Botulism in horses is rather rare, but is usually fatal. It is caused by toxins
produced by the bacteria known scientifically as Clostridium botulinum. The
botulism toxins act on the peripheral nervous system by preventing transmission of the
nervous impulses. These toxins are found in the soil and in decaying plant or animal
matter. Adult horses and foals usually less than 8 months old can be affected.
Horses that have phosphorous or protein deficiencies often ingest the toxins that cause
Botulism. The signs will develop within 3 to 7 days. Foals will show signs of impaired
suckling, inability to swallow, decreased eyelid and tail tone and dilated pupils. The
adults will exhibit many of the same signs and eventually show muscle weakness, tremors
and collapse. Death is due to respiratory paralysis in both the foal and the adult.
Horses are among the most susceptible species. If caught early, there is a polyvalent
equine antitoxin (an antibody produced in response to a toxin from the bacteria) that is
active against several types of the organism. This antitoxin has improved the chances of
survival in the horse.
The toxins produced from Clostridium botulinum can be avoided by insuring a
good source of clean hay, feeding areas, and grazing locations.
For more information see: http://vm.cfsan.fda.gov/%7Emow/Chap2.html
Equine Encephalomyelitis, also called "Blind Staggers" or "Sleeping
Sickness", is an infectious disease that affects the brain of the horse. There are
three strains that have been identified: Eastern, Western and Venezuelan - with the
Eastern strain occurring more frequently and having the highest mortality.
The cause of Encephalomyelitis is a virus. Reservoir hosts include birds, reptiles and
rodents. The mosquito acts as the vector that transmits the virus from the reservoir to
the horse. Therefore, most infections are apparent from mid-summer to frost. Although
horses can spread the disease to one another by rubbing noses or sharing feed and water
containers, they are considered dead end hosts because they have such a low viral count
that it is highly unlikely that feeding mosquitoes can pick up the virus from them.
Clinical signs are first seen 5 days after infection. The symptoms start off with fever
and depression. They then progress to diarrhea, an overall drowsy appearance and no desire
to move. Some owners have described personality changes including self-mutilation,
hyperexcitability, irritability and a refusal of food and water. CNS signs include
incoordination, head pressing, circling, paralysis, convulsions and coma. Death occurs 2-3
days after the first signs appear.
Treatment is mainly supportive in a shaded well padded area. If symptoms are severe,
food and water may need to be forced into and manually evacuated from the animal. If lying
down for long periods of time, the horse will need to be rotated to prevent sores.
Mortality is high and if the horse survives, it is usually considered a "dummy".
As for prevention, immunization and mosquito control are recommended. The first vaccine
should be given prior to mosquito season in the spring or early summer and be followed by
a second vaccination in two to four weeks. Immunization lasts six months and needs to be
repeated yearly.
Equine Infectious Anemia (EIA), or Swamp Fever, is a viral disease which occurs
worldwide. Signs include a high fever, labored breathing, a pounding heartbeat, and
exhaustion. As the disease progresses, signs of anemia develop. Horses that recover
usually remain carriers of the disease. Most infected horses die within 30 days of getting
the disease.
The disease is usually spread by horse flies biting an infected horse, then biting a
healthy horse. The disease can also be transmitted by the use of non-sterile needles and
blood contaminated surgical instruments.
There is no cure for EIA so prevention is the key to controlling the disease. The
Coggins Test is a simple blood test that is widely accepted as a way of determining
carriers of the disease. A Coggins Test is often required to transport, show, sell, or
board a horse. Coggins Tests should be updated yearly. Owners of positive horses have to
make the choice to put the horse down (euthanized), or have the animal permanently
quarantined.
For more information see: Equine Infectious Anemia.at http://www.horseadvice.com
James Rooney, a recently retired Doctor of Veterinary medicine from the University of
Kentucky, identified a mysterious neurologic condition in 1964 that later gained the name Equine
Protozoan Myeloencephalitis. The name literally means Horse disease caused by a
protozoan (organism) that affects the muscles of the central nervous tissue. Ten years
later research teams recognized the protozoa and learned the extent of distribution of
what was once thought a rare disease.
The organism, Sarcocystis neurona, a single celled animal, can cause a
neurological disease in equines of any age, sex, and location throughout the USA. The
parasite cycle involves two animals: birds eat both plants and other animals of prey that
carry the sporocysts of the organism. The opossum, the host responsible for ultimately
carrying the protozoan to the horse, eats birds killed by the effects of the disease. The
organism reproduces sexually in the opossum and is passed out in the feces. The horse
picks up the organism by eating opossum feces dropped in feed or hay. The horse is a
dead-end host, meaning the horse is non-contagious.
A growing problem? Many scientists and veterinarians alike have come to a realistic
idea that this disease has been present for longer than twenty years, while considering
the rise of incidence. In the start of the infection horses will display asymmetric
incoordination (or incoordination on one side of the horse or the other), and loss of
proprioception (or loss of sense of awareness of the position of the limbs). People may
confuse this with a lameness . Not all horses exposed to EPM will show signs and some may
develop an immunity and fight off the disease. Variations of the clinical signs depends on
how much tissue damage is done, and may include various levels of seizure, muscle atrophy
(leading to loss of ability to use muscles), and facial paralysis.
Antiprotozoal drugs are used in treating EPM, which drugs which kill the protozoan. The
most common is trimethoprim-sulfamethoxazole, an antimicrobial. Anti-inflammatory therapy
is recommended and supplements of vitamins E and folic acid may aid in treatment. The
prognosis is variable. Approximately 60% respond to the therapy. Some undesirable effects
of treatment may occur, and depending on the amount of nerve tissue damage, there is no
reversibility with treatment.
The best preventative to EPM is to control the contact between opossums and your horses
in and around your barn. Keeping all food covered and out of range is an essential
practice (especially if there is cat food around). Any person with a trained and precise
eye should consider EPM when evaluating a lame horse. The key is to catch the disease
early in order to effect a full recovery. There is also a higher incidence in stressed
horses; for example, a race track may have an 80-90% occurrence rate. It is helpful to
know that the disease takes a minimum of two weeks to two years from exposure to time it
shows signs. There is presently no vaccine, and labs estimate 20 years before an effective
vaccine is available.
Founder or laminitis is the is the swelling of the inner lining of the hoof. The feet
are hot to the touch due to the increased arterial blood supply. Some signs that horses
may show are weight shifting between feet or walking abnormally. The horse may refuse to
eat, sweat and tremble. The hooves may begin to grow unusually and should be trimmed
often.
Causes of founder vary. It may be linked to excessive amounts of grain or lush pasture,
drinking a lot of cold water while still hot from exercise or severe exercise on hard
surfaces may also cause founder, although some causes are still unknown.
Treatment depends on the severity of founder. Acute founder is treated by change of
diet or cooling of the feet with ice baths or standing the horse in thick mud. Encouraging
but not forcing the horse to walk on soft ground, which may increase circulation in the
hoof, may be recommended. Chronic or long term founder is treated with prescribed
anti-inflammatory drugs and corrective trimming and shoeing.
Osteochondrosis Dissecans is a major bone disease in young horses. This condition can
be seen in any joint through out the horse's leg. OCD can cause lameness to come on
quickly or it may not show up until the horse is stressed by hard exercise.
The major cause of lameness is that the cartilage in the joint starts to flake away
from an area around the joint. This is usually due to a nutritional problem that developed
in the first few months of the foals life. The foal may have had a lack in nutritional
needs, excessive levels of zinc in the diet, uneven levels of calcium and high levels of
phosphorus.
To help prevent OCD in foals you should try the following. Raise the foal on a pasture
with little stall time; feed the foal a high quality diet; being careful about feeding
grains to foals that are rapidly growing ; and lastly regular feeding of alfalfa hay (give
1% of body weight).
Once a horse becomes lame with OCD there are only a few choices to consider when
thinking of treatment. Surgery may be performed to remove loose cartilage around the
joint, therapy could be a consideration, or enforcing rest and lowering the nutritional
diet.
Nutrition is a very important key in prevention of OCD and should be greatly
considered. Evaluation of your horses diet maybe needed to take the proper precautions
against this disease.
For more information see: Osteochondrosis Dissecans (OCD) in
Horses at http://www.horseadvice.com/
Rabies is a highly fatal, contagious disease that affects the central nervous system.
The rabies virus is transmitted from animal to animal, or animal to human through direct
contact with saliva of an infected animal. This direct contact can be a bite wound, or
from getting saliva into an existing wound. In horses, a direct bite wound is the most
common means of transmission. Domestic dogs and cats, along with skunks, foxes, raccoons,
and bats can carry the rabies virus.
The two main signs of rabies in horses are depression and incoordination. Along with
these signs, a horse with rabies will also have signs similar to those of lameness and
colic. More signs of rabies are a fever, loss of appetite, muscle spasms of the third
eyelid, blindness, urinary incontinence, and restlessness.
Rabies in horses is always fatal. A proper diagnosis is nearly impossible since the
signs resemble those of more common horse diseases. The best prevention of rabies in
horses is to properly vaccinate the animal once a year. If the animal is a new addition to
a stable, and no vaccination history is known, then contact a local veterinarian and set
up a vaccination schedule immediately.
For more information see: Rabies in Horses at http://www.horseadvice.com
Scratches is a chronic skin infection of the pasterns and fetlock regions (lower leg).
Other names for this include Seborrheic Dermatitis, Grease Heel, Mud Fever, and Scratched
Heels. Predisposing factors are white legs, heavy horses, and unsanitary conditions.
A number of causes can lead to Scratches. The one most often blamed is the bacteria, Staphylococcus
aureus. Others included mange, fungal infections, photosensitization, and immune
problems. Secondary bacterial infections are also common. Usually, rear limbs are affected
and if not treated it can lead to severe lameness.
Swelling, pain, hair loss, and ulceration at the heels are the beginning stages. This
can lead to eventual thickening of skin and abnormal masses. Lameness ranges from mild to
very severe at all stages.
Clipping the hair and cleansing with warm soapy water are the first steps taken. All
scabs should be removed before a topical astringent is applied. Other popular remedies
include petroleum products and antibiotic salves. In chronic or severe cases, antibiotics
(steroids) and cauterization or cryosurgery on the affected area might be necessary.
Keeping horses out of muddy pastures or unsanitary conditions cuts down on the
likelihood of acquiring Scratches. The prognosis greatly increases with early detection
and treatment. Daily grooming and a conscientious owner will help your horse friend lead a
Scratch free life.
Strangles is a highly contagious upper respiratory infection of horses. The cause has
been identified as a bacteria. The disease has a low mortality rate yet the economic
ramifications due to long recovery periods can be of great consequence. The disease is
contracted through environmental contamination, nasal discharge, or direct contact with
infected animals.
Within two to seven days after contamination the infected animal will run a high fever
of 103-106 F. They will exhibit a loss of appetite, a moist cough, and a clear nasal
discharge that will become yellow, and difficulty in breathing and swallowing (hence the
name). This upper- respiratory inflammation then spreads to the submandibular lymph nodes
(below the jaw) which eventually abscess. Signs can range from minor to major. The most
severe form involves inflammation of all lymph nodes (Bastard Strangles).
Treatment consists of supportive care, which involves keeping the animal warm and dry,
isolating the patient from other animals, and offering soft foods. Hot packing of the
abscesses speeds up formation of pus. The antibiotic of choice is penicillin if used
before abscess development. Penicillin used after abscess formation slows recovery.
There is a vaccination available yet efficacy is low and the duration is short. The
best prevention is to isolate new animals, optimally for a month. Any horses with upper
respiratory signs should be avoided and/or watched closely for further problems.
Tetanus, also known as Lockjaw, is an extremely serious disease of the central nervous
system that kills thousands of horses in the U.S. every year. The bacteria causing tetanus
is found worldwide and therefore every unvaccinated horse is a potential victim.
The disease is caused by a toxin released by the bacteria Clostridium tetani.
This bacteria is normally found in the intestinal tract of horses and is passed in the
feces. The spores are always present in the soil in any horse facility. The bacteria is
anaerobic, meaning that it multiplies in areas where oxygen is not present. Deep puncture
wounds that are contaminated with dirt are ideal locations for tetanus to flourish.
Tetanus may lie dormant in the animal for as long as 6 months. Therefore the onset of
signs may be months after the original injury. The veterinarian may have to rely on signs
rather than the presence of a contaminated wound to diagnose the disease.
The first sign is often the inability to open the mouth to eat and drink. The eyes will
be wide open and the ears rigid. This is followed by stiffness and rigidity of the entire
body. The horse becomes extremely sensitive to sounds, sights and touch. One way to
distinguish tetanus from other neurological diseases is the movement of the third eyelid.
It will close uncontrollably when the horse is stimulated by clapping your hands.
General stiffness progresses to convulsions and death in 75-80% of cases. If the horse
makes it through the first week chances of recovery are good but full recovery may take
many months.
Treatment is mainly supportive. The horse should be kept in a dark, quiet place with
plenty of padding to prevent injury. Adequate nourishment and fluid intake must be
monitored. Sedatives and muscle relaxers should be administered along with the tetanus
antitoxin.
Vaccination with tetanus toxoid is a highly effective preventive. It is given in two
doses four to eight weeks apart followed by a booster every year thereafter. Broodmares
should be vaccinated four to eight weeks before foaling in order to impart passive
immunity to the foal. The foal can then receive its first injection at three months of age
since maternal immunity will not interfere with the vaccine.
If an unvaccinated horse is wounded, it should be given the tetanus antitoxin to confer
immediate protection. However, this protection is short-lived so the horse should be given
the toxoid vaccine at the same time and then be boostered in 4 weeks.
For more information see:
Guidelines for Vaccination of Horses at http://www.thehorse.com/archives/forum_0695.html
Cervical Stenotic Myelopathy (CSM) is also known as Wobblers. It is characterized by
poor coordination and weakness because it attacks the spinal cord by the cervical
vertebrae. The exact cause is not well known, but CSM is believed to be hereditary in some
cases. Male horses under the age of 3 years are most susceptible.
There are many signs of CSM, but they are all related to the incoordination. You may
see clumsiness, swaying body, misplaced steps, or exaggerated leg action. Rear limbs are
most severely effected. A horse may drag its toes or knuckle over at the fetlock. Signs
may worsen when the horse is circled or its head is elevated. You may see neck pain and
muscle deterioration if nerve roots are involved.
Wobblers may be diagnosed by finding abnormal ossification or hardening of parts of the
vertebrae. Dislocation of adjacent vertebrae, or overgrowth of the top layer of vertebrae
may also be seen. Overall abnormalities of vertebrae may help single out the disease as
well. Narrowing of the vertebral canal, the canal the spinal cord is covered by, may also
conclude CSM. To definitely diagnose CSM, a myelogram, a recording of the spinal cord
after a dye has been injected into it, can be performed.
For more information see: Wobblers at http://www.horseadvice.com
1 By Tracy Campbell, Becky Huber, Pam Fuller, and Liz Kaestner, Blue
Ridge Community College Veterinary Technician Program Class of 1997
2 By Toni Daughtry, Tracy Diehl, and Christine Lacy, Blue Ridge Community
College Veterinary Technology Program Class of 1997
3 By Katie Beeson, Robbie Johnson, and Carrie Miller, Blue Ridge
Community College Veterinary Technology Program Class of 1998
4 By Niki Grow, Susan Molden, and Amie Reynolds, Blue Ridge Community
College Veterinary Technology Program Class of 1998
