Understanding FPV and its Threat to Our Cats

Understanding FPV and its Threat to Our Cats

 

Maigan Espinili Maruquin

 

The Feline Panleukopenia (FPL) is an important disease in cats.  It is highly contagious and is often fatal to cats (Van Brussel, Carrai et al. 2019). This is caused by feline parvovirus (FPV; formerly FPL virus) and canine parvovirus (CPV), however, CPV infections in cats are uncommon (Barrs 2019). The FPL is also known to be the oldest known viral disease in cats wherein several epizootics that killed domestic cat populations in the 1800s could have been infected by FPV (Fairweather 1876, Barrs 2019) (Scott FW, 1987).

 

Structure

Fig. 01 A front view 60- meric assembly of FPV by Protein Data Bank in Europe containing 60 copies of Capsid protein VP1

( https://www.ebi.ac.uk/pdbe/entry/pdb/1fpv )

 

The current taxonomic entity of FPV shares with CPV (Tattersall, 2006) wherein after crossing species barriers, CPVs evolved from FPV by acquiring five or six amino acid changes in the capsid protein gene (Truyen, 1999) (Appel, Scott et al. 1979, Black, Holscher et al. 1979, Osterhaus, van Steenis et al. 1980, Parrish 1990, Johnson and Spradbrow 2008, Stuetzer and Hartmann 2014, Barrs 2019).

 

The causative agent FPV is a member of the genus Protoparvovirus in the family Parvoviridae with 5.2 kb long single stranded DNA genome, containing two open reading frames (ORFs): the first ORF encodes two non-structural proteins, NS1 and NS2; and the second ORF encodes two structural proteins, VP1 and VP2 (Reed, Jones et al. 1988, Zhou, Zhang et al. 2017).

 

At first, FPV was thought not to infect cats (Truyen, Evermann et al. 1996). It replicates in thymus and bone marrow but not within the intestinal tract of dogs (Truyen and Parrish 1992, Truyen, Gruenberg et al. 1995). The pathway of viral entry into cells is not fully characterized, however through the feline transferrin receptor (TfR), FPV binds and uses the receptor to infect feline cells (Parker, Murphy et al. 2001, Hueffer, Govindasamy et al. 2003). However, CPV-2b and CPV-2c variants emerged, with only a single amino acid position different from CPV-2a, and infect cats both naturally and experimentally (Mochizuki, Horiuchi et al. 1996, Truyen, Evermann et al. 1996, Ikeda, Mochizuki et al. 2000, Nakamura, Sakamoto et al. 2001, Gamoh, Shimazaki et al. 2003, Decaro, Desario et al. 2011, Zhou, Zhang et al. 2017, Van Brussel, Carrai et al. 2019).

 

FPV Infection

The virus may be shed in feces even in the absence of clinical signs (subclinical infections), or before clinical signs are detected (Barrs 2019).

 

The major portals of the FPV are the gastrointestinal (GI) tract and, less commonly, the respiratory tract. Generally, CPV is an uncommon cause of FPL and to date, no large-scale outbreaks of FPL have been confirmed to be caused by CPV (Barrs 2019). There were cases of indistinguishable CPV from FPV clinical signs in several cats (Mochizuki, Horiuchi et al. 1996, Miranda, Parrish et al. 2014, Byrne, Beatty et al. 2018, Barrs 2019). Moreover, coinfections of CPV and FPV were also reported in cats with clinical disease (Battilani, Balboni et al. 2011, Battilani, Balboni et al. 2013, Barrs 2019).

 

The FPV can remain latent in peripheral blood mononuclear cells of healthy cats with high virus-neutralizing titers (Ikeda, Miyazawa et al. 1999, Miyazawa, Ikeda et al. 1999, Nakamura, Ikeda et al. 1999, Barrs 2019).

 

The development of immunity of an unvaccinated cat to FPV is likely to increase with age (DiGangi, Levy et al. 2012). However, FPL mostly infects unvaccinated and incompletely vaccinated kittens. The age susceptibility correlates with the declining maternally derived antibodies (MDAs) as well as “the immunity gap” in incompletely vaccinated kittens (Barrs 2019).

 

Clinical Signs/ Pathogenesis

The FPV is resistant to heating (80C for 30 min) and low pH (3.0) (Goto, Yachida et al. 1974). Virions enter cells by endocytosis (Hueffer, Palermo et al. 2004). Viral DNA is released from the capsid and replicates through double-stranded RNA intermediates in the nucleus of the cell using the host’s DNA polymerase (Barrs 2019).

 

It can be transmitted by the faecal-oral route and a contact with infected body fluids, faeces, or other fomites, as well as by fleas primarily spreads the virus. Viral replication primarily occurs in lymphoid tissue, bone marrow and intestinal mucosa in infected cats older than 6 weeks of age (Csiza, De Lahunta et al. 1971, Csiza, Scott et al. 1971, Parker, Murphy et al. 2001). Infection outcome ranges from subclinical to peracute infections with sudden death within 12 h (Stuetzer and Hartmann 2014). Initially, non-specific signs such as fever, depression, and anorexia during the acute stage (Addie, Jarrett et al. 1996). However, vomiting unrelated to eating occurs commonly and, less often, cats develop watery to haemorrhagic diarrhoea later in the course of disease, while some cats show extreme dehydration. Cats typically die of complications. Viral DNA can persist for long periods even after infectious virus has been lost, thus detection of DNA does not necessarily signify an active infection (Stuetzer and Hartmann 2014).

 

Utero infection in early pregnancy can result in foetal death, resorption, abortion, and mummified fetuses while in later pregnancy may damage the neuronal tissue. The main clinical signs of FPV infection for new- born kittens include neurological, with ataxia, hypermetric movements and blindness, while some also shows signs of cerebellar dysfunction, forebrain damage (with seizures) with a range of severity and neurological signs. Although some kittens acquire MDAs, they can still get the virus  for up to 2 months after birth (Csiza, Scott et al. 1971, Csiza, Scott et al. 1971, Stuetzer and Hartmann 2014). Infections occurring up to 9 days of age can also affect the cerebellum. Cats having mild cerebellar dysfunction may retain good quality of life. On the other hand, FPV can also cause retinal degeneration in infected kittens, with or without neurological signs (Percy, Scott et al. 1975, Stuetzer and Hartmann 2014).

 

Diagnosis

It is important to have the FPV detected early using accurate testing methods to prevent disease transmission (Stuetzer and Hartmann 2014). The closeness in structure and antigenic relationship of FPV and CPV (Mochizuki and Akaboshi 1988, Parrish 1991, Stuetzer and Hartmann 2014) allows the cats to test for FPV using canine test kits (Stuetzer and Hartmann 2014).

 

Several tests can also confirm the presence of FPV: fecal antigen tests, polymerase chain reaction, and virus isolation, which uses feces, blood, or infected tissues (Schunck, Kraft et al. 1995, Schatzberg, Haley et al. 2003, Stuetzer and Hartmann 2014, Barrs 2019). In cases of tests are negative on point-of-care fecal antigen tests but displays clinical presentations suggestive of disease, PCR assays can be used to confirm. Usually, quantitative PCR is used but may not distinguish between feline (FPV) and canine (CPV) strains (Barrs 2019).

 

Vaccine and Disease Managements

Cats that are diagnosed with FPV are recommended to be hospitalised and kept in isolation for at least 2 weeks to avoid viral transmission (Stuetzer and Hartmann 2014) and for treatment that is, ideally, physically separated from the rest of the shelter whereas staff working in the isolation area should not enter other areas of the shelter, requiring minimum handling to reduce stress and the risk of fomite transmission (Barrs 2019). Disinfection of contaminated surfaces like cage, food and water bowls and of room is very important (Stuetzer and Hartmann 2014).

 

Supportive therapy and good nursing significantly decrease mortality in FPL infected cats, wherein symptomatic treatment will need restoration of fluid, electrolytes and acid–base balance, preferably by intravenous drip. Sepsis caused by invasive bacteria should be treated, considering the side effects of the drug that will be used (Truyen, Addie et al. 2009). The combination of choice in cats with panleukopenia is amoxicillin/clavulanic acid used with a third generation cephalosporin, however gentamycin should only be used in well hydrated cats due to renal toxicity (Stuetzer and Hartmann 2014).

 

Antiemetics might be required if there is persistent vomiting (Truyen, Addie et al. 2009, Stuetzer and Hartmann 2014) and oral intake of water and food might be restricted (feeding should be continued for as long as possible, and restarted as soon as possible).  A highly digestible diet is preferred however, should the cat rejects food, any diet is better than no food intake at all. Further, vitamin supplements, particularly B vitamin complex, can be given to prevent thiamine deficiency. Also, hypoproteinaemic cats may require plasma or whole blood transfusions to restore an oncotic pressure (Truyen, Addie et al. 2009).

 

Immune serum containing FPV antibodies can be used to prevent infection of susceptible cats (Truyen, Addie et al. 2009). Although feline recombinant interferon-omega showed effective treatment on parvoviral enteritis in dogs and also inhibited replication of FPV in cell culture (Mochizuki, Nakatani et al. 1994, Miyazawa, Ikeda et al. 1999, Martin, Najbar et al. 2002, de Mari, Maynard et al. 2003, Truyen, Addie et al. 2009), no data is available yet on its efficacy in FPV-infected cats, but it is expected to perform well – if not better – in the homologous host (Truyen, Addie et al. 2009).

 

Due to the serious consequences of FPL and the ubiquity of the virus, vaccination is highly recommended (Truyen, Addie et al. 2009). With proper administration, cats that respond adequately to primary vaccination against FPV maintain a solid immunity for 7 or more years (Scott and Geissinger 1999, Lappin, Andrews et al. 2002, Stuetzer and Hartmann 2014). Susceptible kittens and unvaccinated older animals should not be in contact with other cats until they are properly immunized (Truyen, Addie et al. 2009).

 

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