Acute flaccid paralysis by non-polio exteroviruses before, during and after eradication of poliomyelitis

Episodes of acute flaccid paralysis (AFP) by one or more coxsackieviruses, type A 4, 6, 7, 9, 11, 14, 21, type B 1 to 6, echovirus type 1 to 4, 6, 7, 9, 11, 14, 16, 18, 19 and 30 or enterovirus type 70, 71 and 72, infections have been described for many decades. Following international plans to eradicate poliomyelitis by the end of the century, non-poliovirus enteroviruses were reported to cause acute flaccid paralysis in Latin America even after a successful eradication of poliovirus-induced AFP. Recently, enterovirus 71 was incriminated for infantile AFP in Brazil with a clinical picture similar to paralytic poliomyelitis. Well-designed laboratory support is needed to ascertain the role of non-polio enteroviruses (NPEV) in episodes of AFP in various countries irrespective of the national polimyelitis eradication or control activities. MRT examination for the central nervous system pathology with sagittal spin-echo proton density and T-2 weighted images should localize hyperintense bands corresponding to anatomic location of ventral horn and other target nuclei for NPEV lesions. An early lead towards neuronal involvement could ensure therapeutic usage of interferon-alpha to alter disease progression, with an uneventful recovery. Apart from MRT, demonstration of poliovirus or NPEV-specific IgM in saliva or CSF, by rapid, simple, assay procedures, could guide the clinicians to a prompt therapy in patients with AFP. As a prelude to control of NPEV-induced AFP in future, it would be desirable to obtain base-line data for neurovirulence in simian nervous tissues as collected with polioviruses during the 1940's. Fiscal allocation towards basic research including a specific, rapid NPEV diagnosis would be more than cost-effective.