Published Clinical Studies
View and download clinical studies to stay up-to-date and educated on the efficacy of Nobivac vaccines.
Groups of 15 laboratory-bred beagles were vaccinated and boosted with either a placebo or adjuvanted bivalent bacterin comprised of a traditional Borrelia burgdorferi strain and a unique ospA- and ospB-negative B. burgdorferi strain that expressed high levels of OspC and then challenged with B. burgdorferi-infected Ixodes scapularis ticks. The vaccinated dogs produced high titers of anti-OspA and anti-OspC borreliacidal antibodies, including borreliacidal antibodies specific for an epitope within the last seven amino acids at the OspC carboxy terminus (termed OspC7) that was conserved among pathogenic Borrelia genospecies. In addition, spirochetes were eliminated from the infected ticks that fed on the bacterin recipients, B. burgdorferi was not isolated from the skin or joints, and antibody responses associated specifically with canine infection with B. burgdorferi were not produced. In contrast, B. burgdorferi was recovered from engorged ticks that fed on 13 (87%) placebovaccinated dogs (P < 0.0001), skin biopsy specimens from 14 (93%) dogs (P < 0.0001), and joint tissue specimens from 8 (53%) dogs (J’ = 0.0022). In addition, 14 (93%) dogs developed specific antibody responses against B. burgdorferi proteins, including 11 (73%) with C6 peptide antibodies (P < 0.0001). Moreover, 10 (67%) dogs developed Lyme disease-associated joint abnormalities (P < 0.0001), including 4 (27%) dogs that developed joint stiffness or lameness and 6 (40%) that developed chronic joint inflammation (synovitis). The results therefore confirmed that the bacterin provided a high level of protection against Lyme disease shortly after immunization.
CIRDC refers to a contagious cough caused by one or more viral or bacterial pathogens. Laymen often refer to CIRDC as “kennel cough” because of its frequent association with dogs that have been recently housed in kennels or shelters. These settings allow for physical proximity of animals (which facilitates contagion spread) and contribute to disease susceptibility and morbidity in other ways, too. Difficulties associated with sanitation in large groups of dogs, poor air quality, the continual exposure to new animals with additional new pathogens, and the stress associated with kenneling cannot be overestimated as a proximate factor in CIRDC. In fact, potentially pathogenic microbes that often cause subclinical infection or very mild illness in well-acclimated, laboratory-raised dogs can cause severe disease in dogs exposed in less favorable settings.
Healthy dogs with low antibody titer to Bordetella bronchiseptica were vacci-nated intranasally with an avirulent live vaccine, subcutaneously with an antigen extract vaccine, or subcutaneously and intranasally with a placebo. Intranasally vaccinated dogs developed B. bronchiseptica–specific IgA titers in nasal secre-tions that remained at high levels until the end of the study; dogs vaccinated subcutaneously with the antigen extract or placebo did not develop measurable antigen-specific IgA titers in nasal secretions. Dogs were challenged with viru-lent live B. bronchiseptica 63 days after vaccination. Intranasally vaccinated dogs had significantly lower cough scores (P ≤ .0058) and shed significantly fewer challenge organisms (P < .0001) than dogs in either of the other groups. Cough scores of subcutaneously vaccinated dogs were not significantly differ-ent from placebo-vaccinated dogs.
The purpose of this study was to compare the efficacy of two commercially available feline leukemia vaccines, NobivacFeline 2-FeLV (inactivated whole virus vaccine) and PureVax Recombinant FeLV (live canarypox virus-vectored vaccine) following challenge with virulent feline leukemia virus.
Three groups of healthy dogs with low antibody titers to Bordetella bronchisepti-ca (Bb), canine parainfluenza virus (CPI), and canine adenovirus type 2 (CAV-2) were used in this study. One group was vaccinated with a single dose of mono-valent attenuated Bb vaccine and one group with a trivalent vaccine containing attenuated Bb, CPI, and CAV-2; dogs were vaccinated intranasally with a single dose of the respective vaccines. The third group served as unvaccinated controls. All vaccinated dogs subsequently developed serum antibody titers to Bb that per-sisted for at least 1 year. Following Bb challenge 1 year after vaccination, all vac-cinated dogs, regardless of group, showed significantly fewer clinical signs and shed significantly fewer challenge organisms than unvaccinated controls. These results demonstrate that intranasal administration of a single dose of monovalent attenuated Bb vaccine or trivalent vaccine containing attenuated Bb, CPI, and CAV-2 provides 1 year of protection against Bb.
Leptospirosis, a zoonotic disease of worldwide significance, is caused by spirochetes of the genus Leptospira. Leptospirosis has been thought to most commonly affect young-adult, large-breed, outdoor dogs; however, small dogs in urban areas can also contract the disease. Pathogenic serovars infecting dogs include icterohaemorrhagiae, canicola, pomona, bratislava, grippotyphosa and autumnalis. Although serovar identification is of interest from an epidemiologic stand point, clinical disease is similar for all serovars and treatment is the same. Therefore, determining whether a dog has leptospirosis is much more important than identification of which specific serovar is involved.
Revention of Disease and Mortality in Vaccinated Dogs Following Experimental Challenge With Virulent Leptospira.
R LaFleur, J Dant, T Wasmoen. Intervet / Schering Plough Animal Health, Elkhorn, NE.
Canine Leptospirosis can vary from subclinical infection to illness that ranges from mild to severe, including death, depending on the susceptibility of the dog, virulence of the organism, and route and degree of infection. The objective of this study was to evaluate the ability of a canine Leptospira bacterin to prevent infection and disease following challenge with virulent Leptospira canicola, L. pomona, L. grippotyphosa, or L. icterohaemorrhagiae. Groups of 8-week-old beagles were vaccinated (day 0) and boosted (day 21) with placebo (n = 10) or the 4-way bacterin (n ≥ 20) and subsequently challenged with each serovar. The results demonstrated that blood and various tissue samples from placebo-recipients became reliably infected, and the dogs developed typical clinical signs of Leptospirosis including loss of appetite, ocular congestion, depression, dehydration, jaundice, hematuria, melena, vomiting, petechiae, and death. In addition, placebo-recipients developed kidney and liver dysfunction. In contrast, some vaccine-recipients became infected, but the organisms were cleared quickly from the blood. Vaccinated dogs failed to develop severe clinical disease requiring medical intervention, and no animals died (p > 0.001). A few of the vaccinated dogs developed clinical abnormalities, but the clinical signs remained mild and were self-limiting (p < 0.0001 for each serovar). Administration of the bacterin also prevented thrombocytopenia (p < 0.0001), kidney complications caused by L. canicola (p < 0.0001), L. icterohaemorrhagiae (p < 0.0001), and L. pomona (p = 0.012), and liver dysfunction caused by L. pomona (p < 0.0001) and L. grippotyphosa (p < 0.0001). The results therefore confirmed that vaccinating dogs with the 4-way Leptospira bacterin provided a high degree of protection (99.5%-100%) against the clinical signs of Leptospirosis including mortality.
Three groups (n = 9 or 10) of 12-week-old canine parvovirus type 2 (CPV-2) antibody–negative puppies were vaccinated: one group with a product con-taining modified-live CPV-2b (Galaxy DA2PPv; Schering-Plough Animal Health), one group with a product containing modified-live CPV-2 (Continuum DAP, Intervet), and one group (controls) with sterile saline. All puppies receiv-ing CPV-2 and CPV-2b vaccines developed antibody as determined by the hemagglutination inhibition assay. All groups of puppies were challenged with a combination of virulent CPV-2b and CPV-2c 5 weeks after vaccination. All puppies in the CPV-2 and CPV-2b vaccinated groups were protected from dis-ease, whereas all control group puppies developed disease and 50% died or were euthanized. This study demonstrated that the CPV-2 and CPV-2b vac-cine components of the Continuum DAP and Galaxy DA2PPv products, re-spectively, provided protection against the CPV-2b virus and also provided complete protection against the new CPV-2c variant.
Since ﬁrst emerging in the North American canine population in 2004, canine inﬂuenza virus (CIV) subtype H3N8 has shown horizontal transmission among dogs, with a high level of adaptation to this species. The severity of disease is variable, and coinfection by other respiratory pathogens is an important factor in the degree of morbidity and mortality. The ﬁrst inﬂuenza vaccine for dogs, an inactivated vaccine containing CIV subtype H3N8, was conditionally approved by the U.S. Department of Agriculture (USDA) for licensure in May 2009 and fully licensed in June 2010. This study evaluates the efﬁcacy of this vaccine to reduce the severity of illness in dogs cochallenged with virulent CIV and Streptococcus equi subsp. zooepidemicus.
To examine the effectiveness of canine influenza vaccination to reduce pulmonary lesions in dogs co-challenged with CIV and S. equi subsp. zooepidemicus. In this study, four groups of 7- to 10-week-old, CIV-naive beagles (32 dogs total) were used. One group was vaccinated with CIV vaccine (group 4) and the remaining 3 groups (groups 1, 2 and 3) were not vaccinated. Group 1was challenged with CIV, group 2 was challenged with S. equi subsp. zooepidemicus and groups 3 and 4 were co-challenged with CIV and S. equi subsp. zooepidemicus. Following challenge, histopathological lung lesion scores were most severe in non-vaccinated dogs co-challenged with CIV combined with S. equi subsp. zooepidemicus. Dogs challenged with CIV alone had mild to severe histopathological lung lesion scores and dogs challenged with S. equi subsp. zooepidemicus alone developed little or no histopathological lung lesion scores. Histopathological lung lesion scores were markedly diminished in dogs vaccinated with CIV vaccine and then co-challenged. The findings confirm the results of previous studies indicating that CIV can cause respiratory disease, leading to severe bronchointerstitial pneumonia and the disease is exacerbated following secondary bacterial co-infection. Importantly, vaccination of dogs with CIV vaccine significantly reduces the severity of disease caused by this viral-bacterial co-infection.
Canine influenza virus (CIV) subtype H3N8 is an emerging pathogen with sustained horizontal transmission in the dog population in the United States. This study evaluated the efficacy of an inactivated CIV vaccine in 6- to 8-week-old beagle pups challenged with virulent CIV. One group of CIV-seronegative pups was vaccinated with two doses of a CIV vaccine 3 weeks apart; a second group of pups received adjuvanted placebo as a control. Blood samples were collected at various times to determine antibody titers. All pups were challenged with a virulent CIV isolate 13 days after the second vaccination and monitored for clinical signs of respiratory disease, virus shedding, and lung consolidation. Vaccinated pups developed hemagglutination inhibition antibody titers after vaccination. The severity of clinical signs (P < .001) and the magnitude and duration of virus shedding (P < .0001) were significantly lower in vaccinated pups compared with control pups. These results demonstrate that the CIV vaccine used in this study provides protection against virulent CIV challenge in dogs.
Canine influenza virus (CIV) subtype H3N8 has emerged as a new pathogen with sustained transmission in the dog population in the United States. In this study, we report the experimental induction of respiratory disease in dogs using three CIV field isolates. Young (14 to 15 weeks of age) CIV-seronegative pups were challenged with one of three CIV isolates and monitored for clinical signs of respiratory disease, nasal virus shedding, seroconversion, lung lesions, and virus isolation from the lower respiratory tract. The challenged pups developed clinical signs and lung lesions typical of influenza virus infection, shed virus in their nasal secretions for 7 to 8 days after challenge, and exhibited serum antibodies at 7 and 14 days after challenge. Lung tissues and tracheal swabs collected at 3 and 6 days after challenge exhibited active virus replication. These results demon-strate that CIV causes respiratory disease in dogs.
Twenty young adult specific pathogen-free cats were randomly divided into two groups of 10 animals each. One group was vaccinated with two doses of feline leukemia virus vaccine according to the manufacturer’s recommendations. All 20 cats were challenge exposed oronasally (4 times over a I-week period), beginning 3 weeks after immunization, with a virulent subgroup A strain of FeLV (CT600-FeLV). The severity of the FeL V infection was enhanced by treating the cats with methylprednisolone acetate at the time of the last FeL V exposure. Ten of 10 non vaccinated cats became persistently viremic compared with 0/10 of the vaccinates. ELISA antibodies to whole FeLV were present at high concentrations after immunization in all of the vaccinated cats, and there was no observable anamnestic antibody response after challenge exposure. ELISA antibodies to whole FeL V appeared at low concentrations in the serum of nonvaccinated cats after infection but disappeared as the viremia became permanently established. Virus neutralizing antibodies were detected in 3 /10 vaccinates and O /10 non vaccinates immediately before FeLV challenge exposure, and in 8/10 vaccinates and 1/10 nonvaccinates 5 weeks later. Although vaccination did not consistently evoke virus neutralizing antibodies, it appeared to immunologically prime cats for a virus-neutralizing antibody response afterinfection. Active FeL V infection was detected in bone marrow cells taken 14 weeks after infection from 10/10 nonvaccinates and 0/10 vaccinates. Latent FeLV infection was not detected in bone marrow cells from any of the vaccinated cats 14 weeks after challenge exposure. (Journal of Veterinary Internal Medicine 1993; 7:34-39)
Laboratory-reared beagles were vaccinated with a placebo or a bacterin comprised of Borrelia burgdorferi S-1-10 and ospA-negative/ospB-negative B. burgdorferi 50772 and challenged after 1 year with B. burgdorferiinfectedlxodes scapu/aris ticks. For the placebo recipients, spirochetes were recovered from 9 (60%) skin biopsy specimens collected after 1 month, and the organisms persisted in the skin thereafter. Ten (67%) dogs also developed joint infection (3 dogs), lameness or synovitis (7 dogs), or B. burgdorferi-specifi.c antibodies (8 dogs). For the vaccine recipients, spirochetes were recovered from 6 (40%) skin biopsy specimens collected after 1 month. However, subsequent biopsy specimens were negative, and the dogs failed to develop joint infection (P = 0.224), lameness/synovitis (P = 0.006), or Lyme disease-specific antibody responses (P = 0.002). The bacterin provided a high level of protection for 1 year after immunization, and the addition of the OspCproducing B. burgdorferi 50772 provided enhanced protection.
Canine infectious respiratory disease complex (CIRDC) is a common disease complex caused by many different viruses and bacteria, including Bordetella bronchiseptica, Mycoplasma cynos, adenovirus type 2, distemper, influenza A virus, parainfluenza virus, pneumovirus and respiratory coronavirus. In March 2015, veterinarians in the Chicago area noted an increase in incidence of signs of canine infectious respiratory disease in dogs. Nasal and pharyngeal swabs from dogs showing clinical signs were submitted to the Cornell University Animal Health Diagnostic Center (AHDC). A canine respiratory polymerase chain reaction (PCR) screening panel was utilized which allows identification of the following CIRDC pathogens: B. bronchiseptica, Mycoplasma cynos, adenovirus type 2, distemper, influenza A, parainfluenza virus, pneumovirus and respiratory coronavirus.
An inactivated virus vaccine was developed J or prevention of FeL V infection in domestic cats. When given in 2 doses, 3 weeks apart, to cats that were ‘2:9 weeks old at the time of first vaccination, the vaccine prevented persistent viremia from developing in 132 of 144 (92%) vaccinates after oronasal challenge exposure with virulent FeL V. In contrast, persistent viremia developed after oronasal challenge exposure with FeLV in 39 of 45 (87%) age-matched nonvaccinated control cats. Transient viremia, indicated by early detection of p27 by ELISA in serum of cats protected from persistent viremia at 12 weeks after challenge exposure, was found in 10 of 132 (8%) vaccinates. Cats that were aviremic 12 to 16 weeks after challenge exposure were examined for reactivation of latent FeLV infection; 4 weekly doses of methylprednisolone were administered, followed by in vitro culture of bone marrow cells. Latent infection was readily reactivated in 6 of 8 (75%) nonvaccinated control cats that had been transiently viremic after challenge exposure. However, latent infection was reactivated in only 5 of 48 (10%) protected vaccinates, and in none of 38 vaccinates in which transient viremia had not been detected. ln a safety field trial, only 34 mild reactions of short duration were observed after administration of 2,379 doses of vaccine to cats of various ages, breeds, and vaccination history, for a 1. 4 3% reaction rate. Results indicate that the aforementioned inactivated virus vaccine is safe and efficacious for the prevention of infection with FeLV.
A challenge-of-immunity study was conducted to demonstrate immunity in dogs 3 years after their second vaccination with a new multivalent, modified-live vaccine containing canine adenovirus type-2, canine parvovirus (CPV), and ca-nine distemper virus (CDV). Twenty-three seronegative pups were vaccinated at 7 and 11 weeks of age. Eighteen seronegative pups, randomized into groups of six dogs, served as challenge controls. Dogs were kept in strict isolation for 3 years following the last vaccination and then challenged sequentially with viru-lent canine adenovirus type-1 (CAV-1), CPV, and CDV. For each viral challenge, a separate group of six control dogs was also challenged. Clinical signs of CAV-1, CPV, and CDV infections were prevented in 100% of vaccinated dogs, demonstrating that the multivalent, modified-live test vaccine provided protec-tion against virulent CAV-1, CPV, and CDV challenge in dogs 7 weeks of age or older for a minimum of 3 years following second vaccination.
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