Maureen Anderson

Maureen Anderson has no picture

Maureen Anderson is currently a post-doctoral fellow in the Department of Pathobiology at the University of Guelph. She grew up in Montreal, Quebec. In 1998 she moved to Guelph, Ontario where she completed her veterinary degree in 2003. Following a year and a half in mixed animal private practice in Listowel, Ontario, she returned to the University of Guelph for graduate studies in infectious disease and a residency in Large Animal Internal Medicine. She completed her thesis on methicillin-resistant Staphylococcus aureus (MRSA) in horses in December 2007, and became board certified with the American College of Veterinary Internal Medicine (ACVIM) in the spring of 2008. She has two cats named Bonnie and Clyde.


Articles By This Author

Follow Up On Iceland Outbreak

The massive outbreak of infectious upper respiratory tract disease that hit Iceland four months ago is finally slowing down, and there is now a little more information available about what they've been seeing and what authorities believe has been going on.

There is a fairly clear description of the clinical signs seen in affected horses (as previously described), although signs vary from horse to horse.  Typically illness begins with a serous (clear) nasal discharge which then becomes mucopurulent (snotty).  There is sometimes mild conjunctivitis (e.g. red puffy eyes) and most commonly a dry cough.  Horses that are examined using endoscopy show signs of laryngitis.  Signs generally last 4-6 weeks, but this can vary.

There's also more information about the epidemiology of the disease (i.e. the pattern of spread).  Morbidity seems to be close to 100%, meaning almost every horse that is exposed gets sick.  Fortunately no mortality has been associated with the disease, meaning all the horses eventually recover.  The incubation period (the time from exposure to illness) is 1-4 weeks.  It seems to be spread mostly by direct contact, but indirect transmission is also possible, as even free-roaming herds with little contact with other horses or people have been affected.  Horses are not completely immune after recovering (meaning they can get sick again if they are re-exposed), but there is evidence that the "herd immunity" of the horse population in Iceland is increasing, and the outbreak seems to be dissipating.  It is still lingering in some horse groups where there are naive (unexposed) horses coming into contact with infected horses.

The way this disease has spread is very typical of a virus burning through a naive population which has never been previously exposed to or vaccinated against the disease.  Even the clinical signs are very typical of an upper respiratory virus.  However, extensive testing has been done using both PCR and antibody titres for a multitude of viruses including (but not limited to): equine herpesviruses 1, 2, 4 and 5, equine arteritis virus, equine influenza virus, equine reoviruses, and equine rhinitis viruses.  None of these viruses appear to be the culprit, despite early suspicions that the cause was in fact equine herpesvirus.  They are still testing for new/unknown viruses using viral culture, but this is a difficult and very time-consuming task.

What authorities have been able to find in affected horses is Streptococcus equi subsp. zooepidemicus, which is what is currently being blamed for the outbreak.  They say it has been cultured from almost all coughing horses and all horses with mucopurulent nasal discharge.  But that's not really surprising, as S. zooepidemicus is a very common commensal bacterium that is even carried by healthy horses in their upper respiratory tracts.  It's also a very common opportunistic pathogen in horses, meaning when the animal gets sick for another reason (for example, if a horse is infected with a respiratory virus), then S. zooepidemicus moves in and causes a secondary bacterial infection, which can make the clinical signs worse or last longer, and may lead to other complications.  In this case they are trying to make S. zooepidemicus out to be the primary pathogen, but it would have to be a very unusual strain of the bacterium - very virulent, highly infectious and totally novel to the horse population in Iceland - to cause an outbreak of this scale.  They are doing additional testing to characterize the strain they have isolated from infected horses and to compare it to other strains previously isolated from horses in Iceland.

The good news is that after the horse industry in Iceland was paralyzed by this outbreak for almost four months, equestrian activities are now resuming under the supervision of the Icelandic Food and Veterinary Authority.  That shouldn't pose a problem to the Icelandic horses, as there are very few naive horses left in the country that would still be highly susceptible to this still somewhat mysterious disease.  However, export of horses from Iceland is slated to recommence on September 15.  There are still quarantine requirements preceding export (horses must not be sick nor be in contact with a sick horse for 30-60 days prior, depending on what country they're going to), which always are and will remain very important for infectious disease control.  However, with the cause of the outbreak still being somewhat unclear, it is unknown if any horses may now be healthy carriers of the outbreak pathogen, be it an unusual strain of S. zooepidemicus or an unidentified virus.  If horses in other countries start getting sick a few weeks after exposure to exported Icelandic horses, strict control measures will have to be rapidly implemented to possibly prevent similar outbreaks from developing.

Photo credit: David Blaikie (source: http://commons.wikimedia.org)

Wound Myiasis: Maggots By Any Other Name

'Tis the season... fly season.  And just like every other living thing on the planet, the flies need to reproduce too, which means sooner or later you're going to find the maggots.  Maggots really aren't so bad... until you find them living in the hide of some poor creature, usually in the decaying tissue of a wound that happened a few days earlier, which a few species of flies thought would make a good nursery.  At that point I think most people would agree that maggots have a pretty high "ick" factor.

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 In Arizona

Vesicular stomatitis (VS) has been identified in three horses on a farm in Arizona.  This is a reportable disease in the US and Canada that makes periodic appearances in various states.  Last year it was found in Texas and New Mexico. The farm where the virus was discovered has been quarantined. The owners were advised to separate affected animals unaffected animals, implement on-farm insect control programs and use protective measures when handling affected animals to avoid human exposure to the disease.  All good pieces of advice.

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/)

Review Of CEM and Implications For Canada

Hard to believe that the whole conundrum about contagious equine metritis (CEM) that is still affecting the Canadian equine industry started a little bit more than a year ago, when a Quarter Horse stud in Kentucky tested positive for the causative agent, Taylorella equigenitalis. Tracing the contacts of that stud lead to the quarantine and testing of 990 horses in 40 states, as well as 19 mares in Canada, including 9 in Ontario. Out of 274 exposed stallions, 22 were ultimately found to be positive, none of which had any detectable clinical signs that they were infected, meaning if they hadn’t been tested, they may have kept on going about their business breeding – and possibly infecting – mares for years to come. The rest of the exposed horses were mares, five of which turned out to be infected. One particularly interesting fact was that four of these mares had been bred by artificial insemination - previous to this it was thought that CEM was only readily transmissible by live cover from an infected stud, not via semen shipped in a straw.

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)

Case: Antibiotic-Induced Diarrhea

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

Case Presentation: Chronic Weight Loss

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).

equIDblog - Thanks To Our Readers!

equIDblog has now been active for one year, and look how far it’s come! Just this week we surpassed 75 000 unique hits since our launch. We now regularly have over 700 unique hits on the site per day during the week, and the numbers are still growing. It's great that we're able to provide a reliable source of information about equine infectious diseases to such a wide and diverse audience.

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)

Antibiotic Awareness Day

European Antibiotic Awareness Day is an initiative of the European Centre for Disease Prevention and Control.  This year it falls on November 18.  The aim of the Day is to provide an annual opportunity for raising awareness about the threat to public health of antibiotic resistance and how to use antibiotics responsibly.

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.

Infectious Agents In Foal Diarrhea

A new study was recently published in the Journal of Veterinary Internal Medicine (Frederick et al. 2009) which looked at infectious agents found in the feces of foals with diarrhea. Specifically, they looked for rotavirus, Clostridium perfringens, C. difficile, Salmonella, parasite eggs and Cryptosporidium oocysts.

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)

Papillomavirus Part 4: Equine Canker

From Guest Author Dr. Angelika Schoster, Department of Clinical Studies, University of Guelph.

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)

Older Entries

November 3, 2009 — Putting A New Spin On Old Drugs

October 27, 2009 — Case Presentation: Neurologic Mare

October 19, 2009 — Think Globally, Treat Locally!

October 16, 2009 — Papillomavirus Part 3: Sarcoid Stresses

September 25, 2009 — New Zealand Trainers Banned For Strangles

September 16, 2009 — Weanling ADR (Ain't Doing Right)

May 25, 2009 — Papillomavirus Part 2: Plaque Problems

May 21, 2009 — Papillomavirus Part 1: Wart Worries

May 12, 2009 — Rhodococcus equi in Horses and People

May 7, 2009 — Rhodococcus equi: More Than Just Pneumonia

March 25, 2009 — An Alternate Point of View on West Nile Vaccination

March 9, 2009 — Urinary Tract Infections in Horses

February 15, 2009 — Mare Mastitis

January 23, 2009 — Foals Gone Wrong - See The Signs

January 21, 2009 — Foals Gone Wrong - One Bad Thing To Another

January 19, 2009 — Canadian Update on CEM Outbreak

January 14, 2009 — Transportation and "Shipping Fever"

January 12, 2009 — Potomac Horse Fever

January 8, 2009 — Contagious Equine Metritis - USA Outbreak

January 7, 2009 — Molecular Diagnostic Testing: Pros and Cons

December 24, 2008 — Rabies Vaccination in Horses: Core Issues

December 19, 2008 — EPM in Horses - Eliminate Possum Muck

December 15, 2008 — Equine Infectious Anemia - Eradication From Ireland

December 13, 2008 — Lawsonia intracellularis - New Horizons

December 8, 2008 — Pulmonary Fibrosis - Latest & Greatest From The AAEP Forum

November 25, 2008 — Sporotrichosis: Stop And Smell The Fungus

October 31, 2008 — Your Mother Was Right! Wash Your Hands

October 31, 2008 — Horses and MRSA

October 31, 2008 — Eastern Equine Encephalitis in Ontario

October 31, 2008 — Preventing West Nile Virus Infection

October 31, 2008 — Deadly Hendra Virus Resurfaces in Australia

October 31, 2008 — Eastern Equine Encephalitis - Not Just For Horses

October 27, 2008 — Equine Infectious Disease Information Sheets

October 27, 2008 — University of Guelph Infection Control Resources

October 27, 2008 — Other Infectious Disease Resources