Feline parvovirus infection is probably the greatest major disease threat to any rescue facility and infection carries a very high mortality rate, particularly in unvaccinated kittens. Parvoviruses can survive for long periods (up to several years) in the environment and are resistant to many disinfectants. It is spread by direct faecal–oral contact, and indirectly following contamination of the environment or objects. Cats infected with feline parvovirus can continue to excrete the virus for a variable period, which may be several weeks following infection. The virus can also be transmitted by dogs. Fluid therapy and nursing care is the cornerstone of treatment for infected cats.
Feline parvovirus (FPV) is a highly contagious pathogen of cats. It is also known as feline panleukopenia virus and feline infectious enteritis. FPV can be seen in any age of cat, but infection is most common in kittens and adolescent cats, as their maternally derived antibodies (MDA) wane, and they encounter the virus for the first time.
In common with the closely related canine parvovirus (CPV) in dogs, FPV is a small virus that travels light and carries little of its own equipment. This strategy means that it targets the most rapidly dividing cells in a cat’s body, to enable it to hijack the existing replication mechanism. Since the crypt cells of the small intestine are constantly turning over, this makes them the ideal environment for the virus. The other main favoured location is the bone marrow, which can result in severe damage to the haemopoietic stem cells. This means that affected cats have a severely impaired immune response, which is an important factor in the high mortality rates often seen.
Key point: FPV causes severe damage to the lining of the intestine leading to acute onset haemorrhagic vomiting and diarrhoea.
Although in some cases the clinical presentation can be similar to the closely related CPV, that is characterised by lethargy, vomiting and diarrhoea, there appears tobe a wider range of possible presentations seen in cats (Figure 1).
Some cats will present initially as lethargic, inappetent and pyrexic for some time before vomiting or diarrhoea occur. Dribbling owing to nausea can be seen. Cases of sudden death are seen relatively commonly, where an apparently healthy cat is found dead or dying, usually due to peracute sepsis secondary to the damage FPV has inflicted on the gut.
Wherever a clinical suspicion of FPV exists, patient-side tests are usually the first port of call. They vary in their exact method of action, but they all fundamentally detect parvovirus antigen in the faeces. Since many practices see more CPV than FPV, CPV tests may be more accessible. While it is certainly possible to use canine tests, they do vary in their sensitivity for FPV (some cats with panleukopenia may be infected with the canine virus) . Additionally, clinical signs may show before shedding begins, or parvovirus particles may be bound in the faeces by gut-associated antibodies. Therefore, in the presence of strong clinical suspicion, a negative test should not always be taken at
In these cases, it is recommended either to retest with a patient-side test, or to send for PCR confirmation of results. While recent administration of a live vaccine can occasionally give rise to a false positive test, when vaccine virus is shed in the faeces, this is uncommon. However, this fact can cause some concern when clinical signs of FPV occur soon after vaccination. In these cases it is likely that the kitten was vaccinated while asymptomatic in the incubation period; if necessary this can be confirmed by selective PCR or sequencing to determine the strain of the virus present. Haematology can be an extremely useful test, both as an adjunct to diagnosis and to inform prognosis and treatment. Marked anaemia is common, and usually poorly regenerative. Many of these cats will have severe deficiencies of all of the white cell lines as well (as indicated by the name ‘panleukopenia’ meaning ‘totally no white blood cells’). Where finances are constrained, assessment of a blood smear is a useful and cheap alternative.
Key point: In cases of FPV, severe panleukopenia is considered an indicator of a poor prognosis.
When kittens are infected with FPV in utero or in the very early neonatal period, the virus can damage the rapidly dividing cells of the brain, and this can lead to cerebellar hypoplasia (CH).1 CH-affected kittens are usually wobbly, with an intention tremor owing to the lack of fine motor control. They have a wide-based stance, exaggerated high-stepping gait, and fall over a lot. Within a litter, kittens can be variably affected, with some having severe signs and others appearing almost unaffected. Provided they can eat and use a litter tray, these kittens can still be happily rehomed (Figure 2); they usually have no other additional deficits and no additional needs beyond a soft surface to land on when they fall and restricted access to roads and other hazards.
Treatment of FPV infection
The cornerstone of FPV treatment is nursing care. Ensuring fluid and electrolyte balances are closely monitored is essential (Figure 3). Keeping cats clean and warm will improve their comfort. Nausea and vomiting can be managed with maropitant, which also potentially has some analgesic effects. Other sources of analgesia may include buprenorphine or methadone. Treatment with broad spectrum antimicrobials such as potentiated amoxicillin and metronidazole is usually recommended due to the severity of compromise of the intestinal barrier. Omega interferon appears to have some efficacy, especially if used early in the course of disease. Deworming affected kittens is usually a sensible step, to reduce additional damage to the gut.
Early enteral nutrition has been shown to have a strong impact on survival in puppies; while evidence is currently lacking for its efficacy in kittens, calorie supplementation, if necessary by nasogastric tube, is likely to be helpful as soon as vomiting and nausea are controlled. Even with treatment, the prognosis must be guarded, with mortality of up to 80% reported .
Vaccination against FPV is highly effective. However, efficacy can be hindered by the presence of MDA at the time of vaccination. MDA are acquired from kittens suckling the colostrum during the first 24 h of life, and since it is metabolised at a steady rate, how long MDA last for depends entirely on how much each kitten received during that critical period (Figure 4). The level of MDA can be affected by numerous factors, including:
• immunity of the queen (owing to previous exposure or vaccination);
• birth order;
• mothering ability;
• litter size; and
• health and nutrition of the queen
For this reason, the level of MDA can vary from virtually none to high levels that can persist for 18–20 weeks. It is very difficult to accurately predict how much MDA an individual kitten will have. Therefore in high risk environments such as shelters, it may be helpful to consider starting vaccinations early (from 4 to 6 weeks) and vaccinating every 2–3 weeks until the kitten is rehomed or reaches 16–20 weeks of age. Although this may require use of vaccines off-licence, there is considerable precedent for this, including the World Small Animal Veterinary Association Guidelines .
Outbreaks of FPV occasionally occur, often in shelters or other high population environments such as veterinary clinics. Since FPV is a non-enveloped virus, it is extremely hardy and can survive for very long periods in the environment. This allows it to spread via fomites, which have usually been contaminated by virus shed in the faeces.
Outbreaks can be devastating, with large numbers of cats affected. The risk is likely to be higher in the spring and summer, as cats’ semi-seasonal breeding habits mean there are large numbers of susceptible kittens present that may be affected. This is often also a time when shelter populations are at their highest levels, which can place additional pressures on staff time.
Recognising an outbreak early is essential, and swift isolation measures implemented in any case with a clinical suspicion of FPV is key. Ideally, cats suspected to be infected should be kept away from the main population, and especially other kittens. This includes any cats with consistent clinical signs, and any known or suspected contacts. Incubation is typically 4–7 days, so suspected in-contacts should be isolated for a minimum of 1 week before relaxing any restrictions. In situations where outbreaks have affected large proportions of a shelter population, mass euthanasia and decontamination has been used to control the spread. This of course is a last resort and should only be used when absolutely unavoidable (Figure 5).
Isolated cats should be attended by a single member of staff who, if possible, does not have contact with any cats from the rest of the population. If this is not possible, affected cats should be cared for last, after all other cats have been handled. Husbandry equipment such as food and water bowls, bedding and litter trays should either be easy to clean and disinfect, or disposable and burned or sent to clinical waste after use. Staff should wear appropriate personal protective equipment and have excellent hand hygiene (Figure 6).
It is important to ensure any equipment used is cleaned with detergent before being decontaminated with a parvocidal disinfectant. Many disinfectants are inactivated by organic matter, so it is important to emphasise that cleaning and disinfection are carried out in the correct order. The author has certainly seen outbreaks maintained where cleaning was inadequate or disinfectant not diluted correctly.
Unlike the situation in dogs, asymptomatic shedding of FPV has been reported, especially in shelter environments. It is as yet unclear what the significance is of finding FPV in a cat that is otherwise well or experiencing mild diarrhoea, and it is not known whether these asymptomatic cats shed at high enough levels to transmit infection. However, a cautious approach, including isolation and retesting, may be the safest course until the situation becomes more clear.
Key point: Following on from an FPV outbreak, it is essential to perform a critical incident review, to determine if measures can be implemented to prevent further outbreaks in the future. It is important to include all members of the team in this exercise, and to emphasise that it is not about finding fault or blame, but improving practice going forward.
Cats and dogs?
There are some key differences in the clinical presentations of CPV and FPV. However, there are some really important areas of interaction between the two diseases (Figure 7).
FPV itself was first recognised almost 100 years ago, and a vaccine was first developed in the 1950s. When CPV first emerged and started killing dogs worldwide in 1978, it was initially thought to be a mutation of FPV. However, we now know that both FPV and CPV are likely to have evolved independently from the same parent strain of the virus, which was probably circulating among wild foxes or mustelids.
Initially the situation was simple; FPV in cats and the original CPV strain, CPV-2, in dogs. Since then, however, the main canine strains are CPV-2a and CPV-2b, both of which can infect cats as well as dogs. A third strain, CPV-2c, also affecting both species, has been seen around the world, although it is not yet established in the UK. This means that cats with signs of panleukopenia could potentially be infected with CPV-2a or CPV-2b, meaning they could be infectious to dogs. Similarly, puppies with parvovirus will almost certainly be shedding CPV-2a or CPV-2b, and therefore potentially infectious to cats. For this reason, it is essential to avoid using the cat ward as an isolation area for puppies with parvovirus (or vice versa) in case of cross-species transmission.
FPV is a challenging disease to manage. Its ability to spread quickly and cause very high mortality rates means that, especially in a shelter or other multi-cat environment, a strong emphasis on prevention is key. Treatment of affected animals and control of spread are challenging, and will be most successful if an outbreak is identified early and strong measures implemented quickly and decisively. Vaccination is a useful component in protection, and, where the risk of disease is high, population-based vaccine strategies should be considered. Parvovirus vaccines
are highly effective and their cost-benefit ratio is excellent when the direct and indirect costs of disease are taken into account. With these measures in place, hopefully it should be possible to minimise cases of this devastating and very preventable disease.
References 1 Truyen U, Addie D, Belak S, et al. Feline panleukopenia: ABCD guidelines on prevention and management. J Feline Med Surg 2009; 11: 538–546.
2 Neurer FF, Horlacher K, Truyen U, et al. Comparison of different in-house test systems to detect parvovirus in faeces of cats. J Feline Med Surg 2008; 10: 247–251.
3 Porporato F, Horzinek MC, Hofmann- Lehmann R, et al. Survival estimates and outcome predictors for shelter cats with feline panleukopenia virus infection.
J Am Vet Med Assoc 2018; 253: 188–195.
4 Day MJ, Horzinek MC, Schultz RD, et al. WSAVA guidelines for the vaccination of dogs and cats. J Small Anim Pract 2016; 57: E1–E45.
Jenny Stavisky qualiﬁed as a vet from the University of Edinburgh, UK, in 2002. After starting out in mixed practice, she moved to the University of Liverpool, UK, to take a PhD in epidemiology and virology. In 2010, she moved to the University of Nottingham School of Veterinary Medicine and Science, UK, where she is currently clinical assistant professor in shelter medicine. She is a founder member of the Association of Charity Vets and also co-founded the Vets in the Community Clinic. She received the CEVA Chris Laurence Vet of the Year Award in 2017.