Feline panleukopenia

What it is

Feline panleukopenia is caused by feline parvovirus (FPV), a small, non-enveloped DNA virus closely related to canine parvovirus. The variants of canine parvovirus type 2 (CPV-2a, 2b and 2c) also infect cats and produce an indistinguishable disease. The virus replicates only in rapidly dividing cells: after oronasal infection it multiplies in oropharyngeal lymphoid tissue, spreads by viraemia and infects the intestinal crypt epithelium, the bone marrow and lymphoid tissues. Loss of the crypts prevents renewal of the villi and breaks down the intestinal barrier; destruction of marrow precursors causes the leukopenia that gives the disease its name, with a risk of sepsis from intestinal bacteria.

Transmission is faecal-oral, mostly indirect: the virus is shed in large amounts in faeces, survives for months in the environment and travels on shoes, clothing, bowls and cages, so cats kept indoors can also be infected. It resists many common disinfectants, such as alcohol and many quaternary ammonium compounds. In the pregnant queen the virus crosses the placenta and causes resorption, abortion or stillbirths; infection late in gestation or in the first weeks of life damages the developing cerebellum. It is not a zoonosis.

Who it affects

Cats of any age without immune protection, but above all unvaccinated or incompletely vaccinated kittens, once maternal antibodies wane. It is common in shelters, colonies and breeding catteries, where many young cats and a high environmental virus load coincide. The virus also infects other felids and raccoons, mink and foxes.

Anatomy involved

• Small intestine: the jejunum and ileum are the most affected. The loops are dilated, with a thickened or oedematous wall and sometimes serosal haemorrhages; histologically there is crypt necrosis and shortened, fused villi. Damage to the mucosal barrier lets bacteria and endotoxins into the blood.
• Brain: in kittens infected in utero or in the first weeks of life, the virus destroys the external germinal layer of the cerebellum, which is still dividing. The result is cerebellar hypoplasia: a small cerebellum that causes non-progressive ataxia. Retinal dysplasia and hydranencephaly can also occur.
• Spleen: part of the target lymphoid tissue. There is lymphoid depletion of the spleen, thymus, lymph nodes and Peyer's patches, together with destruction of bone marrow precursors; hence the neutropenia, lymphopenia and, later, thrombocytopenia and immunosuppression.

Clinical signs

• Enteric form: sudden fever, depression and anorexia, followed by vomiting, diarrhoea (sometimes haemorrhagic, and it may be absent at first), rapid dehydration and abdominal pain; the intestinal loops may feel thickened on palpation. Some kittens die peracutely, with sepsis or hypothermia, with hardly any digestive signs.
• Cerebellar hypoplasia: kittens with ataxia, hypermetria, a wide-based stance and intention tremor that become noticeable when they start to walk. The signs do not progress and many of these cats adapt and live well.
• Infection of pregnant queens shows up as reproductive failure.

Diagnosis

• Complete blood count: leukopenia (neutropenia and lymphopenia) strongly supports the diagnosis; thrombocytopenia and anaemia may follow.
• Rapid faecal antigen test: tests designed for canine parvovirus also detect FPV. They are useful for screening but can give false negatives, and modified-live vaccine can cause positive results in the days after vaccination.
• PCR on faeces or blood: more sensitive, but it also detects vaccine virus; it is interpreted together with the clinical picture and the date of the last vaccine.
• Serology is not used for diagnosis because it cannot distinguish infection from vaccination.
• Necropsy and histopathology: crypt necrosis confirms the diagnosis. Cerebellar hypoplasia is recognised from the clinical signs and brain imaging.

Treatment and prevention

There is no antiviral of proven efficacy; treatment is intensive supportive care: intravenous fluids with correction of potassium and glucose, antiemetics, early enteral nutrition, analgesia and broad-spectrum parenteral antibiotics to cover bacterial translocation during neutropenia. Colloids or plasma are used for hypoalbuminaemia. Sick cats are isolated, and surfaces are cleaned and disinfected with products active against parvovirus, such as sodium hypochlorite, potassium peroxymonosulfate or accelerated hydrogen peroxide.

Vaccination against FPV is core for all cats, including those kept indoors. Modified-live vaccines protect sooner than inactivated ones, but are not used in pregnant queens or in kittens under 4 weeks of age. Maternal antibodies can block the vaccine, so the WSAVA and AAHA/AAFP guidelines recommend vaccinating kittens every 2–4 weeks until 16 weeks of age or older, revaccinating between 6 and 12 months of age and then boosting no more often than every 3 years. The vaccine also protects against the canine parvovirus variants that infect cats.

Key studies

• ABCD guidelines (Truyen et al., 2009): European consensus document on prevention and management. It describes mortality of over 90% in kittens, advises against serology for diagnosis, notes that supportive therapy and good nursing greatly reduce mortality and lists sodium hypochlorite, peracetic acid, formaldehyde and sodium hydroxide as effective disinfectants. Its vaccination schedule predates current guidelines.
• Kruse et al. (2010), retrospective study of 244 cats with panleukopenia at a university hospital in Munich. 51.1% survived. The relative risk of death with fewer than 1,000 leukocytes/µl was 1.77 times that with 1,000–2,500/µl and 1.85 times that with more than 2,500/µl; thrombocytopenia, albumin below 30 g/l and potassium below 4 mmol/l were also associated with death. None of the vaccinated cats had received a dose after 12 weeks of age. It is a single-centre study.
• Porporato et al. (2018), retrospective cohort of 177 shelter cats. Median survival after admission was 3 days and only 20.3% survived to discharge. Lethargy, a rectal temperature below 37.9 °C and low body weight at admission were associated with death; unlike other studies, leukopenia at admission was not associated with outcome, but leukopenia on days 3, 4 and 7 was. Interferon omega was not associated with survival. It is an observational study, and associations with treatments do not prove efficacy.
• Patterson et al. (2007), prospective controlled study in 64 specific-pathogen-free kittens vaccinated with 8 commercial vaccines. After a single dose, 1, 4 and 13 kittens tested positive with each of the 3 faecal antigen tests, and only 1 tested positive on all three. At 14 days, 85% of kittens given modified-live vaccines and 31% of those given inactivated vaccines had protective titres. Vaccine interference exists, but it is uncommon and varies with the test.
• Jakel et al. (2012), field study of 64 kittens from 16 litters vaccinated at 8, 12 and 16 weeks. Despite three doses, 36.7% did not seroconvert; even low titres of maternal antibodies blocked the response, and some kittens still had them at 20 weeks. It is a study in German breeding catteries with a small sample, but it shows that maternal antibodies can block the vaccine even with the last dose at 16 weeks.