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The following points highlight the two main groups of slow virus disease. The groups are: 1. Animal Infection 2. Human Infection.
Slow Virus Disease: Group # 1. Animal Infection:
a. Visna:
It is caused by viruses which are classified under the family lendviridae (See AIDS) as retro viruses and also cause a demyelinating disease in sheep with incubadon period of 2 years. Pathological changes are observed in brain, lungs, and reticulo-endothelial system.
The disease has an insidious onset with paresis, total paralysis and death. The virus can be isolated from CSF, saliva or blood of infected sheep and by tissue culture of choroid plexus. CNS manifestation appears to be an antigen-antibody reaction on the surface of infected glial cells.
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b. Maedi:
Maedi virus is closely related to visna and belongs to subfamily lendviridae. Incubation period is about 2-3 years. Maedi is a slowly progressive haemorrhagic pneumonia of sheep with fatal termination.
c. Scrapie:
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It is a slow virus encephalopathy of sheep. Different breeds of animals are susceptible to scrapie. Incubation period is 2 years. The infection remain confined to nervous system and exhibits reactive astrocytosis. The animal becomes irritable and later dies of paralysis. The virus has been maintained in brain tissue explant cultures by serial passages.
d. Mink:
Mink encephalopathy is similar to scrapie in all aspects except that it occurs in minks. The causative agent may be a strain of scrapie virus.
Slow Virus Disease: Group # 2. Human Infection:
a. Kuru:
It is a unique disease affecting only the members of cannibalistic fore tribe of Eastern highlands of New Guinea. It is a slow viral infection with an incubation period of 5-10 years and is transmitted by the tribal practice of eating infected brains of relatives after a “non- sterilising” ritual cooking.
Grey matter of CNS is degenerated, most marked in cerebellum. This degeneration causes progressive ataxia and tremors. The disease ends fatally in 3-6 months.
b. Creutzfeldt-Jacob Disease (CJD):
It is a sub-acute encephalopathy which develops gradually and is characterised by progressive dementia, epilepsy, myoclonus and extrapyramidal motor neuron signs. It may be accidently transmitted to man from corneal transplant from infected inadequately sterilised neurological instruments and implanted ECG electrodes.
c. Sub-Acute Sclerosing Pan-Encephalitis (SSPE):
It is a rare disease of children and young adults and develops as a very late complication of measles many years after the initial infection. The disease is characterised by slowly progressive demyelination in the CNS with gradual loss of mental and motor function and as a result there is death in 1-3 years.
Electron microscopy and serological test of brain cells of SSPE patients show measles virus infection. A defective virus closely resembling measles virus has been isolated from lymph node and brain material by co-cultivation with He La cells.
Long after administration of live measles virus vaccine, SSPE may also develop. Similar illness may rarely occur in parents with congenital rubella. SSPE may represent a tolerant infection of latent measles virus due to defective CMI.
d. Progressive Multi-Focal Leuco-Encephalopathy (PML):
In old patients whose immune system is impaired as a result of malignancy (chronic leukaemia, Hodgkin’s disease lymphoma) or immunosuppression, PML is a progressive demyelinating disease (multifocal encephalopathy) resulting from infection of oligodendrocytes by papova virus.
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PML is a rare complication of CNS and is characterised by progressive loss of motor function, speech and vision — death occurs in 3-4 months.
Table 67.3. Slow and atypical agents
