Isolation of feline calicivirus and feline herpesvirus from domestic cats 1980 to 1989

Isolation rates of feline herpesvirus (FHV) and feline calicivirus (FCV) from oropharyngeal swabs, taken from 6866 cats in 1980 to 1989 were studied retrospectively. FCV was isolated from 1364 (19.9 per cent) and FHV from 285 (4.2 per cent). The ratio of FCV:FHV isolations varied from 1.3:1 to 15:1 in individual years with an overall ratio of 4.8:1. Isolation of both viruses was fairly uniform for each year and there was no breed or sex disposition to either virus. Of 872 cats shedding FCV and 213 cats shedding FHV, of known age, 447 (51.3 per cent) with FCV and 140 (65.7 per cent) with FHV were under one year old, compared to only 35.3 per cent of the whole population sampled. For the years 1985 to 1989, more information was obtained about the cases. Of 4626 cats tested, 1180 (25.5 per cent) had acute upper respiratory tract disease (URTD) of which 348 (29.5 per cent) were shedding FCV and 162 (13.7 per cent) FHV. A further 597 had chronic URTD and of these, 102 (17.1 per cent) were shedding FCV and 18 (3 per cent) FHV. In 120 cases of suspected vaccine reaction/breakdown, FCV was isolated from 34 (28.3 per cent) and FHV from only two (1.7 per cent). FHV was not isolated from any of 412 cases presenting with chronic gingivitis/stomatitis alone; 181 (43.9 per cent) were shedding FCV and when cats with other signs in addition to chronic gingivitis were included, this proportion increased to 70.4 per cent.(ABSTRACT TRUNCATED AT 250 WORDS)     

Detection of feline calicivirus antigens in the joints of infected cats

Twelve specific pathogen free cats were used to investigate the role of calicivirus in causing lameness. These were divided into two groups each of six cats; one group of cats had previously been vaccinated, the other had not. Three cats in each group were given live vaccine virus (F9 related) by the subcutaneous route and two in each group were challenged intranasally with field virus (A4), either four or seven days before euthanasia. The other two cats were controls. Virus was isolated from the oropharynx of five cats and the conjunctiva of a single cat. Four of these cats had been given the field virus and two the vaccine strain; the latter two cats had been previously immunised and had high circulating neutralising antibodies to calicivirus. No virus was isolated from the joints of any cat but immunofluorescence examination revealed viral antigens within the synovial macrophages of 14 joints from five cats, three having been given the field virus and two the vaccine virus seven days before euthanasia. Immunofluorescence also demonstrated the presence of immunoglobulin and complement within synovial macrophages suggesting that the virus was in the form of an immune complex. No lameness was reported in any cat and the synovial histological changes were minimal.(ABSTRACT TRUNCATED AT 250 WORDS)     

Quantification of viral ribonucleic acid in plasma of cats naturally infected with feline immunodeficiency virus

OBJECTIVE: To assess plasma viral RNA concentration in cats naturally infected with feline immunodeficiency virus (FIV). ANIMALS: 28 FIV-infected cats. PROCEDURE: Cats were categorized into 1 of the 3 following stages on the basis of clinical signs: asymptomatic (nonclinical) carrier (AC; n = 11), acquired immunodeficiency syndrome-related complex (ARC; 9), or acquired immunodeficiency syndrome (AIDS; 8). Concentration of viral RNA in plasma (copies per ml) was determined by use of a quantitative competitive polymerase chain reaction (QC-PCR) assay. Total lymphocyte count, CD4+ cell and CD8+ cell counts, and the CD4+ cell count-to-CD8+ cell count ratio were determined by use of flow cytometry. RESULTS: Plasma viral RNA concentration was significantly higher in cats in the AIDS stage, compared with cats in AC and ARC stages. Most (5/7) cats in the AIDS stage had low total lymphocyte, CD4+ cell, and CD8+ cell counts. CONCLUSIONS AND CLINICAL RELEVANCE: Concentration of plasma viral RNA is a good indicator of disease progression in FIV-infected cats, particularly as cats progress from the ARC to the AIDS stage. Determination of CD4+ and CD8+ cell counts can be used as supportive indicators of disease progression.     

Comparison of prevalence of feline herpesvirus type 1, calicivirus and parvovirus infections in domestic and leopard cats in Vietnam

A serosurvey of feline herpesvirus type 1 (FHV-1), feline calicivirus (FCV), and feline parvovirus (FPV) in cats from Ho Chi Minh City area in southern Vietnam was conducted in December 1998, and we compared the results with our previous results in northern Vietnam (Hanoi area). The positive rate of FHV and FCV in domestic cats were 44% and 74%, respectively. They were rather higher than those in Hanoi area, while the seropositivity of FPV (44%) was similar to that in Hanoi area. In leopard cats, the positive rate of FPV was high (3/4) and it indicated that FPV was prevailing in leopard cats in Vietnam.     

Clonality analysis of various hematopoietic disorders in cats naturally infected with feline leukemia virus

The clonality analysis of the bone marrow cells was carried out by detecting the integrated proviruses of feline leukemia virus (FeLV) to understand the pathogenesis of FeLV-associated hematopoietic disorders in cats. Bone marrow cells from 4 cases with acute myeloid leukemia (AML), 9 cases with myelodysplastic syndromes (MDS), 2 cases with pure red cell aplasia (PRCA) and 3 healthy carriers infected with FeLV were subjected to Southern blot analyses using an exogenous FeLV probe. Clonal hematopoiesis was found in all the cases with AML and in 6 of the 9 cases with MDS, but not in the cases with both PRCA and healthy carriers infected with FeLV. In the 2 cases with MDS, it was thought that the same clones of the hematopoietic cells might proliferate before and after the progression of the disease irrespective of the changes of the hematological diagnoses by cytological examination. This study indicates that MDS in cats is a disease manifestation as a result of clonal proliferation of hematopoietic cells and can be recognized as a pre-leukemic state of AML.     

Tissue distribution of virus replication in cats experimentally infected with distinct feline calicivirus isolates.

Four specific pathogen-free (SPF) cats were each inoculated with one of two genetically and antigenically well characterized feline caliciviruses originally isolated from cats with acute respiratory disease (FCV-KS100/2), or with chronic stomatitis (FCV-KS20). Two cats of each group were euthanized at day 10 post infection and two cats at day 28. No clear differences between the clinical disease induced by the two isolates could be observed, and no apparent differences in the tissue spectrum were seen between day 10 and 28. No persistent virus shedding was observed over the 4-week period of this experiment.     

Laboratory and clinical findings and their association with viral and proviral loads in cats naturally infected with feline leukemia virus

This study was conducted to correlate clinical, laboratory, and bone marrow (BM) changes in cats naturally infected with feline leukemia virus and their association with viral loads in blood and BM and proviral loads in BM. Cats were classified into five groups based on antigenemia, clinical and/or laboratory findings and viral/proviral loads, according to a prospective study: symptomatic progressive (GI); asymptomatic progressive (GII); regressive (GIII); unclassified (GIV); or healthy (GV). |Correlations between these five groups and viral/proviral loads were evaluated. High viral and proviral loads were detected in GI and GII and viral loads were significantly associated with laboratory signs. Proviral loads detected in BM were significantly lower in GIII and GIV. GI cats were more likely to develop hematopoietic disorders than those from the other groups. Hematological and clinical disorders and disease severity are related to higher viral blood and proviral BM loads.     

Comparison of T-cell subpopulations in cats naturally infected with feline leukaemia virus or feline immunodeficiency virus

T-cell subsets were studied by flow cytometry in 58 feline leukaemia virus (FeLV)-positive cats with naturally acquired FeLV infection to determine whether the changes in CD4⁺ or CD8⁺ T cell populations differed from those observed in 55 feline immunodeficiency virus (FIV)-positive cats with naturally acquired FIV infection. The sole criterion for inclusion into the study was seropositivity. Mean (SD) CD4⁺ T cell values of FeLV positive cats were decreased to 31·1 (8·0) per cent and their CD8⁺ T cell values were increased to 22·8 (6·3) per cent in comparison with uninfected control cats (37·9 [9·5] per cent CD4⁺; 15·2 [6·3] per cent CD8⁺). The CD4⁺/CD8⁺ ratio was reduced to 1·5 (0·7), compared with 3·0 (1·5) in 39 FeLv- and FIV-negative control cats. Differences from control values were significant, but there was no significant difference between CD4⁺ and CD8⁺ lymphocytes of FeLV- versus FIV-infected cats. These findings indicate that FeLv and FIV have similar effects on T lymphocyte subsets. Both retrovirus infections can induce immunodeficiency, both viruses infect a broad range of lymphohaemopoietic cells, despite having different primary target cells, and can induce the killing of lymphocytic cells in vitro. It is concluded that a decreased CD4⁺/CD8⁺ ratio is not restricted to FIV infections but may also occur in FeLv infection.     

Prevalence and risk factors for hemoplasmas in domestic cats naturally infected with feline immunodeficiency virus and/or feline leukemia virus in Rio de Janeiro--Brazil

The aim of this study was to determine the prevalence and risk factors for Mycoplasma haemofelis (Mhf) and 'Candidatus Mycoplasma haemominutum' (Mhm) infections in domestic cats tested for feline immunodeficiency virus (FIV) and feline leukemia virus (FeLV) with a commercial enzyme-linked immunosorbent assay (ELISA) kit. Based on serological testing, cats were grouped as i) FIV-positive (n=25); ii) FeLV-positive (n=39); iii) FIV/FeLV-positive (n=8); and iv) FIV/FeLV-negative (n=77). Complete blood counts were followed by DNA extraction, species-specific polymerase chain reaction (16S rRNA gene) for Mhf and Mhm and Southern blotting for all animals. Mhf DNA was found in 4.0, 2.6, 12.5 and 7.8% of the cats from groups i, ii, iii and iv, respectively, while 32, 5.1, 50 and 5.2% of these animals had an Mhm infection. Cats with FIV (OR=4.25, P=0.009) and both FIV and FeLV (OR=7.56, P=0.014) were at greater risk of being hemoplasma infected than retroviral-negative cats, mainly due to Mhm infection (OR=8.59, P=0.001 and OR=18.25, P=0.001, respectively). Among pure-breed cats, FIV-positive status was associated with hemoplasma infection (OR 45.0, P=0.001).     

Pathologic, immunohistochemical, and electron microscopic findings in naturally occurring virulent systemic feline calicivirus infection in cats

Infection with feline calicivirus (FCV) is a common cause of upper respiratory and oral disease in cats. FCV infection is rarely fatal, however, virulent, systemic strains of FCV (VS-FCV) that cause alopecia, cutaneous ulcers, subcutaneous edema, and high mortality in affected cats have recently been described. Seven cats with natural VS-FCV infection all had subcutaneous edema and ulceration of the oral cavity, with variable ulceration of the pinnae, pawpads, nares, and skin. Other lesions that were present in some affected cats included bronchointerstitial pneumonia, and pancreatic, hepatic, and splenic necrosis. Viral antigen was present within endothelial and epithelial cells in affected tissues as determined by immunohistochemical staining with a monoclonal antibody to FCV. Mature intranuclear and intracytoplasmic virions in necrotic epithelial cells were identified by transmission electron microscopy. VS-FCV infection causes epithelial cell cytolysis and systemic vascular compromise in susceptible cats, leading to cutaneous ulceration, severe edema, and high mortality.     

Local pulmonary immune responses in domestic cats naturally infected with Cytauxzoon felis

Cytauxzoonosis is a hemoprotozoal disease of cats and wild felids in the South and Southeastern United States caused by Cytauxzoon felis. Although the causative agent has been recognized since the seventies, no study has examined the local immune response in affected organs, such as the lung, and compared them to the lungs of uninfected domestic cats. Previous studies have suggested that the histopathologic findings in the lungs of C. felis-infected cats are caused by the release of pro-inflammatory mediators, such as cytokines and increased production of inducible nitric oxide synthase (iNOS), by the infected macrophages. Our laboratory had previously found an upregulation of the adhesion molecule CD18, which can stimulate the release of these pro-inflammatory mediators. The objective of this study was to characterize local pulmonary immune responses in cats naturally infected with C. felis. Immunohistochemistry was performed to detect tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, iNOS, and major histocompatibility complex (MHC) II in 19 lungs from affected cats that died between 2005 and 2013. Results showed increased expression of all of these molecules when compared to lungs from uninfected, healthy cats. Furthermore, MHC II is expressed in the endothelium of C. felis naturally infected cats. These results support that there is a marked, local, pro-inflammatory immune response that can contribute to the pathogenesis of cytauxzoonosis in the lungs.     

High viral loads despite absence of clinical and pathological findings in cats experimentally infected with feline coronavirus (FCoV) type I and in naturally FCoV-infected cats

Specified pathogen-free cats were naturally infected with FCoV or experimentally infected with FCoV type I. Seroconversion was determined and the course of infection was monitored by measuring the FCoV loads in faeces, whole blood, plasma and/or monocytes. Tissue samples collected at necropsy were examined for viral load and histopathological changes. Experimentally infected animals started shedding virus as soon as 2 days after infection. They generally displayed the highest viral loads in colon, ileum and mesenteric lymph nodes. Seroconversion occurred 3-4 weeks post infection. Naturally infected cats were positive for FCoV antibodies and monocyte-associated FCoV viraemia prior to death. At necropsy, most animals tested positive for viral shedding and FCoV RNA was found in spleen, mesenteric lymph nodes and bone marrow. Both experimentally and naturally infected cats remained clinically healthy. Pathological findings were restricted to generalized lymphatic hyperplasia. These findings demonstrate the presence of systemic FCoV infection with high viral loads in the absence of clinical and pathological signs.     

Isolation of feline herpesvirus-1 and feline calicivirus from healthy cats in Swedish breeding catteries

Feline calicivirus (FCV) could be isolated from four cats (2.6%) and feline herpesvirus-1 (FHV) from none of 152 clinically healthy cats from 22 Swedish breeding catteries. These cats had all previously shown signs of respiratory tract disease or conjunctivitis, although several years ago. The results suggest that carriers of FCV and FHV were uncommon in Swedish breeding catteries studied. Prevalence rates in other European countries and North America are usually higher, especially of FCV. The lower prevalence rates in our study might be explained by test group selection, differences in factors such as management, environment, or genetic constitution of the cats, or by sample handling. It was concluded that the presence of an FCV shedder in the cattery does not mean that all cats in the group are infected, but special measures are recommended to avoid infection of susceptible cats.     

The kinetics of feline leukaemia virus shedding in experimentally infected cats are associated with infection outcome

Feline leukaemia virus (FeLV) infection in felids results mainly from oronasal exposure to infectious saliva and nasal secretions, but the potential for viral transmission through faeces and urine has not been completely characterized. In order to assess and compare potential FeLV transmission routes, we determined the viral kinetics in plasma, saliva, faeces and urine during early experimental FeLV infection (up to week 15 post-exposure) in specific pathogen-free cats. In addition to monitoring p27 antigen levels measured by ELISA, we evaluated the presence of infectious particles by cell culture assays and quantified viral RNA loads by a quantitative real-time TaqMan polymerase chain reaction. RNA load was associated with infection outcome (high load-progressive infection; low load-regressive infection) not only in plasma, but also in saliva, faeces and urine. Infectious virus was isolated from the saliva, faeces and urine of infected cats with progressive infection as early as 3-6 weeks post-infection, but usually not in cats with regressive infection. In cats with progressive infection, therefore, not only saliva but also faeces and to some extent urine might represent potential FeLV transmission routes. These results should be taken into account when modelling FeLV-host interactions and assessing FeLV transmission risk. Moreover, during early FeLV infection, detection of viral RNA in saliva may be used as an indicator of recent virus exposure, even in cats without detectable antigenaemia/viraemia. To determine the clinically relevant outcome of FeLV infection in exposed cats, however, p27 antigen levels in the peripheral blood should be measured.     

Natural cases of polyarthritis associated with feline calicivirus infection in cats

Veterinary Research Communications - The limping syndrome is occasionally reported during acute feline calicivirus (FCV) infections or as consequence of vaccination. In this retrospective study,...     

Lethal outbreak of disease associated with feline calicivirus infection in cats

Recently, in the USA, virulent mutants of feline calicivirus (FCV) have been identified as the cause of a severe and acute virulent systemic disease, characterised by jaundice, oedema and high mortality in groups of cats. This severe manifestation of FCV disease has so far only been reported in the USA. However, in 2003, an outbreak of disease affected a household of four adult cats and an adult cat from a neighbouring household in the UK. Three of the adult cats in the household and the neighbouring cat developed clinical signs including pyrexia (39.5 to 40.5 degrees C), lameness, voice loss, inappetence and jaundice. One cat was euthanased in extremis, two died and one recovered. A postmortem examination of one of the cats revealed focal cellulitis around the right hock and right elbow joints. The principal finding of histopathological examinations of selected organs from two of the cats was disseminated hepatocellular necrosis with mild inflammatory infiltration. Immunohistology identified FCV antigen in parenchymal and Kupffer cells in the liver of both animals and in alveolar macrophages of one of them. In addition, calicivirus-like particles were observed by electron microscopy within the hepatocytes of one cat. FCV was isolated from two of the dead cats and from the two surviving cats. Sequence analysis showed that they were all infected with the same strain of virus, but that it was different from strains of FCV associated with the virulent systemic disease in cats in the USA. The outbreak was successfully controlled by quarantine in the owner's house.     

Two outbreaks of virulent systemic feline calicivirus infection in cats in Germany

Over the last years, several outbreaks of virulent systemic feline calicivirus (VS-FCV) infection have been described in the USA and several European countries. The paper describes two outbreaks of VS-FCV infection in cats in Germany. Data concerning clinical, laboratory, and histopathological features ofVS-FCV infection were collected from two outbreaks affecting 55 and 4 cats, respectively. Presence of feline calicivirus was confirmed by PCR followed by sequencing of the PCR-products. Clinical signs were variable, including severe upper respiratory tract infection, dyspnoea, oral and footpad ulceration, facial oedema, enteritis, pneumonia, bleeding disorder, high fever, and icterus. Both outbreaks were characterized by a high mortality rate.The present report describes the first documented outbreaks of VS-FCV infection in cats in Germany. Clinical and histopathological features are comparable to outbreaks described in the USA and Europe. However, phylogenetic analysis of the virus genome suggests that virus strains involved in these outbreaks were different from each other and from virulent strains isolated before, confirming the known genetic variability of FCV.     

Quasispecies evolution of a hypervariable region of the feline calicivirus capsid gene in cell culture and persistently infected cats.

The study determines the sequence evolution of feline calicivirus both in cell culture and in persistently infected cats and relates this to changes in virus neutralisation.