In recent years there has been a shift in the U.S. horse population, with aged horses (15 years or older) an increasing percentage (20-30%). Many of these older horses remain actively involved in equestrian sport competitions, are still being bred, or serve as companion animals. Thus, further understanding of how the biology of aging affects the older horse has become increasingly important and valid, given the greater demand for veterinary care and management of these animals. Unfortunately, as with elderly people, old horses suffer from age-related diseases, such as arthritis, congestive heart failure, Cushing's syndrome, and cancer. They also experience age-related changes in immune function.
A decline in the function and regulation of the immune system is a hallmark of aging, termed "immunosenescence." It greatly affects the ability of this aged population to resist infection and respond effectively to vaccination. In fact, it has been shown that like elderly humans, geriatric horses are susceptible to influenza virus infection despite pre-existing immunity to the virus. With age, all components of immunity are affected. These components include innate and adaptive responses to prevent infection and respond satisfactorily to vaccination. This process is very complex; however, changes in T lymphocyte (or T-cells, a specific type of white blood cell that recognize that the horse has been infected by a virus and react before the virus has had a chance to replicate) function underlie much of the age-related decline in the protective immune response. Proper T-cell function is crucial in combating invading organisms and maintaining a pool of memory cells to handle future encounters with the same antigen. The exact causes of immunosenescence are not clear, although it is becoming more evident that this process is multifactorial and correlates with universally observed processes across species, including:
- Thymic involution (attributing to a decreased pool of naive T-cells capable of responding to new pathogens);
- Chronic antigenic stimulation due to persistent infections (predominantly causing clonal exhaustion of memory T-cells), and
- Signal transduction changes in immune cells.
Collectively, these alterations contribute to the diminished ability of the immune system to respond to vaccination, enhancing susceptibility of this age group to infectious disease.
It's important that vaccines and vaccination strategies are developed that keep pace with the changing risk profile of an aging horse population. Vaccines are only effective, however, if the immune system is capable of responding to them. Research efforts are being directed at furthering our understanding of how different formulations of vaccines may overcome immunosenescence in the aged horse.
It is also important to recognize how different vaccine constructs stimulate the immune system. Inactivated or "killed" vaccines are processed and recognized by the immune system as exogenous antigens; they induce primarily an antibody response but poor cell-mediated immune (CMI) responses. "Live" vaccines are processed by the immune system as endogenous antigen, which mimics how a natural viral infection is processed; these antigens elicit both antibody and strong CMI responses. Indeed, it has been shown that older horses are capable of responding to a vectored, or live, influenza vaccine. Further research is needed to improve our understanding of vaccine effectiveness in aged horses.
Areas of current investigation include using high-dose vaccines, multiple administration of vaccines, DNA vaccines with immunostimulatory properties, and vaccines containing new adjuvants. It is also important to recognize that other factors, such as chronic diseases, age associated inflammation ("inflamm-aging"), frailty, stress, and nutritional status likely contribute to impaired immune responses to infectious agents and vaccinations with age. These types of studies will help provide a platform on which to further investigate mechanisms responsible for a decline in immune responses with advancing age.
CONTACT: Amanda Adams, PhD, 859/ 218-1097, email@example.com, Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, Ky.
This is an excerpt from Equine Disease Quarterly, funded by underwriters at Lloyd's, London, brokers, and their Kentucky agents.
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Disclaimer: Seek the advice of a qualified veterinarian before proceeding with any diagnosis, treatment, or therapy.