Polio As a Disease - Ministry of Public Health Afghanistan

Polio As a Disease


Poliomyelitis is an acute, viral and contagious disease which cause by polio virus from entero virus family that almost affecting (acute flaccid paralysis) the under five years old children.

Epidemiology of Polio
The polioviruses

There are three serotypes of poliovirus, labeled P1, P2, and P3, defined by the fact that infection with one serotype does not confer protection against disease caused by either of the other two. Within a serotype, different strains can also be recognized, chiefly on the basis of differences in nucleic acid sequence. The most frequent cause of epidemic polio is poliovirus type 1.It has been observed in countries with successful eradication programs that the first poliovirus serotype to disappear is P2 due to the high immunogenicity of the vaccine against that strain. In fact P2 has been successfully eradicated as it has not been detected anywhere in the world since October of 1999.

In general, 1% of infections with a serotype 1 virus progress to clinical poliomyelitis, the figure being tenfold lower for serotype 3, and even lower for serotype 2. This means that virus, particularly P3, can be very widespread before the first paralytic case is seen, and circulate unobserved for many months if the surveillance is not very sensitive. The reasons for the differences between the serotypes and why some individuals succumb to poliomyelitis, whereas most people are asymptomatic, are not known. The symptoms of the major disease of poliomyelitis are the same for all three serotypes.

Spectrum of Disease
In 90-95% of infected individuals, poliovirus infection is not apparent. Minor illness will result in 4-8% of infections characterized by low-grade fever, sore throat, vomiting, abdominal pain, loss of appetite, and malaise. Recovery is rapid and complete, and there is no paralysis. This form of poliovirus infection is called “abortive poliomyelitis”. It cannot be distinguished from other mild, viral infections.

Following poliovirus exposure, viral replication occurs in the oropharynx and the intestinal tract. Viremia follows, which may result in infection of central nervous system cells. A specific receptor is needed for the virus to enter cells. Aseptic meningitis can also occur, which will resolve untreated as with any other viral meningitis. In less than 1% of infection, the virus invades and replicates in motor neurons of the anterior horn and brain stem resulting in cell destruction and causing the typical clinical manifestations of poliomyelitis. The actual clinical signs depend on which region of the central nervous system is affected. Spinal paralysis results from the infection of the lower motor neurons and typically affects only one leg. The more serious bulbar poliomyelitis involves neurons in the brainstem and, therefore, affects breathing. It was this latter manifestation of the disease that led to the development of the iron lung as an artificial respirator during the 1950s. Encephalitis results from the infection of the brain itself; it makes up ~1% of all cases and is usually fatal. Progression to maximum paralysis is rapid (2–4 days), usually associated with fever and muscle pain, and rarely continues after the temperature has returned to normal. Spinal paralysis is typically asymmetric (i.e. one side affected to a greater degree than the other), more severe proximally than distally, and deep tendon reflexes are absent or diminished. Of paralytic cases, as many as 5–10% are fatal, 10% recover completely and the remainder may have partial recovery with residual paralysis.

Following the acute episode, many patients recover muscle function at least partially, and prognosis for recovery can usually be established within 6 months after onset of paralytic manifestations. Infection with poliovirus results in lifelong, type-specific immunity.

Poliovirus is spread through person-to-person, fecal-oral contact. The virus is intermittently excreted in the stool for one month or more after infection. After initial infection with poliovirus, the virus is shed intermittently in faeces (excrement) for several weeks. The heaviest faecal excretion of the virus occurs just prior to the onset of paralysis and during the first two weeks after paralysis occurs. Individuals with antibody deficiencies may excrete virus for a prolonged period of time, perhaps years and are at higher risk of paralytic disease. Where hygiene and sanitation are poor, young children are especially at risk of infection and young children who are not yet toilet-trained are a ready source of transmission, regardless of their environment. Polio can also be spread by food or drink contaminated by faeces, but is more often spread directly from child to child. There is also evidence that flies can passively transfer poliovirus from faeces to food. Because of the silent transmission and the rapid spread of the disease, one case of paralytic illness generally represents widespread circulation of virus in a community. Poliomyelitis is preventable either by vaccination or by the administration of immunoglobulin containing antibodies that are specific for poliovirus. The rationale of either approach is to prevent the virus reaching the nervous system and producing irrevocable damage. However, even children protected from paralytic illness by vaccination, may have transient virus replication in the intestine and be able to spread it to other children. OPV is the most effective means of boosting intestinal immunity and stopping transmission

Protective immunity against poliovirus infection develops by immunization or natural infection. Immunity to one poliovirus type does not protect against infection with other poliovirus types. Immunity following natural infection or administration of live oral polio vaccine (OPV) is believed to be life long. The duration of protective antibodies after administration of inactivated polio vaccine (IPV) is unknown, and does not result in the same level of intestinal immunity as OPV. Therefore, IPV may not be as effective as OPV in preventing carriage and spread of wild virus from immunized individuals. Infants born to mothers with high antibody levels against poliovirus are protected for the first several weeks of life. In endemic countries such as Afghanistan, nearly all children have acquired natural immunity by the age of 5 years.

Poliovirus infects only human beings and there is no animal reservoir. The virus does not survive long in the environment outside the human body. There is no long-term carrier state. Table 1: Survival of wild polioviruses in the environment Environment Time for virus infectivity to fall by 90%
1. Soil Summer 1.5 days Winter 20 days
2. Sewage At 23Cº 26 days At 2 Cº 180 days
3. Surface water Fresh 5.5 days Sea 2.5 days
AFP_surveillance_Guidelines_2010 4

Poliomyelitis has now been eradicated in the Western hemisphere and most industrialized countries. Incidence is highest in developing countries, where immunization coverage is low and sanitation is poor. The disease is seasonal, occurring more frequently during the rainy season in tropical climates and in summer and early autumn in temperate climates.

Risk Factors for Paralysis after Infection
No one knows why only a small percentage of infections lead to paralysis. Several key risk factors have been identified as increasing the likelihood of paralysis in a person infected with polio virus. These include:
• Intramuscular injections
* Immune deficiency
• Pregnancy
* Removal of the tonsils (tonsillectomy)
• Strenuous exercise
• Injury

Rationale for Polio eradication
Polio is one of only a limited number of diseases (other include measles, small pox has already been eradicated) that can be eradicated. Polio can be eradicated because:
• Polio only affects human, and there is no animal or environmental reservoir An effective, inexpensive vaccine in the shape of OPV exists
• Immunity is life-long The virus can only survive for a very short time in the environment and does not enjoy a carrier state. Other diseases can be controlled through immunization, but never eradicated. For example, in the case of tetanus, the bacterium that causes the disease (Clostridium tetani) is widespread in the environment and can survive independently of a human host

Clinical aspects of polio

Clinical course of paralytic disease

Although the virus is highly contagious, at least 90% of all persons who acquire it have no signs of illness and are never aware they have been infected. Once the symptoms of the disease appear there is currently no treatment, although physical therapy is useful for regaining some function in the recovery phase. The likelihood of developing paralytic illness varies widely between the strains of virus from 100:1 for P1 infections to 1000:1 for P3. Two phases of acute poliomyelitis can be distinguished: a non-specific febrile illness (minor illness) followed, in a small proportion of patients, by aseptic meningitis and/or paralytic disease (major illness). The time between infection and onset of paralysis is 07-14 days (range 4 - 35 days). The minor phase of paralytic disease consists of symptoms similar to those of abortive poliomyelitis (Figure 1). The major phase of illness begins with muscle pain, spasms and the return of fever. This is followed by rapid onset of flaccid paralysis that is usually complete within 72 hours. “Spinal paralytic poliomyelitis” affecting the muscles of the legs, arms and/or trunk is the most common form of paralytic poliomyelitis. The affected muscles are floppy and reflexes are diminished. The sense of pain and touch remain normal. The paralysis is usually asymmetric, affecting one side more than the other, affecting the legs more often than the arms, and the proximal parts of the extremities more often than the distal parts. Residual flaccid paralysis is usually present after 60 days. Figure 1: Phases of occurrence of symptoms AFP_surveillance_Guidelines_2010 5 In severe cases, quadriplegia may develop with paralysis of the trunk, abdominal and thoracic muscles. More rarely, “bulbar polio” occurs, affecting the motor neurons of the cranial nerves. This may result in respiratory insufficiency and difficulty in swallowing, eating and speaking. The risk of death from bulbar polio is high. Certain factors, if present during infection with poliovirus, increase the likelihood of paralysis; these include administration of intramuscular injections, strenuous exercise, pregnancy, tonsillectomy, and injury.

Differential diagnosis
Case Definition for Acute Flaccid Paralysis:
Recent onset of floppy weakness or paralysis in a child aged less than 15 years of age, due to any cause including Guillian-Barre syndrome (GBS); or any paralytic illness in a person of any age when polio is suspected by the clinician The diagnoses that cause acute flaccid paralysis include paralytic poliomyelitis, Guillain-Barré syndrome and Transversemyelitis (Table 2). Less common etiologies are traumatic neuritis, encephalitis, meningitis and tumors. All should be reported to the AFP surveillance system. Distinguishing characteristics of paralytic polio are asymmetric flaccid paralysis, fever at onset, rapid progression of paralysis, residual paralysis after 60 days, and preservation of sensory nerve function, however, clinical features alone are not enough to clearly distinguish poliomyelitis from other causes of AFP. For this reason it is important to obtain stool specimens for Virological testing from all cases regardless of the clinical picture.
Table 2: Differential diagnosis of poliomyelitis AFP_surveillance

Polio vaccines
There are two types of polio vaccine:
1-Oral (live, attenuated) polio vaccine
– Trivalent (tOPV)
– Monovalent (mOPV)
– Bivalent (bOPV)
2-Injectable, Inactivated or killed polio vaccine (IPV).

Trivalent oral polio vaccine (tOPV)
Trivalent oral polio vaccine consists of live, attenuated polioviruses, and is a safe and effective vaccine.

Vaccination schedule through Routine Immunization
WHO currently recommends that children receive five doses of OPV before one year of age. One dose should be given at birth or as close to birth (within 14 days) as possible. This is called the “birth dose”, or “zero-dose”. Three doses should be given at least four weeks apart and usually at the same time as DPT and Hepatitis B. The fifth dose of OPV should be given at least one month after the third one. It is given at the time of measles immunization. Doses administered during the Supplemental Immunization Activities (NIDs and SNIDs) do not replace the primary schedule of vaccination through Routine Immunization and they are only supplemental to the primary doses.

Dosage and administration
One dose of OPV from most manufacturers consists of 2 drops of vaccine administered directly into the mouth. Due to the safety of the vaccine, there is no upper limit to the number of doses of OPV that can be administered. The only requirement is that at least four weeks are required
between two doses for an effective humoral response to occur