Parvoviridae – parvus, small

1. Parvoviridae – parvus, small • Properties of Parvoviruses • Nonenveloped icosahedral virion • Negative strand single stranded DNA genome • Replicate in nucleus of dividing cells • Produce large intranuclear inclusion bodies • Most member viruses hemagglutinate red blood cells • Viruses are very stable • Cat with cerebellar hypoplasia at left

2. Parvoviridae • Subfamilies and Genera • Subfamily Parvovirinae • Contains parvoviruses of vertebrates • Genus Parvovirus – • Replicate autonomously • Cannot grow in stationary cells • Replicate in cells undergoing mitosis – do not code for enzymes required for replication, BUT • Rely on the enzymes of the replicating cell to perform this function • Resistance – very stable to environmental conditions – extremes of pH and heat – disinfection DIFFICULT

3. Diseases caused by Parvovirus • Genus Parvovirus • Virus – Feline parvovirus – Feline panleukopenia • Canine Parvovirus 1 – mild diarrhea • Canine parvovirus 2 - enteritis, leukopenia, myocarditis etc. • Subtypes 2a and 2b • Porcine parvovirus – Reproductive disorders – SMEDI • Mink parvovirus – panleukopenia, enteritis • Pathogenesis - • Determined by the need for mitotic cells for viral replication • Fetus or newborn – Pantropic – Virus may infect a wide range of cells in various tissues and organs • Older neonates – narrower range of cells affected • All age groups – the continuous division of cells of the lymphoid tissue, bone marrow and intestinal epithelium are target sites – leukopenia and enteritis

4. Feline Panleukopenia • Highly contagious often fatal disease of cats • Most severe in kittens • Synonyms – Feline distemper, feline infectious enteritis • Etiologic agent – feline parvovirus – One serotype • Antigenically related to canine parvovirus 2 and mink parvovirus • Distribution – worldwide • Hosts – all members of the cat family, both domestic and wild are susceptible • Raccoon, mink, coatimundi etc. • Epidemiology – virus is ubiquitous due to its contagious nature and resistance and persistence in the environment

5. Feline Panleukopenia • Epidemiology continued – • Most subclinical – 75-85% of unvaccinated cats has developed significant antibody titers by one year of age • Unvaccinated kittens are protected through maternal antibodies for up to 3 months • Recovered cats are solidly immune, but can EXCRETE virus in FECES AND URINE FOR 6 WEEKS (OR LONGER) • Extreme resistance of the virus to inactivation and the high rates of viral excretion – 109 the infective dose/ gram of feces – • Results in high levels of environmental contamination – Virus may survive for more than one year in a suitable environment and can be transported via fomites • Owners should NOT adopt an unvaccinated kitten and bring it into the house if parvovirus was ever present

6. Feline Panleukopenia • Transmission – cats infected ORONASAL route by exposure to infected animals or their secretions – urine, saliva, feces and vomitus or fomites • Mechanical vectors – fleas, humans, flies, etc. • Pathogenesis of Feline Panleukopenia • If exposed in utero – Early fetus will die and be resorbed • Mid-late gestation – abort mummified fetuses • Late gestation – eye, cerebrum and hydranencephaly • **Feline parvovirus produces variable effects on kitttens from the same litter** • Early neonatal – lymphoid tissue affected, cerebellar hypoplasia, bone marrow • Older postnatal – SPF – lymphoid tissue 18-24 hours for replication – adequate titer • Inadequate titer – viremia, 2-7 days in all body tissues either result in DIC and death or recovery

7. Panleukopenia • Results from destruction of various white blood cell elements – lympocytes, neutrophils, monocytes – including both those present in the circulation and those in the lymphoid organs – • Thymus, bone marrow, spleen, lymph nodes, and Peyer’s Patches • Platelets are also destroyed • Enteritis – • Feline parvovirus multiplies in the rapidly dividing intestinal epithelial cells – crypts of Lieberkuhn. • Normally the epithelial cells at the tips of the intestinal villi are continuously lost into the lumen, replaced by the dividing cells of the crypts • With disease, the villous cells are not replaced, resulting in short non-absorptive cells • Diarrhea and poor absorption results

8. Central Nervous System Infection and DIC • The CNS, optic nerve, and retina are susceptible to damage by FPV during prenatal or early neonatal development • Cerebellar hypoplasia is the most common • Cerebellar hypoplasia – observed in fetuses infected during the last two weeks of pregnancy and the first two weeks of life • Neonatal cerebellum damaged by FPV is reduced in size and has disordered cell layers • ********************************************************************* • Disseminated intravascular coagulation • Kittens with feline panleukopenia are susceptible to secondary bacterial infection with enteric microflora • Gram negative endotoxemia with or without bacteremia is a common sequelae of systemic FPV infection • DIC results from endotoxic activation of the alternative complement pathway

9. Feline Panleukopenia and DIC • Clinical signs – most common in kittens 3-5 months of age • Incubation period – 5 days (2-10 day range) • Fever, depression, anorexia, rough coat, repeated vomiting, profuse persistent bloody diarrhea • Dehydration – secondary bacterial infections, and DIC are the major causes of death • Cerebellar hypoplasia. Kitten is permanently ataxic • Usually not apparent until the kitten begins to walk at 3-4 weeks of age • Diagnosis – Clinical signs, hematological examination, and postmortem findings • Virus isolation in cell culture. Swabs from pharynx or rectum, spleen, ileum or mesenteric lymph node • Direct ELISA or immunofluorescence for antigen in tissues • PCR assay for the detection of viral DNA in tissues • Direct hemagglutination of pig or rhesus RBCs by virus present in feces • Paired serum samples. • Virus neutralization test, ELISA, or hemagglutination inhibition test to check for 4 fold increase in antibody titer

10. Feline Panleukopenia and DIC • Treatment – supportive measures • Good nursing care, fluid therapy, and withholding food in early stages of the disease to lessen vomiting and slow intestinal mitotic activity • Administration of broad-spectrum antibiotics • Control – • Large catteries – strict hygiene and quarantine of incoming animals • Disinfection – virus survives disinfection with 70% alcohol, various dilutions of organic iodines, phenolics, and quaternary ammonium compounds – QUATS • FPV – INACTIVATED BY BLEACH – 6% sodium hypochlorite, 4% formaldehyde, and 1% glutaraldehyde in 10 minutes at ROOM TEMPERATURE • Immunity –neutralizing antibodies can be detected within 3-5 days of infection • Immunity after natural infection appears to be lifelong • Attenuated – modified live-virus vaccine and inactivated vaccine are used • MLV should not be administered to cats that are pregnant, immunosuppressed or sick or to kittens less than 4 weeks old

12. Canine Parvovirus • Canine Parvovirus disease first recognized in 1978 when it caused a worldwide pandemic – severe gastointestinal illness • Etiologic agent – Canine parvovirus 2 – 2a, 2b • In North America, disease is caused mostly by CPV-2b. Both 2a and 2b are circulating in Europe in other parts of the world • Canine parvovirus 1 – was isolated in feces of dogs in 1967 but is not a major cause of disease • Hosts – domestic and wild canidae – • self-limiting in cats with no clinical signs • Epidemiology – similar to that of feline parvovirus – CPV-2 can persist on fomites for 5 months or longer. • Disease now has lower morbidity and mortality rates as immunity has built up in the dog population

13. Canine Parvovirus • Transmission –similar to feline panleukopenia • Pathogenesis same as feline, but no cerebellar hypoplasia in puppies • Clinical features – three distinct age-related syndromes have been recognized • 2-12 days – generalized neonatal disease – uncommon • 3-8 weeks – myocarditis –can also develop from infection in utero. Usually all puppies are affected in litter. • Sudden death or a pup may succumb after a short episode of illness • Less common now

14. Canine Parvovirus • 2-4 months – panleukopenia/ enteritis – most common • Diagnosis – same as feline panleukopenia • Direct ELISA kit for feces detection • IgM capture ELISA used to determine recent infection • Control – same as feline panleukopenia • Immunity – same as feline panleukopenia. Immunity after natural infection appears to be lifelong • Attenuated live and inactivated vaccines available

15. Porcine Parvovirus - PPV • Porcine Parvovirus infection – 47th day of gestation • Worldwide and endemic in many swine herds • Virus as been isolated in association with respiratory disease and vesicular disease of the feet and mouth in young pigs and neonatal systemic disease • Transmission – oronasal in the dam followed by transplacental transmission • Venereal transmission – possible because infected boars shed virus in the semen for protracted periods

16. Porcine Parvovirus • Pathogenesis – • virus replicates in lymphoid tissues or organs, salivary glands and other organs • Replicates well in peripheral blood lymphocytes – T and B and NK cells • Reproductive failure is due to exposure of nonimmune females to PPV any time during the first 8 weeks of gestation • Embryo or fetus – less than 30 days – embryo or fetus dies and is resorbed • Early fetus – 30-70 days – fetuses die and become relatively dehydrated – mummified • Late fetus – more than 70 days – develop lesion by nay develop in utero and produce antibody to PPV – immunocompetence of pig fetuses starts at 55-70 days • Boars, sows and gilts – mostly inapparent or subclinical infections • Diagnosis – • Fluorescent antibody staining of frozen sections of fetal tissues results in rapid diagnosis

17. Porcine Parvovirus • Control – • inactivated and attenuated vaccines are widely used • Nonimmune swine may be exposed to virulent virus several weeks before breeding to establish immunity • E.g. commingling gilts and boars with other swine that may be shedding PPV – like older breeding stock • Unlike most parvoviruses, swine parvovirus causes persistent infection with chronic shedding • SMEDI – other causes include: • Porcine enterovirus 2-11 • Porcine herpesvirus 1 – pseudorabies • Porcine arterivirus – porcine reporductive and respiratory syndrome