17.5
Poliomyelitis
Poliomyelitis is caused by the poliovirus, a non-enveloped RNA virus from the Picornaviridae family.
In young children, the virus enters the body through the fecal-oral route, typically by ingesting contaminated food or water.
Once inside, the virus replicates in the mucosal lining of the throat and intestines, remaining mostly asymptomatic.
In symptomatic cases, the virus then spreads to the lymph nodes and enters the bloodstream, causing primary viremia.
As the infection progresses, the virus reaches the central nervous system, particularly the spinal cord.
The virus may also reach the spinal cord through retrograde axonal transport from peripheral nerves.
There, it targets and replicates in the anterior horn of the spinal cord.
This results in the destruction of motor neurons that control muscle movement, leading to motor impairment.
This condition is known as paralytic poliomyelitis, and it is characterized by the sudden onset of asymmetric flaccid paralysis, often affecting the legs.
Poliomyelitis is caused by poliovirus, a small, non-enveloped, positive-sense RNA virus of the Picornaviridae family and Enterovirus genus. Transmission occurs primarily via the fecal-oral route, often through ingestion of contaminated water or food. The virus initially replicates in the oropharynx and intestinal mucosa, particularly in lymphoid tissues such as the tonsils, Peyer’s patches, and regional lymph nodes. Primary viremia follows, allowing dissemination throughout the body.
In most cases (over 90%), infection is asymptomatic or causes minor illness (abortive poliomyelitis) with nonspecific symptoms such as fever, headache, sore throat, and malaise. In about 1–2% of cases, the virus invades the central nervous system (CNS), leading to nonparalytic poliomyelitis with signs of meningeal irritation, including neck stiffness and muscle spasms. Paralytic poliomyelitis, the most severe form, occurs in fewer than 2% of infections and results from viral replication in the anterior horn cells of the spinal cord or cranial nerve motor nuclei. This leads to flaccid, asymmetric paralysis. Bulbar involvement can impair respiratory function, sometimes necessitating mechanical ventilation.
Vaccination and Eradication Efforts
Two main vaccines have been developed to combat poliomyelitis. The inactivated poliovirus vaccine (IPV), developed by Jonas Salk in 1955, is administered by injection and induces systemic immunity (mainly serum IgG). It prevents paralytic disease but does not significantly interrupt viral transmission.
The oral poliovirus vaccine (OPV), developed by Albert Sabin in 1961, is a live attenuated vaccine that induces both systemic and mucosal immunity (serum IgG and secretory IgA). It is orally administered and more effective at interrupting fecal-oral transmission. However, OPV carries a rare risk of reversion to neurovirulence, potentially causing vaccine-associated paralytic poliomyelitis (VAPP) or circulating vaccine-derived poliovirus (cVDPV).
Global eradication efforts have dramatically reduced polio incidence, with endemic transmission now limited to a few countries. IPV is currently preferred in many regions due to its safety, while OPV remains critical in areas with active transmission.
Poliomyelitis is caused by the poliovirus, a non-enveloped RNA virus from the Picornaviridae family.
In young children, the virus enters the body through the fecal-oral route, typically by ingesting contaminated food or water.
Once inside, the virus replicates in the mucosal lining of the throat and intestines, remaining mostly asymptomatic.
In symptomatic cases, the virus then spreads to the lymph nodes and enters the bloodstream, causing primary viremia.
As the infection progresses, the virus reaches the central nervous system, particularly the spinal cord.
The virus may also reach the spinal cord through retrograde axonal transport from peripheral nerves.
There, it targets and replicates in the anterior horn of the spinal cord.
This results in the destruction of motor neurons that control muscle movement, leading to motor impairment.
This condition is known as paralytic poliomyelitis, and it is characterized by the sudden onset of asymmetric flaccid paralysis, often affecting the legs.
From Chapter 17:
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