Tetanus Routine Immunizations Prevent Eleva Term paper
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AbstractThe mortality rate among untreated tetanus patients remains significantly high despite the availability of vaccinations, and implementation of immunization programs for children. Periodic boosters of the vaccine are also strongly recommended.1,2 Although the incidence of tetanus has decreased, the death rate that still exists due to the disease is alarming. The largest challenge of reducing this statistic lies in convincing healthy persons, patients, and health care providers to consider tetanus immunization.2 Tetanospasmin, or tetanus toxin, is the toxin produced by the gram-positive, spore forming bacilli Clostridium tetani.1,2 Tetanus toxin is responsible for the clinical manifestations of tetanus, which presents itself in various degrees of severity. The disease is diagnosed solely through physical evaluations since microbiological and blood tests do not exist to confirm diagnosis of tetanus.1 Treatment for infected patients includes airway maintenance and stabilization of patient, tetanospasmin absorption inhibition, elimination of the pathogen, and other supportive measures. Infection of tetanus shows an inadequate immunization against the neurotoxin. Tetanus is a prime example of a serious preventable disease that remains a threat even in developed countries, such as the United States.2 Over the last fifty years, the incidence of tetanus has steadily decreased. Despite the widespread availability of a safe and effective vaccine against tetanus, the mortality rate among untreated patients remains significantly high.1 The success in the reduction of tetanus cases in the United States can be contributed to the immunization program for children and the recommendation of routine booster shots for patients every 10 years.1,2 However, the high percentage of tetanus related death, is of concern. This serious disease can be thwarted with preventative measures. The challenge lies in convincing healthy persons, patients, and health care providers to consider tetanus immunization.2 Clostridium tetani (C. tetani), the pathogens responsible for tetanus, or "lock jaw," are gram positive, spore-forming bacilli that are found primarily in the soil and feces.1,2 Under anaerobic conditions, the spores of C. tetani germinate to produce two toxins: tetanolysin and tetanospasmin. Tetanolysin is a hemolysin that has not been recognized to exhibit pathologic activity. Tetanospasmin, or tetanus toxin, is the toxin responsible for the clinical manifestations of tetanus. C. tetani require a compromise of the host's skin barrier for inoculation to occur.1 Infection most commonly originates in a minor wound.1,2 The germination and conversion to toxin-producing vegetative form of the bacilli occurs only in wounds favorable to the proliferation of C. tetani, which includes low oxygen tension.1 When the bacteria die and lyse, the neurotoxin, tetanospasmin, is released.3 Tetanospasmin is synthesized by the bacteria as a single 151-kd chain. It is subsequently cleaved to generate toxins with two chains joined by a single disulfide bond. The neurotoxin's heavy chain is responsible for specific binding to neuronal cells and for transport proteins.2 The light chain of tetanospasmin, a zinc endopeptidase, selectively cleaves the synaptic vesicle membrane protein synaptobrevin. The cleavage prevents exocytosis and release of inhibitory neurotransmitters (gamma-aminobutyric acid and glycine) at synapses within the spinal cord motor nerves.1 Tetanospasmin reaches the central nervous system either by blood-borne delivery to peripheral nerves or by retrograde intraneuronal transport, which takes from two to 14 days.1,2With inhibitory control suppressed, the resting firing rate of motor neurons increases, leading to muscle rigidity and spontaneous muscle contraction.1 The autonomic nervous system is also effected. Sympathetic overactivity is caused by the inhibition of acetylcholine, norepinephrine, and enkephalin release at neuromuscular junctions.Muscle rigidity, generalized spasms, and autonomic instability characterize generalized tetanus, the most common form of the disease.1 Incubation periods range from a few hours to greater than one month, but periods less than 7 days correlate with severe disease and complications. Approximately 75% of the cases begin with stiffness in the masseter muscles, commonly referred to as "lock jaw." The patient may also have stiffness in the shoulders and back muscles. As this form of the disease progresses over the next one to four days, reflex muscles spasms begin to occur. Complications, such as hypoxia, aspiration, and pneumonia may result in death if treatment is not received promptly and properly. Recovery, if not severe tetanus, usually takes three weeks to two months.A rarer manifestation of tetanus is cephalic tetanus, which is associated with head wounds and chronic otitis media.1 Patients inflicted with this form present with trismus (lockjaw) and cranial nerve damage. Cephalic tetanus may progress to generalized tetanus, which indicates poor prognosis for the patient.Local tetanus, a less severe form of the disease, is associated with muscle spasm and rigidity restricted to the area of the infection site.1 Muscle rigidity may be mild and persist for several months, or it may progress to generalized tetanus or chronic abnormalities in muscle function. Although the prognosis for local tetanus is quite favorable, this presentation of the disease is rare.Neonatal tetanus is more prevalent in underdeveloped countries.1,2 A degree of passive immunity is passed from an immunized mother to fetus. In countries that do not have an immunization program such as that of the United States, children are at risk for developing neonatal tetanus. This generally occurs due to unsterile manipulations of the umbilical cord. Clinical manifestations of neonatal tetanus exhibit irritability, generalized weakness, rigidity, opisthotonos, and an irritability to nurse within 10 days of their birth. Progression to generalized tetanus is very common. Infant mortality, once contracting the disease, is approximately 90 percent.The diagnosis of tetanus is exclusively based upon physical evaluation and patient history.1,2 Laboratory findings are generally used to rule out other possibilities. Microbiological or blood tests do not exist to confirm diagnosis of tetanus. Results from lab tests, including cerebrospinal fluid values, are generally normal. Other conditions must be ruled out, however, including strichnine poisoning, which can mimic the symptoms of tetanus in exclusion of abdominal rigidity and trismus. Patients who receive proper treatment for tetanus have good potential for recovery...
1. Ernst Michael E, Klepser Michael E, Fouts Michelle, Marangos Markos N. Tetanus: Pathophysiology and Management. The Annals of Pharmacotherapy. 1997 December;31:1507-13. 2. Sanford Jay P. Tetanus--Forgotten But Not Gone. The New England Journal of Medicine. 1995 March 23;332(12). 3. Prescott Lansing M, Harley John P, Klein Donald A. Microbiology 3rd Edition. Dubuque, IA: Wm. C. Brown Publishers; 1996, pp. 764-66. 4. Green Peter J, et al. A Population-Based Serologic Survey of Immunity to Tetanus in the United States. The New England Journal of Medicine. 1995 March 23;332(12):761-66. 5. Dal-Re Rafeal, Gil Angel, Gonzalez Antonio, Lasheras Luisa. Does Tetanus Immune Globulin Interfere with the Immune Response to Simultaneous Administration of Tetanus-Diphtheria Vaccine? A Comparative Clinical Trial in Adults. Journal of Clinical Pharmacology. 1995;35:420-425. 6. Booy R, et al. Immunogenicity of combined diphtheria, tetanus, and pertussis vaccine given at 2, 3, and 4 months versus 3, 5, and 9 months of age. Lancet. 1992 Feb 29;339(8792):507-10.MLA Style
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