updated November 10, 2015
The Feline Panleukopenia guidelines were first published in the J Feline Med Surg 2009; 11: 538-546 and updated in J Feline Med Surg 2013; 15: 530-531; the present update has been authorised by Uwe Truyen and edited by Karin Möstl.
Click here to download the Feline Panleukopenia file
Feline panleukopenia virus (FPV) is the prototype of closely related parvoviruses isolated from dogs, mink, raccoons, raccoon dogs, foxes and other canids (Parrish, 1990). They were initially named after the hosts from which they had been isolated. Current taxonomy defines canine parvovirus and feline panleukopenia virus as a single entity (Tattersall, 2006), but in the present guidelines, FPV refers to the parvovirus in cats.
Virions contain single-stranded genomic DNA, are not enveloped (naked), sometimes penetrated by stain; they are 18-22 nm in diameter, of icosahedral symmetry, but appear to be round and hexagonal in electron micrographs (Fig. 1).
Unlike most other DNA viruses, parvoviruses are unable to activate DNA synthesis in host cells. Their replication is in the nucleus (Fig. 2, 3), and the infected cells must be actively mitotic.
This explains why tissue damage occurs predominantly in rapidly dividing cells, like those in the intestine, bone marrow, and in embryonic tissue.
FPV infects cats and other members of the Felidae, as well as raccoons, mink, and foxes (Steinel et al., 2001). It also infects dogs, where FPV replication was seen in lymphoid tissues (thymus, spleen, bone marrow) and not in the gut, but the virus is not shed (Truyen and Parrish, 1992).
In 1978, a new parvovirus, closely related to FPV, was first described in dogs (Carmichael, 2005). It was named canine parvovirus type 2 (CPV-2), to distinguish it from another parvovirus isolated from dogs in 1970, which is now called “canine minute virus”. CPV-2 has evolved from FPV by acquiring 5 or 6 amino acid changes in the capsid protein gene (Parrish, 1990; Truyen, 1999) and is no longer able to infect cats. However, during further adaptation to the canine host, which most likely occurred in the raccoon, the raccoon virus acquired the amino acid changes that had enabled the new virus to better bind to the canine cellular receptor but also retained its ability to infect cats (Hueffer and Parrish, 2003; Allison et al., 2012). This led to the generation of the new type CPV-2a, that acquired further mutations including those at amino acid 426 of the VP2, which determine the different antigenic types 2a, 2b, and 2c. The parvoviruses now circulating in the dog populations worldwide - genetically and antigenically defined as types CPV-2a, -2b, and “–2c” - can infect cats and may even cause disease (Truyen et al., 1995, 1996; Mochizuki et al., 1996). However, CPV infections of cats are rare in Europe and the USA, and the virus has only sporadically been found in diagnostic material (Truyen et al., 1996). CPV was isolated from feline peripheral blood lymphocytes after numerous blind passages, and viral DNA was demonstrated by PCR (Ikeda et al., 2000). Recently, however, a case of CPV-2c infection in a cat with severe clinical signs was described in Portugal (Miranda et al., 2014).
During the evolution from FPV to CPV-2 with its various antigenic types, neutralizing epitopes have been affected such that cross-neutralization by FPV antisera is markedly lower against the new viruses (Truyen and Parrish, 2013).
FPV is non-enveloped and highly resistant to physical factors and chemical substances. In contaminated environments, it may remain infectious for weeks or even months (Uttenthal et al., 1999). Diseased carnivores shed virus at high titres (up to 109 TCID50 per gram of faeces), and virus quickly accumulates in affected shelters and catteries. As it is highly contagious, susceptible animals may still become infected, even after a seemingly thorough disinfection of the premises. It is therefore recommended that only successfully vaccinated kittens and cats should enter such an environment.
Although few data on FPV prevalence are available, particularly breeding catteries and rescue shelters are at risk (Addie et al., 1998; Cave et al., 2002).
Persistent infections and persistent viral shedding are rare; using PCR, healthy cats have been found positive in faeces over weeks; it is unknown whether this is of epidemiological significance (Jakel et al 2012). Interestingly, CPV-2 viruses could be isolated from feces of healthy cats in the UK in two shelters. It is unclear if this is of epidemiological importance (Clegg et al., 2012).
After intrauterine infection, FPV antigen is present in the cerebellum of kittens for weeks (Csiza et al., 1971).
The analysis of parvovirus sequences recovered from wild carnivores (pumas, coyotes, raccoons, and others) revealed a broad range of virus types. This implicates the infection of predators by their prey, if the latter was infected with parvoviruses, and thus a new route of infection (Allison et al., 2013).
FPV causes a systemic infection. The virus is transmitted via the faecal-oral route, initially replicates in tissues of the oropharynx and is then distributed via cell-free viraemia to virtually all tissues. Replication of the parvoviral single-stranded DNA requires cells in the S-phase of division and is therefore restricted to mitotically active tissues; in the gut, this results in enteritis (Figs. 4, 5). Parvoviruses require cellular DNA polymerases to synthesize the complementary DNA strand, which is the first step in replication and a prerequisite for transcription.
The virus infects lymphoid tissues where it may cause cellular depletion and a functional immunosuppression. Lymphopenia may arise as a result of lymphocytolysis but also indirectly, from lymphocyte emigration into tissues. The bone marrow is affected, and virus replication has been described in early progenitor cells, with dramatic effects on virtually all myeloid cell populations (Parrish, 1995). “Panleukopenia”, i.e. the deficiency of all white cell populations is the result (Truyen and Parrish, 2000).
The hallmark of FPV replication is the shortening of the intestinal villi due to a sometimes complete loss of epithelial cells in the gut (Parrish, 2006). The virus replicates in the rapidly dividing cells in the crypts of Lieberkühn, which impairs regeneration of the epithelium and results in the lesions described above (Fig. 6). Their severity correlates with the epithelial turnover rate, and co-infection with enteric viruses - like feline coronavirus - may enhance the severity of disease.
Intrauterine transmission or perinatal infection may affect central nervous system development. “Feline ataxia syndrome” results from an impaired development of the cerebellum due to lytic infection of the Purkinje cells in the kitten (Figs. 7, 8) Csiza et al., 1971; Kilham et al., 1971). - An FPV-like virus has been described as the cause of reproductive disorders in pregnant foxes (Veijalainen and Smeds, 1988).
Foetal infection may induce immunological tolerance, so that kittens continue shedding virus for extended periods of time (Pedersen, 1987).
Foetuses infected between the 35th and 45th days of gestation have depressed T-lymphocyte mediated immunity. In adult cats, infection leads to a transient decrease in the immune response: neutrophil counts decrease severely, and lymphocytes disappear from the circulation, lymph nodes, bone marrow and thymus (Pedersen, 1987; Ikeda et al., 1998).
Foetuses infected between the 35th and 45th days of gestation have depressed T- lymphocyte mediated immunity. In adult cats, infection leads to a transient decrease in the immune response: neutrophil counts decrease severely, and lymphocytes disappear from the circulation, lymph nodes, bone marrow and thymus (Ikeda et al., 1998; Pedersen, 1987).
Feline panleukopenia virus infection: pathological consequences and clinical manifestations
|Affected cells||Consequences||Clinical manifestation|
|Adapted from: Chandler, Feline Medicine and Therapeutics, 3rd Ed, 2004.|
|Intestinal crypt epithelium||Villous collapse, enteritis||Diarrhoea|
|Lymph node, thymus||Germinal centre depletion, apoptosis of lymphocytes, thymic atrophy||Lymphopenia|
|Bone marrow||Stem cell depletion||Neutropenia (later also thrombocytopenia and anaemia)|
|Foetal death||Most cells in the foetus||Abortion|
|Cerebellar ataxia||Developing cerebellum||Cerebellar hypoplasia|
Adapted from: Chandler, Feline Medicine and Therapeutics, 3rd Ed, 2004.
Passive immunity acquired via colostrum
In the kitten, maternal antibodies have a biological half-life of about ten days (Scott et al., 1970; Pedersen 1987). When antibodies have waned below a titre of 40 to 80 (as measured by haemagglutination inhibition) they do not reliably protect against infection but may interfere with active immunisation (Fig.9). Most cats have maternal antibodies at protective titres until weeks 6 to 8. Later immunisations are effective (Dawson et al., 2001; EBM grade I), which makes ABCD recommend vaccinations at 15 to 16 weeks of age, as explained in the present Guidelines.
The endotheliochorial placentation of the cat restricts maternofetal passage of solutes, and IgG can only cross the placenta barrier in the last trimester of gestation. This immunoglobulin transfer accounts for <10 % of the kitten’s maternal immunity. Therefore ingesting sufficient colostrum is essential for acquiring protective levels of neutralising antibodies from the queen. Maximum absorption is around the 8th hour of life. Later, the kitten’s intestinal cells are replaced by new epithelium that no longer absorbs and transports antibodies.
Kitten serum antibody titres are generally about half of those of the dam. Their levels depend on the individual colostrum intake, which explains the large variations between litter mates. The titres decrease in the first weeks of life, by decay and by dilution in the growing organism. In analogy with canine parvovirus, an immunity gap around 6 to 10 weeks of age is expected to exist, when antibody levels are too low to protect against natural infection, but still high enough to interfere with vaccination.
Active immune response against FPV
Antibodies play an important role in the immune response to FPV. Maternally-derived antibodies (MDA) efficiently protect kittens from fatal infection. This passively acquired immunity is later replaced by an active immune response obtained by vaccination or as a consequence of a natural infection.
Acquired immunity is solid and long lasting (Thiry, 2002a) and can be induced by both inactivated and modified live virus (MLV) vaccines. FPV antiserum can be used for passive immunisation when unvaccinated animal are likely to be exposed to virus before the initiation of a vaccine-induced, active response (Barlough et al., 1997).
Parvoviruses induce a range of immune responses including T-helper CD4+ lymphocytes and CD8+ cytotoxic T lymphocytes. Parvovirus uptake occurs by phagocytosis but also by other non-phagocytic mechanisms such as fluid pinocytosis or receptor-mediated endocytosis (Sedlik et al., 2000).
In practice, FPV antigen detection in faeces is usually carried out using commercially available latex agglutination or immunochromatographic tests (Veijalainen et al., 1986; Addie et al., 1998). These tests have a good specificity and acceptable sensitivity when compared to reference methods (Neuerer et al., 2008; Schmitz et al., 2009; EBM grade I). Tests marketed for the detection of FPV antigen as well as those for detecting canine parvovirus antigen may be used to diagnose FPV in faeces.
Diagnosis by electron microscopy has lost its importance due to more rapid and automated alternatives. Specialised laboratories offer PCR-based test on whole blood or faeces. By PCR, healthy cats tested positive in faeces over weeks, but the epidemiological significance of this finding is unknown. Clinicians need to bear this in mind when interpreting diagnostic data.
A cat showing clinical signs of feline panleukopenia, substantiated by laboratory evidence should be kept in isolation. Supportive therapy and good nursing care significantly decrease s mortality caused by FPV. The severe dehydration accelerates disease progression (Fig. 10, 11). Restoration of fluid and electrolyte, and of the acid-base balance preferably by intravenous drip is most important in symptomatic treatment (Fig. 12).
As the gut barrier often is destroyed in FPV-infected cats, intestinal bacteria may invade the blood stream. Bacteriaemia may ensue, facilitated by the existing neutropenia, and leading to sepsis in these immunocompromised patients. Prevention of sepsis is essential, and a broad-spectrum antibiotic with a proven efficacy against gram-negative and anaerobic bacteria is recommended. Examples are amoxicillin/clavulanic acid or piperacillin in combination with aminoglycosides, fluoroquinolones, cephalosporins or piperacillin/tazobactam. The potential side effects of these drugs should be taken into consideration. Antibiotics should be administered parenterally (preferentially intravenously).
Oral intake of water and food should only be restricted if vomiting persists, and feeding should be continued as long as possible, and restarted as soon as possible. Beneficial effects of early enteral nutrition have been reported in canine parvovirosis (Mohr et al., 2003). A highly digestible diet is preferred, but if the cat does not accept it, any diet is better than no food intake at all. If vomiting persists, anti-emetics should be considered. Vitamin supplements, particularly of the B vitamin complex can be given to prevent development of thiamine deficiency, an infrequent sequel, which occurs infrequently.
Cats that develop hypoproteinaemia may require plasma or whole blood transfusions to restore oncotic pressure. Plasma transfusion in combination with heparin may control disseminated intravascular coagulation (DIC), as it supplements anti-thrombin III and other important plasma proteins. In cats that are anorexic or show severe vomiting and/or diarrhoea, or in patients with persisting hypoproteinaemia, full or partial parenteral nutrition is required, preferably via a central venous catheter in the jugular vein (Hartmann and Hein, 2002).
Table 2. Overview of treatment in cats with FPV (all measures are EBM level 4)
|anti-FPV serum||anti-CPV serum effective in dogs||beneficial effects in cats expected|
|feline recombinant Interferon-omega||effective in dogs||beneficial effects in cats expected|
|fluid therapy||to control dehydration and restore electrolyte and acid base balance||necessary in every cat with vomiting and diarrhea|
in combination with
- aminoglycosides or
- fluoroquinolones* or
- cephalosporins, third generation.)
|prevention of sepsis||broad-spectrum antibiotic with proven efficacy against gram-negative and anaerobic bacteria recommended|
|highly digestible diet||feeding should be continued as long as possible and restarted as soon as possible||any diet is better than no food|
|Antiemetics||to control vomiting||recommended for vomiting animals|
|B vitamin complex||prevention of thiamine deficiency||recommended|
|plasma or wholie blood transfusion||to restore oncotic pressure||recommended in cats with hypoproteinaemia|
|full or partial parenteral nutrition||to restore oncotic pressure and meet energy requirements||recommended in cats with anorexia, severe vomiting/diarrhea or persisting hypoproteinaemia|
|Low- molecular heparin (fragmin)||to control DIC||recommended in cats with DIC|
Anti-FPV serum can be used to prevent infection of susceptible animals following after exposure. The therapeutic efficacy of immune serum has been demonstrated in dogs (Meunier et al., 1985), and similar beneficial effects may be expected in cats.
Feline recombinant interferon-omega is effective in the treatment of parvoviral enteritis in dogs (Minagawa et al., 1999; Martin et al., 2002; De Mari et al., 2003) and also inhibits replication of FPV in cell culture. So far no data are available on its efficacy in FPV-infected cats.
Due to the extreme physicochemical stability of FPV, contaminated cages, litter trays, food dishes, water bowls, shoes and clothing can play an important role in transmission. Therefore attention to hygiene is of utmost importance. The virus is resistant to many common disinfectants, but can be inactivated by products that contain peracetic acid, formaldehyde, sodium hypochlorite, or sodium hydroxide. Commercially available chemical disinfectants proven effective against non-enveloped viruses or a disinfectant (solution or dry fog) based on formaldehyde or peracetic acid can be used for room disinfection.
Susceptible kittens and unvaccinated older animals should not be in contact with other cats until they are properly immunized. Once a disease outbreak occurs, passive immunization can be used to protect susceptible cats (young kittens with an incomplete vaccination history, colostrum-deprived kittens or unvaccinated cats). Anti-FPV serum can be given subcutaneously or intraperitoneally and may protect for 2-4 weeks. If a commercial product of equine origin is used, repeated administration is not recommended as this may lead to anaphylactic reactions. Since the administered immunoglobulins will bind to parvoviral epitopes, these animals should not be vaccinated within the first three weeks after passive immunization.
General recommendations on vaccine type and vaccination protocol
Both MLV and adjuvanted inactivated FPV vaccines are available for administration by injection, and both provide solid immunity against disease. In an immune-competent cat capable of mounting an appropriate response, MLV vaccines generally result in a more rapid protection (Levy et al. 2006; EBM grade II). However, even a single dose of an inactivated FPV vaccine may rapidly induce good antibody responses in naïve cats within a short time span (Fischer et al., 2007). There are no data to suggest that particular vaccine brands are more efficacious than others.
In most situations, there is no reason to prefer one vaccine type to the other in an individual cat; MLV products are being used more generally, because of the more rapid onset of protection and a better resistance to MDA. There may be considerations affecting this decision:
MLV FPV vaccines should not be used in pregnant queens because of the risk of placental virus passage to the foetus and damage, especially to the developing cerebellum (Pollock and Postorino, 1994). In some countries, inactivated FPV vaccines are licensed for use in pregnant queens, but their vaccination should generally be avoided.
MLV FPV vaccines should never be administered to kittens under 4 weeks of age for the same reason: to avoid damage to the cerebellum, which is still developing in young neonates (Pollock and Postorino, 1994).
Because of the ubiquity of the virus and the serious consequences of an infection, vaccination is recommended for every cat: the FPV vaccine is defined as a core vaccine. Even cats with an indoor lifestyle cannot always avoid encountering FPV, since the virus is so stable in the environment and can be transmitted on fomites (Pollock and Postorino, 1994).
Primary vaccination course
Most kittens are protected by MDA in the first weeks of life. However, without serological testing, the level of protection and the point at which a kitten will become susceptible to infection and/or can respond immunologically to vaccination is unknown; also, there is considerable variation between individuals.
In general, MDA will have waned by 8 to 12 weeks of kitten age to a level that allows an active immunological response, and an initial vaccination at 8 to 9 weeks of age followed by a second vaccination 3 to 4 weeks later is commonly recommended. The data sheets of many vaccines contain recommendations to this effect. However, kittens with poor MDA may be vulnerable (and capable of responding to vaccination) at an earlier age, while others may possess MDA at such high titres that they are incapable of responding until some time after 12 weeks of age.
No single primary vaccination policy will therefore cover all potential situations. These are ABCD’s recommendations:
All kittens should receive FPV vaccines
A minimum of two doses – one at 8 to 9 weeks of age and a second 3 to 4 weeks later (at a minimum of 12 weeks of age) should be administered to cats living in low risk situations.
In higher risk situations, a third vaccination at 16 weeks is recommended. Maternal antibodies may persist beyond week 12 in some cats, as field data suggest (Jakel et al., 2012; Dawson et al., 2001), such that vaccination at 12 weeks may fail to induce protection (Kruse et al., 2010). Therefore, a third kitten vaccination at 16 weeks of life should be given to kittens in e.g. breeding catteries or cat shelters. A 16-week-vaccination should also be considered for kittens born to queens with high antibody titres, as these are likely to transmit high levels of MDA that may persist for more than 12 weeks in their kittens (e.g. queens that have recovered from disease, that have lived in a high-exposure environment, or have received vaccination close before or during pregnancy).
If prophylactic administration of immunoglobulins is not possible, additional earlier vaccinations should be considered, especially if MDA is known or suspected to be poor and/or if the kitten is in a high risk situation (EBM grade I). If a kitten is vaccinated at or before 4 weeks of age, this should only be done using an inactivated product, and repeat vaccinations can be done at 3 to 4 week intervals until ≥12 weeks of age.
Adult cats of unknown vaccination status should receive a single initial FPV vaccine injection (MLV) followed by a booster vaccination one year later.
Cats that respond to FPV vaccination maintain a solid immunity for at least seven years – the latest point in time tested - in the absence of any repeat vaccination or natural challenge (Scott and Geissinger, 1999; Lappin et al. 2002; EBM grade II). Nevertheless, the ABCD recommends the following revaccination protocol:
All cats receive a first booster 12 months after completion of the primary vaccination course (this will ensure adequate vaccine-induced immunity for cats that may not have adequately responded to the primary course)
Following this first booster, subsequent revaccinations are recommended at intervals of three years or longer, unless special conditions apply (EBM grade II).
While most cases of feline panleukopenia are caused by infection with FPV, variants of canine parvovirus (CPV-2a, CPV-2b, CPV-2c) have emerged that infect cats and may cause disease. Current FPV vaccines appear to afford protection against these new CPV variants (Chalmers et al., 1999; Nakamura et al. 2001; EBM grade II).
Control in specific situations
Random source populations with unknown vaccination histories, continuous turnover, and high risk for infections characterize most shelters. The cost of a vaccine is a significant management aspect; therefore, only those antigens that demonstrate a clear benefit against common and significant shelter diseases should be considered.
Feline panleukopenia is such a disease. FPV has re-emerged as a cause of cat mortality in cats in shelters and rescue homes throughout Europe and the United States. With rare exceptions, all kittens and cats over 4 to 6 weeks of age should therefore be vaccinated, regardless of their housing status. - For sick or pregnant cats, any decision about vaccination has to be taken for the individual cat, but vaccination is recommended whenever and as soon as justifiable. Pregnant cats should never receive a live FPV vaccine. Alternatively passive immunisation with FPV antiserum may be considered (or anti-CPV-2 canine globulin). Kittens should be vaccinated beginning at 4 weeks of age in the face of an outbreak, otherwise at 6 weeks of age. MLV vaccines are recommended because of their faster onset of action, greater efficacy at overcoming maternal antibody, and a greater likelihood of conferring sufficient immunity. Although concerns have been raised regarding strain reversion to virulence, this has never been documented. Vaccination should be repeated every 3 to 4 weeks until 16 weeks of age. If adult cats are ill or otherwise compromised at the time of initial vaccination, another injection should be considered when the cat is again in good health (at least two weeks after the initial vaccine). - Cats of unknown status should not be housed together.
Passive immunisation can be used in shelters when available. It is useful at admission if other diseases are present or in an environment with high infection pressure, as it provides immediate protection. The efficacy of immunoglobulins to prevent infection, including FPV, has been proven in experimental studies and in the field some 50 years ago. It depends upon the antibody titre against the specific agent, the volume administered, the importance of antibodies in controlling a particular infection, and the timing of administration.
Multivalent hyperimmune immunoglobulin preparations for cats are commercially available in some European countries - horse sera containing antibodies against FPV, FHV-1, and FCV. They are marketed for prophylactic (usually one injection of 1 vial/animal subcutaneously) and therapeutic (usually 3 injections of 1 vial/animal subcutaneously every 24 hours) use. Protection lasts for about 3 weeks. During this period, active immunization (vaccination) must be avoided, because the immunoglobulins will bind to the vaccinal antigens, tying them up in immune complexes. Although large amounts of foreign protein are administered, allergic reactions and side effects are rare if a cat is treated for the first time. Repeated treatment (with an interval of more than 1 week) is discouraged because cats can develop anaphylactic reactions to the equine protein (Hartmann and Hein, 2002).
Customised homologous (hyper)immune serum can be prepared and administered. Serum is obtained from healthy cats or from groups of animals that have recovered from a disease, whereas hyperimmune serum comes from animals that had been repeatedly vaccinated. The antibody content and hence the duration of protection of such sera are unknown.
Like all exogenous proteins, administered antibodies are quickly eliminated from the body.
Feline immune sera can be prepared in veterinary practice, but the blood donors must be screened for insidious infections (e.g. FIV, FeLV, Bartonella infection). The blood type of donor and recipient should match. The minimum amount required for protection is unknown, but the dose recommended for cats is 2 to 4 ml serum per kilogram body weight. Attention must be paid to sterility during collection, storage and administration. Jugular vein puncture is preferred, and the area over the jugular vein should be shaved and disinfected. Blood should be collected (at least twice the amount of required serum) into sterile tubes without additives and allowed to clot. Serum can be stored at -20° C in single dose aliquots, as IgG is very stable, and can be kept for up to a year if frozen promptly after collection (Levy and Crawford, 2000; EBM grade II). Usually, sera are given subcutaneously; intraperitoneal injection is more feasible in kittens. If for an instant effect intravenous administration is required, plasma (instead of serum) should be used (Greene and Schultz, 2005). For details see the ABCD Guidelines Blood transfusion and Pennisi et al. (2015).
As FPV and CPV are closely related viruses that a high degree of cross-neutralization, it may be expected that hyperimmune sera raised against CPV are also effective against FPV. This is of particular importance in countries where commercial anti-FPV serum is not available. The remarks above about heterologous preparations apply.
Vaccination schedules used recommended for privately owned cats are appropriate in for most breeding catteries. Queens not up-to-date on vaccinations may receive booster vaccines injections before prior to breeding, to maximize delivery of MDA to kittens (Lawler and Evans, 1997; EBM grade I). As a consequence, their kittens from such queens may need an extra primary vaccination at 16 to 20 weeks, because of a longer in case of persistpersistence ofing MDAs. As stated before, routine vaccination of pregnant cats should be avoided.
Lactation is not known to interfere with the immune response. However, administration of any vaccine may stress the queen and may result in a temporary deterioration of mothering ability and milk production. Vaccination of lactating queens should therefore be avoided.
Vaccination of immunocompromised cats
Vaccines cannot generate optimum protection in animals with conditions that compromise their immune function. Such conditions include genetic immunodeficiencies, but also deficient nutrition, genetic immunodeficiencies, systemic disease, concurrent administration of immunosuppressive drugs, and environmental stress. Efforts should be made to correct the latter conditions before vaccination, and to protect cats from exposure to infectious agents and to correct these conditions if possible prior to vaccination; if this cannot be assured, vaccination should be performed nevertheless and repeated after the animal is fully recovered.
In immunocompromised individuals, inactivated FPV vaccines are recommended. Modified live FPV vaccines should be used with caution in severely immunocompromised individuals, as the failure to control viral replication could potentially lead to clinical signs.
In cats receiving corticosteroids, vaccination should be considered carefully. Depending on dosage and duration of treatment, corticosteroids may cause functional suppression of particularly cell-mediated immune responses, but pertinent studies are lacking. In dogs, corticosteroids do not hamper effective immunization if given for short periods of time at low to moderate doses (Nara et al., 1979; EBM grade IV). However, the use of corticosteroids at the time of vaccination should generally be avoided.
In cats with chronic illness vaccination may sometimes be necessary. Manufacturers evaluate vaccine safety and efficacy in healthy animals and accordingly label their vaccines for use in healthy animals only. Nonetheless, cats with stable chronic conditions such as chronic renal disease, diabetes mellitus or hyperthyroidism should receive vaccines at the same frequency as healthy cats. In contrast, cats with acute illness, debilitation, or high fever should not be vaccinated, unless there are compelling reasons to do so. In these cases, inactivated preparations should be used.
Retrovirus-infected cats should be kept indoors and isolated, to diminish the likelihood of infecting other cats and to reduce exposure to other infectious agents. FeLV-infected cats should be vaccinated against FPV. Although there is no evidence that FeLV-infected catsthey are at an increased risk of vaccine-induced disease from residual virulence of MLV vaccines, noninactivated (“killed”)-infectious vaccines products are preferred if availablerecommended. FeLV-infected cats may not be able to mount adequate immune responses to rabies vaccines,ation and perhaps also not to other vaccines. Therefore, more frequent vaccination should be considered in these cats.
FIV-infected cats are capable of mounting immune responses to administered antigens except during the terminal phase of infection; also primary immune responses may be delayed or diminished (Dawson et al., 1991; Reubel et al., 1994; Foley et al. 2003; EBM grade III). In one study, cats experimentally infected with FIV developed vaccine-induced panleukopenia when given MLV FPV vaccines (Buonavoglia et al., 1993; EBM grade III). Immune stimulation of FIV-infected lymphocytes in vitro promotes virus production, and in vivo, vaccination of chronically infected cats with a synthetic peptide was associated with a decrease in the CD4+/CD8+ ratios (Lehmann et al.1992; Reubel et al. 1994). Therefore, a potential trade-off to protection from secondary disease is the progression of FIV infection due to increased virus production (EBM grade III). Thus only FIV cats at high risk of exposure to infectious agents should be vaccinated, and only with killed products.
Allison AB, Harbison CE, Pagan I, Stucker KM, Kaelber JC, Brown JD, Ruder MG, Keel MK, Dubovi EJ, Holmes EC, Parrish CR (2012). Role of Multiple Hosts in the Cross-Species Transmission and Emergence of a Pandemic Parvovirus. J Virol 86: 865- 872.
Allison AB, Kohler DJ, Fox KA, Brown JD, Gerhold RW, Shearn-Bochsler VI, Dubovi EJ, Parrish CR, Holmes EC (2013). Frequent cross-species transmission of parvoviruses among diverse carnivore hosts J Virol 87: 2342-2347.
Barlough, JE, Barr M, Scott FW, Richards JR (1997). Viral Diseases, In The Cornell Book of Cats, 2nd ed., Ed. M Siegal
Buonavoglia C, Marsilio F, Tempesta M, Buonavoglia D, Tiscar PG, Cavalli A, Compagnucci M (1993). Use of a Feline Panleukopenia modified-live virus vaccine in cats in the primary stage of Feline immunodeficiency virus-infection. J Vet Med B-Zbl Vet B- Infect 40:343-346
Carmichael, LE (2005). An annotated historical account of canine parvovirus. J Vet Med B Infect Dis Vet Public Health 52, 303-311
Casseleux, G, Fontaine E (2006). Gestion de la parvovirose en élevage canin. Le Point Vétérinaire 37:42-46
Cave TA, Thompson H, Reid SW, Hodgson DR (2002). Kitten mortality in the United Kingdom: a retrospective analysis of 274 histopathological examinations (1986 to 2000). Vet Rec 151(17):497-501
Chalmers, WSK, Truyen U, Greenwood NM, Baxendale W (1999). Efficacy of feline panleucopenia vaccine to prevent infection with an isolate of CPV2b obtained from a cat. Vet Microbiol 69:41-45.
Chandler EA (2004). In Feline Medicine and Therapeutics3rd ed. Blackwell Science (UK)
Clegg SR, Coyne KP, Dawson S, Spibey N, Gaskell RM, Radford AD (2012). Canine parvovirus in asymptomatic feline carriers. Vet Microbiol 157: 78-85.
Csiza, CK, A De Lahunta, FW Scott & JH Gillespie (1971). Pathogenesis of Feline Panleukopenia Virus in Susceptible Newborn Kittens II. Pathology and Immunofluorescence. Infect Immun 3:838-846
Dawson S, Smyth NR, Bennett M, Gaskell RM, McCracken CM, Brown A, Gaskell CJ (1991). Effect of primary-stage feline immunnodeficiency virus infection on subsequent feline calicivirus vaccination and challenge in cats. J Acq Immun Defic Syndrome 5:747-750
Dawson S, Willoughby K, Gaskell RM, Wood G, Chalmers WSK (2001). A field trial to assess the effect of vaccination against feline herpesvirus, feline calicivirus and feline panleucopenia virus in 6-week-old kittens. J Fel Med Surg 3:17-22
De Mari K, Maynard L, Eun HM, Lebreux B (2003). Treatment of canine parvoviral enteritis with interferon-omega in a placebo-controlled field trial. Vet Rec 152:105- 8
Fiscus, SA, Mildbrand MM, Gordon JC, Teramoto YA, Winston S (1985). Rapid enzyme- linked immunosorbent assay for detecting antibodies to canine parvovirus. Am J Vet Res 46:859-863
Foley JE, Leutenegger CM, Dumler JS, Pedersen NC, Madigan JE (2003). Evidence for modulated immune response to Anaplasma phagocytophila sensu lato in cats with FIV-induced immunosuppression. Comp Immunol Micribiol Infect 26:103-113
Goto, H (1975). Feline panleukopenia in Japan. II. Hemagglutinability of the isolated virus. Nippon Juigaku Zasshi 37:239-245
Greene CE, Addie DD (2005). Feline panleukopenia. In Infectious diseases of the dog and cat, Ed. CE Greene, WB Saunders Company, Philadelphia. pp 78-88
Greene CE, Schultz RD (2005). Immunoprophylaxis and immunotherapy. In Infectious diseases of the dog and cat, Ed. C.E. Greene, W.B. Saunders Company, Philadelphia pp 1069-1119.
Hartmann K, Hein J (2002). Feline Panleukopenie. Praxisrelevante Fragen anhand eines Fallbeispiels. Tierärztl Prax 30: 393-9
Hofmann-Lehmann R, Fehr D, Grob M, Elgizoli M, Packer C, Martenson JS, O'Brien SJ, Lutz H (1996). Prevalence of antibodies to feline parvovirus, calicivirus, herpesvirus, coronavirus and immunodeficiency virus and of feline leukemia virus antigen and the interrelationship of these viral infections in free-ranging lions in east Africa. Clin Diagn Lab Immunol 3:554-562
Hueffer, K, Parrish CR (2003). Parvovirus host range, cell tropism and evolution. Curr Opin Microbiol 6:392-398
Ikeda Y, Mochizuki M, Naito R, Nakamura K, Miyazawa T, Mikami T, Takahashi E (2000). Predominance of canine parvovirus (CPV) in unvaccinated cat populations and emergence of new antigenic types of CPVs in cats. Virology 278:13-19
Ikeda Y, Shinozuka J, Miyazawa T, Kurosawa K, Izumiya Y, Nishimura Y, Nakamura K, Cai J, Fujita K, Doi K, Mikami T (1998). Apoptosis in feline panleukopenia virus- infected lymphocytes? J Virol 72:6932-6
Jakel V, Cussler K, Hanschmann K-M, Truyen U, König M, Kamphuis E, Duchow K (2012). Feline Panleukopenia in Norwegian Forest breeding cats. BMC Veterinary Research 8: 62.
Kilham, L, Margolis, G Colby ED (1971). Cerebellar ataxia and its congenital transmission in cats by feline panleukopenia virus. J Am Vet Med Assoc. 158:888-901
Köhler C, Manteufel J, Roeder I, Roesler U, Truyen U (2009). Comparative investigations on tenacity of different model viruses for testing chemical disinfectants (in German). Hyg Med; 34: 224-32
Kruse BD, Unterer S, Horlacher K, Sauter-Louis C, Hartmann K (2010). Prognostic factors in cats with feline panleukopenia. J Vet Intern Med. 24(6):1271-6
Lappin, MR, Andrews J, Simpson D, Jensen WA (2002). Use of serologic tests to predict resistance to feline herpesvirus 1, feline calicivirus and feline parvovirus infection in cats. J Am Vet Med Assoc 220:38-42
Lawler DH, Evans RH (1997). Strategies for controlling viral infections in feline populations. In Consultations in Feline Internal Medicine 3., J.R. August (Ed). WB Saunders Company, Philadelphia. pp 603-610
Lehman R, von Beust B, Niederer E, Condrau MA, Fierz W, Aubert A, Ackley CD, Cooper MD, Tompkins MB, Lutz H (1992). Immunization-induced decrease of the CDA+:CD8+ ratio in cats experimentally infected with feline immunodeficiency virus. Vet Immunol Immunopathol 35:199-214
Levy JK, Crawford PC (2000). Failure of passive transfer in neonatal kittens: correction by administration of adult cat serum. J Vet Intern Med 14:362
Levy JK, Fisher SM, Quest CM, Tucker SJ (2006b). Serological responses of feral cats to vaccination in trap-neuter-return programs. J Vet Int Med 20:711
Levy JK, Patterson EV, Reese MJ, Tucker SJ (2006a). Impact of vaccination on parvovirus testing in kittens. J Vet Int Med 20:711
Lutz, H, Castelli I, Ehrensperger F, Pospischil A, Rosskopf M, Siegl G, Grob M, Martinod S (1995). Panleukopenia-like syndrome of FeLV caused by co-infection with FeLV and feline panleukopenia virus. Vet Immunol Immunopathol 46:21-33
Macintire DK, Smith-Carr S, Jones R, Swango L (1999). Treatment of dogs naturally infected with canine parvovirus with lyophilized canine IgG. Proceedings 17th Annual Conference of the American College of Veterinary Internal Medicine. June 10-13, 1999, abstract 118, p 721
Martin V, Najbar W, Gueguen S, Grousson D, Eun HM, Lebreux B, Aubert A (2002) Treatment of canine parvoviral enteritis with interferon-omega in a placebo- controlled challenge trial. Vet Microbiol 89(2-3):115-27
Meunier PC, Cooper BJ, Appel MJ, Lanieu MF, Slauson DO (1985). Pathogenesis of canine parvovirus enteritis: sequential virus distribution and passive immunization studies. Vet Pathol 22:617-24
Minagawa T, Ishiwata K, Kajimoto T (1999). Feline interferon-omega treatment of canine parvovirus infection. Vet Microbiol 69:51-53
Miranda C, Parrish CR, Thompson G (2014). Canine parvovirus 2c infection in a cat with severe clinical disease. J Vet Diagn Invest 26: 462-464.
Miyazawa T, Y Ikeda, K Nakamura, R Naito, M Mochizuki, Y Tohya, D Vu, T Mikami, E Takahashi (1999). Isolation of feline parvovirus from peripheral blood mononuclear cells of cats in northern Vietnam/ Microbiol Immunol 43:609-612
Mochizuki M, Horiuchi M, Hiragi H, San Gabriel MC, Yasuda N, Uno T (1996). Isolation of canine parvovirus from a cat manifesting clinical signs of feline panleukopenia. J Clin Microbiol 34:2101-2105
Mochizuki M, Nakatani H, Yoshida M (1994). Inhibitory effects of recombinant feline interferon on the replication of feline enteropathogenic viruses in vitro. Vet Microbiol 39:145-52
Mohr AJ, Leisewitz AL, Jacobson LS, Steiner JM, Ruaux CG, Williams DA (2003). Effect of early enteral nutrition on intestinal permeability, intestinal protein loss and outcome in dogs with severe parvoviral enteritis. J Vet Intern Med 17(6):791-8
Nakamura K, Ikeda Y, Miyazawa T, Tohya Y, Takahashi E, Mochizuki M (2001). Characterisation of cross-reactivity of virus neutralising antibodies induced by feline panleukopenia virus and canine parvoviruses. Res Vet Sci 71:219-222
Nara PL, Krakowka S, Powers TE (1979). Effects of prednisolone on the development of immune response to canine distemper virus in beagle pups. Am J Vet Res 40(12):1742-7
Neuerer F, Horlacher K, Truyen U, Hartmann K (2008). Comparison of different in-house test systems to detect parvovirus in feces of cats. J Fel Med Surg, 10:247-51
Parrish CR (1990). Emergence, natural history and variation of canine, mink and feline parvoviruses. Adv Virus Res 38:403-450
Parrish, CR (1995). Pathogenesis of feline panleukopenia virus and canine parvovirus. Baillière’s Clin Haematol 8:57-71
Parrish CR (2006). Pathogenesis of feline panleukopenia virus and canine parvovirus In Parvoviruses, Eds J Kerr, SF Cotmore, ME Bloom, RM Linden, CR Parrish, Oxford University Press, New York, USA pp 429-434
Pedersen, NC (1987). Feline Panleukopenia Virus, In Virus Infections of Carnivores, Ed M J Appel, Elsevier, Amsterdam pp 247-254
Pennisi MG, Hartmann K, Addie DD, Lutz H, Gruffydd-Jones T, Boucraut-Baralon C, Egberink H, Frymus T, Horzinek MC, Hosie MJ, Lloret A, Marsilio F, Radford AD, Thiry E, Truyen U, Möstl K (2015). Blood transfusion in cats. ABCD guidelines for minimising risks of infectious iatrogenic complications. J Feline Med Surg 17: 588-593.
Pollock RVH, Postorino NC (1994). Feline panleukopenia and other enteric viral diseases In The Cat: Diseases and Clinical Management, 2nd Edition Ed R G Sherding, Churchill Livingstone, New York pp 479-487
Reubel GH, Dean GA, George JW, Barlough JE, Pedersen NC (1994). Effects of incidental infections and immune activation on disease progression in experimentally feline immunodeficiency virus-infected cats. J Acq Immun Defic Syndrome 7:1003-1015
Ryser-Degiorgis MP, Hofmann-Lehmann R, Leutenegger CM, Af Segerstad CH, Morner T, Mattsson R, Lutz H (2005). Epizootiologic investigations of selected infectious disease agents in free-ranging Eurasian lynx from Sweden. J Wildl Dis 41:58-66
Schmitz S, Coenen C, Koenig M, Thiel HJ, Neiger R (2009). Comparison of three rapid commercial Canine parvovirus antigen detection tests with electron microscopy and polymerase chain reaction. J Vet Diagn Invest 21: 344–345.
Schunck, B, Kraft W, Truyen U (1995). A simple touch-down polymerase chain reaction for the detection of canine parvovirus and feline panleukopenia virus in feces. J Virol Methods 55:427-433
Scott, F, Csiza CK, Gillespie JH (1970). Maternally derived immunity to feline panleukopenia. J Am Vet Med Assoc 156:439-453
Scott FW, Geissinger CM (1999). Long-term immunity in cats vaccinated with an inactivated trivalent vaccine. Am J Vet Res 60(5):652-8
Schmitz S, Coenen C, Koenig M, Thiel HJ, Neiger R (2009). Comparison of three rapid commercial Canine parvovirus antigen detection tests with electron microscopy and polymerase chain reaction. J Vet Diagn Invest 21:344–5
Sedlik C, Dadaglio G, Saron MF, Deriaud E, Rojas M, Casal SI, Leclerc C (2000). In vivo induction of a high-avidity, high-frequency cytotoxic T-lymphocyte response is associated with antiviral protective immunity. J Virol 74:5769-75
Steinel A, Parrish CR, Bloom ME, Truyen U (2001). Parvovirus infections in wild carnivores. J Wildlife Dis 37:594-607
Tattersall, P (2006). The evolution of parvovirus taxonomy In Parvoviruses, Eds J Kerr, SF Cotmore, ME Bloom, RM Linden, CR Parrish, Oxford University Press, New York pp 5-14
Thiry E (2002a). Panleucopénie féline, In Virologie clinique du chien et du chat, Editions du Point Vétérinaire, Maisons-Alfort, France, pp 137-142
Thiry E (2002b). Parvovirose canine In Virologie clinique du chien et du chat, Editions du Point Vétérinaire, Maisons-Alfort, France, pp 29
Thiry E (2002c). Virologie clinique du chien et du chat, Editions du Point Vétérinaire, Maisons-Alfort, France, p 38
Truyen, U (1999). Emergence and recent evolution of canine parvovirus. Vet Microbiol 69:47-50
Truyen U, Evermann JF, Vieler E, Parrish CR (1996). Evolution of canine parvovirus involved loss and gain of the feline host range. Virology 215:186-189
Truyen U, Gruenberg A, Chang SF, Veijalainen P, Obermaier B, Parrish CR (1995). Evolution of the feline subgroup parvoviruses and the control of canine host range. J Virol 69:4702-4710
Truyen U, C R Parrish (1992). Canine and feline host ranges of canine parvovirus and feline panleukopenia virus Distinct host cell tropisms of each virus in vitro and in vivo. J Virol 66:5399-5408
Truyen U, Parrish CR (2000). Epidemiology and pathology of autonomous parvoviruses In Contributions to Microbiology: Parvoviruses, Eds S Faisst and J Rommelaere Karger AG, Basel, vol 4:149-162
Truyen U, Parrish CR (2013). Feline panleukopenia virus: Its interesting evolution and current problems in immunoprophylaxis against a serious pathogen. Vet Microbiol 165: 29–32.
Uttenthal A, Lund E, Hansen M (1999). Mink enteritis parvovirus. Stability of virus kept under outdoor conditions. Acta Pathologica, Microbiologica, et Immunologica Scandinavica 107:353-358
Veijalainen P, Smeds E (1988). Pathogenesis of blue fox parvovirus on blue fox kits and pregnant vixens. Am J Vet Res 49:1941-1944
Veijalainen PM, Neuvonen E, Niskanen A, Juokslahti T (1986). Latex agglutination test for detecting feline panleukopenia virus, canine parvovirus and parvoviruses of fur animals. J Clin Microbiol 23:556-559