What is canine parvovirus?
Canine parvovirus is a highly contagious and serious disease
caused by a virus that attacks the gastrointestinal tract
of puppies, dogs, and wild canids. It was first identified
in 1978 and is seen worldwide.
How is parvovirus spread?
Puppies and dogs usually become infected when they ingest
virus that is passed in the faeces (stool) of an infected
dog. Canine parvovirus is resistant to changes in environmental
conditions and can survive for long periods of time. Trace
amounts of faeces containing parvovirus may serve as reservoirs
of infection and the virus is readily transmitted from place
to place on the hair or feet of dogs or via contaminated cages,
shoes, or other objects. Canine parvovirus affects dogs and
other canids, but not other types of animals or people.
What dogs are at risk?
All dogs are at risk, but puppies less than four months old
and dogs that have not been vaccinated against canine parvovirus
are at increased risk of acquiring the disease. Certain breeds
(e.g. Rottweiler and Doberman Pinscher) appear to have a high
risk of experiencing severe disease.
What are some signs of parvovirus infection?
Canine parvovirus causes lethargy; loss of appetite; fever;
vomiting; and severe, often bloody, diarrhoea. Vomiting and
diarrhoea can cause rapid dehydration, and most deaths from
parvovirus occur within 48 to 72 hours following onset of
clinical signs. If your puppy or dog shows any of these signs,
you should contact your veterinarian promptly.
How is canine parvovirus diagnosed and treated?
Veterinarians diagnose canine parvovirus on the basis of clinical
appearance and laboratory tests. No specific drug is available
that will kill the virus in infected dogs. Treatment should
be started immediately and consists primarily of efforts to
combat dehydration by replacing electrolyte and fluid losses,
controlling vomiting and diarrhoea, and preventing secondary
infections. Sick dogs should be kept warm, receive good nursing
care, and be separated from other dogs. Proper cleaning and
disinfection of contaminated kennels and other areas where
infected dogs are housed is essential to control the spread
How is parvovirus prevented?
Vaccination and good hygiene are critical components of canine
Vaccination — Vaccination is important. Young puppies
are very susceptible to infection, particularly because the
natural immunity provided in their mothers' milk may wear
off before the puppies' own immune systems are mature enough
to fight off infection. If a puppy is exposed to canine parvovirus
during this gap in protection, it may become ill. An additional
concern is that immunity provided by a mother's milk may interfere
with an effective response to vaccination. This means even
vaccinated puppies may occasionally succumb to parvovirus.
To narrow gaps in protection and provide optimal protection
against parvovirus during the first few months of life, a
series of puppy vaccinations are administered.
To protect their adult dogs, pet owners should be sure that
their dog's parvovirus vaccination is up-to-date. Ask your
veterinarian about a recommended vaccination program for your
Hygiene — Until a puppy has received its complete series
of vaccinations, pet owners should use caution when bringing
their pet to places where young puppies congregate (e.g. pet
shops, parks, puppy classes, obedience classes, doggy day
care, and grooming establishments). Reputable establishments
and training programs reduce exposure risk by requiring vaccinations,
health examinations, good hygiene, and isolation of ill puppies
and dogs. Contact with known infected dogs and their premises
should always be avoided.
Finally, do not allow your puppy or dog to come into contact
with the faecal waste of other dogs while walking or playing
outdoors. Prompt and proper disposal of waste material is
always advisable as a way to limit spread of canine parvovirus
The Virus in the Environment/Disinfection
Because the canine parvovirus is not enveloped in fat the way the distemper virus is, canine parvovirus is especially hardy in the environment. It is readily carried on shoes or clothing to new areas (which accounts for its rapid worldwide spread shortly after its original appearance). It is able to
over-winter freezing temperatures in the ground outdoors plus many household disinfectants are not capable of killing it indoors.
Given that this is such a tough virus to destroy, many people want to know exactly what they must do to disinfect an area that has contained an infected dog or how long they must wait before safely introducing a new dog to a previously contaminated area.
Here is what we know about how contaminated an environment is likely to be:
Infected dogs shed virus (in their stool) in gigantic amounts during the 2 weeks following exposure. Because such enormous amounts of virus are shed, there is a HUGE potential for environmental contamination when a infected dog has been there.
It is important to realize that because the canine parvovirus is so hardy in the environment, it is considered "ubiquitous." This means that NO ENVIRONMENT is free from this virus unless it is regularly disinfected.
A parvoviral infection can be picked up ANYWHERE though it is easier to pick up an infection in an area where an infected dog has been present simply because of the larger amounts of virus present in a contaminated area.
Whether an individual dog gets infected or not depends on the number of viral particles the dog experiences, what kind of immune experience the dog has had with the virus before (vaccinated? previously infected? how much past exposure?), and how strong the individual dog is (stress factors, diet etc.)
A typical/average infectious dose for an unvaccinated dog is 1000 viral particles. For some dogs far less is needed. For other dogs, far more is needed. An infected dog sheds 35 million viral particles (35,000 TIMES the typical infectious dose) per OUNCE of stool.
Indoors, virus loses its infectivity within one month; therefore, it should be safe to introduce a new puppy indoors one month after the active infection has ended.
Freezing is completely protective to the virus. If the outdoors is contaminated and is frozen, one must wait for it to thaw out before safely introducing a new puppy.
Shaded areas should be considered contaminated for seven months.
Areas with good sunlight exposure should be considered contaminated for five months.
Of course, the above presupposes that no decontamination steps (other than waiting) have been taken. In most households, owners want to know how to disinfect their homes to create a safer environment for the other dogs there or to create a safe environment for a new or replacement puppy.
Here's what we know about disinfection:
Despite the introduction of new cleaners with all sorts of claims, parvovirus remains virtually impossible to completely remove from an environment. The goal of decontamination is to reduce the number of viral particles to an acceptable level.
The best and most effective disinfectant against viruses (including
parvoviruses) is BLEACH. One part bleach is mixed with 30 parts water and is applied to bowls, floors, surfaces, toys, bedding, and anything contaminated that is colorfast or for which color changes are not important.
Bleach completely kills parvovirus
Disinfection becomes problematic for non-bleachable surfaces such as carpet or lawn. Outdoors, if good drainage is available, thorough watering down of the area may dilute any virus present. Since carpet is indoors, it may be best to simply wait a good month or so for the virus to die off before allowing any puppies access to the area.
Date Published: 1/1/2001
By Wendy C. Brooks DVM, DABVP
Parvo Treatment Made Simpler, Cheaper
A new therapy developed at the Auburn University College of Veterinary Medicine, Auburn, Alabama, allows tremendous cuts in cost and time required to treat dogs showing signs of parvovirus infection. The usual $500-800 in medication and supportive care and seven-day hospital stay can now be sliced in half, while reducing mortality from 16 to 10 percent.
The new approach involves injections of lyophilised canine immunoglobulin (Ig) G which has been extracted from the serum of dogs that have recovered from parvovirus infection. In clinical trials, patients receiving this IgG in addition to regular treatment recovered more quickly than dogs not receiving the IgG. Furthermore, none of the IgG patients required IV nutrition,
hetastarch, or plasma transfusion.
"Canine immunoglobulin reduces the time needed for a dog to regain its appetite and return to a normal stool," said Douglass
Macintire, D.V.M., associate professor in Auburn's Department of Small Animal Surgery and Medicine and member of the research team.
"Parvo is still not totally curable, but...currently, the infected puppy needs extensive hospital care and intravenous fluids, nutrition, antibiotics and expensive plasma or hetastarch for protein." Even with the new therapy, she noted, "supportive care is still the only treatment; it simply does not take as long when IgG is added. When the illness has run its course, recovery is usually complete, and dogs appear to develop lifelong immunity against reinfection."
The disease is most frequently seen in puppies between six weeks and six months of age. Most adult canines gain immunity either through vaccination or natural infection - an immunity that is passed on to newborns through maternal antibodies. Susceptibility is increased by keeping puppies outside, where parvovirus can last in the soil for up to two years, or in contact with other dogs.
Canine parvovirus (CPV) is a member of the genus Parvovirus of the family Parvoviridae. Canine parvovirus infection emerged in the late 1970s most likely as a variant of feline panleukopaenia virus (FPV) or a closely related parvovirus. FPV-like viruses have been isolated from cats, raccoons, mink, and the arctic fox, and are genetically very similar although distinct from CPV-like viruses from dogs and raccoons. Besides the well-known FPV, new antigenic types of CPV, namely CPV-2a and CPV-2b, are also able to replicate and cause disease in cats. These new antigenic types are the predominant types in dog populations worldwide.
CPV has a worldwide distribution. Serological surveys indicate that severe clinical disease with high mortality is the exception. Most naturally occurring infections with CPV are subclinical or result in mild signs of disease that do not require veterinary care. Age, stress, breed, intestinal parasites, and concurrent infections all can affect the pathophysiological consequences of infection with CPV so that morbidity and mortality in pups can exceed 90% and 50% respectively.
Infection in the dog takes place via the oronasal route. Initial viral replication occurs in extra-intestinal lymphoid tissues. Virus is then spread through the blood to other lymphoid tissues where the cycle is repeated, eventually resulting in intestinal epithelial infection. Thus, viraemia always precedes intestinal epithelial infection.
Infection and destruction of lymphoid tissues are prominent features of parvovirus infection. This is characterized by extensive loss and sometimes depletion of lymphocytes from the cortex of lymph nodes, especially the mesenteric and retropharyngeal nodes. Parvovirus is able to replicate in both T and B-lymphocytes. Intestinal lesions are characterized by extensive necrosis of crypt epithelial cells accompanied by collapse of the lamina propria and a minimal inflammatory infiltrate in both. Lesions are most severe in the ileum and duodenum, with mild lesions in the colon. There is extensive depletion of lymphocytes in the intestinal lymphoid nodules and Peyer's patches.
The most consistent haematological change in CPV infection is transient lymphopaenia.
IgA antibodies appear in the intestinal tract and faeces by day 4 after infection with CPV. Some dogs can develop high titres of humoral antibody but little IgA antibodies in the intestinal lumen. These dogs are more likely to have severe disease.
The severity of intestinal lesions determines the severity of clinical disease, and is in turn dependant on the dose of virus reaching the intestine from the blood. Thereafter, additional virus replication within intestinal lymphoid tissues and the intestinal epithelium further elevates the intestinal virus titre.
The disease is seen mostly in dogs between the ages of 6 weeks to 6 months. Early clinical signs are listlessness, anorexia, vomiting, and fever. The disease progresses to weakness, dehydration, and severe vomition and diarrhoea. In advanced cases, septic/hypotensive shock develops.
Clinical signs especially with a poor/no vaccination history are indicative of the disease.
- Electron microscopy on faecal specimens.
- Serum antibody titres by the haemagglutination inhibition test or the indirect immunofluorescent antibody test.
- Post mortem examination.
- Virus isolation from either serum or faeces.
- Gentamycin at 2 mg/kg TID or 3mg/kg BID for 3-5 days.
Only once patient is rehydrated.
Check for RTE cells in urine.
- Replacement or maintenance fluids.
0.2-0.4 mg/kg tid-qid.
1-2 mg/kg/day as a constant rate infusion.
- Prochlorperazine at 0.5 mg/kg tid or a piece of a suppository. Has no prokinetic effect.
- Ondansetron at 0.1-1 mg bid-qid.
- Feed once rehydrated, which should be approximately 4-12 hours after admission.
- Feed minimum of 1/3 of nutritional requirements in first 24 hours.
- With severe vomition, miss out 1-2 hours and/or reduce quantity.
- Naso-oesophageal tube if necessary.
- Plasma transfusion at 10-20 ml/kg if albumin < 20 g/l.
- Blood transfusion if not improving and Ht <15-20%.
- Deworm if necessary.
- Sucralfate 1ml/3kg tid-qid with severe vomiting to control flux oesophagitis.
- Cimetidine 10 mg/kg tid or ranitidine 2 mg/kg bid.
- Temgesic 0.01mg/kg tid with severe abdominal pain.
Body weight, blood glucose, haematocrit, total serum proteins, and serum potassium should be monitored at admission, after 2 hours of fluids and then on a daily basis in all patients that are still ill.
Remo Lobetti, BVSc, MMedVet (Med), DECVIM (Internal Medicine)
Internist, Bryanston Veterinary Hospital, Professor, Department of Companion Animal Clinical Studies, Faculty of Veterinary Science, University of Pretoria
Onderstepoort, Bryanston, South Africa