TY - JOUR
T1 - Chronic Progressive Poliomyelitis Secondary to Vaccination of an Immunodeficient Child
AU - Davis, Larry E.
AU - Bodian, David
AU - Price, Donald
AU - Butler, Ian J.
AU - Vickers, James H.
PY - 1977/8/4
Y1 - 1977/8/4
N2 - We investigated an immunodeficient child in whom chronic progressive poliomyelitis developed after she had received live oral poliovirus vaccine. Poliovirus, Type II, was isolated from throat and stool during life and from several sites within the brain at autopsy. The brain isolate was classified as vaccine-like on the basis of temperature sensitivity and antigenic markers. However, in the monkey neurovirulence test, the brain isolate produced moderately severe lesions throughout the spinal cord and brain-stem and appeared nonvaccine-like. Thus, the brain isolate demonstrated a dissociation between the antigenic and neurovirulence markers. Our observations suggest that, under unusual circumstances, such as immunodeficiency, attenuated poliovirus can produce a chronic progressive neurologic disease. This case also emphasizes the need to diagnose immunodeficiency as early as possible, so that live-virus vaccines will not be administered. (N Engl J Med 297:241–245, 1977) The typical patient with poliomyelitis has an asymmetrical onset of weakness, fasciculations and areflexia, which rapidly progress to reach maximum severity within one to two weeks. Although pathologic involvement of the anterior horn cells of the spinal cord is the hallmark of this disease, lesions in the tegmentum of the brain-stem, roof nuclei of the cerebellum, thalamus and motor cortex are well recognized.1 Occasionally, patients with acute poliomyelitis may also have clinical signs suggesting involvement of the brain-stem and cerebellum, such as nystagmus, ocular flutter, intention tremors, bulbar muscle weakness, myoclonic jerks, vermiform tongue movements, Babinski signs and mental changes.
AB - We investigated an immunodeficient child in whom chronic progressive poliomyelitis developed after she had received live oral poliovirus vaccine. Poliovirus, Type II, was isolated from throat and stool during life and from several sites within the brain at autopsy. The brain isolate was classified as vaccine-like on the basis of temperature sensitivity and antigenic markers. However, in the monkey neurovirulence test, the brain isolate produced moderately severe lesions throughout the spinal cord and brain-stem and appeared nonvaccine-like. Thus, the brain isolate demonstrated a dissociation between the antigenic and neurovirulence markers. Our observations suggest that, under unusual circumstances, such as immunodeficiency, attenuated poliovirus can produce a chronic progressive neurologic disease. This case also emphasizes the need to diagnose immunodeficiency as early as possible, so that live-virus vaccines will not be administered. (N Engl J Med 297:241–245, 1977) The typical patient with poliomyelitis has an asymmetrical onset of weakness, fasciculations and areflexia, which rapidly progress to reach maximum severity within one to two weeks. Although pathologic involvement of the anterior horn cells of the spinal cord is the hallmark of this disease, lesions in the tegmentum of the brain-stem, roof nuclei of the cerebellum, thalamus and motor cortex are well recognized.1 Occasionally, patients with acute poliomyelitis may also have clinical signs suggesting involvement of the brain-stem and cerebellum, such as nystagmus, ocular flutter, intention tremors, bulbar muscle weakness, myoclonic jerks, vermiform tongue movements, Babinski signs and mental changes.
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U2 - 10.1056/NEJM197708042970503
DO - 10.1056/NEJM197708042970503
M3 - Article
AN - SCOPUS:0017404593
SN - 0028-4793
VL - 297
SP - 241
EP - 245
JO - New England Journal of Medicine
JF - New England Journal of Medicine
IS - 5
ER -