Kittens from vaccinated queens obtain maternal antibodies (MDA) via colostrum. The MDA titre in kittens depends on both the antibody titre of the queen as well as the amount of colostrum ingested during the first day of life. In most kittens, MDA will not persist for longer than 12 weeks.
MDA have been demonstrated even in sera of fox cubs whelped by orally immunized vixens [Vos et al, 2003].
Passive immunity may neutralize vaccine antigens, thereby inhibiting the immunoglobulin production, interfering in the immunization process during the first weeks of life. Therefore, it is generally recommended to perform the primary vaccination against rabies in kittens not earlier than at 12 weeks of age.
Although rabies antigens are highly immunogenic and capable of eliciting the full spectrum of protective immune responses, the virus is not highly cytopathic, since no cell lysis occurs during replication or maturation. Therefore, little antigen is presented to the immune system. Neither humoral nor cell-mediated specific responses can be detected during the early stages of movement of virus from the site of the bite to the central nervous system [Green 1997]. Hence, infection of naive animals with rabies virus most often results in disease and death. Such sequelae may be averted by prompt immunization following exposure, demonstrating that the development of anti-rabies viral immunity prior to extensive infection of neurons is protective. It is well documented that virus neutralizing antibody is a crucial factor in this immunity. Rabies is an example of a “Th-2 healing disease” in which activation of B lymphocytes, with the help of CD4 T cells, is important for protection [Garenne and Lafon 1998]. When activated, primarily by the N protein of the rabies virus, CD4 T cells produce cytokines (i.e. IL-4) that stimulate B cells to produce antibodies. In contrast, rabies-specific CD8 T cells cause neuronal damage when a Th-1 response (IFN-? and TNF-a) predominates [Lafon 2002, Hooper 2005]. However, published reports exist that describe vaccinated animals that had no detectable virus neutralizing antibody and yet survived rabies challenge, indicating that other mechanisms may also protect against this disease [Aubert 1992, Hooper et al, 1998].
After intramuscular infection, the virus replicates locally for several weeks in the myocytes or nervous tissue. In vaccinated cats with adequate serum antibody titres, the virus is often neutralized during this early incubation period. In contrast, unvaccinated cats exposed to rabies virus can produce an antiviral immune response, usually late in the clinical course, that fails to prevent disease [Johnson et al, 2006]. However, protection against the early stages of infection is provided by non-specific immunity, in which interferon seem to play a critical role. High levels of interferon are detectable in sera of mice inoculated with rabies virus by peripheral or intracerebral routes [Marcovistz et al, 1984, 1994; Johnson et al, 2006]. It is not clear how effective these mechanisms are in naturally exposed naive cats. It is believed that factors, determining morbidity include the amount and strain of the virus, the age and immunocompetence of the cat and the bite, such that in unvaccinated cats the risk of developing rabies is higher (and the incubation period shorter) in a young animal that has been bitten severely in the head, with a high saliva deposit in the wound, compared to the risk for an adult cat, bitten in a limb, especially after extensive bleeding [Pastoret et al, 2004].
In natural infections of unvaccinated animals, neutralizing antibody appears usually after the virus has entered the central nervous system. Hence, once symptoms are evident, recovery from rabies is exceedingly rare, although there have been reports of humans and animals that have recovered following confirmed clinical rabies [Bernard 1985, Fekadu 1991]. Furthermore, antibodies to lyssaviruses have been detected occasionally in domestic or wild cats with no history of vaccination, consistent with a non-fatal disease or subclinical infection [Tjørnehøj et al, 2004; Deem et al, 2004].