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Poliovirus is usually spread from person to person through infected fecal matter entering the mouth.[1] It may also be spread by food or water containing human feces and less commonly from infected saliva.[1][2] Those who are infected may spread the disease for up to six weeks even if no symptoms are present. The disease may be diagnosed by finding the virus in the feces or detecting antibodies against it in the blood.[1]
The disease is preventable with the polio vaccine; however, a number of doses are required for it to be effective.[2] The United States Center for Disease Control recommends polio vaccination boosters for travelers and those who live in countries where the disease is occurring.[4] Once infected there is no specific treatment.[2] In 2013 polio affected 416 people down from 350,000 cases in 1988.[2] In 2014 the disease was only spreading between people inAfghanistan, Nigeria, and Pakistan.[2] In 2015 Nigeria had stopped the spread of wild poliovirus.[5]
Poliomyelitis has existed for thousands of years, with depictions of the disease in ancient art.[1] The disease was first recognized as a distinct condition byMichael Underwood in 1789[1] and the virus that causes it was first identified in 1908 by Karl Landsteiner.[6] Major outbreaks started to occur in the late 19th century in Europe and the United States.[1] In the 20th century it became one of the most worrying childhood diseases in these areas.[7] The first polio vaccine was developed in the 1950s by Jonas Salk.[8] It is hoped that vaccination efforts and early detection of cases will result in global eradication of the disease by 2018.[9] In 2013; however, there were reports of new cases in Syria[10] and in May 2014, the World Health Organization declared a public health emergency of international concern due to outbreaks of the disease in Asia, Africa and the Middle East.[11] The disease does not naturally occur in any other animals.[1]
The oral polio vaccine (OPV) was developed in 1961 by Albert Sabin. Also called “trivalent oral polio vaccine” or “Sabin vaccine”, OPV consists of a mixture of live, attenuated (weakened) poliovirus strains of all three poliovirus types.
OPV produces antibodies in the blood to all three types of poliovirus. In the event of infection, these antibodies protect against paralysis by preventing the spread of wild poliovirus to the nervous system.
OPV also produces a local, mucosal immune response in the mucous membrane of the intestines. In the event of infection, these mucosal antibodies limit the replication of the wild poliovirus inside the intestine. This intestinal immune response to OPV is thought to be the main reason why mass campaigns with OPV can rapidly stop person-to-person transmission of wild poliovirus.
OPV is an extremely safe vaccine. All OPV used in supplementary immunization activities for the Global Polio Eradication Initiative is pre-qualified by WHO and procured through UNICEF. In 2006, WHO issued a statement to affirm the quality and safety of OPV.
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| Oral polio vaccine is usually provided in vials containing 10–20 doses of vaccine. A single dose is usually two drops |
OPV is highly effective against all three types of wild poliovirus. When this vaccine is used however, there is competition among the three viruses to cause immunity, which results in protection but not with equal efficiency for each type: it is most effective against type 2.
One dose of OPV produces immunity to all three poliovirus serotypes in approximately 50% of recipients. Three doses produce immunity in more than 95% of recipients. Immunity is long-lasting and probably life-long.
In most countries, OPV remains the vaccine of choice in routine immunization schedules and supplementary immunization activities.
Where more than one type of wild poliovirus is circulating, OPV is epidemiologically and operationally the best vaccine to use because protection develops to each of the three types of polio virus.
In 1950, William Hammon at the University of Pittsburgh purified the gamma globulin component of the blood plasma of polio survivors.[48] Hammon proposed 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.[49] It was also shown to reduce the severity of the disease in patients who developed polio.[48] Due to the limited supply of blood plasma gamma globulin was later deemed impractical for widespread use and the medical community focused on the development of a polio vaccine.[50]
Two types of vaccine 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).[51]
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 27 February 1950.[52] 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.[53]
The second inactivated virus vaccine was developed in 1952 by Jonas Salk at the University of Pittsburgh, and announced to the world on 12 April 1955.[54] 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.[21] 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.[1]
Subsequently, Albert Sabin developed another live, oral polio vaccine (OPV). It was produced by the repeated passage of the virus through nonhuman cells at subphysiological temperatures.[55] 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.[56] A single dose of Sabin's oral polio vaccine produces immunity to all three poliovirus serotypes in about 50% of recipients. Three doses of live-attenuated OPV produce protective antibody to all three poliovirus types in more than 95% of recipients.[1] Human trials of Sabin's vaccine began in 1957,[57] and in 1958 it was selected, in competition with the live vaccines of Koprowski and other researchers, by the US National Institutes of Health.[53] Licensed in 1962,[57] it rapidly became the only polio vaccine used worldwide.[53]
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.[58] On very rare occasions (about one case per 750,000 vaccine recipients), the attenuated virus in OPV reverts into a form that can paralyze.[24]Most industrialized countries have switched to IPV, which cannot revert, either as the sole vaccine against poliomyelitis or in combination with oral polio vaccine.[59]
There is no cure for polio. The focus of modern treatment has been on providing relief of symptoms, speeding recovery and preventing complications. Supportive measures include antibiotics to prevent infections in weakened muscles, analgesics for pain, moderate exercise and a nutritious diet.[60] Treatment of polio often requires long-term rehabilitation, including occupational therapy, physical therapy, braces, corrective shoes and, in some cases, orthopedic surgery.[43]
Portable ventilators may be required to support breathing. Historically, a noninvasive, negative-pressure ventilator, more commonly called an iron lung, was used to artificially maintain respiration during an acute polio infection until a person could breathe independently (generally about one to two weeks). Today, many polio survivors with permanent respiratory paralysis use modern jacket-type negative-pressure ventilators worn over the chest and abdomen.[61]
Other historical treatments for polio include hydrotherapy, electrotherapy, massage and passive motion exercises, and surgical treatments, such as tendon lengthening and nerve grafting.[15]
Patients with abortive polio infections recover completely. In those who develop only aseptic meningitis, the symptoms can be expected to persist for two to ten days, followed by complete recovery.[62] 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.[62] Half the patients with spinal polio recover fully; one-quarter recover with mild disability, and the remaining quarter are left with severe disability.[63] 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.[36] Spinal polio is rarely fatal.[37]
Without respiratory support, consequences of poliomyelitis with respiratory involvement include suffocation or pneumonia from aspiration of secretions.[61] Overall, 5–10% of patients with paralytic polio die due to the paralysis of muscles used for breathing. The case fatality rate (CFR) varies by age: 2–5% of children and up to 15–30% of adults die.[1] Bulbar polio often causes death if respiratory support is not provided;[44] with support, its CFR ranges from 25 to 75%, depending on the age of the patient.[1][64] When intermittent positive pressure ventilation is available, the fatalities can be reduced to 15%.[65]
Many cases of poliomyelitis result in only temporary paralysis.[15] Nerve impulses return to the formerly paralyzed muscle within a month, and recovery is usually complete in six to eight months.[62] 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.[66] Paralysis remaining after one year is likely to be permanent, although modest recoveries of muscle strength are possible 12 to 18 months after infection.[62]
One mechanism involved in recovery is nerve terminal sprouting, in which remaining brainstem and spinal cord motor neurons develop new branches, or axonal sprouts.[67] These sprouts can reinnervate orphaned muscle fibers that have been denervated by acute polio infection,[68] restoring the fibers' capacity to contract and improving strength.[69] Terminal sprouting may generate a few significantly enlarged motor neurons doing work previously performed by as many as four or five units:[38] 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.[68][70]
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.[70]
Residual complications of paralytic polio often occur following the initial recovery process.[14] 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.[71] 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).[71] Osteoporosis and increased likelihood of bone fractures may occur. An intervention to prevent or lessen length disparity can be to perform an epiphysiodesis on the distal femoral and proximal tibial/fibular condyles, so that limb's growth is artificially stunted, and by the time of epiphyseal (growth) plate closure, the legs are more equal in length. Alternatively, a person can be fitted with custom made footwear which corrects the difference in leg lengths. Other surgery to re-balance muscular agonist/antagonist imbalances may also be helpful. 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.[44][72] 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.[44][72]
