Canine parvovirus (CPV), first recognized as an emerging virus of dogs in 1978, resulted from a successful cross-species transmission. CPV emerged from the endemic feline panleukopenia virus (FPV), or from a closely related parvovirus of another host. Here we refine our current understanding of the evolution and population dynamics of FPV and CPV. By analysing nearly full-length viral sequences we show that the majority of substitutions distinguishing CPV from FPV are located in the capsid protein gene, and that this gene is under positive selection in CPV, resulting in a significantly elevated rate of molecular evolution. This provides strong phylogenetic evidence for a prominent role of the viral capsid in host adaptation. In addition, an analysis of the population dynamics of more recent CPV reveals, on a global scale, a strongly spatially subdivided CPV population with little viral movement among countries and a relatively constant population size. Such limited viral migration contrasts with the global spread of the virus observed during the early phase of the CPV pandemic, but corresponds to the more endemic nature of current CPV infections.

Feline panleucopenia virus (FPLV) was introduced in 1977 on Marion Island (in the southern Indian Ocean) with the aim of eradicating the cat population and provoked a huge decrease in the host population within six years. The virus can be transmitted either directly through contacts between infected and healthy cats or indirectly between a healthy cat and the contaminated environment: a specific feature of the virus is its high rate of survival outside the host. In this paper, a model was designed in order to take these two modes of transmission into account. The results showed that a mass-action incidence assumption was more appropriate than a proportionate mixing one in describing the dynamics of direct transmission. Under certain conditions the virus was able to control the host population at a low density. The indirect transmission acted as a reservoir supplying the host population with a low but sufficient density of infected individuals which allowed the virus to persist. The dynamics of the infection were more affected by the demographic parameters of the healthy hosts than by the epidemiological ones. Thus, demographic parameters should be precisely measured in field studies in order to obtain accurate predictions. The predicted results of our model were in good agreement with observations.

To study the effect of interferon on feline leukemia virus (FeLV) infection, 30 specific pathogen free (SPF) cats were infected with the apathogenic FeLV A Glasgow. Unexpectedly, between 5 and 8 weeks after FeLV infection, all 19 cats with persistent FeLV infection but not the FeLV-negative cats died from a panleukopenia-like syndrome. No feline panleukopenia virus (FPLV) antigen was found in feces by latex agglutination, enzyme-linked immunosorbent assay (ELISA) or immunoelectron microscopy. No enteropathogenic bacteria were found. Histopathology revealed changes resembling those of FPLV infection such as destruction of crypts and pancytopenia of bone marrow. Neither clinical signs nor seroconversion to FPLV could be induced by transmitting intestinal extracts to two SPF cats. However, FPLV antigen was demonstrated by immunofluorescence assay in intestinal cryostat sections of diseased animals. FPLV could also be demonstrated in intestinal extracts by immunoelectron microscopy, by latex agglutination and ELISA after anti-FPLV antibodies were removed from immune-complexed FPLV by ultracentrifugation over a CsCl gradient at pH 2.0. From these experiments it was concluded that the panleukopenia-like syndrome of FeLV may not be caused by FeLV alone but at least in some cases by co-infection with FeLV and FPLV. In addition, some form of 'cooperation' between FeLV and FPLV must be postulated because neither virus alone induced symptoms.

A pilot study was carried out among 22 Vietnam-era male US veterans with multiple sclerosis (MS) and 55 age- and sex-matched controls for prior exposure to dogs, cats, and animals with a distemperlike illness. No difference in dog ownership, or sick animals, and subsequent human illness was found in the group with MS or the control group. However, the distribution of dogs by indoor-outdoor status, as reported by patients with MS or controls, showed significant variation by tier of residence. Indoor dogs were more common in northern than southern latitudes, and this may be an important finding in light of the variation in the risk of MS with latitude.

Feline panleukopenia (FPL) was diagnosed in 185 of 7043 feline admissions (2.63%) at a university veterinary hospital over an eight-year period. FLP has a distinct seasonal pattern, occurring during July, August and September. Seasonal peaks were noted in all the years studied. Cats less than one year of age accounted for 70% of the total morbidity. The birth of felines in the United States also assumes a distinctly seasonal pattern. Analysis of 47,786 purebred litters born during 1970-1972 revealed a peak during April, May and June with a national median of May 29. A unifying hypothesis is presented to account for the seasonal occurrence of FPL. An influx of susceptible cats occurs annually following the birth of large numbers of kittens each spring, and disappearance of maternal immunity during the next two to three months. The addition of a large number of susceptible kittens leads to the development of summertime epidemics and serves to exemplify the principles of "herd immunity."