Tuesday, April 20, 2010


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

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