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History of poliomyelitis: The effects of polio have been known since prehistory; Egyptian paintings and carvings depict otherwise healthy people with withered limbs, and children walking with canes at a young age. The first clinical description was provided by the English physician Michael Underwood in 1789, where he refers to polio as "a debility of the lower extremities". The work of physicians Jakob Heine in 1840 and Karl Oskar Medin in 1890 led to it being known as Heine-Medin disease. The disease was later called infantile paralysis, based on its propensity to affect children.
-Before the 20th century, polio infections were rarely seen in infants before six months of age, most cases occurring in children six months to four years of age. Poorer sanitation of the time resulted in a constant exposure to the virus, which enhanced a natural immunity within the population. In developed countries during the late 19th and early 20th centuries, improvements were made in community sanitation, including better sewage disposal and clean water supplies. These changes drastically increased the proportion of children and adults at risk of paralytic polio infection, by reducing childhood exposure and immunity to the disease.
-Small localized paralytic polio epidemics began to appear in Europe and the United States around 1900. Outbreaks reached pandemic proportions in Europe, North America, Australia, and New Zealand during the first half of the 20th century. By 1950 the peak age incidence of paralytic poliomyelitis in the United States had shifted from infants to children aged five to nine years, when the risk of paralysis is greater; about one-third of the cases were reported in persons over 15 years of age. Accordingly, the rate of paralysis and death due to polio infection also increased during this time. In the United States, the 1952 polio epidemic became the worst outbreak in the nation's history. Of nearly 58,000 cases reported that year 3,145 died and 21,269 were left with mild to disabling paralysis. Intensive-care medicine has its origin in the fight against polio. Most hospitals in the 1950s had limited access to iron lungs for patients unable to breathe without mechanical assistance. The establishment of respiratory centers to assist the most severe polio patients, was hence the harbinger of subsequent ICUs.
-The polio epidemics changed not only the lives of those who survived them, but also affected profound cultural changes; spurring grassroots fund-raising campaigns that would revolutionize medical philanthropy, and giving rise to the modern field of rehabilitation therapy. As one of the largest disabled groups in the world, polio survivors also helped to advance the modern disability rights movement through campaigns for the social and civil rights of the disabled. The World Health Organization estimates that there are 10 to 20 million polio survivors worldwide. In 1977 there were 254,000 persons living in the United States who had been paralyzed by polio. According to doctors and local polio support groups, some 40,000 polio survivors with varying degrees of paralysis live in Germany, 30,000 in Japan, 24,000 in France, 16,000 in Australia, 12,000 in Canada and 12,000 in the United Kingdom. Many notable individuals have survived polio and often credit the prolonged immobility and residual paralysis associated with polio as a driving force in their lives and careers.
-The disease was very well publicized during the polio epidemics of the 1950s, with extensive media coverage of any scientific advancements that might lead to a cure. Thus, the scientists working on polio became some of the most famous of the century. Fifteen scientists and two laymen who made important contributions to the knowledge and treatment of poliomyelitis are honored by the Polio Hall of Fame, which was dedicated in 1957 at the Roosevelt Warm Springs Institute for Rehabilitation in Warm Springs, Georgia, USA. In 2008 four organizations (Rotary International, the World Health Organization, the U.S. Centers for Disease Control and UNICEF) were added to the Hall of Fame.
-Symptoms of poliomyelitis :http://www.mayoclinic.com/images/nav/clear.gif
-Although polio can cause paralysis and death, the vast majority of people who are infected with the poliovirus don't become sick and are never aware they've been infected with polio.
-Some people who develop symptoms from the poliovirus contract nonparalytic polio - a type of polio that doesn't lead to paralysis (abortive poliomyelitis). This usually causes the same mild, flu-like signs and symptoms typical of other viral illnesses.
Signs and symptoms, which generally last two to 10 days, include:
Back pain or stiffness
Neck pain or stiffness
Pain or stiffness in the arms or legs
Muscle spasms or tenderness
2-Paralytic polio :
-Fewer than 1 percent of people infected with poliovirus develop paralytic polio, the most serious form of the disease. Initial signs and symptoms of paralytic polio, such as fever and headache, often mimic those of nonparalytic polio. Between one and 10 days later however,
signs and symptoms specific to paralytic polio appear, including:
Loss of reflexes
Severe muscle aches or spasms
Loose and floppy limbs (acute flaccid paralysis), often worse on one side of the body,The onset of paralysis may be sudden.
-Classification of poliomyelitis:
-In around 1% of infections, poliovirus spreads along certain nerve fiber pathways, preferentially replicating in and destroying motor neurons within the spinal cord, brain stem, or motor cortex. This leads to the development of various forms of paralytic poliomyelitis, which vary only with the amount of neuronal damage and inflammation that occurs, and the region of the CNS that is affected. Paralytic polio is classified depending on the location of the nerve cell destruction into 3 categores :
1)Spinal polio: http://upload.wikimedia.org/wikipedia/commons/thumb/3/3a/Polio_spinal_diagram.PNG/220px-Polio_spinal_diagram.PNG
-Spinal polio is the most common form of paralytic poliomyelitis; it results from viral invasion of the motor neurons of the anterior horn cells, or the ventral (front) gray matter section in the spinal column, which are responsible for movement of the muscles, including those of the trunk, limbs and the intercostal muscles.Virus invasion causes inflammation of the nerve cells, leading to damage or destruction of motor neuron ganglia
With the destruction of nerve cells, the muscles no longer receive signals from the brain or spinal cord; without nerve stimulation, the muscles atrophy, becoming weak, floppy and poorly controlled, and finally completely paralyzed. Progression to maximum paralysis is rapid (two to four days), and is usually associated with fever and muscle pain. Deep tendon reflexes are also affected, and are usually absent or diminished; sensation (the ability to feel) in the paralyzed limbs, however, is not affected.
Sometimes the neurons are only damaged, in which case you may recover some degree of muscle function. But if the neurons are completely destroyed, the paralysis is irreversible, although you still retain your sense of feeling, unlike after many spinal cord injuries.
-Making up about 2% of cases of paralytic polio, bulbar polio occurs when poliovirus invades and destroys nerves within the bulbar region of the brain stem. The bulbar region is a white matter pathway that connects the cerebral cortex to the brain stem. These nerves are involved in your ability to see, hear, smell, taste and swallow. They also affect the movement of muscles in your face and send signals to your heart, intestines and lungs.
Bulbar polio can interfere with any of these functions but is especially likely to affect your ability to breathe, speak and swallow and can be fatal without respiratory support.
3) Bulbospinal polio :
-Approximately 19% of all paralytic polio cases have both bulbar and spinal symptoms; this subtype is called respiratory polio or bulbospinal polio. Here the virus affects the upper part of the cervical spinal cord (C3 through C5), and paralysis of the diaphragm occurs. The critical nerves affected are the phrenic nerve, which drives the diaphragm to inflate the lungs, and those that drive the muscles needed for swallowing.
By destroying these nerves this form of polio affects breathing, making it difficult or impossible for the patient to breathe without the support of a ventilator. It can lead to paralysis of the arms and legs and may also affect swallowing and heart functions.
-Prognosis of poliomyelitis :
-Patients with abortive polio infections recover completely. In those that develop only aseptic meningitis, the symptoms can be expected to persist for two to ten days, followed by complete recovery. In cases of spinal polio, if the affected nerve cells are completely destroyed, paralysis will be permanent; cells that are not destroyed but lose function temporarily may recover within four to six weeks after onset. Half the patients with spinal polio recover fully; one quarter recover with mild disability and the remaining quarter are left with severe disability. The degree of both acute paralysis and residual paralysis is likely to be proportional to the degree of viremia, and inversely proportional to the degree of immunity. Spinal polio is rarely fatal.
Without respiratory support, consequences of poliomyelitis with respiratory involvement include suffocation or pneumonia from aspiration of secretions. Overall, 5-10% of patients with paralytic polio die due to the paralysis of muscles used for breathing. The mortality rate varies by age: 2-5% of children and up to 15-30% of adults die. Bulbar polio often causes death if respiratory support is not provided; with support, its mortality rate ranges from 25 to 75%, depending on the age of the patient. When positive pressure ventilators are available, the mortality can be reduced to 15%.
-Many cases of poliomyelitis result in only temporary paralysis. Nerve impulses return to the formerly paralyzed muscle within a month, and recovery is usually complete in six to eight months. The neurophysiological processes involved in recovery following acute paralytic poliomyelitis are quite effective; muscles are able to retain normal strength even if half the original motor neurons have been lost. Paralysis remaining after one year is likely to be permanent, although modest recoveries of muscle strength are possible 12 to 18 months after infection.
-One mechanism involved in recovery is nerve terminal sprouting, in which remaining brainstem and spinal cord motor neurons develop new branches, or axonal sprouts. These sprouts can reinnervate orphaned muscle fibers that have been denervated by acute polio infection, restoring the fibers' capacity to contract and improving strength. Terminal sprouting may generate a few significantly enlarged motor neurons doing work previously performed by as many as four or five units: a single motor neuron that once controlled 200 muscle cells might control 800 to 1000 cells. Other mechanisms that occur during the rehabilitation phase, and contribute to muscle strength restoration, include myofiber hypertrophy-enlargement of muscle fibers through exercise and activity-and transformation of type II muscle fibers to type I muscle fibers.
-In addition to these physiological processes, the body possesses a number of compensatory mechanisms to maintain function in the presence of residual paralysis. These include the use of weaker muscles at a higher than usual intensity relative to the muscle's maximal capacity, enhancing athletic development of previously little-used muscles, and using ligaments for stability, which enables greater mobility.
-Residual complications of paralytic polio often occur following the initial recovery process. Muscle paresis and paralysis can sometimes result in skeletal deformities, tightening of the joints and movement disability. Once the muscles in the limb become flaccid, they may interfere with the function of other muscles. A typical manifestation of this problem is equinus foot (similar to club foot). This deformity develops when the muscles that pull the toes downward are working, but those that pull it upward are not, and the foot naturally tends to drop toward the ground. If the problem is left untreated, the Achilles tendons at the back of the foot retract and the foot cannot take on a normal position. Polio victims that develop equinus foot cannot walk properly because they cannot put their heel on the ground. A similar situation can develop if the arms become paralyzed. In some cases the growth of an affected leg is slowed by polio, while the other leg continues to grow normally. The result is that one leg is shorter than the other and the person limps and leans to one side, in turn leading to deformities of the spine (such as scoliosis). Osteoporosis and increased likelihood of bone fractures may occur. Extended use of braces or wheelchairs may cause compression neuropathy, as well as a loss of proper function of the veins in the legs, due to pooling of blood in paralyzed lower limbs. Complications from prolonged immobility involving the lungs, kidneys and heart include pulmonary edema, aspiration pneumonia, urinary tract infections, kidney stones, paralytic ileus, myocarditis and cor pulmonale.
- Post-polio syndrome (PPS) is a condition that affects polio survivors anywhere from 10 to 40 years after recovery from an initial paralytic attack of the poliomyelitis virus. PPS is characterized by a further weakening of muscles that were previously affected by the polio infection. Symptoms include fatigue, slowly progressive muscle weakness and, at times, muscular atrophy. Joint pain and increasing skeletal deformities such as scoliosis are common. Some patients experience only minor symptoms, while others develop spinal muscular atrophy, and very rarely, what appears to be, but is not, a form of amyotrophic lateral sclerosis (ALS), also called Lou Gehrig's disease. PPS is rarely life-threatening.
-Prevention of poliomyelitis:
-In 1950, William Hammon at the University of Pittsburgh purified the gamma globulin component of the blood plasma of polio survivors. Hammon proposed that the gamma globulin, which contained antibodies to poliovirus, could be used to halt poliovirus infection, prevent disease, and reduce the severity of disease in other patients who had contracted polio. The results of a large clinical trial were promising; the gamma globulin was shown to be about 80% effective in preventing the development of paralytic poliomyelitis. It was also shown to reduce the severity of the disease in patients that developed polio. The gamma globulin approach was later deemed impractical for widespread use, however, due in large part to the limited supply of blood plasma, and the medical community turned its focus to the development of a polio vaccine.
-Two types of vaccines are used throughout the world to combat polio. Both types induce immunity to polio, efficiently blocking person-to-person transmission of wild poliovirus, thereby protecting both individual vaccine recipients and the wider community (so-called herd immunity). http://upload.wikimedia.org/wikipedia/commons/thumb/2/20/Poliodrops.jpg/220px-Poliodrops.jpg
-The first candidate polio vaccine, based on one serotype of a live but attenuated (weakened) virus, was developed by the virologist Hilary Koprowski. Koprowski's prototype vaccine was given to an eight-year-old boy on February 27, 1950. Koprowski continued to work on the vaccine throughout the 1950s, leading to large-scale trials in the then Belgian Congo and the vaccination of seven million children in Poland against serotypes PV1 and PV3 between 1958 and 1960.
-The first inactivated virus vaccine was developed in 1952 by Jonas Salk, and announced to the world on April 12, 1955. The Salk vaccine, or inactivated poliovirus vaccine (IPV), is based on poliovirus grown in a type of monkey kidney tissue culture (Vero cell line), which is chemically inactivated with formalin. After two doses of IPV (given by injection), 90% or more of individuals develop protective antibody to all three serotypes of poliovirus, and at least 99% are immune to poliovirus following three doses.
-Subsequently, Albert Sabin developed another live, oral polio vaccine (OPV). It was produced by the repeated passage of the virus through non-human cells at sub-physiological temperatures. The attenuated poliovirus in the Sabin vaccine replicates very efficiently in the gut, the primary site of wild poliovirus infection and replication, but the vaccine strain is unable to replicate efficiently within nervous system tissue. A single dose of Sabin's oral polio vaccine produces immunity to all three poliovirus serotypes in approximately 50% of recipients. Three doses of live-attenuated OPV produce protective antibody to all three poliovirus types in more than 95% of recipients. Human trials of Sabin's vaccine began in 1957, and in 1958 it was selected, in competition with the live vaccines of Koprowski and other researchers, by the US National Institutes of Health. It was licensed in 1962 and rapidly became the only polio vaccine used worldwide.
-Because OPV is inexpensive, easy to administer, and produces excellent immunity in the intestine (which helps prevent infection with wild virus in areas where it is endemic), it has been the vaccine of choice for controlling poliomyelitis in many countries. On very rare occasions (about 1 case per 750,000 vaccine recipients) the attenuated virus in OPV reverts into a form that can paralyze. Most industrialized countries have switched to IPV, which cannot revert, either as the sole vaccine against poliomyelitis or in combination with oral polio vaccine.
-Polio survivors often ask if there is a way to prevent post-polio syndrome. Presently, no intervention has been found to stop the deterioration of surviving neurons. But physicians recommend that polio survivors get the proper amount of sleep, maintain a well-balanced diet, avoid unhealthy habits such as smoking and overeating, and follow an exercise program as discussed above. Proper lifestyle changes, the use of assistive devices, and taking certain anti-inflammatory medications may help some of the symptoms of post-polio syndrome.