Surviving rabbits may be contagious for up to 2 months. Contaminated fomites such as clothing, food, cages, bedding, feeders, and water also spread the virus. Flies, fleas, and mosquitoes can carry the virus between rabbits. Predators and scavengers can also spread the virus by shedding it in their feces. Caliciviruses are highly resistant in the environment, and can survive freezing for prolonged periods. The virus can persist in infected meat for months, and for prolonged periods in decomposing carcasses. Importation of rabbit meat may be a major contributor in the spread of the virus to new geographic regions. RHD outbreaks tend to be seasonal in wild rabbit populations, where most adults have survived infection and are immune. As young kits grow up and stop nursing, they no longer receive the antibodies provided in their mother's milk and become susceptible to infection. Thus, RHD epizootics occur more often during the rabbits' breeding season. Generally, high host specificity exists among lagoviruses. Classic RHDVa only affects European rabbits, a species native to Europe and from which the domestic rabbit is descended. The new variant RHDV2 affects European rabbits, as well, but also causes fatal RHD in various Lepus species, including Sardinian Cape hares (L. capensis mediterraneus), Italian hares (L. corsicanus), and mountain hares (L. timidus). Reports of RHD in Sylvilagus species have been coming from the current outbreak in the United States. RHD caused by RHDV and RHDVa demonstrates high morbidity (up to 100%) and mortality (40-100%) in adult European rabbits. Young rabbits 6–8 weeks old are less likely to be infected, and kits younger than 4 weeks old do not become ill. The more recently emerged RHDV2 causes death and disease in rabbits as young as 15 days old. Mortality rates from RHDV2 are more variable at 5-70%. Initially less virulent, the pathogenicity of RHDV2 has been increasing and is now similar to that found with RHDV and RHDVa. Deaths from RHDV2 have been confirmed in rabbits previously vaccinated against RHDVa. Pathophysiology These viruses replicate in the liver and by mechanisms not fully elucidated, trigger the mass death of hepatocytes which can in turn lead to disseminated intravascular coagulation, hepatic encephalopathy, and nephrosis. Bleeding may occur, as clotting factors and platelets are used up. Clinical signs The incubation period for RHDVa is 1–2 days, and for RHDV2 3–5 days. Rabbits infected with RHDV2 are more likely to show subacute or chronic signs