Parvoviridae Flashcards
General properties of Parvo
Noneveloped ,iscosahedral virion, small 18-25 nm in diameter. Virion capsid is composed of 60 protein subunits, T=1. ssDNA genomes which are linear approximately 4-6 kb in size. Most viruses hemagglutinate RBC. Very stabile resisting 60C for 60 mins and pH3-pH9
Where does replication occur>
Occurs in rapidly dividing cells in the nucleusVirus replication only occurs in cells that pass through mitosis S phase cannot replicate in stationary cells as they rely on enzymes of actively dividing cells, mitosis.
Infection leads to large intranuclear inclusion bodies? True or False?
True dat
For funs, name the 5 genera
Parvovirus, Dependovirus, Amdovirus, Erythrovirus, Bocavirus
Genus Erythrovirus aka Fifth Disease, Slap cheek rash
Replicates autonomously, includes human parvovirus B19, B19 causes Mild rash, also called erythema infection, aplastic anemia in children, painful joints.No evidence of transmission of B19 to humans from dogs or cats, or vice versa.
Genus Dependovirus
Viruses are themselves replication defective and do not cause disease as they are UNABLE to replicate except in the presence of a helper virus usually an ADENO virus. Includes goose and Duck parvovirus and provisionally bovine parvovirus 2.
Genus Bocavirus
Unique as they contain a third ORF. Open reading frame between non structural and structural coding regions. These viruses generally infect the gastrointestinal and respiratory tracts. found in human dogs,and cattle
Family Parvoviridae, Etiology: Feline parvovirus and Feline Panleukopenia is the disease FPV.
Other names, feline distemper, feline infectious enteritis.
Hosts of FPVq
All family Felidae are most susceptible. Highly contagious, often fatal in cats. Severe in kittens. Also in related families such as raccoon, mink, etc Distribution is worldwide.
FPV epidemiology.
Contagious and capacity for persistence in the environment. All cats are exposed and infected within first year of life. Most infections are subclinical as much as 75% of unvaccinated healthy cats have demonstrable antibody titers by 1 year of age.
How do cats shed FPV
Through urine or feces for a max of 6 weeks after recovery.
Transmission of FPV
Cats are infected oro nasally by exposrue to infected animals, their feces, secretions or contaminated fomites. In utero transmission occurs, Mechanical transmission by flies. Very stable in the ENV.
Pathogenesis of FPV
After virus enters the oropharynx, initial virus replication occurs in the pharyngeal lymphoid tissue. There is cell associated viremia to other organs and tissue via the blood stream. Cells that have appropriate receptors and are in the S phase of the cell cycle are infected and killed or prevented from entering mitosis.
What is the hallmark of the disease? FPV
The more severe the Leukopenia the poorer the prognosis. The characteristic profound leukopenia involves destruction of all white blood cell elements, including lymphocytes, neutrophils, monocytes and platelets. Cells present in circulation [consequence of virus adsorption and cytotoxic lysis] as well as those in lymphoid organs, including the thymus, bone marrow, lymph nodes, spleen, and Peyer’s patches are destroyed. Thromobyctopenia due to damage to bone marrow may accompany leukopenia. `
Enteritis in FPV
Virus selectively damages replicating cells deep in the crypts of the intestinal mucosa. Differentiating adsorptive cells on the surface of the villi are non-dividing and are not affected. villi become atrophied, Severe diarrhea, Lymph nodes and spleen shows hemorrhages.
Gross lesions seen during necropsy?
Hemorrhagic Spleen, Intestines and mesenteric lymph nodes, dark hemorrhagic jejunum and ileum. Dilation with accumulation of undigested food and gas.Hyperplasia and necrosis.
Histopathology shows basophilic intranuclear inclusion bodies
Yes, and you would see that the smal intestine epithelial necrosis and hyperplasia.
In Utero FPV infections in early in uter infection?
early in utero infection in pregnant queen can result in ? Early fetal death and resorption with infertility, abortions, birth of mummified fetuses.
In utero FPV infections in closer to end gestation?
Birth of live kittens with varying degree of damage to the late developing neural tissues. Variable effects on kittens from the same litter.
CNS infection . the CNS optic nerve and retina are susceptible to damage by FPV during prenatal or early neonatal development. What is most commonly reported with neurological lesions?
Cerebellar damage, Cerebellar hypoplasia observed in fetuses infected during the last 2 weeks of pregnancy and the first two weeks of life.
Cerebellar hypoplasia
Destroyed mitotic external germinal layer, Damaged purkinje’s cells, Dysplasia of granule cell layer. Lysis of mitotic cells of the external germinal layer, impaired cerebellar development
FPV leads to marked ataxia.
yas and also you can get hydranecephaly, no development of the brain bur the space is filled with fluid.
Disseminated Intravascular Coagulation
Kittens with FPV infection are also susceptible to secondary bacterial infection
Gram negative endotoxemia, with or without bacteremia is a common sequelae of systemic FPV infection
Endotoin LPS induces expression of tissue factor [factor III} on endothelial cells
Tissue factor is a potent activator of coagulation, resulting in DIC, followed by hemorrhages.
Clinical signs of FPV
Most common in kittens 3 to 5 months of age
Incubation period ranges from 2-10 days [5 days]
