Important features of modified live virus vaccines — A comment

Dear Editor,

I read with interest the Case Report by Galán et al in the April 2014 CVJ (1). The report is well-documented and illustrates an unusual acute neurological form of adult canine distemper in previously vaccinated dogs, but some points need to be addressed.

First, it is not uncommon for vaccinated dogs (or cats) to harbor viruses for which they had been adequately immunized and thus protected from disease. The important point is that these vaccinates do not show clinical signs of the disease. Modified live virus (MLV) vaccines are effective because they provide the same immunity (cellular, humoral, systemic, and local) produced by natural exposure (2).

Properly immunized animals have sterilizing immunity that not only prevents clinical disease but the presence of antibody also prevents infection. Furthermore, the animal doesn’t need and should not be revaccinated since the vaccine could elicit an adverse reaction (hypersensitivity disorder). It is best to avoid vaccinating animals that are already protected (2–4).

Second, MLV canine distemper (CD) vaccine viruses are capable of reverting to virulence, especially if these vaccines contain the potent Rockborn strain of CD virus (CDV) (5,6). They also are known to produce post-vaccinal encephalitis (PVE) (2,5,6). The Onderstepoort or recombinant CDV vaccines do not produce PVE (2). In rare cases, disease expression could occur from latent virus infection, if the animal then became immune compromised from illness or immunosuppressant therapy (2–4).

Third, the authors state incorrectly that “protective immunity induced by live modified vaccines persists for no more than 3 y”. The dog in question (Case # 4), had been vaccinated yearly until adulthood, but not in the prior 3 years. Regardless, if the dog had been truly immunized against CDV from prior vaccinations, immunity should have lasted for at least 9 years and perhaps a lifetime (2–4,7–11). Published challenge studies have documented this long-lived protection from CDV, canine parvovirus (CPV-2), and canine hepatitis (adenovirus) (CAV-2), even in the absence of viral exposure or revaccination (4).

The persistence of antibody to these vaccine or native viruses comes from a population of long-lived plasma cells known as “memory effector B cells” which continue to produce the specific antibody long after vaccination (2). Memory B and T cells should provide an anamnestic (secondary) humoral- and cell-mediated immune response that limits virus replication and prevents disease. MLV vaccines, like CDV, and the other “core” vaccines (CPV-2 and CAV-2), always stimulate both humoral- and cell-mediated immunity (2).

Last, the authors discussed possible reasons for vaccine failures (p. 377) but did not mention the possibility of genetically based vaccine non- or low-responders. About 1 in 5000 dogs is estimated to be genetically incapable of developing an immune response to CDV vaccines, and certain breeds or families of dogs are suspected to have a higher prevalence than in the general canine population (2).