Rabbit myxomatosis is a very contagious viral disease with a high mortality rate. It is caused by the myxoma virus, genus Leporipoxvirus of the Poxviridae family, a double-stranded DNA virus with different strains of variable virulence; it belongs to the same genus of the Shope fibroma virus. The virus is very resistant in the environment and to heat and humidity variations, but it is sensitive to common disinfectants (e.g. sodium hypochlorite 10%). The virus is antigenically related to the Shope fibroma virus and to the hare fibroma virus, with cross-immunity against both viruses.
The virus was isolated for the first time in Uruguay in 1896 by the Italian researcher Giuseppe Sanarelli from a naturally infected rabbit. It later turned out that the virus was endemic in South America where the natural host is the leporidespecies Sylvilagus brasiliensis, in which it is the cause of a benign fibroma. A different strain is found in California, with the leporide Sylvilagus bachmani as the natural host and also in this case the virus is benign. The virus can infect only lagomorphs as the genus Lepus is extremely resistant.
In 1950 the virus was deliberately spread into Australia to control the devastating proliferation of imported rabbits. In 1952 a French citizen spread the virus to control the local population of wild rabbits; the viral replication was particularly successful, the virus invaded Europe and reached the UK in the following year.
The virus spreads through secretions and excretions. The infection can be transmitted by direct route from sick animals or carriers to healthy ones, via aerosol, or indirectly via contaminated objects (i.e. infected needles) and insect vectors (mosquitoes, simulidae, fleas, lice, ticks, mites, Cheyletiella spp.) which act as passive carriers. The virus can survive for many months in insect vectors. After a single blood meal a mosquito can remain infectious for up to 220 days. Healed animals remain carriers of the virus for 2-3 weeks. In animals that overcome the infection immunity is weak and transient.
The incubation time is of 5-15 days. Once the infection is present, the virus replicates locally in dendritic cells and subsequently in epidermal cells, causing cell proliferation and cell disruption with a swelling of the mucosa of the underlying dermis. In 2-3 days this leads to the formation of a primary nodular lesion (myxoma), which may go unnoticed. Propagation continues through the lymphatic tissue and viraemia, with dissemination to all organs. Proliferation of the dermal connective tissue is stimulated, with formation of nodules in particular on the head and genitals. Myxomas are rich in viral particles which are passed to the biting insects that feed on the sick rabbit. The virus has the ability to inhibit the antiviral immune activity and the activation of macrophages and T cells, resulting in immunosuppression. In 8-10 days secondary bacterial infections appear affecting the respiratory system.
In rabbits the disease occurs in two forms, nodular (classic) and amyxomatous (respiratory). In pet rabbits the classic form is usually present. The classic form is characterized by depression, fever up to 42°C, blepharoconjunctivitis, mucopurulent ocular discharge, skin swellings on the head (especially of the eyelids, Figs. 1a and 1b, the nasal region and ears, Fig. 3) and limbs, inflammation of the genitals (vulva, Fig. 3, and scrotum). The skin lesions consist of erythematous plaques of varying sizes, from a few millimeters to a few centimeters. Because of the swelling the eyelids remain closed (Fig. 4) and abundant purulent material accumulates underneath, preventing the rabbit from seeing. The eyeballs are not affected. Death occurs within 1-2 weeks from complications caused by secondary bacterial infections of the respiratory tract by gram negative bacteria and by a probable multiple organ dysfunction. The mortality rate is high and depending on the strain involved it can vary from 50 to 100%.
More attenuated strains may have a slower evolution and a lower mortality rate. In rabbits that survive, the skin lesions become crusty and fall off, leaving areas of scarring alopecia (Figs. 5-8). Chronic respiratory infections and areas of pulmonary consolidation may persist. In young subjects a hyperacute form may be present, with death in 48 hours, with high fever as the only symptom and a mortality rate of 100%. In acute and hyperacute forms the pathogenic mechanism of death has not been clarified. The suspected cause is pulmonary oedema, massive lymphocyte destruction, extensive damage to skin cells and subsequent septic shock.
The amixomatous (respiratory) form, enzootic in farms, is characterised by conjunctivitis and respiratory symptoms, with very mild skin lesions and swelling of the genitals.
The diagnosis can be made in view of the characteristic skin lesions that are pathognomonic. The examination of internal organs reveals scarce lesions: splenomegaly can be present. The hystological examination is generally deprived of lymphocytes. At microscopic level the cells of the ocular conjunctiva exhibit the presence of large eosinophilic cytoplasmic inclusion bodies.
Diagnostic certainty is achieved with the use of electron microscopy, with laboratory tests that search for the antigen or with serology. Within 6-10 days specific IgM appear, and IgG after 10 days, which persist for at least two years and may be detected with an ELISA test. Other possible assays are complement fixation, serum neutralization and gel immunodiffusion.
Myxomatosis is endemic in Northern Italy, it is present in Central Italy and in the Region Campania while it is uncommon in the rest of Southern Italy and on the islands. It is considered not eradicable due to the presence of a susceptible host, the wild rabbit. The peak incidence of the classic form is observed in late summer/fall; this is related to the presence of the insect vectors. The respiratory form is present throughout the year on farms.
No effective therapy exists and also with eventual intensive supportive care the mortality rate would still be very high. In Italy, the Veterinary Police regulation provides for the removal and destruction of infected or suspected infected subjects, with communication of any immunising treatment to the local Health Authorities.
The vaccines against myxomatosis are all live attenuated (the inactivated vaccine is poorly immunogenic) and are based on viral strains of myxomatosis (homologous vaccines from Borghi or SG33 strains) or of the Shope fibroma virus (heterologous vaccines). Homologous vaccines confer a more solid and lasting immunity than the heterologous ones, but the latter do not cause side effects or immunosuppression. Monovalent vaccines as well as vaccines associated with the vaccine against viral haemorrhagic disease (VHD) are present on the market. A new bivalent vaccine contains the MR24 strain, from which the two virulence factors have been eliminated.
The age of the rabbit at first vaccination and for the subsequent boosters depends on the type of vaccine used. In pet rabbits booster vaccinations are to be repeat lifelong, on a semi-annual or annual basis depending on the type of vaccine used.