Transmission
The feline panleukopenia virus is considered ubiquitous, meaning it is in virtually every place that is not regularly disinfected. The infection is highly contagious among unvaccinated cats.Antibodies against FPLV, produced by the adaptive immune system, play an important role in the feline response to the virus. Maternally-derived antibodies (MDA) efficiently protect kittens from fatal infection. This passively acquired immunity is later replaced by an active immune response obtained by vaccination or as a consequence of a natural infection. In kittens, the period of greatest susceptibility to infection is when maternal antibodies are absent, or waning, and vaccine-induced immunity has not yet fully developed.Free-roaming cats are thought to be exposed to the virus during their first year of life. Those that develop a subclinical infection or survive acute illness mount a robust, long-lasting, protective immune response.An infected cat sheds large amounts of virus in all body secretions including feces, vomit, urine, saliva, and mucus during the acute phase of illness. It can continue to shed the virus for as long as 6 weeks after recovery. Subclinically ill cats can also shed the virus in body secretions. The virus can be carried or transferred on an infected object (such as bedding, food dishes, fur) or by other animals, fleas, and humans  (see: fomites). It persists long after evidence of the original body secretion has faded away, and can be transported long distances. Like all parvoviruses, FPLV is extremely resistant to inactivation and can survive for longer than one year in a suitable environment.
The macrophages that clear these cells are unable to eliminate the waste product, which accumulates in fibrils, and turn into Gaucher cells, which appear on light microscopy to resemble crumpled-up paper.The exact mechanism of neurotoxicity is not understood, but it is thought to involve a reaction to glucosylsphingosine.Different mutations in the GBA (beta-glucosidase) gene determine the remaining activity of the enzyme. In type I, there is some residual activity of the enzyme, accounting for the lack of neuropathology in this type. Although there is some correlation between genotype and phenotype, neither the amount of stored lipids, nor the residual enzyme activity correlates well with disease symptoms. This circumstance has called for alternative explanations accounting for disease symptoms including

jamming of the endo/lysosomal system
ER stress
altered lipid composition of membranes throughout the cell, including the plasma membrane, and consequent changes in the dynamic and signaling properties of the cell membrane
inflammation caused by cytokine secretion as a result of sphingolipid accumulation, and neurodegeneration caused by the accumulation of glucosylsphingosine, a neurotoxinHeterozygotes for particular acid beta-glucosidase mutations carry about a five-fold risk of developing Parkinsons disease, making this the most common known genetic risk factor for Parkinsons.Cancer risk may be increased, particularly myeloma. This is thought to be due to accumulation of glucosylceramide and complex glycosphingolipids.The role of inflammatory processes in Gaucher disease is poorly elucidated. However, sphingolipids are known to participate in inflammation and apoptosis, and markers of macrophage activation are elevated in people with Gaucher disease.