Pathogenesis of PPR
The virus contaminates "naive" animals through their oral and nasal passages. After entering into the organism, it multiplies first in the oropharynx and local lymphoid tissues. All of the immune cells (lymphocytes, macrophages, reticular cells) can be a target for virus multiplication. The newly formed virions spread throughout the host's organs and tissues with a preference for digestive, pulmonary, and respiratory mucosa and the immune system.
Lesions
On the macroscopic scale
The resulting tissue damage, which can be observed post-mortem, is responsible for the clinical manifestations of the disease: discharge, lacrimation, diarrhoea.
On the microscopic scale
Biochemical and enzyme analyses show changes in kidney function (high urea and creatinine) through the multiplication of the virus in its cells and low blood parameter values (erythrocytes and haematocrit) linked to internal intestinal and renal haemorrhaging.
In parallel, the PPRV infection induces cell death through apoptosis in immune cells, leading to severe immunosuppression. This weakening of the animal's natural defences through leukopenia[1] opens the door to secondary bacterial and viral infections which interfere with the normal progression of the disease and complicate its diagnosis. These opportunistic infections significantly increase the mortality rate associated with PPR.
Fundamental :
The animals which recover are protected against PPRV for the remainder of their economic life.
