In our observations of wild horses and burros coming off the range there are several health concerns commonly noted. Most of the concerns are not specific to wild populations and are common threats to any equine population housed in large numbers in confined space. Most of the conditions do not represent life-threatening illness but create a compound stress that could influence animal health over the long term. We are concerned that most of these conditions remain untreated in the wild equines taken into captivity but would create immediate intervention in a domestic population in all but a “feed lot” (animals awaiting slaughter) situation.
Ringworm is a contagious fungus (not a parasite) that lives in soil, manure or any dark damp place. Crowded conditions (present at a stable or facility) can predispose animals to contacting ringworm through soil and common use of equipment. The ringworm fungi attach themselves to a horse where they live off of dead tissue in the horse’s skin and hair follicles.
Ringworm presents as small, circular patches of hair loss with scabbed or flaky skin beneath. If left untreated, these circular lesions will grow into large, irregular areas of broken hairs and blisters with scabs. Lesions are most typically seen around the girth and saddle areas, on the face and around the eyes, and on the legs.The lesions usually become extremely itchy. Itching and irritation generally starts on the chest or hindquarters and spreads to other parts of the body. These areas are susceptible to secondary skin infections so it is important to treat Ringworm symptoms proactively to prevent complications.
Ringworm is also very contagious, often spreading between horses and even from horses to humans. So, an affected horse should be isolated while being treated and any shared grooming tools should be disinfected after each use.
Treatment usually requires a combination of components: shaving of infected areas, application of anti-fungal and keeping manure and damp areas clean.
Equine papillomavirus is the virus that causes the development of benign, proliferative skin tumors in horses. Microscopic evidence indicates that two different clinical presentations occur in the equine from the papillomavirus: (1) warts, and (2) aural plaques. The warts are highly contagious. Transmission occurs by direct contact (nose to nose) and indirectly.
Equine papilloma virus has an incubation period of about 60 days.
The warts reach maturity after a growth period of four to eight weeks and usually disappear spontaneously about three to four months later. In this respect, they resemble human warts in that one day they can be extremely unpleasant, and then the next will suddenly vanish. However some cases may last longer than a year. Cases present for two years may suggest immune deficiency.
The virus may also cause aural plaques. They are benign, raised, white to pink lesions that occur bilaterally on the inner surface of the ear. They respond poorly to treatment and do not spontaneously regress. Animals should be monitored.
Disinfection of the premises and equipment with lye, formaldehyde, iodine, and chlorhexidine helps decrease spread of the virus.
Strangles is a highly contagious and serious infection of horses and other equids caused by the bacterium, Streptococcus equi. The disease is characterized by severe inflammation of the mucosa of the head and throat, with extensive swelling and often rupture of the lymph nodes, which produces large amounts of thick, creamy pus.
Strangles commonly affects young horses (weanlings and yearlings), but horses of any age can be infected. Vaccination against S. equi is recommended on premises where strangles is a persistent endemic problem or for horses that are expected to be at high risk of exposure. Following natural infection, a carrier state of variable duration may develop and intermittent shedding may occur.
The organism is transmitted by direct contact with infected horses or sub-clinical shedders, or indirectly by contact with water troughs and equipment. Streptococcus equi has demonstrated environmental survivability particularly in water sources and when protected from exposure to direct sunlight and disinfectants, and can be a source of infection for new additions to the herd.
Below is taken from http://www.omafra.gov
The main and often fatal complications of strangles are:
Bastard strangles, which describes the dissemination of infection to unusual sites other than the lymph nodes draining the throat. For example, abdominal or lung lymph nodes may develop abscesses and rupture, sometimes weeks or longer after the infection seems to have resolved. A brain abscess may rupture causing sudden death or a retropharyngeal lymph node abscess may burst in the throat and the pus will be inhaled into the lung.
Purpura haemorrhagica, which is an immune-mediated acute inflammation of peripheral blood vessels that occurs within 4 weeks of strangles, while the animal is convalescing. It results from the formation of immune complexes between the horse’s antibodies and bacterial components. These immune complexes become trapped in capillaries where they cause inflammation, visible in the mucous membranes as pinpoint haemorrhages. These haemorrhages lead to a widespread severe edema of the head, limbs, and other parts of the body. Purpura can also be a complication of routine vaccination.
Minor, non-fatal complications include:
Post strangles myocarditis (inflammation of heart muscle), which may follow strangles in a small proportion of horses. An electrocardiogram (ECG) can determine that a horse can return to heavy work or to training after an episode of strangles.
Purulent cellulitis (inflammation of the subcutaneous tissue), which is an unusual occurrence where infection spreads locally in the subcutaneous tissue to the head.
Laryngeal hemiplegia, which involves paralysis of the throat muscles. It is commonly referred to as “roaring”. The condition may follow abscessation of cervical lymph nodes.
Anaemia (low red blood cell count), during the convalescent period because of immune-mediated lysis of red blood cells.
Guttural pouch empyaema (filled with pus), which may be concurrent with classic strangles, or follow in the immediate convalescent period. The 2 guttural pouches are large mucous sacs; each is a ventral diverticulum of the Eustachian tube. They are present only in Equidae and are situated between the base of the cranium dorsally and the pharynx ventrally. (3) They open into the nasal pharynx and each has a capacity of about 300 mL. (4) Persistent infection in the guttural pouch may lead to inspissation (drying) of pus and, in some cases, the formation of a solid, stone-like, concretion called a chondroid. Animals that have persistent infection of the guttural pouches become the carriers, the major source of infection to spark outbreaks in susceptible horses with which they are mixed.
Apart from the problem of long-term guttural pouch carriers, discussed below, recovered horses may shed S. equi from their nose and in their saliva for up to 6 weeks following infection. Therefore, isolate all horses that have had strangles from susceptible animals for 6 weeks following infection.
A series of 3 nasopharyngeal swabs (e.g., swabs introduced through the nose and collecting material from the back of the throat), evenly spaced over 2 or 3 weeks, will result in the detection of about 60% of carriers using isolation and identification of the organism, or of about 90% of carriers using PCR. For the detection of carriers, the laboratory should use a selective medium (Columbia blood agar with nalidixic acid and colistin).
Investigation of carriers should be done either before a new animal is introduced into a stable or herd, or at least 30 days following recovery of a horse from strangles. Animals should be isolated until there have been 3 consecutive negative cultures and/or PCR reactions.
Isolate clinically affected animals or identified carriers immediately in a quarantine area, and clean and disinfect their water buckets or feed containers daily. Bedding can be burned or alternatively composted under a plastic sheet (to prevent spread by flies). Scrub with water and detergent any areas contaminated by infected horses, then disinfect by steam cleaning and/or applying effective disinfectants. Fly control is required to prevent spread during an outbreak.
Under optimal conditions, the bacteria can survive probably 6–8 weeks in the environment. Jorm (1991) has shown that S. equi survived for 63 days on wood at 2°C and for 48 days on glass or wood at 20°C. (6) The organism is readily killed by heat (60°C) or disinfectants (particularly povidone iodine, chlorhexidine). Rest contaminated pasture areas for 4 weeks, since the natural antibacterial effects of drying and of ultraviolet light will kill the organism.
Have quarantine area staff change their coveralls and boots before leaving the quarantine area, and wash their arms and hands carefully with chlorhexidine soap.
Farms with large populations and movement of horses, particularly of older foals and yearlings, will want to maintain a routine immunization program of all horses to reduce the incidence and severity of disease. On these farms, depending on the vaccination program including the type of vaccine used, all incoming horses should be isolated for 2 to 3 weeks and, although expensive, a series of nasal or preferably nasopharyngeal swabs taken during this time for demonstration of the organism or its DNA. Only then should these isolated horses join the rest of the group.
To date, the most important factors associated with increased risk of infection have been identified as:
1) Age: Horses 1 to 5 years old are more susceptible. Older horses are generally less susceptible to infection, but immunity can be overwhelmed in horses frequently exposed at shows or similar athletic events.
2) Serum concentrations of influenza virus-specific antibody: The importance of local mucosal protection is difficult to quantitate by methods currently available.
3) Frequent contact with large numbers of horses.
Although mortality rates are low, Equine influenza is highly contagious and the virus spreads rapidly through groups of horses in aerosolized droplets dispersed by coughing. The severity of clinical signs depends on the degree of existing immunity, among other factors. Horses that are partially immune can become subclinically infected and shed virus. Immunity to the same (homologous) strain of virus following natural infection persists for approximately one year.
Pneumonia was listed as the cause of fatalities at Broken Arrow with frequency. Pneumonia is a complication of various illnesses and not the cause of infection.
These symptom variations depend upon the cause of the pneumonia (fungi, virus or bacteria), the age of the horse (foals under 6 months of age, foals older than 6 months or horses of other ages) and the stress and living conditions the horse is experiencing at the time of his illness. There are two types of horse pneumonia: aspiration and rhodococcus. Aspiration is experienced most by newborn foals, and rhodococcus afflicts older foals more often, as well as adult horses with compromised immune systems.
Pneumonia in foals is very serious and often fatal in foals up to eight months of age. Failure to receive colostrum, overcrowding, cold and damp quarters, inadequate vaccination and deworming programs, recent viral respiratory illness, or any physical condition that weakens the foal may lead to reduced resistance to pneumonia.
Concerns involving moldy hay, salmonella and botulism remain high.
This list in incomplete and will be updated soon.