Epizootic canine distemper virus infection among wild mammals

In the spring of 2007, seven raccoon dogs and a weasel were captured near the city of Tanabe in Wakayama prefecture, Japan. The causative agent of the animals' death 1-2 days after capture was identified as canine distemper virus (CDV) by virus isolation, immunostaining with an anti-CDV polyclonal antibody, and a commercially available CDV antigen-detection kit. Sequence analysis of hemagglutinin genes indicated the isolated viruses belong to genotype Asia-1 and possess the substitution from tyrosine (Y) to histidine (H) at position 549 that is associated with the spread of CDV to non-canine hosts. A serosurvey for CDV was then conducted among wild animals in the region. The animals assayed consisted of 104 raccoons, 41 wild boars, 19 raccoon dogs, five Sika deer, two badgers, one weasel, one marten, one Siberian weasel and one fox. Virus-neutralization (VN) tests showed that, except for fox and weasel, all of the species assayed had VN antibodies to CDV. Interestingly, 11 of the 41 wild boars (27%) and two of the five Sika deer assayed possessed VN antibodies to CDV. These findings indicate that CDV infection was widespread among wild mammals during this epizootic.     

Spontaneous Aleutian disease in a ferret

A 3-year-old female ferret died five days after admission to a veterinary clinic for treatment of acute dyspnea and posterior paresis. Blood chemistry showed no hypergammaglobulinemia. Histopathological examination revealed mild to severe inflammatory infiltrates, composed mostly of plasma cells, in multiple organs. Lesions were especially severe in the kidneys, where focal segmental membranous glomerulopathy was also present. In the liver, in addition to lymphocytic and plasmacytic infiltration in periportal areas, dilatation and proliferation of the bile ducts were seen. On analysis of PCR products, using primers directed against the gene encoding Aleutian disease (AD) viral capsid and formalin-fixed kidney samples, we detected a single band of about 400 bp, specific to the AD virus.     

Molecular survey of Mycoplasma haemofelis and 'Candidatus mycoplasma haemominutum' infection in cats in Yamaguchi and surrounding areas

A molecular survey of hemoplasma (Mycoplasma haemofelis and 'Candidatus Mycoplasma haemominutum') in Yamaguchi Prefecture and surrounding areas was performed by using molecular methods. PCR-RFLP with HindIII revealed that 2 cats were infected with M. haemofelis, and 16 with 'C. Mycoplasma haemominutum' among 102 randomly selected cats. Partial 16S rRNA gene sequences of M. haemofelis and 'C. Mycoplasma haemominutum' determined in this study showed percent similarities of 98.3-99.8% and 96.4-100%, respectively, with those from other countries. Hemoplasma infections were more frequently detected in free-roaming cats than inside cats. Also, the status of FeLV infection was another significant risk factor for hemoplasma infection.     

Molecular cloning of canine RCAS1 cDNA

Receptor-binding cancer antigen expressed on SiSo cells (RCAS1) is a novel cancer cell-surface antigen, strongly expressed in invasive cancers. RCAS1 inhibited the in vitro growth of immunocytes, and induced apoptotic cell death. The cloning of canine RCAS1 cDNA was carried out and identified from the mammary gland tumor of a dog. A canine RCAS1 cDNA of 864 bp in length has an open reading frame of 642 bp nucleotides encoding a protein of 213 deduced amino acids. The predicted amino acid sequence of canine RCAS1 showed 96.2% and 96.7% homologies with those of human and mouse RCAS1 respectively. Canine RCAS1 has an N-terminal transmembrane segment and a coiled-coil structure in the C-terminal protein, which are highly conserved in mouse and human RCAS1.     

The effects of the loop diuretics furosemide and torasemide on diuresis in dogs and cats

Torasemide is a new loop diuretic that combines the effects of furosemide and spironolactone. There are no reports on the effects of torasemide in cats and dogs. This study compared the diuretic effects of furosemide and torasemide in cats and dogs. Cats with pressure overload cardiac hypertrophy were given oral placebo, torasemide 0.3 mg/kg, or furosemide 1 mg/kg or 3 mg/kg. Control and mitral regurgitation dogs were given oral placebo, torasemide 0.2 mg/kg, and furosemide 2 mg/kg for 7 days. Urine samples were obtained at baseline and 1, 2, 3, 4, 5, 6, 8, 12, and 24 hr after each drug dose. Urine volume and urine Na(+) and K(+) were measured. Both furosemide and torasemide increased urine volume 1 hr after administration. Furosemide caused a dose-dependent increase in urine volume that peaked at 2-3 hr in cats and dogs. The diuretic effect of furosemide disappeared 6 hr after administration, while that of torasemide peaked 2-4 hr after administration and persisted for 12 hr in cats and dogs. In MR dogs, torasemide for 7 days significantly decreased urine potassium excretion. Plasma aldosterone increased with torasemide, whereas there was no change with furosemide. In conclusion, about 1/10 concentration of torasemide was as potent as furosemide and had a longer diuretic effect in cats and dogs. These data suggest that torasemide is useful for treating congestive heart failure or edema in cats and dogs.     

Detection of centrosome amplification as a surrogate marker of dysfunction in the p53 pathway –p53 gene mutation or MDM2 overexpression

In human and canine cancers, the inactivation of p53 protein as well as p53 gene mutation and MDM2 overexpression result in centrosome amplification that in turn contributes to chromosomal instability. To explore the usefulness of the detection of centrosome amplification as a surrogate marker of dysfunction in the p53 pathway, we systematically analysed centrosome amplification, p53 overexpression, p53 gene mutation and MDM2 overexpression in canine tumours. Centrosome amplification was detected in 16 of 51 (31%) naturally developing tumours in dogs. All the tumour specimens with aberrations in the p53 pathway, including p53 overexpression, p53 gene mutation or MDM2 overexpression, showed centrosome amplification, suggesting that the detection of centrosome amplification could serve as a preliminary surrogate marker of dysfunction in the p53 pathway.     

Infestivity of Demodex canis to hamster skin engrafted onto SCID mice

We demonstrated that Demodex canis was transferred to skin xenografts of a dog and a hamster onto severe combined immunodeficiency mice. After the transfer of mites, the number of eggs, larvae, nymphs and adult mites per gram of canine and hamster xenografts increased, whereas no live mites were detected on murine allograft. These results indicate that D. canis proliferates in hair follicles of dog and hamster skins but not in murine allograft. Therefore, D. canis may have host preference but not strict host-specificity.