Clostridium tetani

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Pathology

For more information, see: Tetanus.

Clostridium tetani spores enter body tissue through wounds, lacerations, and burns, settling in dead cells that lack oxygen. Initially unnoticed, the spores are then able to germinate and spread its toxin, long before diagnosis and pursuit of treatment. All identified strains have been found to produce a common toxin called tetanospasmin. The potent neurotoxin blocks the release of necessary neurotransmitters in the central nervous system's transmission of inhibitory nerve impulses [1]. It is the inhibitory neuron messages that allow the muscles of the body to relax by halting the release of acetylcholine from excitatory neurons, which stimulate muscle contraction. The resulting effect in humans begins with muscle spasms at the sight of infection. As the infection spreads along neurons of the spinal chord and brain, it could lead to spastic paralysis and may be fatal. The most recognized associated manifistation of the disease is trismus, or lockjaw. The muscles and nerves of the neck and jaw are commonly the first to be affected before spreading to other parts of the body. Death is usually the result of breathing difficulties that arise due to the spasms and lead to respiratory arrest.

Symtoms

Tetanus has been known to take up to 10 years before manifestations may be observed. Aside from lockjaw, difficulty in swallowing, drooling, and persistent back spasms are among early signs. Later symtoms include perfuse sweating, hyperthermia, cardiac arrythmias and fluctuations in blood pressure. These manifestations indicate the toxic affects of both the somatic and autonomic nervous systems that involve voluntary and involuntary muscle contractions, respectively. The disease can also be transferred to a fetus by a mother with no immunity through the placenta, where nutrients are absorbed into the blood of the developing baby via the umbilical chord. This is a neonatal infection and the baby is born with the disease [2].

Treatment and Prevention

Therapy for suspected cases and diagnoses include antibiotics, such as penicillin and tetracyclines, in addition to antitoxin treatment and prompt surgical care of the infected wounds and tissues. Vaccination is available for proactive prevention. Individuals are actively immunized with DPT (diphtheria, pertussis, tetanus) toxoid as infants, and should continue vaccination in ten year intervals. The toxoid prompts human cells to make neuralizing antibodies against the binding component of the tetanus toxin. Individuals are passively immunized with tetanus immuno globulin [3].

The tetanus disease is relatively uncommon in North America and industrialized countries. The condition pccurs more often in underdeveloped countries where immunizations are not widely available and agricultural regions where contact with animal fecal matter is likely.

  1. http://bioweb.uwlax.edu
  2. Todar, Ken. Pathogenic Clostridia. Ken Todar's Microbial World. University of Wisconsin: Madison. 2005 <http://bioinfo.bact.wisc.edu/themicrobialworld/clostridia.html>
  3. Kaiser, Dr. Gary E."Tetanus." 7 Jan 2005<http://student.ccbcmd.edu>