By Diana Woodworth
Etiologic agent: Poliomyelitis, or infantile paralysis, is a viral disease that can affect nerves and may cause some form of paralysis (8, 9). Poliomyelitis means inflammation of the gray (poliós) marrow (myelós), in the spinal cord (8). Polio is caused by the poliovirus, a member of the enterovirus subgroup, family Picornaviridae (4). While the disease once reached epidemic proportions in the United States and several other countries, due to vaccination efforts, polio has now been eliminated from the Western Hemisphere (3).
Transmission: Poliovirus is transmitted by direct person-to-person contact, contact with infected mucus or phlegm from the nose or mouth, or contact with infected feces (9). This enterovirus enters through the mouth and multiplies, at the site of implantation, in the throat and gastrointestinal tract. Most often, the virus is present in the throat and stool before the onset of illness. When illness begins, there is less virus found in the throat, however virus is excreted in the stool for several weeks (4). Poliovirus is also absorbed and spread through the blood and lymph system. This path may eventually lead to the central nervous system, and other areas where the polio virus receptors may be found. These CD155 receptors are expressed in spinal cord anterior horn cells, dorsal root ganglia, skeletal muscle, motor neurons and some cells of the lymphoid system (8). The incubation time for polio ranges from 5 - 35 days (average 7 - 14 days) (9).
Reservoirs: Humans are the only known reservoir of poliovirus (4). However, cockroaches and flies may serve as vectors for the subgroup enterovirus (1).
Specific characteristics: The poliovirus, a member of the enterovirus subgroup, family Picornaviridae. The Picornaviridae family consists of icosahedral, nonenveloped, and small (22 to 30 nm) virions (1). The capsid proteins, of the virus, sheath a sense RNA strand consisting of approximately 7,500 nucleotides. The RNA houses a covalently bound noncapsid viral protein (VPg) at its 5’ end and a polyadenylated tail at its 3’ end (1). The poliovirus, along with all enteroviruses, thrives in low pH conditions. The acid stability of these viruses is what allows them to can pass into the gastrointestinal tract and set up additional infections in the intestinal mucosa (8).
P1, P2, and P3 are three poliovirus serotypes. There is minimal heterotypic immunity between the three serotypes. Meaning, immunity to one serotype does not guarantee immunity to the other serotypes (4). All three serotypes bind to the CD155 receptor protein, or polio virus receptor protein. However, not all polio cases spread to the central nervous system, where CD155 receptors can be found (8). Most disease results from infection of P1 serotype poliovirus (8).
The poliovirus can be rapidly inactivated by heat, formaldehyde, chlorine, and ultraviolet light (4).
Specific tests for identification: There are three ways of testing for presence of poliovirus. These testing methods include: viral isolation, serology, and use of cerebrospinal fluid (4).
Viral isolation is the recovery of poliovirus from the stool or throat of a person with poliomyelitis. Virus isolation from an acute flaccid paralysis case must be tested further, using oligonucleotide mapping (fingerprinting) or genomic sequencing. This secondary testing determines if the virus is “wild type” (causes polio disease) or vaccine type (could derive from a vaccine strain) (4).
Serology is used to detect for antibodies during a suspected polio infection. Neutralizing antibodies appear early, in the disease, and may reach high levels by the time the infected patient is hospitalized. This means, a fourfold rise in antibody titer may not be demonstrated (4).
Poliovirus isolation from the cerebrospinal fluid (CSF) rarely accomplished, but serves as a diagnostic tool. In a poliovirus infection, the CSF generally contains a significantly elevated number of white blood cells (10–200 cells/mm3, primarily lymphocytes) and a mildly elevated protein (40–50 mg/100 mL) (4).
Signs and symptoms: Poliovirus infections can manifest themselves in varying degrees of severity. Most individuals (90 to 95 percent) experience inapparent infection, or no symptoms at all. Three other categories of poliomyelitis include: abortive poliomyelitis, nonparalytic poliomyelitis, and paralytic poliomyelitis (5).
Abortive poliomyelitis is classified as a mild, short course of the disease. It may involve one or more of the following symptoms: fever (up to 103 degrees F), decreased appetite, nausea and/or vomiting, sore throat, body aches, constipation, and abdominal pain (5).
Nonparalytic poliomyelitis causes similar symptoms as abortive poliomyelitis. However, patients with nonparalytic polio may also feel ill for a couple of days, appear to improve, then get increasing sick. Additional symptoms may include: pain of muscles in the neck, trunk, arms, and legs and stiffness in the neck and spine (5).
Paralytic poliomyelitis causes the same symptoms as the nonparalytic and abortive cases, plus some addition symptoms. Patients experiencing paralytic polio may experience total muscle weakness or wasting, severe constipation, weakened breathing, difficulty swallowing, weak coughing, flushed or blotchy skin, bladder and/or muscle paralysis, irritability, poor mood control, drooling, and abdominal bloating (5).
Perminant states of paralysis, due to poliomyelitis, can be characterized as acute flaccid paralysis (AFP) or bulbar polio. AFP can occur when the virus enters the blood stream and infiltrates the central nervous system. As the virus grows, it destroys the nerve cells that activate muscles. This makes the muscles no longer functional and the limb becomes floppy and lifeless. This usually occurs in the legs, and is irreversible (7). More extensive paralysis, involving the trunk and muscles of the thorax and abdomen, may result in quadriplegia (irreversible functionality of all four limbs). Bulbar polio occurs in the most severe cases of infection. It is caused by poliovirus attacking the nerve cells of the brain stem, reducing breathing capacity and causing difficulty in swallowing and speaking (7).
Historical information: It is thought that polio has tormented humans for thousands of years. The first records of poliomyelitis come from an Egyptian carving from the 18th dynasty (1580-1350 BCE) showing a casualty of the disease with a withered leg (8). The first to describe and recognize poliomyelitis as a paralytic disease in children was the Englishman Michael Underwood, in 1789. The first outbreaks in Europe were recorded in the early 19th century, and outbreaks in the United States were first reported in 1843 (4). However, polio reached epidemic proportions in the early 1900s (3). Between the late 1940s to the early 1950s, outbreaks in the United States increased in size and frequency. The public was frightened to let children go outside, especially in the summer when the virus infections peaked (2).
In the early 1950s, Dr. Jonas Salk developed the inactivated polio vaccine (IPV) and in the early 1960s Dr. Albert Sabin developed the oral polio vaccine (OPV) (2). After the introduction of effective vaccines, polio incidence declined rapidly. The last case of “wild-type” virus polio acquired in the United States was in 1979 (4). Due to widespread vaccination efforts, polio was eliminated from the Western Hemisphere in 1994 (3).
Virulence factors: In order for the poliovirus to infect tissue, a cell surface glycoprotein poliovirus receptor (CD155) must be present. When the virus binds to the CD155 receptor, the promoter releases the VP4 protein. This allows viral RNA to leave the nucleocapsid when the virus is taken into the endocytic pathway (8). Once in the acidic endosome, the nucleocapsid disassembles. Poliovirus protein synthesis can be detected within 15 minutes of initial infection (8).
CD155 is expressed in several types of tissue, including: spinal cord anterior horn cells, dorsal root ganglia, skeletal muscle, motor neurons and some cells of the lymphoid system. Embryonic structures giving rise to spinal cord anterior horn motor neurons are capable of expressing CD155. According to Dr. Richard Hunt, “this may explain the restrictive host cell tropism of polio virus for this cellular compartment of the central nervous system.” (8).
Control and treatment: Poliomyelitis can be prevented by the Salk-type (inactivated) and Sabin-type (live) attenuated poliovirus vaccines. Control may be achieved by public education on transmission modes and personal hygiene, proper sewage disposal, and supply of uncontaminated water supplies (1).
There is no cure for those infected with poliomyelitis, but there is treatment for symptoms experienced by those infected. These treatments include: analgesics for pain, bed rest, balanced diet, reduction in exercise, and heat packs for muscle pain (1).
Prevention and vaccine information: There are two vaccines available for preventing polio, the inactivated poliovirus vaccine (IPV) and the oral poliovirus vaccine (OPV). Currently, the IPV is the only polio vaccine given in the United States, because it is a killed vaccine and cannot cause the disease. OPV, however, is still used in vaccination programs in other areas of the world (4).
The inactivated poliovirus vaccine was developed by Dr.Jonas Salk, in the early 1950s. TheIPV contains all three serotypes of polio vaccine virus (4). The virus serotypes are grown in a type of monkey kidney tissue (Vero cell line) and inactivated, or killed, with formaldehyde. The vaccine is preserved by 2-phenoxyethanol, and contains small amounts of neomycin, streptomycin, and polymyxin B. It is produced in a single-dose prefilled syringe and is given by either subcutaneous or intramuscular injection (4).
The oral poliovirus vaccine was developed by Dr. Albert Sabin, in the early 1960s. It too contains all three serotypes of the polio virus vaccine. However, the three virus serotypes are live attenuated strains, in a 10:1:3 ratio (4). Like the IPV viruses, the OPV viruses are grown in Vero cells (monkey kidney cells). The OPV contains neomycin and streptomycin and is distributed in single 0.5-mL doses. No preservative is needed, because the virus is not killed. Live attenuated polioviruses multiply in the intestinal mucosa, lymphoid cells and, lymph nodes that drain the intestine. The viruses are excreted in stool, for up to 6 weeks after a dose. This means that the virus is able to spread from the recipient to persons who come in contact with fecal matter of the vaccinated individual (4).
Current outbreaks (local): Polio has been eradicated from the Western Hemisphere since 1994 (3). It has been eradicated from United States since 1979 (2).
Current outbreaks (global): Although polio has been eradicated from most of the world, there are still cases of the disease in Asia and Africa (2). Polio cases have decreased from around 350,000 cases in 1988, to 1,352 reported cases in 2010 (6). The reduction of polio cases is due to the global effort to eradicate the disease. In 2012, only, Afghanistan, Nigeria, and Pakistan remain polio-endemic. This is down from more than 125 countries that were endemic in 1988 (6). Continual pockets of polio transmission in northern Nigeria and the border between Afghanistan and Pakistan are where the polio eradication initiative is currently focused. In 1988, the forty-first World Health Assembly, pledged to eradicate polio internationally. The Global Polio Eradication Initiative, spearheaded by WHO, Rotary International, the US Centers for Disease Control and Prevention (CDC) and the United Nations Children’s Fund (UNICEF) was launched (6). They continue to fight for total eradication of polio.
1) Marguerite Yin-Murphy and Jeffrey W. Almond. National Center for Biotechnology Information. “Picornaviruses.” 1996. http://www.ncbi.nlm.nih.gov/books/NBK7687/#A2844 accessed 3-6-12.
2) Centers for Disease Control and Prevention. “A Polio-Free US Thanks to Vaccine Efforts.” February 7, 2011. http://www.cdc.gov/Features/PolioFacts/ accessed 3-6-12.
3) The College of Physicians of Philadelphia. “History of Polio.” 2012. http://www.historyofvaccines.org/content/timelines/polio accessed 3-6-12.
4) Centers for Disease Control and Prevention. “Poliomyelitis: Epidemiology and Prevention of Vaccine-Preventable Diseases.” April 15,2011. http://www.cdc.gov/vaccines/pubs/pinkbook/polio.html accessed 3-6-12.
5) Johns Hopkins Medicine. “Poliomyelitis (Polio).” 2012. http://www.hopkinsmedicine.org/healthlibrary/conditions/adult/infectious_diseases/poliomyelitis_polio_85,P00643/ accessed 3-6-12.
6) World Health Organization. “Poliomyelitis.” February 2012. http://www.who.int/mediacentre/factsheets/fs114/en/index.html accessed 3-7-12.
7) Polio Global Eradication Initiative. “Polio and Prevention.” 2010. http://www.polioeradication.org/Polioandprevention.aspx accessed 3-7-12.
8) Dr. Richard Hunt. “ENTEROVIRUSES AND GENERAL FEATURES OF PICORNAVIRUSES.” April 12, 2010. http://pathmicro.med.sc.edu/virol/picorna.htm accessed 3-7-12.
9) PubMed Health. “Poliomyelitis.” August 24, 2011. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002375/ accessed 3-7-12.