Tetanus

MRSA Slideshow

• Tetanus Overview
• Tetanus Causes
• Tetanus Symptoms
• When to Seek Medical Care
• Exams and Tests
• Tetanus Treatment
• Self-Care at Home
• Medical Treatment
• Next Steps
• Follow-up
• Prevention
• Outlook
• Vaccine (Shot) Complications (Side Effects)
• Information
• Synonyms and Keywords
• Authors and Editors

Tetanus Overview

Tetanus is an infectious disease caused by contamination of wounds from bacteria that live in the soil. The causative bacterium Clostridium tetani is a hardy organism capable of living many years in the soil in a form called a spore. The bacterium was first isolated in 1899 by S. Kitasato while he was working with R. Koch in Germany. Kitasato also found the toxin responsible for tetanus and developed the first protective vaccine against the disease.

Tetanus occurs when a wound becomes contaminated with bacterial spores. Infection follows when spores become activated and develop into gram-positive bacteria that multiply and produce a very powerful toxin (poison) that affects the muscles. Tetanus spores are found throughout the environment, usually in soil, dust, and animal waste. The usual locations for the bacteria to enter your body are puncture wounds, such as those caused by rusty nails, splinters, or insect bites. Burns, any break in the skin, and IV drug access sites are also potential entryways for the bacteria Tetanus is acquired through contact with environment; it is not transmitted from person to person.

Tetanus results in severe, uncontrollable muscle spasms. The jaw is "locked" by muscle spasms, causing the disease to sometimes be called "lockjaw." In severe cases, the muscles used to breathe can spasm, causing a lack of oxygen to the brain and other organs that may possibly lead to death.

The disease in humans is the result of infection of a wound with the spores of the bacteria Clostridium tetani. These bacteria produce the toxin (poison) tetanospasmin, which is responsible for causing tetanus. Tetanospasmin binds to motor nerves that control muscles, enters the axons (filaments that extend from nerve cells), and travels in the axon until it reaches the body of the motor nerve in the spinal cord or brainstem (a process termed retrograde intraneuronal transport). Then the toxin migrates into the synapse (small space between nerve cells critical for transmission of signals among nerve cells) where it binds to presynaptic nerve terminals and inhibits or stops the release of certain inhibitory neurotransmitters (glycine and gamma-aminobutyric acid). Because the motor nerve has no inhibitory signals from other nerves, the chemical signal to the motor nerve of the muscle intensifies, causing the muscle to tighten up in a huge continuous contraction or spasm. If tetanospasmin reaches the bloodstream or lymphatic vessels from the wound site, it can be deposited in many different presynaptic terminals resulting in the same effect on other muscles.

In the United States, because of widespread immunization and careful wound care, the total annual number of cases has averaged about 40-50 cases per year since 1995. In developing countries of Africa, Asia, and South America, tetanus is far more common. The annual worldwide incidence is between 500,000-1 million cases. The majority of new cases worldwide are in neonates in Third World countries.

• The disease can show four possible types:



• Generalized tetanus can affect all skeletal muscles. It is the most common as well as the most severe form of the four types.



• Local tetanus manifests with muscle spasms at or near the wound that has been infected with the bacteria.



• Cephalic tetanus primarily affects one or several muscles in the face rapidly (in one to two days) after a head injury or ear infection. Trismus ("lockjaw") may occur. The disease can easily progress to generalized tetanus.



• Neonatal tetanus is similar to generalized tetanus except that it affects a baby that is less than 1 month old (called a neonate). This condition is rare in developed countries.