POLIOMYELITIS

POLIOMYELITIS
- destruction of motor neurons in spinal cord → flaccid paralysis

-         very restricted host range → natural infection occurs only in humans.

-         Grows readily in tissue cultures of primate origin.

 PATHOGENESIS

-         transmitted by faeco- oral route.

-         Virus multiplies initially in epithelial cells of AC (Oropharynx or intestine) and the lymphatic tissue ( tonsils / payers patches).

-         Regularly present in throat and stools before the onset of illness.

-         Then spreads to the regional lymph nodes and enters blood stream (minor / 2⁰ viraemia) across the BBB.

-         Direct neural transmission may also occur eg after tonsillectomy..

-         In the CNS, Virus multiplies selectively in the neurons destroys the anterior horn cells of spinal cord.

-         Earliest change is degeneration of Nissils bodies.

-         When degeneration becomes irreversible, necrotic cell lyses or is phagocytosed.

-         Viruses don’t multiply in muscle in vivo.

-         Changes that occur in peripheral nerves and voluntary muscles are secondary to destruction of nerve cells.

Clinical findings

-         Incubation period 7-14 days.

-         Inapparent infection: 90-95% cases; only seroconversion.

-         Abortive poliomyelitis: 4-8%; minor illness.
- Fever, malaise, drowsiness, headache, nausea, vomiting, constipation.
- Recovery in few days.

-         Non- paralytic poliomyelitis ( aseptic meningitis) – 1-2%
- above symptoms + stiffness and pain in back and neck; 2-10 days.

-         Paralytic poliomyelitis: 0.1-2%
- flaccid paralysis resulting from lower motor neuron damage.
- Maximal recovery with in 6 months, with residual paralysis lasting much longer.

-         Progressive post – poliomyelitis muscle atrophy: rare
- recrudescence of paralysis and muscle wasting.
- Decades after experience with paralytic poliomyelitis.
- doesn’t appear to be a consequence of persistent infection rather a result of physiologic and aging changes.

Lab diagnosis
specimen: throat swabs, rectal swabs / stool, blood, CSF ( uncommon).

No permanent carriers known.

Specimen should be kept frozen during transmit to lab.
A. Isolation of virus.
- can be isolated from blood and pharyngeal aspiration during 10 viraemia,(3-5 days after infection). From feces → upto 5 weeks.

-         After processing specimen, inoculated into tissue culture.

      •Primary monkey kidney cells, typical CPE in 2-3 days.

       • Identification by neutralization tests with pooled and specific antisera.

-         Virus isolation from feces must be interpreted along with clinical and serological evidence.

B. direct demonstration of virus by electron microscopy
c. serology: less often employed.
- paired serum specimens to show a rise in antibody titer

-         Only 1^st infection produces strictly type- specific responses.

Prophylaxis

Passive immunization is of little value.

Salk killed vaccine
- viral pools of adequate titer filtered and inactivated with formalin (1:4000) 37⁰C / 12-15 days.

-         given by injection, IPV

-         3 doses given 4-6 weeks apart + booster 6 months later.
1^st dose to babies after age of 6 months.

Sabin live vaccine ( OPV).

-         developed by plaque selection in monkey kidney tissue culture on HDCC.

-         Stringent precautions to be taken to ensure freedom from extraneous agents like SV40 and B- virus.

-         Issued either in monovalent or trivalent form; 3 doses at 4-8 weeks interval.

-         Vaccine stabilized by MgCl2; shelf life at 4-80C is 4 monts and at -200C is 2 yrs.

-         Improper storage conditions and cold chain failure partly responsible for apparent failure of OPV.

-         Live vaccines infects, multiplies and disseminated in the community.

-         Produces not only IgM and IgG but also IgA in the intestine, and then becomes resistant to re- infection.

o       Both killed and live vaccines protect the CNS, but gut develops a far increased degree of resistance after administration of live – virus vaccine.

o       OPV not safe in immunodeficient or immuno- suppressed subjects.

o       Interference → if alimentary tract of a child infected with another enterovirus at the time vaccine is given, establishment of polio infection and immunity may be blocked.

o       Frequent diarrhoeal diseases prevent colonization by vaccine virus.

o       Breast feeding immediately before or after vaccine may neutralize the vaccine virus.

o       IG provides protection for a few weeks against paralytic disease, but doesn’t prevent subclinical infection.

o       Effective only if given shortly before infection; no value after clinical symptoms develop.