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Biomedical subjects

R V Pollock

Publications and source records attributed to R V Pollock.

At least 19 recordsLinked to original sources

Source of acquisition as a risk factor for disease and death in pups.

Data were obtained and analyzed for 2,144 pups examined at 65 veterinary hospitals in the northeastern United States to determine whether there were significant differences in the frequency of disease and death among pups acquired from private owners, Societies for the Prevention of Cruelty to Animals/pounds, breeders, or pet stores. All health problems reported by owners and veterinarians in the first 2 weeks of ownership were tabulated. The prevalence of serious disease among pups (resulting in death, euthanasia, return, or extensive treatment) was < 4% for all sources and did not differ significantly between pet stores and other sources. Pups from pet stores had more respiratory tract disease, but fewer fleas and parasites of the intestinal tract. Data supplied by the veterinarians indicated that the risk of intestinal tract diseases was significantly (P < or = 0.01) higher among pups from pet stores and Societies for the Prevention of Cruelty to Animals/pounds, compared with those from private owners. The prevalence of reported behavioral and congenital problems did not differ among the 4 sources.

Animals

Canine parvovirus.

Canine parvovirus is a truly new pathogen of dogs that emerged in the late 1970s. Initially seen as epidemic disease in all dogs, parvoviral enteritis is now primarily a disease of 1- to 6-month-old dogs. Maternal antibody interference with immunization accounts for the vast majority of vaccine "breaks." Molecular virologic methods have revealed continued evolution of the virus, but this appears to be of greater academic than practical interest. Clinical diagnosis can be definitive in fulminant cases but requires laboratory support--usually demonstration of virus in the feces--in less clear-cut cases. Treatment remains symptomatic, based simply on principles of good supportive care. As the virus is firmly entrenched in both the wild and domestic canine population, elimination of the virus is impossible, and CPV-2 will remain a concern for the small animal practitioner indefinitely.

Animals

Long-term follow-up study of cats vaccinated with a temperature-sensitive feline infectious peritonitis vaccine.

The long-term safety of a temperature-sensitive feline infectious peritonitis (FIP) vaccine was evaluated. Five hundred eighty-two healthy cats of various age groups were vaccinated with 2 doses of the vaccine. Seventy-eight percent, or 453 cats, were available for follow-up. The mean follow-up period was 541 days. At the end of the follow-up period, 427 cats (94%) were alive. FIP was not diagnosed in any cat during the follow-up period, but 1 cat died of FIP after completion of the follow-up period. Fifty cats (11%) presented with a problem during the follow-up period, but there were typical of those seen in a feline practice. The temperature-sensitive FIP vaccine appears to be safe for use in the general cat population. It does not appear to sensitize cats to develop FIP, nor do there appear to be any other systemic problems associated with use of the vaccine.

Administration, Intranasal

Year two of follow-up evaluation of a randomized, blind field trial of a commercial feline leukemia virus vaccine.

A blind randomized field trial of a commercial FeLV vaccine was conducted. Cats on study were vaccinated with either a commercial FeLV vaccine or a placebo, then housed with FeLV-positive cats in a ratio of approximately 2 study cats to 1 infected cat (results of the first 12 months of the study have been reported). All surviving placebo-treated and FeLV-vaccinated cats were re-vaccinated 1 year after initial exposure to FeLV-infected cats. Exposure continued for an additional 12 months, and the viremia status of the cats was monitored by immunofluorescent antibody (IFA) and ELISA testing at 4-month intervals. During the second year of observation, 1 additional FeLV-vaccinated cat had positive results of 2 consecutive ELISA tests, but remained IFA negative. Classifying this cat as persistently viremic reduced the estimate of the preventable fraction, but did not alter the conclusions drawn earlier, viz, that vaccination appreciably reduces the number of cats that become persistently viremic after long-term natural exposure.

Animals

Evaluation of three techniques to demonstrate retrograde transport of horseradish peroxidase.

Three methods of tracing neural connections by the use of horseradish peroxidase (HRP) were evaluated: (1) endoneurium injection, (2) injection followed by crushing at site of injection, and (3) nerve transection followed by capping of the proximal stump with a silicone cylinder containing HRP. The capping technique resulted in increased uptake and more uniform distribution of HRP in the nerves under study.

Animals

Randomized blind trial of a commercial FeLV vaccine.

A randomized blind trial of a commercial FeLV vaccine was conducted to evaluate its performance in cats under conditions of long-term natural exposure. Seventy-nine nonviremic, seronegative cats were randomized into 2 groups. Cats were given 3 doses of either FeLV vaccine or placebo (killed rabies virus vaccine) sc at weeks 0, 3, and 9 of the trial. Six weeks later, 44 known-viremic cats were added to the colony. Cats were housed in a single large room and food dishes and litter pans were used in common. Blood samples were collected at 4, 8, and 12 months after the addition of the viremic cats and were assayed for viremia by use of ELISA. Twelve-month samples were also assayed independently by use of indirect fluorescent antibody testing. Investigators conducted assays on coded samples without knowledge of the cat's vaccination status; neither the investigators nor colony personnel knew which cats had been given the FeLV vaccine and which had been given the placebo until the twelfth month of exposure. After 12 months of cohabitation with infected cats, vaccinated cats had a significantly (P less than or equal to 0.02) lower incidence of persistent viremia (defined as 2 positive ELISA test results at least 8 weeks apart or 1 positive indirect fluorescent antibody test result), compared with the placebo-inoculated cats. The incidence of persistent viremia was approximately 3 times greater among the placebo-inoculated cats than among vaccinates.

Animals

Sensitivity, specificity, and predictive values of ClinEase-Virastat saliva test for feline leukemia virus infection.

Detection of virus in saliva using a commercial enzyme-linked immunosorbent assay (ELISA), ClinEase-VirastatR, was compared to evidence of FeLV infection by the indirect immunofluorescent antibody assay (IFA) and plasma ELISA. The sensitivity and specificity of the saliva ELISA were derived by comparison to IFA and plasma ELISA in 103 cats from a large colony in New York State. The sensitivity of the saliva test in relation to IFA and plasma ELISA was approximately 100% and 93%, respectively. The specificity of the saliva ELISA in relation to IFA and plasma ELISA was approximately 85% and 92%, respectively. This test appears to be particularly suitable as a screening test for FeLV infection, especially in populations where the expected prevalence is low. Because of its high sensitivity, the saliva test has a high negative predictive value, particularly in populations where the disease is rare. Since the specificity is moderate, however, the predictive value of a positive test will be poorest in cats originating from places where the infection is rare (e.g. single cat households, or free roaming cats), and better among cats from environments having a high prevalence of FeLV (e.g. multiple-cat households).

Animals

Esophageal, gastric, and intestinal disorders of young dogs and cats.

Digestive tract disorders are common diagnostic and therapeutic problems among young dogs and cats. Prompt and effective symptomatic therapy is necessary in all cases, and is sufficient in many. Parasitic and protozoal problems require attention to kennel management as well as to individual treatment. Chronic and congenital disorders are often extremely challenging diagnostic dilemmas.

Animals

Response of puppies to canine-origin parvovirus vaccines.

Pups 9-18 1/2 weeks old were given a single dose of 1 of 4 commercial, live, canine-origin parvovirus vaccines. All 4 vaccines evoked high levels of antibody in seronegative pups, but variable response in those with low levels of maternally derived antibodies. Vaccinal virus spread to unvaccinated contact controls and elicited essentially equivalent titers. No clinical signs of parvovirus infection were observed in vaccinates or controls.

Animals

Canine viral enteritis.

Canine viral enteritis should be suspected in dogs with an acute onset of vomiting and diarrhea, especially in puppies and where several animals are affected simultaneously. Definitive diagnosis requires laboratory confirmation, most often detection of viral particles in the stool. No diagnostic test is entirely specific or absolutely sensitive, however, and laboratory findings should be weighed accordingly. Immunization is the key to successful control. Effective vaccines for canine parvovirus are available. Maternal antibody suppresses response to vaccination in young pups and is the major problem in the control of infection. Vaccines against canine rotavirus and coronavirus are not available. The need for such vaccines and the feasibility of their effective use have not yet been clearly demonstrated.

Animals

Use of modified live feline panleukopenia virus vaccine to immunize dogs against canine parvovirus.

Modified live feline panleukopenia virus (FPLV) vaccine protected dogs against canine parvovirus (CPV) infection. However, unlike the long-lived (greater than or equal to 20-month) immunity engendered by CPV infection, the response of dogs to living FPLV was variable. Doses of FPLV (snow leopard strain) in excess of 10(5.7) TCID50 were necessary for uniform immunization; smaller inocula resulted in decreased success rates. The duration of immunity, as measured by the persistence of hemagglutination-inhibiting antibody, was related to the magnitude of the initial response to vaccination; dogs with vigorous initial responses resisted oronasal CPV challenge exposure 6 months after vaccination, and hemagglutination-inhibiting antibodies persisted in such dogs for greater than 1 year. Limited replication of FPLV in dogs was demonstrated, but unlike CPV, the feline virus did not spread to contact dogs or cats. Adverse reactions were not associated with living FPLV vaccination, and FPLV did not interfere with simultaneous response to attenuated canine distemper virus.

Animals

A modified live canine parvovirus vaccine. II. Immune response.

The safety and efficacy of an attenuated canine parvovirus (A-CPV) vaccine was evaluated in both experimental and in field dogs. After parenteral vaccination, seronegative dogs developed hemagglutination-inhibition (HI) antibody titers as early as postvaccination (PV) day 2. Maximal titers occurred within 1 week. Immunity was associated with the persistence of HI antibody titers (titers greater than 80) that endured at least 2 years. Immune dogs challenged with virulent CPV did not shed virus in their feces. The A-CPV vaccine did not cause illness alone or in combination with living canine distemper (CD) and canine adenovirus type-2 (CAV-2) vaccines, nor did it interfere with the immune response to the other viruses. A high rate (greater than 98%) of immunity was engendered in seronegative pups. In contrast, maternal antibody interfered with the active immune response to the A-CPV. More than 95% of the dogs with HI titers less than 10 responded to the vaccine, but only 50% responded when titers were approximately 20. No animal with a titer greater than 80 at the time of vaccination became actively immunized. Susceptibility to virulent CPV during that period when maternal antibody no longer protects against infection, but still prevents active immunization, is the principal cause of vaccinal failure in breeding kennels where CPV is present. Reduction, but not complete elimination, of CPV disease in large breeding kennels occurred within 1-2 months of instituting an A-CPV vaccination program.

Animals

Maternally derived immunity to canine parvovirus infection: transfer, decline, and interference with vaccination.

Antibody to canine parvovirus (CPV) was transferred from an immune bitch to her pups through the placenta and colostrum. Colostral transfer accounted for approximately 90% of the maternally-derived CPV antibody. After suckling, pups and hemagglutination-inhibition titers that averaged 50% of their dam's titer. Maternally derived CPV antibody declined with a half-life of 9.7 days. Pups with hemagglutination-inhibition titers greater than or equal to 1:80 were immune to oronasal challenge with virulent CPV, but any detectable hemagglutination-inhibition antibody (titer greater than or equal to 1:10) interfered with active immunization by modified-liver feline panleukopenia virus, inactivated feline panleukopenia virus, or inactivated CPV vaccines.

Animals

Experimental canine parvovirus infection in dogs.

In specific pathogen-free dogs, clinical signs of experimental canine parvovirus infection were mild, inconsistent and transient. Clinical signs were more pronounced in conventionally-raised dogs, but the severe disease reported in field cases was not reproduced in either group. A pronounced plasma viremia occurred on the 2nd to 4th day post-infection (d.p.i.) in dogs challenged oronasally. Antibody was detectable on the 5th d.p.i. Marked pyrexia was rare, but a significant temperature rise usually coincided with the appearance of antibody and the cessation of viremia. Significant lymphopenia, but not leukopenia, occurred on the 3rd to 7th d.p.i. Virus could be readily isolated from fecal matter on the 3rd to 8th d.p.i.; a few dogs continued to shed virus for up to 12 days. In dogs challenged parenterally, the onset of elevated temperatures, viral shed and antibody production occurred 24-48 hours sooner. Convalescent dogs were no longer contagious for susceptible contact animals 25 days or longer after challenge, although infectious virus persisted in feces for more than 6 months at room temperature. Active giardiasis seemed to exacerbate the clinical syndrome, although treatment with corticosteroids or anti-thymocyte serum did not.

Animals

Dog response to inactivated canine parvovirus and feline panleukopenia virus vaccines.

Inactivated canine parvovirus (CPV) and inactivated feline panleukopenia virus (FPV) vaccines were evaluated in dogs. Maximal serologic response occurred within 1-2 weeks after vaccination. Antibody titers then declined rapidly to low levels that persisted at least 20 weeks. Immunity to CPV, defined as complete resistance to infection, was correlated with serum antibody titer and did not persist longer than 6 weeks after vaccination with inactivated virus. However, protection against generalized infection was demonstrated 20 weeks after vaccination. In unvaccinated dogs, viremia and generalized infection occurred after oronasal challenge with virulent CPV. In contrast, viral replication was restricted to the intestinal tract and gut-associated lymphoid tissue of vaccinated dogs. Canine parvovirus was inactivated by formalin, beta-propiolactone (BPL), and binary ethylenimine (BEI) in serum-free media; inactivation kinetics were determined. Formalin resulted in a greater loss of viral HA than either BEI of BPL, and antigenicity was correspondingly reduced.

Animals

A modified live canine parvovirus strain with novel plaque characteristics. I. Viral attenuation and dog response.

A canine parvovirus (CPV) strain (C-780916) was found attenuated for pups at 80, but not after 51 serial passages in dog kidney cell (DKC) cultures. A variant viral population ('large plaque') emerged after prolonged cultivation in DKC cultures that may be associated with reduced native virulence. Dogs vaccinated with modified CPV developed high hemagglutination-inhibiting (HI) antibody titers within 4 days of incoluation and antibody persisted. Vaccinated animals shed small amounts of virus in the feces that spread to contact dogs. After five back-passages in dogs the modified strain was not pathogenic for pups and the plaque characteristics of the virus isolated from the feces were typical of the attenuated strain. The modified live CPV did not cause infection of the fetus when inoculated parenterally into pregnant bitches at various stages of gestation. It was not pathogenic for neonatal pups. These results suggest that a safe and effective live homologous (CPV) vaccine has been developed which should aid substantially in controlling CPV infection.

Animals