Experimental infection of dogs with Brucella abortus

Thirteen female dogs, which included eight principals that were fed approximately 4.4 X 10(10) colony forming units (cfu) of Brucella abortus strain 2308 and five sentinels that were housed with the principals, were examined for serologic responses, blood culture, tissue distribution of the organisms and pathologic lesions. Serum samples from each dog were tested on the day of exposure and on post exposure days 5, 7, 10, 14, 21, 28, 35, 42 and 49 for antibodies to B. abortus, using the brucellosis card (BC), standard tube agglutination (STA), 2-mercaptoethanol (ME) and rivanol (RIV) tests. Antibodies were detected in the principals by day 5 and increased through day 21. The STA test was the first to become positive, followed by the BC, ME and RIV tests. After 28 days, the serologic titers receded. From day 14 through day 42, all principals had greater than or equal to 1:50 STA titers. On day 49, seven principals had greater than or equal to 1:50 STA titers and one had a 1:25 STA titer. The sentinels were negative for all tests, except sentinel number 9 which had STA titers ranging from 1:25 to 1:50 on day 14 through day 35. Blood cultures that were obtained from each principal at intervals from one hour after exposure through 49 days were negative. Brucella abortus was isolated from various lymph nodes of the eight principals and from sentinel number 9, which was apparently infected by ingesting brucellae contaminated feces from the principals. Microscopic lesions were not observed in the culture-positive tissues examined.     

Experimental infection of dogs with Campylobacter jejuni

Three groups of conventional puppies were inoculated orally with Campylobacter jejuni biotype 2 which had been isolated from the small intestine of a dog with enteritis. Mild enteric disease was observed in one group. There was superficial intestinal colonization by the organism but penetration of intestinal epithelial cells was not apparent. C jejuni was isolated from the blood and viscera of inoculated dogs which showed no histological evidence of disease.     

Presence of infectious RD-114 virus in a proportion of canine parvovirus isolates

We recently found that certain canine live attenuated vaccines produced using `non-feline' cell lines were contaminated with an infectious feline endogenous retrovirus, termed RD-114 virus. We suspected that RD-114 virus may have contaminated the seed stock of canine parvovirus (CPV) during the production of the contaminated vaccines. In this study, we collected stock viruses of CPVs propagated in a feline cell line, and checked the presence of infectious RD-114 virus. Consequently, we found that RD-114 viral RNA was present in all stock viruses, and 7 out of 18 stock viruses were contaminated with infectious RD-114 virus. We also found that RD-114 virus was stable physically and is capable of retaining its infectivity for a long period at -80°C.     

Carrier-state infection of feline T-lymphoblastoid cells with feline calicivirus

The susceptibility of feline T lymphocytes to feline calicivirus (FCV) in vitro was investigated using feline T-lymphoblastoid cell lines, namely MYA-1 and FL74 cells. The virus titers of supernatants in FCV-infected MYA-1 and FL74 cell cultures increased rapidly, and FCV antigens were also detected in the FCV-infected cells. There were slight differences in the molecular weights of capsid proteins expressed in FCV-infected MYA-1, FL74 and Crandell feline kidney cells. MYA-1 and FL74 cells were productively and persistently infected with FCV, and FCV antigens were observed in the FCV-infected cells for more than one month. At 3 months post infection, FCV-infected FL74 cells that stopped producing infectious FCV could be reinfected with FCV. However, no cytopathic effects were observed.     

Experimental parvovirus infection in dogs.

Five eight week old dogs were inoculated orally and intranasally with cell culture origin canine parvovirus. Three dogs became depressed and anorectic and developed a mild (one dog) to severe diarrhea five days postinfection. The remaining dogs had subclinical infections but developed a lymphopenia followed by a transient lymphocytosis. The ill dogs developed mild (one dog) to severe neutropenia and a moderate lymphopenia. One died nine days postinfection. Recovery was associated with cessation of viral excretion and with lymphocytosis and antibody production. Two of three dogs challenged intragastrically developed mild clinical signs and a moderate panleukopenia four to eight days postinfection. The pathological changes of the experimental disease were very similar to that of spontaneous disease. Bone marrow changes included a severe granulocytic and mild erythroid depletion. The pathogenesis of canine parvovirus infection is discussed.     

Experimental infection of recent field isolates of feline herpesvirus type 1

Two field isolates of feline herpesvirus type 1 (FHV-1) designated as 00-015 and 00-035, were obtained from cats diagnosed as feline viral rhinotracheitis (FVR) in Japan. To analyze the character of recent FHV-1, these two isolates and our laboratory strain C7301 were inoculated experimentally to specific-pathogen-free cats. Although all cats showed typical FVR symptoms, more severe clinical symptoms were observed on cats infected with the isolates 00-015 and 00-035 compared with those of C7301-infected cats. Severe ocular lesions including conjunctivitis were found in the cats infected with the isolates, indicating that the recent FHV-1 has a potential to induce severe FVR symptoms including ocular lesions.     

Experimental infection of equine herpesvirus 9 in dogs

Equine herpesvirus 9 (EHV-9), a new neurotropic equine herpesvirus, was inoculated intranasally at 107 plaque-forming units in five dogs to assess its pathogenicity. Dogs showed weight loss, pyrexia, anorexia, and neurologic signs on the fourth day. The EHV-9 virus was recovered from the examined brains. Histologically, dogs had a fulminant nonsuppurative encephalitis characterized by severe neuronal degeneration and loss, with intranuclear inclusions, slight glial reactions, perivascular cuffing, and multifocal hemorrhage. The olfactory bulb and the frontal and temporal lobes were predominantly affected. Immunohistochemistry revealed reactivity for EHV-9 antigen in neurons. All dogs had mild bronchopneumonia and various degrees of lymphoid necrosis. These findings indicate that dogs are fully susceptible to EHV-9 and that EHV-9 can cause fulminant encephalitis with high mortality in dogs, as in gazelles and goats.     

Experimental infection of Japanese encephalitis virus in dogs

A previous serosurvey of Japanese encephalitis virus (JEV) among dogs suggested that dogs are well suited for use as sentinels for assessing the risk of JEV transmission to humans. To examine the clinical symptoms and duration of anti-JEV antibodies in dogs, three dogs were experimentally challenged with JEV. All JEV-infected dogs did not show any clinical signs or abnormal blood tests, except for C-reactive protein. Virus-neutralization titers rapidly increased and were maintained until 70 days postinfection, and neither the virus nor the viral genome was detected in blood. Thus, since dogs live in close proximity to humans as companion animals, they are well suited for use as sentinels for surveying the human risk of JEV infection.     

2008 American Association of Feline Practitioners' feline retrovirus management guidelines

Feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) are among the most common infectious diseases of cats. Although vaccines are available for both viruses, identification and segregation of infected cats form the cornerstone for preventing new infections. Guidelines in this report have been developed for diagnosis, prevention, treatment, and management of FeLV and FIV infections. All cats should be tested for FeLV and FIV infections at appropriate intervals based on individual risk assessments. This includes testing at the time of acquisition, following exposure to an infected cat or a cat of unknown infection status, prior to vaccination against FeLV or FIV, prior to entering group housing, and when cats become sick. No test is 100% accurate at all times under all conditions; results should be interpreted along with the patient's health and risk factors. Retroviral tests can diagnose only infection, not clinical disease, and cats infected with FeLV or FIV may live for many years. A decision for euthanasia should never be based solely on whether or not the cat is infected. Vaccination against FeLV is highly recommended in kittens. In adult cats, antiretroviral vaccines are considered non-core and should be administered only if a risk assessment indicates they are appropriate. Few large controlled studies have been performed using antiviral or immunomodulating drugs for the treatment of naturally infected cats. More research is needed to identify best practices to improve long-term outcomes following retroviral infections in cats.     

Early events in the immunopathogenesis of feline retrovirus infections.

Feline leukemia virus and feline immunodeficiency virus (FIV) are lymphotropic retroviruses that cause a wide range of diseases in domestic cats. Although it is known that both viruses are capable of infecting T lymphocytes and that infected cats are lymphopenic, it was not known how infection with either virus might alter specific lymphocyte subpopulations. Using a panel of monoclonal antibodies to feline lymphocyte subpopulations, we examined, by use of flow cytometric analysis, lymphocyte changes in cats naturally infected with FeLV or FIV and explored the early stages in the immunopathogenesis of experimentally induced infection with these viruses. Both groups of naturally infected cats had T-cell lymphopenia. In the FIV-infected cats, the T-cell decrease was principally attributable to loss of CD4+ cells, whereas CD8+ and B-cell numbers remained normal. This led to inversion of the CD4+ to CD8+ ratio in these cats. In contrast, the T-cell lymphopenia in FeLV-infected cats resulted from decrease in CD4+ and CD8+ cells, which led to a CD4+ to CD8+ ratio within normal limits. Experimentally induced infection with these 2 viruses supported these findings. Infection with FIV induced early (10 weeks after infection), chronic inversion of the CD4+ to CD8+ ratio. In contrast, infection with FeLV did not alter CD4+ to CD8+ ratio in the first 20 weeks after infection.