Christine King BVSc, MANZCVS (equine), MVetClinStud
Thoughts on EHV-1
Note for Australian readers: I wrote this article while I was living and working in the Seattle area, in the midst of an outbreak of equine herpesvirus type 1 (EHV-1) in Quarter Horses returning home from a large cutting-horse show in Ogden, Utah in 2011. By the end of the outbreak, more than 2,000 horses in 10 states had been exposed, either at the show or via horses returning from the show. For all that, only 90 horses tested positive for EHV-1, and 13 horses with neurologic disease (equine herpes myeloencephalopathy) died or were euthanised.
It’s May 23rd, 2011. We’re now more than 2 weeks into the latest outbreak of neurologic disease caused by equine herpes virus type 1 (EHV-1), and I wanted to share some additional thoughts on this disease.
First, a quick reminder:
• the virus is EHV-1
• the neurologic disease it occasionally causes is EHM, for equine herpes
myeloencephalopathy (disease of the spinal cord and brain)
But it’s important to realize that EHV-1 and EHM are not the same thing, and these terms are not interchangeable. Most horses with EHV-1 do not have, and never will have, EHM.
There has been a lot of research on EHV-1 in the past decade, but still we have more questions than answers. One of the most pressing questions is why only a few horses with EHV-1 develop EHM. What are the factors involved in individual susceptibility to EHM?
Equine herpes primer
Equine herpes viruses, particularly EHV-1 and EHV-4, are very common in horses. In fact, it would not be too great a stretch to use the word “ubiquitous.” Most horses are first infected as young foals, picking up the virus from their mothers, other broodmares on the farm, or other foals. The virus establishes long-term residence in the young horse, remaining probably for life in most cases, being dormant most of the time and reactivating only during periods of stress.
This common characteristic of herpes viruses is called latency: the infection is latent or dormant most of the time and active only occasionally. If you get cold sores when you’re stressed or sick, then you’ll be very familiar with this dynamic, as cold sores are caused by a human herpes virus.
Population studies in horses suggest that at least 60% of horses, and with the more sensitive diagnostic methods, almost 90% of horses in some populations, have at least one strain of EHV-1 in residence. A recent statement by the American College of Veterinary Internal Medicine included this telling remark: “For practical purposes, clinicians should presume that the majority of horses are latently infected with EHV-1.”
And yet, despite the prevalence of this virus, neurologic disease caused by EHV-1 is very uncommon. The outbreaks of EHM get a lot of attention when they occur, but given the size of the horse population here in the US and how much horses are moved around the country these days for competitions, breeding, sale, family relocation, etc. — for such a common virus, these outbreaks of EHM are strikingly uncommon.
Also, during an outbreak, the incidence of EHM in exposed horses typically is less than 10%. For example, although we’re only midway through this latest outbreak, the incidence of EHM in the more than 1,000 horses exposed either at the show or by horses returning home from the show is currently less than 3%. We’re not done with this outbreak yet, but we’ve likely seen the bulk of the EHM cases already, so although that figure will probably increase before all is said and done, it is not likely to climb out of the single digits. As a point of comparison, the incidence of fetal foal loss during outbreaks of EHV-1 abortion in broodmares may be over 50%.
A lot of attention has been paid to the different strains or genetic variants of EHV-1 and their disease potential. Here’s a brief summary of what we know:
But here’s where it gets really interesting. There is some evidence that the N variant is the more recent adaptation this virus has made to the various selection pressures it has experienced over its generations. Evidently, the N variation provides some selective advantage over the D strain. For one, the N strain causes less harm to its host.
The vast majority of cases of EHV-1 infection are seen in young horses, especially yearlings and 2-year-olds just starting in training and competition. In these horses it causes its primary disease: rhinopneumonitis, or inflammation of the upper and lower airways (rhino = nose; pneumo = lungs). Hence its common name, “rhino.” It causes usually mild, flu-like symptoms, and unless it is complicated by some other infection (e.g., bacterial pneumonia), the recovery rate is 100%.
Similarly, in outbreaks of EHV-1 abortion in mares, the recovery rate is pretty much 100%. The incidence of fetal or neonatal death is high, but few, if any, mares die from EHV-1 infection during these outbreaks. And typically, the affected mares don’t even show obvious signs of illness, other than spontaneous premature delivery or abortion.
In contrast, horses with EHM can be quite ill. A high fever is common at some point during the disease, and the neurologic signs can be quite severe, in some cases progressing to an inability to stand. The mortality rate, whether from natural causes or euthanasia, is at least 25% in horses with neurologic signs.
The D strain appears to be quite old. For example, it has been identified in a sample collected from a horse in 1941. In fact, there is some evidence that it may be the original genotype of EHV-1. In other words, the virus probably began as the D variant, but at some point and for some reason, it mutated to the N variant.
This mutation is not stable, meaning that it is not consistently inherited in subsequent viral generations. But that just lends weight to the speculation that this mutation is a positive adaptation, made to ensure the on-going survival of the virus in its host. Internal parasites face the same issue: it is not a good long-term survival strategy to kill one’s host!
The fact that this mutation is relatively unstable suggests that the virus is keeping its options open. What further adaptations EHV-1 might make, both at this specific N/D gene site and at others, remain to be seen. In recent decades EHV-1 has had to contend with widespread and intensive vaccination practices. Immunostimulant use has also increased in young performance horses — primarily for the control of respiratory infections! So, to ensure its continued survival, this virus may have to adopt even more stealthier habits.
Thus far, we’ve established that the less neuropathic N variant is the most common strain of EHV-1 now in circulation. That takes us partway in understanding why EHM outbreaks occur so infrequently and affect so few horses: the more neuropathic D strain is relatively uncommon.
But might there be more going on? And what is it about the D strain that makes it more likely to cause neurologic disease?
We don’t yet know, but the possibilities include higher circulating levels of virus (i.e., greater degree of viremia) with the D strain, so greater potential for damage; and differences between strains in their ability to attach to the cells lining the blood vessels (endothelial cells) of the spinal cord and brain.
Yes, but why the central nervous system with the D strain? (And why the uterus and placenta with the N strain?) Why not other organs or tissues?
That’s what really interests me: why certain cell types, tissues, organs, or body parts are affected and not others. Same for cancer as well as for infectious diseases, injuries, and pretty much any other medical condition. Why there? is the question I keep asking myself. What does it mean that it’s happening in one site or system and not another? And what does that mean for how we treat and prevent this disease?
I’m also fascinated by the concept that viruses are little more than genetic code. They primarily consist of relatively short strands of DNA or RNA — in other words, encoded information which directs the functions of a cell. For the most part, viruses are quite species-specific. They also tend to be quite organ- or tissue-specific. So, infection by a particular virus or a particular strain of a virus tells us something about the individual host’s vulnerability.
Here are some things to ponder about EHV-1, particular in regard to EHM:
Combine that with the small percentage of horses latently infected with a D strain of EHV-1, and we gain a better understanding of why outbreaks of EHM occasionally occur at these events and seldom, if ever, at home. From the data we have, it seems clear that horses can be latently infected with a D strain of EHV-1 for life and never develop EHM. It’s not just about the virus. It’s never just about the virus.
Back to the vulnerability theory, a viral infection shows us where we are most vulnerable. With EHM, it is the spinal cord and brainstem — the parts that are responsible for core functions of information processing and response; especially response. It is interesting that the herpes viruses of all types have a habit of latency, re-emerging during periods of stress (i.e., increased vulnerability) to show us where we need to shore up our boundaries and otherwise address our vulnerabilities.
So, what does this mean for the prevention of EHM? I would suggest that, in addition to good food, plenty of rest, loving social bonds, and all the other fundamentals of good health and well-being, we ought to be encouraging as much self-determination, self-direction, and control as possible for the individual horse under the specific circumstances. How you go about that will depend on your horse and your situation. But no matter how you accomplish it, if my theory is even partially correct, enabling your horse to feel a bit more in control of what happens to him will likely go a long way toward reducing his vulnerability to EHM.
Or, you could just vaccinate and cross your fingers...
Copyright © 2011 Christine M. King. All rights reserved.