IN-DEPTH: IMMUNOLOGY/VACCINATION/PARASITE CONTROL


will aid in preventing damage from the presence of the organism or prevent infection altogether. An example of protection involves tetanus vaccination, which provides antibodies that bind even low levels of exotoxin liberated at that time of challenge. An added mechanism by which antibody proteins provide protection at the time of challenge includes the production of neutralizing antibodies. Neutral- izing antibodies are capable of preventing infection by viral pathogens.


4. Host Specific Factors That Impact Immunity


Additional factors for consideration include host im- munity at the time of vaccination. Horses that have undergone a stressful event such as long dis- tance transport, exertion,1 or have received immu- nosuppressive therapy2 should not be vaccinated during times of immune suppression. It should be noted that vaccine formulation should be consid- ered when characterizing the impact of physiologic stress on the equine patient. For instance, al- though exertional exercise may impede an op- timal immune response, mucosal immunity appears effective in response to intranasal influenza vacci- nation in ponies despite high intensity exercise.3 Specific therapeutic medications that should be taken into consideration at the time of vaccination include both corticosteroids and non-steroidal anti- inflammatory (NSAID) therapy. Previous work has demonstrated that routine doses of immunosup- pressive corticosteroid therapy results in immuno- suppression when used at the time of vaccine administration resulting in suppressed IgG expres- sion.4 Even though immunosuppressed horses are capable of producing antibody in response to vacci- nation, the levels of protective IgG antibody are markedly reduced when compared to IgG production in healthy horses that had not received immuno- suppressive corticosteroid therapy.4 Therefore, corticosteroid therapy is not recommended at the time of vaccination in horses. More recent data has demonstrated that the administration of an NSAID at the time of vaccination and continued for a total of 3 days can attenuate cellular and antibody re- sponses.5 Collectively, administration of medica- tions that have the intended purpose of attenuation of inflammation should be used with caution if used at the time of vaccination. Attention to health programs for young foals


should be specifically designed for at risk individu- als. Foals that ingest adequate colostrum will be protected from a variety of pathogen challenges dur- ing the first four to six months of life. From an immunologic standpoint, the optimal time to ini- tiate a preventative health vaccine program is when maternal antibodies have waned, likely as the foal approaches 1 year of age.6 From a practical stand- point, however, this is not possible, so the goal of management is to wait until maternal antibodies have fallen to a sufficient level that endogenous immunity is capable of responding with a pro-


nounced memory response that will provide specific and long lasting protection. We recently evaluated healthy foals that received adequate colostrum for their ability to respond to vaccination beginning at 3 months of age.7 Mea- sures of immunity were characterized by IgG anti- body expression and CD4 and CD8 cellular cytokine production. When compared with foals that were initially vaccinated at 6 months of age, the foals vaccinated at 3 months of age demonstrated a similar immune profile for cellular cytokine expres- sion including IL-4 and interferon gamma. When immune responses were examined at 11.5 months of age, similar cellular expression of interferon gamma was observed in CD4 and CD8 lympho- cytes in response to Eastern equine encephalomye- litis (EEE), Western equine encephalomyelitis (WEE), West Nile virus (WNV), influenza, and equine herpesvirus (EHV-1/4) indicating that the foals vaccinated at 3 months of age responded in a similar manner to foals vaccinated at 6 months of age (P  0.05). In addition, the foals vaccinated at 3 months of age demonstrated a greater than four- fold increase in IgG expression when receiving a booster vaccine against influenza, EHV-1/4, and tet- anus administered at 11 months of age. These data provide evidence that when healthy foals are ini- tially vaccinated at 3 months of age, they are capa- ble of demonstrating an antigen specific immune response.


Age-associated changes in immunity have been investigated in a variety of mammalian species.8–10 Collectively, these investigations have demon- strated that there is an overall age-associated re- duction in circulating T lymphocytes. Similarly, the concentration of circulating lymphocytes is re- duced in aged horses.11–13 Additional age-related changes involve lymphocyte subset concentrations. Consistent with a reduction in total lymphocyte numbers, there is a reduction in the total number of CD4, CD8, and B lymphocytes in circulation. However, older horses display an increased percent- age of CD4 lymphocytes.14 Subsequently, the CD4:CD8 ratio is altered in older horses resulting in an apparent proinflammatory immune bias similar to what has been reported to occur in older people.10 An important characterization of lymphocyte function is the assessment of cellular proliferation induced by cytokine, mitogen, or antigen specific response in vitro. Similar to elderly humans, an impairment of lymphocyte proliferation has been observed in horses.14,15 Regardless of the methods used to enhance this response, such as with IL-2 supplementation or changes in CD25 (IL-2 receptor) expression, cellular proliferation is not restored to adult-age responses. The conclusion from this find- ing is that similar to geriatric humans, horses have reduced T lymphocyte proliferation that may con- tribute to impaired immune function, in particular, with regard to antigen specific responses at the time of vaccination.


AAEP PROCEEDINGS  Vol. 60  2014 393


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