Aujeszky's disease virus was pathogenic for developing
fowl embryos, young chicks, mice and rats. It induced cytopathic
effects on kidney cell cultures derived from different species of
mammals, on fibroblasts from fowl embryos and on kidney cells prepared
from chickens of different ages.
In experimentally infected chickens, the mean duration of
clinical disease was significantly influenced by the route of infection;
the intracerebral route being the most effective. Chickens infected
intranasally, intraocularly or intraderma1ly survived longer than those
infected intramuscularly or subcutaneously. In general, the mortality
pattern was significantly related to the age of the birds at the time
of infection, the route of infection and the dose of virus injected.
The results of experiments in chickens of different ages infected intracerebrally,
intramuscularly or subcutaneously with different doses of
either the McFerran, Hungarian or Weybridge strain of virus, clearlyshowed
that the relationship between the percentage of deaths and the
age at the time of infection was inverse, linear or curvilinear and
significant, and that the influence of age on the mortalities was
independent of the dose of virus and the route of infection.
Deaths in chickens due to the introduction of Aujeszky's
virus by different peripheral routes were always associated with the
presence of virus in the brain. The virus titres were influenced
neither by the age of the chickens at the time of infection nor by the
dose of virus injected; but the rate of replication of the virus in
the brain was related to the age at which the chickens were infected.
Likewise, the mean duration of viraemia in the infected chickens was
inversely- related to age. Virus distribution in the different tissues
of experimentally infected chickens depended on the strain of virus
used. Intracerebral or intramuscular infection of chicks less than
24 hours old with the Hungarian strain of virus resulted in virus
dissemination in the heart, lung, liver, spleen and kidney as well as
in the brain and spinal cord. On the other hand, in chicks of similar
ages infected with the McFerran strain, the virus was rarely detected
in these tissues although, in intramuscularly infected birds, the virus
was frequently present in the muscle tissue at the sites of inoculation
and in the spinal cord.
In chickens surviving intracerebral, intramuscular or
subcutaneous infection with Aujeszky's virus, resistance to intracerebral
challenge infection was not conditioned by the age of the birds at the
time of the first inoculation but was directly and significantly related
to the amount of virus contained in the primary inocula. Specific
resistance to intracerebral challenge developed as early as the fourth
day after primary infection. Recovery from experimental infection was
accompanied by the development of humoral virus neutralising antibodies,
the titres of which were significantly higher in chickens receiving
two or more doses of live virus than in those inoculated with inactivated
virus.
In general, the symptoms in infected rodents were of a
varied nature but were more pronounced in rats than in mice. The chief
clinical hallmark of experimental Aujeszky's infection in both species
was hyperaesthesia of the skin. In infected mice and rats, the mean
incubation periods ranged from 28 to 83 hours, the shortest being that
induced by intracerebral infection. Rats and mice were equally
susceptible to experimental Aujeszky's virus infection.
Virus was present in.the brain of all mice and rats dying
of experimental Aujeszky's disease, but there were differences in the
distribution of virus in the parenchymatous organs. These differences
were related to the routes of infection. As with chickens, exposure
of rats and mice to Aujeszky's virus resulted in some resistance to
challenge infection, but the degree of resistance was not absolute.
