An Epidemic of Paralytic Poliomyelitis Characterized by Dual Infections With Poliomyelitis and Coxsackie Viruses

Abstract

The first known epidemic of poliomyelitis in Easton, Pennsylvania, occurred in 1949, and was unusual in the high proportion of paralytic to non-paralytic cases. Both poliomyelitis and Cosxackie, or C, viruses were isolated from more than half the patients studied during the acute stage of the disease. One month later C virus was only occasionally recovered. Classification of the 28 strains of C virus which were isolated revealed that 24 belonged to one antigenic type, Easton-2 (related to Albany type 1 virus). Patients from whom C virus was isolated showed a rise during convalescence to the Easton-2 or homologous type antibody. Two patients with paralytic poliomyelitis were studied for the quantitative development of antibodies to the poliomyelitis virus and to the C virus found in their stools. Using the neutralization test in monkeys and in newborn mice, respectively, a simultaneous rise in antibodies to both agents was observed. The situation at present can be summarized as follows:—Poliomyelitis virus or C virus may produce infection in man, with a specific antibody response. Both agents may be carried, particularly in the intestines, without causing any serious illness and healthy carrier states have been observed for each. Both viruses can be found in nature in flies and in sewage. However there has been no evidence to suggest that these two viruses bear a relationship to each other, even when isolated from the same patient. Thus, when both viruses are found in a patient with paralysis, it is not yet possible to say with any degree of accuracy to what extent each is responsible in the over-all pattern of the disease. How frequently dual infections of this nature may occur remains for future investigations to determine. Certainly all cases of poliomyelitis are not complicated by a superimposed infection with a C virus. However, this will have to be one more item to consider in epidemic poliomyelitis.

Intra- and interpatient evolution of enterovirus D68 analyzed by whole-genome deep sequencing

“…Three patients showed evidence of dual infection with two different EV-D68 variants. Even though coinfections with different enteroviruses has been reported for poliovirus (PV) and non-polio enteroviruses (NPEV) (Isaacs et al, 2018;Melnick et al, 1951;Parks et al, 1967), this is to our knowledge the first report of dual infections with EV-D68. Dual infections during the 2016 outbreak are not completely surprising in view of the high EV-D68 incidence during the outbreak (Dyrdak et al, 2016) and the fact that the present study showed multiple introductions of the B3 subclade into Stockholm.…”

Factors Influencing the Occurrence of Illness During Naturally Acquired Poliomyelitis Virus Infections1

“…Dalldorf and Wiegand (1958) have presented experimental evidence that some Coxsackie viruses of group A may act synergistically with poliovirus to increase the likelihood of paralytic illness. Epidemiological evidence of an association of group A Coxsackie viruses with poliovirus in paralytic cases has been reported repeatedly (Melnick et al, 1951) and has been noted specifically not to occur on other occasions (Curnen and Melnick, 1951). If a second infectious agent is indeed an important factor in making "proximate" pollution a dangerous mode of spread of poliovirus, it may be presumed that more distant pollution is less dangerous because the agent is lost by dilution or by instability in cold water.…”

Problems Associated With Viral Identification and Classification in 1956

“…In the examples shown in TABLE 6, it can be seen that, in patients from whom both a Type 1 poliovirus and a Type A1 Coxsackie virus were isolated, both antibodies rose together during the course of illness and convalescence. 26 We know of cases in which only one agent has been isolated, but in which antibodies not only against the isolated virus but also against another virus appeared during the course of the illness. Therefore it is generally agreed that the isolation of a Coxsackie virus alone and a corresponding rise in antibody in a paralytic patient are not sufficient evidence to incriminate the isolated Coxsackie virus as the etiological agent of the paralytic disease.…”