Hosts: Sheep, goat

Life cycle: Both the free-living and parasitic phases of the life cycle are similar to those of the bovine species, O. ostertagi.

Geographical distribution: Worldwide

Pathogenesis: In clinical infections, this resembles the situation in cattle and similar lesions are present at necropsy, although the morocco leather appearance of the abomasal surface seen in cattle is not common in sheep and goats. In subclinical infections, it has been shown under both experimental and natural conditions that T. circumcincta causes a marked depression in appetite and this, together with losses of plasma protein into the gastrointestinal tract and sloughed intestinal epithelium, results in interference with the post-absorptive metabolism of protein. In lambs with moderate infections of T. circumcincta carcase evaluation can show poor protein and fat deposition. Skeletal growth can also be impaired.

Clinical signs: The most frequent clinical sign is a marked loss of weight. Diarrhoea is intermittent and although stained hindquarters are common, the fluid faeces, that characterise bovine ostertagiosis, are less frequently seen.

Diagnosis: This is based on clinical signs, seasonality of infection and faecal egg counts and, if possible, postmortem examination, when the characteristic lesions can be seen in the abomasum. Plasma pepsinogen levels are above the normal of about 0.8 IU tyrosine and usually exceed 2.0 IU in sheep with heavy infections.

Pathology: The pathology is similar to that described for O. ostertagi in cattle. The developing parasites cause distension of parasitised gastric glands, leading to a thickened hyperplastic gastric mucosa similar to that seen in cattle (see Fig. 2.5). In heavy infections these nodules coalesce and the abomasal folds are often very oedematous and hyperaemic.

Epidemiology: In sheep, T. circumcincta and O. trifurcata are responsible for outbreaks of clinical disease, particularly in lambs. In Europe a clinical syndrome analogous to type I bovine ostertagiosis occurs from August to October; thereafter arrested development of many ingested larvae occurs and a type II syndrome has been occasionally reported in late winter and early spring, especially in young adults. In subtropical areas with winter rainfall outbreaks of disease occurs primarily in late winter.

Temperate regions

In Europe, the herbage numbers of T. circumcincta L₃ increase markedly from mid-summer onwards and this is when most disease appears. These larvae are derived mainly from eggs passed in the faeces of ewes during the periparturient period, from about 2 weeks prior to lambing until about 6 weeks post-lambing. Eggs passed by lambs, from worm burdens which have accrued from the ingestion of overwintered larvae, also contribute to the pasture contamination. It is these eggs deposited in the first half of the grazing season from April to June which give rise to the potentially dangerous populations of L₃ from July to October. If ingested prior to October, the majority of these larvae mature in 3 weeks; thereafter, many become arrested in development for several months and may precipitate type II disease when they mature.

Immunity is acquired slowly and usually requires exposure over two grazing seasons before a significant resistance to infection develops. Subsequently, adult ewes harbour only very low populations of Teladorsagia except during the annual periparturient rise (PPR).

Subtropical regions

The epidemiology in subtropical areas is basically similar to that in temperate zones, except that the seasonal timing of events is different. In many of these areas lambing is geared to an increase in the growth of pasture, which occurs with the onset of rain in late autumn or winter. This coincides with conditions which are favourable to the development of the free-living stages of Teladorsagia and so infective larvae accumulate during the winter to cause clinical problems or production loss in the second half of the winter; arrested larval development occurs at the end of the winter or early spring. The sources of pasture contamination are again the ewes during the PPR and the lambs following ingestion of larvae, which have survived the summer. The relative importance of these sources in any country varies according to the conditions during the adverse period for larval survival. Where the summer is very dry and hot, the longevity of L₃ is reduced, except in areas with shade and these can act as reservoirs of infection until the following winter. Although L₃ can persist in sheep faeces during adverse weather conditions the protection is probably less than that afforded by the more abundant bovine faecal pat.

Ostertagia trifurcata

In temperate regions this is similar to T. circumcincta. In tropical and subtropical zones where the summer is very dry and hot, the longevity of L₃ is reduced except in areas with shade and these can act as reservoirs of infection until the following winter. Although L₃ can persist in sheep faeces during adverse weather conditions the protection is probably less than that afforded by the more abundant bovine faecal pat. In winter rainfall areas the numbers of Ostertagia and Teladorsagia larvae on pasture reach a maximum in late winter and decline markedly through spring into summer as the pastures dry out.

Treatment: Ovine teladorsagiosis often responds well to treatment with any of the modern benzimidazoles or pro-benzimidazoles, levamisole, which in sheep is effective against arrested larvae, or the avermectins/milbemycins. However, the widespread prevalence of isolates of Teladorsagia circumcincta that are resistant to the benzimidazoles, and increasingly resistant to levamisole and even some macrocyclic lactones, dictates that farmers must monitor the resistance status of their flocks to ensure that an effective anthelmintic is used. Treated lambs should preferably be moved to safe pasture and, if this is not possible, treatment may have to be repeated at 6-weekly intervals until the pasture larval levels decrease in late autumn.

Many of the anthelmintics recommended for sheep are not registered for use in goats. Where goat milk or milk products are used for human consumption, milk-withholding periods for different drugs should be observed. Thiabendazole has anti-fungal properties and should not be used when milk is processed for cheese.

Control: See The treatment and control of parasitic gastroenteritis (PGE) in sheep (below)

Notes: Considered to be a polymorphic species with at least two male morphs, Teladorsagia circumcincta and Ostertagia trifurcata, and possibly a third, Teladorsagia davtiani. The females cannot be differentiated but are distinguishable from other ostertagian females.

The treatment and control of parasitic gastroenteritis (PGE) in sheep

The recommendations outlined below are applicable to temperate areas of the northern hemisphere, but the principles can be adapted to local conditions in other regions.

Treatment

Because of the short period between birth and marketing, the treatment of PGE in lambs is an inferior policy compared with the preventive measures discussed below. However, when necessary, treatment with any of the benzimidazoles, levamisole or an avermectin/milbemycin will remove adult worms and developing stages, unless resistance to these drugs is present in the flock. Following treatment, lambs should be moved to pasture not grazed by sheep that year, otherwise they will immediately become reinfected. The occasional outbreaks of type II teladorsagiosis (ostertagiosis) in young adult sheep in the spring may be treated with the same anthelmintics. Unlike O. ostertagi in calves, the arrested stages of the common sheep nematodes are susceptible to the benzimidazoles and levamisole.

Control

Although the control of PGE in sheep is based on the same principles as that described for O. ostertagi in cattle, its practice is somewhat different for the following reasons:

Summary of guidelines for the control of gastrointestinal nematodes and use of anthelmintics in sheep and goats

Anthelmintic usage

Control strategies

In selecting the best method of prophylaxis much depends on whether the farm consists primarily of permanent pasture or has pastures which are rotated with crops so that new leys or hay and silage aftermaths are available each year.

Prophylaxis on farms consisting of mainly permanent pasture

On such farms control may be obtained either by anthelmintic prophylaxis or by alternate grazing on an annual basis with cattle and sheep. The former is the only feasible method where the farm stock is primarily sheep while the latter can be used where cattle and sheep are both present in reasonable proportions.

Prophylaxis by anthelmintics

Intensive chemoprophylaxis is not a long-term option for the sustainable control of ovine and caprine PGE.

The prophylactic programmes outlined above are relatively costly in terms of drugs and labour but are currently the only practicable options available where the enterprise is heavily dependent on one animal species.

Prophylaxis by alternate grazing of sheep and cattle

On farms where sheep and cattle are both present in significant numbers, effective control is theoretically possible by alternating the grazing of pasture on an annual basis with each host, due to the relative insusceptibility of cattle to sheep nematodes and vice versa. However, Nematodirus battus can infect young susceptible calves and this may inadvertently contaminate pasture which is being prepared for next season’s lambs. In practice, control is best achieved by exchanging, in the spring, pastures grazed by sheep and beef cattle over the previous year, preferably combined with anthelmintic treatment at the time of exchange.

Prophylaxis on farms with alternative grazing

In these mostly intensive farms, rotation of crops and grass is often a feature, and therefore new leys and hay and silage aftermaths are available as safe pastures each year and can be reserved for susceptible stock. In such a situation, control should be based on a combination of grazing management and anthelmintic prophylaxis.

Ostertagia leptospicularis

Synonym: Ostertagia crimensis, Skrjabinagia kolchida, Grosspiculagia podjapolskyi

Predilection site: Abomasum

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Hosts: Deer (roe deer), cattle, sheep, goat, camel

Geographical distribution: Many parts of the world, particularly Europe and New Zealand

For more details see Chapter 2: Cattle

Marshallagia marshalli

Synonym: Ostertagia marshalli, Ostertagia tricuspis

Predilection site: Abomasum

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Description, gross: Similar to Ostertagia spp and can be differentiated by its greater length (males 10–13 mm; females 15–20 mm).

Description, microscopic: Males have a long thin dorsal ray, which bifurcates near the posterior extremity. The end of the spicule is divided into three small processes. The ellipsoidal eggs are much larger than Ostertagia spp (>150 μm) and resemble those of Nematodirus battus.

Hosts: Sheep, goats, deer and wild small ruminants

Life cycle: The life cycle is similar to Ostertagia except that L₂ can hatch from the egg. Following ingestion, larvae burrow into the abomasal mucosa and form small greyish white nodules, which may contain several developing parasites. The young L₅ emerge from the nodules around day 16 post-infection and egg laying is usually apparent by 3 weeks. Arrested development of larvae can occur.

Geographical distribution: The tropics and subtropics including southern Europe, USA, South America, India and Russia.

Pathogenesis and clinical signs: Generally M. marshalli is not considered to be an important pathogen.

Diagnosis: Adults are readily identified based on the structure of the male spicules. Eggs are recognised in faecal samples by their large size.

Epidemiology: Wild ruminants serve as an important reservoir of infection.

Treatment and control: Anthelminitcs used to treat other gastrointestinal nematodes are likely to be effective.

Notes: Other species include M. mongolica, which is found in the abomasum of sheep, goats and camels in parts of Mongolia. M. schikhobalovi and M. dentispicularis occur in sheep in Russia.

Haemonchus contortus

Synonym: Haemonchus placei (see notes)

Common name: Barber’s pole worm

Predilection site: Abomasum

Parasite class: Nematoda

Family: Trichostrongyloidea

Description, gross: The adults are easily identified because of their specific location in the abomasum and their large size (2.0–3.0 cm). In fresh specimens, the white ovaries winding spirally around the blood-filled intestine produce a ‘barber’s pole’ appearance (Fig. 3.2).

Description, microscopic: The male has an asymmetrical dorsal lobe and barbed spicules (Fig. 3.3a); the female usually has a vulval flap. In both sexes there are cervical papillae and a tiny lancet inside the buccal capsule (Fig. 3.3b). Infective larvae have 16 gut cells, the head is narrow and rounded and the tail of the sheath is offset. The egg is medium-sized (74 × 44 μm), a regular broad elipse with barrel-shaped sidewalls and numerous blastomeres, which nearly fill the entire egg.

Fig. 3.2 Adult H. contortus on the surface of the abomasum.

Fig. 3.3 (a) Barbed spicules and bursa of a mature H. contortus male worm. (b) Anterior of Haemonchus contortus showing the position of the cervical papillae.

Hosts: Sheep, goat, cattle, deer, camel, llama

Life cycle: This is direct and the preparasitic phase is typically trichostrongyloid. The females are prolific egg layers. The eggs hatch to L₁ on the pasture and may develop to L₃ in as short a period as 5 days but development may be delayed for weeks or months under cool conditions. After ingestion, and exsheathment in the rumen, the larvae moult twice in close apposition to the gastric glands. Just before the final moult they develop the piercing lancet which enables them to obtain blood from the mucosal vessels. As adults they move freely on the surface of the mucosa. The prepatent period is 2–3 weeks in sheep and 4 weeks in cattle.

Geographical distribution: Worldwide. Most important in tropical and subtropical areas.

Pathogenesis: Essentially the pathogenesis of haemonchosis is that of an acute haemorrhagic anaemia due to the blood-sucking habits of the worms. Each worm removes about 0.05 ml of blood per day by ingestion and seepage from the lesions, so that a sheep with 5000 H. contortus may lose about 250 ml daily. In acute haemonchosis anaemia becomes apparent about 2 weeks after infection and is characterised by a progressive and dramatic fall in the packed red cell volume. During the subsequent weeks the haematocrit usually stabilises at a low level, but only at the expense of a two- to three-fold compensatory expansion of erythropoiesis. However due to the continual loss of iron and protein into the gastrointestinal tract and increasing inappetence, the marrow eventually becomes exhausted and the haematocrit falls still further before death occurs. When ewes are affected, the consequent agalactia may result in the death of the suckling lambs. Less commonly, in heavier infections of up to 30 000 worms, apparently healthy sheep may die suddenly from severe haemorrhagic gastritis (Fig. 3.4). This is termed hyperacute haemonchosis.

Perhaps as important as acute haemonchosis in tropical areas is the lesser known syndrome of chronic haemonchosis. This develops during a prolonged dry season when reinfection is negligible, but the pasture becomes deficient in nutrients. Over such a period the continual loss of blood from small persisting burdens of several hundred worms is sufficient to produce clinical signs associated primarily with loss of weight, weakness and inappetence rather than marked anaemia.

Fig. 3.4 Abomasal haemorrhages in acute haemonchosis.

Fig. 3.5 Anaemia and submandibular oedema characteristic of haemonchosis.

Clinical signs: In hyperacute cases, sheep die suddenly from haemorrhagic gastritis.

Acute haemonchosis is characterised by anaemia, variable degrees of oedema, of which the submandibular form and ascites are most easily recognised, lethargy, dark coloured faeces and falling wool (Fig. 3.5). Diarrhoea is not generally a feature. Chronic haemonchosis is associated with progressive weight loss and weakness, neither severe anaemia nor gross oedema being present.

Diagnosis: The history and clinical signs are often sufficient for the diagnosis of the acute syndrome especially if supported by faecal worm egg counts. Necropsy, paying attention to both the abomasum and the marrow changes in the long bones, is also useful. Changes are usually evident in both, although in sheep, which have just undergone ‘self cure’ (see below) or are in a terminal stage of the disease, the bulk of the worm burden may have been lost from the abomasum. In hyperacute haemonchosis, only the abomasum may show changes since death may have occurred so rapidly that marrow changes are minimal. The diagnosis of chronic haemonchosis is more difficult because of the concurrent presence of poor nutrition and confirmation may have to depend on the gradual disappearance of the syndrome after anthelmintic treatment.

Pathology: In cases of acute haemonchosis, at necropsy, there may be between 2000 and 20 000 worms present on the abomasal mucosa which shows numerous small haemorrhagic lesions. The abomasal contents are fluid and dark brown due to the presence of altered blood. The carcase is pale and oedematous and the red marrow has expanded from the epiphyses into the medullary cavity.

Epidemiology: The epidemiology of H. contortus is best considered separately, depending on whether it occurs in tropical and subtropical or in temperate areas.

Tropical and subtropical areas

Because larval development of H. contortus occurs optimally at relatively high temperatures, haemonchosis is primarily a disease of sheep in warm climates. However, since high humidity, at least in the microclimate of the faeces and the herbage, is also essential for larval development and survival, the frequency and severity of outbreaks of disease is largely dependent on the rainfall in any particular area.

Given these climatic conditions, the sudden occurrence of acute clinical haemonchosis appears to depend on two further factors. First, the high faecal worm egg output of between 2000 and 20 000 epg, even in moderate infections, means that massive pasture populations of L₃ may appear very quickly. Second, in contrast to many other helminth infections, there is little evidence that sheep in endemic areas develop an effective acquired immunity to Haemonchus, so that there is continuous contamination of the pasture.

In certain areas of the tropics and subtropics, such as Australia, Brazil, the Middle East and Nigeria, the survival of the parasite is also associated with the ability of H. contortus larvae to undergo hypobiosis. Although the trigger for this phenomenon is unknown, hypobiosis occurs at the start of a prolonged dry season and permits the parasite to survive in the host as arrested L₄ instead of maturing and producing eggs, which would inevitably fail to develop on the arid pasture. Resumption of development occurs just before the onset of seasonal rains. In other tropical areas such as East Africa, no significant degree of hypobiosis has been observed and this may be due to more frequent rainfall in these areas making such an evolutionary development unnecessary.

The survival of H. contortus infection on tropical pastures is variable depending on the climate and degree of shade, but the infective larvae are relatively resistant to desiccation and some may survive for 1–3 months on pasture or in faeces.

In areas of endemic haemonchosis it has often been observed that after the advent of a period of heavy rain the faecal worm egg counts of sheep infected with H. contortus drop sharply to near zero levels due to the expulsion of the major part of the adult worm burden. This event is commonly termed the self-cure phenomenon, and has been reproduced experimentally by superimposing an infection of H. contortus larvae on an existing adult infection in the abomasum. The expulsion of the adult worm population is considered to be the consequence of an immediate-type hypersensitivity reaction to antigens derived from the developing larvae. It is thought that a similar mechanism operates in the naturally occurring self-cure when large numbers of larvae mature to the infective stage on pasture after rain.

Although this phenomenon has an immunological mechanism it is not necessarily associated with protection against reinfection since the larval challenge often develops to maturity.

Another explanation of the self-cure phenomenon as it occurs in the field is based on the observation that it may happen in lambs and adults contemporaneously and on pasture with insignificant numbers of infective larvae. This suggests that the phenomenon may also be caused, in some non-specific way, by the ingestion of fresh growing grass. Whatever the cause, self-cure is probably of mutual benefit to both host and parasite. The former gains a temporary respite from persistent blood loss while the ageing parasite population is eventually replaced by a vigorous young generation.

Temperate areas

In the British Isles, the Netherlands and presumably in other parts of northern Europe and in Canada, which are among the least favourable areas for the survival of H. contortus, the epidemiology is different from that of tropical zones. From the information available, infections seem to develop in two ways. Perhaps most common is the single annual cycle. Infective larvae, which have developed from eggs deposited by ewes in the spring are ingested by ewes and lambs in early summer. The majority of these become arrested in the abomasum as EL₄ and do not complete development until the following spring. During the period of maturation of these hypobiotic larvae, clinical signs of acute haemonchosis may occur and in the ewes this often coincides with lambing. The epidemiology is unknown, but is perhaps associated with pasture contamination by that proportion of ingested larvae, which did not undergo hypobiosis in early summer.

Treatment: When an acute outbreak has occurred the sheep should be treated with one of the benzimidazoles, levamisole, an avermectin/milbemycin or salicylanilide and immediately moved to pasture not recently grazed by sheep. When the original pasture is grazed again, prophylactic measures should be undertaken, as enough larvae may have survived to institute a fresh cycle of infection. Chronic haemonchosis is dealt with in a similar fashion. If possible the new pasture should have a good nutritional value; alternatively some supplementary feeding may be given.

Control: In the tropics and subtropics this varies depending on the duration and number of periods in the year when rainfall and temperature permit high pasture levels of H. contortus larvae to develop. At such times it may be necessary to use an anthelmintic at intervals of 2–4 weeks depending on the degree of challenge. Sheep should also be treated at least once at the start of the dry season and preferably also before the start of prolonged rain to remove persisting hypobiotic larvae whose development could pose a future threat. For this purpose, one of the modern benzimidazoles or an avermectin/milbemycin is recommended. In some wool-producing areas where Haemonchus is endemic, closantel, which has a residual prophylactic effect, may be used. Because of long withdrawal periods this is of limited use in meat-producing animals.

Apart from anthelmintic prophylaxis, some studies, especially in Kenya, have indicated the potential value of some indigenous breeds of sheep, which seem to be naturally highly resistant to H. contortus infection. Presumably such breeds could be of value in developing areas of the world where veterinary surveillance is poor. Rapid rotation through a series of paddocks can be effective in certain wet tropical areas (for details refer to The treatment and control of PGE in sheep – prophylaxis by grazing management alone).

In temperate areas, the measures outlined for the control of parasitic gastroenteritis in sheep are usually sufficient to pre-empt outbreaks of haemonchosis.

Currently trials are in progress to determine the efficacy of a recombinant vaccine based on a membrane glycoprotein of intestinal microvilli of parasitic stages of H. contortus.

Notes: Until recently the sheep species was called H. contortus and the cattle species H. placei. However there is now increasing evidence that these are the single species H. contortus with only strain adaptations for cattle and sheep.

Trichostrongylus axei

Synonym: Trichostrongylus extenuatus

Common name: Stomach hairworm

Predilection site: Abomasum or 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: In T. axei, the male spicules are dissimilar and unequal in length, the right being shorter than the left (Fig. 3.6a).

Hosts: Cattle, sheep, goat, deer, horse, donkey, pig and occasionally man

Life cycle: This is direct and the preparasitic phase is typically trichostrongyloid. The prepatent period in sheep is about 3 weeks.

Fig. 3.6 Comparison of spicules of Trichostrongylus spp. (a) T. axei male showing the dissimilar unequal length spicules. (b) Male T. colubriformis showing the characteristic thick spicules of equal length with a barb tip. (c) T. vitrinus male showing the thick spicules of equal length which terminate in a point.

Geographical distribution: Worldwide

Pathogenesis: The extent of the lesions in the abomasum or stomach is dependent on the size of the worm population. Small irregular areas, showing diffuse congestion and whitish grey raised flat, circular lesions may be present in the pyloric and fundic regions. These lesions are about 1–2 cm in diameter and have been termed plaques or ringworm lesions (Fig. 3.7). In heavy infections, shallow ulcers may be seen. The changes induced in the gastric mucosa are similar to those of Ostertagia with an increase in pH and an increased permeability of the mucosa, leading to an increase in plasma pepsinogen concentration and hypoalbuminaemia.

Fig. 3.7 Raised plaques in abomasum due to Trichostrongylus axei.

Clinical signs: The principal clinical signs in heavy infections are rapid weight loss and diarrhoea. At lower levels of infection, inappetence and poor growth rates, sometimes accompanied by soft faeces, are the common signs.

Diagnosis: This is based on clinical signs, seasonal occurrence of disease and, if possible, lesions at postmortem examination. Faecal egg counts are a useful aid to diagnosis, although faecal cultures are necessary for generic identification of larvae. At necropsy, T. axei is easily identified from washings and digests of the abomasum or stomach.

Pathology: In sheep, there is often extensive desquamation of the superficial epithelium of the mucosa. A mucoid hyperplasia is seen in the plaques and in longer-established infections there may be shallow ulcers in the neck regions of the glands. Cellular infiltration of the lamina propria occurs, particularly an influx of eosinophils and lymphocytes. In most cases there is not a marked reduction in the number of parietal or zymogen cells. Over time, infection can lead to a chronic proliferative inflammation and shallow depressed ulcers may be present.

Epidemiology: The embryonated eggs and infective L₃ of T. axei can survive under adverse conditions. Larval numbers increase on pasture in late summer/autumn often giving rise to clinical problems during the winter and early spring. Immunity is slowly acquired and age immunity is not well developed.

Treatment and control: See Treatment and control of parasitic gastroenteritis (PGE) in sheep.

Parabronema skrjabini

Predilection site: Abomasum

Parasite class: Nematoda

Superfamily: Spiruroidea

Description, gross: The white slender adult worms (up to 3.6 cm long) resemble Haemonchus spp somewhat in gross form and size, but without the red spiral coloration, while the younger worms are closer to Ostertagia in appearance. Males are 15–18 mm with one spicule.

Description, microscopic: The genus is readily distinguished from the other abomasal worms by the presence of large cuticular shields and cordons in the cephalic region. The tail of the male is spiral with four pairs of pre-anal papillae.

Final host: Sheep, goat, cattle, camel

Intermediate host: Muscid flies of the genera Stomoxys and Lyperosia

Life cycle: Eggs or L₁ are passed in the faeces and the L₁ are ingested by the larval stages of various muscid flies that are often present in faeces. Development to L₃ occurs synchronously with the development to maturity of the fly intermediate host. When the fly feeds around the mouth, lips and nostrils of the host the larvae pass from its mouthparts on to the skin and are swallowed. Alternatively infected flies may be swallowed whole in feed and drinking water. Development to adult takes place in the glandular area of the abomasum.

Geographical distribution: Central and East Africa, Asia, and some Mediterranean countries, notably Cyprus

Pathogenesis: Parabronema is usually regarded as non-pathogenic, although it can cause nodular lesions in the abomasal wall.

Clinical signs: Usually inapparent

Diagnosis: Abomasal worms may be found in abomasal scrapings on postmortem.

Pathology: Non-specific. An abomasitis may be found and lesions may become nodular.

Epidemiology: The seasonality of infection is related to the activity of the fly vectors.

Treatment: Treatment is normally not required.

Control: Any measures to reduce fly populations will be beneficial.

Notes: This genus in ruminants is equivalent to Habronema in equines.

SMALL INTESTINE

Trichostrongylus

Species of Trichostrongylus are small, light brownish red, hair-like worms, and difficult to see with the naked eye. Males measure around 4.0–5.5 mm and females 5.5–7.5 mm in length.

Description, microscopic: The worms have no buccal capsule. A useful generic character is the distinct excretory notch in the oesophageal region. The male bursa has long lateral lobes, while the dorsal lobe is not well defined. Spicules are stout, ridged and pigmented brown, and a gubernaculum is present. Species identification is based on the shape and size of the spicules (Table 3.1; Fig. 3.6). The female tail is bluntly tapered and there is no vulval flap. Eggs are thin-shelled and typically strongyle.

Life cycle: This is direct and the preparasitic phase is typically trichostrongyloid; eggs developing to the infective L₃ in about 7–10 days under optimal conditions. Following ingestion and exsheathment, larvae penetrate the mucosa of the small intestine (Fig. 3.8) and after two moults the fifth-stage worms are present under the intestinal epithelium around 2 weeks after initial infection. The prepatent period is 2–3 weeks.

Diagnosis: This is based on clinical signs, seasonal occurrence of disease and, if possible, lesions at postmortem examination. Faecal egg counts are a useful aid to diagnosis, although faecal cultures are necessary for generic identification of larvae. At necropsy, the small intestine is often inflamed and the mucosa thickened with an increase in mucus. There may be flattened, red areas that are demarcated from the surrounding mucosa. Digestion of the gut in warm physiological saline for 2–3 hours will release the small hair-like worms for examination.

Fig. 3.8 Developing Trichostrongylus vitrinus in the small intestinal mucosa.

Table 3.1 Identification of Trichostrongylus spp found in sheep and goats based on spicule morphology.

Pathology: Microscopically, there is villous atrophy and fusion of villi with elongation and dilation of the intestinal crypts and an increase in the number of mucus-secreting goblet cells. This is accompanied by marked cellular infiltration of the laminar propria, in particular an increase in eosinophils. Intraepithelial globule leucocytes are numerous, often in the more normal surrounding areas of the mucosa.

Epidemiology: The embryonated eggs and infective L₃ of Trichostrongylus can survive under adverse conditions. In temperate areas the L₃ survive the winter, occasionally in sufficient numbers to precipitate clinical disease in the spring, but more commonly, larval numbers increase on pasture in summer and autumn giving rise to clinical problems during these seasons. Hypobiosis plays an important part in the epidemiology, the seasonal occurrence being similar to that of Ostertagia spp. In contrast to other trichostrongyles hypobiosis occurs at the L₃ stage although their role in outbreaks of disease has not been fully established.

In the southern hemisphere larvae accumulate in late winter and outbreaks are usually seen in spring. In Australia and Africa, following a period of drought the advent of rain has been shown to rehydrate large numbers of apparently desiccated L₃ (anhydrobiosis) which then become active and rapidly available to grazing animals. T. colubriformis also survives adverse environmental conditions as adult parasites within the host and these can persist for many months.

Immunity to Trichostrongylus, as in Ostertagia, is slowly acquired and in sheep, and probably goats, it wanes during the periparturient period.

Treatment: This is as described for ostertagiosis and parasitic gastroenteritis in sheep.

Control: See Treatment and control of parasitic gastroenteritis (PGE) in sheep

Notes: Trichostrongylus is rarely a primary pathogen in temperate areas, but is usually a component of parasitic gastroenteritis in ruminants. By contrast, in the subtropics it is one of the most important causes of parasitic gastroenteritis.

Trichostrongylus colubriformis

Synonym: Trichostrongylus instabilis

Common name: Black scour or bankrupt worm

Predilection site: Duodenum and anterior small intestine

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Description, gross: Males measure around 4.0–5.5 mm and females 5.5–7.5 mm in length.

Description, microscopic: In T. colubriformis, the spicules are thick, brown, unbranched, of equal length and terminate in a barb-like tip (Table 3.1; Fig 3.6b).

Hosts: Sheep, goat, cattle, camel and occasionally pig and man

Geographical distribution: Worldwide. Although T. colubriformis occurs in temperate regions, it is mainly a parasite of subtropical and tropical zones.

Pathogenesis: Following ingestion, the larvae penetrate the mucosa and developing worms are located in superficial channels sited just beneath the surface epithelium and parallel with the luminal surface, but above the lamina propria. When the sub-epithelial tunnels containing the developing worms rupture to liberate the young worms about 10–12 days after infection, there is considerable haemorrhage and oedema and plasma proteins are lost into the lumen of the gut leading to hypoalbuminaemia and hypoproteinaemia. Grossly there is an enteritis, particularly in the duodenum; the villi become distorted and flattened and the mucosa is inflamed, oedematous and covered in mucus. However many areas may superficially appear normal. Where parasites are congregated within a small area, erosion of the mucosal surface is apparent with severe villous atrophy (Fig. 3.9). In heavy infections diarrhoea occurs, and this, together with the loss of plasma protein into the lumen of the intestine and an increase in turnover of the intestinal epithelium, leads to an impairment in protein metabolism for growth and is reflected as weight loss. Reduced deposition of body protein, calcium and phosphorus and efficiency of food utilisation may occur. Heavy infections can induce osteoporosis and osteomalacia of the skeleton.

Fig. 3.9 Erosions characteristic of intestinal trichostrongylosis.

Clinical signs: The principal clinical signs in heavy infections are rapid weight loss and diarrhoea, often dark coloured. Deaths can be high, particularly if animals are also malnourished and they receive a high larval challenge over a short period. At lower levels of infection, inappetence and poor growth rates, sometimes accompanied by soft faeces, are the common signs. It is often difficult to distinguish the effects of low infections from malnutrition.

Trichostrongylus vitrinus

Common name: Black scour worm

Predilection site: Duodenum and small intestine

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Fig. 3.10 Scanning electron micrograph of small intestine showing villus atrophy in areas where worms are present.

Description, gross: The adults are small, hair-like and light brownish red when fresh. Males measure around 4–6 mm and females 5–8 mm in length.

Description, microscopic: The spicules are thick, unbranched, of equal length and end in a point (Table 3.1; Fig. 3.6c). Eggs are slightly ‘brazil nutshaped’ and measure 93–118 × 41–52 μm.

Hosts: Sheep, goat, deer, camel, occasionally pig and man

Geographical distribution: Mainly temperate regions of the world

Pathogenesis: The macroscopic lesions in the intestine are similar to those described for T. colubriformis, although they tend not to be as extensive and appear to resolve earlier, possibly being indicative of an earlier expulsion of worms than with T. colubriformis. Frequently shallow red depressed areas, demarcated from the more normal coloured surrounding mucosa, are present on the surface of the intestine. These have been termed ‘finger print’ lesions (Fig. 3.10). These affected areas are devoid of villi, or the villi appear as rounded protruberances, and numerous worms are embedded in the surface mucosa. Infection can induce similar adverse effects on protein and mineral metabolism to those described for T. colubriformis.

Clinical signs: The principal clinical signs in heavy infections are weight loss and diarrhoea. At lower levels of infection, inappetence and poor growth rates, sometimes accompanied by soft faeces, are the common signs.

Trichostrongylus longispicularis

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Description, gross: The adults are similar in size to T. colubriformis.

Description, microscopic: The spicules are stout, brown, unbranched, slightly unequal in length and terminate in a tapering blunt tip that has a small semi-transparent protrusion (Table 3.1).

Hosts: Cattle, sheep, goat, deer, camel, llama

Life cycle: This is direct and typically trichostrongyloid. See T. colubriformis for details.

Geographical distribution: Ruminants in Australia; and cattle in America and parts of Europe

There are a number of other species of Trichostrongylus found in the small intestine of sheep and goats (T. rugatus, T. falculatus, T. probolurus, T. drepanoformis and T. capricola). These have a more local distribution. The species in rabbits, T. retortaeformis and T. affinus, have occasionally been recovered from small ruminants.

Cooperia curticei

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Description, gross: C. curticei is moderately small with a large bursa. The most notable feature is the ‘watch spring-like’ posture. Males measure around 4.5–6.0 mm and females 6.0–8.0 mm in length. When fresh they appear pinkish white.

Description, microscopic: The main generic features are the small cephalic vesicle and the transverse cuticular striations in the oesophageal region. The body possesses longitudinal ridges. The spicules are short and stout and have a distinct wing-like expansion in the middle region, which often bears ridges; there is no gubernaculum. The females have a long tapering tail. Eggs are oval and thin-shelled.

Hosts: Sheep, goat, deer

Life cycle: This is direct and typical of the superfamily. Ingested L₃ exsheath, migrate into the intestinal crypts for two moults and then the adults develop on the surface of the intestinal mucosa. The prepatent period is around 2 weeks. The bionomic requirements of the free-living stages are similar to those of Teladorsagia.

Geographical distribution: Worldwide

Pathogenesis: C. curticei is generally considered to be a mild pathogen in lambs and kids although in some studies it has been associated with inappetence and poor weight gains. A partial immunity to reinfection develops after about 8–12 months of exposure to infective larvae.

Clinical signs: Low to moderate infections are often asymptomatic but heavy worm burdens can lead to loss of appetite and poor growth rates.

Diagnosis: Eggs of Cooperia spp are all very similar morphologically. Faecal culture will allow identification of infective larvae.

Pathology: Cooperia do not tunnel into the epithelium but coil among the intestinal villi causing adjacent villous atrophy. In heavy infections there is more widespread villous atrophy in the small intestine leading to loss of brush border enzymes and digestive disturbance.

Epidemiology: In temperate areas, this is similar to that of Teladorsagia. Hypobiosis at the EL₄ is a regular feature during late autumn and winter in the northern hemisphere, and spring and summer in the southern hemisphere. Generally, first year grazing animals are most likely to accumulate moderate worm populations. Exposure to infective pasture enables animals to acquire a good level of immunity and as adults they usually show little clinical signs of infection but act as carriers, shedding low numbers of eggs in their faeces. Infective larvae survive well on pasture, being tolerant of cold conditions.

Treatment: The principles are similar to those applied in PGE in sheep. Cooperia is one of the dose-limiting species and one should consult the manufacturer’s data sheets for efficacy of anthelmintics against adult and L₄ stages.

Control: Similar to that recommended for Teladorsagia

Notes: In temperate areas, members of the genus Cooperia usually play a secondary role in the pathogenesis of PGE of small ruminants although they may be the most numerous trichostrongyle present.

Cooperia surnabada

Synonym: Cooperia mcmasteri

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Hosts: Cattle, sheep, goat, camel

Geographical distribution: Parts of Europe, North America and Australia

For more details see Chapter 2 (Cattle).

Fig. 3.11 Anterior of Nematodirus battus illustrating the small cephalic vesicle.

Nematodirus battus

Common name: Thread-necked worm

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Description, gross: The adults are slender, the males measuring around 11–16 mm and females 15–25 mm in length. The anterior of the worm is thinner than the posterior region and the cuticle possesses longitudinal ridges.

Microscopic: A small but distinct cephalic vesicle is present (Fig. 3.11). Males are characterised by having only one set of divergent rays in each bursal lobe and the tips of the spicules are fused in a small, flattened oval-shaped projection (Fig. 3.12c). The female worm has a long pointed tail and the large egg is brownish with parallel sides.

Hosts: Sheep, goat and occasionally cattle (calves)

Life cycle: The preparasitic phase is almost unique in the trichostrongylids in that development to the L₃ takes place within the eggshell. Hatching of most eggs requires a prolonged period of chill followed by a mean day/night temperature of more than 10°C, conditions which occur in late spring. Hence most of the eggs from one season’s grazing remain unhatched on the ground during the winter and only one generation is possible each year for the bulk of this species. However, some N. battus eggs deposited in the spring are capable of hatching in the autumn of the same year resulting in significant numbers of L₃ on the pasture at this time. The ingested L₃ penetrate the mucosa of the small intestine and moult to the L₄ stage around the fourth day. After moulting to the L₅ the parasites inhabit the lumen, sometimes superficially coiled around villi. The prepatent period is 14–16 days.

Fig. 3.12 Comparison of spicules of (a) Nematodirus filicollis, (b) N. spathiger and (c) N. battus.

Geographical distribution: N. battus is most important in the British Isles, but also occurs in Norway, Sweden, the Netherlands and parts of Canada.

Pathogenesis: Nematodirosis, due to N. battus infection, is an example of a parasitic disease where the principal pathogenic effect is attributable to the larval stages. Following ingestion of large numbers of L₃ there is disruption of the intestinal mucosa, particularly in the ileum, although the majority of developing stages are found on the mucosal surface. Development through L₄ to L₅ is complete by 10–12 days from infection and this coincides with severe damage to the villi and erosion of the mucosa leading to villous atrophy. The ability of the intestine to exchange fluids and nutrients is grossly impaired, and with the onset of diarrhoea the lamb rapidly becomes dehydrated.

Clinical signs: In severe infections, yellowy-green diarrhoea is the most prominent clinical sign and can occur during the prepatent period. As dehydration proceeds, the affected animals become thirsty and in infected flocks the ewes continue to graze, apparently unaffected by the larval challenge, while their inappetent and diarrhoeic lambs congregate round drinking places. At necropsy, the carcase has a dehydrated appearance and there is often an acute enteritis. The intertwining of the thin, twisted worms in the intestine can produce an appearance similar to that of cotton wool. Mortalities can be high in untreated animals. Concurrent infection with pathogenic species of coccidia can exacerbate the severity of disease.

Diagnosis: Because the clinical signs appear during the prepatent period faecal egg counts are of little value in early diagnosis which is best made on grazing history, clinical signs and, if possible, a postmortem examination. Nematodirosis should be differentiated from coccidiosis.

Pathology: Gross pathological changes may be limited to fluid mucoid contents in the upper small intestine with occasional hyperaemia of the mucosa of the duodenum with excess mucus on the surface. Worm counts may reveal tangled, cottony masses of elongate, coiled nematodes. The presence of large numbers of larvae is associated with villous atrophy and fusion, whilst crypts may appear elongate and dilated. Local erosions may occur if villous atrophy is severe and on histopatholgy there is a mixed inflammatory response with large numbers of lymphocytes, plasma cells and eosinophils in the lamina propria.

Epidemiology: The three most important features of the epidemiology of N. battus infections are:

Treatment: Several drugs are effective against Nematodirus infections: levamisole, an avermectin/milbemycin or one of the modern benzimidazoles. However, Nematodirus is one of the dose-limiting species and the manufacturer’s data sheets should be consulted as there are differences in efficacy against adults and L₄ stages between oral and parenteral administration for some macrocyclic lactones. The response to treatment is usually rapid and, if diarrhoea persists, coccidiosis should be considered as a complicating factor.

Control: Due to the annual hatching of N. battus eggs in spring, the disease can be controlled by avoiding the grazing of successive lamb crops on the same pasture. Where such alternative grazing is not available each year, control can be achieved by anthelmintic prophylaxis, the timing of treatments being based on the knowledge that the peak time for the appearance of N. battus L₃ is May to early June. Ideally, dosing should be at 3-week intervals over May and June and it is unwise to await the appearance of clinical signs of diarrhoea before administering the drugs. Forecasting systems are based primarily on soil temperature in the early spring which can predict the likely severity of nematodirosis. In years when the forecast predicts severe disease, three treatments are recommended during May and June; in other years two treatments in May should suffice.

Notes: As anthelmintic resistance is rare in Nematodirus species it may be advisable to use a benzimidazole against specific Nematodirus infection and in this way reduce the selection pressure on the other families of drugs.

Nematodirus filicollis

Common name: Thread-necked worm

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Description, gross: The adults are slender worms, males measuring 10–15 mm and females 15–24 mm in length.

Description, microscopic: A small but distinct cephalic vesicle is present. The male has two sets of parallel rays in each of the main bursal lobes. The spicules are long and slender with fused tips and terminate in a narrow pointed swelling (Fig. 3.12a). The female has a truncate blunt tail with a small spine (similar to N. spathiger), and the egg is large, ovoid, thin-shelled and colourless and twice the size of the typical trichostrongyle egg.

Hosts: Sheep, goat, occasionally cattle and deer

Life cycle: The preparasitic phase is almost unique in the trichostrongyloids in that development to the L₃ takes place within the egg shell. N. filicollis does not have the same critical hatching requirements as N. battus. Hatching occurs over a more prolonged period and so larvae often appear on the pasture within 2–3 months of the eggs being excreted in the faeces. The parasitic phase within the host is similar to that of N. battus. The prepatent period is 2–3 weeks.

Geographical distribution: Cosmopolitan, but more prevalent in temperate zones

Pathogenesis: Similar to that of N. battus but of lesser severity

Clinical signs: Low to moderate infections may produce no obvious clinical manifestations. In severe infections, diarrhoea can occur during the prepatent period and young animals may become dehydrated.

Diagnosis: Examination of faeces will enable the colourless eggs to be differentiated from the brown eggs of N. battus. At necropsy the tips of the male spicules will allow diagnosis from other Nematodirus species.

Pathology: Third-stage larvae enter the deep layers of the mucosa, penetrating into the crypts. Larvae emerge as fourth- or fifth-stage larvae and coil among the villi with their posterior ends protruding into the lumen. The presence of large numbers of worms leads to the development of villous atrophy, crypt dilation and elongation. If villous atrophy is severe the worms may not be able to maintain their position in the intestine.

Epidemiology: The hatch of L₃ from the eggs occurs over a more prolonged period than with N. battus, numbers of larvae accumulate on pasture and often peak in late autumn to early winter. More than one annual generation is possible. Although N. filicollis has been associated with outbreaks of nematodirosis in small ruminants it is more common to find it in conjunction with the other trichostrongyles that contribute to ovine PGE.

Treatment: See Nematodirus battus.

Control: Disease due to monospecific Nematodirus filicollis infections is rarely seen. They are usually part of the worm burden of trichostrongyloid species that are responsible for the syndrome of PGE in sheep and as such may be controlled by the measures outlined elsewhere.

Nematodirus spathiger

Common name: Thread-necked worm

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Description, gross: The adults are slender worms, males measuring around 10–14 mm and females 15–24 mm in length.

Description, microscopic: A small but distinct cephalic vesicle is present. The male has two sets of parallel rays in each of the main bursal lobes. The spicules are long and slender with fused tips and terminate in a spoon-shaped tip (Fig. 3.12b). The female has a truncate blunt tail with a small spine (similar to N. filicollis), and the egg is large, ovoid, thin-shelled and colourless and twice the size of the typical trichostrongyle egg.

Hosts: Sheep, goats, occasionally cattle and other ruminants

Life cycle: The preparasitic phase is almost unique in the trichostrongyloids in that development to the L₃ takes place within the egg shell. N. spathiger does not have the same critical hatching requirements as N. battus. Larvae can appear on the pasture within 3–4 weeks of eggs being excreted in the faeces; more than one annual generation is therefore possible. The parasitic phase is similar to that of N. battus. The prepatent period is 2–3 weeks.

Geographical distribution: Cosmopolitan

Pathogenesis: Similar to that of N. battus but of lesser severity

Clinical signs: Low to moderate infections may produce no obvious clinical manifestations. In severe infections, diarrhoea can occur during the prepatent period and young animals may become dehydrated.

Diagnosis: Examination of faeces will enable the colourless eggs to be differentiated from the brown eggs of N. battus. At necropsy the tips of the male spicules will allow diagnosis from other Nematodirus species.

Pathology: As for N. filicollis

Epidemiology: The eggs do not usually exhibit delayed hatching, and the pattern of infection is similar to that of Trichostrongylus species.

Treatment and control: See Nematodirus battus

Bunostomum trigonocephalum

Synonym: Monodontus trigonocephalum

Common name: Hookworm

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Ancylostomatoidea

Description, gross: Bunostomum is one of the larger nematodes of the small intestine of ruminants, being 1.0–3.0 cm long, stout, greyish white and characteristically hooked at the anterior end with the buccal capsule opening anterodorsally.

Description, microscopic: The large buccal capsule opens anterodorsally and bears on the ventral margin a pair of chitinous cutting plates and internally a large dorsal cone. Dorsal teeth are absent from the buccal capsule but there is a pair of small sub-ventral lancets at its base. In the male the bursa is well developed and has an asymmetrical dorsal lobe. The right externodorsal ray arises higher up on the dorsal stem and is longer than the left. It arises near the bifurcation of the dorsal ray, which divides into two tri-digitate branches. The spicules are slender, twisted and relatively short. In the female the vulva opens a short distance in front of the middle of the body.

The infective larva is small with 16 gut cells and a short filamentous tail. The eggs is medium sized (90 × 51 μm), irregular broad elipse in shape, with dissimilar sidewalls and 4–8 blastomeres.

Hosts: Sheep, goat, camel, deer

Life cycle: Infection with the L₃ may be percutaneous or oral. After skin penetration, the larvae travel to the lungs and moult to fourth-stage larvae before re-entering the gastrointestinal tract after approximately 11 days. Ingested larvae usually develop without a migration. Further development continues in the gut. The prepatent period is 4–8 weeks.

Geographical distribution: Worldwide

Pathogenesis: The adult worms are blood-suckers and infections of 100–500 worms can produce progressive anaemia, hypoalbuminaemia, loss of weight and occasionally diarrhoea. Worm burdens of around 600 may lead to death in sheep.

Clinical signs: The main clinical signs are progressive anaemia, with associated changes in the blood picture, hydraemia and oedema, which show particularly as submandibular oedema (‘bottle jaw’). The animals become weak and emaciated and the appetite usually decreases. The skin is dry and the wool of sheep falls out in irregular patches. Diarrhoea may occur, and the faeces may be dark because of altered blood pigments. Collapse and death may occur.

Diagnosis: The clinical signs of anaemia and perhaps diarrhoea in young sheep are not in themselves pathognomonic of bunostomosis. However, in temperate areas, the epidemiological background may be useful in eliminating the possibility of Fasciola hepatica infection. In the tropics, haemonchosis must be considered, possibly originating from hypobiotic larvae. Faecal worm egg counts are useful in that these are lower than in Haemonchus infection, while the eggs are more bluntly rounded, with relatively thick sticky shells to which debris is often adherent. For accurate differentiation, larval cultures should be prepared.

Pathology: The carcase is anaemic and cachexic. Oedema and ascites are seen. The liver is light brown and shows fatty changes. The intestinal contents are haemorrhagic and the mucosa is usually swollen, covered with mucus, and shows numerous lesions resulting from the worms feeding. The parasites may be seen still attached to the mucosa or free in the lumen.

Epidemiology: Pathogenic infections are more common in the tropics and subtropics and, in some areas, the highest worm burdens are found at the end of the dry season apparently due to the maturation of hypobiotic larvae. Young animals are most susceptible. In temperate countries, high worm burdens are usually uncommon. The prophylactic dosing regimes, adopted for the control of trichostrongyles, has contributed to the low prevalence of Bunostomum.

Treatment: The prophylactic anthelmintic regimes advocated for other gastrointestinal nematodes are usually sufficient.

Control: A combination of strategic dosing with anthelmintics and pasture management as used in the control of ovine PGE is effective. Larvae are susceptible to dessication, and the infection is mainly found on permanently or occasionally moist pastures. Avoiding or draining such pastures is an effective control measure. The ground around water troughs should be kept hard and dry, or treated with liberal applications of salt. Housed sheep and goats should be protected by ensuring the floors and bedding are kept dry and that faeces are removed frequently and are not allowed to contaminate food and water.

Gaigeria pachyscalis

Common name: Hookworm

Predilection site: Duodenum and small intestine

Parasite class: Nematoda

Superfamily: Ancylostomatoidea

Description, gross: Adult males are up to 2 cm; females are up to 3 cm long.

Description, microscopic: The buccal capsule contains a large dorsal cone, but no dorsal tooth, and a pair of sub-ventral lancets, which have several cusps each. The male bursa has small lateral lobes joined together ventrally, and a large dorsal lobe. The anterolateral ray is short and blunt and is separated widely from other lateral rays. The externo-dorsal rays arise from the main stem of the dorsal ray, which is split for about a quarter of its length, the two short branches ending in very small digitations. The spicules are slender with recurved barb ends.

Hosts: Sheep, goat, wild ruminants

Life cycle: The life cycle is thought to be direct; the main route of infection is percutaneous. Infective L₃ larvae are susceptible to desiccation.

Geographical distribution: South America, South Africa, Indonesia and parts of Asia

Pathogenesis: The parasite is a voracious blood sucker; as few as 100–200 worms are sufficient to produce death in sheep within a few weeks.

Clinical signs: Causes severe anaemia and death.

Diagnosis: Demonstration of the characteristic large eggs in the faeces

Pathology: As for B. trigonocephalum

Epidemiology: As for B. trigonocephalum

Treatment and control: As for B. trigonocephalum

Strongyloides papillosus

Common name: Threadworm

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Rhabditoidea

Description, gross: Slender, hair-like worms generally less than 1.0 cm long

Description, microscopic: Only females are parasitic. 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 (Fig. 3.13). Strongyloides eggs are oval, thinshelled and small, being half the size of typical strongyle eggs. In herbivores it is the larvated egg which is passed out in the faeces, but in other animals it is the hatched L₁.

Hosts: Sheep, cattle, other ruminants and rabbits

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. 3.13 Adult Strongyloides female.

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