Diagnosis of Poliomyelitis

Poliomyelitis should be considered in any unimmunized or incompletely immunized child with paralytic disease. VAPP should be considered in any child with paralytic disease occurring 7–14 days after receiving the orally administered polio vaccine (OPV). VAPP can occur at later times after administration, and should be considered in any child with paralytic disease in countries or regions where wild-type poliovirus has been eradicated and the OPV has been administered to the child or a contact. The combination of fever, headache, neck and back pain, asymmetric flaccid paralysis without sensory loss, and pleocytosis does not regularly occur in any other illness.

Identification of Poliovirus in Stool:
The World Health Organization (WHO) recommends that the laboratory diagnosis of poliomyelitis be confirmed by isolation and identification of poliovirus in the stool, with specific identification of wild-type and vaccine-type strains. In suspected cases of acute flaccid paralysis, 2 stool specimens should be collected 24–48 hr apart, as soon as possible after the diagnosis of poliomyelitis is suspected. Poliovirus concentrations are high in the stool in the 1st week after the onset of paralysis, which is the optimal time for collection of stool specimens. Polioviruses may be isolated from 80–90% of acutely ill patients, whereas <20% may yield virus within 3–4 wk after onset of paralysis. Because most children with spinal or bulbospinal poliomyelitis have constipation, rectal straws may be used to obtain specimens; ideally a minimum of 8–10 g of stool should be collected. In laboratories that can isolate poliovirus, isolates should be sent to either the Centers for Disease Control and Prevention or to 1 of the WHO-certified poliomyelitis laboratories where DNA sequence analysis can be performed to distinguish between wild poliovirus and neurovirulent, revertant OPV strains. With the current WHO plan for global eradication of poliomyelitis, most regions of the world (the Americas, Europe, Australia) have been certified wild-poliovirus free; in these areas, poliomyelitis is most often caused by vaccine strains. Hence it is critical to differentiate between wild-type and revertant vaccine-type strains.

CSF Examination:
The CSF, while often normal during the minor illness, with CNS involvement demonstrates a pleocytosis of 20–300 cells/mm3. The cells in the CSF may be polymorphonuclear early during the course of the disease but shift to mononuclear cells soon afterward. By the 2nd week of major illness, the CSF cell count falls to near-normal values. In contrast, the CSF protein is normal or only slightly elevated at the outset of CNS disease but usually rises to 50–100 mg/dL by the 2nd week of illness. In polioencephalitis, the CSF may remain normal or show minor changes. Serologic testing demonstrates seroconversion or a 4-fold or greater increase in antibody titers, when measured during the acute phase of illness and 3–6 wk later.

Differential Diagnosis:
Poliomyelitis should be considered in the differential diagnosis of any case of paralysis, and is only 1 of many causes of acute flaccid paralysis in children and adults. There are numerous other causes of acute flaccid paralysis . In most conditions, the clinical features are sufficient to differentiate between these various causes, but in some cases nerve conduction studies and electromyograms in addition to muscle biopsies may be required.

The possibility of polio should be considered in any case of acute flaccid paralysis even in countries where polio has been eradicated. The diagnoses most often confused with polio are VAPP, West Nile virus, and other enteroviruses, as well as Guillain-Barré syndrome, transverse myelitis, and traumatic paralysis. In Guillain-Barré syndrome, which is the most difficult to distinguish from poliomyelitis, the paralysis is characteristically symmetric and sensory changes and pyramidal tract signs are common; these are absent in poliomyelitis. Fever, headache, and meningeal signs are less notable, and there are few cells but an elevated protein level in the CSF. Transverse myelitis progresses rapidly over hours to days, causing an acute symmetric paralysis of the lower limbs with concomitant anesthesia and diminished sensory perception. Autonomic signs of hypothermia in the affected limbs are common, and there is bladder dysfunction. The CSF is usually normal. Traumatic neuritis occurs from a few hours to a few days after the traumatic event, is asymmetric, acute, and affects only 1 limb. There is reduced or absent muscle tone and deep tendon reflexes in the affected limb with pain in the gluteus. The CSF is normal.

Conditions causing pseudoparalysis do not present with nuchal-spinal rigidity or pleocytosis. These causes include unrecognized trauma, transient (toxic) synovitis, acute osteomyelitis, acute rheumatic fever, scurvy, and congenital syphilis (pseudoparalysis of Parrot).