Post by Master Kim on Jan 26, 2015 12:22:51 GMT -5
Botulism - en.wikipedia.org/wiki/Botulism
Botulism (Latin, botulus, a sausage) (pronounced /ˈbɒtʃʉlɪzəm/) is a rare and potentially fatal paralytic illness caused by a toxin produced by the bacteria Clostridium botulinum. The disease begins with weakness, trouble seeing, feeling tired, and trouble speaking. This may then be followed by weakness of the arms, chest muscles, and legs. The disease does not usually affect consciousness or cause a fever.
Botulism can occur in a few different ways. The bacterial spores that cause it are common in both soil and water. They produce botulinum toxin when exposed to low oxygen levels and certain temperatures. Foodborne botulism happens when food containing the toxin is eaten. Infant botulism happens when the bacteria develops in the intestines and releases toxin. Typically this only happens in children less than six months of age as after that protective mechanisms develop. Wound botulism is found most often among those who inject street drugs. In this situation spores enter a wound and, in the absence of oxygen, release toxin. It is not passed directly between people. The diagnosis is confirmed by finding the toxin or bacteria in the person in question.
Prevention is primarily by proper food preparation. The toxin is destroyed by heating to more than 85 °C (185 °F) for longer than 5 minutes. It is not recommended to give honey to children who are less than one year of age due to the risk with this food. Treatment is with an antitoxin. In those who lose their ability to breathe on their own, mechanical ventilation potentially for months may be required. Antibiotics may be used for wound botulism. Death occurs in 5 to 10% of people. Botulism can affect a number of other animals.
Five days after sustaining a compound fracture of his right arm, this 14-year-old boy noticed that he had blurred vision. Four days later, he could not swallow, move his lips, or protrude his tongue. Other findings included bilateral total ophthalmoplegia with ptosis (left) and dilated, fixed pupils (right). His mental status and sensory examination were normal. When symmetric, descending cranial nerve paralysis develops four to 14 days after an open injury and spares mental and sensory function, think of wound botulism. In this patient, culture of serosanguineous fluid from the fracture site grew Clostridium botulinum.
Signs and symptoms
The muscle weakness of botulism characteristically starts in the muscles supplied by the cranial nerves. A group of twelve nerves controls eye movements, the facial muscles and the muscles controlling chewing and swallowing. Double vision, drooping of both eyelids, loss of facial expression and swallowing problems may therefore occur, as well as difficulty with talking. The weakness then spreads to the arms (starting in the shoulders and proceeding to the forearms) and legs (again from the thighs down to the feet).
Severe botulism leads to reduced movement of the muscles of respiration, and hence problems with gas exchange. This may be experienced as dyspnea (difficulty breathing), but when severe can lead to respiratory failure, due to the buildup of unexhaled carbon dioxide and its resultant depressant effect on the brain. This may lead to coma and eventually death if untreated.
In addition to affecting the voluntary muscles, it can also cause disruptions in the autonomic nervous system. This is experienced as a dry mouth and throat (due to decreased production of saliva), postural hypotension (decreased blood pressure on standing, with resultant lightheadedness and risk of blackouts), and eventually constipation (due to decreased peristalsis). Some of the toxins (B and E) also precipitate nausea and vomiting.
Clinicians frequently think of the symptoms of botulism in terms of a classic triad: bulbar palsy and descending paralysis, lack of fever, and clear senses and mental status ("clear sensorium").
Signs and symptoms
The muscle weakness of botulism characteristically starts in the muscles supplied by the cranial nerves. A group of twelve nerves controls eye movements, the facial muscles and the muscles controlling chewing and swallowing. Double vision, drooping of both eyelids, loss of facial expression and swallowing problems may therefore occur, as well as difficulty with talking. The weakness then spreads to the arms (starting in the shoulders and proceeding to the forearms) and legs (again from the thighs down to the feet).
Severe botulism leads to reduced movement of the muscles of respiration, and hence problems with gas exchange. This may be experienced as dyspnea (difficulty breathing), but when severe can lead to respiratory failure, due to the buildup of unexhaled carbon dioxide and its resultant depressant effect on the brain. This may lead to coma and eventually death if untreated.
In addition to affecting the voluntary muscles, it can also cause disruptions in the autonomic nervous system. This is experienced as a dry mouth and throat (due to decreased production of saliva), postural hypotension (decreased blood pressure on standing, with resultant lightheadedness and risk of blackouts), and eventually constipation (due to decreased peristalsis). Some of the toxins (B and E) also precipitate nausea and vomiting.
Clinicians frequently think of the symptoms of botulism in terms of a classic triad: bulbar palsy and descending paralysis, lack of fever, and clear senses and mental status ("clear sensorium").
Infant botulism
Infant with botulism. He is unable to move or open his eyes. His cry was weak. He is not asleep or sedated.
Infant botulism (also referred to as floppy baby syndrome) was first recognized in 1976, and is the most common form of botulism in the United States. There were 17 diagnosed cases of infant botulism in the United States in 2013. Infants are susceptible to infant botulism in the first year of life, with more than 90% of cases occurring in infants younger than six months. Infant botulism results from the ingestion of the C. botulinum spores, and subsequent colonization of the small intestine. The infant gut may be colonized when the composition of the intestinal microflora (normal flora) is insufficient to competitively inhibit the growth of C. botulinum and levels of bile acids (which normally inhibit clostridial growth) are lower than later in life.
The growth of the spores releases botulinum toxin, which is then absorbed into the bloodstream and taken throughout the body, causing paralysis by blocking the release of acetylcholine at the neuromuscular junction. Typical symptoms of infant botulism include constipation, lethargy, weakness, difficulty feeding and an altered cry, often progressing to a complete descending flaccid paralysis. Although constipation is usually the first symptom of infant botulism, it is commonly overlooked.
Honey is the only known dietary reservoir of C. botulinum spores linked to infant botulism. For this reason honey should not be fed to infants less than one year of age. Other cases of infant botulism are thought to be caused by acquiring the spores from the natural environment. Clostridium botulinum is a ubiquitous soil-dwelling bacterium. Many infant botulism patients have been demonstrated to live near a construction site or an area of soil disturbance.[citation needed]
Infant botulism has been reported in 49 of 50 US states, and cases have been recognized in 26 countries on five continents.
Complications
Infant botulism has no long-term side effects, but can be complicated by nosocomial adverse events. The case fatality rate is less than 1% for hospitalized infants with botulism.
Botulism can result in death due to respiratory failure. However, in the past 50 years, the proportion of patients with botulism who die has fallen from about 50% to 7% due to improved supportive care. A patient with severe botulism may require mechanical ventilation (breathing support through a ventilator) as well as intensive medical and nursing care, sometimes for several months. Patients who survive an episode of botulism poisoning may have fatigue and shortness of breath for years and long-term therapy may be needed to aid their recovery.
Botulism (Latin, botulus, a sausage) (pronounced /ˈbɒtʃʉlɪzəm/) is a rare and potentially fatal paralytic illness caused by a toxin produced by the bacteria Clostridium botulinum. The disease begins with weakness, trouble seeing, feeling tired, and trouble speaking. This may then be followed by weakness of the arms, chest muscles, and legs. The disease does not usually affect consciousness or cause a fever.
Botulism can occur in a few different ways. The bacterial spores that cause it are common in both soil and water. They produce botulinum toxin when exposed to low oxygen levels and certain temperatures. Foodborne botulism happens when food containing the toxin is eaten. Infant botulism happens when the bacteria develops in the intestines and releases toxin. Typically this only happens in children less than six months of age as after that protective mechanisms develop. Wound botulism is found most often among those who inject street drugs. In this situation spores enter a wound and, in the absence of oxygen, release toxin. It is not passed directly between people. The diagnosis is confirmed by finding the toxin or bacteria in the person in question.
Prevention is primarily by proper food preparation. The toxin is destroyed by heating to more than 85 °C (185 °F) for longer than 5 minutes. It is not recommended to give honey to children who are less than one year of age due to the risk with this food. Treatment is with an antitoxin. In those who lose their ability to breathe on their own, mechanical ventilation potentially for months may be required. Antibiotics may be used for wound botulism. Death occurs in 5 to 10% of people. Botulism can affect a number of other animals.
Five days after sustaining a compound fracture of his right arm, this 14-year-old boy noticed that he had blurred vision. Four days later, he could not swallow, move his lips, or protrude his tongue. Other findings included bilateral total ophthalmoplegia with ptosis (left) and dilated, fixed pupils (right). His mental status and sensory examination were normal. When symmetric, descending cranial nerve paralysis develops four to 14 days after an open injury and spares mental and sensory function, think of wound botulism. In this patient, culture of serosanguineous fluid from the fracture site grew Clostridium botulinum.
Signs and symptoms
The muscle weakness of botulism characteristically starts in the muscles supplied by the cranial nerves. A group of twelve nerves controls eye movements, the facial muscles and the muscles controlling chewing and swallowing. Double vision, drooping of both eyelids, loss of facial expression and swallowing problems may therefore occur, as well as difficulty with talking. The weakness then spreads to the arms (starting in the shoulders and proceeding to the forearms) and legs (again from the thighs down to the feet).
Severe botulism leads to reduced movement of the muscles of respiration, and hence problems with gas exchange. This may be experienced as dyspnea (difficulty breathing), but when severe can lead to respiratory failure, due to the buildup of unexhaled carbon dioxide and its resultant depressant effect on the brain. This may lead to coma and eventually death if untreated.
In addition to affecting the voluntary muscles, it can also cause disruptions in the autonomic nervous system. This is experienced as a dry mouth and throat (due to decreased production of saliva), postural hypotension (decreased blood pressure on standing, with resultant lightheadedness and risk of blackouts), and eventually constipation (due to decreased peristalsis). Some of the toxins (B and E) also precipitate nausea and vomiting.
Clinicians frequently think of the symptoms of botulism in terms of a classic triad: bulbar palsy and descending paralysis, lack of fever, and clear senses and mental status ("clear sensorium").
Signs and symptoms
The muscle weakness of botulism characteristically starts in the muscles supplied by the cranial nerves. A group of twelve nerves controls eye movements, the facial muscles and the muscles controlling chewing and swallowing. Double vision, drooping of both eyelids, loss of facial expression and swallowing problems may therefore occur, as well as difficulty with talking. The weakness then spreads to the arms (starting in the shoulders and proceeding to the forearms) and legs (again from the thighs down to the feet).
Severe botulism leads to reduced movement of the muscles of respiration, and hence problems with gas exchange. This may be experienced as dyspnea (difficulty breathing), but when severe can lead to respiratory failure, due to the buildup of unexhaled carbon dioxide and its resultant depressant effect on the brain. This may lead to coma and eventually death if untreated.
In addition to affecting the voluntary muscles, it can also cause disruptions in the autonomic nervous system. This is experienced as a dry mouth and throat (due to decreased production of saliva), postural hypotension (decreased blood pressure on standing, with resultant lightheadedness and risk of blackouts), and eventually constipation (due to decreased peristalsis). Some of the toxins (B and E) also precipitate nausea and vomiting.
Clinicians frequently think of the symptoms of botulism in terms of a classic triad: bulbar palsy and descending paralysis, lack of fever, and clear senses and mental status ("clear sensorium").
Infant botulism
Infant with botulism. He is unable to move or open his eyes. His cry was weak. He is not asleep or sedated.
Infant botulism (also referred to as floppy baby syndrome) was first recognized in 1976, and is the most common form of botulism in the United States. There were 17 diagnosed cases of infant botulism in the United States in 2013. Infants are susceptible to infant botulism in the first year of life, with more than 90% of cases occurring in infants younger than six months. Infant botulism results from the ingestion of the C. botulinum spores, and subsequent colonization of the small intestine. The infant gut may be colonized when the composition of the intestinal microflora (normal flora) is insufficient to competitively inhibit the growth of C. botulinum and levels of bile acids (which normally inhibit clostridial growth) are lower than later in life.
The growth of the spores releases botulinum toxin, which is then absorbed into the bloodstream and taken throughout the body, causing paralysis by blocking the release of acetylcholine at the neuromuscular junction. Typical symptoms of infant botulism include constipation, lethargy, weakness, difficulty feeding and an altered cry, often progressing to a complete descending flaccid paralysis. Although constipation is usually the first symptom of infant botulism, it is commonly overlooked.
Honey is the only known dietary reservoir of C. botulinum spores linked to infant botulism. For this reason honey should not be fed to infants less than one year of age. Other cases of infant botulism are thought to be caused by acquiring the spores from the natural environment. Clostridium botulinum is a ubiquitous soil-dwelling bacterium. Many infant botulism patients have been demonstrated to live near a construction site or an area of soil disturbance.[citation needed]
Infant botulism has been reported in 49 of 50 US states, and cases have been recognized in 26 countries on five continents.
Complications
Infant botulism has no long-term side effects, but can be complicated by nosocomial adverse events. The case fatality rate is less than 1% for hospitalized infants with botulism.
Botulism can result in death due to respiratory failure. However, in the past 50 years, the proportion of patients with botulism who die has fallen from about 50% to 7% due to improved supportive care. A patient with severe botulism may require mechanical ventilation (breathing support through a ventilator) as well as intensive medical and nursing care, sometimes for several months. Patients who survive an episode of botulism poisoning may have fatigue and shortness of breath for years and long-term therapy may be needed to aid their recovery.
subdue LU10, ST41, SP2, BL60, KI2, GB38 and LR2.