About Equine Worms

Information kindly provided by Merial Animal Health

Parasite life cycles

Figure 3.1. Trichostrongylus axei

ENDOPARASITES

Nematodes – Roundworms

Stomach

Trichostrongylus axei (Stomach hairworm)

Also known as hairworms. T. axei generally infect ruminants but can parasitise horses if grazed on the same pasture. Burdens are usually low.

Morphology: Up to 7.0mm long, small and hair-like
in appearance.

Prepatent period: Approximately 25 days.

Figure 3.2. Muscid Fly

Life cycle: T. axei has a direct life cycle with infection caused by ingestion of L3 larvae from infected pasture. Once ingested, larvae infest the gastric mucosa where they complete their life cycle.

Pathogenesis: Lesions within the gastric mucosa can cause haemorrhage, with loss of plasma proteins and reduced absorption of nutrients.

Clinical signs: Rapid weight loss and diarrhoea with heavy burdens. Loss of appetite, soft faeces and poor growth with lower burdens.

Habronema spp. (Large-mouthed stomach worm)

Adult Habronema in the stomach rarely cause any serious clinical concern but the larvae can cause persistent ‘summer sores’ in warm countries.This is one of the few nematode species that requires an intermediate host (housefly or stable fly).

Morphology: 1.0-2.5cm long, white in colour.

Prepatent period: 6-8 weeks.

Figure 3.3. Summer sores'

Life cycle: L1 are passed in faeces and ingested by housefly or stable fly maggots feeding in dung. Larvae develop within the maggots and become infective to coincide with the fly emerging from the pupa. Infective larvae of Habronema are then transferred from the mouthparts of the fly onto the lips, nostrils and wounds of horses during feeding. Larvae deposited around the horse’s mouth are swallowed and mature in the stomach to become adult worms. Larvae deposited in skin wounds or around the eye burrow into tissue but cannot develop into adults to complete their life cycle.

Pathogenesis: In the stomach, adult worms may cause mild gastritis but skin lesions caused by larvae deposited in wounds (cutaneous Habronemiasis) are far more important.They cause intense irritation and non-healing wounds known as ‘summer sores’ that spread and tend to become infected.They may require surgical treatment. Larvae deposited in the eye cause persistent conjunctivitis and ulcers.

Clinical signs: ‘summer sores’ from cutaneous Habronemiasis, persistent conjunctivitis and mild gastritis.

SMALL INTESTINE

Figure 3.4. S westeri

Strongyloides westeri (Intestinal threadworm)

A parasite of the small intestine and a problem in newborn foals, usually infected from larvae in the mare’s milk.These larvae move into the mare’s udder from dormant (resting) stages in the tissues
of the mare’s abdomen around foaling time. Infection can also be via larvae entering through the skin or by ingestion from pasture. Natural immunity develops by six months of age and so adult horses rarely show signs of infection.

Morphology: Slender hair-like worms. Less than 1.0cm long.

Prepatent period: 8 to 14 days.

Figure 3.5. Life cycle of S.westri

Life cycle: Strongyloides are unique because they are capable of both parasitic and completely free-living life cycles. Infective larvae (L3) enter the host through the skin or by ingestion.They migrate via the blood stream to the lungs, move up the trachea and are then swallowed to reach the small intestine, completing their development into adults in a few days. Worms in the parasitic life cycle are all females capable of laying larvated eggs (eggs containing larvae). Under favourable conditions (warm, humid weather) eggs passed in the faeces can develop into both male and female worms which reproduce in the environment to complete a free-living life cycle. When conditions are unfavourable the parasitic life cycle takes over.

Pathogenesis: Adult worms damage the lining of the intestine, interfering with digestion causing loss of appetite, diarrhoea and dullness.

Clinical signs: Seen in foals – particularly 1-4 weeks of age – to coincide with the mare’s first heat after foaling (the ‘foaling heat’). Diarrhoea, cough and localised dermatitis from penetration by infective larvae. Heavy infections can be fatal with foals developing severe diarrhoea, rapid dehydration, weight loss and anaemia.

Ascarids

Figure 3.6. P. equorum.

Parascaris equorum (Large roundworm)

This is the largest nematode of horses and affects younger animals under 2 years old. Horses acquire immunity at approximately 18 months of age.

Morphology: Large and white in colour. May reach 40.0cm in length.

Prepatent period: The minimum period is 10-16 weeks.

Life cycle: A direct life cycle. Adult worms live in the small intestine and produce huge numbers of eggs (up to 200,000 per day), which are passed in the faeces.The L2 develop within the egg in 10 – 14 days, and horses become infected by ingesting these eggs which hatch to release the larvae.They penetrate the wall of the intestine and are carried by the blood to the liver. Eventually they reach the lungs, migrating through the blood vessels into the airways and up the trachea.They are coughed up and swallowed to reach the small intestine to mature into adult worms. The eggs are able to survive in the environment for several years due to their protective sticky outer coat. A parasitized foal could shed up to 30 million eggs per day resulting in a very high risk of reinfection. Control programmes must therefore include good stable and pasture management to help reduce this risk because the cycle of infection is largely maintained by survival of the eggs and transmission from one generation of foals to the next.

Pathogenesis: Migrating larvae can cause damage to the liver and lungs and pneumonia in heavy infections. Intestinal stages can result in impaction, leading to fatal rupture of the small intestine and peritonitis, although this is rare. Heavy burdens are more likely to compete with the host for nutrients.

Clinical signs: Coughing, grey nasal discharge (migrating larvae), unthriftiness and poor growth rates.

LARGE INTESTINE

Figure 3.7. O.equi adult

Oxyuris equi (Pinworm)

Infection with the horse pinworm Oxyuris equi, is common – especially in stabled animals.

Morphology: Large white worms. Females may reach 10.0cm in length. Males are less than 1.0cm.

Prepatent period: 5 months.

Life cycle: Adult worms live in the caecum and colon. Adult females migrate to the anus to lay eggs on the skin surrounding the anus.This causes intense irritation. The L3 develop within the egg in 4-5 days.The eggs are contained within a sticky substance that dries out and crumbles, spreading 1000s of eggs which are rubbed off into the environment.They attach themselves to feeding troughs, walls and floors of stables from where they can easily be ingested. Once in the small intestine the larva is released from the egg and moves to the large intestine to complete the life cycle.The L4 develops within 10 days and the emerging L4s feed on the mucosa before moulting to the immature adult L5.

Pathogenesis: The feeding L4 larvae can cause small lesions within the intestinal mucosa. The major effect is irritation around the anus from the eggs.

Clinical signs: Parasites in the intestine rarely cause serious clinical signs.The main clinical sign associated with pinworm is itching and rubbing of the rump and tail head. The skin and underside of the tail should be regularly cleaned with a disposable cloth, combined with a high level of stable hygiene.

Strongyles (Redworms)

The strongyles are categorised into small and large redworms.The term ’redworm’ results from the red colour of the worm after feeding.They are found in the large intestine in the caecum and colon.
The term strongylosis describes disease caused by infection with the large strongyles (Strongylus spp, Triodontophorus spp) and/or small strongyles (Trichonema/Cyathostomum spp).

Trichonema/Cyathostomum spp. (Small redworms)

Figure 3.8. Small Redworms feeding on gut lining

There are over 50 species recognised and they are the most common and important parasites to affect horses.They make up at least 90% of the total worm burden and are the main target for treatment. Small strongyles are non-migratory with the whole life cycle taking place inside the lumen and within the wall of the intestine.

Morphology: Up to 2.5cm long, thin and red in colour.

Prepatent period: 6-12 weeks.

Life cycle: Adults in the caecum and colon live and feed attached to the intestinal lining. They lay thin-shelled oval eggs which are passed out in the faeces to develop into infective third-stage larvae (L3) on pasture. Infection is caused by the ingestion of the third-stage larvae. They burrow into the gut wall and then develop into L4 within a few weeks without interruption, or undergo hypobiosis (state of inhibited development) for several months during the late summer and autumn. These hypobiotic stages can account for more than 50% of the total worm population, and are difficult to kill.

Pathogenesis: Severe damage is caused by mass emergence of larvae from hypobiosis, when they emerge from the gut wall and return to the lumen of the intestine, typically in late winter/early spring.
The disease syndrome is called acute larval cyathostomosis and is potentially fatal.

Clinical signs: Usually seen in younger horses up to 2-3 years of age. Symptoms include unthriftiness, anaemia and sometimes diarrhoea. Rapid and massive emergence of hypobiotic larvae is characterised by severe diarrhoea, rapid weight loss, oedema (fluid collection) in the lower parts of the body (e.g. jaw, lower legs, prepuce), colic and rise in temperature. Although older horses acquire some age-related immunity, this is incomplete and so life-long treatment is needed for small strongyles.

Large redworms

Figure 3.9. S.vulgaris

There are three major species of migratory large strongyles – Strongylus vulgaris, Strongylus edentatus and Strongylus equinus – and one non-migratory species, Tridontophorus.The use of modern wormers has been very effective in reducing the large redworm population so that they are now relatively uncommon in the UK.

Morphology: The adults are dark red in colour.
S. vulgaris, 1.5-2.5cm with two rounded teeth.
S. endentatus, 2.4-4.5cm with no teeth.
S. equinus, 2.5-5.0cm with three conical teeth.

Prepatent period:
S. vulgaris, 6-7 months.
S. edentatus, 10-12 months.
S. equinus, 8-9 months.

Life cycle of migratory large redworms

S. vulgaris used to be a major cause of colic in horses and the migratory larval stages were considered to be the most damaging of the intestinal parasites. The infective L3 penetrate the intestinal mucosa and moult into L4s in the submucosa. They then enter small arteries from where they migrate to the cranial mesenteric artery, a major artery supplying blood to the intestine. The L4s develop here over several months. Once they have moulted, the L5s migrate back to the intestine where they burrow into the intestinal mucosa and form nodules. Upon rupture of these nodules, adult parasites are released back into the gut lumen. Adults live attached to the mucosa in the caecum, and sometimes in the large colon.

S. edentatus. The L3s penetrate the intestinal mucosa and migrate via the portal (blood) system to the liver. Two weeks later they moult into L4s and migrate further through the liver. After four months the final moult takes place and the L5s migrate back to the large intestine where they form large purulent nodules, which subsequently rupture to release young adult parasites.

S. equinus. Less is known about the migration of this parasite, but it involves migration through the liver and pancreas before returning to the large intestine.

Pathogenesis: The adults cause damage to the intestinal mucosa during feeding. They are ‘plug feeders’ with large mouths (buccal capsules) and are able to ingest large plugs of intestinal lining (mucosa).
Accidental damage to blood vessels can cause haemorrhage.The tissue damage and loss of blood and tissue fluids is in part responsible for anaemia and ill thrift, but the larvae are far more dangerous.

During the migratory stage of S. vulgaris, the larvae damage the cranial mesenteric artery resulting in the formation of thrombi (blood clots) with marked thickening of the arterial wall. This leads to narrowing of the diameter of the artery and reduced blood flow.

Clinical signs: Colic is the most common sign. Other signs may include loss of appetite, weight loss, poor performance, ill thrift, anaemia, lameness in the hind legs after exercise (from thrombi in arteries supplying the back legs), neurological signs (from erratic larval migration into the nervous system) and sudden death (from damage to coronary arteries). Sometimes the wall of the artery above the narrowed part becomes dilated (an aneurism). This can rupture, causing sudden death from internal haemorrhage.

Figure 3.5. Life cycle of S.vulgaris

Triodontophorus spp. (Non-migratory large redworms)

Parasites belonging to the genus Triodontophorus are non-migratory large strongyles in the colon.

There are four major species: T. serratus,T. tenuicollis,T. brevicauda and T. minor.

Morphology: 1.0 – 2.5cm long, red in colour.

Life Cycle: There is little information available.

Pathogenesis: These are less damaging than the ‘strongylus’ family.They are uncommon but where present add to the damage caused by other species of worms.

RESPIRATORY SYSTEM

Dictyocaulus arnfieldi (Lungworm)

Donkeys are the main reservoir of infection.They act as carriers (usually without showing symptoms), so lungworm is only seen in horses and foals grazing with an infected donkey.The prevalence is unknown.

Morphology: Long slender worm; males 3-8cm, females 5-10cm

Prepatent period: 2-4 months

Life cycle: Infection is caused by the ingestion of infective L3 from pasture.The larvae migrate from the intestine through the lymphatic system and blood to the lungs, where they mature.The adult females lay larvated eggs which are passed out in faeces and hatch almost immediately into L1s.

Larvae are spread across pasture in two ingenious ways.When eaten by earthworms they pass through the digestive system undamaged having been transported some distance across the pasture.They are also dispersed via the fruiting bodies of a microscopic fungus (Pilobolus) that develops on dung.When mature, the fruiting bodies explode, dispersing spores several metres away and carrying the larvae with them.

Pathogenesis: Adults living in the airways cause inflammation and damage to the respiratory tract. Horses of all ages can be affected but foals are more susceptible than adults.

Clinical signs: Vary from none to chronic cough, bilateral discharge from nostrils, increased respiratory rate and effort, wheezing, audible lung sounds (heard via a stethoscope) and pneumonia. In severe infections horses may show loss of appetite, rapid weight loss and death within a few weeks.

SKIN

Onchocerca spp. (Neck threadworm)

Adults are found in nodules in ligaments. Infection is transmitted by blood sucking midges during feeding.
As a result, immature worms (microfilariae) are found in tissue spaces of the skin.
Two species of Onchocerca can parasitise the ligaments of horses. O. reticulata is found commonly in the suspensory ligament of the fetlock joint and O. cervicalis in the ligamentum nuchae (main ligament along
the top of the neck).

Morphology: Adults: 6-75cm in length, slender and live tightly coiled in nodules.
Microfilariae: ~0.2mm long.

Life cycle: Horses become infected when L3 (microfilariae) are inoculated via the bites of female midges (Culicoides spp.) during feeding.The microfilariae then migrate through the superficial layers of the skin to ligaments.
Conversely, midges become infected by ingesting microfilariae from an infected horse during a blood meal. Having passed through the insect’s stomach the microfilariae develop into infective L3 stages in the mouthparts of the midge and are transmitted back to horses during feeding.

Clinical signs: Irritated skin and swelling of ligaments.There is no effective treatment against adult worms, although nodules may be removed surgically. Treatment of immature stages produces a marked clinical improvement of onchocercal dermatitis.

Figure 3.11. Adult worms of the genus Onchocerca, after extraction from nodules on the ligaments

Figure 3.12.Skin lesions caused by Onchocerca microfilariae

Cestodes – Flatworms

Anoplocephala spp. (Tapeworm)

Figure 3.14. A. perfoliata

Anoplocephala perfoliata, A. magna and Paranoplocephala mamillana are tapeworms which affect horses. A. perfoliata is the most common. P. mamillana seems to be extremely rare.They are flat segmented worms.

Morphology: A. perfoliata: 4-8cm in length; A. magna: 20-80cm.
White in colour.

Prepatent period: 1-2 months.

Life cycle: Adult tapeworms are attached to the intestinal lining by means of hooks at the ‘head’ end of the worm. Mature segments are passed in faeces from the ‘tail end’ and release eggs as they disintegrate.The tapeworm eggs are ingested by Oribatid forage mites and hatch to release a single cysticercoid larva. Infected mites are ingested by horses during grazing with adult tapeworms developing in 6-10 weeks. Adult worms live for 4 to 6 months. Mites survive the winter in an arrested state in soil and reactivate in spring. Horses therefore become infected in spring, with infection levels reaching a peak in autumn.

Pathogenesis: Formerly considered to be relatively harmless, but recent studies have shown that the prevalence is often very high and heavy infections can lead to severe clinical signs. A. perfoliata is usually located at the ileo-caecal junction and can cause ulceration at the site of attachment, which frequently becomes infected or abscessed.Tapeworms play a major role in certain types of colic, while intestinal obstruction and perforation of the intestinal wall have been noted in cases of heavy infections.

Clinical signs: Range from none in most cases to loss of condition, digestive disturbances, colic and death.

Insects

Gasterophilus spp. (Bots)

Figure 3.14. Bot fly

Members of the genus Gasterophilus spp. (G. intestinalis, nasalis, haemorrhoidalis, pecorum) are insects known as ‘bot flies’; their larvae are called ‘bots’. Bots spend most of their life cycle developing in the stomach of horses over the winter months, after infection of horses the previous summer. They are not considered to be particularly pathogenic, but can cause problems, especially in large numbers.
The flies are active during June – September in the hottest part of the day.They live for only 2-3 weeks and are unable to feed due to their poorly developed mouthparts.

Morphology:
Adults:The flies are dark and 1-2cm long.
Larvae: 16-20mm long. Reddish-orange in colour.

Life cycle: Each adult fly lays 400-1000 eggs on the hairs of the forelegs and shoulders. These hatch in 5-10 days under the influence of heat and moisture, and either crawl into the horse’s mouth or are ingested when the animal licks or nibbles its coat. The larvae then penetrate the tongue or mucosa of the mouth and gums where they can stay for many weeks.They can be hidden well below the gum line in pockets of pus around the root sockets of the molar teeth. The L2 larvae become fixed at the base of the tongue and then travel to the stomach where they attach to the gastric mucosa (stomach lining),
remaining there for 10-12 months over the winter and developing into the final L3 stage.The following spring they detach from the mucosa and are carried out through faeces. The larvae then pupate in the
ground with adult flies emerging 1-2 months later.

Pathogenesis: Adult flies worry horses when laying their eggs. Larvae in the mouth and tongue may cause ulcers but this is rare. Larvae of G. intestinalis can produce ulcers in the wall of the stomach at the site of attachment, and occasionally perforate the wall with fatal results. They have also been found in groups of up to 6cm in diameter in the duodenum, causing inflammation and early abscess formation.

Clinical signs: Range from none to inflammation of mouth, gums and stomach, colic and difficulty eating. Loss of condition and poor growth rates, with large numbers in young animals reducing the available stomach volume.

Figure 3.15. Diagram of the bot life cycle

ECTOPARASITES

Flies

Flies belong to the order Diptera. As adults, they feed intermittently on vertebrate blood, saliva, tears or mucus – and can cause severe irritation throughout the months of April to October. They are broadly divided into those with non-biting mouthparts (e.g. houseflies) and biting mouthparts (e.g. stable flies, horse flies).

Musca domestica (House flies)

Non-biting flies feeding on secretions.

Morphology: Up to 9mm in length. Light to dark grey in colour. Their mouthparts are designed for sucking semi-liquid food.

Length of life cycle: Usually around 3 weeks, but can be as little as 10-14 days under optimal conditions.

Life cycle: The females lay up to 100 creamy-white, banana-shaped eggs in batches, in faeces or decaying organic matter. Eggs hatch in 12-24 hours and the larvae (maggots) emerge. They undergo three larval stages within a few days to 3 weeks – depending on the temperature and availability of food – before moving to a drier area to pupate. The adult fly emerges in 3-26 days. Although adult flies are attracted to a variety of food material, their mouth parts only allow them to ingest liquid materials. Solid materials are liquefied by means of regurgitated saliva.

Pathogenesis: Cause irritation and are important in transmitting numerous pathogens: bacteria, viruses, helminths and protozoa.They are also an intermediate host for Habronema spp (Large-mouthed stomach worm of horses).

Stomoxys calcitrans (Stable flies)

Biting flies that feed on blood.

Morphology: 6-7mm long, looks very similar to the house fly. They are a greyish-brown colour with a bayonet-like proboscis (mouth part) that protrudes forward from the head.

Length of life cycle: Usually 2-3 weeks depending on temperature.

Life cycle: Males and females are blood feeders. Adult females require several blood meals before they are able to reproduce.They then lay eggs singly or in batches of 25-50 in moist decaying organic matter. Eggs hatch in 1-4 days and the larvae mature in 11-30 days or longer, depending on the availability of food. After the third growth stage the maggot will pupate for 6 to 20 days.

Pathogenesis: Painful bites cause great irritation.The fly usually lands on the host with its head pointing upwards and inflicts painful bites that puncture the skin and bleed freely.These flies do not move around on the host and usually attack the neck, lower legs and underbelly, causing horses to shake their heads and stamp. Feeding takes between two to five minutes. Stable flies are mechanical vectors for a number of diseases, including anthrax and equine infectious anaemia. They are also an intermediate host for Habronema spp. (Large-mouthed stomach worm of horses).

Tabanus spp. (Horse flies)

Biting flies. Only the females feed on blood. Males feed on plant juices.

Morphology: Largest in the dipteran group (up to 3.5cm long).They are swift fliers with powerful wings, very large eyes and lacerating scissor-like mouthparts.

Life cycle: Adult horse flies lay 300-600 eggs, usually on plant leaves near open water.The eggs hatch in 4-7 days and the maggot-like larvae drop off into water or mud, often buried deep at the bottom of lakes and ponds.They feed on small crustacean or even one another and grow for 2-3 months before pupating. The whole life cycle takes 4-5 months or longer if the temperature is less than optimum.

Pathogenesis: The mouthparts are adapted to lacerate the skin and lap up oozing blood (0.1-0.3ml of blood at a single feed). Bites are painful and irritating and horses become restless when the flies are present. They prefer the underside of the belly around the navel, the legs or the neck and withers.They feed a number of times in multiple feeding sites before they become replete.They may act as mechanical transmitters of a number of diseases, including anthrax and the virus of equine infectious anaemia.

Lice

Figure 3.16. Louse

Lice are wingless, flattened insects.

Horse biting louse (Damalinia equi) – feeds on skin scales and scurf.
Horse sucking louse (Haematopinus asini) – blood feeders.

In temperate regions such the UK, lice are most abundant during the colder months and often very difficult to find in the summer. Lice are largely host-specific, living on one species or several closely related species.

D. equi, the horse biting louse, prefers the finer hairs of the body and is found on the sides of the neck, the flanks and the tail base. Sucking lice usually move more slowly and are often found with mouthparts embedded in the skin.
H. asini, the horse sucking louse, is normally found on coarser hair at the roots of the forelock and mane, around the base of the tail and on the hairs just above the hoof.

Morphology: Usually 2-4 mm long. Biting lice are easily differentiated from sucking lice by the size of the head relative to the pro-thorax.The head is wider in biting lice and narrower in sucking lice.

Life cycle: Lasts approx 3-4 weeks depending on the species. Females lay eggs (nits) which are glued to the hair by secretions.The eggs hatch into nymphs (looking and behaving like small adults), which undergo three moults before reaching maturity.Transmission usually occurs by direct horse-to-horse contact. Lice dropped or pulled from the horse die in a few days, but detached eggs may continue to hatch over 2-3 weeks in warm weather and so act as a potential source of infestation in stables.

Clinical signs: Itching and skin irritation leads to rubbing and biting of infested areas causing matting, hair loss and a generally unthrifty appearance. Heavy infestations with sucking lice can cause anaemia.

Culicoides spp. (Midges)

Culicoides spp. are vicious biters and suck the blood of their hosts, both humans and livestock, causing intense irritation and annoyance.There are many different species.

Morphology: 1.5-5.0mm depending on the species.

Life cycle: The eggs are laid in damp ground or decaying organic matter near water.All culicoides larvae need a certain amount of free water to complete their life cycle.The eggs generally hatch within 3 days to a week, but this can take more than 4 months, depending on the species and ambient temperature. There are four larval stages, taking from 2-4 weeks to seven months. Pupae, from which adult flies emerge, are found at the edge of water.

Pathogenesis: Adult midges fly only in the warm months of the year and are most active before and during dusk. They tend to feed on the mane, tail and belly of horses. Horses and ponies can become allergic to the bites, causing intense irritation resulting in scratching and rubbing, abrasions and marked skin thickening. This is known as ‘Sweet-itch’ and typically affects the withers and the base of the tail. Culicoides are also responsible for the transmission of the nematode Onchocerca spp. (neck threadworm), inoculating horses with the immature stages (microfilariae) during feeding. Some species of Culicoides also transmit the bluetongue virus in sheep and cattle.

Mites

Six different types of mite affect horses:
Sarcoptic mange mite (Sarcoptes scabiei var equi)
Psoroptic mange mite (Psoroptes equi)
Chorioptic mange mite (Chorioptes equi) – Leg mange
Demodectic mange mite (Demodex equi)

Harvest mites
Forage mites

Sarcoptes scabiei var equi – These are burrowing mites.The fertilised female burrows into the skin and lays eggs in the tunnel she has made. The eggs hatch in 3-5 days to produce a six legged larva. Some larvae remain in the parent tunnel or side pockets, whilst others crawl to the skin surface and burrow into the top layers of the skin to form new ‘moulting pockets’. There are 2 nymphal stages before adult male and female mites are produced. Once the adults emerge, fertilisation takes place and the females burrow back into the skin. The life cycle is complete within 17-21 days.
Sarcoptic mange of horses is the most severe type of mange but is now very uncommon. The first sign is intense itching due to hypersensitivity to the mites, with signs appearing first on the head, neck and shoulders. Left untreated it can spread to involve the whole body with crusts and marked thickening of the skin. This leads to emaciation, general weakness and anorexia.

Psoroptes equi – These are non-burrowing mites. Female mites lay eggs (approximately 90 eggs during her life-time) which hatch to develop through the larval and nymph stages to maturity in about 12 days. Psoroptic mange of horses is very rare in the UK and there have been no reported cases for many years. Signs are seen on thickly haired regions of the body e.g. under the forelock, mane and tail.

Chorioptes equi – (Leg mange). The life cycle is similar to Psoroptes. As the name implies, this mite affects the legs of horses. Chorioptic mange is common in heavy horses and feathered breeds, causing irritation, crusting and thickening of the skin around the hoof and fetlock.When left untreated it can spread up the legs to the underbelly.

Demodex equi – Mites live in the hair follicles and sebaceous glands of the body, eyelids or muzzle, depending on the species. Demodectic mange can cause patchy areas of hairloss and scaling – or skin nodules – but no irritation. It is rare in horses.

Harvest mites – Adult harvest mites live on invertebrates and plants. The larvae normally feed on small rodents, but given the opportunity will also feed on domestic animals – including cats, dogs and horses – as well as humans. They are just visible with the naked eye as tiny red dots and cause intense irritation.

Forage mites – These mites usually feed on organic material in straw and grain but can infest horses. They cause itching, with skin lesions appearing on the face and neck if horses are fed from a hay rack – and on the muzzle and legs if fed from the ground.

Summary – clinical signs: Severe itching, irregular skin lesions, scabs and alopecia.

Ticks

Figure 3.5. Life cycle of S.westri

Ticks belong to the same class as spiders (Arachnida) and are blood feeders. Horses can be affected by both Ixodid ticks (hard ticks) and soft ticks (Argasidae) worldwide, but only hard ticks are
found in the UK. The most common of these to feed on horses is Ixodes ricinus (the ‘castor bean tick’), which can be picked up from pasture, typically during March-June and August-November. Ticks
are temporary parasites and only spend a short time attached to the host during feeding.

Morphology: Female 3-3.6mm, engorged female 11mm, male 2.4-2.8mm, unfed nymph 1.3-1.5mm.
Adults are grey in colour, bean-shaped with four pairs of legs.

Length of life cycle: 3 years in UK.

Life cycle: Ixodes ricinus is a three-host tick requiring a different host for each stage of the life cycle. The life cycle usually takes three years in the UK. In the first year the tick is a larva, in the second year it is a nymph and in the third year it reaches maturity and is in adult form. Ticks only feed once each year at each stage of the life cycle.
Fertilisation takes place on the host. The female feeds for approximately 14 days then drops to the ground, lays thousands of eggs in sheltered spots such as under stones and clods of soil, in wall crevices and cracks of wood near the ground, then dies.The larvae hatch, feed for a few days and then drop off and moult. In the second year the nymph feeds, drops off and then becomes an adult to complete the cycle. Nymphs and larvae target small mammals such as rodents, rabbits, birds, reptiles and bats. Adult ticks target medium to large mammals, including sheep, cattle, dogs, deer, horses and man.

Pathogenesis: When ticks feed they bury their mouthparts into the skin causing localised lesions which may become infected. Ticks are also important as transmitters of a great variety of infectious agents.

Clinical signs: Localised skin reactions and a number of tick-borne diseases.