Background
Acute poliomyelitis is a disease of the anterior horn motor neurons of the spinal cord and brain stem caused by poliovirus. Flaccid asymmetric weakness and muscle atrophy are the hallmarks of its clinical manifestations, due to loss of motor neurons and denervation of their associated skeletal muscles. Because of the success of poliovirus vaccine, poliomyelitis, once one of the most feared human infectious diseases, is now almost entirely preventable by proper immunization (see image below).
The typical contractures of postpolio residual paralysis. In 1988, the World Health Organization initiated the Global Polio Eradication Initiative to eradicate poliomyelitis; at the time, it was endemic in 125 countries. As of 2006, only 6 countries were endemic for polio; however, the worldwide campaign to eradicate polio continues today, as do efforts to prevent transmission of the disease into polio-free areas.[1, 2, 3]
Pathophysiology
Acute poliomyelitis is caused by small ribonucleic acid (RNA) viruses of the enterovirus group of the picornavirus family. The single-stranded RNA core is surrounded by a protein capsid without a lipid envelope, which makes poliovirus resistant to lipid solvents and stable at low pH. Three antigenically distinct strains are known, with type I accounting for 85% of cases of paralytic illnesses. Infection with one type does not protect from the other types; however, immunity to each of the 3 strains is lifelong.
The enteroviruses of poliomyelitis infect the human intestinal tract mainly through the fecal-oral route (hand to mouth). The viruses multiply in oropharyngeal and lower gastrointestinal tract mucosa during the first 1-3 weeks of the incubation period. Virus may be secreted in saliva and feces during this period, causing most host-to-host transmission. After the initial alimentary phase, the virus drains into the cervical and mesenteric lymph nodes and then into the blood stream. Only 5% of infected patients have selective nervous system involvement after viremia. It is believed that replication in extraneural sites maintains the viremia and increases the likelihood that the virus will enter the nervous system.
The poliovirus enters the nervous system by either crossing the blood-brain barrier or by axonal transportation from a peripheral nerve. It can cause nervous system infection by involving the precentral gyrus, thalamus, hypothalamus, motor nuclei of the brainstem and surrounding reticular formation, vestibular and cerebellar nuclei, and neurons of the anterior and intermediate columns of the spinal cord. The nerve cells undergo central chromatolysis along with an inflammatory reaction while multiplication of the virus precedes onset of paralysis. As the chromatolysis process goes on further, muscle paralysis or even atrophy appears when fewer than 10% of neurons survive in the corresponding cord segments. Gliosis develops when the inflammatory infiltrate has subsided, but most surviving neurons show full recovery.[4, 5]
Epidemiology
Frequency
United States
Because of widespread use of the poliovirus vaccine, the incidence rate has been less than 0.01 cases per 100,000 population since 1965. The last case of wild-type polio in the United States was in 1979. Only a few cases of paralytic poliomyelitis are reported each year in the United States. Vaccine-derived poliovirus infections are seen primarily in low-vaccination communities. Rare cases of poliomyelitis are reported due to live attenuated poliovirus vaccine. Small pockets of poliomyelitis epidemics still exist among isolated religious sects, such as the Amish. These groups usually choose not to participate in government-sponsored public health services, such as immunizations for infectious diseases.
International
Acute poliomyelitis has a worldwide distribution, with the peak season being from July to September and the concentration being in tropical areas of the Northern Hemisphere. As of 2006, 6 countries were endemic to polio: Afghanistan, Egypt, India, Niger, Nigeria, and Pakistan. The condition continues to occur epidemically in nonimmunized populations in developing regions. Poor sanitation and crowded circumstances are 2 additional factors associated with dissemination. Internationally, importation of polio continues to occur into polio-free countries. From 2002-2005, 21 previously polio-free countries experienced a resurgence of wild-type polio.[6] In 8 of those countries, the cases were limited and no further spread was observed. In the remaining 13 countries, multiple cases were observed, with the outbreak lasting less than 6 months.[7, 8]
Mortality/Morbidity
Of acute poliovirus infections, 4-8% show only nonspecific illness, and 1-2% of infections finally result in neurologic symptoms. The incidence of paralytic diseases increases with young age, advanced age, recent hard exercise, tonsillectomy, pregnancy, and impairment of B-lymphocyte defenses. The mortality from acute paralytic poliomyelitis is 5-10%, but it can reach 20-60% in cases of bulbar involvement.
Race
Acute poliomyelitis has no racial predilection.
Sex
The male-to-female ratio for acute poliomyelitis is 1:1.
Age
Most cases of acute poliomyelitis occur in the pediatric population. Infection or immunization against poliovirus provides lifelong protection.
Henderson DA. The eradication of smallpox - An overview of the past, present, and future. Vaccine. Dec 19 2011;[Medline].
Progress toward poliomyelitis eradication--Afghanistan and Pakistan, January 2010-September 2011. MMWR Morb Mortal Wkly Rep. Nov 11 2011;60:1523-7. [Medline].
Global routine vaccination coverage, 2010. MMWR Morb Mortal Wkly Rep. Nov 11 2011;60:1520-2. [Medline].
Kindberg E, Ax C, Fiore L, Svensson L. Ala67Thr mutation in the poliovirus receptor CD155 is a potential risk factor for vaccine and wild-type paralytic poliomyelitis. J Med Virol. May 2009;81(5):933-6. [Medline].
Racaniello VR. One hundred years of poliovirus pathogenesis. Virology. Jan 5 2006;344(1):9-16. [Medline].
Resurgence of wild poliovirus type 1 transmission and consequences of importation--21 countries, 2002-2005. MMWR Morb Mortal Wkly Rep. Feb 17 2006;55(6):145-50. [Medline]. [Full Text].
Wild poliovirus type 1 and type 3 importations--15 countries, Africa, 2008-2009. MMWR Morb Mortal Wkly Rep. Apr 17 2009;58(14):357-62. [Medline]. [Full Text].
Progress toward interruption of wild poliovirus transmission--worldwide, 2008. MMWR Morb Mortal Wkly Rep. Apr 3 2009;58(12):308-12. [Medline]. [Full Text].
Tsai HC, Hung TH, Chen CC, et al. Prevalence and risk factors for upper extremity entrapment neuropathies in polio survivors. J Rehabil Med. Jan 2009;41(1):26-31. [Medline].
[Best Evidence] Oncu J, Durmaz B, Karapolat H. Short-term effects of aerobic exercise on functional capacity, fatigue, and quality of life in patients with post-polio syndrome. Clin Rehabil. Feb 2009;23(2):155-63. [Medline].
Adams RD, Victor M, Ropper AH. Viral infection. In: Poliomyelitis. Principles of Neurology. 6th ed. 1997:136-7.
Alcala H. [The differential diagnosis of poliomyelitis and other acute flaccid paralyses]. Bol Med Hosp Infant Mex. Feb 1993;50(2):136-44. [Medline].
Birk TJ. Poliomyelitis and the post-polio syndrome: exercise capacities and adaptation--current research, future directions, and widespread applicability. Med Sci Sports Exerc. Apr 1993;25(4):466-72. [Medline].
Centers for Disease Control and Prevention. Poliovirus infections in four unvaccinated children--Minnesota, August-October 2005. MMWR Morb Mortal Wkly Rep. Oct 21 2005;54(41):1053-5. [Medline].
Frustace SJ. Poliomyelitis: late and unusual sequelae. Am J Phys Med. Dec 1987;66(6):328-37. [Medline].
Howard RS. Poliomyelitis and the postpolio syndrome. BMJ. Jun 4 2005;330(7503):1314-8. [Medline]. [Full Text].
Kidd D, Williams AJ, Howard RS. Poliomyelitis. In: Classic Diseases Revisited. 1996:641-647.
Miller MA, Sutter RW, Strebel PM, Hadler SC. Cost-effectiveness of incorporating inactivated poliovirus vaccine into the routine childhood immunization schedule. JAMA. Sep 25 1996;276(12):967-71. [Medline].
Price RW, Plum F. Poliomyelitis. In: Handbook of Clinical Neurology. Vol 32. 1978:2091-2092.
Rowland LP. Viral infections of the nervous system: syndrome of acute anterior poliomyelitis. In: Merritt's Neurology. 10th ed. 2000:764-767.

