Monday 29 February 2016

CANINE PARVOVIRUS




Canine Parvovirus (CPV) infection is a relatively new disease that appeared for the first time in dogs in 1978. Because of the severity of the disease and its rapid spread through the canine population, CPV has aroused a great deal of public interest. The virus that causes this disease is very similar to feline panleukopenia (feline distemper) and the two diseases are almost identical. 

Parvo is caused by Canine Parvovirus type 2 which is a small non-enveloped single stranded DNA virus belonging to the genus Parvovirus, subfamily Parvovirinae and family the Parvoviridae family. CPV-2 replicates in dividing cells especially intestinal, lymphoid, bone marrow and fetal tissues and is severely pathogenic. This virus is known simply as canine parvovirus or CPV.
Three slightly different strains of canine parvovirus, named CPV-2a, CPV-2b and CPV-2c, are recognized. They cause the same disease and vaccines give protection against all the variants. These current variants have different antigenic structures, increased pathogenicity, and a shorter incubation period (4-5 days vs 5-8) than CPV-2. These variants also replicate efficiently in cats.

Important clinical features of the virus
Parvoviruses- resistant to inactivation; can remain infectious outside the host > 5 months.
CPV stable in the environment and is resistant to the effects of heat, detergents, alcohol, and many disinfectants.
CPV-2 hemagglutinates RBCs from a number of species so hemagglutination assays are
useful for diagnosis.

Host range and Epidemiology
Almost all Canidae are susceptible. Within domestic dog populations, Dobermans
pinschers, Rottweilers, English Springer Spaniels, American Pit bull terriers and German Shepherds are at higher risk of severe illness.
Parvo may affect dogs of all ages, but is most common in dogs less than one year of age. Young puppies less than five months of age are usually the most severely affected, and the most difficult to treat.
Age and immunity determine whether CPV infection results in myocardial disease or enteritis. Cardiac myocyte replication is sufficient enough only to support virus until 2 weeks of age. Although myocarditis is seen in pups at 6 to 8 weeks of age, it is the result of infection
several weeks earlier.
Enteritis is commonly seen in pups 6 to 16 weeks of age.
Intact male dogs seem more predisposed to infection than intact females. Unvaccinated dogs - about 13 times more likely to become infected than vaccinated dogs.
Concurrent infection with other gastrointestinal pathogens (Giardia, hookworms and
roundworms, coronavirus) may exacerbate the severity of CPV infection.
Stress of overcrowding, poor nutrition, and age at infection can dictate the outcome of infection.

Fecal-oral route: A vast amount of virus is shed in the faeces of clinically infected dogs.
However, the persistence of virus in the environment is thought to be more important than
chronic carriers in perpetuating disease – not clear if carrier state exists?
Susceptible dogs become infected by ingesting the virus. Active shedding of virus occurs up to the first 2 weeks post inoculation. Generally, dogs that recover from infection do not transmit disease to susceptible kennel mates.
Due to its stability, the virus is easily transmitted via the hair or feet of infected dogs, contaminated shoes, clothes, and other objects or areas contaminated by infected faeces.

The clinical signs and symptoms of CPV disease can vary, but generally they include severe vomiting and diarrhea. The diarrhea often has a very strong smell, may contain lots of mucus and may or may not contain blood. Additionally, affected dogs often exhibit a lack of appetite, marked listlessness and depression, and fever. It is important to note that many dogs may not show every clinical sign, but vomiting and diarrhea are the most common and consistent signs; vomiting usually begins first.

Diagnosis
The clinical signs and symptoms of CPV are variable and dependent on age, immunity, co-pathogens (parasites, enteric bacteria, viruses) and infective dose of the virus. These signs can mimic many other diseases that cause vomiting and diarrhea hence the diagnosis of CPV is often a challenge for the veterinarian.
A tentative diagnosis is often based on the presence of a reduced white blood cell count (leukopenia), clinical signs and epidemiology. The positive confirmation of CPV infection requires the demonstration of the virus or virus antigen in the stool 2-4 days after onset of disease by commercial fecal ELISA tests, or the detection of anti-CPV antibodies in the blood serum. Occasionally, a dog will have parvovirus but test negative for virus in the stool. Fortunately, this is an uncommon occurrence. If further confirmation is needed, stool or blood can be submitted to a veterinary laboratory for additional tests. The absence of a leukopenia does not mean the dog does not have CPV infection. Some dogs that become clinically ill may not have a low white blood cell count.

Treatment
There is no treatment to kill the virus once it infects the dog. However, the virus does not directly cause death; rather, it causes loss of the lining of the intestinal tract, and destroys some blood cell elements. The intestinal damage results in severe dehydration (water loss), electrolyte (sodium and potassium) imbalances, and infection in the bloodstream (septicemia and bacteremia).
The first step in treatment is to correct dehydration and electrolyte imbalances. This requires the administration of intravenous fluids containing electrolytes. Antibiotics (Cephalosporins, enrofloxicins, or combinations such as IV ampicillin and gentamicin) and anti-inflammatory drugs are given to prevent or control septicemia. Antispasmodic drugs are used to inhibit the diarrhea and vomiting that perpetuate the problems.

Survival Rate
Most dogs with CPV infection recover if aggressive treatment is used and if therapy is begun before severe septicemia and dehydration occur. Some breeds, notably the Rottweiler, Doberman pinscher and English Springer spaniel, have a much higher fatality rate than other breeds.

Prevention
The best method of protecting your dog against CPV infection is proper vaccination. Puppies receive a Parvo vaccination as part of their multiple-agent vaccine given at 6, 9 and 12 weeks of age. After the initial series of vaccinations, all dogs should be given a booster vaccination at one year. Thereafter your veterinarian will discuss with you an appropriate schedule of revaccination. Dogs in high exposure situations (i.e., kennels, dog shows, field trials, etc.) may be better protected with a booster every six months. Pregnant females might be boostered with a killed Parvo vaccine within two weeks before whelping in order to transfer protective antibodies to the puppies. Your veterinarian should make the final decision about a proper vaccination schedule.

Client Education
The stability of the CPV in the environment makes it important to properly disinfect contaminated areas.
This is best accomplished by cleaning food bowls, water bowls, and other contaminated items with a solution of 1/2 cup of chlorine bleach in a gallon of water (133 ml in 4 liters of water). It is important that chlorine bleach be used because most disinfectants, even those claiming to be effective against viruses, will not kill the canine parvovirus.

Dr. Moses Bwana
Post-grad at the University of Nairobi [Applied Microbiology]
Department of Veterinary Pathology, Microbiology and Parasitology

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