NAME OF DISEASE:     Polio
                                        Poliomyelitis

ETIOLOGICAL AGENT:     Poliovirus (a picornavirus), types I, II, III

THE DISEASE:

    An acute infection of both the meninges and the motor neurons of the spinal cord and the brainstem. The latter produces a permanent paralysis.

EPIDEMIOLOGY:

    Spread by the fecal-oral route but sometimes by the respiratory route.

PATHOLOGY:

    The virus is ingested with fecally contaminated food or water. The initial multiplication occurs in the lymphatic tissue of the oropharynx (tonsils) and intestine (appendix). Dissemination to the regional lymphatics is followed by viremia.

    The mechanism by which circulating viruses cross the blood- brain barrier is probably by transcapillary diffusion. The term poliomyelitis indicates that:

    1.     The gray matter (polio) of the spinal cord (myel) is inflamed (itis).

    2.     Motor neurons are involved, but the lesions are not usually confined to the anterior horns of
            the cord.

    3.     In fatal cases, destruction is found in the cerebral ganglia, reticular formation, cerebellar
            nuclei, hypothalamus, thalamus and cerebral cortex.

    When the brain is cut during postmortem examination, damage is grossly evident as swelling, softening, congestion and petechial hemorrhage.

    The non-neural aspects of poliomyelitis, so critical to the pathogenesis of the disease, are reflected not only in the lymph nodes but also in the spleen, liver, kidneys and other viscera.

    One sees:

        Gross Pathology

            Enlargement
            Softening

        Microscopic Pathology

            Congestion
            Interstitial edema
            Infiltration with lymphocytes
            Hyperplasia (increase in volume caused by the formation and growth of new cells)

DIAGNOSIS:

    Some 6-20 days after exposure, nonspecific symptoms occur in most clinically apparent cases. These include:

    1.     Moderate fever             )
    2.     Headache                     )
    3.     Vomiting                       ) Often misdiagnosed as
    4.     Constipation                 ) intestinal flu
    5.     Coryza                         )
    6.     Sore throat                   )

    Two to 6 days after onset, the illness may subside entirely (abortive poliomyelitis), abate temporarily or progress directly to CNS involvement. Early in paralytic poliomyelitis the patient exhibits:

    1.     Signs of meningeal irritation
    2.     Weakness
    3.     Hyperesthesia (increased sensitivity to stimuli)
    4.     Severe muscle pain
    5.     Spasm of involved muscle
    6.     Normal or accentuated tendon reflexes

    This phase is followed rapidly by loss of motor function. One or both legs are involved in 60% of cases; one or both arms in 25% of cases. Involvement of the diaphragm and intercostal muscles reduces breathing capacity. Cranial nerve motor loss is most often evident in the distribution of the facial nerve and extraocular innervation, but loss of lower cranial motor neurons is sufficiently frequent to cause respiratory obstruction, regurgitation and aspiration problems. Damage to the medullary respiratory center usually results in death. Sensory losses and signs of extra-pyramidal involvement are rare in polio.

    Routine laboratory tests are usually within normal limits except for those of the CSF where:

    1.     Leukocyte count is 100 (pmns initially predominate but later monocytes are most numerous)

    2.     Protein is initially normal, reaches abnormal limits in 3 weeks and remains high for 8 weeks.

PROGNOSIS:

    Only 1 out of 1,000 cases are paralytic. Probability of paralysis is increased:

    1.     With age

    2.     In infection with type I

    3.     In infection with an epidemic strain

    4.     In pregnancy

    5.     With excessive physical exercise at or just before the onset of clinical symptoms.

    6.     With local trauma

TREATMENT:

    There is no specific therapy. Supportive care includes:

    1.     Blood pressure monitoring - bulbar (oblongata) damage may produce either hypertension
            or shock

    2.     Aid in ventilation

    3.     Examination for vocal cord weakness - vagal paralysis can produce respiratory obstruction

    4.     Monitoring ability to handle secretions

    5.     Monitoring of ability to swallow

    6.     Examination of breath sounds for evidence of pulmonary edema, atelectasis (incomplete
            expansion or collapse of pulmonary alveoli) or pneumonitis.

    7.     Monitoring of ability to void

    8.     Examination for evidence of thrombophlebitis.

    Rest and close observation are essential. Once the acute phase has passed, physical therapy and orthopedic surgery are required.

PREVENTION:

    Two vaccines are available:

    1.     Inactivated virus vaccine (Salk)

    2.     Attenuated virus vaccine (Sabin) - do not give to immunosuppressed patients

    Vaccination schedule for Sabin vaccine is one dose at 2, 4 and 6 months of age and then another dose when the patient begins school (about 5 years of age).