Clinical signs: The presence of adult worms in the stomach causes very little clinical disturbance. Cutaneous habronematidosis presents as intense itching of the affected skin. Non-healing granulomatous lesions, raised above the surface of the skin may be a feature (see Habronema).
Diagnosis: Usually only low numbers of eggs or larvae are present in the faeces. Eggs may be demonstrated in gastric lavage taken via a stomach tube. Sometimes larvae can be identified in the small granulomatous skin lesions.
Pathology: Adult worms burrow into the submucosa of the stomach producing large tumour-like nodules causing the mucosa to protrude into the gastric lumen. The worms provoke a surrounding granulomatous reaction, which contains a central core of necrotic and cellular debris and large numbers of eosinophils. Burrowing larvae in the conjunctivae cause an ulcerative, weeping lesion at the medial canthus, which becomes progressively more nodular as the lesion becomes more granulomatous. Mineralised granules, caseous debris and larvae may be found in the lesion. Larvae in the skin cause lesions that are rapidly progressive and proliferative in nature, comprising ulcerated masses of granulation tissue that haemorrhages readily. Lesions may be single or multiple and range in size from 5-15 cm. On section, the lesions are caseous and histologically there are aggregates of eosinophils scattered throughout the connective tissue, which contains a few macrophages and multinucleate giant cells surrounding degenerating larvae. The surface of the lesion is usually covered with a fibronecrotic exudate overlying a highly vascular granulation tissue infiltrated with neutrophils.
Habronema microstoma
Synonym: Habronema majus
Predilection site: Stomach
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: Slender white translucent worms 1.5–2.5 cm long; adult males are 16–22 mm and females 15–25 mm. The male has wide caudal alae and the tail has a spiral twist.
Description, microscopic: The pharynx contains a dorsal and ventral tooth in its anterior part. The male has four pairs of pre-cloacal papillae. Spicules are uneven in length with the slender left one longer than the right. The elongated, oval, small eggs are thin-shelled, 45–59 × 16 μm and larvated when shed in faeces.
Geographical distribution: Worldwide
Pathogenesis: The adult Habronema in the stomach may cause a mild catarrhal gastritis with excess mucus production. More important are the granulomatous lesions of cutaneous habronematidosis, commonly known as ‘summer sores’, and the persistent conjunctivitis with nodular thickening and ulceration of the eyelids associated with invasion of the eyes. Larvae have also been found associated with small lung abscesses.
Clinical signs: These are usually absent in gastric habronematidosis. Lesions of cutaneous habronematidosis are most common in areas of the body liable to injury and occur during the fly season in warm humid countries, although it also occurs in temperate regions. During the early stages, there is intense itching of the infected wound or abrasion, which may cause further self-inflicted damage. Subsequently a reddish brown, non-healing cauliflower-like granuloma develops that protrudes above the level of the surrounding skin and may be up to 8.0 cm in diameter. These lesions are known as ‘summer sores’ in acute cases. Later the lesion may become more chronic, fibrous and inactive, but will not heal until the advent of cooler weather when fly activity ceases (Fig. 4.2). Invasion of the eye produces a persistent conjunctivitis with nodular ulcers, especially at the medial canthus. Sometimes larvae invade the skin of the prepuce and glans penis of stallions.
Diagnosis: This is based on the finding of nonhealing, reddish cutaneous granulomas. The larvae, recognised by spiny knobs on their tails, may be found in material from these lesions. Gastric infection is not easily diagnosed since Habronema eggs and larvae are not readily demonstrable in the faeces by routine techniques.
Fig. 4.2 Ulcerated granuloma on commissure of lips of horse due to cutaneous habronematidosis.
Pathology: Adult worms in the mucosa of the stomach have been associated with a mild ulceration. Burrowing larvae in the conjunctivae cause an ulcerative, weeping lesion at the medial canthus, which becomes progressively more nodular as the lesion becomes more granulomatous.
Habronema muscae
Predilection site: Stomach
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: Slender white translucent worms, 1.0–2.5 cm long; adult males are 8–14 mm and females 13–22 mm. The male has wide caudal alae and the tail has a spiral twist. It is unlikely to be confused with other nematodes in the stomach since Draschia is associated with characteristic lesions and Trichostrongylus axei is less than 1.0 cm in length.
Description, microscopic: There are two lateral trilobed lips; the pharynx is cylindrical and has a thick cuticular lining. There are four pairs of pre-cloacal papillae and one or two papillae behind the cloaca. The cloacal region is covered with small cuticlar ridges. Spicules are uneven in length with the slender left one longer than the right. The vulva is situated near the middle of the body and opens dorsolaterally. The elongated, oval, small eggs are thin-shelled, 40–50 × 10–12 μm and larvated when shed in faeces.
Final host: Horse and other equines
Intermediate hosts: Dipteran flies of the genera Musca, Stomoxys and Haematobia (Lyperosia)
Geographical distribution: Worldwide
Trichostrongylus axei
Synonym: Trichostrongylus extenuatus
Common name: Stomach hairworm
Predilection site: Stomach
Parasite class: Nematoda
Superfamily: Trichostrongyloidea
Description, gross: The adults are small, hair-like, light brownish red and difficult to see with the naked eye. Males measure around 3–6 mm and females 4–8 mm in length.
Description, microscopic: The male spicules are dissimilar and unequal in length (the right being shorter than the left (see Table 3.1, Chapter 3: Sheep and goats).
Hosts: Cattle, sheep, goat, deer, horse, donkey, pig and occasionally man
Life cycle: This is typically trichostrongylid and is described in detail under Sheep and goats in Chapter 3. The prepatent period is about 4 weeks in the horse.
Geographical distribution: Worldwide
Clinical signs: T. axei is responsible for gastritis in horses.
Pathology: In the horse, initial lesions are circumscribed areas of hyperaemia in the gastric mucosa, which progresses to catarrhal or lymphocytic inflammation and erosion of the epithelium. This may be associated with necrosis. Over time, infection can lead to a chronic proliferative inflammation and shallow depressed ulcers may be present.
Treatment and control: This is as described under treatment and control of strongylosis in the horse.
Gasterophilus
Species of Gasterophilus, known as bots, are obligate parasites of horses, donkeys, mules, zebras, elephants and rhinoceroses. Nine species are recognised in total, six of which are of interest as veterinary parasites of equids.
Description, adults: Bot flies are robust dark flies, 10–15 mm in length (Fig. 4.3). The body is densely covered with yellowish hairs. In the female the ovipositor is strong and protuberant. The wings of adult Gasterophilus characteristically have no cross-vein dm-cu (Fig. 4.4).
Fig. 4.3 Gasterophilus spp.
Fig. 4.4 Adult female Gasterophilus intestinalis (reproduced from Castellani and Chalmers, 1910).
Description, larvae: When mature and present in the stomach or passed in faeces the larvae are cylindrical, 16–20 mm long and reddish orange with posterior spiracles (Fig. 4.5). Differentiation of mature larvae of the various species can be made on the numbers and distribution of the spines present on various segments (Fig. 4.6).
Fig. 4.5 (a) Third-stage larva of Gasterophilus intestinalis. (b) Ventral view of pseudocephalon of G. pecorum. Eggs of (c) G. nasalis; (d) G. intestinalis; (e) G. haemorrhoidalis; (f) G. inermis (reproduced from Zumpt, 1965).
Life cycle: The life cycles of the various species differ only slightly; key differences will be highlighted below.
Geographical distribution: All species of Gasterophilus were originally restricted to the Palaearctic and Afrotropical regions, but three species, Gasterophilus nasalis, G. haemorrhoidalis and G. intestinalis, have been inadvertently introduced into the New World.
Pathogenesis: The presence of larvae in the buccal cavity may lead to stomatitis with ulceration of the tongue. On attachment by their oral hooks to the stomach lining, larvae provoke an inflammatory reaction with the formation of funnel-shaped ulcers surrounded by a rim of hyperplastic epithelium (Fig. 4.7). These are commonly seen at postmortem examination of horses in areas of high fly prevalence and although dramatic in appearance their true pathogenic significance remains obscure.
Fig. 4.6 Mouth hooks (top) and ventral spines (bottom) of the fifth segment of (a) Gasterophilus intestinalis-, (b) G. inermis; (c) G. nasalis; (d) G. haemorrhoidalis; (e) G. pecorum (reproduced from Zumpt, 1965).
Fig. 4.7 Gasterophilus larvae in the stomach of a horse.
Clinical signs: Burrowing of the first-stage larvae in the mouth lining, tongue and gums can produce pus pockets, loosen teeth and cause loss of appetite in the host. Larvae attached to the gastrointestinal mucosa cause inflammation and ulceration. The adult fly can cause irritation and intense avoidance reactions when hovering around the host and laying eggs on the skin. Ovipositing females may be tenacious, laying eggs on mobile as well as stationary animals. Females will pursue galloping horses and immediately resume oviposition when the horse stops.
Diagnosis: The adult flies may be visible and recognisable on and around the host. The eggs are also easily recognisable on the host and may be identified by colour and location. Damage to the mouth and tongue may be detected. The presence of larval parasites in the stomach is difficult to identify except by observation of the larvae in faeces.
Pathology: The burrowing of first- and second-stage Gasterophilus larvae in the tissues of the tongue and mouth may result in lesions, the appearance of which is dependent on the degree of burrowing activity. Active tunnelling removes virtually all tissue in the path of the larvae including nerves and capillaries leading to haemorrhage and exocytosis into the tunnels, which fill with erythrocytes mixed with macrophages, lymphocytes and some eosinophils. The tunnels may become infected with bacteria, which result in microabscesses, composed of clotted erythrocytes, bacteria, disintegrating epithelial cells and large numbers of neutrophils. Cells surrounding the tunnel exhibit pyknosis, epithelial hydropic degeneration and became separated from each other.
Interdental gingiva invaded by larvae appear hyperaemic and denuded of epithelia. Recession and ulceration of the gingiva produces periodontal pockets. Extensive invasion by larvae leads to compound periodontal pockets.
The attachment of third-stage larvae results in ulceration at the site of attachment with intense fibrosis below the ulcer. The cephalic portions of embedded larvae become surrounded by a cellular exudate containing erythrocytes and mononuclear cells.
Epidemiology: Adult flies are most active during late summer.
Treatment: The most widely used specific drugs included trichlorphon and dichlorvos, but these have generally been replaced by broad-spectrum macrocyclic lactone compounds, such as ivermectin and moxidectin.
Control: The most effective means of control of this parasite is to remove the eggs from the host’s coat. This requires, where possible, daily examination of the animal, paying particular attention to the area around the lips. If eggs are found during the summer and autumn, subsequent infection can be prevented by vigorously sponging with warm water containing an insecticide. The warmth stimulates hatching and the insecticide kills the newly hatched larvae.
From the life cycle it is clear that in temperate areas during the winter almost the entire Gasterophilus population will be present as larvae in the stomach, since adult fly activity ceases with the advent of the first frosts in autumn. A single treatment during the winter, therefore, should effectively break the cycle. In certain areas, where adult fly activity is prolonged by mild conditions, additional treatments may be required. Despite the lack of understanding of the pathogenic effect of bots, treatment is usually recommended as owners are concerned when larvae appear in the faeces. Treatment, however, does reduce fly populations and thus the fly worry associated with egg-laying.
Gasterophilus haemorrhoidalis
Common name: Bot flies
Predilection site: Stomach
Parasite class: Insecta
Family: Oestridae
Description: In G. haemorrhoidalis, the spines on the ventral surface of the larval segments are arranged in two rows. The head segment has only lateral groups of denticles and the dorsal row of spines on the eighth segment is not broadly interrupted medially. The mouth hooks are uniformly curved dorsally and directed laterally (Fig. 4.6d). The body spines are sharply pointed.
Hosts: Horse, donkey
Life cycle: G. haemorrhoidalis lays batches of 150–200 eggs around the lips. The adult flies have a short lifespan and females can deposit all of their eggs within 2–3 hours if the weather is mild and a suitable host is available. The eggs are easily seen: they are 1–2 mm long and usually black in colour. They either hatch spontaneously in about 5 days or are stimulated to do so by warmth, which may be generated during licking and self-grooming. Larvae either crawl into the mouth or are transferred to the tongue during licking. The larvae can burrow into the epidermis of the lips and from there migrate into the mouth. These then penetrate the tongue or buccal mucosa and burrow through in these tissues for several weeks while feeding, before moulting and passing via the pharynx and oesophagus to the stomach where they attach to the gastric epithelium. The larvae remain and develop in the stomach for periods of 10–12 months. When mature in the following spring or early summer, they detach and are passed in the faeces. In this species, the larvae reattach in the rectum for a few days before being passed out. Pupation takes place on the ground, and after 1–2 months the adult flies emerge. These do not feed, and live for only a few days or weeks, during which time they mate and lay eggs. If suitable hosts are unavailable the flies move to high points to aggregate and mate, following which the females initiate a longer-distance search for hosts. There is therefore only one generation of flies per year in temperate areas.
Geographical distribution: Worldwide
Gasterophilus inermis
Common name: Bot flies
Predilection site: Stomach
Parasite class: Insecta
Family: Oestridae
Description: In G. inermis the spines on the ventral surface of the larval segments are arranged in two rows. The head segment has only lateral groups of denticles and the dorsal row of spines on the eighth segment are not broadly interrupted medially. The mouth hooks are strongly curved, with their tips directed backwards and approaching the base (Fig. 4.6b). The body spines are sharply pointed. Body segment 3 has three complete rows of spines, and body segment 11 has one row of spines interrupted by a broad median gap.
Hosts: Horse, donkey, zebra
Life cycle: The adult female lays up to 300 eggs on the cheeks and around the mouth of the host animal. These are each attached individually to the base of a hair in these regions. The eggs are easily seen, being 1–2 mm in length and usually creamy white in colour. The eggs either hatch spontaneously in about 5 days or are stimulated to do so by warmth, which may be generated during licking and self-grooming. After hatching, the larvae burrow into the epidermis, and migrate towards the mouth. The migration route of the larvae can be detected by the presence of a track along which the hair has fallen out. The larvae enter at the corner of the mouth and penetrate the mucous membranes of the cheek. The second- and third-stage larvae migrate to the rectum where they reattach. The larvae remain and develop in the host for periods of 10–12 months. When mature in the following spring or early summer, they detach and are passed in the faeces. Pupation takes place on the ground, and after 1–2 months the adult flies emerge. These do not feed and live for only a few days or weeks, during which time they mate and lay eggs. There is therefore only one generation of flies per year in temperate areas.
Geographical distribution: Northern Europe, northern Asia, Africa
Gasterophilus intestinalis
Common name: Bot flies
Predilection site: Stomach
Parasite class: Insecta
Family: Oestridae
Description: In G. intestinalis, the mouth hooks are not uniformly curved dorsally and the body spines have blunt tips (Fig. 4.6a).
Hosts: Horse, donkey
Life cycle: Eggs are laid on the hairs of the forelegs and shoulders. Several eggs may be glued to each hair and up to 1000 eggs may be deposited by a female G. intestinalis during its lifetime of only a few days. The eggs are easily seen, being 1–2 mm in length and usually creamy white in colour; they either hatch spontaneously in about 7 days or are stimulated to do so by warmth, which may be generated during licking and self-grooming. Larvae either crawl into the mouth or are transferred to the tongue during licking. These then penetrate the tongue or buccal mucosa at the anterior end of the tongue where they excavate galleries in the sub-epithelial layer of the mucous membrane. The larvae wander in these tissues for several weeks before exiting the tongue and moulting. Second-stage larvae attach for a few days to the sides of the pharynx, before moving to the oesophageal portion of the stomach where they cluster at the boundary of glandular and non-glandular epithelium. Larvae remain and develop in this site for periods of 10–12 months. When mature in the following spring or early summer, they detach and are passed in the faeces. Pupation takes place on the ground and after 1–2 months the adult flies emerge. These do not feed and live for only a few days or weeks, during which time they mate and lay eggs. There is therefore only one generation of flies per year in temperate areas.
Geographical distribution: Worldwide
Gasterophilus nasalis
Common name: Throat bot flies
Predilection site: Stomach
Parasite class: Insecta
Family: Oestridae
Description: G. nasalis have spines on the ventral surface of the larval segments arranged in a single row. The first three body segments are more or less conical and the third segment has a dorsal row of spines and sometimes ventral spines (Fig. 4.6c).
Hosts: Horse, donkey and zebra
Life cycle: The throat bot fly, G. nasalis, lays its eggs in the intermandibular area. Eggs are laid in batches of up to 500, usually with one egg attached per hair. The eggs are easily seen, being 1–2 mm in length and usually creamy white in colour. Eggs either hatch spontaneously in about 7 days or are stimulated to do so by warmth, which may be generated during licking and self-grooming. Larvae either crawl into the mouth or are transferred to the tongue during licking. These then burrow into the spaces around the teeth and between the teeth and gums. This may result in the development of pus sockets and necrosis in the gums. The first larval stage lasts 18–24 days, following which larvae moult and second-stage larvae move via the pharynx and oesophagus to the stomach, where they attach to the gastric epithelium. In the stomach, the yellow G. nasalis larvae attach around the pylorus and sometimes the duodenum. Larvae remain and develop in this site for periods of 10–12 months. When mature in the following spring or early summer, they detach and are passed in the faeces. Pupation takes place on the ground, and after 1–2 months the adult flies emerge. These do not feed and live for only a few days or weeks, during which time they mate and lay eggs. There is therefore only one generation of flies per year in temperate areas.
Geographical distribution: Worldwide, particularly the Holarctic
Gasterophilus nigricornis
Common name: Bot flies, broad-bellied horse bot
Predilection site: Stomach
Parasite class: Insecta
Family: Oestridae
Description: In G. nigricornis spines on the ventral surface of the larval segments are arranged in a single row. The first three body segments are more or less cylindrical, showing sharp constrictions posteriorly, and the third segment is without spines dorsally or ventrally.
Hosts: Horse, donkey
Life cycle: Female flies alight on the host’s cheek to oviposit. The eggs are easily seen; they are 1–2 mm long and usually creamy white in colour. The larvae hatch in 3–9 days and burrow directly into the skin. They then burrow to the corner of the mouth and penetrate the mucous membranes inside the cheek. Once they have reached the central part of the cheek (about 20–30 days after hatching) they moult and leave the mucous membranes. The second-stage larvae are then swallowed, following which they attach themselves to the wall of the duodenum. Larvae remain and develop in this site for periods of 10–12 months, and when mature in the following spring or early summer they detach and are passed in the faeces. Pupation takes place on the ground and after 1–2 months the adult flies emerge. These do not feed and live for only a few days or weeks during which time they mate and lay eggs. There is therefore only one generation of flies per year in temperate areas.
Geographical distribution: Middle East, southern Russia and China
Gasterophilus pecorum
Common name: Bot flies, dark-winged horse bot
Predilection site: Stomach
Parasite class: Insecta
Family: Oestridae
Description: G. pecorum has spines on the ventral surface of the larval segments, which are arranged in two rows. The head segment has two lateral groups of denticles and one central group, the latter situated between the antennal lobes and mouth hooks. The dorsal rows of spines are broadly interrupted medially on the 7th and 8th segments. The 10th and 11th segments have no spines.
Hosts: Horse, donkey
Life cycle: Adult G. pecorum are most active in late summer and unlike other species, the dark-coloured eggs are laid on pasture and are ingested by horses during grazing. Up to 2000 eggs are laid in batches of 10–115. The eggs are highly resistant and the developed larva may remain viable for months within its egg until ingested by horses. In the mouth, the eggs hatch within 3–5 minutes. First-stage larvae immediately penetrate the mucous membrane of the lips, gums, cheeks, tongue and hard palate and burrow towards the root of the tongue and soft palate, where they may remain for 9–10 months until fully developed. They may also be swallowed and settle in the walls of the pharynx, oesophagus or stomach. When mature in the following spring or early summer, the larvae detach and are passed in the faeces. Pupation takes place on the ground and after 1–2 months the adult flies emerge. These do not feed and live for only a few days or weeks, during which time they mate and lay eggs. There is therefore only one generation of flies per year in temperate areas.
Geographical distribution: Europe, Africa, Asia
Pathogenesis: Gasterophilus pecorum is the most pathogenic species in the genus. Large numbers of attached larvae can cause inflammation, hinder swallowing and may eventually lead to death resulting from constriction of the oesophagus.
Clinical signs: Burrowing of the first-stage larvae in the mouth lining, tongue and gums can produce pus pockets, loosen teeth and cause loss of appetite in the host. Large numbers of attached larvae can cause inflammation, choking and hinder swallowing.
Diagnosis: Larvae present in the pharynx can usually be seen on direct inspection. Larvae further down the digestive tract can only be detected by observation of the mature detached larvae in faeces.
SMALL INTESTINE
Strongyloides westeri
Common name: Threadworm
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Rhabditoidea
Description, gross: Slender, hair-like worms, 6–9 mm long. Only females are parasitic.
Description, microscopic: The long oesophagus may occupy up to one third of the body length and the uterus is intertwined with the intestine giving the appearance of twisted thread. Unlike other intestinal parasites of similar size the tail has a blunt point. Strongyloides eggs are oval, thin-shelled and small, 40–52 × 32–40 μm, being half the size of typical strongyle eggs (Fig. 4.8). The hatched L1 is passed out in the faeces.
Hosts: Horse, donkey, zebra, rarely pig
Life cycle: Strongyloides is unique among the nematodes of veterinary importance, being capable of both parasitic and free-living reproductive cycles. The parasitic phase is composed entirely of female worms in the small intestine and these produce larvated eggs by parthenogenesis, i.e. development from an unfertilised egg. After hatching, larvae may develop through four larval stages into free-living adult male and female worms and this can be followed by a succession of free-living generations. However under certain conditions, possibly related to temperature and moisture, the L3 can become parasitic, infecting the host by skin penetration or ingestion and migrating via the venous system, the lungs and trachea to develop into adult female worms in the small intestine.
Fig. 4.8 Egg of Strongyloides westeri.
Foals may acquire infection immediately after birth from the mobilisation of arrested larvae in the tissues of the ventral abdominal wall of the dam, which are subsequently excreted in the milk. The prepatent period is from 8–14 days, depending on the mode of infection.
Geographical distribution: Worldwide
Pathogenesis: Mature parasites are found in the duodenum and proximal jejunum and if present in large numbers may cause inflammation with oedema and erosion of the epithelium. This results in catarrhal enteritis with impairment of digestion and absorption. Migration of larvae through the lungs can cause severe haemorrhage and respiratory distress. Skin penetration may result in irritation and dermatitis.
Clinical signs: Foals with heavy burdens show acute diarrhoea, weakness and emaciation. Older animals may harbour large burdens without showing clinical signs.
Diagnosis: The clinical signs in very young animals, usually within the first few weeks of life, together with the finding of large numbers of the characteristic eggs or larvae in the faeces are suggestive of strongyloidosis. It should be emphasised, however, that high faecal egg counts may be found in apparently healthy animals.
Pathology: Adult worms establish in tunnels in the epithelium at the base of the villi in the small intestine. In large numbers they may cause villous atrophy, with a mixed mononuclear inflammatory cell infiltration of the lamina propria. Crypt epithelium is hyperplastic and there is villous clubbing.
Epidemiology: Infections are very common especially in warm and humid environments. Strongyloides infective larvae are not ensheathed and are susceptible to extreme climatic conditions. However, warmth and moisture favour development and allow the accumulation of large numbers of infective stages. A second major source of infection for the very young animal is the reservoir of larvae in the tissues of their dams and this may lead to clinical strongyloidosis in foals in the first few weeks of life. Successive progeny from the same dam often show heavy infections.
Treatment: Specific control measures for infection are rarely called for. Not all anthelmintics show high efficacy, but most of the modern benzimidazoles are effective. Macrocyclic lactones are effective against against adult worms.
Control: Reduction in numbers of free-living larvae by removal of faeces and provision of dry bedding and areas may limit numbers and transmission. On stud farms, foals are often given an anthelmintic treatment at 1–2 weeks of age against S. westeri.
Parascaris equorum
Synonym: Ascaris equorum, Ascaris megacephala
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Ascaridoidea
Description, gross: This very large rigid, stout, whitish nematode, up to 40 cm in length, cannot be confused with any other intestinal parasite of equines. Males measure 15–25 cm and females up to 40 cm.
Description, microscopic: The adult parasites have a simple mouth opening surrounded by three large lips and in the male the tail has small caudal alae. The dorsa lip has two double papillae and each ventrolateral lip has one double subventral, and a small lateral papilla. Spicules are long and stout. The egg of P. equorum is almost spherical, 50–75 × 40–50 μm, brownish and thick-shelled with an outer, pitted coat.
Hosts: Horse, donkey
Life cycle: The life cycle is direct and migratory involving a hepato-pulmonary route. Eggs produced by the adult female worms are passed in the faeces and can reach the infective stage containing the L2 in as little as 10–14 days, although development may be delayed at low temperatures. After ingestion and hatching the larvae penetrate the intestinal wall and within 48 hours have reached the liver. By 2 weeks they have arrived in the lungs where they migrate up the bronchi and trachea, are swallowed and return to the small intestine. The site of occurrence and timing of the parasitic larval moults of P. equorum are not precisely known, but it would appear that the moult from L2 to L3 occurs between the intestinal mucosa and the liver and the two subsequent moults occur in the small intestine. The minimum prepatent period of P. equorum is 10 weeks; longevity is up to 2 years. There is no evidence of prenatal infection.
Geographical distribution: Worldwide
Pathogenesis: During the migratory phase of experimental infections, up to 4 weeks following infection, the major signs are frequent coughing, accompanied in some cases by a greyish nasal discharge, although the foals remain bright and alert. Light intestinal infections are well tolerated, but moderate to heavy infections will cause unthriftiness in young animals with poor growth rates, dull coats and lassitude. A wide variety of other clinical signs, including fever, nervous disturbances and colic, has been attributed to field cases of parascariosis, but these have not been observed in experimental studies.
Clinical signs: Adult worms in heavy infections can cause severe enteritis resulting in alternating constipation and foul-smelling diarrhoea. Large numbers of larvae may cause coughing, with fever and anorexia.
Diagnosis: This depends on clinical signs and the presence of spherical, thick, brownish, rough-shelled eggs on faecal examination. Occasionally, atypical thick-walled eggs are seen that lack the dark outer shell. If disease due to prepatent infection is suspected, faecal examination having proved negative, diagnosis may be confirmed by administration of an anthelmintic when large numbers of immature worms may be observed in the faeces.
Pathology: Gross changes are provoked in the liver and lungs by migrating P. equorum larvae. In the liver, larvae cause focal haemorrhages and eosinophilic tracts that resolve, leaving whitish areas of fibrosis. Larval migration in the lungs also leads to haemorrhage and infiltration by eosinophils, which are later replaced by accumulations of lymphocytes, while subpleural greyish green lymphocytic nodules develop around dead or dying larvae; these nodules are more numerous following reinfection. These liver and lung lesions are usually of little pathological significance.
Although the presence of worms in the small intestine (Fig. 4.9) is not associated with any specific lesions, heavy infections have occasionally been reported as a cause of impaction and perforation leading to peritonitis. Adult worms may cause catarrhal enteritis and intermittent diarrhoea. However, under experimental conditions, unthriftiness is a major sign and despite maintaining a good appetite infected foals lose weight and may become emaciated. Competition between a large mass of parasites and the host for nutrients may be the underlying cause of this weight loss.
Fig. 4.9 Parascaris equorum from the intestine of an infected horse.
Epidemiology: Infection with Parascaris equorum is common throughout the world and is a major cause of unthriftiness in young foals. There are two important factors in the epidemiology of infection. First is the high fecundity of the adult female parasite, some infected foals passing millions of eggs in the faeces each day. Secondly, the extreme resistance of the egg in the environment ensures its persistence for several years. The sticky nature of the outer shell may also facilitate passive spread of eggs.
In the northern hemisphere, summer temperatures are such that many eggs become infective at a time when a population of susceptible foals is present. The infections acquired by these result in further contamination of pasture with eggs which may survive during several subsequent grazing seasons. Although mature horses may harbour a few adult worms and act as carriers, heavy burdens are usually confined to yearlings and to foals, which become infected from the first month or so of life; infection is maintained largely by seasonal transmission between these groups of young animals. Exposed foals often develop immunity, resulting in partial or total loss of the worm population.
Treatment: Benzimidazoles (such as fenbendazole, oxfendazole, oxibendazole), pyrantel, ivermectin and moxidectin are all effective against adult and larval stages when given orally.
Control: Since transmission is largely on a foal-to-foal basis it is good policy to avoid using the same paddocks for nursing mares and their foals in successive years. Treatment should start when foals are about 8 weeks old and be repeated at appropriate intervals depending on the anthelmintic used.
Notes: Infection with Parascaris equorum is common throughout the world and is a major cause of unthriftiness in young foals.
Tapeworms
Several tapeworm species are found in horses, donkeys and other equines. Intermediate hosts for all species are forage mites of the family Oribatidae, in which the intermediate cysticercoid stages are found.
Life cycle: Mature segments are passed in the faeces and disintegrate, releasing the eggs. These are ingested by forage mites in which they develop to the cysticercoid stage in 2–4 months. The adult tapeworms are found in the intestine of horses 1 or 2 months after the ingestion of infected mites in the herbage.
Diagnosis: Where clinical signs occur they may be difficult to differentiate from more common causes of unthriftiness and digestive upsets. However, it may be possible to confirm the presence of Anoplocephala by the demonstration of the typical eggs on faecal examination or on postmortem.
Epidemiology: Horses of all ages may be affected, but clinical cases have been reported mainly in animals up to 3–4 years of age.
Treatment: Specific treatment for Anoplocephala infection is rarely called for but a number of compounds have been reported as effective, including pyrantel at increased dosage rates (38 mg/kg). Praziquantel at 1 mg/kg is also effective.
Control: Control is difficult, since forage mites are widespread on pasture. Treatment with an effective anthelmintic before the animals enter new grazing may help to control Anoplocephala infections in areas where problems have arisen.
Anoplocephala perfoliata
Predilection site: Terminal ileum, caecum
Parasite class: Cestoda
Family: Anoplocephalidae
Description, gross: A. perfoliata is up to 4–8 cm in length by 1.2 cm wide.
Description, microscopic: There is a small, rounded scolex, 2–3 mm in diameter, with a lappet behind each of the four suckers, but there is neither a rostellum nor hooks. It has a very short neck and the strobila widens rapidly, individual proglottids being much wider than they are long. Eggs are irregularly spherical or triangular, 65–80 μm in diameter. The oncosphere is supported by a pair of projections – the pyriform apparatus.
Geographical distribution: Worldwide
Pathogenesis: Anoplocephala perfoliata has been considered to be relatively non-pathogenic but there is increasing evidence that heavy infections may cause severe clinical signs and may even prove fatal. A. perfoliata is usually found around the ileocaecal junction (Fig. 4.10) and causes ulceration of the mucosa at its site of attachment; these lesions have been incriminated as a cause of intussusception. Cases of intestinal obstruction and perforation of the intestinal wall have been recorded associated with massive infections.
Fig. 4.10 Anoplocephala perfoliata tapeworms around the ileocaecal junction.
Clinical signs: In most infections there are no clinical signs. However, when there are significant pathological changes in the intestine there may be unthriftiness, enteritis and colic. Perforation of the intestine will prove rapidly fatal.
Pathology: The mucosa at the site of attachment may be inflamed, thickened and ulcerated, particularly in the areas of the ileocaecal junction where it may lead to partial or fatal occlusion of the ileocaecal orifice.
Anoplocephala magna
Common name: Dwarf equine tapeworm
Predilection site: Small intestine, rarely stomach
Parasite class: Cestoda
Family: Anoplocephalidae
Description, gross: A. magna is similar morphologically to A. perfoliata but much longer, up to 80.0 cm.
Description, microscopic: The scolex is large, 4–6 mm wide with suckers opening anteriorly, and there are no lappets on the scolex. The neck is short, as are the segments. The genital organs are single and the pores are unilateral. Eggs are similar to A. perfoliata.
Geographical distribution: Worldwide
Pathogenesis: Heavy infections of Anoplocephala magna may cause catarrhal, haemorrhagic or ulcerative enteritis. Cases of intestinal obstruction, colic and perforation of the intestinal wall have been recorded associated with massive infections.
Clinical signs: Rare, but infection causes diarrhoea and colic.
Pathology: The mucosa at the site of attachment may be inflamed, thickened and ulcerated.
Paranoplocephala mamillana
Synonym: Anoplocephaloides mamillana
Predilection site: Small intestine, rarely stomach
Parasite class: Cestoda
Family: Anoplocephalidae
Description, gross: P. mamillana is only 6–50 × 4–6 mm in size.
Description, microscopic: There are no lappets on the narrow scolex and the suckers are slit-like. The scolex is large and without rostellum and hooks. The gravid segments are wider than they are long. Eggs are irregularly spherical or triangular, 51 × 37 μm in diameter.
Geographical distribution: Worldwide
Pathogenesis: Paranoplocephala is usually considered to be relatively non-pathogenic.
Clinical signs: In most infections there are no clinical signs.
Diagnosis: It may be possible to confirm the presence of Paranoplocephala by the demonstration of the typical eggs on faecal examination or on postmortem.
Pathology: Infection is rarely associated with lesions but occasionally the site of attachment is inflamed and slightly ulcerated.
Epidemiology: Horses of all ages may be affected.
Coccidiosis
Several species of coccidia have been reported from horses. Few details are available on the life cycles, pathogenesis and epidemiology and pathogenesis. Similarly, little is also known about treatment and control of equine coccidiosis, but by analogy with other hosts, sulphonamides can be tried. Prevention is based on good management and hygiene. Young animals should be kept off heavily contaminated pastures when they are most susceptible. Good feeding of dams prior to parturition and rearing of animals of similar ages limits the build-up and spread of oocysts.
Eimeria leuckarti
Synonym: Globidium leuckarti
Predilection site: Small intestine
Parasite class: Sporozoasida
Family: Eimeriidae
Host: Horse, donkey
Description: Oocysts are ovoid or pyriform, flattened at the small end and very large, measuring 70–90 × 49–69 μm (mean 80 × 60 μm), with a thick dark shell and distinct micropyle. Sporocysts are elongate, 3043 × 12–15 μm, with a Stieda body and residuum. The sporozoites are up to 35 μm long, lie lengthwise head to tail in the sporocysts and have a clear globule at the broad end.
Life cycle: Complete details of the life cycle are not known and merogony stages have not been described. Early gamonts are in the cells of the intestinal lamina propria of the small intestine. The prepatent period is 15–33 days and sporulation time is 15–41 days.
Geographical distribution: Worldwide
Pathogenesis: Occurs in the small intestine of horses and donkeys and has been incriminated as the cause of an intermittent diarrhoea.
Diagnosis: Diagnosis is difficult, and because of the heavy nature of the oocysts, sedimentation techniques should be employed or, if flotation is used, a concentrated sugar solution is necessary.
Pathology: The pathology includes marked inflammatory changes in the mucosa and a disruption of villous architecture due to the presence of large meront stages (Fig. 4.11).
Fig. 4.11 ‘Giant’ meront of Eimeria leuckarti.
Eimeria solipedum
Predilection site: Small intestine
Parasite class: Sporozoasida
Family: Eimeriidae
Host: Horse, donkey
Description: Oocysts are spherical, orange to yellowish brown, 15–28 μm in diameter, without an oocyst residuum or micropyle. Sporocysts are ellipsoid to oval, 5 × 3 μm.
Geographical distribution: Russia, CIS
Pathogenesis: Has been reported to cause intermittent diarrhoea.
Diagnosis: Identification of oocysts from faecal samples
Epidemiology: Almost 10% of horses in the former Soviet Union (now Russia and CIS) were found to be infected.
Eimeria uniungulati
Predilection site: Small intestine
Parasite class: Sporozoasida
Family: Eimeriidae
Host: Horse, donkey
Description: Oocysts are oval or ellipsoid, light orange, 15–24 × 12–17 μm, without an oocyst residuum or micropyle. Sporocysts are oval, 6–10.5 × 4–6 μm with a central sporocyst residuum.
Geographical distribution: Russia, CIS
Pathogenesis: Not reported.
Epidemiology: Infection has been reported in 1–10% of horses in the former Soviet Union (now Russia and CIS).
Other protozoa
Cryptosporidium parvum
Predilection site: Small intestine
Parasite class: Sporozoasida
Family: Cryptosporidiidae
Hosts: Cattle, sheep, goat, horse, deer, man
Description: Mature oocysts are ovoidal or spheroidal, 5.0 × 4.5 μm (range 4.6–5.4 × 3.8–4.7 μm) and a length: width ratio of 1.19.
Geographical distribution: Worldwide
Pathogenesis: Cryptosporidiosis has been reported in immunodeficient foals as a cause of diarrhoea.
Clinical signs: Clinically the disease is characterised by anorexia and diarrhoea.
Epidemiology: Several mammals act as hosts to C. parvum but little is known of the importance of their involvement in transmitting infection to, or maintaining infection in domestic livestock. In the UK, surveys in horses have shown the presence of C. parvum in 28% of thoroughbred foals although there was no association between infection and diarrhoea. Subsequent studies have demonstrated the genotype in horses to be genotype 2.
Treatment: There is no known effective drug therapy, and where cryptosporidiosis is diagnosed, supportive treatment, in the form of antidiarrhoeals and fluids, is usually sufficient.
For more details see Chapter 2 (Cattle).
Giardia intestinalis
Synonym: Giardia duodenalis, Giardia lamblia, Lamblia lamblia
Predilection site: Small intestine
Parasite class: Zoomastigophorasida
Family: Diplomonadidae
Description: The trophozoite has a pyriform to ellipsoidal, bilaterally symmetrical body, 12–15 μm long by 5–9 μm wide. The dorsal side is convex and there is a large sucking disk on the ventral side. There are two anterior nuclei, two slender axostyles, eight flagellae in four pairs and a pair of darkly staining median bodies. The median bodies are curved bars resembling the claws of a hammer. Cysts are ovoid, 8–12 × 7–10 μm and contain four nuclei.
Hosts: Man, cattle, sheep, goat, pig, horse, alpaca, dog, cat, guinea pig, chinchilla
Geographical distribution: Worldwide
Pathogenesis: Infection in horses is considered non-pathogenic.
Clinical signs: No associated clinical signs
Treatment and control: Not required
Notes: There is still controversy over the classification of Giardia spp. The current molecular classification places isolates into eight distinct assemblages. Some authors give separate specific names to organisms isolated from different hosts although species specificity of many isolates is unknown. Phylogenetic data suggest that G. intestinalis is a species complex composed of several species that are host specific.
For more details see Chapter 2 (Cattle).
LARGE INTESTINE
Cyathostomins (‘small strongyles’)
The group ‘small strongyles’ embraces over 40 species, popularly known as trichonemes, cyathostomes or cyathostomins. For many years there has been a great deal of confusion in the classification of this group of parasites and in a new revision it has been proposed that the genus Trichonema be discarded and replaced by four main genera, namely Cyathostomum, Cylicocyclus, Cylicodontophorus and Cylicostephanus, these being collectively referred to as cyathostomes or more recently, cyathostomins. Other genera of unknown significance included in this group are Poteriostomum, Craterostomum and Oesophagodontus. Since the majority of species involved are similar both morphologically and in behaviour they will be referred to in this text as cyathostomins or small strongyles. Fifteen species of small strongyles are commonly present in large numbers.
The following general descriptions apply to all species of small strongyles.
Pathogenesis and clinical signs: Small strongyles are extremely prevalent, and grazing horses usually carry a mixed burden of large and small strongyles. The major clinical signs associated with heavy infections in animals up to 2–3 years of age are unthriftiness, anaemia and sometimes diarrhoea. Marked clinical signs are less common in older animals, although general performance may be impaired. In temperate countries an acute syndrome of catarrhal and/or haemorrhagic enteritis with severe diarrhoea, leading to emaciation and in some cases death, in horses and ponies in the spring has been reported; this is associated with the simultaneous mass emergence of cyathostome L4 from the intestinal mucosa and submucosa. This may have aetiological and epidemiological similarities to type II ostertagiosis in young cattle and is often referred to as acute larval cyathostomosis.
Diagnosis: Diagnosis is based on the grazing history and clinical signs of loss of condition and anaemia. Although the finding of typical, oval, thin-shelled strongyle eggs on faecal examination may be a useful aid to diagnosis, it is important to remember that substantial worm burdens may be associated with faecal egg counts of only a few hundred eggs per gram (epg) due either to low fecundity of adult worms, the long prepatent period or to the presence of many immature parasites. On postmortem, it may be possible to visualise the L4 larvae as tiny grey spots in the intestinal mucosa using the transmural illumination technique. On some occasions when heavy cyathostome infections in the spring cause severe diarrhoea, thousands of bright red cyathostome L4, apparently unable to establish, may be present in the faeces.
Fig. 4.12 Developing small strongyle larvae in the mucosa of the caecum.
Pathology: Parasitic larval development of most species takes place entirely in the mucosa of the caecum and colon, but a few penetrate the muscularis and develop in the submucosa. The entry of larval cyathostomes (Fig. 4.12) into the lumina of the tubular glands generally provokes an inflammatory response together with marked goblet cell hypertrophy. Emergence of the bright red L4 into the gut lumen appears to be associated with a massive infiltration of the gut mucosa with eosinophils. Many thousand L4 may be present, but their pathogenic significance has been little studied. There are, however, reports of heavy natural infections of adult worms and larvae associated with catarrhal and haemorrhagic enteritis, with thickening and oedema of the mucosa, especially in animals of 6 months to 3 years of age.
Mature parasites are frequently present in large numbers in the lumen of the large intestine; during feeding those species with small buccal capsules take in only glandular epithelium, while large species may damage deeper layers of the mucosa. Although the erosions caused by individual parasites may be slight, when large numbers are present a desquamative enteritis may result.
Epidemiology: Strongylosis is most frequently a problem in young horses reared on permanent horse pastures, although cases of severe disease may occur in adult animals kept in suburban paddocks and subjected to overcrowding and poor management. Although the preparasitic larval requirements of the horse strongyles are similar to those of the trichostrongyles of ruminants, adult horses, unlike cattle, may carry substantial worm burdens and therefore have a considerable influence on the epidemiology of infection. Thus there are two sources of infection during the grazing season in temperate areas. First there are infective larvae, which developed during the previous grazing season and have survived on pasture over winter. The second and probably more important source of infective larvae are the eggs passed in the current grazing season by horses, including nursing mares, sharing the same grazing area. Pasture larval levels increase markedly during the summer months when environmental conditions are optimal for rapid development of eggs to L3 and may lead to the accumulation of large infections in the autumn.
At present there is little evidence for a consistent periparturient rise in faecal egg output in breeding mares due to a relaxation of immunity, since the egg rise in the spring occurs in both breeding and nonbreeding animals and is often unrelated to parturition.
There is increasing evidence that many cyathostome L3 ingested during the autumn show a degree of hypobiosis and remain in the large intestinal mucosa until the following spring. Mass emergence of these larvae results in the severe clinical signs described previously.
Treatment: Treatment for clinical strongylosis should not be necessary if prophylactic measures are adequate. There are several broad-spectrum anthelmintics, including the benzimidazoles, pyrantel and the avermectins/milbemycins (macrocyclic lactones), which are effective in removing lumen-dwelling adult and larval strongyles and these are usually marketed as in-feed or oral preparations. The macrocyclic lactones have the additional advantage of activity against larvae of horse bot flies (Gasterophilus spp), which develop in the stomach. Some modern benzimidazoles and macrocyclic lactones are also efficient against both developing cyathostome larvae in the gut wall and some migrating stages of the large strongyles.
Control: Since horses of any age can become infected and excrete eggs, all grazing animals over 2 months of age should be treated every 4–8 weeks with an effective broad-spectrum anthelmintic. This regimen will also control infections with other intestinal parasites such as Parascaris equorum and Oxyuris equi. Any new animals joining a treated group should receive an anthelmintic and be isolated for 48–72 hours before being introduced. If possible, a paddock rotation system should be adopted so that nursing mares and their foals do not graze the same area in successive years. Avoid overstocking.
If horses are housed in the winter, treatment at that time with an anthelmintic effective against larval cyathostomes will reduce the risk of disease due to their mass emergence in the spring.
There is evidence that some species of cyathostomes are becoming resistant to benzimidazole compounds, pyrantel and piperizine, and to avoid this it is suggested that these should be used strategically alternated with chemically unrelated anthelmintics on an annual or a 6–monthly basis. Faecal samples from groups of horses should be examined at regular intervals to monitor drug efficiency.
The introduction of pasture management techniques may be feasible for some enterprises, such as pasture cleaning twice a week (vacuuming or sweeping) or the alternate grazing of pasture by ruminant livestock.
Cyathostomum spp
Synonym: Trichonema spp
Common name: Small strongyles, cyathostomins, cyathostomes, trichonemes
Predilection site: Large intestine
Parasite class: Nematoda
Superfamily: Strongyloidea
Family: Strongylidae
Subfamily: Cyathostominae
Description, gross: Small (5–12 mm in length), bursate nematodes ranging in colour from white to dark red, the majority being visible on close inspection of the large intestinal mucosa or contents (Fig. 4.13).
Description, microscopic: The well developed short buccal capsule is cylindrical, without teeth, and species differentiation is based on characteristics of the buccal capsule, and the internal and external leaf crowns. Cyathostomum have a moderately high mouth collar, with cephalic papillae not very prominent. The buccal capsule is broader than deep and has no dorsal gutter. Elements of the external leaf crown are larger, broader and fewer than elements of the internal leaf crown. Inner leaf crown is deep in the buccal capsule and has sclerotised extra-chitinous supports at or near the anterior edge of buccal capsule. The dorsal ray of the male bursa is split to the origin of the externo-dorsal rays and the spicules are filiform, equal in length with ‘pickshaped’ tips. In the female, the vulva is close to the anus. The tail may be straight or bent dorsally with a ventral bulge, anterior to the vulva.
Fig. 4.13 Adult and larval small strongyles on the mucosa of the large intestine.
Table 4.1 Cyathostomum species.
Hosts: Horse, donkey
Life cycle: Hatching of eggs and development to L3 is complete within 2 weeks during the summer in temperate areas, after which the larvae migrate from the faeces on to the surrounding herbage. After ingestion, the L3 exsheath and invade the wall of the ileum and large intestine where they develop to L4 before emerging into the gut lumen and moulting to become young adult worms. The prepatent periods of members of this genus are generally between 2 and 3 months, although this may be extended due to hypobiosis in some species.
Geographical distribution: Worldwide
Cylicocyclus spp
Synonym: Trichonema spp
Common name: Small strongyles, cyathostomins, cyathostomes, trichonemes
Predilection site: Large intestine
Parasite class: Nematoda
Superfamily: Strongyloidea
Family: Strongylidae
Subfamily: Cyathostominae
Description, gross: Small to medium size (10–25 mm in length), bursate nematodes ranging in colour from white to dark red, the majority being visible on close inspection of the large intestinal mucosa or contents.
Description, microscopic: The well developed short buccal capsule is cylindrical, without teeth, and species differentiation is based on characteristics of the buccal capsule, and the internal and external leaf crowns. Cylicocyclus have a high mouth collar with broad lateral papillae. Elements of the external leaf crown are larger, fewer and broader than those of the inner leaf crown, the latter being short, with thin rods at or near the anterior edge of the buccal capsule. The buccal capsule is short, broader than deep, with thin walls tapering anteriorly, with a hoop-shaped thickening around the posterior margin. In the male the dorsal ray is split to the region of origin of the externodorsal rays and the spicules are filiform, of equal length with pick-shaped tails. In females, the vulva is near the anus and the tail is usually straight but may be bent slightly dorsally.
Hosts: Horse, donkey and other equids
Geographical distribution: Worldwide
Cylicodontophorus spp
Synonym: Schultzitrichonema
Common name: Small strongyles, cyathostomins, cyathostomes, trichonemes
Predilection site: Large intestine
Parasite class: Nematoda
Superfamily: Strongyloidea
Family: Strongylidae
Subfamily: Cyathostominae
Description, gross: Small (7–14 mm in length), bursate nematodes ranging in colour from white to dark red, the majority being visible on close inspection of the large intestinal mucosa or contents.
Description, microscopic: The well developed short buccal capsule is cylindrical, without teeth, and species differentiation is based on characteristics of the buccal capsule, and the internal and external leaf crowns. Cylicodontophorus have a high mouth collar, with inconspicuous lateral papillae and short and conical submedian papillae. The buccal capsule is short, thick walled, of nearly uniform thickness, and broader than deep. Inner leaf crown elements are longer, broader and less numerous than the external leaf crown elements, and are inserted near the anterior edge of the buccal capsule. The dorsal ray of the male bursa is split only to the proximal branch, and the spicules are filiform, equal in length with ‘hook-shaped’ tips. In the female, the tail is short with a sharp tip and a prominent ventral bulge may be present anterior to the vulva.
Hosts: Horse, donkey
Geographical distribution: Worldwide
Cylicostephanus spp
Synonym: Schultzitrichonema, Petrovinema
Common name: Small strongyles, cyathostomins, cyathostomes
Predilection site: Large intestine
Parasite class: Nematoda
Superfamily: Strongyloidea
Family: Strongylidae
Subfamily: Cyathostominae
Description, gross: Small (4–10 mm in length), bursate nematodes ranging in colour from white to dark red, the majority being visible on close inspection of the large intestinal mucosa or contents.
Table 4.2 Cylicocyclus species.
Table 4.3 Cylicodontophorus species.
Table 4.4 Cylicostephanus species.
Description, microscopic: The well developed short buccal capsule is cylindrical, without teeth, and species differentiation is based on characteristics of the buccal capsule, and the internal and external leaf crowns. Cylicostephanus have a depressed mouth collar, with inconspicuous lateral papillae and prominent submedian papillae. The buccal capsule is slightly narrow anteriorly, with a wall of varying thickness, and with a dorsal gutter. External leaf crown elements are longer, broader and less numerous then the internal leaf crown elements, which are short thin rods inserted near the anterior edge of the buccal capsule. The dorsal ray of the male bursa is split only to the proximal branch, and the spicules are filiform, equal in length with ‘pick-shaped’ tips. In the female, the vulva is near the anus, and the tail is usually straight.
Hosts: Horse, donkey
Geographical distribution: Worldwide
Poteriostomum imparidentatum
Common name: Non-migratory large strongyles
Predilection site: Large intestine
Parasite class: Nematoda
Superfamily: Strongyloidea
Family: Strongylidae
Subfamily: Cyathostominae
Description, gross: Males are 9–14 mm and females 13–21 mm.
Description, microscopic: This genus is closely related to the genus Cylicodontophorus. The two genera are easily separated based on characteristics of the buccal capsule, especially the point of insertion of the internal leaf crown and the character of the dorsal ray. In P. imparidentatum six elements of the internal leaf crown are markedly longer than the others.
Hosts: Horse, donkey
Geographical distribution: Worldwide
Poteriostomum ratzii
Common name: Non-migratory large strongyles
Predilection site: Large intestine
Parasite class: Nematoda
Superfamily: Strongyloidea
Family: Strongylidae
Subfamily: Cyathostominae
Description, gross: Males are 9–14 mm and females 13–21 mm.
Description, microscopic: This genus is closely related to the genus Cylicodontophorus. The two genera are easily separated based on characteristics of the buccal capsule, especially the point of insertion of the internal leaf crown and the character of the dorsal ray. In P. ratzii all elements of the internal leaf crown are of equal length.
Hosts: Horse, donkey
Geographical distribution: Worldwide
Craterostomum acuticaudatum
Synonym: Cylicostomum acuticaudatum, Cylicostomum mucronatum, Craterostomum mucronatum
Predilection site: Large intestine
Parasite class: Nematoda
Superfamily: Strongyloidea
Family: Strongylidae
Subfamily: Cyathostominae
Description, gross: Small worms, 6–10 mm long
Description, microscopic: The buccal capsule is of greatest diameter in the middle, the wall is thickened behind the anterior edge. The dorsal gutter is strongly developed. The shallow oesophageal funnel has three small triangular teeth that do not project into the buccal cavity. Elements of the external leaf crown are large and transparent and less numerous than the short, broad elements of the inner leaf crown that ring the anterior ridge of the buccal capsule. Sub-median papillae extend beyond the depressed mouth collar. In the female the tail is long and pointed and the vulva is relatively far from the anus.
Hosts: Horse, donkey
Geographical distribution: Africa, Asia, Europe
Craterostomum tenuicauda
Predilection site: Large intestine
Parasite class: Nematoda
Superfamily: Strongyloidea
Family: Strongylidae
Subfamily: Cyathostominae
Description, gross: Small worms, 6–10 mm long
Description, microscopic: The buccal capsule is of greatest diameter in the middle, the wall is thickened behind the anterior edge. The dorsal gutter is strongly developed. The shallow oesophageal funnel has three small triangular teeth that do not project into the buccal cavity. The elements of the external leaf crown (nine) are large and transparent and less numerous than short, broad elements of the inner leaf crown (18) that ring the anterior ridge of the buccal capsule. Submedian papillae are unnotched and extend beyond the depressed mouth collar. In the female, the tail is short and pointed and the vulva is relatively far from the anus.
Hosts: Horse, zebra
Geographical distribution: Africa, Asia
Pathogenesis: Not reported
Oesophagodontus robustus
Predilection site: Large intestine
Parasite class: Nematoda
Superfamily: Strongyloidea
Family: Strongylidae
Subfamily: Cyathostominae
Description, gross: Male worms are 15–16 mm and females 19–22 mm. There is a slight constriction between the anterior end and the rest of the body.
Description, microscopic: The buccal capsule is shaped like a funnel with a thickened ring encircling its posterior margin. The oesophageal funnel has three lancet-like teeth that do not project into the buccal capsule. There is no dorsal gutter.
Hosts: Horse, donkey
Geographical distribution: Worldwide
Large strongyles
Members of the genus Strongylus live in the large intestine of horses and donkeys and, with Triodontophorus, are commonly known as the large strongyles. Since members of these genera form only one component of the total parasitic burdens of the large intestine of the horse, general aspects on their epidemiology, treatment and control have been described under the general introduction to small strongyles.
Diagnosis of these migratory species is difficult during the migratory prepatent phase and is based on grazing history and clinical signs. Due to the long prepatent period, clinically apparent strongylosis may be associated with no, or low, faecal egg counts. Species or generic diagnosis is not usually required but may be undertaken by specialist laboratories based on morphology of larvae or adult worms.
Strongylus edentatus
Synonym: Alfortia edentatus
Common name: Large strongyles
Predilection site: Large intestine
Parasite class: Nematoda
Superfamily: Strongyloidea
Family: Strongylidae
Subfamily: Strongylinae
Description, gross: Robust dark red worms which are easily seen against the intestinal mucosa (Fig. 4.14). The well developed buccal capsule of the adult parasite is prominent, as is the bursa of the male. Male are 2.3–2.8 cm in size and females 3.3–4.4 cm. The head end is wider than the rest of the body.
Description, microscopic: Species differentiation is based on size and the presence and shape of the teeth in the base of the buccal capsule. The buccal capsule is wider anteriorly than at the middle and contains no teeth (Fig. 4.15a).
Hosts: Horse, donkey
Fig. 4.14 Strongylus edentatus feeding on the mucosa of the large intestine.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
