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Clinical outcome of 73 cases with feline panleukopenia
Abstract
Feline panleukopenia is still considered an important disease, although some time has passed since identification of its aetiology as a virus in 1932. In the past, prognosis has often been described as very poor with up to 90 % mortality in diseased cats; however, little is known about prognostic factors in feline panleukopenia or the current mortality rate in patients treated with intensive care. In this retrospective study of 73 cats with feline panleukopenia, animals with anorexia, hypothermia, reduced skin elasticity, poor nutritional condition, lymphopenia, thrombocytopenia or hypoalbumenaemia had a significantly higher probability to die. Adjuvant application of antibodies against panleukopeniavirus, rhinotracheitisvirus and calicivirus (Feliserin®) improved the chance of survival. In contrast, treatment with either a single or two different antibiotics had no influence on survival rate. The average duration of hospitalization was five days, and mean costs for the owners of surviving cats amounted to 579 Euro. The mortality rate of 61 intensively treated cats was 49 %, indicating a survival rate of 51 %. Thus with aggressive treatment, the prognosis seems to be morefavourable than described in the past. Owners informed about this fact might be more willing to attempt treatment for their cats suffering from parvovirus infection.
... The FPLV infection is characterized by steep drop in the leucocyte count that can be effectively corrected by using rHGSF [27,28]. The rHGSF is a glycoprotein that stimulates bone marrow and produce granulocytes, the majority of the case fatalities in FPLV are due to secondary bacterial infection due to resulting leukopenia [29,30]. The first serological evidence of circulating viruses among wild felids was reported in 1991 [31]. ...
Background
Feline Panleukopenia is an important disease of cats and has been reported worldwide. The disease is caused by a non-enveloped, single-stranded DNA virus; Feline Panleukopenia Virus (FPLV), belonging to the Parvoviridae family. The disease causes significant mortality in unvaccinated kittens. The disease has been well documented in companion animals. However, only a few reports have surfaced from the wild.
Case presentation
An orphan leopard cub was presented to Wildlife Rescue Centre, Nagpur, for further care; the leopard was kept under quarantine. On day 22 of the quarantine, the leopard showed inappetence, lethargy and depression and did not consume the offered carabeef (Day 0 of treatment). The leopard was examined clinically and was found to have a temperature of 102°F; blood was collected and analysed. On day one, the leopard exhibited bloody diarrhoea, inappetence, fever and depression. The leopard was rationally treated with fluids, antibiotics, multi-vitamins, haemostatics and haematinics. To gain qualitative insights into the epidemiological aspect of the disease, molecular investigation, including Polymerase Chain Reaction (PCR) and qPCR (Quantitative Polymerase Chain Reaction), were utilized to confirm the infection. The amplicon was sequenced and was found to be similar to sequences of FPLV reported domestic cats and other wild felids from India and abroad. Phylogenetic analysis was performed to understand the evolutionary relationship of the virus with previously reported sequences of FPLV. Sequences were submitted to National Center for Biotechnology Information (NCBI) and were allotted accession numbers.
Conclusion
The infection in endangered leopard cubs could be managed with prompt fluid therapy, antibiotics and support treatment, ensuring an uneventful recovery. Molecular investigation and sequencing efforts can provide valuable data on epidemiology and the evolutionary relationship of the virus with the circulating strains in the field. The study has implications in the preventive management of FPLV in captivity and the selection of strains for inclusion in vaccines meant for the wild felids.
... lamasi (interleukin-1) yang selanjutnya akan meningkatkan sintesis prostaglandin oleh preoptic hypotalamus anterior hingga meningkatkan suhu tubuh kucing(Singh dan Singh, 2010). MenurutPurnamaningsih et al. (2020), demam terjadi pada kasus akut dengan masa inkubasi virus rata-rata (2-7 hari) setelah masuk dan bereplikasi dalam tubuh secara viremia.Wolfesberger et al. (2012), mencatat terdapat 73 ekor kucing yang terkena FPV mengalami demam serta beberapa tanda klinis lainnya seperti muntah, lesu, dan diare.Kucing kasus dapat mengalami demam yang disebabkan oleh adanya infeksi FPV.Pemeriksaan darah lengkap menunjukkan bahwa kucing mengalami leukopenia, granulositopenia, dan trombositopenia. Hal serupa dilap ...
Feline panleukopenia virus (FPV) merupakan penyakit infeksius yang menyerang kucing baik diumur muda maupun dewasa. Seekor kucing kampung bernama Bumbi berumur tiga bulan berjenis kelamin betina dibawa ke Rumah Sakit Hewan Pendidikan, Universitas Udayana. Menurut pemilik kucing kasus tidak mau makan dan minum selama sehari, muntah cacing setelah diberikan obat cacing pada hari yang sama, dan diare berwarna coklat dengan konsistensi semisolid. Pemeriksaan klinis menunjukkan kucing kasus lemas, dehidrasi, turgor kulit melambat, mukosa gusi pucat, cermin hidung yang kering, dan demam (39,6℃). Pemeriksaan laboratorium hematologi menunjukkan kucing kasus mengalami leukopenia, granulositopenia, dan anemia normositik hiperkromik. Pemeriksaan penunjang dengan tes kit FPV memperlihatkan hasil positif terhadap virus FPV. Kucing kasus diberikan pakan basah urgent care a/d Hill’s® Prescription Diet, terapi cairan menggunakan ringer laktat 30 mL/kgBB/hari secara intravena (IV), injeksi antibiotik Cefotaxime sodium (50 mg/kg BB, IV q12h) selama empat hari, injeksi antiemesis Ondansetron HCl (0,2 mg/kg BB, IV, q12h) selama dua hari, dan Raniditine HCl (2,5 mg/kg BB, IV q12h) selama empat hari. Terapi suportif diberikan injeksi vitamin C (30 mg/kg BB, IV, q12h) selama empat hari, vitamin B kompleks sebanyak 1 mL/ekor drop pada cairan infus, kaolin-pektin sirup (1 mL/kg BB, PO, q12h). Pengobatan rawat jalan diberikan Cefadroxil (22 mg/kg BB, PO, q24h) selama lima hari, multivitamin (vitamin A, vitamin D, vitamin B1, vitamin B2, vitamin B6, vitamin B12, vitamin C, vitamin E, Mangan, Zinc, Fluor, dan Iodium) sebanyak 1 mL/hari selama tiga hari dan obat cacing pyrantel pamoat 20 mg/kg BB sebagai terapi kecacingan. Kucing kasus dirawat secara intensif dan memperlihatkan kemajuan mulai hari ketiga dan pulang pada hari keempat.
... In feline panleukopenia, the negative prognostic factors are leukopenia, thrombocytopenia, hypoalbuminemia, and hypokalemia. The In-shelter environments, survival rates of 20%-51% have been reported in cats with supportive treatment in hospital [4], [23], [24]. In a study by [23] indicated that survival rate was 51.1% and there was no significant correlation between the outcome of treatment and living conditions, age, vaccination status, or severity of clinical signs. ...
Feline panleukopenia is a fatal and contagious viral disease caused by the family of Parvoviridae. Feline panleukopenia virus (FPV) is synonymously called as feline distemper and feline Parvo. FPV infects all felids, raccoons, mink and foxes. FPV infected animals generally have compromised health conditions. Cats of all ages are mostly affected by FPV, but kittens are highly susceptible with higher mortality. The virus is resistant to many disinfectants and normally survives in the environment for several months. Transmission occurs through direct contact of faeces contaminated feeds as well as by indirect contact of fomites, and through intrauterine route. Clinical symptoms include vomition, diarrhoea, lymphopenia and neutropenia, followed by thrombocytopenia and anaemia, immunosuppression, cerebellar ataxia and abortion. Commercially available test kits are used to detect FPV antigen in faeces. Fluid therapy, antibiotics, metronidazole, supportive therapy, and good nursing care are the common treatment practice in Central Referral Veterinary Hospital (CRVH), Nepal. The disease can be controlled by isolation of infected cats, routine vaccination and disinfection of premises. The higher incidence in Nepal is due to lack of vaccination practice against FPV. Disinfectants containing sodium hypochlorite (bleach), potassium peroxymonosulfate and accelerated hydrogen peroxide are found effective. The aim of this paper is to review the current status of the disease, epidemiology, pathophysiology, diagnosis, treatment and control measures for prevention and management of feline panleukopenia infections in developing countries like Nepal.
Feline panleukopenia (FPL) is caused by a Carnivore protoparvovirus infection. Feline parvovirus (FPV) causes most cases. When Canine parvovirus 2 (CPV-2) first emerged, it could not replicate in cats. All current CPV variants (CPV-2a-c) can infect cats to cause subclinical disease or FPL. Feline panleukopenia has re-emerged in Australia in shelter cats associated with failure to vaccinate. Parvoviruses can remain latent in mononuclear cells post-infection. Molecular methods such as polymerase chain reaction are used to determine the infecting strain. Current perspectives on causes, epidemiology, diagnosis, treatment, prognostic indicators, and management of outbreaks in shelters are reviewed.
ABSTRACT: Parvoviruses of carnivores include three closely related autonomous parvoviruses: canine parvovirus (CPV), feline panleukopenia virus (FPV) and mink enteritis virus (MEV). These viruses cause a variety of serious diseases, especially in young patients, since they have a remarkable predilection for replication in rapidly dividing cells. FPV is not the only parvovirus species which infects cats; in addition to MEV, the new variants of canine parvovirus, CPV-2a, 2b and 2c have also penetrated the feline host-range, and they are able to infect and replicate in cats, causing diseases indistinguishable from feline panleukopenia. Furthermore, as cats are susceptible to both CPV-2 and FPV viruses, superinfection and co-infection with multiple parvovirus strains may occur, potentially facilitating recombination and high genetic heterogeneity. In the light of the importance of cats as a potential source of genetic diversity for parvoviruses and, since feline panleukopenia virus has re-emerged as a major cause of mortality in felines, the present study has explored the molecular characteristics of parvovirus strains circulating in cat populations. The most significant findings reported in this study were (a) the detection of mixed infection FPV/CPV with the presence of one parvovirus variant which is a true intermediate between FPV/CPV and (b) the quasispecies cloud size of one CPV sample variant 2c. In conclusion, this study provides new important results about the evolutionary dynamics of CPV infections in cats, showing that CPV has presumably started a new process of readaptation in feline hosts.
Feline panleukopenia virus (FPV) is a significant pathogen of cats. Rapid virus detection is critical for treatment and management, especially in populations in which spread may occur. This study investigated the ability of the SNAP Canine Parvovirus Antigen Test Kit (SNAP Parvo, IDEXX Laboratories) to detect FPV with confirmation of viral identity by polymerase chain reaction (PCR) assay and genetic sequencing on fecal samples (n = 97) from cats with suspected FPV infection. Fifty-five samples were positive by SNAP Parvo; 54 of 55 were also positive by conventional PCR assay and were identified as FPV by genetic sequencing. This study demonstrates that SNAP Parvo can detect FPV in clinical samples.
Feline parvovirus (FPV) causes leukopenia in naturally infected cats. We investigated the mechanism of hematopoietic depression by this virus in feline bone marrow cultured in vitro. In suspension cultures we demonstrated FPV propagation and replication using DNA molecular hybridization. Viral RNA and DNA were observed by in situ hybridization in about 10% of marrow cells at day 3. Granulocytes and their precursors were virtually absent from infected cultures after six days. Infected cells showed viral capsid protein predominantly in nuclei by immunofluorescence. In clonal assays, FPV most efficiently inhibited hematopoietic colony formation by myeloid progenitor cells (CFU-GM), but erythroid colony formation (BFU-E and CFU-E-derived) was also depressed in the presence of virus. Inhibition of colony formation could be abrogated by physical inactivation of the virus or preincubation with specific neutralizing antibodies. Recombinant human colony stimulating factors GM-CSF and G-CSF supported feline myelopoiesis in progenitor assays, and FPV completely inhibited factor dependent colony formation.
The in vivo pathogenicity of canine parvovirus (CPV) type 2c (strain V203) and of CPV type 2a (strain V154) against cats was investigated. Our results indicate that both types of CPV have the potential to induce disease in cats.
The clinical efficacy of a recombinant feline interferon (IFN) (type omega) was evaluated under field conditions for the treatment of dogs with parvoviral enteritis. In this multicentric, double-blind, placebo-controlled trial, 94 dogs from one to 28 months old were randomly assigned to two groups which were treated intravenously either with IFN (2.5 million units/kg) or placebo once a day for three consecutive days, and monitored for clinical signs and mortality for 10 days. Each dog received individual supportive treatment The data from 92 interpretable cases (43 IFN-treated and 49 placebo) showed that the clinical signs of the IFN-treated animals improved significantly in comparison with the control animals, and that there were only three deaths in the IFN group compared with 14 deaths in the placebo group (P = 0.0096) corresponding to a 4.4-fold reduction. Alternative analyses of the data taking into account the prior vaccination status of the dogs against canine parvovirus suggested that the IFN therapy resulted in a 6.4-fold reduction in mortality (P = 0.044) in the unvaccinated cohort, a significant reduction when compared with the vaccinated cohort.
Canine parvovirus type-2a (CPV-2a) and type-2b (CPV-2b) have recently been isolated from domestic cats. The pathogenicity of CPV-2b in domestic cats is still unclear. In this study, we performed infection tests to examine the pathogenicity of CPV-2b, FP84 strain, isolated from a domestic cat. The results demonstrated that the CPV strain FP84 is able to infect and replicate well in domestic cats. Two of the 3 cats used in the test died. They showed loss of appetite, diarrhea, leukopenia and dehydration. Since FP84 was found to be virulent to domestic cats, it is necessary to examine the efficacy of inactivated feline panleukopenia virus vaccines against CPV infection in domestic cats.
The aim of this study was to evaluate differences between young cats (< 6 months) and adult cats (≥ 6 months) with feline panleukopenia with respect to clinical signs, laboratory abnormalities, environmental conditions, vaccination status, and outcome.
Medical records of 244 cats diagnosed with panleukopenia between 1990 and 2007 at the Clinic of Small Animal Medicine, Ludwig-Maximilians University of Munich, Germany, were evaluated retrospectively. Cats that tested positive for feline panleukopenia virus (FPV) via electron microscopy, polymerase chain reaction (blood, faeces), antigen ELISA (faeces), or that had histopathological lesions consistent with panleukopenia at necropsy were included. Cats were excluded if they had been vaccinated against FPV within 3 weeks before admission.
In total 43.3% of cats were older than 6 months. There was no statistically significant difference between the two age groups regarding outcome, breed, sex, environmental conditions, vaccination status, clinical signs, and laboratory parameters with the exception of haematocrit: cats < 6 months had significantly lower haematocrit on the day of presentation than cats ≥ 6 months.
Feline panleukopenia is predominantly in young cats, but older cats can also suffer from the disease. Although young cats are at a higher risk of infection, cats at the age of < 6 months suffering from clinical disease do not have a higher risk of death. Clinical presentation, laboratory abnormalities, prognosis, and outcome did not differ significantly between cats younger versus older than 6 months of age.
The objectives of this matched case-control study in a veterinary teaching hospital were to investigate the influence of signalment and historical data on the odds of occurrence of canine parvovirus (CPV) enteritis and the potential usefulness of the clinical signs and clinicopathologic abnormalities recorded on admission as prognostic indicators of mean duration of hospitalization (DOH) and outcome of the disease. Ninety-four puppies with natural CPV enteritis and 188 age-matched controls were studied. The odds to develop CPV enteritis were higher in purebreds compared to mixed-breed puppies. Vomiting and depression at the time of admission were associated with a prolongation of DOH by 2 and 1.75 days, respectively. The lymphopenic and hypoalbuminemic dogs were hospitalized for 1.9 and 2.5 more days, respectively, compared to those without these abnormalities. The odds of non-survival were higher in those puppies with evidence of systemic inflammatory response syndrome (SIRS) at the time of admission.
DMSO has multiple known pharmacological properties. In addition to those referred to include: cryoprotective action, radioprotective effect, influence on serum cholesterol in experimental hypercholesteremia, and platelet aggregation antagonism. How the multiple properties of this chemical affect therapy in clinical medicine must yet be explained. It is clear, however, that DMSO does affect biological systems, and that this influence has many clinical applications. Perhaps one of the most interesting and significant properties of DMSO is its ability to move other drugsthrough membranes. When mixed with DMSO, many drugs appear to be potentiated in their physiologic effect; thus smaller doses are required and less toxicity is demonstrated. In cancer chemotherapy, this value already has practical use. Some of the studies to be reported in this monograph will describe additional, almost unbelievable observations. Perhaps the mechanism of action of these clinical phenomena will be found in one or more of the pharmacological properties described. It would not be surprising, however, if we were to conclude with a resolution to search for new explantations of the mystery of DMSO, for it would appear that DMSO is really a new principle in medicine and cannot always be measured by existing standards.
Antiviral activities of a recombinant feline interferon (rFeIFN) KT-80 were evaluated against feline enteropathogenic viruses in feline and canine cell lines. Sensitivity to antiviral activities of the rFeIFN varied with cell types; Felis catus whole fetus (fcwf-4) cells were more sensitive than Crandell feline kidney cells, but no sensitivity was found for Madin-Darby canine kidney cells when vesicular stomatitis virus was used as a challenge virus. Reductions were generally IFN dose-dependent and were more consistent when the cells were continuously treated with the rFeIFN than when they were pretreated only before viral challenge. Compared with each virus control culture of fcwf-4 cells, yields of rotavirus, feline panleukopenia virus (FPLV), feline calicivirus and feline infectious peritonitis coronavirus were reduced by ranges of 1.3 to < or = 3.1 log10, 0.6 to 1.6 log2, 0.8 to 3.7 log10 and 0.5 to 0.6 log10, respectively, in the cultures continuously treated with 10 to 10000 U of the rFeIFN. The yield reduction of FPLV was considered to be in part attributable to inhibition of cell growth by the rFeIFN supplemented in the medium.
The recombinant hG-CSF Filgrastim was used in severe cases of neutropenia in the dog caused by parvovirosis, hyperestrogenism, treatment with antineoplastic agents, an aplastic syndrome and in the cat in cases of infectious panleukopenia. Increases of the numbers of leukocytes were observed in all groups of diseases in the dog, but not in feline infectious panleukopenia. Filgrastim is indicated in neutropenias associated with disturbance of the general condition accompanied by fever, but not in cases of transitory leukopenias.
Dogs with clinical signs consistent with parvoviral enteritis and leukopenia (total leukocyte count < 5.0 x 10(9) l(-1)) were included in this randomised double-blind study (treatment group: n = 22; control group: n = 21). The dogs in the treatment group received a subcutaneous daily injection of 10 microg kg(-1) of recombinant human granulocyte colony-stimulating factor (rhG-CSF) for 5 days. Clinical and blood investigations were performed prior to the first injection, daily during the treatment period and on the day after treatment ended, and then once more, 26 days after the first injection. During the study, no significant differences were found between the two groups with respect to survival rate (treatment group: 68 per cent; control group: 71 per cent, P > 0 4, Fisher-Test) and other clinical findings. Similarly the total leukocyte count, neutrophil count and other haematologic and biochemical parameters did not differ significantly between the groups, based on differences from initial values (P > 0 05). Consequently, the use of rhG-CSF in the treatment of dogs with parvoviral enteritis cannot be recommended.
Administration of recombinant feline interferon-omega (rFeIFN) has been proposed for the prophylaxis of canine and feline parvovirosis. In the present study, the influence of the administration of rFeIFN on blood markers of inflammation (alpha-globulins, alpha(1)-acid glycoprotein) and immune system activation (gamma-globulins, IgG, IgM, specific anti-feline parvovirus IgG or IgM) was evaluated in a cattery developing an outbreak of feline panleukopenia due to feline parvovirus (FPV) infection few days after initial administration of rFeIFN. Kittens (n=23) were injected with rFeIFN (1MU/kg subcutaneously, once a day for 3 days) and their blood parameters were compared with those of 17 untreated cats. Cats that survived the outbreak were vaccinated and re-sampled 1 month after the last rFeIFN administration. Time of emergence of clinical signs and survival rate were not significantly different between the two groups. Controls and treated cats surviving the infection had high levels of gamma-globulins, total- and anti-FPV specific IgGs, likely due to passive transfer of maternal immunity. Compared to controls, treated kittens had lower levels of alpha(1)-globulins and higher mean values of gamma-globulins and immunoglobulins. Data from samples collected after vaccination revealed a higher level of gamma-globulins, total- and anti-FPV specific IgGs in treated kittens, compared with controls, suggesting that rFeIFN stimulates antibody production. Based on this results, rFeIFN should be administered to the queen, to increase passive maternal immunity, or to kittens before introduction in a potentially contaminated environment.
D-Galactosamine (D-Galn: 300 mg/kg) was intraperitoneally administered to rats. After 6 h the activity of plasma GOT and GPT was significantly higher than that of the control group and plasma GOT and GPT activities increased thereafter. These results indicated that the necrotic process was initiated at about 6 h and developed thereafter. With coadministration of DMSO (1 h before administration of D-Galn: 2.5 mL/kg, oral), plasma GOT and GPT were significantly lower, showing that DMSO inhibited the necrotic action of D-Galn. After 6-24 h of D-Galn administration, the hepatic level of vitamin C, the most sensitive indicator of oxidative stress, decreased significantly, indicating that oxidative stress was significantly enhanced 6 h after D-Galn intoxication and thereafter. DMSO significantly restored the liver vitamin C level 24 h after D-Galn injection, demonstrating that DMSO effectively ameliorated the oxidative stress caused by D-Galn, resulting in the prevention of necrosis of the liver. Phosphorylated JNK and phospho-ERK were significantly increased transiently 6-12 h after treatment with D-Galn. These results indicated that oxidative stress and the activation of JNK took place almost simultaneously. Phosphorylated p38 MAPK was not changed and DMSO treatment did not affect the change of these MAPKs by D-Galn.
Despite treatment, many dogs still die of complications related to canine parvoviral (CPV) enteritis. Effective prognostication would be beneficial in managing this disease.
We hypothesize that the occurrence of leukocytopenias at admission and at 24 and 48 hours after admission, and changes in absolute leukocyte counts over time, could be used to predict outcome.
Sixty-two puppies with confirmed CPV.
A prospective study was performed. CBC was performed daily until discharge or death (in which case a postmortem examination was performed).
Of the nonsurvivors (10/62; 16%), 9 died because of complications of the disease and 1 was euthanized because of a poor prognosis. There was a statistical significant difference in the occurrence of leukocytopenias between groups at 24 and 48 hours postadmission. The survivors showed a significant increase over time in certain leukocyte types (specifically lymphocytes) compared with values at admission. The positive predictive value for survivors was high. Nonsurvivors had marked thymic and lymphoid atrophy and marked bone marrow hypocellularity.
An accurate prognosis could be obtained at 24 hours after admission by evaluating the change in total leukocyte, band neutrophil, lymphocyte, monocyte, and eosinophil counts.