Skin Diseases

1. Ringworm (Dermatophytosis) "Girth Itch"

A fungal infection commonly transmitted from cats, rodents, or other horses.

Occasionally cattle will transmit ringworm.

A) Transmission

Direct contact via tack, brushes, animals, and environment that have the infected hair shaft or crust. Fungal spores can be infectious for over 12 months and thrive during fall and winter months. Wet warm weather with short daylight is an ideal fungal environment. Younger horses are most commonly infected due to decreased immunity. Abrasions are necessary to start ringworm therefore lesions are common around tack areas. Incubation is 1-4 weeks.

B) Diagnosis

Clinical appearance, hair loss, crusts and flaky skin. A fungal
culture of the hair roots is the best diagnostic aid.

C) Therapy

1)Self limiting and usually resolved in 1 to 3 months

D) Topical Treatment

1) Povidone iodine shampoo or solution.
2) Captan 2 Tbsp./gallon water (use sprayer or gloves - a known carcinogen)
3) .5% Bleach (1:200 dilution)
4) Thibendazole - 5% solution in 90% DMSO.
5) Sunshine
6) Good Nutrition
7) Chlorhexidine

E) Systemic Fulvicin/Griseofulvicin - Dosage has not been established and
effectiveness is questionable. Very expensive. Teratogenic (DO
NOT USE ON PREGNANT MARES)

F) Prevention

Isolate infected horses. Have individual tack and don't share
grooming equipment. Clean and wash all tack and equipment with
6% Clorox bleach at 1:15 dilution, povidone iodine, 3% Captan, 1%
lime plus 1.5% copper sulfate. Handle infected horses last and
always wash, it is contagious to people, especially children.

Matted tufts of hair and crusts. Occurs over the back and
shoulders, muzzle, eyes and legs. Most prevalent during rainy
and short sunlight days. Very similar in appearance and
pathogenesis to ringworm. Organism enters via abrasions in moist
skin areas. Sweating can cause generalized skin infections.

A) Diagnosis-Impression smears, culturing, and biopsy.

B) Clinical signs-The bacteria has a railroad track appearance on microscopic exam.

C) Treatment-Similar to ringworm

1. Maintain in a dry environment.
2. Usually self-limiting (4 weeks) if rainy season is not prolonged.
3. Clip and clean wounds. Wounds are painful. Responds to
antiseborrheic shampoo to remove crusts and debris followed by
daily antiseptic shampoos of providine/iodine, or
chlorhexidine.
4. Systemic procaine penicillin in severe non-responsive cases

 3. Papillomas (Warts)

Caused by the papilloma virus commonly found in young horses on the lips and muzzle, penis, prepuce, and occasionally generalized.

Self limiting but very contagious to young horses. Has incubation period of 30-60 days. Spread via insects, skin abrasions and punctures.

A) Therapy
Surgical removal or cryosurgery is the best. Spontaneous regression in 3-4
months. IV Immunostimulants have a reported success in prevention
and treatment. (EQ-STIM) Autogenous vaccines in severe cases. Don't use cattle wart vaccines.

4. Sarcoids (Non-Malignant tumor)

A common skin cancer of horses that occurs at any location of
the body. They may appear wart-like, nodular, ulcerative, or flat
sarcoids which mimic ringworm lesions. Sarcoids never metastasize internally but can spread through the skin.

A) Cause - Unknown-Spontaneous fibroblastic tumor

B) Therapy
1. Surgical excision and cryosurgery
2. No treatment
3. Immuno-therapy BCG- Injection into nodular lesions less than
2-3 inches in diameter every 1-2 weeks.
4. Chemotherapy - Cisplatin intralesional.
5. Indian Mud

1) Predisposed to older Grey mares.
2) May metastasize internally
3) Common under the tail and reproductive area.
4) Only remove if interfering with reproduction or urination.
5) Cimetidine and surgical removal show promise in control of
melanomas.

Common on the non-pigmented eyes and limbal region of the eyeball.

Also seen on the penis and prepuce. Surgically remove and cryosurgery.

Wear sun protection; shade during the day or fly mask to reduce UVA exposure.

Tattoo non-pigmented eyelids.

Benign ear lesions caused from chronic irritation from black fly bites.

Multiple smooth depigmented (white) plaques located on the inner surface of the ear pinna.

Occasionally located on anus, penis, and vulva. Lesions appear to be precancerous-like cells.

A) Diagnosis- Location and appearance

B) Treatment- Control with insect repellents and topical panalog or Desitin.

Multifractorial crusty, scabby, cracking dermatitis of the caudal pastern region.

Factors include moisture and dirt, photosensitivity (White areas), and infectious bacteria and fungus. Chorioptic mites maybe involved in refractory cases
especially in draft horses.

A) Therapy
1. Remove crusts - antiseborrheic or antibacterial shampoo
2. Clip and shave wounds
3. Topical treatment - best results if used under a soft wrap for
longer contact time. 
    a) Forte topical
    b) Panolog 
    c) Home made mix of DMSO, Thibendazole, dexamethazone, 
        and sulfanilamide.
    d) Silvadine cream
4. Penicillin or SMZ-TMP may be needed in resistant cases

9. Cutaneous Onchocerciasis
Hairlike parasite in the neck ligament (ligament UN nuchae). The adult worms produce larvae (microfilaria) that localize in the ventral central skin areas and the iris of the eye.

A) Clinical signs:
    1.Hair loss, dermatitis of the skin ventral midline.
    2.Recurrent uveitis
B) Treatment:
    1. Ivermectin- will kill the microfilaria only. Repeat at 3 week intervals
    2.Dermatitis - therapy
    3.Uveitis- See previous therapy

Influenza

1. History

A/equine 1 - Praque Czech-1956

A/equine 2 - Miami Florida-1963

A/equine 2 - Only virus isolated the last two decades. There are many

antigenetic variants including prototypes of A/E2 in 1979, 1981, up to 1996.

The most recent has been A/E2 Kentucky 93 incorporated in the flu

vaccine "Fluvac EHV 4/1 Plus".

The best vaccine in our opinion is the Intranasal Flu-> Modified Live Virus A/E2.

2. Pathogenesis
A) Inhaled aerosol, direct contact, water source, trailers, and personnel.
B) Incubation period is 1-5 days.

3. Clinical Signs
Dry cough, fever, serous nasal discharge, anorexia, muscle soreness. Lasts 1 to 3 weeks in the uncomplicated flu. Complicated by stress and secondary bacterial infections, may last several weeks. Continuous fever greater than 5 days with mucopurulent discharge indicates bacterial involvement. Flu can induce COPD (heaves).

4. Mortality
Rare - young foals with no maternal antibodies or CID. Morbidity - High in susceptible horses.

5. Diagnosis
Clinical signs are difficult to differentiate from Herpes/Strep in early stages, but all are treated the same. Nasal swabs within 48 hours of the fever, viral transport media - ice. Virus is hard to isolate. Serology - Two samples 3 weeks apart.

6. Treatment
A) Rest in clean, dry, dust free environment that is well ventilated. Recommend 1 week of rest for every day of elevated temperature.
B) Antipyretic if fever lasts longer than 3 days or is above 104 degrees.
C) Antibiotics should be given if a fever persists greater than 5 days and a muco- purulent nasal discharge occurs. Give penicillin 3cc per 100# of body weight in the muscle twice daily, SMZ/TMP 960 mg tablets - 12 tablets per 1000# body weight twice daily, or give Tucoprim (Sulfa) - 1 scoop per 500# body weight once daily in grain.
D) Immunostimulant drugs for quicker recovery. Can use Equimune IV weekly as needed.
E) Vaccinate with "Fluvac EHV4/1 Plus" to stimulate immunity.
F) Clenbuterol- bronchodiolator
G) Supportive care - Fluids, electrolytes, and food

7. Control
A) Vaccinate every 6 months with intranasal vaccine (The intramuscular flu may Only last 1-2 months).
B) Vaccinate every 1 1/2 to 2 months in high-risk environment.
C) Isolation of sick animals. Virus can be shed up to 18 days.
D) Reduce stress and provide clean, well-ventilated environment.
Avoid common water sources. 

1. History

EVH-1 - The most virulent and can cause respiratory disease, abortion, CNS paralysis and foal death.

EVH-3 - Coital Exanthema-VD

EVH-4 - A milder form causes respiratory disease and occasional abortions. Immunity is short lived in EVH-4 and is commonly seen as the "snots" in foals and yearlings. EVH-1 horses have immunity up to 1 year.

2. Pathogenesis
Same as influenza (coughing is not as common as with flu)

3. Clinical signs
Same as influenza
Latent carriers in lymphnodes and is expressed with stress.

Duration:
A) Respiratory form lasts 1 to 4 weeks.
B) Abortion - 10 to 20 days after exposure. Fetus is delivered
fresh in placenta. Occurs primarily during the last trimester.
C) Foal death - without maternal protection or if infected near term and born with herpes. The foals are weak and die within 7 days.
D) CNS - 8 to 10 days. Mild ataxia to paralysis and death. Can be progressive. Recovery is possible. "Dog sitting"position, loss of tail tone, and fecal and urine incontinence.

4. Mortality
Same as influenza

5. Morbidity
Same as influenza

6. Diagnosis
A) Same as influenza
B) Abortion: Send fetus to Clinical Pathology Lab
C) CNS - Send brain tissue
D) Serology - C
F) Test is valuable since titers increase and decrease very quickly. Need 2 samples two weeks apart.

7. Treatment
A) Same as influenza
B) Rest
C) Antipyretics with fever greater than 3 days.
D) Antibiotics with fever greater than 5 days.
E) Immunostimulants
F) Clenbuterol
G) Supportive therapy

8. Prevention
A) Slower to spread so isolate animals, quarantine new arrivals, two to four weeks.
B) Separate paddocks with no common water source. This will isolate the disease.
C) Abortions - Dispose and burn all tissues except for the use of laboratory diagnosis. Disinfect premises.
D) Vaccinate with Pneumabort K (killed) Herpes at 3,5,7, and 9 months of pregnancy.
E) Booster vaccinate foals and adults every 6 months. Vaccine is not effective in protection, but reduces the severity of the clinical signs and amount of virus shed.
Vaccinate every 6 months with Intranasal Influenza Vaccine in high-risk environment.

Equine Viral Arteritis

1. History
Rare, severe vasculitis and respiratory disease, with a high rate of abortions and stallions can be carriers and shed the virus in their semen. Estimated that 30-50% of stallions are carriers once exposed to EVA.
2. Clinical signs
Respiratory form - like flu and herpes. Edema in legs, head and prepuce, diarrhea.

Abortions - fetus severely autolyzed and can be at any stage of gestation.

3. Diagnosis
Serology - VN - Strong response and lasts for years. Virus is shed up to 14 days except in stallions. Viral isolation.

4. Treatment
A) Same as influenza
B) Control swelling

5. Control
A) Quarantine new animals.
B) Test stallion before breeding.
C) Vaccinate stallions in breeding operations. This is questionable because the vaccination may cause viral shedding in the semen.

Strangles/Distemper/Strep Equine

1. History
Worldwide bacterial disease of the upper respiratory tract called streptococcus equi.

2. Pathogenesis
Ingestion or inhalation initially causes an acute pharyngitis (throat) /rhinitis then localizes in the retropharyngeal and sub-mandibular lymph nodes within 3 days. Lymph node abscesses rupture and drain within 10 to 14 days, some cases are very prolonged.

3. Clinical signs- (incubation period of 3-20 days) Fever of 103 to 105 degrees, depression, mucopurulent nasal discharge, outstretched neck, pain when swallowing, difficulty breathing (dyspnea), enlarged lymph nodes. Some cases become disseminated to the lymph nodes in the body and are usually fatal, called Bastard Strangles. Purpura hemorrhagica is a rare sequela to strangles. Horses can spread disease for 45-60 days after clinical signs disappear.

4. Mortality
Rare, bastard strangles, purpura hemorrhagica

5. Morbidity
Near 100% in susceptible horses

6. Diagnosis
Clinical signs and culture. Strep zooepidemicus can abscess like s. equi.

7. Treatment
A) Rest in warm, dry, well ventilated area
B) Soft palatable feed with difficulty swallowing. May require tube feeding and water in severe cases.
C)Antibiotics - controversial - Antibiotics have recently been found to help Strangles and not cause Bastard Strangles
D) Hot pack and poultice abscessed lymph nodes. Numotizine is an excellent poultice.
E) Flush draining abscesses with 3% povidone/iodine solution. Establish good drainage.
F) Retropharyngeal abscesses can cause severe breathing and eating problems. See a veterinarian for feeding, hydration, and possible tracheostomy.
G) Bastard Strangles - Rarely respond to high doses of antibiotics. See your veterinarian.

8. Prevention
A) Hygiene - strep equi can remain viable for 2 months in a moist environment.
B)Some animals continue to shed several weeks after recovery in nasal secretions (45-60 days).
C) Quarantine new arrivals for 4 weeks.
D) Vaccination may reduce incidence and severity, especially in a face of an outbreak. Some vaccines require 1 to 2 boosters, then revaccinate annually. Protection immunity that follows an attack is short-lived. Individuals can suffer repeated attacks at 6-month intervals if a challenge is virulent (natural).

Purpura Hemorrhagica

1. Clinical signs
Severe swelling of the legs. A vasculitis secondary to strep infections, EVA, EIA, Potomic Horse Fever, or photosensitivity.

2. Treatment
A) Penicillin IM twice daily
B) Dexamethasone 25mg/1000# IV once daily and gradually reduce
10% per day over 2 to 3 weeks.
C) Banamine/Butezolidin
D) Hydrotherapy and walking

Chronic Obstructive Pulmonary Disease (Heaves)

1. History

Caused by allergies to molds in hay and straw, dusty, poorly ventilated environments and secondary to bacterial and viral respiratory infections. Also there is an increased chance of COPD with close contact between chickens and horses. Sources of mold are from bedding and forage. Bedding - straw is the highest source of mold, sawdust, peat, shavings and shredded paper are best.

Forage: Avoid moldy hay. Your eyes and nose cannot eliminate all moldy hay!!!

Avoid close contact between chickens and horses.

A) Wash down hay thoroughly before feeding. Don't allow drying. Feed on the ground. Soak hay for 30 minutes minimum.
B) Pasture is best.
C) Cubed or pelleted alfalfa and oats, but watch for stable vices or eating their feces caused by processed hay.
D) Clenbuterol is approved in the USA for horses.
E) Skin testing and hypoallergenic serums have questionable value.

2. Clinical signs
Alert, no fever, an occasional cough and exercise intolerant. Coughing increases with the progression of the COPD while eating or exercising. In severe cases there is an increase respiration rate, double expiratory effort and flared nostrils.

"Heave Line" develops along chest.

3. Diagnosis
Response to atropine, but can cause paralytic ileus and severe abdominal pain

4. Treatment
A) Corticosteroids - Dexamethasone, prednisone, Predef 2X, Vetalog
B) Bronchodiolators - Clenbuterol - (side effects are increased heart rate and sweating at higher doses) Increases mucociliary transport.

Anterior Uveitis (Recurrent uveitis), Moon Blindness

The leading cause of blindness in one or both eyes.

1. Acute uveitis
Usually traumatic related, corneal ulcers, neoplasia, onchocerciasis, or systemic infectious disease. Usually a good prognosis unless it becomes a recurrent uveitis.

2. Chronic recurrent uveitis
The cause is usually unknown but leptospirosis and onchaerca are occasionally diagnosed. Repeat episodes of inflammation followed by variable periods of clinical quiesense. Very poor prognosis for curing, but you can control or slow the gradual loss of vision. Appaloosas have the highest rate of uveitis.

3. Clinical signs:
A) Conjunctivitis
B) Glepharospasm
C)Corneal edema
D) Keratitis with vascularization
D) Iritis
E)Aqueous hemorrhage and precipitates
F)Synechia
G)Cataracts
H)Glaucoma

4. Treatment
A) Topical atropine 1% ointment 2 to 6 times daily
B) Topical anti-inflammatory ointments: .1% Dexamethasone, Decadron, Maxidex
C) Systemic treatments with Banamine twice daily for 1 to 2 days.
D) Systemic treatment with Bute or aspirin twice daily until swelling has resolved. E) Oral prednisolone (.25mg/# twice daily) used in resistant cases
F) Subconjunctival (eye injection) - Triamcinolone (Vetalog) S.C. or DepoMedrol every 2 to 4 days in severe cases and difficult treatment situations. Atropine S.C. Avoid cortisone in corneal ulceration.

5. Antibiotic ointments only in corneal ulceration.

6. Ocufen - Flurbiprofen - non-steroidal agent used in combination with cortisone in severe cases and in the face of ulceration. Diclofenac Sodium (Voltaren R), Indomethacin (Indophthal R)

7. Optimune Cyclosporin - shows promise in controlling uveitis.

Equine Protozoal Myeloencephalitis (EPM)

1. History
Protozoal parasite affecting the brain and spinal cord. Cultured and identified for the first time in 1991 as sarcocystis neurona. Primarily found in the eastern US and west coast mirroring the opossum habitat. Opossums the definitive hosts and birds are the intermediate hosts. Horses are an aberrant intermediate host.

2. Clinical signs
The "3A" presentation is signs of asymmetrical, ataxia and atrophy. Signs are variable since the lesions are located in different sites in the brain and spinal cord. Some include cranial nerve deficits (facial paralysis, unable to swallow, atrophy of muscles, etc.) falling, stumbling, ataxic, progressive to recumbancy. Long term lameness that can't be localized. Some seizure. Signs can occur at any age over 2 months. Incubation time of 1 month to 2 years.

3. Diagnosis
Immunoblot assay of serum or CSF fluid. CSF at lumbosacral region is most sensitive and specific due to persistent antibodies in the blood. Exposure rate in Oregon has been 45% via serology. Response to treatment in the first 2 weeks.

4. Treatment
A) Sulfadiazine 10mg/# twice daily orally.
B) Pyrimethamine .5mg/# once daily orally, an antifolate drug so folate supplementation may be necessary at 40mg/day. Give orally not on feed.
C) Anti-inflammatory IV DMSO, Bute or Banamine
D) Vitamin E supplementation 9,000iu per day
E) Treat a minimum of 4 months.

5. Prevention
Relapses are possible months later. No vaccines available. Limit opossum access from feed, garbage cans, dog and cat food, and maintain cleanliness.
Potomac Horse Fever

1. History
Ehrlichia risticii is the causative agent. This rickettsial disease is seasonal (Spring, Summer, Fall) and commonly associated with large water bodies. Suspect an insect, bird,or snail vector as a transmission agent. Three cases I've seen have been in the late summer / early fall in Central Oregon. Endemic in Northern California and Klamath Falls, OR. Very sporatic- Not direct transmission.

2. Clinical signs- Incubation period of 2 weeks.

Biphasic (2 rises) fever, diarrhea, limb edema, icterus, ataxia, petechiae of mucous membranes, ileus, colic, laminitis (can affect all 4 feet), death. Clinical signs last 3 to 16 days.

3. Diagnosis
Serology fourfold increase or decrease, granular inclusions in the cytoplasm of neutrophils and eosinophils in spoke wheel shapes.

4. Treatment
Tetracycline - aggressive fluid therapy and prevent laminitis

5. Prevention
Vaccines are 80% effective with short 2-4 month duration. Insect control and quarantining new horses have not helped. We need to find the carrier first.

Bacterial abscesses caused by bacteria called Corynebacterium Pseudo Tuberculosis. Occurs primarily during the summer and is spread possible by a fly vector. The last outbreak in Central Oregon was 9 years ago and associated with a drought period.

1. Clinical signs
Fever, lameness, nodular swellings develop commonly in the chest region hence the "pigeon breast" appearance. Abscesses have occurred commonly in the groin, prepuce and facial regions. Clinically looks like distemper (strangles) but is a different bacteria.

2. Morbidity
Moderate outbreaks appear cyclic every 7-10 years.

3. Treatment
Hot pack and poultices to bring the abscess to a "head". Establish good drainage to prevent persistence and recurrence. Have seen a couple cases go several months before finally breaking and draining. Avoid antibiotics unless the horse is lethargic and not eating. Use high doses of penicillin or erythromycin at 5-7mg/# four times daily in combination with rifampin 2.5mg/# twice daily. Also, SMZ-TMP with Penicillin.

4. Prevention
Fly control and repellants. Sanitation reduces flies. Drainage of exudate in a sealed container and proper disposal may avoid an outbreak. Permethrin is the longest acting fly repellant on the market. Distemper/strep vaccine has been used in an outbreak situation but is not effective in preventing the Rhodococcus or Corynebacterium abscesses.

5. Mortality
8% External Abscesses/ 40% Internal Abscesses.

Tetanus

1. History-Wounds, muscle and sole bruises, castration, foal navels, neuritis, dystocia, injuries, retained placentas, etc… caused by a clostridium bacteria. In an anaerobic (no oxygen) tissue environment, the bacteria release potent exotoxins. Clos. Tetani is a common inhabitant of the intestinal tract of humans and animals and is abundant in the soil. Horses have a high susceptibility to tetanus exotoxin. Species susceptibility in order is sheep, goats, horses, cattle, humans, dogs, cats, and rodents. Due to the high incidence of wounds and punctures, horses are a prime candidate for acquiring tetanus.

2. Clinical signs
Three days to several weeks depending upon the proximity to the CNS. Average is 2 weeks. Prolapse of the 3rd eyelid, flared nostrils, sawhorse stance, raised croup, muscle spasms and paralysis. Masseter muscle is usually the first affected then spasms progress to the muscles of the neck, trunk, and finally the limbs. Convulsions (seizures) occur with external stimuli. Salivation and reluctance to eat especially off the ground is common. Duration is approximately 6 weeks and muscle spasms may persist for months. Death results from respiratory (diaphragm) failure.

Secondary signs: Laminitis, myositis, Aspiration Pneumonia, and pleuropneumonia.

3.Treatment- IV catheterization is best to avoid inducing seizures with intramuscular administrations of medications.
    A) TAT 100 units/kg x 500 = 50,000 units every 3-5 days SQ, IM or IV 
    B) TAT intrathecal (in brain cavity) via cistern puncture; 30ml in foal, 50ml 
    in adult equine
    C) Penicillin 3cc/100# twice daily
    D) Clean and debride obvious wounds
    E) Tranquilizer (Acepromazine or Chlorpromazine)
    F) Dark, quiet stalls. Cotton in ears. 
    G) Supportive care as needed for water and nutrition.

4. Prevention
    A) Tetanus toxoid annually and repeat tetanus toxoid with an injury if vaccine   
    has been longer than 6 month ago.
    B) Tetanus antitoxin in unvaccinated or young foals last 3 weeks. Serum
    hepatitis is a risk with antitoxin. Injury in horses with questionable vaccine
    history need a tetanus toxoid and antitoxin with a toxoid booster in 3 weeks.

1. History
Viral disease (Lentivirus). Spread primarily via horse flies, deer flies, needles, equipment, or transplacentally. The virus only survives 1-2 hours out of the horse.

2. Signs
Fever, anemia, ventral edema, and weight loss.

3. Testing
Blood sample taken by your veterinarian and sent to your state laboratory to have a Coggins Test performed.

4. Treatment
None Known.

The viruses exist in a host population of birds. The viruses are spread by mosquitoes to horses. It affects all ages of horses, but is rare in foals.

1. Clinical signs:
    A) Docile horses can become aggressive.
    B) Anorexia
    C) Will not drink
    D)Fever/Depression
    E)Head pressing, circling, and blindness
    F)Seizure, coma, death

2. Prognosis:
    A) Poor- recommend euthanasia

3. Prevention:
    A) Vaccinate in the spring or when traveling south or east!!

This is a neuromuscular disease. The Botulism toxin blocks the acetylcholine release at the N-M junction. The horse is always bright and alert with no depression. This disease is so easy to differentiate from other CNS diseases because of clinical signs.

1.Cause:
    A) Contaminated feed or stagnant water.

2. Clinical signs:
    A) Progressive flaccid paralysis
    B) Difficulty swallowing, salivation, dropping food
    C) Short gait- difficulty breathing
    D) Death from respiratory failure

3. Treatment:
Botulism Antitoxin- Used in human medicine for muscle spasms.

4.Prevention:
1. Clean food and water sources
    A)Vaccines are good

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