University of Kentucky College of Agriculture, Food & Environment

 

Gluck Center > Equine Disease Quarterly > April 2014

 

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Commentary

The report of my death was an exaggeration. -- Mark Twain, 1897

The explosion of social media has not changed human nature. The inclination to share rumors, speculation, gossip, and scandalous accusations— with or without credible verification—has been a part of human nature as long as language itself. The speed at which social media now moves such information through the horse industry is, however, both novel and alarming.

For example, the 2011 multistate equine herpesvirus-1 outbreak traced to a cutting horse event in Ogden, Utah, vividly reflects the financial and emotional impacts a crisis event can have on the horse industry. Some information shared on social media regarding the outbreak was accurate and served a legitimate purpose. Other postings were exaggerated or outrightly false and generated erroneous perceptions and unwarranted overreactions.

Successful crisis communication in a world obsessed with social media involves individuals at all levels of the horse industry. Two decades of research by risk and crisis communication experts offer some feasible suggestions for all of us in combatting inaccurate messages shared during crises:

1. Those with knowledge must communicate openly and honestly. The disastrous impact of falsifying or withholding public information is well known. Doing so endangers the well-being of horses and undermines public trust.

2. Know your network and spokespersons in advance. Although every industry is vulnerable to crises, relatively few regularly engage in crisis planning. Having a network in place and the means for credible spokespersons to communicate through that network is essential. Social media outlets such as Twitter and Facebook give agencies and industry leaders an unprecedented opportunity to proactively establish such a network.

3. Acknowledge public concern. Even if we believe a problem making its way through social media is false, our failure to respond creates space for rumors to spread. We must often provide a substantial response to unsubstantiated problems.

4. Communicate early and often. Case studies and experiments reveal that sources are perceived more credibly if they communicate early in an event. Waiting until a story spreads widely to make a response significantly reduces credibility.

5. Acknowledge both sides of the story. Message testing research in crisis communication reveals an overwhelming advantage to speakers who acknowledge the accusations that are shared and then systematically explain why they are or are not true. Simply disregarding accusations presumed or known to be false and then advocating your position is seen as arrogant and far less credible by audiences.

6. Give those who are alarmed something meaningful to do. Surprisingly, an extensive review of crisis messages shared through traditional and new media reveal far more content emphasizing the threat than recommendations for selfprotection. Providing suggestions for avoiding the threat or seeking treatment greatly enhances credibility and can legitimately diminish the impact of a crisis.

Following these six suggestions based on considerable research may make the difference between success and failure in a crisis response.

CONTACT:
Dr. Timothy Sellnow, (859) 257-7805, tim.sellnow@uky.edu
Department of Communication
University of Kentucky Lexington, Kentucky

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Fourth Quarter 2013*

The International Collating Center, Newmarket, United Kingdom, and other sources reported the following disease outbreaks.

Outbreaks of strangles were reported by Denmark, France, Germany, Sweden, and the USA. Denmark confirmed the disease in 15 of 50 horses in a riding school of which two had to be euthanized. Four outbreaks were recorded in France. One case was diagnosed in Germany. Strangles was considered endemic in Sweden and the USA with numerous outbreaks confirmed in several US states including but not exclusive of Indiana, Kentucky, North Carolina, and Virginia.

Germany, the UK and the USA recorded outbreaks of influenza. Isolated cases of the disease were diagnosed in Germany (one outbreak) and the UK (two outbreaks). The USA reported outbreaks in several states, California, Indiana, and New Jersey, among others, with horses exhibiting signs of varying clinical severity.

The USA was the only country to report limited serological evidence of equine arteritis virus infection in breeding stock in a few states.

Equine herpesvirus 1 and 4 (EHV-1, -4) related diseases were recorded in France, Germany, Ireland, Japan and the UK. Respiratory disease caused by EHV-4 was confirmed in France (12 outbreaks), Germany (seven cases on four premises), and the UK (five outbreaks with limited numbers of affected horses). Abortions due to EHV-1 were reported from Germany (one outbreak), Ireland (four outbreaks), Japan (three cases on two premises), Sweden (one outbreak), the UK (two outbreaks), and the USA (three outbreaks). Most affected premises had isolated cases of the disease.

EHV-1 related neurologic disease was confirmed in France (one outbreak in a riding school) and the USA (two outbreaks). One occurred at a racetrack and was associated with a non-neuropathogenic genotype strain of the virus. The second US outbreak occurred at a riding school: Four horses died or had to be euthanized, and five other febrile in-contact horses were also confirmed infected with a neuropathogenic genotype strain of EHV-1.

A limited number of cases of EHV-2 and EHV-5 infection were reported in the USA.

Reports on equine piroplasmosis were received from France (endemic) and the USA (Theileria equi infection in one Quarter Horse racehorse).

Germany and the USA reported isolated cases/ outbreaks of Salmonella infection. One case was recorded in Germany, and 13 cases of Group B salmonellae involving multiple premises were confirmed in the USA.

Equine proliferative enteropathy due to Lawsonia intracellularis was reported in foals in several states including Kentucky (16 cases) and Ohio (one case).

The USA recorded one case of equine monocytic ehrlichiosis in Texas.

Cases of clostridial enteritis due to C. perfringens type A were reported from several states in the USA. Two cases of C. difficile were also diagnosed, both on premises in Kentucky.

Abortion due to leptospiral infection was recorded in France (one case) and the USA (six cases).

During the fourth quarter, the USA confirmed 40 cases of Eastern equine encephalomyelitis out of an annual total of 183 from 22 states. South Carolina (49), Florida (34), and Georgia (25) had the highest number of cases for 2013.

Reports of West Nile Virus encephalitis were received from the USA. Over a three month period, 201 cases were diagnosed in a total of 41 states. The greatest number of cases was diagnosed in Texas (60), Oklahoma (41), and Montana (27).

Equine Hendra virus infections were reported in Australia during the 3rd quarter of 2013. Isolated cases occurred on four separate premises in New South Wales and on one premises in Queensland.

Switzerland reported a single case of atypical myopathy.

*Third Quarter Report for Australia

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Emergence of Methicillin-Resistant Staphylococcus aureus Sequence Type 398 in Horses

In the Netherlands in 2005, a small number of unexpected methicillin-resistant Staphylococcus aureus (MRSA) infections in people with pig contact led to identification of a novel MRSA clone, sequence type (ST) 398. This clone was quickly called “‘livestock-associated” MRSA, although recent evidence suggests that it originated in humans as a methicillin-susceptible strain that subsequently moved to pigs, became methicillin-resistant, and lost some human-adaptive traits.

Nonetheless, whatever it is termed, ST398 MRSA is an important issue in people and animals in some regions. The organism has been identified in pigs (and to a lesser degree other livestock such as cattle and poultry) worldwide and is commonly found in people that have contact with livestock. In some northern European countries, it is the leading cause of MRSA infection in people.

Equine MRSA infections were first reported in the late 1990s, and it soon became apparent that MRSA was endemic in the horse population in many regions, being found in a small percentage (typically <3%) of healthy horses and causing sporadic infections and outbreaks.

Abnormally high rates of MRSA colonization of horse owners and equine veterinarians have also been reported, along with smaller numbers of zoonotic infections. Until the late 2000s, the vast majority of MRSA isolates from horses were common human epidemic clones (e.g. ST8), suggesting that equine MRSA was ultimately human in origin.

Yet recent years have ushered in a potential new concern, with identification of ST398 in horses. ST398 has now been reported in horses in many European countries as well as in a single Canadian horse. Zoonotic infection from a horse has also been reported. Highly variable colonization rates (0.5-11%) have been described, and ST398 has displaced other strains to become the leading cause of MRSA infection in horses in some areas of Europe. As is typical for any MRSA strain, a wide range of clinical infections has been reported, including skin and soft tissue infections, surgical site infections, pneumonia, catheter site infections, mastitis, and metritis.

Whether the emergence of ST398 in horses indicates a clinically relevant change for the horse population, a concern restricted to certain regions or farm types, or simply a shift in predominant strains with limited clinical relevance remains to be seen. While ST398 appears to be rare (at this time) in horses outside of northern Europe, the highly mobile nature of the horse population indicates a potential for horses to assist with global dissemination of this animal and human pathogen.

Horse owners and veterinarians should be aware of the risk of MRSA (ST398 and others), and use:

1. Basic infection control practices at all times

2. Enhanced infection control practices for any animal with an infection

3. Antimicrobials prudently

4. Bacterial culture and susceptibility testing routinely on animals with opportunistic infections

Emergence of this livestock-associated MRSA clone also highlights the often-overlooked potential for pathogen exposure of horses that have direct or indirect contact with food animals.

CONTACT:
Dr. J. Scott Weese, (519) 824-4120, Ext. 54064, jsweese@uoguelph.ca
Ontario Veterinary College, University of Guelph
Guelph, Ontario
Canada

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Epizootic Lymphangitis

Epizootic lymphangitis is a systemic infection of equids, caused by the dimorphic soil fungus Histoplasma capsulatum var. farciminosum. Donkeys are less commonly affected than horses and mules. It has been reported in camels, cattle and anecdotally in humans.

The disease has been eradicated from many countries, but remains a problem for equids, particularly in northern Africa, Asia, and the Middle East. It is contagious, spreading between animals through inhalation, skin contact with infected discharges, fomites, and insect vectors. Skin wounds are common entry sites for the organism.

Three forms of the disease exist: cutaneous, ocular and respiratory. The cutaneous form is most common, causing a chronic, suppurative, ulcerating pyogranulomatous dermatitis and lymphangitis. Initial nodules appear anywhere on the body but commonly on lower limbs, chest, and neck. Nodules rupture, discharging thick pus, the ulcerated lesions subsequently scarring and healing. Lesions progress locally along lymphatics, which become beaded and rope-like with enlarged regional lymph nodes. Repeated cycles of ulcerating and healing nodules occur.

Keratoconjunctivitis with mucopurulent discharge characterizes the ocular form and is more common in donkeys. The respiratory form results in a mucopurulent nasal discharge and subsequent coughing and difficult breathing.

In all three forms the disease’s chronic nature leads to debility and anorexia. Working animals can no longer perform, leading to abandonment by their owners, especially where veterinary care is unavailable or unaffordable or euthanasia not easily accepted. Some animals appear to recover, but the mechanism of immunity and the possibility of carrier states are unclear.

Field diagnosis of epizootic lymphangitis is by organism identification in a smear of material aspirated from an unruptured nodule. The yeast appears as pleomorphic ovoid-to-globose structures, 2-5 μm diameter, found extracellularly and in macrophages. Organisms are usually surrounded by a “halo” when Gram-stained, useful in rapid differentiation from glanders (difficult to differentiate clinically). Culture of the organism is possible but challenging. A Histofarcin skin test (similar to tuberculin and mallein tests) has been developed but requires further validation. Serological techniques have been described but are not commercially available. A polymerase chain reaction (PCR) has been developed for H. capsulatum var. capsulatum, which may prove useful in the future.

Treatment is challenging. Amphotericin B is the drug of choice but, since most cases occur in working animals owned by poor individuals in developing countries, modern antifungals are rarely available or affordable. More commonly systemic iodides (oral potassium iodide or intravenous sodium iodide) and local excision of nodules and topical iodine tincture are used. Treatment is lengthy (3-4 weeks) and owner compliance challenging. Treatment initiation early in the disease increases success rates.

Historically, disease control focused on culling infected animals, strict hygiene, and movement controls to limit disease spread. These methods are usually impractical in endemic areas, particularly in developing countries where control commonly concentrates on educating owners about wound prevention; vector control; management of harnesses, tack, and equipment; early presentation for treatment; and encouraging euthanasia for advanced cases.

This neglected disease has a significant welfare impact on working equids and has economic importance to many resource-poor owners with inadequate access to animal health services who rely on animals for their livelihoods. More research is required to understand fully transmission routes, risk factors and immunity, and develop animal-side diagnostics and simple, affordable, transportable, and stable therapeutics.

CONTACT:
Dr. Karen Reed, karen@thebrooke.org
Head of Animal Welfare and Research
The Brooke, London
United Kingdom

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Equine Botulism

Equine botulism is most frequently observed in Kentucky and the Mid-Atlantic region of the Eastern United States, although it has been reported worldwide. The disease is also known as shaker foal syndrome, forage poisoning, and grass sickness.

Botulism is a neuromuscular disorder of horses caused by neurotoxins of the bacteria Clostridium botulinum that results in flaccid paralysis by the action of the various botulinum neurotoxins in the presynaptic axon, preventing release of acetylcholine into the synapse. Of the three types, botulism Type B occurs throughout the United States but is more predominant in the Mid-Atlantic states and Kentucky. Type A botulism occurs primarily in the west while botulism type C occurs in Florida. Botulism neurotoxins type B and C are the most commonly reported types in foals.

Botulism results from exposure to the toxin by three main routes. Ingestion of pre-formed toxin is the most common form affecting adult horses when they eat feed, such as hay or grain, that contains animal remains. Swallowing the botulism organism with subsequent elaboration of toxin in the intestines is known as shaker foal syndrome, which is associated with one- to three-month-old foals, but can occur as early as one week of age. Rarely, wound infection with Clostridium botulinum occurs and the subsequent release of the toxin in the body causes disease.

Clinical signs after exposure to toxin occur from 12 hours to several days and may be dependent on dose and type of botulinum neurotoxin involved. Sudden, unexplained death of one or more horses may be the initial signal of an outbreak. Decreased eyelid, tongue, and tail tone may be observed early in disease. Horses that can walk may have a stilted, short-strided gait without ataxia. Muscle trembling and weakness may be apparent, particularly in foals. Pupillary dilation with sluggish pupillary light reflexes and difficulty swallowing (dysphagia) is frequently observed. Clinical signs may rapidly progress to recumbency. Tachycardia may occur, particularly in foals. Death is generally attributed to respiratory failure secondary to respiratory muscle paralysis.

Diagnosis is made based on clinical signs. Definitive diagnosis requires detection of the toxin in serum, feces, gastrointestinal (GI) contents, or feed by enzyme-linked immunosorbent assay (ELISA), radioimmunoassay (RIA) or polymerase chain reaction (PCR). Specific toxin activity can be confirmed by a mouse inoculation test and is supported by isolation of C. botulinum from serum, feces, GI contents, or feed.

Treatment consists of blockade of any circulating toxin by intravenous administration of plasma containing specific antibotulism neurotoxin antibodies (generally against types B and/or C). Supportive care, including fluid, nutritional, antimicrobial and respiratory supportive therapies, is critical. Adults and foals with mild respiratory signs can frequently be treated with intranasal oxygen insufflation and positioning in sternal recumbency. Mechanical ventilation can be life-saving in foals. Antimicrobial administration (avoiding procaine penicillin, aminoglycosides, and tetracyclines) is employed to prevent or reduce complications of the disease, such as aspiration pneumonia caused by dysphagia. Nutritional management can be provided to foals by feeding milk or milk replacer via indwelling nasogastric or nasoesophageal tubes while in adult horses, periodic nasogastric intubation of slurry meals or commercially available liquid diets can be provided.

For type B botulism, the survival rate in appropriately treated foals less than six months of age is greater than 90%. Affected adult horses that remain standing have a good prognosis, although a prolonged recovery, while recumbent adults are less likely to survive. Vaccination with Clostridium botulinum type B toxoid is thought to be almost 100% protective against type B in adult horses and should be undertaken in endemic regions. Vaccination of pregnant mares will be at least partially protective to their foals assuming adequate passive transfer of immunity.

CONTACT:
Dr. Pamela Wilkins, (217) 333-2000, pawilkin@illinois.edu
University of Illinois, College of Veterinary Medicine
Champaign-Urbana, Illinois

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Kentucky’s 2013 EIA Surveillance and Testing

During calendar year 2013, 77,001 serum samples purported to represent horses within Kentucky were tested for equine infectious anemia (EIA) with no positive animals being discovered. Of these, 73,549 samples were collected and tested to comply with state regulations governing the sale and exhibition of equine within Kentucky or to meet interstate transportation requirements (private testing). The remaining 3,452 samples were collected and tested as part of our market surveillance program of stockyard animals. Equine sampled and tested in this surveillance model are considered to have an elevated risk of exposure due in part to the environment from which many of these horses originate and the “trading channels” through which they may have passed.

Figure 1.Comparatively, private testing declined 4.7% from 2012 while the market surveillance testing decreased a staggering 70% during this same reporting period. The modest decline in private testing may be a result of a still-recovering economy that likely impacted some interstate movement of horses for recreational purposes. The significant decline in the number of horses sampled through Kentucky’s market surveillance program may also be attributed in part to a depressed economy, but was likely exaggerated by the reality of few sustainable markets for these animals. During the 24-year period of 1990 through 2013, 369,441 samples were collected and tested through the market surveillance program with 129 equine (0.03%) found to be positive. In comparison, private testing had greater than 1.8 million samples tested during this same time period with 92 (0.004%) positive equine identified. The last year a horse in Kentucky tested positive for EIA was in 2007.

Figure 1 shows the number of samples tested annually during the past 24 years overall and in the market surveillance program. These data provide evidence for concern over what is potentially an increasing population of untested equine, historically characterized as having elevated disease risk. Long term, consistent and accurate disease surveillance among identifiable populations can be beneficial in determining prevalence, progression or regression of emerging equine disease and aids in decision making processes to identify and mitigate associated risks.

CONTACT:
E.S. Rusty Ford, (502) 564-3956, Rusty1.ford@ky.gov
Equine Programs Manager, Kentucky Department of Agriculture
Frankfort, Kentucky

www.kyagr.com/statevet/equine/index.htm

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Editors:
Roberta Dwyer
Peter Timoney
Neil Williams
Staff:
Diane Furry
Tawana Brown
Dennis Duross

Correspondence should be addressed to the editors,
Department of Veterinary Science, Gluck Equine Research Center,
University of Kentucky, Lexington, KY 40546-0099;
Phone (859) 257-4757; FAX (859) 257-8542.

 

Maxwell H.Gluck Equine Research Center
Department of Veterinary Science, University of Kentucky
Lexington, Kentucky 40546-0099

Main Office (859) 257-4757
Fax (859) 257-8542