The final stage in the pathogenesis of poliomyelitis is an invasion by and multiplication of the virus in the nervous system. It has been suggested that the area postrema in the medulla oblongata is the site at which the virus leaves the blood and enters the brain. There is evidence, however, that virus may penetrate the nervous system at many points by a direct passage from capillaries to neurons rather than at a single area of specialized vascular permeability.
The spread of the infectious agent takes place along nerve fibers. Two groups of factors determine susceptibility and reaction to the invasion of the central nervous system by poliomyelitis virus: those associated with the host, and those related to the virus. Strains of the infecting agent vary greatly in their ability to invade nervous tissue and to destroy neurons. The repeated passage in animals or tissue cultures may induce changes in invasive capacity without affecting the basic antigenic character of the virus. One of the host factors of importance in determining whether or not involvement of nervous tissue occurs is circulating type-specific neutralizing antibody; this is very often detectable before manifestations of the disease appear.
The presence of “immunity” early is in favor of multiplication of virus in non-nervous tissue and accounts for the short-lived persistence of the agent in the pharynx and blood, sites in which antibody is demonstrable. The fact that the virus remains in the nervous system and intestine for relatively long periods is probably related to the difficulty with which antibody reaches these areas. Inapparent infection and illness without invasion of the nervous system are common in areas where paralytic poliomyelitis occurs; these and clinically recognizable forms of the disease lead to the development of type-specific antibody and resistance to reinvasion by the same serotype, usually for life. Many children and most adults possess antibody to all three types of the virus; this probably accounts for the relative infrequency of infection in older age groups. Infants less than three to six months old rarely get poliomyelitis because of immunity passively transferred from the mother.
pathogenesis of poliomyelitis Babies born to women in the acute. a phase of poliomyelitis may develop the disease shortly after birth, indicating in utero infection or exposure during delivery. Sex plays a role in determining susceptibility. Among children, males are affected more often than females; the opposite is true in adults. Pregnancy increases the risk of clinically apparent poliomyelitis. Multi-parous females are more susceptible than primiparas. The disease is somewhat more frequent in the second than in the first or third trimesters. Menstruation or ovulation appears to heighten susceptibility. Absence of the tonsils and adenoids, regardless of the time of their removal, is associated with an increased incidence of bulbar poliomyelitis.
The chilling or physical exertion of moderate to a severe degree after invasion by the virus leads to more frequent development of paralytic poliomyelitis, especially in adults. Pathology. The anterior horn cells of the spinal cord bear the brunt of the damage produced by the poliomyelitis virus. Although any segment of the cord may be affected, the cervical and lumbar areas are the ones in which damage is most frequent. Disease of. the motor nuclei of the medulla and midbrain is not uncommon. In addition, the vestibular nuclei in the medulla, the reticular formation, and the cerebellar roof nuclei are often involved. Although the grey matter is almost exclusively attacked, extension into the white matter with the destruction of long-fiber path-ways may take place, especially when the brainstem is injured. The lesions are not limited to the anterior grey region of the spinal cord; the posterior and lateral columns, as well as the dorsal root ganglia, are often affected.
Microscopic study reveals intense infiltration of the perivascular spaces with leukocytes, dilatation of and inflammatory reactions in the blood vessels, and small hemorrhages; these are noted throughout the spinal cord. but are least evident in the white matter. Parenchymatous degeneration is most severe in the areas of greatest infiltration. The cellular response becomes primarily lymphocytic in the later stages of the disease. Large numbers of granulocytes and lymphocytes are present in the meninges; this response is secondary to the inflammatory reaction within the tissue.
pathogenesis of poliomyelitis AS the disease activity comes to a halt, the hyperemia, edema, and mild ganglion cell changes in the areas adjacent to degenerated foci gradually recede. As the cells resume function, paralysis of. muscles may disappear. Clinical Manifestations and Laboratory Findings. The incubation period of poliomyelitis varies from 3 to 35 days about 80 percent of cases occur within 6 to 20 days after contact with the virus. Four types of the clinical picture may develop an inapparent infection, “minor illness,” nonparalytic poliomyelitis, and paralytic poliomyelitis. Inapparent Infection. In families in which a clinically recognized case of poliomyelitis appears, inapparent infection usually develops ifs other susceptible members.