One of Regina Chesser's horses was tested for EIA at a Florida veterinary clinic, and the test came up positive. It appears that the horse was healthy and tested so it could be taken to a show, as per standard rules. However, the owner must have somehow had a suspicion that the horse would be positive since she used an alias, along with a false phone number and address when submitting the test.

As with any positive result, local authorities investigated the case. EIA positive horses pose a risk to other horses in the area since they can have the virus in their bloodstream lifelong, and can be a source of infection for other horses through biting insects or improper re-use of blood-contaminated items (e.g. needles).  Because of the risk of transmission and the potential severity of the disease, infected horses must be euthanized or quarantined.

Officials quickly realized that false information had been provided, and after an extensive search the owner's true identity was determined. The infected horse was found. Another horse was found on the property that was also positive. Testing of other horses in the vicinity of the farm has not identified any more infected horses. Now, in addition to the loss of her horses, Ms. Chesser faces some other serious problems.

Yes, EIA control is strict and severe. It's awful to lose a horse that is not showing any signs of disease because of a test result. However, there's a reason such strict measures are used. This is a serious disease and the loss of the odd positive horse, while certainly unfortunate, is necessary to protect many other horses from this devastating disease.

During the 1996 Olympics in Atlanta, concerns about the potential for introduction of piroplasmosis (to the US) led to much angst, and restrictions such as only allowing horses carrying the disease to compete in indoor events. Piroplasmosis concerns have also played a role in planning the World Equestrian Games in Kentucky.

Piroplasmosis is caused by the bloodborne parasites Babesia caballi and Theileria equi, and is spread by ticks (as well as re-using needles and other modes of blood transmission). While it can be a fatal disease, some infected horses appear healthy, and these silent carriers can spread the disease to the ticks, which then spread it to other horses.

What to do regarding piroplasmosis was an important consideration for the World Equestrian Games. To even be awarded the games, a clear and fair plan was required to get approval from both the FEI and US Department of Agriculture. Balancing infectious disease risks with limited disruption of activities isn't easy, and it's not an exact science. Significant efforts have been taken to reduce the potential for piroplasmosis transmission. These include:

• Surveys of the park taken prior to the bid that showed minimal tick activity.
• Planning the event for late September and October because ticks are typically dormant by that time of the year (in Kentucky).
• Trapping small mammals at the park from 2006-2008 to study tick levels and types.

During the games:

• Known piroplasmosis carriers will be housed together in a separate barn that will be treated to eliminate ticks.
• Carriers will be inspected for ticks when they enter or leave the stable area.
• In advance of the event, all horses currently at the park have been inspected and treated for ticks.

You can never guarantee that an infectious disease won't slip through even the most strict measures, but that's the nature of infection control. This seems like a nice evidence-based, logical plan to reduce the risk of piroplasmosis dissemination during the Games.

Photo by Ronald Yochum, 2006 (click for source)

Here are the results, with my commentary:

Small strongyles (cyathostomes): 26.08% (103)

• A narrow victory over large strongyles but a worthy winner. Cyathostomiasis is definitely a problem and it can cause serious disease. It seems to be increasingly common, or at least increasingly diagnosed. Resistance to dewormers among this group of parasites is also becoming a concerning problem.  Cyathostomes are probably the most important overall parasite issue, in terms of real impact on horse health, in most areas.

 Large strongyles (bloodworms): 23.04% (91)

• Large strongyles, particularly Strongylus vulgaris, used to be a major problem, before the advent and widespread use of ivermectin. These worms migrate through blood vessels in the abdomen and can cause blood clots to form, compromising the blood supply to the colon. This used to be a leading (if not main) cause of surgical colics and killed a lot of horses. They are a very rare problem now because of their susceptibility to drugs in the ivermectin family and fenbendazole.

Tapeworms: 15.70% (62)

• It's hard to determine the importance of tapeworms. There have been conflicting studies about their relevance, with some studies indicating they play a role in certain types of colic (e.g. gas colic, ileocecal intussusceptions) and others saying they are not involved in disease. The risks probably vary by region and type of colic, and tapeworms probably play a role in some colics, but it is difficult to quantify just how big a role.

Bots: 11.90% (47)

• It's not surprising that this was a popular choice since people are (hyper)aware of the tiny bot eggs that can be deposited on the horse's haircoat, especially on the lower legs. However, while bot eggs are visible and the sight of adult bot worms attached to the stomach during a gastroscopy can freak people out, bots are pretty innocuous. Adult bots can cause small superficial errosions in the stomach wall where they attach, but this isn't of much relevance to the horse. The main issue with bots is how much the adult flies annoy horses when buzzing around and laying their eggs.

Other 10.13% (40)

• I'm not really sure what people meant when they chose "other." I can't think of any other parasites that would be contenders for "most important."

Ascarids (roundworms): 9.37% (37)

• I'm surprised this isn't higher. Ascarids are controllable but can and do cause disease, particularly in foals. The main issue is when foals are not dewormed properly early in life, and accumulate a large burden of worms. When these foals are eventually dewormed, the worms  die all at once and can cause an intestinal obstruction.

Pinworms: 3.80% (15)

• It's good to see that there's not much concern, but no one should be most concerned about pinworms. Pinworms are, at best, a minor annoyance that can cause tail rubbing.

Little information about the clinical signs is available, but usually it's pretty easy to establish a high index of suspicion based on the typical signs of strangles, particularly during an outbreak. Confirmation of strangles in an outbreak is also usually pretty easy, since isolation of the bacterium is quite straightforward. Results are expected soon.

Strangles outbreaks are not uncommon and this disease is constantly circulating in most horse populations at some level. Some references say that approximately 10% of affected horses die, a number that I think is excessive, but the key point is that strangles can be fatal to a small but not inconsequential percentage of affected horses. The potential severity of disease plus the high infectivity are big reasons why good control measures are needed.

One common problem with strangles control is described by horse trainer Joe Byrne, who said "the most damaging thing with strangles is the attitude of "ignorance and secrecy". Owners with infected stables "straight away clam up, don't tell anyone" and remain operating like nothing has happened and that is very problematic."  Indeed it is.

Photo: A horse with strangles (S. equi infection) showing the characteristic severe swelling of the submandibular lymph nodes (click image for source).

This is quite concerning because it now seems to be a regular event to get a report of piroplasmosis in US horses from different areas and with no clear link to other outbreaks. The disease, caused by the blood parasites Theileri equi and Babesia caballi, can produce a wide range of clinical signs, and kills approximately 20% of infected horses. Some horses can become healthy "silent" carriers, complicating recognition and control. The bloodborne parasites are naturally transmitted by ticks, but can also be spread by other forms of bloodborne transmission, most notably the reuse of needles. Often, poor needle handling practices are blamed by officials for spread of piroplasmosis among groups of horses on a farm, but that doesn't address the most important question - where did it come from in the first place?

PIroplasmosis is considered a foreign disease in the US, but the repeated cases of unknown origin in at least 19 US states suggests that the disease is actually endemic (established) in the US. Any explanation of where the causative parasites keep coming from is pretty much always missing from US piroplasmosis reports. It certainly seems possible, if not likely, that there is an unidentified pool of infected horses and tick species in the affected areas that are able to transmit the infection.

If the US is going to get piroplasmosis under control, a serious effort needs to be undertaken to understand how widespread the infection is and how it's being spread. Tracking known cases and their contacts is important, but a more concerted effort is required. That takes time and money, and often governments are reluctant to spend much of either when it comes to horses (as opposed to food animals), but considering the potential implications of endemic piroplasmosis and the often overlooked economic importance of the horse industry, it's a worthy investment.

EIA, which is sometimes also called swamp fever, is a caused by the un-originally named equine infectious anemia virus. It is a retrovirus (the same type of virus that causes HIV/AIDS in people and feline leukemia in cats) that can cause serious infection but also long-term carriage by apparently healthy horses. The ability of this virus to cause lifelong infection in some horses is a major problem and complicates its control. The infection is not treatable and there is no vaccine. For these reasons, aggressive control measure are in place in most regions. The main component of this is routine testing.

EIA testing is a standard requirement in many areas of the world for horses that are traveling, competing or being sold. Traditionally, the Coggins test has been used for EIA testing. More recently, another test (a cELISA test) has become available. This test is thought to be more sensitive and takes less time to perform, but positive results still need to be confirmed with a standard Coggins test.

Positive results are immediately reported to the appropriate government agency (in Canada, it's the Canadian Food Inspection Agency). Immediate euthanasia of positive horses is the typical response, although keeping the horse in permanent quarantine, with insect control and a minimum distance from any other horse (or donkey or mule) is also an option in some cases. It may seem draconian to euthanize an apparently healthy horse and quarantine the farm, but this is an important disease that is hard to control if it gets established in an area.

The most important EIA control measure is regular testing, which allows for early detection of cases and implementation of appropriate (albeit unfortunate for the horse) measures. Other measures that help reduce the risk of transmission if the virus is in the area include control of biting insects and ensuring that there is no re-use of needles or other equipment or biologics that can transfer blood. 

There's no indication as of yet where the infection originated from in the Missouri horse. That's a very important factor, because the horse had to get it from somewhere, and that means another infected horse, donkey or mule. Finding one positive animal means that there must have been another positive animal somewhere in the vicinity to infect the insect (the most likely vector) that infected this horse. Hopefully, the horse did not pick it up from another animal in the US, but careful tracking of this horse's travel history and detailed surveillance of equids in the area will need to be performed to figure this out.

Image: A black horse fly (Tabanus atratus); members of this genus are capable to transmitting EIA between horses when they bite.  (Photo credit: Mark Cassino, source: USDA Systematic Entomology Laboratory)

It's always tough to say, with confidence, why disease trends occur. EEE is a sporadic disease in many regions, like Michigan, and there can be no cases some years and clusters other years. So, there's no guarantee that vaccination is the problem. However, it makes sense that it could be involved since decreasing vaccination rates increase the number of susceptible horses.

The only saving grace with regard to decreasing EEE vaccination rates is that it only hurts the horses that are not vaccinated. With some diseases, namely those that are spread horse-to-horse, maintaining a high overall vaccination rate in the horse population is critical to reduce the chance of disease transmission. This is the concept of "herd immunity."  With those diseases, when people stop vaccinating their horses, they also in part increase the risk to other horses in the area. With a disease like EEE that is spread by mosquitoes which cannot be infected by other horses, herd immunity doesn't apply. The percentage of horses in the region that are vaccinated has no impact on the likelihood that any single horse will be exposed.

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While a fatal infection at a facility with a lot of horses always (rightfully) raises concerns, this isn't anything for people at Keeneland to be worried about.

• Potomac Horse Fever is not transmitted between horses. Horses are infected by ingesting aquatic insects (e.g. caddis flies, mayflies) that are infected with the causative bacterium. Horses that graze around rivers or creeks can inadvertently ingest these insects while eating or drinking. There is no evidence of horse-to-horse transmission.
• The horse presumably acquired the infection elsewhere. The horse was only at Keeneland for a few days prior to becoming ill. Given what we know about the incubation and normal progression of the disease, it's most likely that the horse was already infected when it arrived but simply was not yet showing signs of illness.

Potomac Horse Fever is one disease for which you need to know what is going on in your area, and what the specific risks are for your farm. If you live in an area where cases are diagnosed every year and your horses have potential access to aquatic insects, then the risk is higher. If you are in an area where the disease is rare and/or your horses don't have access to rivers or creeks (or pasture in close proximity to them) the risk is pretty low.

Knowing the risk is important for ensuring prompt diagnosis. Unfortunately, there aren' t any great preventive measures for PHF, apart from restricting access to areas where aquatic insects might be encountered. A vaccine is available but there's not much evidence that it's effective (it might decrease the severity of disease, but there's no evidence that it prevents disease). The most important thing is recognizing early signs of disease, which may be subtle (e.g. transient mild fever, decreased appetite, general malaise). These vague signs don't necessarily mean the horse has PHF and that it should be treated right away, but getting the horse evaluated and tested ASAP, with close monitoring to see if other signs of of the disease develop, can lead to earlier and better treatment, and likely a better outcome.

Photo credit: David Dew (click for source)

It's concerning that there have been three deaths in Florida so far this year, considering we're still not even far into the typical EEE season. It is suspected that the higher number of cases is the result of a greater percentage of infected mosquitoes (not an increase in total number of mosquitoes).

There is a vaccine for horses, and it is recommended for all horses in areas where EEE virus is expected to be active. There is no vaccine for humans, so the focus is on decreasing mosquito populations and reducing mosquito bites. EEE virus cannot be transmitted from horses to people, and horses cannot pass the virus back to mosquitoes, so they play no role in human infections. The main role of horses in terms of human health is as an indicator that EEE virus is active in the area, since equine cases tend to occur earlier and be more common than human cases. If an infected horse is identified in a particular area, it's an indication that the virus is active and people are at increased risk.

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Good routine cleaning and disinfection practices are important for all barns, but the specific needs vary greatly between facilities. Proper disinfection practices are particularly important in certain situations, such as in foaling stalls, stalls housing sick horses and isolation areas. Because problems are so common, everyone should think about their disinfection program and the disinfectant(s) they use. When in comes to the disinfectant, here are some questions everyone should ask themselves:

Is it actually a disinfectant?

• Some people mistakenly use cleaners as disinfectants. Cleaners help remove debris and make the surface look good (i.e. clean), while disinfectants kill microorganisms through their chemical activity. You need a clean site for disinfectants to work, but using a cleaner in place of a disinfectant won't get rid of the microorganisms that remain after the visible dirt has been removed.

What kind of disinfectant is it?

• Disinfectants are a little like antibiotics. They have a "spectrum of activity" which tells you what types of microorganisms that they kill. Some disinfectants kill a wide range of microorganisms while the activity of others is more limited. Some work well in the presence of some dirt and debris, while others are readily inactivated and essentially won't work at all unless the surface is very clean first. Some are quite toxic and some are pretty innocuous.

What concentration should be used?

• There should be specific instructions on the product. Some are "ready-to-use" and don't need dilution. Most come as concentrates that need to be properly diluted. Excessive dilution will reduce the chance of of the disinfectant working. Inadequately diluting the concentrate ends up costing a lot more because you waste the product, and high concentrations of some disinfectants can be harmful. "Add two splashes to a bucket" is not proper dilution. You need to measure.

What contact time is needed?

• Disinfectants don't work instantly. They need time. Usually, it's anywhere from five to thirty minutes, depending on the disinfectant.

Common disinfection errors or misconceptions

A nice smell means it's clean.

• Clean actually has no smell at all. Products that leave a residual smell do so for aesthetic purposes, not for any real effect.

All disinfectants are created alike.

• Disinfectants are quite variable, in terms of the different organisms they can kill, how well they work in the presence of dirt and debris, how quickly they work, how toxic they are, and other factors.

The label says it kills 99.99% of microorganisms so it must be great.

• This type of advertising is misleading. Killing 99.99% of selected organisms in a lab environment is different than killing the entire range of possible microorganisms encountered in a barn, and in the presence of debris and difficult-to-disinfect surfaces.

If the area is dirty, just use more disinfectant

• Cleaning removes 80-95% of microorganisms, and is the most important step of the disinfection process. If the area isn't cleaned properly and has a lot of dirt and debris, the disinfectant will not be very effective, regardless of how much is used.  There's no substitute for good old fashioned "elbow grease" when it comes to getting a barn clean.

One disinfectant is good, so two must be better

• A single disinfectant with a good disinfection protocol is adequate. There should be no need for multiple products, unless you want to have a higher level disinfectant available for certain situations (e.g. a stall for a horse with diarrhea). However, you should never mix disinfectants, because highly toxic by-products can be produced.

I'm not having any infectious disease problems, so I don't need to worry about my disinfection practices.

• Everyone that has an outbreak can say, right before the outbreak, that they had no infectious disease problems. Just because things are going well today doesn't mean that things will be fine tomorrow. It's a common perception, however, and often we don't find out about peoples' inadequate disinfection (or other infection control) practices until we are dealing with an outbreak. There's no guarantee that a better disinfection program would have prevented the outbreak, but it certainly wouldn't have hurt and may have helped reduce the problem.  It's much easier to review things and make improvements before there are problems.
  

• Nothing happens: This is probably the most common outcome. People get exposed to the virus by being bitten by an infected mosquito, but their immune system fights it off. They may develop antibodies against the virus but they don't get sick.
• West Nile fever (also called West Nile non-neuroinvasive disease): In this scenario, the infected person develops a fever, often along with a headache and joint or muscle pain. This accounts for most of the people that get sick after being infected.
• West Nile neuroinvasive disease: This is the big scary problem, though it fortunately only occurs in a small percentage of infected people. This form is characterized by neurological abnormalities such as meningitis, encephalitis and/or paralysis.

US data indicate that there were 720 cases of West Nile virus disease reported in 2009, 54% of which were non-neuroinvasive and 46% of which were neuroinvasive.  While that may not seem to support my statement above that only a small percentage of infected people get neurological disease, you have to remember that if you don't get sick, you won't get tested. Further, if you just have a headache and muscle or joint aches, it's pretty unlikely you're going to get tested. Therefore, while a large percentage of reported cases were neurological, a very large percentage of non-neurological cases were presumably not identified because they were mild and testing wasn't performed.

Back to horses...

In horses, we pretty much only identify horses that are healthy but have been exposed (based on the presence of antibodies against the virus) and those with neuroinvasive disease. However, that doesn't mean that West Nile fever does not exist in horses. It probably does, we just don't diagnose it.

Horses that develop mild disease of short duration aren't always even examined by a veterinarian. If a veterinarian is called and the horse is just a little "off" with a fever and vague signs of illness, testing for West Nile virus will not be very high on the list of priorities (especially if the horse owner has to pay for testing). Most of these horses, if they are examined, probably get treated empirically with anti-inflammatories and rest, and they get better. So, we really have no idea whether this form of the disease exists or how common it is. In a lot of ways, it doesn't really matter. The main reasons that it would be nice to know whether horses with mild, non-specific disease have West Nile is to know that there is active West Nile virus transmission to horses going on in the area, and for a better general understanding of West Nile virus in horses.

If you have a horse that develops vague signs of disease during the typical West Nile season, especially if there are no major other risk factors for other diseases that typically cause fever and vague illness (e.g. going to shows, new horses in the barn), you should at least consider the possibility that West Nile virus is present. That doesn't necessarily mean you have to get the horse tested or do anything different, but it never hurts to have a better idea of to what infectious diseases your horses might be exposed.

Image source: www.lapublichealth.org (click image to enlarge)

But, does it work?

I've heard many anecdotes about peoples' success (or lack thereof) with feeding their horses garlic or garlic components. Some people have said they thought it worked. Others, probably the majority, didn't think it did anything.

The scientific literature doesn't help much. Despite what you read on internet sites selling garlic, there's no published work on garlic as a mosquito repellent in horses. There's a little research involving humans but no significant effect has been identified. One study involved giving people garlic or a placebo, then exposing them to mosquitoes and counting the number of bites and the weights of the mosquitoes after exposure (the more the blood they ingest, the more they weigh), but the study showed no effect of garlic (Rajan et al 2005). Beyond that, there's nothing else out there.

Lack of scientific evidence doesn't necessarily mean lack of effectiveness. It could just be that adequate studies haven't been performed. However, it doesn't change the fact that there is currently nothing indicating that garlic is an effective mosquito repellent. There's probably no harm in giving reasonable doses of garlic as part of an overall mosquito control program, but it shouldn't be done in place of other activities such as reducing mosquito breeding grounds and avoiding areas where there are large numbers of mosquitoes (particularly at dawn and dusk).

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The good news:

• The infected (and infectious) horse was identified so proper measures can be taken to reduce the risk of spread to other horses.
• The surveillance program that is in place is effective at identifying (at least some) positive horses.

The bad news:

• Still, no one has a good explanation as to why these unrelated cases keep occurring. I can't see any other explanation other than this disease must be present (endemically) in the US and is probably being spread by unrecognized insect vectors. 
• The surveillance that is underway only tests a very small percentage of horses. So, for every infected horse that is detected, there may be many more that go undetected.

Clearly, a concerted and coordinated effort needs to be undertaken to determine the scope of the problem and, more importantly, the source and route of transmission (i.e. the insect vector) of these infections. If at least the vector is not identified, there's no way to properly control this disease.

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We've done several surveillance studies across North America and we consistently find MRSA in a small but not insignificant percentage of horses. In most studies, we see it carried in the nasal passages of 1-5% of horses. A couple of recent studies provide more evidence that this bug has spread widely in horses internationally.

In a retrospective study of bacterial infections in horses at the University Equine Clinic of Bern, Switzerland (Panchaud et al, Schweiz Arch Tierheilkd 2010), MRSA was on the most important bacterium isolated from affected horses. Additionally, screening of horses at admission to the hospital revealed that 2.2% were carriers.

In a retrospective study of samples submitted for bacterial culture from horses in Ireland (Abbott et al, Vet Rec 2010), MRSA accounted for 5.2% (20/383) of isolated bacteria, which was higher than the percentage of MRSA in samples from dogs (1.1%) and cats (0.7%). In the prospective part of the study, MRSA was isolated from only 4.6% (3/65) of infections where clinicians suspected that MRSA was the cause. Its interesting that it was isolated less commonly in cases where people thought MRSA might be the problem than overall.  In contrast, while MRSA was only found in 1.1% of culture samples from dogs, it was found in 8.1% of infections where clinicians suspected an MRSA infection. It's not clear why there was such a difference between horses and dogs. It doesn't mean the equine clinicians are clueless, it just supports the notion that there are few clear indicators of that an infection is being caused by MRSA. MRSA infections occur in horses without any obvious risk factors, which complicates diagnosis and management of the infection.

MRSA must be considered in any situation when a horses has an infection. There's evidence that it's more common in horses that have been recently treated with antibiotics or in a veterinary hospital, but the link is not particularly strong and MRSA infections do occur in horses with no identifiable risk factors. That's why culturing infected sites - rather than just trying different antibiotics and seeing what happens - is critical. Money and effort spent culturing infected sites is a good investment.

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The risk of EEE varies greatly across North America. For EEE to be a problem:

• EEE virus must be present in birds in the area. Birds are the reservoir hosts and are not typically affected by the virus.
• Mosquito populations must be large enough to facilitate transmission of EEE virus between birds and from birds to horses (or humans).
• The types of mosquitoes that are present must be those that like to feed off both birds and horses/humans. These "bridging vector" mosquitoes are critical since they are the ones that allow the infection to spread beyond birds.

Not all mosquitoes are the same in terms of their feeding patterns and likelihood of carrying EEE virus and transmitting it from birds to horses and people. Not all bird species have the same likelihood of carrying EEE virus. These factors play an important role in explaining why EEE can be a major problem in some areas but not in others.

Photo: Aedes vexans, one of the mosquito species capable of transmitting EEE from birds to mammals (click image for source).

EEE causes severe neurological disease in horses and people. Horses and people are infected after being bitten by a mosquito that was infected by feeding from an infected bird. Infection is often fatal.

The keys to prevention (for horses and people) are:

1. Avoid mosquito bites by:

• Reducing mosquito breeding grounds (i.e. standing water)
• Staying away from mosquito-infested areas, particularly at dusk or dawn.
• Wearing clothes that cover your arms and legs
• Wearing a DEET-based repellent when outside

2. Vaccination

• EEE vaccination is important in areas where the disease is present. Ideally, vaccination should be performed approximately one month prior to the time of year when cases start to occur, but late is better than never.

More information about EEE can be found in our archives.

Photo: Horse in a full-body fly sheet.  Good in theory but not very helpful in hot weather. (click image for source)

Salmonella

A report about one high-profile outbreak that occurred a couple of years ago was recently published in the Journal of Veterinary Internal Medicine (Dallap Schaer et al 2010). This was a large outbreak caused by a multidrug resistant strain of Salmonella Newport that hit the University of Pennsylvania's New Bolton Center.

• Ultimately 61 animals were infected, 54 of which were horses.
• 22 (36%) infected animals died. This occurred despite the fact that aggressive treatment was provided and cost issues were minimal because the hospital paid for treatment associated with the outbreak. That's an incredibly high rate and shows how "hot" this strain was.
• Environmental sampling during the outbreak identified persistence of the bacterium in the hospital. Because of this, and ongoing cases, the hospital had to be closed for thorough decontamination. The hospital was closed for approximately three months, and the NICU/ICU was closed for eight months.
• There was extensive renovation of some areas, including sandblasting and resurfacing of 4 cement-block barns, replacing dirt flooring with concrete, installation of a polyurethane-based flooring system in all stalls and animal handling areas, and replacing non-cleanable surfaces throughout the facility. Chlorine gas decontamination was used for the ICU/NICU.
• The financial impact was estimated at over $4 million US. That doesn't include the impact on reputation and morale.
• "A paradigm shift in the relevance of biosecurity in a veterinary teaching hospital and the establishment of a stringent infection control program were integral components of successful hospital re-opening."

A good infection control program is a key component of reducing the risk of outbreaks, but they can still happen in any facility at any time. An infection control program was present in this hospital, but it was later determined to have some weaknesses that were corrected. Analysing an outbreak after the fact and trying to correct any underlying causes is a critical component and is often overlooked. By the time the outbreak is over, people often want to immediately forget that it happened and don't want to look for causes, whether it's directed at the facility, management, protocols or personnel. The goal isn't to blame someone and penalize them, it's to find out how to prevent the problem from happening again.

I commend the authors for publishing this report. I've always taken the approach of publishing and talking about any infection control issues we've run into in our hospital. It's a double edged sword, so some people don't like the fact that I do this. It certainly can lead to negative publicity, but I think it's critical that this information be shared so that problems can be prevented in the future. We've become international leaders in some aspects of infectious diseases and infection control by aggressively pursuing and publishing our "dirty laundry." Personally, I'd much rather take my horse to a hospital that isn't afraid to talk about their issues because it shows they're paying attention, and trying to stay on top of any problems, as compared to a facility that never submits a Salmonella culture from diarrheic horses just so they can say they've never found (which isn't the same as never had) Salmonella in their building.

As I've said before, hope isn't an infection control strategy. You have to work at it to do it right.

Image: New Bolton Center, University of Pennsylvania

Bahrain's chief veterinarian has stated that different testing must be done for camels and that an invalid technique may have been used. There is, however, no evidence supporting this claim, and the Dubai lab is sticking by the diagnosis. There are also anecdotal reports of other camels that might have been infected.  Efforts are better spent exploring this potentially important problem rather than bickering.

Glanders has been previously reported in camels, so it's not a stretch to believe that camels could be infected in the current Bahraini outbreak. It's concerning because of the potentially large number camels that would need to be investigated and tested as part of the outbreak, if camels became involved. It sounds like there's a lot of reluctance to expand investigation and control efforts to this other species, but blaming the test or the lab is never a good approach to outbreak control. It's much better to over-react initially and put extra effort into potential problems than sit back, debate, deny and then have to deal with an even larger problem. Let's hope that these issues get sorted out soon. If not, even if all horses in the country are tested and declared negative, there will continue to be a threat of ongoing infections if the bacterium is able to get a foothold in the camel population.

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In the vast majority of foalings, things go well: the foal comes out on its own, gets up in a normal period of time, starts nursing and ingests an adequate volume of good quality colostrum.

Sometimes, an adequate volume of good quality colostrum is not available. This can be because the mare leaked colostrum before foaling, the mare didn't produce colostrum, the mare rejected the foal or the mare died during foaling. Whatever the reason, lack of colostrum is an emergency and needs to be addressed promptly to reduce the risk of serious infections. There are a few possible ways to do this:

• Get colostrum from another mare that has just foaled: Great idea, but difficult in practice unless you have a large farm or a network of other local breeders that might have a mare who  just foaled and has colostrum to spare.
• Commercial colostrum replacers: Not a great option. They're very convenient, and likely better than nothing if all other options are exhausted, but they just don't do the job like the real thing.
• Plasma: Plasma can be given orally in the first 18-24 hours of life or intravenously after that, to provide antibodies. It doesn't replace all the goodies found in colostrum, and it's expensive, but it's often the best option available to most people.
• Stored colostrum: Banking colostrum by collecting and freezing extra colostrum from mares (or all the colostrum from mares whose foals died during birth) is a cheap and relatively easy approach. It's easiest for large farms with lots of mares, but anyone can do it. (Remember, however, not to deprive a live foal of any of the colostrum it needs so you can build up a store.  Some mares may only produce enough colostrum for their own foals.)  For stored colostrum to be useful, however, it must retain its beneficial properties during storage.

A recent paper in the Journal of the American Veterinary Medical Association (Nath et al 2010) looked at this aspect. They checked colostrum quality in mares at the time of foaling, and if poor quality colostrum was identified, foals were supplemented with stored, frozen colostrum within six hours of birth. Blood antibody levels were checked 24 hours after treatment. Overall, 5.8% of foals had suboptimal antibody levels, but only one foal (0.4%) had true failure of passive transfer of maternal antibodies, with antibody levels <400 mg/dL. The rest of the "low" group had partial failure of passive transfer, meaning they had lower than ideal (400-800 mg/dl) antibody levels, but these levels are not necessarily a problem, particularly in an otherwise healthy foal on a well-managed farm.

It's not exactly an earth-shattering study, and only limited conclusions can be made because of some aspects of study design (e.g. not proving that supplementation was the reason that foals had adequate antibody levels, no statistical comparison of the incidence of failure of passive transfer between foals that were or were not supplemented, treating some foals that didn't fit the study criteria and not treated a couple that did), however this study showed that this type of approach - checking colostrum of mares at birth and supplementing foals whose mares produce poor colostrum - is a practical approach and resulted in a very low percentage of foals with inadequate antibody levels.

The take home message, perhaps, is that you need to pay attention to colostrum quality. If you check colostrum quality of mares that have just foaled and intervene in situations when poor quality colostrum is present, or when the foal can't/won't ingest an adequate amount of colostrum, you can make sure that failure of passive transfer of maternal antibiotics is a rare event.

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

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• Giving a drug by nasogastric tube (stomach tube) used to be common, but is rarely done now because, while you can be sure the drug goes where you want it to go, it has to be done by a veterinarian and is not particularly pleasant for the horse.
• There are injectable versions of ivermectin, but they tend to cause significant pain and reaction at the site of injection, and are not generally recommended for horses.
• Most commonly, dewormers are given as oral pastes. These are easy to get and easy to administer - to some horses. Failure to get the whole dose into the horse is a problem (and some horses are remarkably good at avoiding what they don't want to swallow!).  This can result in underdosing, which can reduce the effectiveness of deworming and likely contributes to the emergence of drug-resistant parasites.

Another approach used by some is topical or "pour-on" administration of dewormers. Pour-on formulations are only available for cattle, so use of them in horses is "off-label". The ease of administration is appealing, but an important question is how well do pour-ons work in horses?

A study published in a recent edition of Veterinary Parasitology (Gokbulut et al 2010) compared oral, intravenous and pour-on ivermectin in horses. (Ivermectin is a common horse dewormer, sold under a variety of brand names.)  The researchers treated three groups of horses witheither ivermectin paste, bovine pour-on or bovine injectable formulations. They then looked at blood and hair/skin levels of ivermectin and fecal egg count reduction. Here are the highlights:

• Ivermectin concentrations were high on the skin and hair at the pour-on site, not surprisingly. Detectable concentrations were found on the skin at distant sites.
• Blood levels of ivermectin were lower in horses treated with the pour-on compared to the paste, but blood levels persisted longer with the pour-on, presumably because of longer, slower absorption. That's not necessarily a good thing, however. Prolonged exposure to low levels of an anthelmintic is a good recipe for resistance. What we want are high (therapeutic) levels for relatively short time to kill susceptible parasites and decrease the emergence of resistance.
• Oral ivermectin produced better reductions in fecal egg counts, meaning it did a better job eliminating parasites in the intestinal tract. Pour-on ivermectin did not work as well, but produced a longer effect.

What does this tell us?

Basically, it  means that pour-on ivermectin is absorbed and can reduce intestinal parasite levels. It can also provide a more long-lasting effect than oral ivermectin. However, it also has the potential for inadequate levels in the intestinal tract and theoretically a greater likelihood of resistance.

Since we have pastes with demonstrated efficacy against intestinal parasites and which are licensed for use in horses ("on-label"), it's hard to justify the use of pour-ons in this species. Perhaps in situations where a particular horse is extremely resistant to oral deworming and there is no way to get the dewormer paste into the horse by any method (after trying many different tricks), topical treatment of that specific horse could be considered. Such treatment of a rare single horse here or there is probably of limited consequence in the broader context, but if people start treating all horses on the farm like this just because one is hard to dose orally, or because they think it's easier, resistance concerns increase greatly.

Photo credit: Lesley Ward (click for source)