ABSTRACT. Infectious tracheobronchitis (ITB), also known as the kennel cough, is a respiratory syndrome of dogs and usually appears to be contagious among dogs housed in groups. Etiologic agent of ITB is multiple and sometimes complex. In the present study, 68 household dogs showing clinical signs of respiratory infection were examined, and 20 dogs (29.4%) were found to be positive for either of following agents. Bordetella bronchiseptica (B.b.) was most frequently detected from nasal and oropharynx sites of 7 dogs (10.3%). Among the viruses examined, canine parainfluenza virus (CPIV) was detected with the highest frequency (7.4%). Other pathogens included in the order of frequency group 1 canine coronavirus (4.4%), canine adenovirus type 2 (2.9%), group 2 canine respiratory coronavirus (1.5%), and canine distemper virus (1.5%). Only 2 cases showed mixed infections. Neither influenza A virus nor canine bocavirus (minute virus of canines) was found in any dogs examined. These results indicate that both B.b. and CPIV are likely to be the principal etiologic agents of canine ITB in Japan, and they may be considered as the target for prophylaxis by vaccination. KEY WORDS: Bordetella bronchiseptica, canine parainfluenza virus, canine respiratory coronavirus, infectious tracheobronchitis, kennel cough.

ABSTRACT. Canine parvovirus type 2 (CPV) is a pathogen that causes severe hemorrhagic gastroenteritis with a high fatality rate in pups worldwide. Since CPV emerged in the late 1970s, its origin has been explored with the conclusion that CPV originated from feline panleukopenia virus or a closely related virus. Both high mutation rate and recombination are assumed to be key factors in the evolution of parvoviruses. Here we provide evidence for natural recombination in CPV isolated from dogs in cell culture. Antigenic and genetic properties of isolates from 10 diseased pups were elucidated. Six pups had been vaccinated beforehand with live combined vaccine containing original antigenic type CPV (CPV-2). Six isolates recovered from 4 vaccinated pups in cell cultures were found to contain either CPV-2 or CPV-2-like viruses. The other isolates, including all those from non-vaccinated pups, were CPV-2b viruses. Antigenic typing of two CPV-2-like isolates, 03-029/M and 1887/f, with a monoclonal antibody panel suggested they were a mixture of CPV-2 and CPV2a (03-029/M) and a recombinant of CPV-2 and CPV-2b (1887/f). Genetic analysis of the VP1 gene indicated that isolate 03-029/M was a mixture of CPV-2, CPV-2a and a recombinant of CPV-2 and CPV-2a viruses, while isolate 1887/f was composed of a recombinant of CPV-2 and CPV-2b viruses. This is the first demonstration of natural CPV recombination in the field and suggests that recombination in the evolution of CPV is a more frequent and important process than previously believed. KEY WORDS: canine parvovirus, cell culture, dog, parvovirus, recombination.J. Vet. Med. Sci. 70(12): 1305-1314 Canine parvovirus type 2 (CPV), one of the feline parvovirus (FPV) subspecies, emerged suddenly throughout the world in the late 1970s as a new pathogen that caused severe hemorrhagic gastroenteritis and myocarditis in domestic dogs [1,2,7,20,23,40]. Mortality rate is usually high, particularly in non-immune pups. The origin of the virus is still not clear but the most likely hypothesis from phylogenetic analysis is that CPV originated from feline panleukopenia virus (FPLV) or a very closely related carnivore parvovirus of feral canids, such as foxes and mink [52,55]. There has been speculation that, during circulation for some time in an European local dog population, this ancestral CPV gradually adapted for domestic dogs and the emergent original CPV (antigenic type 2: CPV-2) rapidly spread globally as a new pathogen of domestic dogs.In the early 1980s, this first CPV-2 disappeared from the field having been replaced by a new antigenic variant designated CPV-2a, and another antigenic variant CPV-2b appeared soon afterwards. These variants can be distinguished by monoclonal antibodies (MAbs) [35,43,[45][46][47]. CPV-2a and 2b use both canine and feline transferrin receptors for binding to cells both in vitro and in vivo [17,42] and consequently can infect dogs as well as cats [34,56]. In contrast, CPV-2 can infect both feline and canine cells in vitro but infects only dogs in vivo [57]...

Specimens obtained from 96 dogs with respiratory and enteric clinical signs in Japan were retrospectively examined for group 2 coronavirus by reverse transcription-PCR. Two dogs were found to be positive. Phylogenetic analysis of the spike gene indicated that they were most probably related to the canine respiratory coronavirus recently described in the United Kingdom.

Previous studies have shown that cellular prion protein (PrPC) plays anti‐apoptotic and anti‐oxidative role against cell death induced by serum‐deprivation (SDP) in an immortalized prion protein gene‐deficient neuronal cell line derived from Rikn prion protein (PrP) gene‐deficient (Prnp–/–) mice, which ectopically produce excess Doppel (Dpl) (PrP‐like glycoprotein). To investigate whether PrPC inhibits apoptotic neuronal cell death without Dpl, an immortalized cell line was established from the brain of ZrchI Prnp–/– mice, which do not show ectopic expression of Dpl. The results using a ZrchI neuronal Prnp–/– cell line (NpL2) showed that PrPC potently inhibited SDP‐induced apoptotic cell death. Furthermore, PrPC expression enhanced the superoxide dismutase (SOD) activity in NpL2 cells. These results indicate that Dpl production did not affect anti‐apoptotic and anti‐oxidative functions of PrP, suggesting that PrPC may be directly correlated with protection against oxidative stress.