Myiasis is the technical term for infestation of the tissues with fly larvae (aka maggots).  There are three kinds of myiasis: obligatory, facultative and accidental.  They all occur when adult flies are attracted to moist or oozing tissues (such as an open wound) in which they then lay their eggs.  The eggs ultimately hatch and the larvae hang around in the local tissue for a few days until they fall off to pupate on the ground to produce more adult flies.  Obligatory myiasis is a reportable disease caused by certain species of Cochliomyia and Chrysomyia, which are commonly known as screwworms.  The reason screwworms in particular are such a concern is the larvae of these species will actually invade and digest healthy, living tissue.  Thankfully we don't have these species in Canada, but they do occur in Central and South America, Africa and Asia.  Facultative myiasis is caused by blowflies and fleshflies of several genera.  These flies lay their eggs in decomposing (dead) tissue, typically in wounds or skin mascerated by moisture or chronic fecal soiling, as well as carcasses of dead animals.  Although the larvae do not invade living tissue like screwworms, they do secrete enzymes which may cause enlargement of the wound.  Accidental myiasis occurs when flies of the Muscidae family lay their eggs in a wound while feeding, even though animal tissues are not normally used by these species for breeding.

Although myiasis may not be common in horses, it certainly does occur.  The presence of maggots, particularly in a wound, indicates that there is necrotic (dying) tissue present, which should be removed.  Furthermore, the maggots you may find on a horse are by no means "medical grade" - the maggots that you may have heard of being used in human medicine are purpose-bred and kept very sterile.  Secondary bacterial infection is common with wound myiasis, and in large or deep wounds this may even result in septicemia.  Larvae-infested wounds are typically painful, with a foul smell and a lot of discharge.  Treatment involves removal of the maggots, debriding all of the dead or unhealthy tissue, cleaning the entire wound, applying an appropriate dressing (if possible), and use of topical insecticides to prevent future infestation.  Antibiotics may be necessary if secondary bacterial infection is present.

There are a few things you can do to help prevent wound myiasis.

• Avoid doing surgical procedures during fly season.  If a procedure must be done, monitor the incision carefully until it is completely closed and keep it as clean and dry as possible so flies aren't attracted to it.  Use of topical insecticides can be very helpful too, but check with your veterinarian about what kinds of fly spray to use around surgical sites. 
• Check your horse carefully on a daily a basis for any flesh wounds, and if you find one make sure it's properly cleaned and treated as soon as possible. 
• It's also important to prevent skin and hair from becoming caked with mud or manure.

People are also susceptible to wound myiasis, but the keys to prevention are the same: keep wounds clean and dry, keep wounds covered if possible (and also keep bandages clean and dry), and keep the adult flies away!

Image: Screwworm larvae armed with sharp mouth hooks that they use to tear at flesh. (source: www.vetmed.ucdavis.edu)

Vesicular stomatitis is caused by a virus from the Rhabdoviridae family (the same family as rabies virus) and is highly infectious.  The most obvious clinical signs of infection are blisters and sores on the lips, gums, tongue and nostrils.  Infection is rarely so severe as to be fatal, but the blisters can be quite painful such that affected horses may not eat.  In addition to being a highly infectious disease among horses, a major concern with VS is that it can infect swine and cattle as well, in which infection looks very similar to Foot and Mouth Disease - a tremendously important foreign animal disease in these other species.  Horses infected with VS must be strictly quarantined, from both other horses and other livestock, to contain the virus.  The virus is shed in the fluid from the blisters, so controlling exposure to insects which may mechanically transfer virus from one animal to another (just by flying from nose to nose), and preventing transmission via people's hands or other equipment is very important.  Some insect species also serve as biological vectors of the virus.  There is no specific treatment, but most animals will recover with supportive care in a few weeks.  People can be infected by VS, but clinical signs are typically limited to flu-like illness and occasionally mild stomatitis (inflammation of the mouth) and the disease is self-limiting.

The Canadian Food Inspection Agency (CFIA) has implemented the following import restrictions to help prevent the disease from getting into Canada:

• No horses originating from Arizona will be allowed into Canada
• Any horse coming to Canada from the US must have been out fo Arizona for at least 21 days
• Any Canadian horse going into Arizona will either have to be out of Arizona a minimum of 21 days before returning or it will require an import permit and an inspection within 15 days by a USDA accredited veterinarian, and a negative ELISA test for VS.

I have to wonder about the allowance for horses to come back from Arizona is less than 21 days - it doesn't make sense to me that a horse in Arizona can be inspected and tested for VS and still considered virus-free up to two weeks later.  The 21-day minimum "layover" between Arizona and coming back to Canada makes much more sense, as any horse that encounters VS should develop clinical signs of infection within this time frame.  If they're still lesion-free three weeks after leaving Arizona, then it's fairly safe to say they're VS-free.

By far the best thing to do for the next several weeks - until they've identified the source of the virus and have the situation well contained - is to keep your horses out of Arizona.

Image: Lesions on the lips of a horse with vesicular stomatits (source: http://wyovet.uwyo.edu/)

Thankfully all of the Canadian mares were negative, but unfortunately the Canadian equine industry is still suffering the consequences of what has happened to our close southern neighbour. Fourteen countries have increased import requirements for Canadian (and obviously US) horses in terms of CEM testing, and another major blow was the loss of Canada’s low-risk status with the UK's Horserace Betting Levy Board (HBLB).

Canada must maintain strict import requirements for horses to prevent CEM from getting into the country. Most of the horses imported into Canada come from CEM-positive countries, and it’s getting more difficult to argue not including the US on that list as well. The risk is constantly present, and remaining diligent about quarantine and testing – and rules like ensuring horses are not on antibiotics for some other reason when they’re cultured – is key. Semen import restrictions for semen coming from the US to Canada will stand for 2010. While this certainly causes a headache for breeders, requiring an import permit and a health certificate for the stud stating that it has not stood on a CEM-quarantined farm, is it enough to protect Canadian horses? The next step would be to require all studs to be tested for CEM before their semen can be imported to Canada. That is no small request. Testing a stud involves culturing the stud himself, and then having him test-breed two mares which then also need to be culture-negative. Anecdotally the entire process can cost in the neighbourhood of $5-7K per horse, which at the moment all needs to be borne by the horse owner. That gives you some idea of what an enormous undertaking it was to quarantine and test 274 exposed stallions during last year’s outbreak.

In the US, 87% of exposed horses have now been cleared, and there have been no new positives in the last 8 months. However, there are still 17 states where there are quarantined farms. There is talk of voluntary testing of over 2000 studs in the US in 2010, as well as targeted surveillance of stallions imported in the last 10 years and those standing at large AI centers. Only time will tell if these extra efforts will serve to calm the fears of countries that are now hesitant to import horses and semen from the US, or whether they will reveal more cases of CEM and confirm the fears that CEM may have unknowingly become endemic in the US in the past decade.

More information on CEM is available in our archives.

This blog is based on a presentation by Dr. Tracey Chenier, a theriogenologist and faculty member at the Ontario Veterinary Collge, given at the recent 2010 Ontario Veterinary Medical Association Conference.

Photo credit: David Campbell (click for source)

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

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).

Everyone involved in equIDblog would like to take this opportunity to thank all the visitors who come to our site, and especially those who keep coming back for more! Please continue to help us spread the word about equine infectious disease control so everyone can do their part to help protect our equine companions, on a local, national and even global scale!  Questions, comments and suggestions are always welcome!  -Scott & Maureen

(Image credit: Tatiana Sapaterio)

Responsible use of antibiotics can help stop resistant bacteria from developing and help keep antibiotics effective for the use of future generations.  Successful national public awareness campaigns are already resulting in more rational use of antibiotics and a reduction in levels of antibiotic resistance in Europe.

Responsible use of antibiotics includes use in people and in animals.  Here are some of the things you can do to help with regard to antibiotic use in your horses:

• Only give your horse antibiotics if directed to do so by your veterinarian.
• Make sure your horse gets the full dose of medication at the correct time(s) of day.  If you are having problems injecting medication or getting your horse to swallow pills, contact your veterinarian as soon as possible.  Your veterinarian may be able to give you advice on some "tricks" for getting your horse to take the medication, or sometimes the medication can be provided in a different form (e.g. a liquid instead of a pill, oral versus injectable).
• Always ensure your horse finishes the entire prescription.  There should be no leftover pills or medication.  Do not stop giving your horse the antibiotics just because it looks/acts like its feeling better.  This is a common mistake that can have disasterous consequences!  You should NEVER "save a few pills for the next time."
• Never give your horse antibiotics that were prescribed for you, another person or any other animal, whether they are expired or not.

This equIDblog entry was originally posted on the Worms & Germs blog on 18-Nov-09.

They found at least one infectious agent in the feces of 122 (55%) of the 233 foals in the study. That means, despite testing for a wide range of pathogens, they could not identify an infectious agent in 45% of the diarrheic foals. This is very similar to the situation typically found in adult horses with diarrhea. This could have happened for a number of reasons:

1. No test is perfect. It’s possible that in some of the cases one of the test results was a “false negative,” meaning it did not detect the infectious agent even though it was there.
2. A few cases may have been caused by other infectious agents that were not included in the diagnostic panel.  For example, Rhodococcus equi is a common cause of respiratory disease in foals, but it has also been associated with diarrhea in some cases.
3. The diarrhea was caused by an agent of which we are unaware, and for which we have no test. Researchers are constantly looking for other bacteria, viruses or parasites that may be capable of causing or contributing to diarrhea in foals and adult horses.
4. The diarrhea was not caused by an infectious agent. For example, the authors failed to discuss foal heat diarrhea as a cause of clinical diarrhea in very young foals. This is a well recognized cause of foal diarrhea, but no infectious agents are involved.

The most commonly identified pathogens were rotavirus (20% of cases), Clostridium perfringens (18%), Salmonella (12%) and C. difficile (5%). Overall 191 (87%%) of the foals survived, and survival was not associated with any pathogen identified in the feces (i.e. in this study, foals were not more likely to die if they had one particular pathogen in their feces than another). This must be interpreted very cautiously, however, because the study does not account for other kinds of illness in these foals, or even whether diarrhea was the primary problem for which they were referred to the hospital. Diarrhea, especially in very young foals, can be very serious because they can dehydrate very quickly and are very susceptible to shock of various kinds.

There were a few other issues with this study that are important to keep in mind as well:

1. The group of foals they looked at ranged in age from newborns to 10-months old. The digestive tract of a foal undergoes drastic changes in the first year of life, and it is well known that certain infectious agents only cause disease in foals of particular ages. For example, different parasites may take weeks to months to develop within the intestine of a foal, so even if a foal is infected as soon as it’s born, these parasites cannot cause disease for quite some time. For this reason, it would have perhaps been more useful to look at the data separately for different age groups.
2. There was no control group in this study. Most of the time, if an animal has diarrhea and the test you perform tells you there is a known diarrhea-causing pathogen in the feces , you assume the diarrhea is due to that agent. This is not necessarily always the case. Some pathogens are carried around by totally normal animals, who may get diarrhea for a completely different reason. So what we really need to know now is: if the authors tested 233 foals with normal feces (and the same ages), how common would each of these pathogens be?

While the data may be interesting to look at, this paper doesn't really tell us anything new that will change the way we treat or manage foals with diarrhea in general.  Nonetheless, the information may still be useful for helping to design and interpret future research studies about these pathogens and diarrheal disease in foals.

Image source: www.bbc.co.uk (credit: George Ring)

Equine hoof canker (pododermatitis chronica verrucosa) is described as a chronic, proliferative dermatitis, beginning in the caudal part of the cleft of the frog and gradually expanding to the sole and wall. Equine canker is not lethal in and of itself, but because of where it occurs on the foot, and because it can be so difficult to treat and it recurs so often, it can severely compromise a horse’s ability to do its job (even if that job is just walking around in a field sometimes). The etiology of equine canker has been a topic of discussion for over 50 years, but so far no specific cause for the disease has been found.

Canker is usually diagnosed based on the appearance of the affected horny tissue and a distinctly fetid odour. The definitive diagnosis has to be confirmed by microscopic examination (histopathology) of biopsies collected from the affected tissue.

Treatment of canker has always been a dilemma for veterinarians and farriers because it is so difficult. Treatments used today can range from surgical intervention (removal of the affected tissue) to conservative medical management using topical medications of many different kinds.

The proliferative but non-metastatic nature of canker is similar to that of equine sarcoids. Like canker, sarcoids also tend to be difficult to treat and often recur. Both canker and sarcoids often include a mixture of proliferative and erosive changes in the skin secondary to overgrowth and thickening of the tissues. Due to these similarities, it has been speculated that bovine papillomavirus (BPV) might also be involved in causing canker. A large study in Europe (which will hopefully be published soon) has found evidence to suggest that a variant of BPV-1 plays a role in the development and/or maintenance of canker lesions in horses. Much more study is still needed, but this is another interesting example of how an infectious pathogen may ultimately play a role in a disease that’s origin has remained a mystery for decades.

More information about papillomaviruses is available in our archives.

Image: Severe canker in the frog of a horse's hoof (source: www.answers.com)

In terms of treating infectious diseases, liposomes can be used to deliver antibiotics to infected tissues.  Because of the targeted delivery system, the toxic/side effects of drugs on the rest of the body can be reduced while still achieving the same (or higher) concentrations of drug at the site of infection.  An example of this is the drug Abelcet (Enzon Pharmaceuticals), which is a liposomal preparation of the very toxic antifungal drug amphotericin B.  Abelcet has been licensed for use in the US and Europe since 1995.

The abstract presented at the ACVS (C. Underwood et al.) described the use of liposomes containing a radioactive marker (99-m Technetium) in horses.  They injected 10 healthy horses with a dose of liposomes, monitored them for adverse effects (of which there were none detected), and then used the radioactive marker to determine where the liposomes accumulate in a horse under normal conditions.  Their ultimate objective is to determine if liposomes can be used to better deliver antimicrobials to areas of infected bone (osteomyelitis), which are typically very difficult to treat.  Liposome technology still has a long way to go before it's being used widely in horses, but this was an important first look at how liposomes can possibly be applied to equine medicine in the future.

Image credit: Kosi Gramatikoff (1999)

A five-year-old Quarter Horse mare was found down in the field in the mid-afternoon.

When the horse arrived at the hospital, she was down on the trailer.  By that time she had a fever, high heart and respiratory rates, and she was dehydrated.  Although she was still aware of things going on around her, she was very depressed.  She was still able to see, and she could move all four legs and her tail.  However, it was even difficult for her to lie on her chest (e.g. sternal recumbency), so she would roll to one side instead (e.g. lateral recumbency).  Her jaw remained rigid, but she could still move her tongue a little.

With a lot of encouragement and help the mare was able to stand up and stumble off the trailer, but she was so weak and uncoordinated in all four legs that she fell down again before she could even walk the 10 metres to her stall.  Eventually she made it to her stall, and she was able to stand for about an hour before she lied down (or fell down) again.  A urinary catheter had to be used to drain the mare's bladder because she did not seem to be able to urinate on her own.

The mare was treated with intravenous fluids (supportive therapy), and anti-inflammatories and steroids to try to reduce the inflammation that was suspected to be going on in her brain and spinal cord.  Despite all this, her condition continued to worsen, and by the next morning the mare could not even sit up and was becoming less aware of her surroundings.  The mare was therefore humanely euthanized.

Post-mortem tests in this mare confirmed there was inflammation in the brain based on a high number of inflammatory cells in her cerebral spinal fluid (CSF).  Because of the clinical presentation, some of the brain tissue also had to be sent away for rabies testing, which was (thankfully) negative.  Once that result was back, samples were also tested for evidence of infection with equine herpes virus (EHV-1), West Nile virus and Sarcocystis neurona (the cause of equine protozoal myeloencphalitis), all of which were also negative.  Botulism was also considered, but this disease is very difficult to test for in horses.  In the end, the final diagnosis, and the cause of the mare's neurological signs, was infection with eastern equine encephalitis (EEE) virus .

This case of EEE was diagnosed in September 2009 in Southwestern Ontario.  The description of the presentation, and how rapidly this mare deteriorated, demonstrates just how devastating and severe this disease can be.    This case also tells us that there are mosquitos in the area that are carrying EEE.  Vaccination of the other horses in the region will not provide protection before the end of this mosquito season, but owners of horses in the same area should seriously consider (and discuss with their veterinarian) vaccination of their horses against EEE in the spring, prior to the next mosquito season.  No one can say for certain if vaccination of this mare would have prevented the infection, or decreased the severity of the infection, but it likely would have helped.  In the meantime, as always, decreasing exposure to mosquitos as much as possible (if there are any left) should be the priority.

Image: TEM of the salivary gland of a mosquito infected with eastern equine encephalitis (EEE) virus (source: CDC Public Health Image Library #7057).

• Treating what counts: Local therapy is targeted at the site of infection - the wound itself.  Some antibiotics that are too toxic to be given systemically, or can't be given safely at a high enough dose to be effective, can be applied directly to the wound at a higher concentration, delivering a more effective blow to the infecting organism.
• Not treating what doesn't count: Avoiding the use of systemic antibiotics decreases exposure of the bacteria that are part of the horse's normal bacterial flora, particularly those in the intestinal tract.  This helps to decrease the risk of disrupting the flora, which can otherwise result in antibiotic-associated diarrhea.  It also helps decrease the risk of other bacteria in the horse's body developing resistance to the antibiotic being used.
• "Taking out the trash": Drainage, debridement and lavage help remove all the "junk" in a wound by getting rid of dirt, pus and dead tissue.  Often times, these are the most important components of treatment, and likely have more of an effect on the outcome than any of the drugs that may be used.  Whatever can be physically removed from the wound decreases the amount of junk and bacteria with which the horse's body needs to deal, and also eliminates material in which bacteria can hide from the immune system.
• Cost savings: Often times local therapy involves more time for cleaning and bandaging, but less drugs, because you're only treating the infected site, not the entire horse.

• It's not easy: As difficult as it sometimes can be to give a horse needles or make it swallow medication, these methods are often chosen because they are perceived as the "easy way out." Local therapy for a wound can be a lot of work - it takes time, it sometimes means getting yourself a little dirty, and some owners don't like the "ick" factor of having to deal directly with the wound itself.  However, systemic antibiotics should not be used as a substitute for proper wound care.
• Every wound (and every horse) is different: Not every infected wound is amenable to local treatment.  Deep wounds can be especially difficult to treat this way, because the deepest parts of the wound simply aren't accessible.  Also, depending on the temperament of the horse and/or the location of the wound, the animal may not tolerate local therapy of the site without sedation, in which case it is best left to your veterinarian.  It is always very important to ensure that you can safely treat your horse.

Even for wounds that do require systemic antibiotic treatment for one reason or another, local therapy should not be neglected, and can be critical to achieving a successful outcome.  It's important to try to resolve infections (of any kind) as quickly and efficiently as possible in order to avoid complications associated with chronic infection, and minimize the risk of antibiotic resistance developing (if antibiotics are used).  That means using all the available tools at our disposal, including simple wound care and local therapy, to treat them. But remember:

• Always wear disposable gloves if you need to clean, treat, bandage or otherwise touch a wound, and wash your hands well with soap and water afterward.  This will help prevent bacteria from the wound from being transmitted to you, and bacteria from your hands from infecting the wound.
• Do not give your horse antibiotics of any kind before consulting your veterinarian.

Papillomaviruses are generally strictly species-specific, meaning a certain type of virus will only infect one animal species. Infection of horses with bovine papillomavirus is the only known example (so far) of cross-species infection within this group of viruses. In cattle, bovine papillomaviruses (BPVs) cause warts, just like equine papillomaviruses cause warts in horses. It is now widely accepted that bovine papillomaviruses (BPV-1 and BPV-2) are also the primary cause of equine sarcoids. More recently, these viruses have also been implicated in some cases of equine dermatitis and equine hoof canker (more on that in another post).

Equine sarcoids are skin tumours that affect horses, donkeys, mules and zebras. They are the most common type of tumour found in horses, and account for 35-90% of all equine skin tumours. Sarcoids are generally not life-threatening – unlike some other tumours, they do not metastasize (i.e. spread to other organs or tissues). However, they can be locally aggressive growths, meaning they may invade deep into the tissues immediately surrounding the primary tumour. They are also very difficult to treat, and therefore can affect a horse’s welfare or quality of life, depending on the size and location of the sarcoid. There is some evidence of a genetic predisposition to sarcoids in some horses as well. Involvement of bovine papillomavirus in the development of sarcoids was first suggested by Olson and Cook in 1951, who were able to reproduce sarcoid-like lesions in horses by inoculating them with tissue from bovine warts. Since then, researchers have used PCR to show that the vast majority of sarcoids contain BPV DNA, whereas normal horses and non-sarcoid skin tumours do not. Although BPV DNA has been found in healthy horses living in close contact with sarcoid-bearing animals, there is currently no evidence that BPV or sarcoids are transmissible horse-to-horse.

Six types of equine sarcoid are described based on their appearance: occult, verrucous, nodular, fibroblastic, mixed or malevolent. Each type tends to occur on different parts of the body, and they also differ in how they behave (i.e. how fast they grow). However, all six types share the tendency to recur and become more aggressive if they are disturbed accidentally (e.g. traumatized) or iatrogenically (e.g. surgically (but incompletely) removed). Unlike warts, sarcoids rarely disappear on their own (resolve spontaneously). Many different techniques have been used to try to treat sarcoids, including surgical removal, cryotherapy (freezing), carbon dioxide laser therapy, hyperthermia (burning), irradiation, photodynamic therapy, immunotherapy, and chemotherapy. Unfortunatley, to date there is no universally effective treatment for sarcoids (which is why so many different things have been tried and continue to be tried).

There is currently no effective vaccine against sarcoids, but knowing that a virus (BPV) is involved may ultimately allow researchers to one day develop a vaccine or other means of prevention. In the meantime, it probably wouldn’t hurt to keep your horse away from any warty cows that may be around.

Photo: A horse with recurrent aggressive sarcoids on the medial aspects of both forelegs (credit: M. Anderson)

All horses from the affected farms are banned from racing facilities for 21 days after the last known case had run its course (reportedly September 16): That's great, but... 21 days is the isolation period typically used to detect clinical cases of strangles (i.e. exposed horses that get sick will usually do so within 21 days).  However, some horses, particularly those recovering from being sick, can shed the strangles bacterium for much longer than this.  In order for such a ban to really be effective, horses from the property should also be tested to ensure they are not shedding Streptococcus equi subsp equi before being allowed in more public facilities.

In a press release issued by NZTR on September 23, it is stated that "An isolation period of six weeks is usually necessary to ensure that the disease is not still incubating before ending the isolation.": Why would they make such a statement and then only isolate these properties for three weeks?

The same press release states "...controls have been put in place, as recommended, and this should ensure that the risk of further spread will be effectively controlled."  If the NZTR thinks that banning horses from the affected farm and the neighbouring properties from the track is going to eliminate the risk of strangles, they're deluding themselves.  As we've said before, strangles is an endemic disease in the horse population, and there are certainly other horses in New Zealand that are carrying strangles.  Any time a large group of horses get together there is risk.    The best way to reduce the risk is to ensure that simple, practical infectious disease control measures are in place, and followed, every day.  Statements like this just give people a false sense of security.

Strangles was initially identified in a horse from a sale that was brought onto the farm over a month earlier.  The horse was isolated on September 8 for being sick, and diagnosed sometime in the following week:  There are a few good points here.  First of all, it demonstrates a classic example of a "normal" carrier animal (the "trojan horse" if you'll forgive the pun) from a sale (making it high risk for carrying infectious diseases) that was brought onto a farm and likely not isolated and tested, ultimately resulting in an outbreak on the farm which is now affecting the ability of all the horses there to race.  Classic.  Furthermore, this horse from the sale arrived on a truck with several other horses which were delivered to three other properties in the area.  There is no indication that these other horses have been tested to see if they are carriers, nor that the other properties have been inspected.  Based on the ban that has been slapped on the currently affected property and its neighbours, I could see trainers and owners being reluctant to report any new cases, or even horses with a fever, for fear of the same thing happening to them.  Also, I have to wonder, if there was a known strangles case on the index farm since at least last week, why did it take until September 23 for the NZTR to issue the ban? 

"...once strangles was diagnosed, all the horses on the Cottle property - minus the infected ones - were vaccinated [for strangles].": Vaccination in the face of an outbreak is actually not recommended according to the strangles consensus statement from the American College of Veterinary Internal Medicine.  Particularly with a known carrier having been on the farm for a month, by that time all the other horses were likely already exposed, and vaccinating them at that point merely puts another drain on their systems.

"The barn yard was disinfected but the bedding was not replaced.":  I've never seen nor heard of a barn yard that could actually be effectively disinfected.  It would have to made entirely of sealed wood/concrete or metal, and even then it would be a momentous task and likely still impossible.  I don't doubt they gave the area a thorough cleaning, but it was not disinfected.  The fact that the bedding was not replaced surprises me - this seems like one of the simpler, easier things to do.  While it also can't guarantee a strangles-free stall, any horse that is shedding the bacterium is likely to have highly contaminated bedding, and removing it at least decreases the environmental pathogen burden.  The article also states that "the bacteria can survive in bedding and soil for at least eight months."  Perhaps under ideal sheltered conditions this may be possible, but a study presented last year showed that in the "real world" S. equi probably only survives in the environment for a few days.

Both the article and the press release do make a few sound recommendations in the end, including adopting hygiene guidlelines such as replacing bedding, disinfecting water troughs and feed buckets and other equipment, avoiding mixing and moving horses, being aware that people are a potential source of cross-contamination, and of course our favorite: "As with any contagious
disease, handwashing is a simple and effective tool."

More information on strangles is available on the equIDblog Resources page and in our archives.

Image: Banned trainer/owner Tim Symes, with his horse Molly O'Reilly (source: www.hawkesbaytoday.co.nz)

Bloodwork on these scraggy foals often shows low - sometimes extremely low - protein levels in their blood.  Blood protein is very important for normal body function and controlling tissue fluid levels, and the body (especially the liver) works very hard to maintain normal levels.  Low blood protein (also called hypoproteinemia) in these animals usually indicates that the protein is being lost from the body, and the most common route for this to happen is through the intestine. (It can also be lost through the kidneys, but renal disease in young animals is generally uncommon.)  Some of these foals have diarrhea as well, or may go on to develop diarrhea if left untreated.

What is it that turns a foal's intestine into a protein sieve?  One possibility, and a hot research topic at the moment, is the bacterium Lawsonia intracellularis, which causes the condition known as proliferative enteropathy.  But any severe infection of the intestine has the potential to affect the barrier that normally keeps blood protein fluids in the bloodstream, so other causes of enteritis and colitis such as Salmonella and Clostridium also need to be considered.  Heavy burdens of intestinal parasites can cause similar problems - some of these may be difficult to test for because the larval stages do not produce eggs that can be found on a fecal test, and developing resistance issues mean that routine deworming cannot guarantee that parasites are not present.  There are no doubt other causes as well that haven't been identified - in half of all diarrhea cases in (adult) horses, a causative agent cannot be identified, even with a complete diagnostic work-up. 

In horses, if only the small intestine is affected (enteritis) - even in severe cases - the animal usually will not have diarrhea.  However, if the infection spreads to the colon, or if the bacterial populations in the colon are affected badly by the foal's poor health status and abnormal "flow" of feed material due to the infected intestine "upstream", then colitis will develop as well, resulting in diarrhea.  Anytime the normal intestinal bacteria of a horse are disrupted, the animal also becomes more susceptible to other bacterial pathogens such as Salmonella and Clostridium as well.

What should be done with these "scraggy" weanlings?

1. Have them examined by your veterinarian as soon as possible.  Don't wait for them to start looking really sick.  These weanlings can be frustrating to diagnose and treat at the best of times, but the farther they're allowed to slip, the harder it is (and the longer it takes) to bring them back.

2. Look for other foals that might be affected.  Especially in larger groups of foals, one particularly sick animal may stand out, but there could be several others flying just under the radar that you may not notice unless you really take the time to look at each foal individually.

3. Separate healthy weanlings from those that aren't 100%.  It may be difficult or impossible to individually isolate all the "scraggy" animals depending on numbers and the facilities available, particularly more severely hypoproteinemic foals that may take weeks to months to recover.  At a minimum, the foals that appear healthy should be separated from and always handled before the ones that may be affected by an intestinal infection.  Any animal with diarrhea should be isolated.  The duration of isolation required will depend on the specific diagnosis (if one can be made).

More information about Lawsonia is available on the equIDblog Resources page and in our archives.

Image source: www.virginiawildhorserescue.com

No, not dental plaque like you get on your teeth - in this case we’re talking about aural plaques, which are a type of skin lesion that some horses develop on the inside surface of their ears. These plaques are usually depigmented, meaning the skin cells of which they are made do not have the same pigment in them as the cells of the surrounding skin, making the lesions appear pale grey or off-white. Other than being considered unsightly in some cases, aural plaques usually don’t cause problems for the horse – they’re not itchy, sensitive or painful. They can occur in any horse, no matter the age, breed or sex. Occasionally some horses may develop similar plaques on the udder or around the anus or vulva (under the tail). The diagnosis of an aural plaque is typically made based on the horse’s clinical signs alone (i.e. a raised, depigmented skin lesion inside the ear that is not associated with any inflammation or discomfort).

The exact cause of aural plaques is still not clear, but using extremely high-powered electron microscopy, researchers have been able to demonstrate that in some cases there is a papillomavirus infecting the cells within these plaques. No one has yet been able to isolate the virus to determine what type of papillomavirus it might be. Aural plaques are not known to be transmissible from horse to horse, but since there may be a virus involved, it's prudent to consider the possibility that virus transmission may play a role in their development (although there are likely many other factors involved as well).  Unlike regular papillomas (i.e. warts, caused by equine papillomaviurs), aural plaques do not disappear on their own. It the past, the only way to remove the plaques was to actually cut them away surgically. In more recent years, successful treatment has been reported using an immune-response modifier cream such as imiquimod (Aldara), which is used in people to treat several different skin conditions, including genital warts.

Photo: Aural plaque on the ear of a horse (source: University of Minnesota - College of Veterinary Medicine)

Papillomaviruses (PVs) are small DNA-based viruses that are recognized causes of disease in many animal species and humans. More than 100 different human papillomavirus types (HPV) have been identified, which can cause a range of problems from annoying (but benign) warts to malignant cervical cancer. The ability of papillomaviruses to cause cancer was first recognized in animals, specifically with cottontail rabbit papillomavirus (CRPV), bovine papillomavirus (BPV) and canine oral papillomavirus (COPV). In general, PV infection causes benign disease in the vast majority of individuals, but the viruses have the potential to cause malignant disease in a small proportion of the mammals they infect as well.

Horses can be infected by both equine papillomavirus (EPV) and some bovine papillomaviruses. Infection with BPV is associated with equine sarcoids – look for more information on BPV in horses in an upcoming post. Infection with EPV (specifically Equuus caballus papillomavirus types I and II) causes cutaneous papillomas – small proliferative skin lesions better known as warts. Warts are benign growths that appear on animals less than two years of age. They typically persist for 6-12 months and then disappear without any specific treatment, and they do not otherwise make the animal sick. Usually warts appear on the muzzle and lips, but rarely genital warts can occur (usually with infection by the type II virus). Occasionally warts can also occur on the lower limbs, ears and eyelids.

Warts can be spread between horses by fomites (e.g. objects, equipment, tack, clothing that has been contaminated with EPV), or by close horse-to-horse contact. Spread is common when young are horses are brought together in large groups for shows, sales or breeding. Infection is usually diagnosed by the characteristic skin lesions, the horse’s history and age - more than 90% of affected horses are less than three years old. Usually the warts regress spontaneously and they do not require treatment. However, if treatment is sought for esthetic reasons, cryosurgery (i.e. freezing, usually with something like liquid nitrogen) can be performed. Caustic chemicals such as trifluoracetic acid can also be used to “burn” the warts off. Even after treatment, though, the warts can recur.

Controlling warts caused by EPV is fairly simple: if you have an affected horse, keep it away from other young horses. Do not allow the horses to have direct contact, and make sure the horse with the warts has its own tack, grooming supplies, water bucket, hay net/trough etc. so the virus is not indirectly transmitted to others. There is no vaccine available for horses for EPV. There are a lot of “voodo” treatments for warts out there, and some people swear by them, but (just like people who treat foal heat diarrhea) that’s usually because they’re treating a condition which goes away on its own anyway. People cannot be infected by EPV.

Photo: Warts on the nose and lips of a horse (source: http://www.yourveterinaryclinic.com)

• Almost all foals are exposed to R. equi as neonates, but most of them never develop signs of infection.
• Giving newborn foals hyperimmune plasma (plasma with extra antibodies against R. equi) may have some beneficial effects on farms where the infection is a recurrent problem, but this practice is still controversial.
• Adult horses are essentially immune to the infection.
• In almost all cases if clinical disease in foals, the R. equi strain involved carries a special gene called vapA.
• Mortality rates in foals vary considerably from 0% to 30%.
• So far, efforts to develop a vaccine to help protect foals have been unsuccessful, but research in this area is ongoing.

People can also be infected with R. equi, and as in foals, pyogranulomatous pneumonia (infection of the lungs which results in the formation of many abscesses) is one of the most common conditions caused by this organism. However, there are a few important differences between infection in people and infection in horses:

• 85% to 90% of people with R. equi infection are immunocompromised, meaning their immune system is weakened or suppressed for some reason, e.g. HIV infection, or immunosuppressive drugs taken by organ transplant or cancer patients.
• Among people infected with R. equi who have normal immune systems (i.e. immunocompetent), about half of the infections are localized, meaning they only affect one small part of the body. Many of these are associated with wound infections.
• Only 20% to 25% of the R. equi isolates in people carry the vapA gene.
• Infection in immunocompetent people can be fatal in approximately 11% of cases, but among HIV-infected patients the mortality rate from R. equi infection can be as high as 50% to 55%.

Rhodococcus equi is actually a soil organism, and this is likely the most common source of the organism for both horses and people. Only approximately 1/3 of humans infected with R. equi report that they have had contact with horses or pigs (pigs can also carry the bacterium). So we don't know how much of a risk an infected foal is to a person.  However, it is prudent for people, particularly those with weakened immune systems, to take precautions to avoid potential transmission of R. equi from horses.

• Try to reduce dust levels on the farm. Because R. equi most often lives in the soil, it can get stirred up into the air in dusty areas, which can then lead to inhalation by animals and people. Doing things like planting grass or other vegetation, installing windbreaks in high-traffic areas, or wetting down dusty stalls or paddocks can help reduce dust levels in the air.
• Keep open wounds and other broken skin covered when working around animals.
• Always wash your hands after handling a foal (or any horse)
• If you have a foal that develops signs of R. equi infection, make sure you have your veterinarian examine it as soon as possible so the diagnosis can be determined and the foal can be treated properly as soon as possible. Some foals with R. equi may develop severe pneumonia very quickly, so it’s important that they are examined right away.

This equIDblog entry was originally posted on the Worms & Germs blog on 09-May-09.

Rhodococcus equi

At the 2008 Forum of the American Association of Equine Practitioners (AAEP), researchers at Texas A&M presented the results of a study they recently completed looking at EPDs in 150 foals with R. equi infection over a 20 year period. Here are some of the highlights:

• 74% of the foals had an EPD associated with their R. equi infection. On average foals had two EPDs each and up to as many as nine EPDs in a single animal.
• Many of the EPDs did not cause separate, detectable clinical signs. These were therefore most often found on necropsy in foals that died.
• The most common EPD was diarrhea, which occurred in 50 foals (33%).
• Immune-mediated polysynovitis (inflammation and swelling of the joints without infection of the joints themselves) was the second most common EPD
• 31 foals (21%) had ulcers and inflammation somewhere in their intestine (ulcerative enterotyphlocolitis), all of which were diagnosed at necropsy
• 25 foals (17%) had abscesses in the abdomen, 71% of which could be detected by ultrasonography

Thirty-nine different EPDs were identified in the group.  Other EPDs included uveitis (inflammation of the eye), hepatitis (inflammation of the liver), septic arthritis (joint infection), lymphadenopathy (enlarged lymph nodes), peritonitis (inflammation of the lining of the abdomen) and septicaemia (bloodstream infection).

• Among the foals with EPDs, 43% survived hospitalization, whereas 82% of foals without EPDs survived.  However it is very important to remember that many EPDs were only detected at necropsy, therefore they were more often found in foals that died, but it is unknown if they actually occurred more commonly in one group or the other.
• Risk factors for foals developing EPDs included longer time from onset of clinical illness to referral (e.g. foals that were sick at home for longer before being sent to the hospital were more likely to have an EPD), higher heart rate on admission and a higher white blood cell count.

It’s important to remember that even though an infectious pathogen may usually affect an animal in a certain way, “the bugs don’t read the textbooks” (as we often say), and they can cause problems in other ways. That’s just one of the reasons it’s so important to have your veterinarian perform a full physical exam of your animal if it is sick - even if it looks similar to something you’ve seen before - in case the pathogen causing the problem starts to affect other parts of the body, which may require more or different kinds of treatment.

Photo credit: M. Anderson

West Nile vaccines are labeled to provide protection for 12 months. Before they can be marketed with such a label, these vaccines have to be tested to prove that they still offer some protection for the animal for at least that long. For some vaccines, like rabies, protection likely lasts much longer than the label claim, but until recently no one’s bothered to study most vaccines beyond one year. I have no doubt that the protective immunity does decrease with time – the protective effects of vaccine are likely highest (as Scott said) about 30 days post vaccination, and lowest at the end of the 12 months. But there is no evidence that the immunity drops off so fast that after 4-6 months the vaccine would require a booster to be adequately, if not maximally, effective. There are vaccines, like herpesvirus and influenza, for which we recommend boosters for horses semi-annually, but this is for animals that are at ongoing high-risk for exposure to these diseases, which are very common. Six months after mid-April is mid-October, and in this part of the world there are very few mosquitoes still flying around at that point.

Scott pointed out that the first part of the summer is likely lower risk in terms of WNV transmission, at least for horses. But there is a time of year when the risk is even lower – October to April, when (as I just said) there are virtually no mosquitoes. If you vaccinate a horse in July, its immunity will be lowest over the first three months of the summer, when there are still birds and mosquitoes around that are carrying WNV. If you vaccinate a horse in April, its immunity is lowest in the late winter, when there’s almost no risk of transmission, so it doesn’t matter! I would rather have a horse protected for the entire mosquito season (May-September), and in the vast majority of cases the animal’s immunity will still be quite adequate come peak season in August, even without an extra booster in July. (Although we want to protect our animals from infectious disease, we also don’t want to give them any more vaccines than we have to.)

I don’t think there’s a right or wrong answer in this case. The best thing to do is talk to your veterinarian about the pros and cons of doing things either way, while taking into consideration the conditions in your specific region in terms of vector populations, disease prevalence, and the health management priorities for your own animals.

Photo: Transmission electron micrograph (TEM) of the West Nile virus (WNV). (Credit: Cynthia Goldsmith, CDC Public Health Image Library ID#10701)