanus toxin vaccine was first produced in 1924 and used extensively for the first time among soldiers during World War II. Currently, the pentavalent vaccine, which protects against diphtheria, tetanus, pertussis, Hib, and hepatitis B (DTP-Hib-HepB), is the most commonly used childhood vaccine worldwide.[4][5]

Pathophysiology

Tetanus is characterized by severe, diffuse muscle contractions. The muscular rigidity and spasms of tetanus are caused by tetanus toxin (tetanospasmin). The transmission of C. tetani is through the exposure of a deep tissue wound to the spores which are present in soil or fecal matter from animals or humans. Given that C. tetani is an obligate anaerobe, the anaerobic tissue wound provides an ideal environment for the replication and growth of C. tetani. Following extensive bacterial replication at the wound site, an expression of the genes encoding the 2 toxins, tetanospasmin, and tetanolysin, occur. Tetanospasmin is taken up at the nerve terminals of the peripheral nervous system and can interfere with the vesicular release of acetylcholine at the neuromuscular junction. Thus, an initial presenting symptom of tetanus is flaccid paralysis which can resemble the effects of C. botulinum. However, the toxin is transported in a retrograde fashion toward the central nervous system and eventually reaching the spinal cord or brainstem. It is here that the tetanus toxin produces its characteristic satellite of symptoms. The toxin causes inhibition of the release of GABA and glycine inside inhibitory nerve terminals that control the activity of the lower motor neurons. Thus, this action causes a hyperactivity effect leading to involuntary contraction of the skeletal muscles.[6]

History and Physical

The incubation period of tetanus is approximately 8 days but ranges from 3 to 21 days.

Neonatal tetanus is seen in children less than 1 month, and have a shorter incubation period. Within the first 7 days, the infant is irritable, develops severe rigidity, and has a poor outcome. Neonatal tetanus still remains a major cause of death in developing countries. It is often due to unsterile transection of the umbilical cord following delivery, in addition to a lack of maternal vaccination.

Generalized tetanus is the most recognizable and well-known form and is characterized by specific clinical findings including trismus, dysphagia, nuchal rigidity, opisthotonus (backward arching of the head, neck, and spine), risus sardonicus (sustained spasm of facial muscles that resembles a grin), systemic rigidity, and tonic contractions. Patients can also experience airway compromise presenting as dyspnea and eventually airway obstruction and apnea. The patient often develops excruciating pain from these contractions which can result in tendon rupture and fractures. The clinical presentation of tetanus can sometimes have an early phase that includes symptoms of autonomic over-activity (irritability, restlessness, sweating, and tachycardia).

Local tetanus is somewhat rare and presents with muscle contractions in a localized body region.

Cephalic tetanus is a form of local tetanus that can present as dysphagia, trismus, and focal cranial neuropathies and sometimes mistaken for a cerebrovascular accident. These cases are rare and may occur after an ear infection or head trauma.

Evaluation

Diagnosis of tetanus is based on the physical exam, immunization history, and the clinical presentation while less emphasis is placed on laboratory testing. Differentiating tests include blood, urine, and tissue assays.[5][7] The spatula test involves touching the oropharynx with a tongue blade and determining if the patient has a gag reflex. If tetanus is present the patient will attempt to bite down on the blade; normal people will immediately gag and expel the spatula.

Treatment / Management

The focus of acute tetanus management should center around toxin mitigation and aggressive symptom management including airway protection. All patients with tetanus-prone wounds should undergo immediate cleansing and debridement to eradicate spores and avoid further spread of the toxin from the tissue to the bloodstream. Patients with signs and symptoms of tetanus should be admitted to the intensive care unit for initial management. Some patients may even require mechanical ventilation. Symptom management is of the utmost importance.

Tetanus toxin binds irreversibly to the tissue, so the focus of neutralization is the unbound toxin. Human tetanus immune globulin should be given as soon as tetanus is suspected at a dose of 500 units. Antimicrobial therapy for the wound is typically given for 7-10 days. It is important to note that antimicrobial therapy plays a relatively minor role in the management of tetanus.

Muscular spasms in the setting of tetanus are life-threatening and can lead to respiratory compromise, aspiration, and exhaustion. Benzodiazepines can be used in controlling the rigidity and spasms associated with tetanus. In situations where sedation is not sufficient, neuromuscular blocking agents such as pancuronium or vecuronium can be used. Infection with C. tetani does not provide immunity, and thus, all patients with the diagnosis of tetanus should receive immunization as soon as possible with tetanus toxoid.[4][8][9]

Autonomic complications may require management with magnesium sulfate in combination with a benzodiazepine. If magnesium is administered intravenously, the patellar reflex should be monitored. If areflexia occurs, the dose of magnesium should be lowered. Morphine can also be used to manage pain and other autonomic symptoms but it can cause hypotension. Patients with bradycardia may need a temporary pacemaker.

Differential Diagnosis

  • Encephalitis
  • Meningitis
  • Dystonia (congenital and acquired)
  • Drug-induced dystonias
  • Intracranial hemorrhage
  • Hepatic encephalopathy
  • Seizure
  • Strychnine poisoning
  • Neuroleptic malignant syndrome

Prognosis

The prognosis following tetanus depends on time to symptoms or incubation period. In general, a short incubation period usually indicates severe disease. Negative prognostic factors including an incubation period of fewer than 48 hours, addiction to narcotics, generalized tetanus, high fever (greater than 104F), acquiring tetanus from surgery, burns, intravenous drug abuse, or a septic abortion. Both cephalic and neonatal tetanus have poor outcomes.

Patients with localized tetanus have low mortality and morbidity. Recovery in most patients is slow but can take months or years for a full recovery. Unfortunately, some patients may remain hypotonic for life. Since tetanus does not provide any immunity, those who survive should be actively immunized.

Complications

  • Respiratory arrest
  • Upper airway obstruction
  • Fractures
  • Cardiac arrhythmias & hypertension
  • Stress ulcers
  • Coma
  • Nerve damage
  • Hypoxic injury
  • Paralytic ileus
  • Coma
  • Cranial nerve palsies
  • Contractures
  • Permanent hypotonia

Deterrence and Patient Education

Tetanus toxin is administered through vaccination with DTP at 2, 4, 6, 12-18 months of age and then at 4-6 years, 11-12 years, and every 10 years thereafter. Pregnancy is not a contraindication to vaccination in the 2nd or 3rd trimester.

Secondary prevention is done by thorough wound cleaning, debridement, and administration of tetanus toxoid. It is not always necessary to wait for 10 years to get the adult tetanus toxoid after the last dose as the duration decrease with increasing age.

Enhancing Healthcare Team Outcomes

Tetanus is a serious life-threatening infection that is associated with high morbidity and mortality. The best way to manage tetanus is to prevent it in the first place. Public health nurses, pharmacists, and primary care clinicians need to educate patients on the importance of childhood tetanus vaccination. Patients should be educated about how tetanus is acquired and when they should seek medical assistance. The key is to see a clinician as soon as possible. Healthcare workers should develop aseptic techniques when doing procedures and emergency room personnel should always ask patients if they have had tetanus immunization. Anytime a nurse manages a wound, he or she should always ask the patient if he or she is up to date with tetanus vaccination. Only through open communication and creating awareness of the morbidity of tetanus can the outcomes be improved. [10]

The prognosis of patients infected with C.Tetani depends on the time of presentation, the inoculation dose, and the time to the first tetanic spasm. Overall, patients who develop tetanus quickly have a poor prognosis. For those who survive tetanus, they may have some residual deficits but the life span is not reduced. However, some patients may have hypotonia for life. Despite active infection, no immunity is created and the patients need active immunization to prevent a recurrence. [11][12](Level V)


References

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