Disinfectant Facts And Fallacies

While it seems straightforward, disinfection is pretty easy to screw up. It's not uncommon for me to find illogical or completely ineffective "disinfection" practices when I do farm investigations. In general, people don't really understand much about disinfectants and disinfection. That's not too surprising because it's not exactly a common or enthralling topic (and I didn't really know much about it until I became focused on infection control).

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.

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Do Horses Get West Nile Fever?

In humans, infection with West Nile virus have a few different possible outcomes:

  • 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)

Garlic, Horses And Mosquitoes

As eastern equine encephalitis (EEE) season is in full swing in some areas and West Nile virus cases should be starting soon, the need to avoid the vectors of these diseases, mosquitoes, is clear. There are various ways to reduce exposure to mosquitoes, but none of them are great in terms of their effectiveness and practicality. In peoples' quests to find alternative approaches, they often come across garlic. Ingestion of garlic has been advertised and used as a mosquito repellent in humans and horses. 

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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Pirplasmosis In The US: A Broken Record

Yet another case of piroplasmosis has been identified in the US. The horse was identified as infected with the bloodborne parasite Babesia caballi through routine testing for interstate movement of horses. Babesia caballi and Theileria equi are both causes of piroplasmosis, and both have been found multiple times in the US over the past year or so. The infected horse is currently under quarantine.

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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More On MRSA In Horses

Methicillin-resistant Staphylococcus aureus (MRSA) is an antibiotic-resistant bacterium and a major concern in both human and veterinary medicine. This bacterium can be carried by healthy horses and is an opportunistic pathogen, meaning it can cause infection in certain situations, particularly when the body's normal defensive barriers (like the skin) are breached (e.g. by surgery, wounds, compromised immune system).

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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EEE Spreading In US

Eastern equine encephalitis (EEE) season is now in full swing in the US. Cases are being reported in horses in several US states, including Florida, Georgia and Louisiana. Infected mosquitoes have been found over a wider range, including as far north as Massachusetts. That’s not particularly surprising because this seasonal mosquito-borne viral infection typically occurs at this time of year in eastern/southeastern coastal regions.

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 In Southeastern US

Eastern equine encephalitis (EEE) season is well underway. EEE is a devastating mosquito-borne disease that can infect (and usually kill) horses and people. It is a regionally important disease that infects many horses in some regions and none elsewhere, mainly based on the types of mosquitoes and birds in the area. The southeastern US is a hotbed, and cases are now being reported in areas such as Florida and Georgia. It is very important that horse owners make themselves aware of infectious disease risks in their own areas, including the risk of EEE. It is equally important for owners to be aware of the disease risks in any areas to which they may take (or send) their horses. Knowing the risks is necessary to develop a logical and effective infection control program.

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 Outbreak Report

Salmonella is the bane of existence of equine hospitals. It's the most common cause of infectious disease outbreaks, some of which can be devastating.

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

Expanding Glanders Range In Bahrain?

A new twist has been encountered in Bahrain's glanders (Burkholderia mallei) outbreak. Controversy and confusion abound, with questions about testing, application of infection control practices and the actual number of infected animals. The latest issue to emerge is a report of diagnosis of glanders in a camel.  Bahraini officials have been adamant that this disease has not spread to camels, but Dubai's Central Veterinary Research Laboratory, one of only two international reference laboratories for the disease, made the diagnosis. This has led to further rounds of accusations and counter-accusations, none of which helps control this problem.

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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Feeding Stored Colostrum

Hopefully, everyone that breeds horses knows the importance of colostrum. Unlike human babies, foals don't get antibodies from their dam before they're born. They need to drink colostrum, the antibody-laden first-milk, to get these antibodies which help fight off early infections. Failure to get adequate antibodies from the mare, known as failure of passive transfer (FPT) of maternal antibodies, is a life-threatening problem that needs to be treated quickly. Like most things, prevention is better than treatment, so efforts aimed at reducing failure of passive transfer are critical.

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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