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The causative agent of polyomyelitis (Poliovirus hominis), discovered by Landsteiner and Popper, is a very small virus (20-30 nm) belonging to the family of enteroviruses (the group of picornaviruses), that family also includes the Coxsackie and ECHO viruses. It contains RNA and is destroyed by heating to 56°C for 30 minutes, by the action of disinfecting agents in normal concentrations, and by ultra-violet rays. The virus is very stable in the external environment, and is resistant to low temperatures and desiccation. It is not destroyed by digestive juices, and is not sensitive to the action of known antibiotics. It is grown on cellular cultures and provokes a cytopathogenic effect. Apart from man, the poliomyelitis virus is pathogenic for monkeys. Certain strains have been experimentally adapted to the organism of cotton rats and mice. Three types of poliovirus (I, II, HI) are known.
Epidemiology
Apart from patients with clinically manifest poliomyelitis, persons suffering from atypical and abortive forms and formes frustes also serve as sources of infection. The number of patients with atypical forms, according to several authorities is much greater than the number with clinically manifest forms of the disease. The infectivity of patients is greatest during the acute stage. Most are free of the virus in 15 to 20 days after an attack, but the carrier state may last as long as 30 to 40 days, and even four to five months. Healthy carriers may also disseminate the disease; and indeed this carrier state is the most common form of the infectious process in poliomyelitis.
The mechanism of infection. Many facts have been accumulated pointing to the great importance of fecal mode of transmission (characteristic of infectious intestinal diseases). It has been demonstrated by virological methods that the poliomyelitis virus is isolated from feces with great constancy (in 70 to 100% of cases) during the first two weeks of the disease. Individual patients become fecal earners of the virus for three to five months. Polio-virus has even been discovered in town sewage. The virus is found much less often in the nasopharynx of patients, and mainly during the first 3 to 7 days. It has been demonstrated experimentally that flies can serve as mechanical vectors. There is also evidence that infection can be conveyed by milk and other foodstuffs.
Many specialists consider all this to characterize poliomyelitis as an intestinal infection, aerial-droplet mode of infection being only of secondary significance — an additional factor mainly seen during epidemic outbreaks. The intensity of the processes of latent immunization observed in poliomyelitis (see below), however permits us to assess the role of aerial-droplet route as highly important, since rapid latent immunization of a population is not typical of intestinal infections. It is probably more correct to consider both modes of communication important in the epidemiology and that one of them may become the leading, cardinal, factor according to the phase of the disease and prevailing conditions.
Judging from the recorded incidence, susceptibility to poliomyelitis is low. Only 0.2 to 1 per cent of the persons exposed to infection fall ill even in the absence of active immunization. The actual incidence, however, is much higher, since there are numerous unrecorded atypical forms. It is most prevalent in children aged under seven years of age (75 to 90% of cases on average). The much less pronounced susceptibility of older children and adults is considered to be the result of latent immunization due to earner state or formes frustes of the disease.
Many authors find that susceptibility to poliomyelitis increases in the presence of hypovitaminosis and overexertion. Development of the disease is often preceded by some infection (measles, whooping-cough, angina, enteritis, etc.) that apparently enfeebles the organism and reduces its resistance. Stable immunity is conferred by an attack, and repeated attacks are very rare.
Pathology
The most pronounced pathological changes in poliomyelitis are in the ventral horns of the grey matter of the cervical and lumbar enlargements of the spinal cord. The nerve cells undergo dystrophic necrotic changes, and perish. Neuronophagia is marked. Less constant are similar but less pronounced lesions of the cells of the brain stem, and subcortical nuclei of the cerebellum, and to an even less extent cells of the motor areas of the cerebral cortex, and dorsal horns of the spinal cord.
These changes in the nerve cells develop rapidly; the process usually ceases to progress during the first days of the paralytic stage. A leukocytic reaction and perivascular infiltrates composed of lymphoid cells with some polymorphonuclear leukocytes are found around the affected cells. Micro-hemoirhages are not uncommon in the ventral horns of the spinal cord. There is very often hyperemia and cellular infiltration of the pia mater.
After the termination of acute phenomena, the dead cells are replaced by glia, with subsequent scarring. The dimensions of the spinal cord (particularly of the ventral horns) dimmish; asymmetry is noted when lesions are unilateral. Atrophy develops in muscles whose innervation is affected.
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