Typhus Group Rickettsiae Antibodies in Rural Mexico

However, rather than suggesting that a single case report "contradicts" the anterior horn cell hypothesis, we suggest that WNV-associated flaccid paralysis be viewed as having a spectrum of causes, one of which certainly is poliomyelitis like illness.The neuropathologic findings in poliomyelitis (due to poliovirus, WNV, or other viruses) are not restricted focally to the anterior horn cells (5).Demonstrating pathologic changes as well as focal anterior horn cell loss in the patient referenced by Holman is in keeping with neuropathologic findings in poliomyelitis.Additionally, the presence of a diffuse axonal polyneuropathy cannot be concluded from Holman's data.Reduced compound motor axon potentials and slowing of conduction velocity could certainly be seen in pathologic conditions affecting anterior horn cells or spinal nerve roots.In addition, reduced sensory nerve action potentials in the median and ulnar nerves alone, without documentation of neuropathy in additional nerves, cannot be used as evidence of a diffuse axonal polyneuropathy, since both of these nerves are commonly prone to entrapment neuropathies.Finally, the context in which the preservation of this patient's reflexes is observed remains unclear.Preserved "normal" deep-tendon reflexes, in the setting of disease that interrupts the reflex arc at any point, are incongruous with established physiologic and clinical concepts.The seven patients observed by our group clearly had a distinct clinical syndrome with similar clinical findings and electrodiagnostic results.However, as demonstrated by prior reports (3,5-7), multiple mechanisms may lead to WNV-associated flaccid paralysis.In fact, we acknowledge a spectrum of cord, root, and nerve involvement with WVN flaccid paralysis.