Poliomyelitis (Heine Medin Disease): Epidemiology, Pathology And Clinical Manifestations

Enteroviruses

These are viruses which are found in the alimentary tract of man. These include poliomyelitis, coxsackie, ECHO and several other viruses. They are isolated from the feces of healthy and sick individuals. Most of them are host specific and antigenically distinct.

Poliomyelitis

Poliomyelitis is an acute contagious disease producing a wide clinical spectrum ranging from a non-paralytic illness in which the patient develops symptoms and signs of meningeal involvement without paralysis to a severe paralytic form in which flaccid paralysis results from affliction of spinal motor neurons and brainstem nuclei. Poliomyelitis viruses belong to the group of picorna viruses. Three types are pathogenic-types I, II and III. Type I is most common and is responsible for the majority of paralytic cases. Types I, II and III do not show cross- immunity.

Epidemiology: The disease is worldwide in distribution (Even though it is presently almost eliminated in the globally), spread by the fecal-oral route. The virus is eliminated in feces by cases and carriers. The disease may occur sporadically or in outbreaks. Majority of cases of infection are unapparent with only transient nonspecific symptoms and a rise in antibody levels. Classical paralytic polio develops only rarely. Poliomeylitis is common in India and Nigeria with an average incidence of 20 to 40/100,000 of the population. About 90% of children aged 5 years and above show the presence of neutralizing antibodies to all the three types of polio viruses.

Pathogenesis and pathology: The virus enters the system by ingestion. It proliferates in the cervical and mesenteric lymph nodes and peyer’s patches. At this stage, the virus may be present in the oropharyngeal secretions and feces. The next stage is one of viremia. The virulence of the virus and immune status of the host determine the localization of the virus to the central nervous system. Even a genetic predisposition to paralytic polio has been postulated. Physical exhaustion, intramuscular injections, tonsillectomy and local injury have all been known to be associated with paralysis localized to the affected part.

In the paralytic cases, the anterior horn cells of the spinal cord and the medullary nuclei are swollen and congested. As the condition proceeds chromatolysis and pericellular infiltration occur. The neurons are totally destroyed. In the early stages, the CSF shows increase in cells, mainly polymorphs, but this gives way to lymphatic increase with the passage of time. Protein level may be moderately increased (up to 150 mg/dl) and the sugar level is normal.

The incubation period is 7 to 14 days. The disease manifests a bimodal pattern, the initial features are due to viremia and the second one is due to neurological damage. Initial symptoms are nonspecific such as fever, headache, muscle pain and diarrhea. The second phase, which sets in after a period of three to four days is characterized by paralysis.

Nonparalytic polio: Features of meningitis develop in nonparalytic polio. These include fever, headache, neck rigidity and muscle pains. Physical examination may reveal signs of meningeal irritation. The condition subsides without further events within a week.

Paralytic Polio: In paralytic polio, paralysis may involved the spinal group of muscles, bulbar muscles or a combination of both.