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Epidemiologic Notes and Reports Case of Paralytic Illness Associated With Enterovirus 71 Infection

On October 1, 1987, an 18-month-old child was admitted to a medical center in central Mississippi 2 days after the onset of severe weakness in his left leg. On September 22, 1987, the child had received measles/mumps/rubella (MMR) vaccine in his right thigh and diphtheria/pertussis/tetanus (DPT) vaccine in his left thigh. Five days after his vaccinations, his mother noted a temperature of 39.3 C (102.8 F) and a decrease in his appetite. On September 29, he began dragging his left leg and was unable to use it 1 day later.

The child received DPT/oral polio vaccine (OPV) at 2, 4, and 6 months of age. He was never breast-fed, had not traveled outside Mississippi, and had no known contact with anyone who had. He began attending a day-care center at the beginning of September 1987. Thirteen of the other 97 attendees had OPV between August 1 and September 22, 1987.

The child was awake and alert and had right-sided otitis and possible tonsillitis when he was admitted to the medical center. The neurological examination was normal, except that the muscles in the left hip and thigh were not functioning, and the muscles below the left knee were weakened. The left knee-jerk reflex was absent; the left ankle-jerk reflex was present but slightly weaker than the right. The plantar reflex was downgoing and equal bilaterally.

Lumbosacral X-ray films, magnetic resonance imaging of the lumbosacral spine, quantitative immunoglobulins, and skin tests for cellular immunity were normal. A lumbar puncture revealed normal glucose and protein and nine white blood cells (98% lymphocytes) in the cerebrospinal fluid. Nerve conduction studies and electro- myograms of the lower left leg were normal except for absent or decreased activation of tested muscles.

A follow-up examination 4 months later showed a partial return of function in the lower left leg. The child was able to walk with a slight limp. Reflexes were present, but they were slightly weaker in the left leg than in the right. There was some atrophy in the left calf. These and other clinical findings were indicative of a lower motor neuron process, such as paralytic poliomyelitis, in the lower left leg.

Stool specimens obtained on October 5, 6, and 8 all grew enterovirus 71 (EV71). Cerebrospinal fluid was not cultured for virus. Sera obtained on October 3, 4, 6, and 29 (7, 8, 10, and 33 days after onset of illness) all showed low but constant titers to the three serotypes of poliovirus (range 1:40 to 1:120), as would be expected for a child who had received three OPV vaccinations. The titers to EV71 were 1:720, 1:1,280, and 1:720 for the first, third, and fourth serum specimens, respectively. Reported by: RR Hanson, MD, Univ Medical Center; H Myers, MD, Voice of Calvary Family Health Center, Jackson; FE Thompson, MD, State Epidemiologist, Mississippi State Dept of Health. Div of Field Svcs, Epidemiology Program Office; Div of Viral Diseases, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: While flaccid paralysis is most often associated with poliovirus infection, several nonpolio enteroviruses, including EV71, have also been associated with paralytic disease. The etiology of this case is likely to be EV71 infection for three reasons. First, the serologic results were consistent with those expected for an 18-month-old child who had received three doses of OPV and had developed an antibody response to all three serotypes. Second, EV71 was the only virus isolated from the specimens under conditions in EV71, have also been associated with paralytic disease. The etiology of this case is likely to be EV71 infection for three reasons. First, the serologic results were consistent with those expected for an 18-month-old child who had received three doses of OPV and had developed an antibody response to all three serotypes. Second, EV71 was the only virus isolated from the specimens under conditions in which poliovirus, if present, would have been isolated. Third, the antibody titers to EV71 were very high, as would be expected with a recent infection.

EV71 is unique among the nonpolio enteroviruses in its ability to occasionally cause outbreaks of severe central nervous system (CNS) disease including encephalitis and polio-like paralysis (1). EV71 was first described in 1974 from cases of CNS disease, including fatal encephalitis, occurring in California from 1969 to 1973 (2). To date, the virus has principally been associated with outbreaks of hand, foot, and mouth disease (HFMD), upper respiratory symptoms, meningitis, encephalitis, and flaccid paralysis very similar to that associated with poliovirus infection (2-8). The clinical symptoms associated with any particular outbreak have varied widely. In California prior to 1973, in Australia in 1972 (3), and in Sweden in 1973 (4), meningitis was the predominant severe illness associated with outbreaks of EV71. In Japan in 1973 and 1978 (5,6), HFMD was the predominant syndrome, although CNS infections were frequently observed. In Bulgaria in 1975 (7), 21% of about 700 patients with laboratory-confirmed EV71 infection developed paralysis, and 44 patients died. Fatal encephalitis occurred among patients in an outbreak of EV71 infection in Hungary in 1978 (8). In the United States, a cluster of 12 laboratory-confirmed cases in the Rochester, New York, area in 1977 included two cases of transient polio-like paralysis (9). While isolates of EV71 have been identified sporadically in the United States, extensive spread of the virus has not been observed.

The enterovirus surveillance system at CDC received 49 reports of EV71 isolates from 1977 through 1987. Fifteen of these occurred in 1977; 11, in 1979; and 8, in 1987. No other year had more than four reported isolates. However, in the last 6 months, the Enterovirus Laboratory at CDC has received and characterized ten additional EV71 isolates including four from Alaska, two from Oklahoma, and four from Pennsylvania, bringing the total for 1987 to 18. Surveillance data on EV71 is probably not a sensitive measure of its presence because of the inability of most diagnostic virology laboratories to isolate or characterize the virus.

EV71 infection can be diagnosed by isolation or serologic studies. A variety of human and primate cell lines, including primary rhesus monkey kidney cells, diploid human lung fibroblast cells, rhabdomyosarcoma cells, and Vero cells, can be used to isolate EV71. Growth of this virus is often slow compared to other enteroviruses, and multiple blind passages are often required to isolate it. Once isolated, the virus can readily be adapted to a wide variety of human and primate cells. Identification of an isolate is complicated by the absence of antisera to EV71 in the common enterovirus typing pools and by the limited availability of type-specific antisera.

Clinicians are encouraged to report suspected cases of paralytic illness due to enteroviruses to their local and state or territorial health departments. Enterovirus isolates from these cases can be sent through the local and state or territorial laboratories to the Division of Viral Diseases, Center for Infectious Diseases, CDC, for typing.


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  2. Schmidt NJ, Lennette EH, Ho HH. An apparently new enterovirus isolated from patients with disease of the central nervous system. J Infect Dis 1974;129:304-9.

  3. Kennett ML, Birch CJ, Lewis FA, Yung AP, Locarnini SA, Gust ID. Enterovirus type 71 infection in Melbourne. Bull WHO 1974;51:609-15.

  4. Blomberg J, Lycke E, Ahlfors K, Johnsson T, Wolontis S, von Zeipel G. New enterovirus type associated with epidemic of aseptic meningitis and/or hand, foot, and mouth disease (Letter). Lancet 1974;2:112.

  5. Tagaya I, Takayama R, Hagiwara A. A large-scale epidemic of hand, foot and mouth disease associated with enterovirus 71 infection in Japan in 1978. Jpn J Med Sci Biol 1981;34:191-6.

  6. Ishimaru Y, Nakano S, Yamaoka K, Takami S. Outbreaks of hand, foot, and mouth disease by enterovirus 71. High incidence of complication disorders of central nervous system. Arch Dis Child 1980;55:583-8.

  7. Shindarov LM, Chumakov MP, Voroshilova MK, et al. Epidemiological, clinical, and pathomorphological characteristics of epidemic poliomyelitis-like disease caused by enterovirus 71. J Hyg Epidemiol Microbiol Immunol 1979;23:284-95.

  8. World Health Organization. Virus diseases surveillance. Wkly Epidem Rec 1979;54:57.

  9. Chonmaitree T, Menegus MA, Schervish-Swierkosz EM, Schwalenstocker E. Enterovirus 71 infection: report of an outbreak with two cases of paralysis and a review of the literature. Pediatrics 1981;67:489-93.

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