Since it has been determined that foals may be most susceptible to R. equi in the first few days of life, the foal can become initially infected at the breeder's farm and bring the resulting contamination
back to the home farm, says Bonnie R. Rush, DVM, MS, Dipl. ACVIM, professor and section head of equine internal medicine at
Kansas State University.
"Therefore, it is important for the owner to understand where the infection came from and to recognize that foals that are
sick are shedding a lot of bacteria and serve as a source of R. equi," she says.
Although a farm did not have a serious heavy load of R. equi previously, once the foal sheds bacteria, it is a reservoir of disease to infect the farm where it is housed. If it is a
farm's only foal, then it should try to confine and contain the spread of infection. It is then important to dispose of the
foal's manure, and try to keep them away from other newborn foals.
"But once the environment is contaminated, it is pretty hard to get it completely clean again," Rush says.
To the contrary, Hines suggests that the evidence that foals are infected only during the first few days of life is really
quite controversial, though they can be infected very early in life; definitely many are in some settings. However, even in
the studies that report the earliest onset of disease, the disease is diagnosed at 40-plus days of age, and there is no experimental
evidence for a 40-plus day incubation period. Foals likely can be infected for a significant period of time, not just in the
first week. Experimentally, foals at 6-10 weeks of age typically have been used, and they have always been susceptible.
Virulence, foals show more susceptibility
There is a particular genetic construct or plasmid of R. equi that is essential to development of the disease. It allows the organism to penetrate and replicate within the macrophage.
This plasmid contains genes that encode for several proteins that have been named virulence associated protein (VAP) and are
noted as 'A through H'.
"VAP A appears to be one of the keys to how this bacterium thrives in macrophages, but we still don't know why," Prescott
explains. "The other VAP genes appear less important, perhaps because they are secreted rather than staying on the bacterial
surface, but what their function is also is still a mystery."
All foal strains contain VAP A and the same other VAP genes. Without VAP A, these strains don't cause disease. The bacterium
seems to like to get into macrophages through the "back door" by getting itself taken up by complement or other receptors.
If it goes through the "front door", that is through antibody receptors, it is more likely to be killed. It really seems to
want to get inside macrophages as the safest place it can find in the body, which is strange because macrophages are usually
bacterial hell, Prescott says.
"Why young foals are so susceptible is probably because of VAP A strains, which are essentially unique to the horse, which
like to take advantage of the window in the immune system when immunoglobulins are at their lowest levels to get inside macrophages
through the back door," Prescott says. "There may also be some heritable predisposition in some foals and perhaps also a general
tendency of young foals not to be good at mounting the correct type of immune response, perhaps because they are overwhelmed
by the numbers of R. equi they encounter, perhaps because they have intercurrent equine herpesvirus-4 infection, or for a combination of these and
"Foals are seeing R. equi for the first time, so they don't have pre-existing immunity," states Hines. "Like any other neonate, their immune system
is just not well developed yet. The big question is do they have the capability to respond as adults do? They do not. I think
part of it is the immaturity of their immune system."