Acute Poliomyelitis

Updated: Feb 11, 2016
  • Author: Christine L Munson, MD; Chief Editor: Stephen Kishner, MD, MHA  more...
  • Print
Overview

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 par The typical contractures of postpolio residual paralysis.

See Pediatric Vaccinations: Do You Know the Recommended Schedules?, a Critical Images slideshow, to help stay current with the latest routine and catch-up immunization schedules for 16 vaccine-preventable diseases.

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 July 2014, only two countries, Pakistan and Afghanistan, were endemic for polio; [1, 2] however, the campaign to eradicate polio continues today, as do efforts to prevent transmission of the disease into polio-free areas. [3, 4, 5]

Next:

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. [6, 7]

Previous
Next:

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 had a worldwide distribution, with a peak season from July to September and a concentration in tropical areas of the Northern Hemisphere. The condition continues to occur epidemically in nonimmunized populations in developing regions. Poor sanitation and crowded circumstances are two 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. [8] In eight 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. [9, 10] In October 2013, Syria reported that, after having been eradicated there 15 years earlier, polio had returned to that country, with 13 cases from the Deir Al Zour province, caused by wild poliovirus type I, having been confirmed. [11] As of July 2014, Pakistan and Afghanistan remained the only two countries where wild-type polio was endemic. [1, 2]

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.

Previous