Canine Parvovirus Still Deadly, but our Knowledge of it has Grown
By Lou Anne Epperley, DVM For Veterinary Practice News
Posted: December 3, 2013, 5:00 p.m. EDT
While parvovirus’s clinical signs and treatment principles haven’t appreciably changed in recent years, our knowledge base on disease transmission and patient prognosis has vastly improved.
At the CVC veterinary conference in Kansas City in August, Stephen C. Barr, BVSc, spoke to attendees on all things parvo. Some of his key points follow.
Parvoviruses are extremely hardy, and remain infectious in the environment for more than five months. Not all disinfectant products work on parvo. Barr recommends a 1:30 bleach solution (5 percent sodium hypochlorite).
Leukocyte numbers, character help track the course of parvo
By Lou Anne Epperley, DVM
For Veterinary Practice News
The ELISA "snap” test for canine parvovirus is an efficient initial diagnostic test. Then, leukocyte counts and character can provide hints of the virus’s progress and the patient’s prognosis, according to Stephen C. Barr, BVSc, infectious disease specialist at Cornell University College of Veterinary Medicine.
Barr told veterinarians at the CVC veterinary conference in Kansas City that CPV-2 infection causes necrolysis of myeloid and erythroid stem cells in bone marrow. While red blood cell changes are slow to show up due to their long half-life, leukocyte counts will nosedive from day three to five post-infection.
Neutropenia, toxic changes in neutrophils, degenerative left shift and often absolute lymphopenia occur concurrently with the onset of clinical signs, about six days post-infection, Barr said.
"Severe, even absolute, lymphopenia is common and helps distinguish the disease from other causes of severe diarrhea, such as hemorrhagic gastroenteritis or salmonellosis.”
In recovery, leukocytosis combined with a left shift in a patient often predicts a successful treatment outcome.
It was recently reported that a white blood cell count greater than 4.5, lymphocyte count greater than 1, monocyte count greater than 0.15 and eosinophil count greater than 0.1 with a left shift are accurate prognostic indicators for recovery, he added.
Specifically, parvovirus survivors develop a left shift, usually degenerative, in neutrophils, but non-survivors don’t, Barr said. Parvo survivors show a marked rise in lymphocyte counts during the first 24 hours after admission for treatment. An increase in monocytes occurs in about three days, a change more quickly observed than an increase in polymorphonuclear cells, which takes about six days, he said.
The appearance of eosinophils bodes for a good prognosis, especially if noted beyond 48 hours after admission for treatment, Barr said.
"The progression of leukopenia can help to set a prognosis,” he said. "When band cells appear in the blood smear, the prognosis improves markedly.”
Infected dogs begin shedding the virus in feces before clinical signs appear—sometimes three days before they get sick, noted Barr, an infectious disease specialist at Cornell University College of Veterinary Medicine. Viral fecal shedding peaks about four to seven days after a dog is infected, but ceases by 12 to 14 days post-infection, and a carrier state has not been demonstrated in dogs.
Spreading the Disease
Once a dog is infected, it doesn’t show clinical signs for four to seven days. Those non-sick days are included in the two-week period where the dog can spread the virus. Therefore, Barr noted that generally, dogs that recover from infection do not transmit parvo to susceptible kennel mates. In other words, the primary route of infection is from viral particles in the environment rather than a "chronic carrier” dog, he said.
Paul Demars, DVM, small-animal community practice specialist at Oklahoma State University’s Center for Veterinary Health Sciences, said most parvo cases treated there are sent home within three to seven days.
"I have not seen any change in the mortality or length of hospitalization with parvo cases” over the past 10 years, said Demars, a diplomate of the American Board of Veterinary Practitioners. "I have not read any articles that suggest the disease is changing, even though the genetics are.”
Three parvoviruses are known to infect dogs, said Barr, a diplomate of the American College of Veterinary Internal Medicine. CPV-1, or minute virus of canines, has been associated with "fading pups.” Symptoms are lethargy, loose stools, respiratory distress and sudden death.
The second, canine adeno-associated virus, is apparently non-pathogenic, he said.
CPV-2 is the severely pathogenic and best-known parvovirus, which is closely related to feline panleukopenia, Barr said. The virus appeared in about 1977.
Current newer isolates of CPV-2 that have been widespread in the U.S. and the world since 2007 have different antigenic structures, increased pathogenicity and a shorter incubation period than the original CPV-2, said Barr, who is co-editor of the textbook "Canine and Feline Infectious Diseases and Parasitology” and wrote the chapter on canine parvovirus infection.
The virus targets puppies under 16 weeks old, with Rottweilers, Dobermans, English springer spaniels, American pit bull terriers and German shepherds at higher risk of severe illness, he said. Intact male dogs seem more predisposed to infection than intact females, and unvaccinated dogs are about 13 times more likely to get parvo than vaccinated dogs.
Parvo is well known for causing profuse vomiting and diarrhea, but it can also cause myocardial disease in very young pups. Barr said cardiac myocyte replication is sufficient enough only to support the virus until 2 weeks of age in puppies. So although myocarditis is seen in puppies at 6 to 8 weeks old, it is the result of infection several weeks earlier.
Because so many bitches in the U.S. have been immunized for parvo, conferring passive immunity to neonatal pups, Barr said myocardial disease is rarely seen in this country.
Commercial fecal ELISA tests for parvo appear to be highly specific and sensitive at detecting virus in the stool for two to four days after onset of the disease, Barr said. However, blood in the stool can cause a false negative test due to antibody binding virus in the stool.
Even though an apparent breakdown in vaccine efficacy against CPV-2c virus was reported in a kennel of dogs from Italy, Barr said experimental evidence in the U.S. and UK suggests that current vaccines against CPV-2b and CPV-2 protect against CPV-2c. Specifically, Barr cited these modified live vaccines: for CPV-2b, Galaxy DA2PPv (Schering-Plough Animal Health); for CPV-2, Continuum DAP (Intervet).
OSU’s Demars concurs.
"With the change in vaccination in the 1990s to a less-attenuated strain with more virus particles in each dose, I have not perceived any lack of efficacy of the vaccine,” he said. "The ‘window period’ issue of the older vaccines has been virtually solved by this change.”
Demars recommends starting parvo vaccinations at 6 to 8 weeks of age and boostering every three to four weeks until a puppy is past 16 weeks of age. He administers a booster vaccination at the first annual wellness visit, and every three years afterwards.
While annual dosing of core vaccines—parvo, distemper and adenovirus-2—is a common practice among veterinarians, American Animal Hospital Association guidelines recommend administering a single dose of a combination vaccine every three years or longer, once the initial series is completed.
Parvo treatment still remains supportive, Demars said.
"Keeping the patient hydrated, treating the bacterial translocation due to the damage to the intestinal epithelium and immune system, keeping their oncotic pressure normalized, controlling vomiting, controlling discomfort, and getting them back on oral nutrition as soon as possible are key components to successful treatment.”
Anti-emetics favored by Barr are metoclopramide and prochlorperazine. He said the serotonin receptor antagonists odansetron and dolastron are also very effective. Once vomiting has stopped, sucralfate, famotidine or even Pepto-Bismol may be given orally as gastric protectants, he said.
Successful parvo immunization hinges on puppy vaccinations
By Lou Anne Epperley, DVM
For Veterinary Practice News
If a dog is to be immunized against canine parvovirus, it needs a modified-live vaccine at 8 weeks, 12 weeks and 16 weeks of age, followed by a single dose not later than one year following the last dose in the initial series, says Richard B. Ford, DVM, MS, a co-author of vaccination recommendations by the American Animal Hospital Association.
Whether dogs need an annual parvovirus vaccination beyond that foundation series is debated among veterinarians.
"For the canine population at large, annual vaccination for distemper, parvovirus and adenovirus-2 is, in a word, unnecessary,” Dr. Ford said. "What we’ve actually been doing for many years is administering vaccines to healthy, previously vaccinated dogs that already have protective levels of circulating antibody to each of these viruses.”
Ford, emeritus professor of medicine at North Carolina State University College of Veterinary Medicine, is a diplomate of the American College of Veterinary Internal Medicine and an honorary diplomate of the American College of Veterinary Preventive Medicine.
"Administering more vaccine annually simply culminates in vaccine interference by existing antibody, in the same way maternal antibody interferes,” he explained. "’Boosting’ titers, which by definition means a fourfold increase in titer, seldom occurs when administering core vaccines annually.”
Robust immune "memory”—not just antibody—results from administration of the initial vaccine series, he emphasized. That "memory” to the antigens persists for at least seven years, and may even last for the patient’s lifetime.
"Even if antibody levels do decline, memory is still present, working in the background,” Ford said. "If the seronegative, previously vaccinated patient is exposed to, say, parvovirus, the memory cells (B lymphocytes) immediately begin producing antibody, in essence, boosting the patient’s immunity. That’s why we don’t see older dogs with distemper, parvovirus or viral hepatitis (adenovirus), even among unvaccinated populations. "
Ford said dogs who have lived long enough to be considered "geriatric” have likely either been previously vaccinated or have been infected and therefore immunized.
With respect to disproportionately high numbers of parvo cases among Rottweilers, Doberman pinschers, English springer spaniels, American pit bull terriers and German shepherds, Ford said it is important to recognize that failure to respond to parvovirus vaccination is not uniquely breed-determined.
"There are, in fact, a number of reasons that dogs of any breed may appear not to respond to vaccination and, therefore, become susceptible to disease if exposed,” he said. "Interference from maternally-derived antibody is certainly the most common reason, especially when the initial series of juvenile ‘puppy’ vaccines is discontinued at 12 weeks of age.”
Ford said some dogs, both mixed-breed and purebred, may be genetic non-responders or low-responders to vaccination.
"Today, it can be assumed that about one in 1,000 dogs don’t respond to parvovirus vaccine, at least initially,” he continued.
"They may respond later in life, if they survive an exposure and infection. It has been estimated that approximately one in 5,000 dogs are genetic non-responders when it comes to canine distemper vaccination; not surprising when, as we all know, no vaccine is ever considered to be 100 percent efficacious.”
Ford said administering more vaccine, more frequently, to a genetic non-responder is not expected to provoke an immune response. Rather, continued vaccination of such a dog would be justified on the basis that its immune system might eventually recognize the parvovirus vaccine antigens and respond.
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Canine Parvovirus Still Deadly, but our Knowledge of it has Grown
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