The words polio (grey) and myelon (marrow, indicating the spinal cord) are derived from the Greek. It is the effect of poliomyelitis virus on the spinal cord that leads to the classic manifestation, paralysis.
Although records from antiquity mention crippling diseases compatible with poliomyelitis, it was Michael Underwood from England who, in 1789, first described a debility of the lower extremities in children that was recognizable as poliomyelitis. The first outbreaks in Europe were reported in the early 19th century, and outbreaks were reported in the United States a few years later. For the next hundred years, epidemics of polio were reported from developed countries in the northern hemisphere each summer and fall. These epidemics became increasingly severe, and the average age of persons affected rose. The increased age of primary infection increased both the disease severity and number of deaths from polio. Polio reached a peak in the United States in 1952, with over 21,000 paralytic cases. Polio incidence fell rapidly following introduction of effective vaccines. The last case of wild-virus polio acquired in the United States was in 1979, and global polio eradication may be achieved within the next decade.
Poliovirus is a member of the enterovirus subgroup, family Picornaviridae. Enteroviruses are transient inhabitants of the gastrointestinal tract, and are stable at acid pH. Picornaviruses are small, ether-insensitive viruses with an RNA genome. There are three poliovirus serotypes (P1, P2, and P3). There is minimal heterotypic immunity between the three serotypes. The poliovirus is rapidly inactivated by heat, formaldehyde, chlorine, and ultraviolet light.
The virus enters through the mouth and primary multiplication of the virus occurs at the site of implantation in the pharynx and gastrointestinal tract. The virus is usually present in the throat and in the stool before the onset of illness. One week after onset there is little virus in the throat, but virus continues to be excreted in the stool for several weeks. The virus invades local lymphoid tissue, enters the blood stream, and then may infect cells of the central nervous system. Replication of poliovirus in motor neurons of the anterior horn and brain stem results in cell destruction and causes the typical manifestations of poliomyelitis.
The incubation period for poliomyelitis is commonly 6 to 20 days with a range from 3 to 35 days. The response to poliovirus infection is highly variable and has been categorized based on the severity of clinical presentation.
Up to 95% of all polio infections are inapparent or asymptomatic. Estimates of the ratio of inapparent to paralytic illness vary from 50:1 to 1,000:1 (usually 200:1). Infected persons without symptoms shed virus in the stool, and are able to transmit the virus to others.
Approximately 4%-8% of polio infections consist of a minor, nonspecific illness without clinical or laboratory evidence of central nervous system invasion. This clinical presentation is known as abortive poliomyelitis, and is characterized by complete recovery in less than a week. Three syndromes observed with this form of poliovirus infection are upper respiratory tract infection (sore throat and fever), gastrointestinal disturbances (nausea, vomiting, abdominal pain, constipation or, rarely, diarrhea), and influenzalike illness.
These syndromes are indistinguishable from other viral illnesses. Nonparalytic aseptic meningitis (symptoms of stiffness of the neck, back, and/or legs), usually following several days after a prodrome similar to that of minor illness, occurs in 1%-2% of polio infections. Increased or abnormal sensations can also occur. Typically these symptoms will last from 2 to 10 days, followed by complete recovery.
Less than 1% of all polio infections result in flaccid paralysis. Paralytic symptoms generally begin 1 to 10 days after prodromal symptoms and progress for 2 to 3 days. Generally, no further paralysis occurs after the temperature returns to normal. The prodrome may be biphasic, especially in children, with initial minor symptoms separated by a 1- to 7-day period from more major symptoms. Additional prodromal signs and symptoms can include a loss of superficial reflexes, initially increased deep tendon reflexes and severe muscle aches and spasms in the limbs or back. The illness progresses to flaccid paralysis with diminished deep tendon reflexes, reaches a plateau without change for days to weeks, and is usually asymmetrical. Strength then begins to return. Patients do not experience sensory losses or changes in cognition.
Many persons with paralytic poliomyelitis recover completely and, in most, muscle function returns to some degree. Patients with weakness or paralysis 12 months after onset will usually be left with permanent residua.
Paralytic polio is classified into three types, depending on the level of involvement. Spinal polio is most common, and accounted for 79% of paralytic cases from 1969-1979. It is characterized by asymmetric paralysis that most often involves the legs. Bulbar polio accounted for 2% of cases and led to weakness of muscles innervated by cranial nerves. Bulbospinal polio accounted for 19% of cases and was a combination of bulbar and spinal paralysis.
The death-to-case ratio for paralytic polio is generally 2%-5% in Poliomyelitis Poliomyelitis children and up to 15%-30% in adults (depending on age). It increases to 25%-75% with bulbar involvement.
LABORATORY DIAGNOSIS VIRAL ISOLATION
Poliovirus may be recovered from the stool or pharynx of a person with presumed poliomyelitis. Isolation of virus from the cerebrospinal fluid (CSF) is diagnostic, but is rarely accomplished. If poliovirus is isolated from a person with acute flaccid paralysis, it must be tested further, using oligonucleotide mapping (fingerprinting) or genomic sequencing, to determine if the virus is wildtype or vaccine-type.
Neutralizing antibodies appear early and may be at high levels by the time the patient is hospitalized and, therefore, a 4-fold rise may not be demonstrated.
(CSF) The CSF in poliovirus infection usually contains an increased number of white blood cells (10 to 200 cells/mm3, primarily lymphocytes) and a mildly elevated protein from 40 to 50 mg/100 ml.
At one time poliovirus infection occurred throughout the world. Transmission of wild poliovirus ceased in the United States in 1979, or possibly earlier. A polio eradication program conducted by the Pan American Health Organization led to elimination of polio through the Western Hemisphere in 1991. The Global Polio Eradication Program has dramatically reduced poliovirus transmission throughout the world. Poliovirus transmission now occurs primarily in the Indian subcontinent, the Eastern Mediterranean, and Africa.
Humans are the only known reservoir of poliovirus, which is transmitted most frequently by persons with inapparent infections. There is no asymptomatic carrier state except in immune deficient persons.
Person-to-person spread of poliovirus via the fecal-oral route is the most important route of transmission, although the oral-oral route may account for some cases.
Poliovirus infection typically peaks in the summer months in temperate climates. There is no seasonal pattern in tropical climates.
Poliovirus is highly infectious, with seroconversion rates in susceptible household contacts of children nearly 100% and over 90% in susceptible household contacts of adults. Persons infected with poliovirus are most infectious from 7 to 10 days before and after the onset of symptoms, but poliovirus may be present in the stool from 3 to 6 weeks.
SECULAR TRENDS IN THE UNITED STATES
Before the 18th century, polioviruses probably circulated widely. Initial infections to at least one type probably occurred in early infancy, when transplacentally acquired maternal antibodies were high. Exposure throughout life probably provided continual boosting of immunity and paralytic infections were probably rare. (This view has been recently challenged based on data of lameness studies in developing countries.)
In the immediate pre-vaccine era, improved sanitation allowed less frequent exposure and increased the age of primary infection. There was infrequent boosting of immunity from natural exposure, accumulation of susceptibles, and ultimately the occurrence of epidemics, with 13,000 to 20,000 paralytic cases reported annually.
In the early vaccine era, the incidence dramatically decreased following IPV introduction in 1955. The decline continued following OPV introduction in 1961. In 1960, a total of 2,525 paralytic cases were reported, compared with 61 in 1965.
The last cases of paralytic poliomyelitis caused by endemic transmission of wild virus in the United States were in 1979, when an outbreak occurred among the Amish in several Midwest states. The virus was imported from the Netherlands.
From 1980 through 1999, a total of 152 confirmed cases of paralytic poliomyelitis were reported, an average of 8 cases per year. Six cases were acquired outside the United States and imported. The last imported case was reported in 1993. Two cases were classified as indeterminant (no poliovirus isolated from samples obtained from the patients, and these persons had no history of recent vaccination or direct contact with a vaccine recipient). The remaining 144 (95%) cases were vaccine-associated paralytic polio (VAPP) caused by live oral polio vaccine.
In order to eliminate VAPP from the United States, ACIP recommended in 2000 that IPV be used exclusively in the United States. The last case of VAPP was reported in 1999.
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