Over the past few weeks, we have had reports of a slight increase in cases of Potomac Horse Fever (PHF) in the Northeast. While this disease is not commonly seen in Connecticut or Rhode Island, a small increase in case numbers is cause for increased vigilance and attention. Knowledge is power, so we thought we'd go through some specific details on PHF in this blog.
Please keep in mind as we go through this information, PHF is fairly uncommon in our region. There is a higher concentration in central New York (near Syracuse), and a much higher concentration in the Potomac River Valley, including Pennsylvania, Maryland, Virginia. While we still watch for it in this area, we don't see or hear of many cases.
Potomac Horse Fever is caused by an intracellular bacteria called Neorickettsia risticii
(side note - it used to be called Erhlichia risticii
, but the microbiologists changed its name on us a decade or so ago. You'll still see the old name kicking around, don't let it confuse you.) Intracellular means it can only live inside a cell - it doesn't live freely in the environment. That also means that it needs a "vector" to get inside a horse. A "vector" is another type of animal (worm, insect, etc) which carries the bacteria and allows it to infect something else. PHF is kind of confusing because there are multiple vectors involved. The bacteria is carried by a small parasitic worm (fluke) that infects freshwater snails followed by aquatic insects. The horse doesn't appear to be directly infected by the fluke, however.
Rather, the horse is infected after it eats the insect which is itself infected. (Whew! There's a reason this is a confusing disease. It doesn't get better from here, but try to stay with us.) What kind of insects are we talking about here? The list seems to be fairly broad, but can include the adult and immature forms of caddisflies, mayflies, damselflies, and stoneflies (see image to right). Recent work by Dr. John Madigan of UC Davis has proven that horses become infected when they ingest the flies that are infected with the bacteria. (Read more about it here.) Under experimental conditions, they were able to cause infection in a horse by feeding just 8 (yes, 8!) caddisflies. Other methods including feeding the snails or feeding the organism directly did not lead to transmission of the disease. It's important to remember that since the fly is the vector, that means the horse doesn't need to drink directly from a river or pond. The disease can come to the horse and land in its water bucket.
Image (edited slightly) from Merial's FAQ page: http://www.equinewnv.com/Pages/faq.aspx
Keep in mind that a horse is an ACCIDENTAL host of the N. risticii bacterium. While there is some fecal shedding of the bacteria in actively infected horses, which can be important in seeding aquatic areas with the bacteria, there is no evidence of direct transmission from horse to horse. So while an active case on a farm can be alarming because it indicates that the bacteria is present and infection of other horses is possible, the infected horse does not pose a direct threat to other horses.
Once a horse is infected, the bacteria enters the monocytes (a type of white blood cell), and then travels to the intestinal tract. The clinical signs of PHF can be quite variable - importantly, the signs can vary from farm to farm and region to region, not just horse to horse. (There is a fair amount of evidence that PHF is actually caused by several different strains of N. risticii, based on the difference in disease severity, response to vaccination, and microscopic appearance in cells.) Technically, PHF is classified as an "enterocolitis" - this means it causes diffuse inflammation of the intestinal tract. Fever is often (but not always) seen, and when seen it's often moderately high - in the 103-106 degrees F range. Depression and inappetance are common, as well as mild colic and a variable degree of diarrhea. Some horses will also develop mild to severe laminitis. In most areas, laminitis is a rare symptom - in other area outbreaks (such as in the Potomac River Valley), it can occur in up to 40% of cases. Laminitis is the most concerning clinical sign - often, we can control the diarrhea, fever, and resulting dehydration, but if there is severe laminitis present, it becomes difficult to treat these horses and have them fully recover.
The one nice thing about PHF is that the treatment is identical to another disease in our area that is MUCH more common, and has slightly similar symptoms ("Anaplasmosis" aka "Ehrlichiosis" which is a tick-borne intracellular bacteria, causing a high fever as its primary clinical sign). These two bacteria are closely related, as evidenced by the "old" name, "Ehrlichia", which is a genus they shared before the microbiologists decided to rename them all!) Both of these bacteria are very responsive to the related antibiotics oxytetracycline, doxycycline or minocycline. Which antibiotic we choose depends on the severity of signs, but a response to treatment is usually seen in about 12 hours after the first dose. The diarrhea associated with PHF takes a bit more time to clear up as the gut needs time to heal. So some supportive care (oral or IV fluids) is often necessary for the next few days if the diarrhea is profound.
Side note: While oxytetracycline is available over the counter (for use in cattle), it's very important NOT to attempt treatment of your horse without a veterinarian. Oxytetracycline is poorly absorbed orally in horses, and must be given IV, diluted in sterile fluid, slowly through an IV catheter. Don't take this on alone!
Like Anaplasmosis, a diagnosis of PHF can be made based on a blood test, most commonly an IFA (indirect fluorescent antibody) titer. PCR and ELISA tests are also available. Testing has its pros and cons, and can sometimes not yield expected results. Often, clinical signs are suggestive enough to start treatment before a blood test is complete, and we generally have confirmation that treatment is successful before we have a positive blood test. But it's nice to have a positive test, especially in an area (like ours) where the disease is uncommon, so we know that the farm has a higher risk than the general area.
Prevention of PHF is actually trickier than it would seem. First off, completely a
voiding aquatic environments altogether isn't really feasible, especially with a trail horse. Reducing fly populations on your farm can be beneficial (check out our newsletter on that
!) Additionally, keeping lights turned off around barns at night can help, since these lights attract insects and may lead to an increase in potential transmission.
There is a vaccine, but it's of variable effectiveness. We do vaccinate horses in our region who seem to be at higher risk (those horses who live in a paddock with a pond or stream in it, or who commonly trail ride in wet areas, or drink from ponds or streams). Since the vaccine isn't particularly protective (only reaching about 78% protectiveness in experimental studies, and certainly less than that in actual infections), and the effect of vaccination wanes quickly (reaching about 50% protective at 6 months, and about 33% after 9 months), if you're going to vaccinate, it's best to do so about a month before cases start to emerge in the area. For the northeast, we start to see cases in July/August, so vaccinating in June makes the most sense. There is some evidence that the vaccine is waning in effectiveness over the past several years, and in some region it seems to be much less effective than in others. This lends support to the idea that we are actually seeing several different strains, and the vaccine may be effective against some, but not others. It's also believed that since the disease is contracted orally, vaccines may need to be reformulated to provide better protection.
In summary, PHF is a confusing disease, and can be difficult to deal with. Fortunately, it's not common for our area. The vaccine may be of benefit for high risk farms, including those who have seen definitive cases. If your horse goes off feed or just seems "off", take a rectal temperature - ask us how to do it at your next appointment if you're not sure. If there's a fever (temperature of 102 or higher), give your vet a call. There are many, many reasons for a horse to have a fever, but PHF will be on the (long) list of possibilities this time of year.
Equine Cushing's disease is a fairly common term in the horse industry. That's because 1 out of 5 horses over the age of 15 have the disorder. But for how common Cushing's is in horses, there remains a lot of misunderstanding about this condition. In this blog, we'll try to make things a little more clear!
Note: While Cushing's disease can contribute to other metabolic disorders (such as insulin resistance), we're going to focus solely on Cushing's disease for the purpose of this post. We'll tackle insulin resistance in another blog post!
The term Equine Cushing's Disease was coined for the similarity to the syndrome in humans and dogs. (Cushing's disease in humans was originally described by a neurosurgeon at Johns Hopkins University named Harvey Cushing
.) In humans and dogs, Cushing's is most commonly caused by either 1) an adrenal tumor or 2) a tumor in the anterior lobe of the pituitary gland which causes hyperplasia (excessive growth) of the adrenal gland. Both of these cause an increase in cortisol (a steroid). In horses, Cushing's is primarily due to a tumor in the intermediate lobe of the pituitary gland, but there is no associated hyperplasia of the adrenal gland. That's why the technical name of it is Pituitary Pars Intermedia Dysfunction (PPID). Whew! If you thought that was scientific, just wait!
In our last post, we discussed (mainly) non-surgical types of large intestinal colic. However, as we all know, sometimes colic goes beyond what we can treat in the field and referral for surgery is necessary. Typically, these result from the colon moving (or displacing) into a place that it shouldn't be. That being said, some of these can be treated medically, however not always successfully. Since we've already gone over the anatomy of the large colon, (See Large Intestinal Colic: Part One
) let's jump right into what might have happened if your horse's bowel becomes blocked.
Right Dorsal Displacement: The left colon is quite mobile and likes to get stuck in places. In a right dorsal displacement (RDD), the left colon slides around to the right side of the abdomen and gets stuck between the cecum and the body wall. The pelvic flexure (the U-shaped area at the top of the picture) moves from the back end of the abdomen (near the rectum) to end up near the diaphragm. This is all kinds of crazy! The large intestine becomes partially occluded and gas distended. In practice, we can see this occur in conjunction with a pelvic flexure impaction. Generally speaking, the blood supply remains intact so the bowel remains healthy. We can sometimes treat these with fluids and withholding feed, but often times surgery is required. At surgery, the colon just needs to be decompressed and repositioned into the appropriate anatomic location. As long as nothing more serious is going on, these horses recover quite well.
Previously, we have discussed small intestinal colic
and gastric ulcers
. However, when discussing colic, we have to determine if it is small intestinal in origin or large intestinal.
Below is a brief list of problems associated with the large colon. Typically, these are non-surgical and can be resolved with some medical management. That's not ALWAYS the case, but for the most part it is. (Part 2 will focus on more severe types of large intestinal colic.)
Colic is a scary word to horse owners and veterinarians. However, some types of colic are much worse than other types. While 90% of colic cases resolve with minimal treatment on the farm, some require more intensive care. One such type of more serious colic is small intestinal strangulation, which is an obstruction of the blood supply and the lumen (the inside of the tube, where food passes through) of the small intestine. 1. Stomach 2. Small intestine 3. Cecum
The horse's gastrointestinal system is quite lengthy - it spans approximately 120 feet, and the majority (70-80 feet) of that is small intestine. Furthermore, it's mostly floating freely in the abdomen, with minimal attachments to the body wall and surrounding organs. This conformation gives lots of opportunities for something to go wrong, whether that's a twist, or some other way that the intestine ends up in the wrong spot.
The small intestine (or SI, for short) is the same in horses as it is in dogs, cats or humans. It's made up of 3 segments - the duodenum, the jejunum and the ileum. The duodenum is the first section, just after it leaves the stomach and for about the next 12-16 inches (that's it - so, not much goes wrong with the duodenum!) The jejunum makes up the bulk of the small intestine, and the ileum comprises the last foot or so before it enters the cecum. There are minor variations in these structures, but we don't have to worry about them here. All this SI is suspended within the abdomen by a sheet of connective tissue called "mesentery". (If you laid a garden hose straight across a towel, then picked the towel up at all 4 corners it would create the same effect.) The mesentery brings blood supply to the intestines.
The equine digestive tract is always a concern for horse owners - and veterinarians! Colic can be caused by many different things, and one possibility is EGUS - Equine Gastric Ulcer Syndrome. Gastric ulcers are actually quite common in horses. There are a variety of reasons for this, but have no fear! While they are common, they are rarely life-threatening and can be cured with appropriate treatment. www.egus.org
First, let's start with an anatomy overview. The equine stomach is divided into two sections - the non-glandular (or squamous) section, and the glandular area. The line dividing these areas is known as the "margo plicatus". Stomach acid is secreted by the glandular area. We typically see ulcers along the margo plicatus on the squamous side of the stomach, but we can also see ulcers throughout the non-glandular and glandular regions. Oh yeah, and just to be clear, gastric ulcers are erosions in the normal lining of the stomach. Pretty simple so far, right?
The eye is a very delicate organ, and horses specifically have eyes which are in a very precarious position. In order to allow for a nearly 360 degree view around them, horse eyes are placed well on the outsides of their heads. This anatomic location combined with a horse's normal "flight" response makes eye injuries quite common. One of the most common things we see are corneal ulcers.
Every so often it happens – your horse just doesn’t seem right and you need to call the vet. When you do, it’s important to have as much information as possible so your vet can get a good picture of what’s going on. Here are five of the most common questions we ask horse owners – know these, and you’re one step ahead of the game!
With the warm fall we've been enjoying, it may be hard to remember that winter is just around the corner. Soon enough, however, we'll be battling snow and frozen ground as we take care of our equine companions. It's important to put some thought and time into preparing your horse and your property before winter sneaks up on us completely. We've outlined a few things to keep in mind to help this transition time be as seamless as possible.
Recently, mosquitoes infected with EEE (Eastern Equine Encephalomyelitis virus) were found in Voluntown, CT. Not only that, but there have been 2 confirmed cases of EEE positive horses in Massachusetts. While it would be nice to hide from it, the fact is that it is in our backyard. But what do we really know about it?
USDA map Oct. 2012
EEE is mainly found in the US east of the Mississippi river, and throughout areas of Central and South America. The virus persists in “reservoirs” – wild animals that carry the disease such as bats, rodents, and birds. A vector (such as a mosquito) becomes infected when it feeds on one of these animals. Most often, EEE is maintained through a transmission cycle between birds and mosquitoes. The mosquito then carries the virus for life and can transmit it through its saliva. If a horse happens to be the source of the next blood meal, then they can become infected and quickly begin to show signs.
Once infected, it takes approximately 5-15 days for signs to show up. These signs can be very mild such as a fever and depression; or severe including blindness, stumbling, seizures or death. Any neurologic signs could be indicative of EEE, however other diseases such as rabies must be considered as well, and a diagnosis should be confirmed via testing. Unfortunately, a diagnosis is often obtained post-mortem. If EEE is suspected, the state veterinarian must be contacted and the disease needs to be reported.