Canine Parvovirus Infection
Parvovirus infection remains one of the most common infectious disorders of dogs. Canine parvovirus emerged in the late 1970s
and caused a worldwide pandemic of illness in dogs. It was initially thought that it may have emerged from FPV, but that now
seems unlikely based on the differences between them. Canine parvovirus is caused by canine parvovirus 2. CPV-2 has mutated
to CPV-2a, CPV-2b, and CPV-2c since it first appeared, and these latter viruses predominate in dogs currently. With this mutation,
the virus has developed the ability to replicate readily in feline cells, and it now appears that CPV may now be causing some
cases of feline viral enteritis, which are being increasingly recognized, perhaps because of poor vaccine cross-reactivity.
A study from the UK showed that parvovirus accounted for 25% of kitten mortality. Concern has been raised about the ability
of the current CPV vaccines to protect against newer CPV strains such as CPV-2c, but one recent study showed good protection
against experimental challenge with CPV-2c.
Research into coagulation problems in dogs with parvoviral gastroenteritis suggests that many dogs may actually be hypercoagulable,
rather than having DIC; the platelet count has typically been normal. Many dogs had evidence of venous thrombosis or phlebitis
in association with catheters. Leukopenia results from sequestration of neutrophils within the gut as well as bone marrow
destruction. The concurrent presence of leukopenia is highly supportive of the diagnosis, but severe gastrointestinal signs
and leukopenia can also occur with other severe infections of the gastrointestinal tract, particularly salmonellosis. Shedding
continues for up to 6 weeks after recovery, and most infectious disease experts recommend isolating dogs for about a month
after discharge from hospital.
Parvovirus myocarditis now appears to be a rare condition because of protection of pups by maternal antibody, but still occasionally
occurs in pups born to isolated, unvaccinated bitches. Investigators have been looking at DCM cases for evidence of parvoviral
DNA but so far it seems that CPV-2 is not associated with DCM in adult dogs.
Neurologic signs may occur in dogs with parvovirus. These may result from intracranial hemorrhage secondary to DIC, hypoxia
due to myocarditis, or profound hypoglycaemia. With the use of PCR, parvovirus has now been detected in both dogs and cats
with cerebellar hypoplasia.
False positive results with the fecal ELISA may occur 5 to 12 days after vaccination with an MLV vaccine. Negative results
do not completely rule out canine parvovirus infection, because virus is often not present in the stool 5 to 7 days after
the onset of clinical illness.
The fecal ELISA developed for detection of CPV-2 will also detect FPV.
PCR has also been used as a sensitive and specific method of detecting viral DNA in tissues, and has been used to detect CPV-2
and FPV. PCR has been used to distinguish between wild type CPV-2 and vaccine CPV-2.
Other treatments that have been examined for CPV infection include anti-endotoxin, rhG-CSF, recombinant bactericidal/permeability
increasing protein (rBP121) and recombinant feline interferon-omega. Anti-endotoxin, rhG-CSF and rBP121 have not been shown
to be convincingly beneficial, and are expensive. In fact, one study showed that treatment of dogs less than 16 weeks of age
with anti-endotoxin was actually associated with a higher mortality. Dogs with parvovirus infection are expected to and do
have high levels of endogenous G-CSF anyway. Recombinant feline interferon-omega has been shown to be of benefit in experimentally
infected dogs, but it has not been used yet to treat dogs with natural infections. A recent study showed early enteral nutrition
via NE tube 12 hours after admission resulted in earlier clinical improvement and significant weight gain compared with using
NPO until vomiting had ceased for 12 hours.
Canine Parvovirus Vaccine Recommendations
Prior to 1994, as many as 20% of dogs retained sufficient maternal antibody to interfere with parvovirus vaccination. Since
then, a new generation of parvovirus vaccines have been introduced that produce superior immunity, and these have reduced
the window of vulnerability down to a few days to two weeks. Killed CPV-2 vaccines produce a weaker response, and should not
be used in contaminated environments, because the window of vulnerability is too great. Current vaccination recommendations
are to vaccinate every 3 weeks from 4-6 weeks of age to 14 to 16 weeks of age. After the first annual booster, vaccination
should be repeated every 3 years. A puppy that recovers from CPV-2 enteritis is immune for at least 20 months after infection,
and possibly for life.