Veterinary DNA viruses I (Parvoviruses)

Why are parvoviruses important to learn about?

• Acute lytic viral infection

• No latency or persistence in the host

• Systemic spread

• Tissue tropism for rapidly dividing cells

• Severe clinical disease in different species

• Clearance by the immune system

What are the properties of parvoviruses?

Parvoviruses are among the smallest viruses known

The genome is a single molecule of single-stranded DNA (ssDNA)

Replication in the nucleus of dividing cells; infection leads to large intranuclear inclusion bodies.

Parvoviruses are nonenveloped → extremely stable to environmental conditions, including extremes of heat and pH

Most viruses hemagglutinate red blood cells (diagnostic tool)

What is feline panleukopenia virus?

• Pan (all) + leuko (leokocytes) + penia (low level): term "panleukopenia" refers to decrease in the number of all WBCs caused by the virus.

• Highly contagious and potentially fatal disease

What is the epidemiology of feline panleukopenia virus?

Epidemiology:

• All members of the family Felidae are susceptible

• Spread worldwide

• Shed: predominantly in the feces, but in the vomitus, urine, and saliva of sick animals

• Modes of transmission: faeco-oral (primary route), direct contact with infected cats or via fomites, intrauterine

• Age: most common in kittens infected around the time of weaning, but cats of all ages are susceptible to infection.

What are the clinical signs of feline panleukopenia virus?

Clinical signs:

• Incubation period is ~ 2-7 days

1. Onset of clinical signs: a profound leukopenia proportional to severity of the disease

2. Fever (greater than 40C), persist for 24 h or more

3. Often repeated vomiting, lassitude, inappetence, a rough coat

4. Persistent diarrhea at day 3-4 → dehydration

Clinical signs in case of intra-uterine infection:

• In pregnant cats, parvovirus cross the placenta and infect dividing cells in the developing cerebellum of kitten:

• Cause cerebellar hypoplasia → noticeably ataxic (wobbly cat syndrome)

• A wide-based stance, exaggerated steps, overshoot the mark

What is the pathogenesis of feline panleukopenia virus?

Entry via the oropharynx: primary virus replication in pharyngeal lymphoid tissue

Spread via free and cell-associated viremia→ infect rapidly dividing cells (progenitor cells) in their S phase in:

• Bone marrow

• Intestinal epithelial stem cells in intestinal crypt

• stimulated lymphocytes in lymph node

• cerebellum in kitten

Shed: predominantly in the feces, but in the vomitus, urine, and saliva of sick animals

Outcome of infecting/destroying rapidly dividing cells in:

• Bone marrow ➔ leukopenia

• Intestinal epithelial stem cells in intestinal crypt ➔ mucosal collapse in the intestine, diarrhea maldigestion and malabsorption, dehydration

• Stimulated lymphocytes in lymph node (LN) ➔ enlarged and edematous LN

• Cerebellum in kitten ➔ affected kittens remain permanently ataxic

Why do parvoviruses target rapidly dividing cells?

Parvoviruses have ssDNA genomes and lack their own DNA polymerase.

They require host DNA replication machinery, which is active in S phase. Only rapidly dividing cells provide nucleotides and enzymes needed for viral replication.

Common cell targets in S phase: bone marrow, intestinal crypts, foetal tissues

✓ Key Point: Parvovirus replication is S-phase dependent.

What is the necropsy/pathology of feline panleukopenia virus?

• Hemorrhages on the bowel serosa

• Histology: attenuation of the lining epithelium

• Widespread destruction of lymphocytes in LN

• In fetus/kitten: cerebellar hypoplasia/atrophy

How is feline panleukopenia virus diagnosed?

✓ Clinical signs

✓ Haematological changes

✓ Postmortem findings

✓ Confirmatory tests:

• PCR for the detection of viral DNA in feces

• Fecal antigen rapid test

How should feline panleukopenia virus be prevented and controlled?

• Vaccination or natural immunity due to infection provide lifelong protection.

• Kittens can acquire passive immunity from their mothers.

• FPV is extremely stable and can survive in the environment for a long time

• In large catteries, strict hygiene and quarantine of incoming cats

• Sick cat should be isolated

What is the epidemiology of canine parvovirus 2?

• Epidemiological features similar to those of FPV (highly contagious and very stable)

• Feacal-oral transmission (exposure of susceptible dogs to virus-contaminated faeces)

• All members of the family canidae are susceptible to natural infection

• Severe disease is most common in rapidly growing pups (6 weeks to 6 months)

What are clinical signs of canine parvovirus 2?

Enteritis syndrome analogous to FPV(leukopenia is often less severe in dogs):

• Vomiting (the initial sign); anorexia, lethargy, and diarrhoea → severe dehydration

• Intestinal haemorrhage ➔ severe diarrhoea (important cause of infectious diarrhoea in young dogs)

• Death is uncommon except in young pups.

Intestine lesions:

• Destruction of enterocytes in intestinal crypts

• mucosal collapse (C)

• Maldigestion and malabsorption

• Diarrhoea

• Mucosal and serosal haemorrhage

Myocarditis syndrome in puppies results from infection in the first week of life:

• Acute heart failure and sudden death in pups, often without preceding clinical signs.

Heart lesions:

• Parvovirus destroys the myocardial myocytes

• Myocardial necrosis and inflammation

• Pulmonary edema and/or hepatic congestion from acute heart failure

• If pup survive (heart hypertrophy)

How is canine parvovirus 2 diagnosed?

• Sudden foul-smelling, bloody diarrhea in young dogs

• Confirmed by:

• Fecal (ELISA) SNAP Test

• Detection of viral DNA using PCR Test

How should canine parvovirus 2 be prevented and controlled?

• Immunity after vaccination/ natural infection is lifelong.

• Passive maternal antibody in colostrum (vaccine failure in weanling pups).

• Problem of high viral loads in shelters, breeding facilities, and veterinary clinic

What is porcine parvovirus?

Ungulate parvovirus 1

Cause of reproductive failure in swine throughout the world.

Losses are most extreme if the virus is introduced into a seronegative herd at a time when many sows are pregnant→

• In susceptible breeding herd cause SMEDI syndrome (Stillbirth, Mummification, Embryonic Death, Infertility).

• Older swine causes only a mild or subclinical disease

What are the clinical signs of porcine parvovirus?

• The major impact of porcine parvovirus results from infection of pregnant gilts or sows, and the stage of gestation

• Runs the full gamut of the SMEDI syndrome.

• In young pigs, infection has been associated with a vesicular disease of the feet and mouth.

Foetus Infection in:

✓ Early gestation (less than 30 d after conception) ➔ embryonic death and resorption

✓ Mid-gestation (30 - 70 d after conception) ➔ no immune response and fetus affected severely/ dies

✓ Late-gestation (70 d or more after conception) ➔ mount an immune response and affected less severe

Immunocompetence of swine fetuses starts at 55-70

days

How is porcine parvovirus diagnosed and prevented?

• Clinical manifestation (suspicion)

• Confirm: Infected fetuses may contain very large amounts of virus.

• Fluorescent antibody test of foetal tissues to detect viral antigen

• PCR

Vaccination is practiced widely as the only means of assuring that all gilts are protected

Parvovirus summary:

• Among the smallest DNA viruses

• Non-enveloped, making them extremely environmentally stable and difficult to eliminate.

• They replicate only in S-phase cells because they depend entirely on host DNA polymerase.

This explains their tropism for:

• Bone marrow

• Intestinal crypt cells

• Lymphoid tissue

• Developing fetal tissues (especially cerebellum)

Feline panleukopenia virus summary:

Key features:

• Profound leukopenia

• Vomiting and diarrhoea due to intestinal crypt destruction

• Dehydration and risk of sepsis

• In utero infection → cerebellar hypoplasia (“wobbly cat syndrome”).

• Diagnosis: clinical signs, haematology, faecal antigen tests, PCR.

• Prevention: lifelong immunity after infection or vaccination; strict hygiene essential due to environmental stability

Canine parvovirus-2 summary:

• Major cause of infectious diarrhoea in young dogs.

Presents with:

• Acute vomiting and haemorrhagic diarrhoea

• Intestinal mucosal collapse

• In very young pups: myocarditis, sudden death.

• Diagnosis: SNAP ELISA, PCR.

• Control: vaccination, hygiene, managing maternal antibody interference.

Porcine parvovirus summary:

Major cause of SMEDI syndrome:

• Stillbirth

• Mummification

• Embryonic Death

• Infertility

Outcome of infection depends entirely on gestational age:

• Early gestation → embryonic death/resorption

• Mid gestation → no fetal immune response → fetus affected severely

• Late gestation → fetus is immunocompetent → may survive with antibodies

• Prevention: vaccination of gilts is essential