Equid Blog : Horse Health & Diseases : University of Guelph : Ontario Veterinary College : Equine Infectious Diseases

The latest edition of the journal Emerging Infectious Diseases contains a paper describing the 2008  Australian Hendra virus outbreak in horses and people.

In this outbreak, there were five horses infected and two humans infected. The horses predominantly had signs of neurological disease, not respiratory disease like some other reports describing this disease. Four horses died. One recovered but was euthanized for public health reasons.

Two people became infected after working with the sick horses, which represents 10% of the total veterinary staff that were exposed to the infected horses.  Both people started off with influenza-like illness, which seemed to improve initially, but then signs of severe neurological disease developed. They were treated with ribavirin, an antiviral drug, as part of an experimental treatment. One of them died after 40 days of illness, the other person survived.

The authors stressed that the effectiveness of ribavirin could not be determined, but they recommend it nonetheless because of the severity of Hendra virus infection and lack of other options. Ribavirin was also used in the 2009 outbreak, but it is clearly not 100% effective since one person died there also.

A number of concerning activities occurred that put people at risk of infection, including a "percutaneous blood exposure while euthanizing an infected horses" (they didn't explain exactly what this was, but it could have been a needlestick), low use of personal protective equipment, and contact with potentially infectious body fluids. This is unfortunately not surprising since the approach to infection control (particularly in terms of zoonotic infections) is often lax in equine medicine. That certainly has to change, particularly in areas where Hendra virus may be present.

Much more information about how to control this potentially devastating virus is needed. Fortunately, infections are uncommon and it is restricted to a fairly small geographic range in Queensland, Australia.

Image source: http://animalphotos.info/

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Equine infectious anemia (EIA) virus, a chronic and potentially devastating bloodborne virus, was identified in two horses in Britain. The two affected horses were from a group of horses imported from Romania via Belgium. They were tested as part of standard import testing regulations designed to do exactly what happened here - diagnose this important infectious disease at the time of importation so that the infected horses cannot spread the disease in the country. The two positive horses will be euthanized, the unfortunate but standard response to this virus, because infected horses can pose a risk of infection to other horses for their entire lives. Other horses on the premises are under quarantine and are likely being tested further. The risk of transmission to other horses during the presumably short period of time they've been on the farm is probably low because, as an insect borne disease, biting fly activity has probably been pretty low during the cold British winter weather. (Transmission by sharing needles or other human-associated ways of cross-contamination of blood is also a concern, and has been a problem in other outbreaks.)

Chief veterinary officer Nigel Gibbens stated that these are the first imported cases of EIA identified since 1976. This is a good example of why we need to continue routine infection control measures such as import testing, even when nothing is found for years. Some people try to argue that since certain problems don't seem to be present, or at least are not identified, that infection control testing or activities should be decreased. This situation illustrates why that's bad thinking. Despite only picking up one incident in the past 34 years, this is a very important finding - failure to detect the positive horses could have lead to widespread infection in the country, which would ultimately make it very difficult and expensive to try to control. You never know when the next outbreak is lurking around the corner, and complacency is a big enemy of infection control.

Image source: www.collectgbstamps.co.uk

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I assume that people wouldn't voluntarily and regularly walk around barefoot on dog feces (or feces of any type), yet it's perplexing that some people regularly clean out horse stalls in bare feet (I've seen it done!). While horse manure may not be as inherently gross as dog poop, it's still feces, and like all feces contains a huge population of various bacteria, some of which can be harmful. The risks of barefoot mucking may also extend to bare feet inside boots, although I don't think sock-averse people need to panic.

An article in the International Journal of Infectious Diseases (Friederichs et al) describes infectious arthritis of the shoulder of a horse owner that was caused by Streptococcus zooepidemicus, a bacterium commonly found in horses but rarely associated with disease in people. The person didn't have a wound in the shoulder area or any other obvious route for the bacterium to get to the shoulder joint. They searched for a source of the infection and all they found was a chronic lesion on the person's foot. This, combined with the patient's history of taking care of his horses in "bare feet in boots", led them to implicate the foot as the source of infection.

The idea, I guess, is that socks would be a barrier to help prevent contamination of the foot wound. That makes sense to a degree - the person could contaminate his foot with S. zooepidemicus from his hands (probably acquired from touching the horse's nose) while removing the boots, or manure could work its way into boots and directly contaminate the wound. Both are possible, but we have to be a little cautious in interpreting these conclusions. However, this is a bacterium that is associated with horses and the foot lesion is certainly a possible route of entry.

Overall, this should be considered an interesting report of a very rare problem, not something that indicates a major concern. However, there are a few good points to take away from this story:

• If you have a wound or chronic lesion of any sort, make sure you take measures to reduce the risk of bacterial contamination when working around horses. This might be as simple as making sure it's covered by clothing, or something more involved like using an impermeable bandage.
• Hands are probably the major source of infection transmission, and good hand hygiene is important after horse or stall contact, particularly if you have an underlying disease.

This equIDblog entry was originally posted on our sister site, Worms & Germs Blog, on 20-Jan-10.

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A three-year-old Standardbred gelding was presented to the hospital for evaluation and treatment of diarrhea (colitis). The previous week the horse had developed a mild hind-limb lameness which seemed to come and go, and it was decided to treat the horse with antibiotics “just in case” it had something to do with an infection. The horse was treated with ceftiofur (an antibiotic, often sold under the brand name Excenel or Naxcel) for five days. On the fifth day, the gelding developed moderate to severe diarrhea. The next morning the horse also had a fever. He was treated with anti-inflammatories and quickly referred to the hospital for intensive care.

On presentation, the gelding was very quiet. He had a very high heart rate, reddish gums and he was significantly dehydrated. Intestinal sounds could not be heard over the abdomen, indicating that the horse’s intestines were not moving normally, and there was a “ping” on the right side of the abdomen, indicating that there was gas accumulating in the cecum (part of the large intestine). Treatment with intravenous (IV) fluids was started right away to try to correct the dehydration and keep up with the amount of fluid the horse was losing in its diarrhea.

By the next morning the horse’s attitude was improved, but his gums were still an abnormal colour (“toxic mucous membranes”, see picture), indicating that there were inflammatory cytokines (substances released by cells when they’re in distress) and likely bacterial toxins in horse’s bloodstream. Also, despite the IV fluids, the gelding was still dehydrated, likely because he was pooling fluid from his body tissues in his intestine, as well as the more obvious loss of fluid in his ongoing diarrhea. This went on for another two days, despite intensive treatment in the hospital. On the fourth day, the gelding developed severe signs of colic. His large colon became progressively more distended with gas, and the contents of his small intestine started to back-up into his stomach. His heart rate became extremely high, and his pain could not be controlled with sedatives or anti-inflammatories. A belly-tap yielded a red-tinged fluid (normally belly fluid is light yellow), and the concern at that point was that the intestines had become twisted (which can happen in horses with diarrhea as a result of their abnormal intestinal motility). Despite the risks, it was decided to take the horse to surgery - but there was no twist in the bowel. The cause of the colic was that the large colon was severely distended with gas and fluid, and it was barely moving at all. The appearance of the large colon was consistent with extreme inflammation, and the tip of the cecum looked so bad that the surgeons decided to remove it because it was likely dead or dying.

The horse recovered from anesthesia, and IV fluid therapy was continued. Later that day, when the horse was offered some pellets, some intestinal sounds were detectable. The horse soon started to pass diarrhea again, but overall his attitude was much brighter, and his hydration status and (remarkably) blood protein levels remained stable.

Unfortunately the day after surgery the gelding became reluctant to move around the stall. Increased digital pulses were detected on the front feet, and the horse was sensitive to hoof testers – the gelding was developing laminitis. Despite additional treatment, the signs of laminitis became worse and worse. In the end the horse was euthanized, less than a week after being admitted to the hospital.

On necropsy, the entire large colon was severely thickened, filled with green-yellow fluid, and the mucosa (inside surface of the intestine) was ulcerated. Signs of severe acute laminitis were present in all four feet. A specific causative agent of the colitis could not be identified – tests for Salmonella and clostridial toxins were all negative. This is not too surprising as no agent is identified in over half of all adult horse colitis/diarrhea cases. But there is no doubt what set this terrible chain of events in motion – treatment with antibiotics, for a condition that may or may not have ever required antibiotic treatment in the first place.

We talk a lot about antibiotic-induced colitis/diarrhea in horses, but until you’ve seen it for yourself, it can be hard to believe that drugs used every day in both people and animals can have such a devastating effect on a horse. Antibiotics certainly do save lives, but unfortunately there are no “miracle cures” that are entirely without drawbacks. This case clearly demonstrates one of the most important reasons why we so strongly advocate prudent use of antibiotics in horses – their use should never be employed lightly. Although this is a “worst case scenario” that overall occurs uncommonly, the potential is there and should always be taken into consideration.

Photo credit: M. Anderson 2007

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I received newsletter today from Intervet (a pharmaceutical company) that is targeted at equine veterinarians. One article discussed rabies in horses. It wasn't bad overall, but I thought the section on what to do when a horse might have been exposed to rabies was worth discussing.

The article asks, "If your client suspects that a horse has been bitten by a rabies-infected animal, what should be done?"

Answer: "Contacting you as the veterinarian is always the first step."

Great first step.  A second step that wasn't mentioned should be, "Try to identify and (safely) capture the animal that bit the horse." This is often impossible but certainly worthwhile if it can be done.  However, if you're trying to catch the offending animal, make sure you don't put yourself at risk of exposure to rabies in the process.  If the animal can be caught, it's rabies status at the time of the bite can be determined (either through testing or quarantine). If it can be shown that the animal wasn't rabid, a lot of stress, hassle and expense can be saved.

"If the horse was previously vaccinated... Then isolate and observe the animal for 45 to 90 days (your clinical evaluation will involve gait analysis, radiography and a spinal tap)."

Boosting the rabies vaccine is also a good idea. The next step, however, needs to be contacting local regulatory officials to find out what you have to do. They determine if, how and how long an animal needs to be quarantined - this is NOT the decision of the local veterinarian nor the animal's owner. Most likely, they will recommend a 45 day quarantine for a vaccinated horse, since this is what is recommended in the NASPHV Compendium on Rabies. The discussion of diagnostic testing makes no sense. There is absolutely no indication to perform diagnostic tests on a horse that has been bitten by a rabies suspect. None. There are no tests that can be used to diagnose rabies in live horses (also exposed horses don't instantly develop signs of rabies). Horses should be monitored closely for signs of rabies during the quarantine period, but that's it.

"...and have the client make a list of all people who had contact with the horse."

This is often done when horses have or are suspected of having rabies, but not horses that are potentially exposed. It is done to help public health personnel contact people that may have been exposed to rabies. A horse that was just bitten by an animal is not a risk for transmission of rabies.  (However, keeping a list of people who have contact with the horse after it's been bitten (i.e. durng the quarantine period) - which should be as short a list as possible - is a reasonable precaution in the unlikely event that the horse does develop rabies.)

"If the animal was not vaccinated, your options are to euthanize and perform a postmortem examination of the brain (the only way to definitely confirm rabies)..."

Euthanasia is one of the options that needs to be considered in an unvaccinated horse that has been exposed, which is one of the reasons that identifying the biting animal and testing it is critical, if it can be done. The last part of the above sentence (from the atricle) is complete nonsense. Why would you test the brain of a normal horse that has been euthanized because it's just been bitten by a potentially rabid animal? The horse isn't being euthanized because it has rabies, it's being euthanized because of the likelihood  of it developing rabies weeks to months later. Testing of the brain will tell you absolutely nothing if the animal was only bitten recently.

"...or isolate and observe the horse for six months and develop the human contact list."

Again, this needs to be decided based on discussions with regulatory personnel who are responsible for dictating what is to be done. A six-month quarantine is a pretty standard recommendation for an unvaccinated animal. Creating a human contact list should not be necessary, since quarantine involves severely restricting contact of people with the horse and only a few (ideally one) person would have any type of contact.

The article wraps up with the very true emphasis on vaccinating horses. It's a cheap measure to prevent a relatively rare but invariably fatal disease.

Click image for source.

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At some point, the US is going to have to admit that piroplasmosis, the bloodborne parasitic infection caused by Theileria equi, is endemic in some regions of the country. It's a declaration that will have major impacts on horse movement to some areas but, it's better for everyone to know what's going on. Piroplasmosis is technically still considered an exotic disease in the US, but there have been many cases identified over the past year and a clear source for the individual outbreaks in lacking, indicating there must be a reservoir in some part(s) of the country.

The latest incident involves the diagnosis of piroplasmosis in three race horses in New Mexico, which were picked up as part of routine screening. There were only three positives out of about 1200 horses tested, so the disease is still rare, but the fact that it was there and none of the positive horses had any link with previous outbreaks is definitely a concern. The OIE report states that transmission is suspected to have been from "artificial" means like sharing needles between horses, not natural tick transmission. This could account for the multiple horses affected but doesn't explain where the disease came from it the first place, and it's unclear how solid that hypothesis really is.

It's quite interesting (surprising, frustrating...) that few comments are put forth in any of these outbreaks indicating where the infections may have originated and why we are seeing recurrent, unrelated infections. Is increased testing in different areas helping to pick up cases that would otherwise have been missed (i.e. were already there), or is piroplasmosis in the US an emerging problem? How confident are they that there are no ticks capable of transmitting T. equi in some of these areas? Is wider screening of horses required to determine the extent of the problem and to determine whether it can be controlled? Is broader screening of ticks in the affected areas needed to see if there are ticks known to be able to transmit T. equi? Are studies needed of other tick species in areas where unexplained cases have occurred to determine if some tick species that are not currently known to be able to spread the parasite can actually do so? Lots of questions... hopefully someone's trying to find some answers.

Click image for source.

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A pony in New Jersey has been diagnosed with equine infectious anemia (EIA) and euthanized. Details are pretty scarce at this point and it's unclear whether the pony was sick or whether EIA was simply diagnosed through routine testing. There's also no indication of where the pony might have acquired the infection, which is a very important question.

Equine infectious anemia is a viral disease of horses and other equids that is characterized by recurrent fever, lethargy, decreased appetite and decreased red blood cell numbers (anemia). Sometimes, the first episode of disease (acute EIA) can be fatal, but most horses recover. Most survivors experience recurrent episodes of illness. In some horses, these episodes become frequent and severe.

A major problem with EIA is that horses are infected (and are infectious) for life. Even if they recover from the acute disease and rarely or never get noticeable recurrent disease, they are still carrying the virus in their blood. Biting flies are the main means of transmission from horse-to-horse, although human-associated transmission through reuse of needles or other procedures that cross-contaminate blood between horses can also be involved.

The combination of life-long infection and an insect vector is BAD. That's why, in areas where EIA is not endemic, infected horses are usually immediately euthanized. In some regions, affected horses can be branded or tattooed to permanently indicate their EIA status and housed at least 200 yards from any other horse (and often with strict insect control measures).

Control of EIA focuses on identification of carriers. Most jurisdictions require regular EIA testing (formerly the "Coggins test") for horses that are traveling or competing, as well as imported horses. While this disease is extremely rare and the vast majority of routine tests are negative, it's a disease that can silently spread in a population if people are not looking for it - routine testing is critical for keeping this disease at bay.

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As foaling season approaches, it's a good idea for people to review proper umbilical care. The umbilicus is an important route of infection in foals, and can be associated with problems including local umbilical abscesses, large abdominal abscesses extending to the liver, and overwhelming body-wide infection (sepsis). The reason the umbilicus is such a critical structure is that it contains three major blood vessels (two arteries and one large vein) and the urachus (which connects the umbilical cord to the foal's bladder) . When the umbilicus ruptures shortly after birth, these structures are exposed to the bacteria-laden environment of the outside world and can be a route of entry for local and deep infections. Care of the umbilicus during the initial high-risk period is a key part of raising a healthy foal.

Do all foal's need specific umbilical care? Not really. Most foals, especially those born normally in a clean environment to a healthy mare and who received adequate colostrum, don't need anything done. However, it's not always easy to differentiate these low-risk foals from others, and it is possible for the healthiest foal born in the cleanest environment with ingestion of an adequate volume of good quality colostrum to develop complications, so most people perform some form of post-birth umbilical care (and that's a good thing). The key is making sure that it's the right umbilical care.

The goals of umbilical care are pretty basic:

• Prevent bacteria from entering the umbilicus.
• Avoid damaging the umbilicus and other body tissues, and avoid delaying normal drying of the umbilicus.

What to use?

• Research has indicated that a 0.5% chlorhexidine solution is the optimal umbilical dip. Other disinfectants can also kill local bacteria on the umbilicus but may not be as effective, may not work as well in the presence of debris (dirt, manure...), or may be irritating to body tissues.

Read the label:

• Make sure you are actually using 0.5% chlorhexidine and that it's a solution (diluted in water), not a tincture (diluted in alcohol). If you don't have 0.5% chlorhexidine solution and are unsure about how to dilute it properly, ask your veterinarian.

More is not better!

• Don't think that since 0.5% is good, 5% must be 10 times better. The stronger the concentration, the greater the chance of damage to local tissues, which can increase the risk of complications. Stick with 0.5%.

More is not better! Part 2

• The umbilicus should be dipped in disinfectant, not marinaded in it! The goal is to cover the umbilicus and not other tissues (e.g. the abdominal wall). You don't need to soak the umbilicus or hold the disinfectant in place over it. Short term contact (dip) is adequate. Dip it and walk away. The umbilicus needs to dry up - repeated soaking isn't helpful.

More is not better! Part 3

• The umbilicus should be disinfected shortly after birth, then every 6-8 hours for the first 24 hours of life. That's usually enough. If the umbilicus still appears wet at that time, it can be dipped again. Continued dipping "just is case" is not needed.
  

Don't tie off the umbilicus:

• Tying off the umbilicus can actually increase the risk of complications such as infection and patent urachus (urination through the umbilicus).

Hands off!

• Don't touch, poke or otherwise make contact with the umbilicus with your hands. It's not needed and it's a great way of transferring bacteria to the umbilicus.

If in doubt, call your veterinarian:

• A proactive call to your veterinarian is much better and cheaper than an umbilical infection, umbilical abscess, septic foal or patent urachus. These are all expensive complications and  often difficult to treat successfully. Foals can change very quickly, and waiting to "see what happens" for a day or two can be the difference between a minor complication and a life-threatening problem.

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An eight-year-old Quarter Horse gelding was presented for examination due to chronic weight loss over several months. Lately he’d also been lying down frequently and exhibiting increased breathing effort, so he was treated for what was suspected to be mild signs of colic, but failed to improve. He’d also collapsed once during mild exercise.

On examination, the gelding was quiet, alert and otherwise physically normal except for his poor body condition. However, on rectal palpation there was a large, firm, non-painful mass within the caudo-dorsal (i.e. upper rear) abdomen. revealed a large (42 centimeter) firm mass in the caudo-dorsal abdomen. The mass was further evaluated using ultrasound via the rectum. the mass was multi-lobulated (i.e. made up of many pockets on the inside) and had a large blood supply. It did not appear that the mass was directly attached to or growing in any abdominal organs (e.g. kidneys, intestine). Blood work showed a high white blood cell count (mature neutrophilia), moderate anemia, and high protein levels due to an abnormal increase in globulins (hyperglobulinemia).

These findings were highly suggestive of a large abdominal abscess, but a cancerous mass could not yet be ruled out. It was decided to take the horse to surgery the next day in order to better evaluate the mass, collect samples and remove it if possible. In surgery, the mass was found to be right at the root of the intestinal mesentery (the large membrane that carries the blood supply to the intestines), and there were a large number of adhesions between the mass and the base of the cecum, as well as to some loops of the small intestine. A needle and syringe were used to remove a sample of the mass’s contents in a sterile manner. The fluid retrieved had the appearance of thick pus, which further supported the tentative diagnosis of an abscess. Unfortunately, due to the location and size of the mass, as well as the number and size of adhesions, it could not be safely removed. The horse was therefore euthanized while still under anesthesia.

Necropsy examination confirmed that the mass was an abscess. The capsule of the abscess was extremely thick and tough, indicating that it had been developing over a very long period of time. A long-standing abscess such as this explained all of the gelding’s clinical signs – weight loss and moderate anemia due to chronic disease, high globulin levels due to constant stimulation of immune cells by the infectious focus, and recumbency and collapse due to discomfort caused by entanglement of the intestines in the adhesions associated with the abscess.

Culture of the fluid sample retrieved at surgery yielded a heavy, pure culture of Streptococcus equi subsp. equi – the bacterium that causes strangles. This horse had what’s known as “bastard strangles,” which is a recognized complication that occurs occasionally in horses that have had the classic upper respiratory infection. In these cases the S. equi invade beyond the respiratory tract and can end up anywhere in the body. Then, just as the bacterium does in the lymph nodes around the head and throat in classic cases, the S. equi can form abscesses. The abscesses may form in internal lymph nodes (which is likely what happened with this gelding) or in organs like the kidneys or even the brain. These abscesses tend to develop slowly and insidiously. Even if they can be identified, they are typically extremely difficult to treat effectively, and unfortunately euthanasia is often the end result. Other bacteria that can cause similar abscesses include Rhodococcus equi, Corynebacterium spp. and Arcanobacterium pyogenes.

Strangles is endemic in the horse population – whenever horses are mixed or brought together in large groups there is a risk of strangles transmission. We cannot eliminate the risk, but we can try to reduce it as much as possible using basic infectious disease control measures. More information about strangles is available on the equIDblog Resources page and in our archives.

Image: A Standardbred in poor body condition due to chronic debilitation as a result of large abdominal abscess, similar to the case described here (photo credit: M. Anderson).

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