Feline Parvo 2024 PDF

Feline Panleukopenia Epidemiology: FPV is non-enveloped and highly resistant to physical factors and chemical substances. In contaminated environments, it may remain infectious for weeks or even months (Uttenthal et al., 1999). Diseased carnivores shed virus at high titres (up to 109 TCID...

Feline Panleukopenia Epidemiology: FPV is non-enveloped and highly resistant to physical factors and chemical substances. In contaminated environments, it may remain infectious for weeks or even months (Uttenthal et al., 1999). Diseased carnivores shed virus at high titres (up to 109 TCID50 per gram of faeces), and virus quickly accumulates in affected shelters and catteries. As it is highly contagious, susceptible animals may still become infected, even after a seemingly thorough disinfection of the premises. It is therefore recommended that only successfully vaccinated kittens and cats should enter such an environment. Pathogenesis: FPV causes a systemic infection. The virus is transmitted via the faecal-oral route, initially replicating in the tissues of the oropharynx and is then distributed via cell-free viraemia to virtually all tissues in the body. Replication of the parvoviral single-stranded DNA requires cells in the S-phase of division and is therefore restricted to mitotically active tissues; in the gut, this results in enteritis. Parvoviruses require cellular DNA polymerases to synthesize the complementary DNA strand of their ssDNA, which is the first step in replication and a prerequisite for transcription. Pathogenesis: The virus infects lymphoid tissues where it can cause cellular depletion and a functional immunosuppression. Lymphopenia can arise as a result of lymphocytolysis but also indirectly, from lymphocyte emigration into tissues. The bone marrow is affected, and virus replication has been described in early progenitor cells, with dramatic effects on virtually all myeloid cell populations (Parrish, 1995). “Panleukopenia”, i.e., the deficiency of all white cell populations, is the result (Truyen and Parrish, 2000). Pathogenesis: The hallmark of FPV replication is the shortening of intestinal villi due to, sometimes, a complete loss of epithelial cells in the gut (Parrish, 2006). The virus replicates in the rapidly dividing cells in the crypts of Lieberkühn, which impairs regeneration of the epithelium and results in the lesions described below (Fig. 6). The severity of the lesions correlates with the epithelial turnover rate, and co-infection with enteric viruses – like feline coronavirus – can enhance the severity of disease. Pathogenesis Pathogenesis: Intrauterine transmission or perinatal FPV infection can affect central nervous system development. So-called “Feline ataxia syndrome” results from an impaired development of the cerebellum due to lytic infection of the Purkinje cells in the kitten Immunity: Passive immunity Antibodies play an important role in the immune response to FPV. Maternally derived antibodies (MDA) efficiently protect kittens from fatal infection. The endotheliochorial placentation of the cat restricts maternofoetal passage of solutes, and IgG can only cross the placenta barrier in the last trimester of gestation. This immunoglobulin transfer accounts for