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At least 19 recordsLinked to original sources
PubMed1976

Seasonality, natality and herd immunity in feline panleukopenia.

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."

Animals↗
PubMed2004

A severe dual infection by feline panleukopenia virus and feline calicivirus in an adult cat.

A dual infection by feline panleukopenia virus (FPV) and feline calicivirus (FCV) in a 7 month-old cat is described. The animal developed a severe illness with depression, anorexia, fever, leucopoenia, nasal and ocular discharge and oral ulcers. Both FPV and FCV were isolated in cell cultures from a rectal swab and the presence of FCV was confimed by polymerase chain reaction. Antibodies to both the viruses were detected in the serum. The severity of the disease induced by the mixed viral infection highlights the need for intensifying FPV vaccination in cats.

Animals↗
PubMed1987

Feline leukemia virus-associated enteritis--a condition with features of feline panleukopenia.

Infection with feline leukemia virus (FeLV) was demonstrated immunohistologically in 218 necropsied cats suffering from enteritis. The animals were divided into three groups according to histopathological criteria. The first group exhibited the signs of feline panleukopenia in intestine, lymphoid tissues, and bone marrow. Only 1.6% of these animals were FeLV-infected. The animals of the second group had histopathological alterations as seen in cats suffering from feline panleukopenia, but these were found only in the intestine and not in lymphoid tissues or bone marrow. Of these 71.9% were infected with FeLV. The third group consisted of all other cats suffering from enteritis of which 6.3% were FeLV-positive. The association between FeLV infection and the lesions seen in the animals of group 1 (feline panleukopenia) and group 3 (other types of enteritis) is statistically not significant whereas the alterations exhibited by the cats of group 2 are significantly FeLV-associated. Cats with FeLV-associated enteritis (group 2) are of a mean age of about 2.5 years and are significantly older than animals with feline panleukopenia which are of a mean age of about half a year. Thus a FeLV-associated enteritis exists as a histopathologically recognizable condition which sometimes might be mistaken for feline panleukopenia in routine post-mortem investigations.

Animals↗
PubMed1994

Characterization of the feline host range and a specific epitope of feline panleukopenia virus.

The feline parvovirus subgroup is comprised of viruses isolated from various carnivores, including the dog, cat, mink, raccoon, Arctic fox, and raccoon dog. Those viruses are > 98% identical in their DNA sequences and are very similar antigenically. We have shown that although canine parvovirus (CPV) replicates in numerous feline cell lines in vitro it does not infect cats after parenteral inoculation (U. Truyen and C. R. Parrish, (1992) J. Virol. 66, 5399-5408). Here we use recombination mapping to locate some viral determinants required for feline host range, and show that the ability to replicate in cats was determined by the right-hand 45% of the genome, most likely a function of the capsid protein gene. Efficient replication in the cat appeared to require feline panleukopenia virus sequences from both ends of the VP2 molecule, which contained differences of VP2 amino acid residues 80, 564, and 568. The difference at amino acid 80 was also associated with expression of an FPV-specific antigenic epitope. The differences which affected the feline host range were located in a region of the capsid structure where three VP2 molecules interact, and the mutations gave rise to changes in the conformation of loops of the three adjoining VP2 monomers. The mechanism(s) of the in vivo feline host range restriction were not defined, and we were unable to show in vitro inhibition of virus infectivity by feline serum components or erythrocytes.

Animals↗
PubMed1998

Apoptosis in feline panleukopenia virus-infected lymphocytes.

Feline panleukopenia virus (FPLV) was shown to induce apoptosis to feline lymphoid cells and to reduce the expression of interleukin-2 receptor alpha on the cells. FPLV-induced apoptosis might be a key element in the pathophysiology of atrophy of lymphoid tissues associated with feline panleukopenia caused by FPLV.

Animals↗
PubMed1996

Isolation of canine parvovirus from a cat manifesting clinical signs of feline panleukopenia.

Twenty-seven feline parvovirus (FPV) isolates were recovered from cats clinically diagnosed with feline panleukopenia (FPL) for assessing antigenic and genomic properties of FPL viruses (FPLV) recently prevalent among cats in Japan. All isolates, with the exception of one novel isolate, FPV-314, possessed homologous properties, and their subgroups in FPVs were identified as FPLV. The FPV-314 isolate, which was from a 1.5-year-old cat which manifested clinical signs of FPL and died on the 13th day after the first medical examination, was finally identified as canine parvovirus (CPV) because it lacked a specific antigenic epitope commonly detected in FPLV and mink enteritis virus and because the nucleotide sequence of the capsid protein gene was almost identical to those of CPV-2a and -2b antigenic type strains recently prevalent among dogs in Japan. The present result together with our previous findings (M. Mochizuki, R. Harasawa, and H. Nakatani. Vet. Microbiol. 38:1-10, 1993) indicates the possibility that CPV and FPLV undergo mutual interspecies transmission between dogs and cats, and it is postulated that they may cause disease in some adventitious hosts.

Animals↗
PubMed1983

Response of mink, skunk, red fox and raccoon to inoculation with mink virus enteritis, feline panleukopenia and canine parvovirus and prevalence of antibody to parvovirus in wild carnivores in Ontario.

Mink virus enteritis, feline panleukopenia and canine parvovirus-2 were inoculated separately into groups of raccoon, mink, red fox and striped skunk. Raccoons were highly susceptible to mink virus enteritis and feline panleukopenia, with animals developing clinical illness, and several dying within six to ten days of inoculation with lesions typical of parvovirus infection. Both viruses were shed in high titre in the feces of infected raccoons, and high antibody titres were stimulated. Raccoons inoculated with canine parvovirus-2 showed no signs; shedding of virus was sporadic though moderate titres of antibody developed. Mink inoculated with mink virus enteritis and feline panleukopenia developed signs and lesions of early parvovirus infection. No signs or significant lesions followed canine parvovirus-2 inoculation. Shedding of virus was heavy (mink virus enteritis) or sporadic (feline panleukopenia and canine parvovirus-2), though good serological responses were elicited to all three viruses. Red fox showed no signs of infection, shed all three viruses only sporadically, and the serological response was strong only to feline panleukopenia. Skunks developed low antibody titres, but no signs, and did not shed virus. Antibody to parvovirus was found in 79.2% of 144 wild red foxes; 22.3% of 112 wild raccoons; 1.3% of 157 wild skunks and 6/7 coyotes in southern Ontario. The likely significance of these viruses to wild and captive individuals and populations of these carnivores is discussed.

Animal Population Groups↗
PubMed1993

[Detection by PCR of genomic markers in canine parvovirus and feline panleukopenia virus].

The NS1 and VP1/VP2 genes of canine parvovirus and feline panleukopenia virus were amplified by the polymerase chain reaction (PCR). The restriction cleavage patterns of the amplified DNA fragments were compared among these parvoviruses including vaccine strains. Differences of the restriction site in the NS1 portions were observed between the vaccine strain and the wild type strain as well as between canine parvoviruses and feline panleukopenia viruses. The restriction patterns of feline panleukopenia viruses were distinct from those of canine parvoviruses, and showed differences between the vaccine strain and its wild type strain. This PCR-based restriction cleavage can be used for ecological study of such viruses.

Feline Panleukopenia Virus↗
PubMed1976

Fine structure of epithelial cells of Lieberkühn's crypts in feline panleukopenia.

Electron microscopic observation was carried out on epithelial cells of Lieberkühn's crypts of cats naturally affected with feline panleukopenia. The most important change was the replication of feline panleukopenia. The most important change was the replication of feline panleukopenia virus in the nucleus with associated alterations in the lining epithelial cells of the crypts. In these cells in the early stage of infection, virus particles 20 nm in average diameter were found either singly or in small regularly arrayed clusters everywhere in the markedly swollen nucleus. In the course of infection, the nucleus of infected cells became rather atrophic with a marked margination of chromatin granules. Its major portion was occupied with masses of fine fibrillar substance. It was a "viral matrix area" in which appeared a large compact aggregate of virus particles showing a crystalline array. At the same time, the outer membrane of the nuclear envelope partially extended and disrupted. Membranous elements related to it in the cytoplasm were regularly distributed almost always with particles indistinguishable from the virus particles in the nucleus. From these results it was suggested that the major portion of the infected nucleus, or the site of viral replication, might correspond to the amphophilic intranuclear inclusion body revealed by light microscopy.

Animals↗
PubMed1995

Pathogenesis of feline panleukopenia virus and canine parvovirus.

Feline panleukopenia virus (FPV) and canine parvovirus (CPV) are autonomous parvoviruses which infect cats or dogs, respectively. Both viruses cause an acute disease, with virus replicating for less than seven days before being cleared by the developing immune responses. The viruses have a broad tropism for mitotically active cells. In neonatal animals the viruses replicate in a large number of tissues, and FPV infection of the germinal epithelium of the cerebellum leads to cerebellar hypoplasia, while CPV may infect the hearts of neonatal pups, causing myocarditis. In older animals the virus replicates systemically, primarily in the primary and secondary lymphoid tissues, and also in the rapidly replicating cells of the small intestinal epithelial crypts. A transient panleukopenia or relative lymphopenia is often observed after FPV or CPV infection, respectively. Whether the reduction in cell numbers in vivo is due to virus replicating in and killing cells, or due to other indirect effects, is not known. However, FPV kills both erythroid and myeloid colony progenitors in in vitro bone marrow cultures, and it has been suggested that virus replication in the myeloid cells in vivo could lead to the reduced neutrophil levels seen after FPV infection of cats.

Animals↗
PubMed1989

Comparison of feline parvovirus subspecific strains using monoclonal antibodies against a feline panleukopenia virus.

Four monoclonal antibodies (mAb) against a feline panleukopenia virus (FPLV) TU 1 strain, one of the host range variants of feline parvovirus (FPV), were produced and applied for antigenic analysis of FPLV, canine parvovirus (CPV) and mink enteritis virus (MEV). All mAbs were considered to be directed at epitopes on the virus capsid surface because they neutralized the infectivity and inhibited the hemagglutination (HA) of the homologous virus as well as other FPV strains. They were of the mouse IgG1 type. High antigenic homogeneity among FPLV strains was confirmed by HA-inhibition (HI) test with the mAbs and polyclonal immune sera against FPLV or CPV. But the TU 11 strain of FPLV was antigenically distinguished from the remaining 14 FPLV strains by both the HI test and the micro-neutralization test with one of the mAbs produced. MEV Abashiri strain was found to be antigenically indistinguishable from FPLV. Most of the CPV strains isolated after 1981 were considered to be antigenically different from earlier CPV isolates when some mAbs were applied in the serological tests, confirming the replacement of CPV by an antigenic variant in Japan. However, antigenically different CPVs were detected at the end of 1984 from unrelated epizootics occurred a month apart in the same area.

Animals↗
PubMed1993

Use of a feline panleukopenia modified live virus vaccine in cats in the primary-stage of feline immunodeficiency virus infection.

Cats in the primary stage of Feline Immunodeficiency Virus (FIV) infection and FIV seronegative cats were vaccinated with a modified live Feline Panleukopenia virus vaccine (FPV-MLV). The FPV-MLV strain was not pathogenic for FIV seronegative cats, whereas in FIV infected cats it produced severe clinical signs, similar to those typically observed in cats naturally infected with field strains of FPV (fever, diarrhoea, leukopenia).

Animals↗
PubMed1985

Cloning and sequence of DNA encoding structural proteins of the autonomous parvovirus feline panleukopenia virus.

Approximately 80% of the genome of feline panleukopenia virus was cloned into pBR322. This DNA included the transcription unit for the major viral mRNA species. The nucleotide sequence of the cloned portion of the genome was determined. Comparison of the feline panleukopenia virus sequence with the sequences of the parvoviruses minute virus of mice and H-1 revealed considerable homology between the three viruses on both the nucleic acid and protein levels. Based on this homology, a model for the generation of the two size classes of viral structural proteins (VP1 and VP2') is proposed.

Amino Acid Sequence↗
PubMed1987

Comparisons of feline panleukopenia virus, canine parvovirus, raccoon parvovirus, and mink enteritis virus and their pathogenicity for mink and ferrets.

Parvoviruses from mink (mink enteritis virus [MEV]), cats (feline panleukopenia virus [FPV]), raccoons (raccoon parvovirus [RPV]), and dogs (canine parvovirus [CPV]) were compared. Restriction enzyme analysis of the viral replicative-form DNA revealed no consistent differences between FPV and RPV isolates, but CPV and MEV isolates could be distinguished readily from other virus types. Feline panleukopenia virus, RPV, and MEV, but not CPV, replicated to high titers in mink. However, on the first passage, disease and microscopic lesions were observed only in mink inoculated with MEV. Feline panleukopenia virus and RPV isolates replicated in ferrets, but disease or microscopic lesions were not observed. Feline panleukopenia virus and RPV isolates could be passaged repeatedly in mink and ferrets. Virulence of FPV and RPV isolates was low compared with that of MEV, and only a single mink inoculated with FPV or with RPV developed clinical disease on the sixth passage of virus.

Animals↗
PubMed1999

Enterocolitis associated with dual infection by Clostridium piliforme and feline panleukopenia virus in three kittens.

Dual infection by Clostridium piliforme and feline panleukopenia virus (FPLV) was found in three kittens. In all cases, we found focal necrosis and desquamation of epithelial cells with occasional neutrophil infiltration in the large intestine. Large filamentous bacilli and spores were observed in the epithelium by using the Warthin-Starry method. Electron microscopy revealed the vegetative forms with characteristic peritrichous flagella and spore forms. Immunohistochemically, these bacilli showed a positive reaction with mouse antisera against the RT and MSK C. piliforme strains. Polymerase chain reaction (PCR) using cecum specimens demonstrated the 196-bp band specific to C. piliforme 16S rRNA. All three kittens were also diagnosed as FPLV-infected on the basis of the characteristic mucosal lesions, including intranuclear inclusions and PCR study for the FPLV genomic DNA. The PCR techniques are useful for confirming the C. piliforme and FPLV infection in spontaneous cases.

Animals↗
PubMed1983

Comparison of the viral proteins of canine parvovirus-2, mink enteritis virus and feline panleukopenia virus.

Canine parvovirus-2 (CPV-2), Mink enteritis virus (MEV) and feline panleukopenia virus (FPV) were produced using identical cell culture and purification techniques. The distributions of the haemagglutinating activity of the three different parvoviruses in a CsCl gradient were similar with haemagglutinating peaks identified at 1.48-1.49, 1.42, 1.36 and 1.30-1.31 g cm-3. The number and distribution of the viral proteins and the equivalent protein molecular weights are similar for all three viruses in SDS-polyacrylamide gels (10%). Four viral proteins were identified and their molecular weights were determined: protein A (77 500-79 500), protein B (63 000-63 500), protein C (61 500-63 000) and protein D (50 000-55 000). The viral protein D although reported for some other parvoviruses has not previously been demonstrated in CPV-2, MEV or FPV.

Animals↗
PubMed1980

A plaque assay for feline panleukopenia virus.

Plaque formation with representative strains of feline panleukopenia virus (FPV) has been obtained using a permanent line of feline kidney cells under agarose overlay. FPV-infected cells appear as white plaques after neutral red staining. Plaque size is determined by the extent of cell division in the infected monolayer. FPV assay by the plaque procedure is rapid and gives infectivity titres which exceed those determined by the common inclusion body and immunofluorescent assays of FPV by a factor of about 100 and 10, respectively. Moreover, the plaque assay offers an effective means for the quantification of neutralizing antibodies in feline sera as well as for the detection of heat-stable substances in bovine sera which strongly interfere with replication of the virus.

Animals↗