Equine Diseases & Conditions

Equine - Diseases & Conditions

Horse head

GASTRO-INTESTINAL PARASITES OF HORSES IN BRITAIN

There are over a dozen different species of worms which infect the gastrointestinal tract of horses.

In Britain all grazing horses acquire a mixed infection with various gastro-intestinal parasites early in life. The development of disease depends on the numbers and species present which, in turn, depends on various environmental and epidemiological factors. Although mixed infection is the rule various specific disease syndromes may emerge. For example, in the young foal strongyloidosis, in the older foal parascariasis and in animals over 3 - 6 months of age strongylosis and oxyuriasis.

STRONGYLOIDOSIS

Infection with the threadworm Strongyloides westeri is common in foals aged two weeks to four months but seldom persists in animals over 6 months of age.

LIFE CYCLE

Only females are parasitic. Foals infected by larvae in mares* milk, or skin penetration.

CLINICAL SIGNS

Uncommon. In severe infections diarrhoea may occur between 2 - 4 weeks of age. Older foals may have high faecal egg counts without any clinical signs.

EPIDEMIOLOGY

The main source of infection for foals appears to be the reservoir of larvae in the tissues of the mare. It is possible that in the immune foal or older animal infective larvae penetrating the skin may be inhibited in development until triggered to migrate to the mammary gland in late pregnancy/early lactation.

DIAGNOSIS

This is based on the presence of large numbers of typical, small, thin-shelled eggs in the faeces.

TREATMENT

Fenbendazole (panacur) or oxbendazole.

PARASCARIASIS

Heavy infections with the roundworm Parascaris equorum are extremely common in foals and yearlings, the main problem is unthriftiness.

LIFE CYCLE

The adult male and female parasites (15-50 cms in length) live in the small intestine and produce circular, sticky eggs which are passed in the faeces. These develop to the infective stage, which is the egg containing the larvae, in a minimum of 10-14 days, and foals are infected by ingesting these eggs. P. equorum larvae migrate through the liver and lungs to their final site in the small intestine. In the susceptible foal this migration is completed within 4 weeks of infection, but the

CLINICAL SIGNS

The clinical signs of parascariasis include fever, nasal discharge, coughing, unthriftiness, colic and, rarely, intestinal rupture with subsequent peritonitis.

EPIDEMIOLOGY

The important factors in the epidemiology of P. equorum are the high egg output of the adult worms and the ability of these eggs to survive for several years in the environment. The sticky outer coat enables the egg to adhere to stable floors, fittings, etc., and may facilitate passive spread of infective eggs.

DIAGNOSIS

Parascariasis should always be considered in the differential diagnosis of unthriftiness in foals. Patent infections may be confirmed by the finding of typical, brown, thick-shelled, spherical eggs in faeces, but faecal egg counts may vary tremendously from day to day.

TREATMENT

All classes of anthelmintic have good efficacy against adult stages but much less effective against migrating/immature ascarids. Proven regimens for larval stages are fenbendazole and ivermectin.

CONTROL

Since it is extremely difficult to remove infective material already present, control measures should be aimed at preventing further contamination of the environment. This will be achieved by 4 - 6 weekly anthelmintic treatment of foals from 1 - 2 months of age onwards to remove developing parasites and thus reduce the number of infective eggs which would otherwise become available for foals of the same or succeeding generations. Where possible mares and foals should avoid, for several years, pastures previously grazed by young animals.

STRONGYLOSIS

Common infection with mixed strongyle species but dominated by cyathostomes. Large strongyles, especially Strongylus vulgaris now very rarely detected (<5% prevalence) in countries where modern anthelmintics widely used. Strongylosis occurs in horses, ponies and donkeys of all ages but young animals are more susceptible.

AETIOLOGY/EPIDEMIOLOGY

2 subfamilies of parasites, the Strongylinae, and the Cyathostominae

PATHOGENESIS

Larval stages rather than adults are responsible for the main pathogenic effects. Ill thrift/weight loss is due to protein losing enteropathy (intestinal damage). Colic may be due to either intestinal motility changes and/or disrupted intestinal blood flow and/or irritation of the gut lining. Large strongyles may cause incidental blood loss when feeding on the gut lining resulting in anaemia. Diarrhoea is a feature of larval cyathostomiasis arising at times of synchronous, mass emergence into the lumen of larvae arrested in development within the large intestinal lining.

CLINICAL SIGNS

ill-thrift/weight loss, poor coat condition
colic; maybe severe, or recurrent bouts
lethargy, poor performance
diarrhoea (cyathostomiasis only)

DIAGNOSIS

Surprisingly difficulty and usually presumptive, faecal and blood tests may help.

TREATMENT

- anthelmintic - larvicidal oral doses:

either ivermectin
or oxfendazole
or fenbendazole
analgesics, antidiarrhoeals etc.

CONTROL

Although control programmes on different horse establishments will vary according to conditions, the following measures will dramatically reduce the level of infection:

Treat ALL animals with a broad spectrum anthelmintic.
Treat new arrivals and isolate for 72 hours before allowing them to join resident animals.
Change to unrelated compounds once yearly to avoid drug resistance problems.
At the end of the grazing season, if the animals are to be housed, treatment with ivermectin, oxfendazole, or a high dose of fenbendazole will reduce the numbers of developing cyathostome larvae and prevent disease in the spring.
Stress management factors such as good stable hygiene; bi-weekly collection

LARVAL CYATHOSTOMIASIS

Commonest cause of diarrhoea in the horse in the U.K. More common in young animals (<4 years, but not foals and may occur in aged animals) during late winter/early spring (but any month possible).

PATHOGENESIS

Mass, synchronous emergence of mucosal larvae from arrested development causes intestinal inflammation giving rise to sudden onset clinical signs which become chronic. The condition varies in severity and some cases may not have obvious disease but show only weight loss.

CLINICAL SIGNS

Diarrhoea
Weight loss - often rapid and may be only sign
colic
peripheral oedema

TREATMENT

Ivermectin, oxfendazole and fenbendazole are effective wormers. Drugs such as codeine phosphate or corticosteroids may be useful along with supportive nutrition in the form of a high protein diet.

PROGNOSIS

Fair, about 40 percent of cases recover.

TAPEWORM INFECTIONS

Anoplocephala spp. are acquired by ingestion of cysticeroids in mites with herbage. Occasionally specimens 4-5 cms long and resembling large flukes are found in faeces.

A. perfoliata occurs in the small intestine and caecum near the ileo-caecal valve, in the lumen of the valve itself, and is often seen in association with erosive change in the gut lining. A. perfoliata infection is very common in healthy horses but it has recently been implicated as a cause of disease e.g. intussusception. Treatment with pyrantel (Strongid-P) is effective.

EQUINE COLIC

Colic is defined as simply being 'abdominal pain'. It is not a diagnosis in itself, purely a clinical sign of an underlying problem. It may be manifest as one of the following.

inappropriate recumbency
flank watching/kicking
abnormal posture
rolling
depression
restless walking
stretching to urinate

Some causes of colic can be fairly easily diagnosed after clinical examination, and the primary aim of the initial examination is to identify those cases with a mild or uncomplicated disease process from those which require further investigation and/or surgery. It is important to bear in mind that disorders associated with colic are dynamic and rapid, with progressive change of the condition commonly occurring. At each examination the veterinary surgeon may have to alter their diagnosis and/or change the treatment plan to deal with the developing situation. The majority of colic cases are however relatively mild and respond to painkilling therapy.

Colic can be caused by a wide variety of problems such as spasmodic colic, impaction, gut stricture, tumours, adhesions of the bowel, infection (enteritis, peritonitis etc), grass sickness, abnormal twisting of bowel, displacement of the bowel, herniation, parasites, inflammatory, or ulcerative disorders.

In approaching a diagnosis your veterinary surgeon will consider the age, sex, breed, management factors, breeding history (if relevant), previous medical history, nature of the current problem, duration, progression, faecal production, degree and location of pain, abdominal distension, temperature, gut movement, and cardiovascular status. In carrying out this assessment rectal palpation, stomach tubing, blood tests, and sampling the peritoneal fluid (abdominal fluid) may provide important information.

Treatment depends entirely on the presumptive diagnosis, in mild colic painkillers/antiflammatories are often sufficient. Drugs to slow, or speed up, intestinal movement are frequently employed, as are compounds to prevent a generalised toxaemia developing secondary to bowel damage. Dehydration may require intravenous fluid therapy for correction. Antibiotics should only be used in cases of colic developing as a result of bacterial infection.

In those cases which do not respond to medical therapy, or a definite diagnosis has been made of a surgical condition then surgery is the next step. Frequently this requires referral to a specialist centre.

It is pointless to attempt to give a comprehensive explanation of colic, the possible causes, symptoms, and treatments here. Every case can be different, always rely on your veterinary surgeon for advice on each individual case.

GRASS SICKNESS

Though principally a disease of horses and ponies it has been recorded occasionally in donkeys and once in Zebra.

Previously it had a limited geographical incidence, being confined mainly to Scotland, but it is now increasingly recognised in England and Wales

AETIOLOGY

The disease is apparently not contagious, but despite intensive investigation its cause is still a mystery. It is virtually always associated with grazing but there appears to he no constant association with any type of grass, pasture or plant. Some confirmed cases have had no access to grass. No infective agent has ever been isolated. No bacterial or other toxic factor has ever been found in intestinal contents. Climatic change, especially mild weather (? with sudden grass growth) following frosty/cold periods, may be associated with occurrence of clinical cases.

EPIDEMIOLOGY

The overall incidence in Scotland is estimated at about 0.5% annually, but the incidence is uneven and varies quite widely from district to district. It is generally higher in the north east of the country. In any particular year cases tend to be concentrated in certain localities. It is quite common to find more than one case on the same premises in the same year. Occasionally the disease assumes ‘outbreak" proportions.

The peak period for Grass Sickness is April/May but seasonal occurrence of this disease is much less marked than previously. Occurrence of Grass Sickness in the winter months is no longer very uncommon.

The disease can occur any any age from 9 months onwards, but most affected animals are between 2 and 7 years old.

The disease is commoner:

on premises where the disease has occurred previously
in horses that have been on the premises for less than two months
in horses kept outdoors all the time
when no supplementary roughage is fed (feeding of concentrates appears to make no difference)

CLINICAL SIGNS

The clinical signs of Grass Sickness are all referable to sympathogotonia (dominance of the sympathetic side of the autonomic nervous system) and subsequent dehydration. Although it is usual to describe acute and chronic forms separately, with intermediate forms classified as subacute, it is probably more appropriate to consider the disease as a single entity whose course and clinical manifestations depend upon the extent and severity of neurone damage in the autonomic ganglia. Acute and subacute cases invariably die but, with dedicated nursing, selected chronic cases very occasionally survivie.

The most striking effects are on the gastrointestinal tract. Peristalsis and gland secretion are inhibited, resulting in intestinal stasis and closure of sphincters throughout the length of the alimentary tract.

Chronic form

emaciated carcass
marked reduction of intestinal size
dry, firm, large intestinal content

TREATMENT

euthanasia
selected chronic cases may survive given nursing/supportive therapy and use of intestinal prokinetic agent, cisapride.

PROPHYLAXIS

There is very little one can ever suggest. It might help to keep horses indoors for at least part of every day during periods of peak incidence. This applies particularly to young or newly-arrived animals, or when a case of grass sickness has already occurred on the premises. Such horses should also be fed supplementary hay.

EQUINE STRANGLES

An inflammatory disease of horses affecting principally the upper respiratory tract with lymphadenitis of adjacent lymph nodes. The cause is Streptococcus equi, but other streptococci may be involved as secondary invaders.

INCIDENCE

The disease is worldwide in distribution amongst young horses, particularly where they are kept in large numbers. The morbidity rate may vary from 10% to nearly 100% in any infected batch and is dependent upon previous exposure and the age of the animals concerned.

Horses of 6 months - 3 years of age are most frequently affected but older animals reared in isolation may be susceptible. The mortality rate is usually low (1-2% at most).

Infection occurs by aerosol and becomes established on the mucosa of the upper respiratory tract and pharynx. Inflammation of these mucosae results from the production of toxins and enzymes and streptococci are carried to the local lymph nodes where they cause lymphadenitis and abscessation. This abscessation may become so pronounced that discharge to the surface takes place. Occasionally systemic spread occurs to other organs to cause meningitis, arthritis or lymphadenitis in other parts of the body.

Local spread of pus in the pharyngeal region may lead to infection of the guttural pouch in up to 45% of cases.

Recovery is associated with the production of antibodies, these prevent further systemic invasion although they do not prevent surface transfer of the organism.

Infection may accompany or complicate viral infections of the respiratory tract and may persist in mesenteric or other lymph nodes when systemic spread has occurred.

EQUINE INFLUENZA

Equine influenza occurs as an epizootic, viral disease characterised by a tracheobronchitis in adult horses and a primary viral pneumonia in foals. Horses of all ages are susceptible but infection is most common in young (<3 yrs) unvaccinated animals. The principal clinical sign is coughing.

INCIDENCE

Worldwide occurrence as a major disease of economic importance. Extensive use of killed vaccines has reduced the severity of clinical disease and degree of viral shedding but when new antigenic variants emerge, explosive outbreaks of disease can occur.

Large amounts of virus are aerosolised due to the frequent cough. Short incubation period (1-3 days) with viral shedding for about 10 days. Rapid transmission of virus over long distances make isolation virtually impossible.

CLINICAL SIGNS

- Cough - sudden onset; group affected; harsh and dry
- fever, dullness, lethargy, anorexia
- bilateral, serous or mucopurulent nasal discharge
- increased respiratory rate and harsh respiratory sounds
- ± conjunctivitis/muscle stiffness/limb oedema.

Signs are less severe in vaccinated animals. Rare complications occur including bacterial bronchopneumonia.

DIAGNOSIS

Based on history and clinical signs, virus isolation form nasopharyngeal swabs and paired serology samples.

TREATMENT

Rest, minimum 3 weeks.
Reduce environmental dust/moulds.
antibiotics prophylaxis.
antiflammatories to reduce fever and muscle stiffness.
+/-bronchodilators and mucolytics to ease respiration.

CONTROL

Outbreak

virtually impossible, aerosol transmission over hundreds of yards.
strict rest and isolation of affected cases.
cease training of susceptible in contacts.
vaccination of healthy in contacts.

Vaccination should be carried out, firstly with 2 doses 3-6wks apart then 6mth booster followed by annual boosters.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

(Chronic Small Airway Disease, Broken Wind, Heaves, Chronic Bronchiolitis, Chronic Emphysema)

INTRODUCTION

COPD is one of the most common causes of chronic coughing in the horse. The disease is thought to be caused primarily by a hypersensitivity to organic dust antigens, though a great many epidemiological factors are important in the development of this disease. The end result of a combination of different insults is the response of the lung manifested as clinical signs which are recognised as COPD.

EPIDEMIOLOGY

In most cases the disease has a seasonal occurrence coinciding with the winter months of the year when horses are housed in often poorly ventilated environments, and exposed to high concentrations of the causative antigens - mostly from poor quality hay and straw. The disease is virtually never seen in animals under 2 years old and incidence increases with age.

AETIOLOGY

Several factors are thought to be involved in the development of COPD either separately or in combination

1.Allergic - there is considerable evidence for an allergic reaction to inhaled organic dust antigens e.g. spores of fungal and thermophilic actinomycetes which are found in high numbers in poor quality hay and straw.

2.Previous Infection - many authors have reported signs identical to COPD following viral respiratory Infections. This is sometimes referred to as a separate entity - Post Viral Cough, but the clinical signs and pathology are identical to COPD. The exact mechanism by which viruses can cause a long lasting airway hypersensitivity is unclear, but it may be more likely to occur when a horse has been given inadequate time to recover from the primary viral infection

3.Genetic Predisposition - it has been suggested that there is a genetic component to susceptibility to COPD, though this is not proven.

CLINICAL SIGNS

Very wide ranging from a decrease in exercise tolerance in mildly affected performance animals to a respiratory cripple In the most severe cases.

chronic intermittent dry cough
nasal discharge (often more apparent after exercise).
increased respiratory rate (depending on severity)
expiratory breathing difficulty (depending on severity) leading to increased abdominal effort on expiration the ‘double expiratory effort* (hypertrophy of abdominal muscles in long-standing cases) can lead to the development of a ‘heaves line*.

Occasionally signs will appear to have sudden onset if a COPD case in clinical remission is exposed to environmental respiratory allergens.

Virtually identical respiratory signs may occur in grazing animals - in which case the condition is referred to as Summer pasture associated obstructive pulmonary disease (SPAOPD).

DIAGNOSIS

In most cases the taking of a thorough history and the combination of clinical signs are sufficient to make a diagnosis of COPD. It is very unlikely that a precise causal agent will be identified.

Where there is doubt, blood or pulmonary function tests may be useful. Cytology from tracheal washes and/or broncho-alveolar lavage reveals large numbers of neutrophils in cases of COPD.

TREATMENT

The most important factor in the treatment of COPD is to place the horse in the correct environment (i.e. turn it out in the open where there is low concentration of organic dust antigens responsible for the development of the disease). Where there is no option other than to stable the horse for part or all of the time, it should be bedded on wood shavings, shredded paper or synthetic bedding in a well ventilated stable, and fed on purely pelleted food, or at the very least fed good quality hay that has been soaked for several hours. Also ensure that affected animal is in a separate airspace (or that all animals within same airspace also have "dust-free") environment). Several drugs can be used as an adjunct to environmental management to speed recovery from COPD, but are unlikely to be effective if the horse remains exposed to the dust antigens.

Bronchodilators, mucolytics, or in severe cases or short term, corticosteroids are all useful.

CONTROL AND PREVENTION

The signs of COPD, except in very long-standing cases, are completely reversible. Prevention of recurrence is very simply achieved by keeping susceptible animals turned out, and minimising contact with organic dust antigens (see above).

Where horses have to be temporarily stabled e.g. at competitions, prophylaxis can be given against developing signs of COPD by the administration of disodium cromoglycate (Cromovet) to animals in clinical remission (i.e. not clinically affected with COPD at the time of administration) prior to the expected time of stabling. Cromoglycate prevents mast cell degranulation so blocking the hypersensitivity response of COPD. It is administered via a special face mask fitted to the horse*s head, the horse inhaling droplets of the drug. Treatment on 1 day gives protection for up to 4 days, whereas treatment for 4 consecutive days gives up to 24 days protection.

TETANUS IN THE HORSE

Tetanus is caused by Clostridium tetani infection and is found throughout the world. Its spores are present in soil and in the intestinal contents of horses and other animals but the clinical disease occurs only sporadically. It can occur in horses of any age and is frequently fatal.

PATHOGENESIS

Clostridium tetani exists outside the body as spores. These are carried into puncture wounds and, where tissue damage allows anaerobic conditions to develop, the spores germinate. A small amount of soil or bacterial infection is often sufficient to allow germination. Puncture wounds of the foot and umbilical infections are the most common sites for germination to occur. The uterus can also become infected at foaling, especially if foetal membranes have to be removed manually.

Toxin production occurs in the puncture wound and the toxin is absorbed, traveling along peripheral nerves to reach the central nervous system. Clinical signs of spasm in voluntary muscles may begin at any time from 7-21 days after infection. Muscle spasm increases until finally the respiratory muscles are paralysed and death occurs.

CLINICAL SIGNS

Skin wounds may be evident. Signs of tetanus appear within 7-21 days of wound contamination. Usually the first signs are associated with chewing/swallowing difficulty and muscle spasm is progressive over head/neck then trunk then limbs with head and neck rigidity and muscle spasm; erect ears and flared nostrils are followed by limb rigidity and a sawhorse stance

DIAGNOSIS

The clinical signs are characteristic and a diagnosis can usually be made very early in the course of the disease. A history of a puncture wound may help.

TREATMENT

- Tetanus antitoxin, probably of little use as toxin becomes fixed to receptors and cannot then be neutralised
- wound should be located, cleaned, exposed to the air, washed with potassium permanganate solution or hydrogen peroxide and treated with penicillin. Antitoxin may also be applied locally
- penicillin
- sedatives and tranquillizers if needed.
- nutritional support.
- darkened, quiet box, raised buckets/manger etc.

PROPHYLAXIS

Vaccination - two injections 4 weeks apart followed by a third 6 months later. Booster doses annually or every two years.

Pregnant mares should always be protected in this way in order that colostral immunity should be passed to the foal. Foals vaccinated from 6 months of age.

Tetanus antitoxin should be given to all unvaccinated horses with wounds or puncture wounds or which undergo surgery. Newborn foals from unvaccinated dams should also be given antitoxin.

Penicillin treatment of animals with puncture wounds may also help to heal the wound and eliminate infection thus preventing the disease.

SPORADIC LYMPHANGITIS (Monday Morning Disease, Monday Morning Leg, Weed)

AETIOLOGY

The sudden onset of symptoms is associated with a period of enforced inactivity. The pathogenesis is not properly understood. Infection probably gains entry via abrasions to the skin of swollen limbs, resulting in inflammation of the lymphatics and lymph nodes, lymph stasis and thickening of affected limbs.

CLINICAL SIGNS

- fever
- anorexia
- unilateral hindlimb diffuse, hot and painful swelling
- skin fissures

TREATMENT

- antibiotics
- corticosteroids
- local treatment;? poultice, massage
- frequent, in-hand walking exercise
- laxative, low protein diet

Although the horse should become fit to work again, the affected leg may remain permanently thickened. Recurrences are common in the same limb, and each time, though the systemic disturbances may be less severe, more fibrous tissue is laid down and the limb becomes progressively more thickened.

PREVENTION

Restrict concentrate feeding during periods of rest and treat superficial wounds promptly.

LIVER DISEASE

A variety of liver diseases occur in the horse: they have few differentiating clinical features and ancillary investigations are often required. Generally the presenting sign of liver failure is weight loss, reflecting the chronic nature of most equine liver diseases but acute failure does occur. Other possible clinical manifestations of liver failure are:

Alterations in appetite
Behavioural abnormalities
Photosensitisation
Bleeding disorders
Colic (less common)
Skin irritation
Diarrhoea
Jaundice
Gastric impaction

Behavioural abnormalities may range from the very subtle, noticeable only to those familiar with the horse, to depression, incoordination, yawning and head-pressing.

DIAGNOSIS

Clinical findings may be suggestive of liver disease but are rarely definitively diagnostic. A pertinent history may also be helpful. Blood tests, liver function tests and ultrasound of the liver are helpful, in some cases a liver biopsy may be required.

Common causes of liver problems include:

RAGWORT POISONING

The plant is normally unpalatable but may be eaten in times of sparse grazing, or inadvertently in hay.

DIAGNOSIS

A history of access to ragwort may support the diagnosis but is often not known. Blood biochemistry indicates liver failure, but definitive diagnosis requires biopsy which reveals characteristic changes.

TREATMENT

Removal of horses from pasture, and/or removal of plants and/or cessation of feeding contaminated hay will not benefit affected horses, but will prevent further damage, and new cases.

Injectable and oral B vitamin complexes may be helpful. Lactulose may be given, to reduce ammonia production by bacteria in the gut. A low-protein diet is indicated for the same reason.

PROGNOSIS

If no noticeable clinical response is apparent within 2-3 days the prognosis is hopeless. Even apparently improving horses generally progress to chronic liver failure (below).

CHRONIC LIVER FAILURE/CIRRHOSIS

An end stage of liver disease. Generally presents as chronic weight loss, but may be more acute if the liver suddenly decompensates after the large functional reserve is passed.

Very poor prognosis but short term improvement may be achieved with symptomatic therapy (above).

LIVER FLUKE

Infection with Fasciola hepatica is rare in the horse, but donkeys may be more susceptible. May be suspected if grazed on wet land with ruminants carrying heavy burden. Faecal fluke egg counts may be diagnostic, but immature forms cause damage prior to patency in which case there may be biochemical evidence of biliary tract damage

BILIARY CALCULI

These stones within the bile ducts occur only rarely and may be asymptomatic, or present as recurrent colic with associated liver signs. Diagnosis by ultrasound examination. Prognosis is guarded to poor, although surgery is an option if hepatic fibrosis secondary to the biliary obstruction is not too severe.

MISCELLANEOUS LIVER DISEASE

Other rarer causes of liver disease such as porto-caval shunt, liver abscesses, lymphosarcoma and chronic active hepatitis should be borne in mind where liver failure is suspected.

PHOTOSENSITISATION

Photosensitisation is defined as an abnormal skin reaction to U.V. light. It is not a single disease entity but a syndrome whose pathogenesis may vary. There are features common to all types: the presence of a photodynamic agent within the skin; concomitant exposure to a sufficient amount of a certain wavelength of light (UV A range 320-400nm) and the fact that skin absorption of UV radiation is greatly facilitated by lack of pigmentation and haircoat.

PATHOGENESIS

The pathogenesis can involve liver disease causing decreased phylloerythrin excretion or ingestion of plants containing photodynamic agents (PDA).

Sunburn is a normal reaction to excessive exposure to sunlight, especially UV B range (290-320nm). Excessive exposure depends on both duration and depigmentation, and in the horse is usually seen in white or lightly-pigmented animals.

CLINICAL SIGNS

In severe cases of photosensitivity, vesicles form and the skin is swollen and tender with a weeping surface. Serum mats the hair and forms a crust, which becomes hard along with the underlying skin. Crust and necrotic skin frequently peel, leaving raw, bleeding areas that eventually heal. Large areas with poor regrowth of hair result. Irritation tends to be more severe in cases secondary to hepatic disease. Animals may show other signs of liver dysfunction, such as jaundice.

DIAGNOSIS

Feed analysis, liver function profile and investigation are the most important diagnostic tools.

TREATMENT

In cases of chronic liver disease prognosis is guarded. Removal of PDA containing feedstuffs and removal of the horse from pasture with plants containing these will usually result in full recovery if the horse is also kept out of the sun for 1 to 2 weeks. Antiflammatories are helpful in controlling inflammation and irritation.

EQUINE COLIC

Colic is defined as simply being 'abdominal pain'. It is not a diagnosis in itself, purely a clinical sign of an underlying problem. It may be manifest as one of the following.

inappropriate recumbency
flank watching/kicking
abnormal posture
rolling
depression
restless walking
stretching to urinate

PARASITIC SKIN CONDITIONS

LICE

Horses are commonly infected especially during late winter and early spring with both sucking and biting lice. Animals in poor condition which are kept together in large numbers and are not groomed regularly often have heavy burdens.

LIFE CYCLE

Adult lice lay eggs which are attached to hairs. The nymph which hatches from the egg resembles the adult and matures through three larval stages the whole cycle taking place on the horse over a period of two to three weeks.

CLINICAL SIGNS

Lice occur particularly in the mane and tail-head areas but may spread anywhere in the body. In most cases there is little or no hair loss with only a moderate increase in skin scales. Loss of hair occurs in severe cases resulting in Irregularly shaped bare areas with ill-defined borders and some reddening of non-pigmented skin. Superficial abrasions may be caused by rubbing. The parasites make the skin itchy and the horse may rub against objects and nibble and lick at the skin. Extremely heavy infections of sucking lice may cause anaemia.

EPIDEMIOLOGY

Lice are host specific and do not live for more than a few days off the horse. Transmission is by direct contact or via grooming equipment, harness or bedding.

TREATMENT

Synthetic pyrethroid sprays (cypermethrin or permethrin) can be used. Selenium sulphide shampoo has been shown to be effective in a controlled clinical study. However, spray (noise) and shampoo (soaking) therapies have some logistical/expense problems for treatment of animals with full, winter haircoat.

CHORIOPTIC MANGE (leg mange, itchy heel)

Infection with non-burrowing mites. The prevalence of infection has been reduced with the fall in the number of heavy horses as it was common in breeds with heavy feather. Chorioptic mange tends to be more common in the winter.

LIFE CYCLE

Eggs are laid on the skin and hatch in 1 to 5 days. The subsequent larval and two nymphal stages do not penetrate below the skin surface and the life cycle is completed in 9 to 10 days.

CLINICAL SIGNS

Irritation caused by this parasite makes the horse stamp its feet and rub its lower limbs together. Lesions are mainly confined to the lower hind limbs but sometimes are present on all four legs and may extend upwards to appear occasionally on the body. The appearance of the lesions is often mild. Hair around the fetlock and pastern becomes broken and matted with dried exudate and in the upper limbs the skin may become bare, dry and visibly scaly

EPIDEMIOLOGY

Transmission is by direct or indirect contact.

TREATMENT

Synthetic pyrethroid sprays or washes, ivermectin orally, selenium sulphide shampoo, or 'Frontline' spray. Treatment should be combined with clipping and topical disinfection.

HARVEST MITE INFECTION

Infection with larvae of the harvest mite is not common in the West of Scotland but is common in the East and in some parts of England. The larvae come off the herbage and live for a few days on an animal causing minor irritation and itching of the horse*s heels without marked skin changes.

The red or orange mite may be just visible with the naked eye.

Horse limbs and faces may be dusted with insecticide once weekly in the autumn to prevent infection as this is the only time of year the condition occurs.

WARBLES

Warble flies rarely lay their eggs on the horse but larvae may migrate and reach the back and sometimes occur on unusual sites. Diagnosis is made on the appearance of the typical hemispherical lesion about 2 cm in diameter which may or may not have a central orifice. Lesions may be treated by incision of the lesion to remove the warble or local application of a recognised warble fly dressing.

STABLE FLIES

Stable flies in large numbers can attack horses, the bites being painful and bleeding easily.

Multiple wheals and papules can develop, evolving into crusts on the back, chest, neck and legs. Lesions may represent arthropod hypersensitivity or may be caused by irritating and toxic components of saliva.

DIAGNOSIS

Diagnosis is by physical examination, and indicated by improvement of lesions if horses are stabled during the day when the flies feed.

TREATMENT

Treatment depends on frequent application of pyrethrin fly repellents and good stable hygiene - removing soiled bedding and manure from the stable and surrounding areas removes the breeding areas.

BLACK FLIES

Black flies are daytime feeders, attacking the sparsely haired areas of horses resulting in itchy, crusted papules and hair loss. Lesions are seen in the lower jaw and pectoral areas, lower body wall and inguinal areas, and also in the ears.

DIAGNOSIS

Diagnosis is again by physical examination and is indicated by response to daytime stabling.

TREATMENT

Treatment involves daytime stabling, frequent insecticide and repellent application.

HORN FLIES

Horn flies cause the syndrome of focal ventral midline dermatitis in horses. This is a seasonal irritation, characterised by one to many foci of hair loss, inflammation and depigmentation, scaling, crusting and excoriation centred around the umbilical area.

TREATMENT

Treatment is clipping and cleansing with mild antiseptic and application of antibiotic/corticosteroid cream to reduce inflammation. Fly repellents in a gel or ointment base provide a physical and chemical barrier against further bites.

HORSE AND DEER FLIES

Horse flies and deer flies inflict painful bites which can result in large wheels. Control is difficult owing to the robust nature of the flies. Heavy and frequent application of pyrethrins with repellents may give some relief. As the files require water for breeding and egg deposition, drainage of breeding grounds or moving horses from fly breeding areas, may be helpful.

URTICARIA

Urticaria is an acute skin condition characterised by the rapid development and equally rapid disappearance of round, elevated, flat-topped, steep-sided areas on the skin surface. These are also known as wheals, hives and plaques.

AETIOLOGY/ PATHOGENESIS

The causative agent is seldom defined. Most but not all urticarias are allergic in nature.

CLINICAL SIGNS

The clinical features of urticaria are diagnostic. As the major component of a wheal is oedema, lesions should pit on pressure. The sides of the neck, shoulders and thorax are the commonest areas to be affected.

Food allergy is associated with the presence of small, itchy lumps mainly over the thorax but many may appear on the head and neck. Severe tail rubbing may be present. Occasionally lumps are rubbed bare of hair and become raw with secondary bacterial infection, resulting in tenderness, swelling, weeping and heat in the area. Food allergy reactions should be treated topically with iodine surgical scrub and topical antibiotics, with systemic antibiotics if cellulitis occurs. Foods frequently causing reactions include distillery wastes, malt, beet pulp, clover, St.John*s wort, glucose, wheat, oats, barley, bran and chicory. Urticarial reaction is more likely to occur when the protein content of the ration is excessive. The mucous membranes of the nose, mouth, anus and vulva are sometimes involved in urticarial lesions, and the pharynx and larynx are infrequently involved, causing impairment of swallowing and breathing.

TREATMENT

Dexamethasone usually produces recovery within 24 hours, but most untreated cases spontaneously regress. Attempts ought to be made to determine the cause of recurrent urticaria although this is unsuccessful in over 50% of cases.

EQUINE SARCOID

A locally aggressive fibropapilloma, the sarcoid is the equine neoplasm most commonly submitted for histopathological examination. The aetiological agent is a papillomavirus and there are reports of outbreaks of the disease occurring In groups of animals. More recent work suggests a genetic predisposition to the disease. The tumour is seen most frequently in young to middle-aged animals. The lesion is very difficult to treat, frequently recurring. Spontaneous rejection is very rare.

CLINICAL SIGNS

Sarcoids are found in three main areas of the body:

Head, especially around the eye.
Ventral body, especially around the genital region.
Limbs.

There are four clinical manifestations of sarcoids. The tumours often appear on the site of a previous injury and the lesions, which can grow to be very large, may become ulcerated and traumatised.

TREATMENT

Sarcoids are notoriously difficult to treat and there are a number of therapies available.

1. Surgical excision may be used on smaller lesions, removing a large margin of normal tissue. Even so, recurrence and the appearance of satellite lesions is common.

2. Cryotherapy is more successful and should be performed after debulking of large tumours.

3.The use of gold and iridium radioactive implants has been successful but the requirement for dedicated premises and operator hazard makes this impossible in the field.

4. BCG has been injected intra-lesionally to stimulate a local cellular immunological response. This should be injected intra-lesionally on 3-4 occasions 2-3 weeks apart.

5. Arsenical ointment - topical applications i.e. chemical cautery.

In practice a combination of the treatments would probably be used. However, due to the difficulty in treatment sarcoids should always carry a guarded prognosis