Poliovirus (Polio, Poliomyelitis)
What is poliovirus?
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. That is, immunity to one serotype does not produce significant immunity to the other 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 less virus in the throat, but virus continues to be excreted in the stool for several weeks. The virus invades local lymphoid tissue, enters the bloodstream, 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.
Clinical Features of Polio Infection
The incubation period for poliomyelitis is commonly 6–20 days with a range of 3–35 days.
The response to poliovirus infection is highly variable and has been categorized on the basis of 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 characterised 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, diarrhoea), and influenza-like 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.
Fewer 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. Weakness or paralysis still present 12 months after onset is usually permanent.
Paralytic polio is classified into three types, depending on the level of involvement. Spinal polio is most common, and during 1969–1979, accounted for 79% of paralytic cases. It is characterised by asymmetric paralysis that most often involves the legs. Bulbar polio leads to weakness of muscles innervated by cranial nerves and accounted for 2% of cases during this period. Bulbospinal polio, a combination of bulbar and spinal paralysis, accounted for 19% of cases. The death-to-case ratio for paralytic polio is generally 2%–5% among children and up to 15%–30% for adults (depending on age). It increases to 25%–75% with bulbar involvement.
- Viral Isolation
Poliovirus may be recovered from the stool or pharynx of a person with 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 “wild type” (that is, the virus that causes polio disease) or vaccine type (virus that could derive from a vaccine strain).
Neutralizing antibodies appear early and may be at high levels by the time the patient is hospitalized; therefore, a fourfold rise in antibody titer may not be demonstrated.
- Cerebrospinal Fluid
In poliovirus infection, the CSF usually contains an increased number of white blood cells (10–200 cells/mm3, primarily lymphocytes) and a mildly elevated protein (40–50 mg/100 mL).
At one time poliovirus infection occurred throughout the world. Transmission of wild poliovirus was interrupted in the United States in 1979, or possibly earlier. A polio eradication programme conducted by the Pan American Health Organization led to elimination of polio in the Western Hemisphere in 1991. The Global Polio Eradication Programme has dramatically reduced poliovirus transmission throughout the world. In 2003, only 784 confirmed cases of polio were reported globally and polio was endemic in six countries.
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 faecal-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 among susceptible household contacts of children nearly 100%, and greater than 90% among 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.
Is there a vaccine against polio virus?
Yes. See polio vaccine.
After an interval of 30–40 years, 25%–40% of persons who contracted paralytic poliomyelitis in childhood experience new muscle pain and exacerbation of existing weakness, or develop new weakness or paralysis. This disease entity is referred to as postpolio syndrome. Factors that increase the risk of postpolio syndrome include increasing length of time since acute poliovirus infection, presence of permanent residual impairment after recovery from the acute illness, and female sex. The pathogenesis of postpolio syndrome is thought to involve the failure of oversized motor units created during the recovery process of paralytic poliomyelitis. Postpolio syndrome is not an infectious process, and persons experiencing the syndrome do not shed poliovirus.
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