The authors know of no systematic study of the potency of antiviral agents in this disease.
Prevention, of course, has proved to be one of the outstanding accomplishments of modern medicine. The cultivation of poliovirus in cultures of human embryonic tissues and monkey kidney cells—the achievement of Enders and associates—made possible the development of effective vaccines. The first of these was the injectable Salk vaccine, containing formalin-inactivated virulent strains of the three viral serotypes. This was followed by the Sabin vaccine, which consists of attenuated live virus, administered orally in two doses 8 weeks apart; boosters are required at 1 year of age and again before starting school. Since 1965, the reported annual incidence rate of poliomyelitis in the United States has been less than 0.01 per 100,000 (compared to a rate of 24 cases per 100,000 during the years 1951 to 1955). Very rarely in the past, poliomyelitis followed vaccination with the attenuated live virus (0.02 to 0.04 cases per 1 million doses). Only the inactivated vaccine is used in the United States and polio is essentially eradicated in the Americas. The only obstacle to eradication of the disease elsewhere is inadequate utilization of vaccine. Conceivably, with an increasing lack of immunity in underdeveloped nations (so-called herd immunity), outbreaks of poliomyelitis could occur once again.
Mortality from acute paralytic poliomyelitis is between 5 and 10 percent—higher in the elderly and very young. If the patient survives the acute stage, paralysis of respiration and deglutition usually recovers completely; in only a small fraction of such patients is chronic respiratory care necessary. Many patients also recover completely from early muscular weakness, and even the most severely paralyzed often improve to some extent. The return of muscle strength occurs mainly in the first 3 to 4 months and is probably the result of morphologic restitution of partially damaged nerve cells. Branching of axons of intact motor cells with collateral reinnervation of muscle fibers of denervated motor units may also play a part. Slow recovery of slight degree may then continue for a year or more. The postpolio syndrome is discussed briefly in “Differential Diagnosis of ALS” in Chaps. 38 and 45.
As indicated earlier, a number of RNA viruses that infections are now the main causes of a sporadic poliomyelitic syndrome. Fifty-two such cases were recorded by the Centers for Disease Control over a 4-year period. Most of them were caused by one of the echoviruses and a smaller number to Coxsackie enteroviruses, and strains 68, 70, and 71. The echovirus illness leaves little residual paralysis, but the Coxsackie viruses, which have been studied in several outbreaks in the United States, Bulgaria, and Hungary, have had more variable effects. Enterovirus 70 causes acute hemorrhagic conjunctivitis in limited epidemics and is followed by a poliomyelitis in 1 of every 10,000 cases. European outbreaks of enterovirus 71, known in the United States as a cause of hand-foot-and-mouth disease and of aseptic meningitis, have resulted in poliovirus-type paralysis, including a few fatal bulbar cases (Chumakov et al). In a recent outbreak of enterovirus 71 in Taiwan, Huang and associates described brainstem encephalitis with myoclonus and cranial nerve involvement in a high proportion of the patients. The tendency of West Nile virus to cause a poliomyelitis has already been mentioned. More recently, clustered outbreaks of respiratory illness from enterovirus 68 have been associated with a polio-like illness but the causal connection has been difficult to establish. Case control studies support such an association but viral isolation has proved elusive.