Pathology: The immature flukes are embedded in the mucosa of the upper ileum and duodenum and are plug feeders, and this can result in severe erosion of the duodenal mucosa. In heavy infections these cause enteritis characterised by oedema, haemorrhage, ulceration and associated anaemia and hypoproteinaemia. At necropsy, the young flukes can be seen as clusters of brownish pink parasites attached to the duodenal mucosa and occasionally also in the jejunum and abomasum.

Epidemiology: Paramphistomosis often depends for its continuous endemicity on permanent water masses, such as lakes and ponds, from which snails are dispersed into previously dry areas by flooding during heavy rains. Paramphistome eggs deposited by animals grazing these areas hatch and infect snails. Subsequent production of cercariae often coincides with receding water levels making them accessible to grazing ruminants. In other areas, the situation is complicated by the ability of the snails to aestivate on dry pastures and become reactivated on the return of rainfall. A good immunity develops in cattle, and outbreaks are usually confined to young stock. However, adults continue to harbour low burdens of adult parasites and are important reservoirs of infection for snails. In contrast, sheep and goats are relatively susceptible throughout their lives.

Treatment: Resorantel and oxyclozanide are considered the anthelmintics of choice against both immature and adult rumen flukes in cattle and sheep.

Control: As in Fasciola gigantica, the best control is achieved by providing a piped water supply to troughs and preventing access of the animals to natural water. Even then snails may gain access to watering troughs and regular application of a molluscicide at source or manual removal of snails may be necessary.

Notes: There is confusion over the classification of paramphistomes and it is likely that many described species, such as those listed below, are synonymous.

Paramphistomum microbothrium

Common name: Rumen fluke

Predilection site: Rumen

Parasite class: Trematoda

Family: Paramphistomatidae

Definitive hosts: Cattle, sheep, goat, deer, buffalo, antelope

Geographical distribution: Africa

Ceylonocotyle streptocoelium

Synonym: Paramphistomum streptocoelium

Common name: Rumen fluke

Predilection site: Rumen

Parasite class: Trematoda

Superfamily: Paramphistomatidae

Definitive hosts: Cattle, sheep, goat and wild ruminants

Geographical distribution: Africa

Cotylophoron cotylophorum

Synonym: Paramphistomum cotylophorum

Common name: Rumen fluke

Predilection site: Rumen, reticulum

Parasite class: Trematoda

Family: Paramphistomatidae

Definitive hosts: Cattle, sheep and wild ruminants

Geographical distribution: India, Australia

Monocercomonas ruminatium

Synonym: Trichomonas ruminantium, Tritrichomonas ruminatium

Predilection site: Rumen

Fig. 2.2 Monocercomonas ruminatium.

Parasite class: Zoomastigophorasida

Family: Monocercomonadidae

Description: The trophozoite is subspherical, 3–8 × 3–7 μm, with a rounded anterior end. The axostyle is curved and may or may not extend beyond the body. A pelta and parabasal body are present. The cytosome and anterior nucleus are anterior. There are three anterior flagella and a trailing one (Fig. 2.2).

Life cycle: The life cycle is simple with trophozoites dividing by binary fission. No sexual stages are known and there are no cysts.

Geographical distribution: Worldwide

Pathogenesis: Not considered to be pathogenic

Diagnosis: Identification of trophozoites based on morphological examination.

Epidemiology: Transmission presumably occurs by ingestion of trophozoites from faeces or rumen contents.

Treatment and control: Not required

Entamoeba bovis

Predilection site: Rumen

Parasite class: Sarcodina

Family: Endamoebidae

Description: Trophozoites are 5–20 μm in diameter. The smoothly granular cytoplasm is filled with vacuoles of various sizes. The nucleus is large with a large central endostome made up of compact granules, with a row of chromatin granules of varying sizes around its periphery. The cysts are 4–14 μm in diameter and contain a single nucleus when mature with irregular clumps of chromatin granules. A large glycogen granule may or may not be present.

Hosts: Sheep, goat

Life cycle: Trophozoites divide by binary fission. Before encysting the amoebae round up, become smaller and lay down a cyst wall. Each cyst has one nucleus. Amoebae emerge from the cysts and grow into trophozoites.

Distribution: Worldwide

Pathogenicity: Non-pathogenic

Diagnosis: Identification of trophozoites, or cysts in large intestinal contents or faeces.

Treatment and control: Not required

ABOMASUM

Cattle can be parasitised by over 18 species of gastrointestinal nematodes, infection causing parasitic gastroenteritis (PGE). The most economically important gastrointestinal nematode in cattle is Ostertagia ostertagi and whilst the diagnosis, epidemiology, treatment and control are described in detail for this parasite, details are similar for other gastrointestinal nematodes.

Ostertagia ostertagi

Synonym: Ostertagia lyrata, Skrjabinagia lyrata

Common name: Brown stomach worm

Predilection site: Abomasum

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Description, gross: Adults are slender, reddish brown worms with a short buccal cavity. Males measure 6–8 mm and females 8–9 mm in length.

Description, microscopic: The cuticle in the anterior region is striated transversely whereas the rest of the body is unstriated and bears around 30 longitudinal ridges. The brown spicules are slightly curved and divided in the posterior region to terminate in three stubby hooked processes (Fig. 2.3a). In the female, the vulva is sited about 1.5 mm from the posterior and is covered with a flap. The tail tapers gradually and ends in a slender, rounded tip.

Fig. 2.3 Spicules of Ostertagia species. (a) O. ostertagi. (b) O. leptospicularis.

Hosts: Cattle, deer and very occasionally goats

Life cycle: The life cycle is direct. Eggs are passed in the faeces, and under optimal conditions, develop within the faecal pat to the infective third stage within 2 weeks. When moist conditions prevail, the L₃ migrate from the faeces on to the herbage. After ingestion, the L₃ exsheaths in the rumen and further development takes place in the lumen of an abomasal gland. Two parasitic moults occur before the L₅ emerges from the gland around 18 days after infection to become sexually mature on the mucosal surface. The entire parasitic life cycle usually takes 3 weeks, but under certain circumstances many of the ingested L₃ become arrested in development at the early fourth larval stage (EL₄) for periods of up to 6 months (also referred to as hypobiosis).

Geographical distribution: Worldwide. Ostertagia is especially important in temperate climates and in subtropical regions with winter rainfall.

Pathogenesis: Large populations of O. ostertagi can induce extensive pathological and biochemical changes and these are maximal when the parasites are emerging from the gastric glands (about 18 days after infection) but these may be delayed for several months when arrested larval development occurs.

In heavy infections of 40 000 or more adult worms the principal effects of these changes are first, a reduction in the acidity of the abomasal fluid, the pH increasing from 2.0 up to 7.0. This results in a failure to activate pepsinogen to pepsin. There is also a loss of bacteriostatic effect in the abomasum. Secondly, there is an enhanced permeability of the abomasal epithelium to macromolecules.

The results of these changes are a leakage of pepsinogen into the circulation, leading to elevated plasma concentrations, and the loss of plasma proteins into the gut lumen, eventually leading to hypoalbuminaemia. In addition, in response to the presence of the adult parasites, the zymogen cells secrete increased amounts of pepsin directly into the circulation.

Although reduced feed consumption and diarrhoea affect liveweight gain they do not wholly account for the loss in production. Current evidence suggests that this is primarily because of substantial leakage of endogenous protein into the gastrointestinal tract. Despite some reabsorption, this leads to a disturbance in post-absorptive nitrogen and energy metabolism due to the increased demands for the synthesis of vital proteins, such as albumin and the immunoglobulins, which occur at the expense of muscle protein and fat deposition.

Clinical signs: Bovine ostertagiosis occurs in two clinical forms. In temperate climates with cold winters the seasonal occurence of these is as follows:

Type I disease is usually seen in calves grazed intensively during their first grazing season, as the result of larvae ingested 3–4 weeks previously; in the northern hemisphere this normally occurs from mid-July onwards. In type I disease, the morbidity is usually high, often exceeding 75%, but mortality is rare provided treatment is instituted early.

Type II disease occurs in yearlings, usually in late winter or spring following their first grazing season and results from the maturation of larvae ingested during the previous autumn and subsequently become arrested in their development at the EL₄ stage. Hypoalbuminaemia is more marked, often leading to submandibular oedema. In type II the prevalence of clinical disease is comparatively low and often only a proportion of animals in the group are affected; mortality in such animals can be high unless early treatment with an anthelmintic effective against both arrested and developing larval stages is instituted.

The main clinical sign in both type I and type II disease is a profuse watery diarrhoea and in type I, where calves are at grass, this is usually persistent and has a characteristic bright green colour. In contrast, in the majority of animals with type II, the diarrhoea is often intermittent and anorexia and thirst are usually present. In both forms of the disease, the loss of body weight is considerable during the clinical phase and may reach 20% in 7–10 days.

Diagnosis: In young animals this is based on:

In older animals, laboratory diagnosis is more difficult since faecal egg counts and plasma pepsinogen levels are less reliable.

Pathology: The developing parasites cause a reduction in the functional gastric gland mass; in particular the parietal cells, which produce hydrochloric acid, are replaced by rapidly dividing, undifferentiated, non-acid-secreting cells. Initially, these cellular changes occur in the parasitised gland (Fig. 2.4), but as it becomes distended by the growing worm these changes spread to the surrounding non-parasitised glands, the end result being a thickened hyperplastic gastric mucosa.

Macroscopically, the lesion is a raised nodule with a visible central orifice; in heavy infections these nodules coalesce to produce an effect reminiscent of morocco leather (Fig. 2.5). The abomasal folds are often very oedematous and hyperaemic and sometimes necrosis and sloughing of the mucosal surface occurs (Fig. 2.6); the regional lymph nodes are enlarged and reactive.

Fig. 2.4 Ostertagia ostertagi emerging from a gastric gland.

Fig. 2.5 Abomasum showing the characteristic nodules produced by the development of O. ostertagi larvae in the gastric glands.

Fig. 2.6 Necrosis of mucosa in severe ostertagiosis.

Epidemiology of ostertagiosis in temperate countries of the northern hemisphere

Dairy herds

Two factors, one management and one climatic, appear to increase the prevalence of type II ostertagiosis.

First, the practice of grazing calves from May until late July on permanent pasture, then moving these to hay or silage aftermath before returning them to the original grazing in late autumn. Such pasture will still contain many L₃ and when ingested they will become arrested.

Secondly, in dry summers the L₃ are retained within the crusted faecal pat and cannot migrate on to the pasture until sufficient rainfall occurs. If rainfall is delayed until late autumn many larvae liberated on to pasture will become arrested following ingestion and so increase the chance of type II disease.

Although primarily a disease of young dairy cattle, ostertagiosis can nevertheless affect groups of older cattle in the herd, particularly if these have had little previous exposure to the parasite.

Acquired immunity is slow to develop and calves do not achieve a significant level of immunity until the end of their first grazing season. Housing over the winter allows the immunity to wane by the following spring and yearlings turned out at that time are partially susceptible to reinfection and so contaminate the pasture with small numbers of eggs. However, immunity is rapidly re-established and any clinical signs which occur are usually of a transient nature. By the second and third year of grazing, adult stock in endemic areas are usually highly immune to reinfection and of little significance in the epidemiology. However, around the periparturient period when immunity wanes, particularly in heifers, there are reports of clinical disease following calving. Burdens of adult Ostertagia spp in dairy cows are usually low and routine treatment of herds at calving should not be required.

Beef herds

Although the basic epidemiology in beef herds is similar to dairy herds, the influence of immune adult animals grazing alongside susceptible calves has to be considered. Thus, in beef herds where calving takes place in the spring, ostertagiosis is uncommon since egg production by immune adults is low, and the spring mortality of the overwintered L₃ occurs prior to the suckling calves ingesting significant quantities of grass. Consequently, only low numbers of L₃ become available on the pasture later in the year. However, where calving takes place in the autumn or winter, ostertagiosis can be a problem in calves during the following grazing season once they are weaned, the epidemiology then being similar to that for dairy calves.

Epidemiology of ostertagiosis in subtropical and temperate countries in the southern hemisphere

In countries with temperate climates, such as New Zealand, the seasonal pattern is similar to that reported for Europe with type I disease occurring in the summer and burdens of arrested larvae accumulating in the autumn. In those countries with subtropical climates and winter rainfall, such as parts of southern Australia, southwest Africa and some regions of Argentina, Chile and Brazil, the increase in L₃ population occurs during the winter and outbreaks of type I disease are seen towards the end of the winter period. Arrested larvae accumulate during the spring and where type II disease has been reported it has occurred in late summer or early autumn. A basically similar pattern of infection is seen in some southern parts of the USA with non-seasonal rainfall, such as Louisiana and Texas. There, larvae accumulate on pasture during winter and arrested development occurs in late winter and early spring with outbreaks of type II disease occurring in late summer or early autumn.

The environmental factors which produce arrested larvae in subtropical zones are not yet fully known.

Treatment: Type I disease responds well to treatment at the standard dosage rates with any of the modern benzimidazoles, the pro-benzimidazoles (febantel, netobimin and thiophanate), levamisole, or the avermectins/milbemycins. All of these drugs are effective against developing larvae and adult stages. Following treatment, calves should be moved to pasture which has not been grazed by cattle in the same year.

For the successful treatment of type II disease it is necessary to use drugs which are effective against arrested larvae as well as developing larvae and adult stages. Only the modern benzimidazoles (such as albendazole, fenbendazole or oxfendazole) or the avermectins/milbemycins are effective in the treatment of type II disease when used at standard dosage levels, although the pro-benzimidazoles are also effective at higher dose rates.

The field where the outbreak has originated may be grazed by sheep or rested until the following June.

In lactating dairy cattle, topical eprinomectin has the advantage that there is no milk withholding period.

Control: Traditionally, ostertagiosis has been prevented by routinely treating young cattle with anthelmintics over the period when pasture larval levels are increasing. However, it has the disadvantage that since the calves are under continuous larval challenge their performance may be impaired. With this system, effective anthelmintic treatment at housing is also necessary using a drug effective against hypobiotic larvae in order to prevent type II disease.

The prevention of ostertagiosis by limiting exposure to infection is a more efficient method of control. This may be acheived by allowing young cattle sufficient exposure to larval infection to stimulate immunity but not sufficient to cause a loss in production. The provision of this ‘safe pasture’ may be achieved in two ways:

Sometimes a combination of these methods is employed. The timing of events in the systems described below is applicable to the calendar of the northern hemisphere.

Prophylactic anthelmintic medication

Since the crucial period of pasture contamination with O. ostertagi eggs is the period up to mid-July, one of the efficient modern anthelmintics may be given on two or three occasions between turn-out in the spring and July to minimise the numbers of eggs deposited on the pasture. For calves going to pasture in early May two treatments, 3 and 6 weeks later, are used, whereas calves turned out in April require three treatments at intervals of 3 weeks. Where parenteral or pour-on macrocyclic lactones are used the interval after first treatment may be extended to 5 or 8 weeks (the interval depends on the anthelmintic used) due to residual activity against ingested larvae.

Several rumen boluses are available which provide either the sustained release of anthelmintic drugs over periods of 3–5 months or the pulse release of therapeutic doses of an anthelmintic at intervals of 3 weeks throughout the grazing season. These are administered to first season grazing calves at turnout and effectively prevent pasture contamination and the subsequent accumulation of infective larvae. Although offering a high degree of control of gastrointestinal nematodes there is evidence to suggest that young cattle protected by these boluses, or other highly effective prophylactic drug regimens, are more susceptible to infection in their second year at grass.

Anthelmintic prophylaxis has the advantage that animals can be grazed throughout the year on the same pasture and is particularly advantageous for the small heavily stocked farm where grazing is limited.

Anthelmintic treatment and move to safe pasture in mid-July

This system, usually referred to as ‘dose and move’, is based on the knowledge that the annual increase of L₃ occurs after mid-July. Therefore if calves grazed from early spring are given an anthelmintic treatment in early July and moved immediately to a second pasture such as silage or hay aftermath, the level of infection which develops on the second pasture will be low.

The one reservation with this technique is that in certain years the numbers of L₃ that overwinter are sufficient to cause heavy infections in the spring and clinical ostertagiosis can occur in calves in April and May. However, once the ‘dose and move’ system has operated for a few years this problem is unlikely to arise.

In some European countries the same effect has been obtained by delaying the turnout of calves until mid-summer.

Alternate grazing of cattle and sheep

This system ideally utilises a 3-year rotation of cattle, sheep and crops. Since the effective lifespan of most O. ostertagi L₃ is under 1 year and cross-infection between cattle and sheep in temperate areas is largely limited to O. leptospicularis, Trichostrongylus axei and occasionally C. oncophora, good control of bovine ostertagiosis should, in theory, be achieved. It is particularly applicable to farms with a high proportion of land suitable for cropping or grassland conservation. In marginal or upland areas reasonable control has been reported using an annual rotation of beef cattle and sheep. The drawback of alternate grazing systems is that they impose a rigorous and inflexible regimen on the use of land. Furthermore, in warmer climates where Haemonchus spp are prevalent, this system can prove dangerous since this very pathogenic genus establishes in both sheep and cattle.

Rotational grazing of adult and young stock

This system involves a continuous rotation of paddocks in which the susceptible younger calves graze ahead of the immune adults and remain long enough in each paddock to remove only the leafy upper herbage. The incoming immune adults then graze the lower more fibrous echelons of the herbage, which contain the majority of the L₃. Since the faeces produced by the immune adults contains few if any O. ostertagi eggs, the pasture contamination is greatly reduced. The optimal utilisation of permanent grassland and the control of internal parasitism without resort to therapy makes it an option for organic systems of production.

Notes: O. ostertagi is perhaps the most common cause of parasitic gastritis in cattle. The disease, often simply known as ostertagiosis, typically affects young cattle during their first grazing season, although herd outbreaks and sporadic individual cases have also been reported in adult cattle.

O. ostertagi is considered to be a polymorphic species with Ostertagia lyrata (syn. Skrjabinagia).

Ostertagia leptospicularis

Synonym: Ostertagia crimensis, Skrjabinagia kolchida, Grosspiculagia podjapolskyi

Predilection site: Abomasum

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Description, gross: Adults are slender, reddish brown worms with a short buccal cavity. Males measure 6–8 mm and females 8–9 mm in length.

Description, microscopic: Distinguished from other ostertagian species by the length of the oesophagus, which is longer than in other species (0.7 mm compared with approximately 0.6 mm). In cattle, the worms are thinner than O. ostertagi and males worms are differentiated on spicule morphology (Fig. 2.3b).

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

Life cycle: Similar to O. ostertagi

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

Notes: Considered to be a polymorphic species with two male morphs, Ostertagia leptospicularis and Skrjabinagia kolchida (Grosspiculagia podjapolskyi).

Details of the pathogenesis, clinical signs, diagnosis, pathology, epidemiology, treatment and control are as for O. ostertagi.

Haemonchus contortus

Synonym: Haemonchus placei (see notes)

Common name: Barber’s pole worm

Predilection site: Abomasum

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

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.

For more details see Chapter 3 (Sheep and goats).

Haemonchus similis

Predilection site: Abomasum

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Description, gross: The adults are 2.0–3.0 cm and reddish in colour.

Description, microscopic: The male has an asymmetrical dorsal lobe and barbed spicules differing from H. contortus in that the terminal processes of the dorsal ray are longer and the spicules shorter.

Hosts: Cattle, deer

Geographical distribution: North America, Europe

Pathogenesis: As for H. contortus

Trichostrongylus axei

Synonym: Trichostrongylus extenuatus

Predilection site: Abomasum or stomach

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

For more details, see Chapter 3 (Sheep and goats).

Mecistocirrus digitatus

Predilection site: Abomasum

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Description, gross: To the naked eye, the worm is indistinguishable from Haemonchus contortus. The males measure up to around 30 mm and the females 42 mm in length.

Description, microscopic: The male is distinguishable from Haemonchus by the presence of long narrow spicules that are fused together for the majority of their length (in Haemonchus the spicules are thicker, separate and barbed at the tips). The female differs from Haemonchus in that the vulva is positioned nearer to the tip of the tail and there is no vulval flap. The cuticle contains many longitudinal ridges and the cervical papillae are readily apparent. The small buccal capsule is armed with a lancet.

Hosts: Cattle, buffalo, zebu, sheep and goat; occasionally the stomach of the pig and rarely man

Life cycle: This is direct and similar to that of Haemonchus. The prepatent period is longer than in Haemonchus, being 60–80 days, partly as the result of the longer duration of the fourth stage in the abomasal mucosa.

Geographical distribution: Tropical and subtropical regions, particularly Central America and parts of Asia

Pathogenesis: In endemic areas, the pathogenesis of this haematophagous parasite is similar to that of H. contortus and it is of similar economic importance.

Clinical signs: Similar to H. contortus, inducing anaemia, weight loss and emaciation.

Diagnosis: See the description of the parasite above.

Treatment and control: See H. contortus for details.

Parabronema skrjabini

Predilection site: Abomasum

Parasite class: Nematoda

Superfamily: Spiruroidea

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

For more details see Chapter 3 (Sheep and goats).

Cryptosporidium andersoni

Synonym: Cryptosporidium muris

Predilection site: Abomasum

Parasite class: Sporozoasida

Family: Cryptosporidiidae

Description: Oocysts, passed fully sporulated, are ellipsoid, 6.0–8.1 × 5.0–6.5 μm (mean 7.4 × 5.5 μm), with a length/width ratio of 1.35.

Life cycle: Oocysts, each with four sporozoites, are liberated in the faeces. Following ingestion, the sporozoites invade the microvillous brush border of the gastric glands and the trophozoites rapidly differentiate to form meronts with four to eight merozoites. Gametogony follows after one to two generations of meronts, and oocysts are produced in 72 hours. The prepatent period is unknown.

Geographical distribution: Reported in USA, Brazil, UK, Czech Republic, Germany, France, Japan and Iran

Pathogenesis: Generally considered to be non-pathogenic

Clinical signs: Usually asymptomatic, although depressed weight gain in calves and milk yields in milking cows have been reported.

Diagnosis: Oocysts may be demonstrated using Ziehl–Nielsen stained faecal smears in which the sporozoites appear as bright red granules. Speciation of Cryptosporidium is difficult, if not impossible, using conventional techniques. A range of molecular and immunological techniques has been developed, that include the use of immunofluorescence (IF) or enzyme-linked immunosorbent assays (ELISA). More recently, DNA-based techniques have been used for the molecular characterisations of Cryptosporidium species.

Pathology: The presence of the endogenous stages of the parasite leads to destruction of the microvilli of peptic glands, leading to elevated concentrations of plasma pepsinogen levels.

Epidemiology: The epidemiology of infection has not been studied although it is likely to be similar to Cryptosporidium parvum in cattle. Many calves are likely to become infected without showing clinical signs but become sources of infection for calves that follow. The primary route of infection is by the direct animal-to-animal faecal-oral route. Thus in calves, for example, overcrowding, stress of early weaning, transport and marketing, together with low levels of hygiene will increase the risk of heavy infections.

Treatment and control: There is no reported treatment. Good hygiene and management are important in preventing disease from cryptosporidiosis. Feed and water containers should be high enough to prevent faecal contamination. Young animals should be given colostrum within the first 24 hours of birth and overstocking and overcrowding should be avoided. Dairy calves should be either isolated in individual pens or kept in similar age groups and cleaned out daily.

Notes: Based on oocyst morphology, C. muris-like oocysts have been found in cattle in several countries around the world. Recent molecular characterisations have indicated that all bovine isolates are C. andersoni.

SMALL INTESTINE

Trichostrongylus colubriformis

Synonym: Trichostrongylus instabilis

Common name: Black scour or bankrupt worm

Predilection site: Duodenum and anterior small intestine

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

For more details see Chapter 3 (Sheep and goats).

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.

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

Details of the pathogenesis, clinical signs, diagnosis, pathology, epidemiology, treatment and control are as for T. colubriformis.

Cooperia oncophora

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Description, gross: In size C. oncophora is similar to Ostertagia but with a large bursa. Males measure around 5.5–9 mm and females 6–8 mm in length. When fresh the worms appear pinkish white.

Description, microscopic: The main generic features are the small cephalic vesicle and the transverse cuticular striations in the oesophageal region (Fig. 2.7). The body possesses longitudinal ridges. The spicules have a distinct wing-like expansion in the middle region and often bear ridges (Fig. 2.8a); there is no gubernaculum. The females have a long tapering tail. Eggs are oval and thin-shelled.

Hosts: Cattle, 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 3 weeks. The bionomic requirements of the free-living stages are similar to those of Ostertagia.

Geographical distribution: Worldwide

Pathogenesis: C. oncophora is generally considered to be a mild pathogen in calves, 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: These are loss of appetite and poor weight gains. Occasionally a heavy infection can induce intermittent diarrhoea.

Fig. 2.7 Anterior of Cooperia spp showing the cephalic vesicle and cuticular striations.

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

Pathology: Moderate to heavy infections can induce a catarrhal enteritis with localised villous atrophy and oedema of the intestinal mucosa.

Fig. 2.8 Spicules of Cooperia species. (a) C. oncophora. (b) C. pectinata. (c) C. punctata. (d) Cooperia surnabada.

Epidemiology: In temperate areas, this is similar to that of Ostertagia. Arrested development (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. Adult animals usually show few signs of infection but act as carriers, shedding low numbers of eggs in their faeces.

In the subtropics, the epidemiology is similar to that of Haemonchus though Cooperia does not have the same high biotic potential and the L₃ survive rather better under arid conditions. Hypobiosis is also a feature during prolonged dry seasons.

Treatment: The principles are similar to those applied in bovine ostertagiosis. 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 described for Ostertagia.

Notes: In temperate areas, members of the genus Cooperia usually play a secondary role in the pathogenesis of parasitic gastroenteritis of ruminants although they may be the most numerous trichostrongyle present. However, in some tropical and subtropical areas, some species are responsible for severe enteritis in calves.

Three further species of Cooperia are found in cattle. Details of the diagnosis, epidemiology, treatment and control are as for C. oncophora

Cooperia punctata

Common name: Cattle bankrupt worm

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Description, gross: Similar to C. oncophora. Males measure around 4.5–6.0 mm, and females 6–8 mm in length.

Description, microscopic: See C. oncophora and Fig. 2.8c for details.

Hosts: Cattle, deer

Life cycle: Similar to C. oncophora but the adults remain closely associated with the mucosa and surface epithelium. The prepatent period is around 2–3 weeks. The bionomic requirements of the free-living stages are similar to Haemonchus.

Geographical distribution: Worldwide

Pathogenesis: C. punctata is a pathogenic parasite since it penetrates the epithelial surface of the small intestine and causes a disruption similar to that of other intestinal trichostrongylid species, which leads to villous atrophy and a reduction in the area available for absorption. In heavy infections, diarrhoea has been reported.

Clinical signs: There is loss of appetite, poor weight gains and diarrhoea and there may be submandibular oedema.

Cooperia pectinata

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Description, gross: Similar to C. oncophora. Males measure around 7–8 mm and females 7.5–10 mm in length.

Description, microscopic: See C. oncophora and Fig 2.8b for details.

Hosts: Cattle, deer

Life cycle: See C. punctata for details

Geographical distribution: Worldwide

Pathogenesis and clinical signs: Similar to C. punctata. A catarrhal enteritis is often present with loss of appetite, poor weight gain, diarrhoea, and in some cases, submandibular oedema.

Cooperia surnabada

Synonym: Cooperia mcmasteri

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Description, gross: The males measure around 7 mm and the females 8 mm in length.

Description, microscopic: The appearance is very similar to C. oncophora, although the bursa is larger and the bursal rays tend to be thinner. The spicules are thinner with a posterior bifurcation and the tips possess a small conical appendage (Fig. 2.8d).

Hosts: Cattle, sheep, camel

Life cycle: Similar to that of C. pectinata and C. punctata. The bionomic requirements of the free-living stages concur with those for Haemonchus.

Geographical distribution: Parts of Europe, North America and Australia

Pathogenesis: Moderate pathogenicity as the worms penetrate the surface of the small intestine and can induce villous atrophy.

Clinical signs: See C. punctata.

Diagnosis: See C. oncophora.

Treatment and control: Refer to C. oncophora.

Nematodirus helvetianus

Common name: Thread-necked worm

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

Description, gross: The adults are slender, males measuring around 11–16 mm and females 17–24 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 and the long, slender spicules end in a fused point with the surrounding membrane being lanceolate. The female has a truncate tail with a small spine, and the egg is large, ovoid and colourless and twice the size of the typical trichostrongyle egg (Fig. 2.9).

Hosts: Cattle, occasionally sheep, goat 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. helvetianus does not have the same critical hatching requirements as N. battus (see Chapter 3) and so the larvae often appear on the pasture within 2–3 weeks of the eggs being excreted in the faeces. More than one annual generation is therefore possible. The parasitic phase within the host is similar to that of N. battus. The prepatent period is around 3 weeks.

Geographical distribution: Worldwide

Pathogenesis: Although this is similar to that of N. battus, there is some controversy over the extent of the pathogenic effect. N. helvetianus has been incriminated in outbreaks of bovine parasitic gastroenteritis but experimental attempts to reproduce the disease have been unsuccessful.

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.

Fig. 2.9 Large egg of Nematodirus helvetianus.

Diagnosis: Examination of faeces will allow the large colourless eggs to be differentiated from those of N. spathiger. At necropsy, the tips of the male spicules will allow diagnosis from other Nematodirus species.

Pathology: Increased mucus production and focal compression and stunting of villi may occur in the small intestine.

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

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

Nematodirus battus

Common name: Thread-necked worm

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

For more details see Chapter 3 (Sheep and goats).

Nematodirus spathiger

Common name: Thread-necked worm

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Trichostrongyloidea

For more details see Chapter 3 (Sheep and goats).

Bunostomum phlebotomum

Synonym: Monodontus phlebotomum

Common name: Cattle hookworm

Predilection site: Small intestine, particularly the anterior jejunum and/or duodenum

Parasite class: Nematoda

Superfamily: Ancylostomatoidea

Description, gross: Bunostomum is one of the larger nematodes of the small intestine of ruminants, being 1–3 cm long, stout, greyish white and characteristically hooked at the anterior end with the buccal capsule opening anterodorsally (Fig. 2.10).

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 are two pairs 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 tridigitate branches. The spicules are very long and slender. 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. Eggs are medium-sized (97 × 50 μm) irregular broad elipse, with dissimilar sidewalls and four to eight blastomeres.

Fig. 2.10 Head of Bunostomum phlebotomum showing the large buccal capsule and cutting plates.

Hosts: Cattle

Life cycle: Infection with the L₃ may be percutaneous or oral. After skin penetration, the larvae travel to the lungs and moult to 4th 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 about 6 weeks after skin penetration, and 7–10 weeks after ingestion.

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 2000 may lead to death in cattle. In stabled cattle, pruritus of the limbs, probably caused by skin penetration by the larvae, is seen.

Clinical signs: There may be inappetence, diarrhoea and emaciation, more frequently seen in young animals. Severe infection can also induce submandibular oedema (‘bottle jaw’). Postmortem examination often reveals hydrothorax and fluid within the pericardium. Older livestock frequently develop sufficient immunity to limit reinfection and in many cases Bunostomum is present asymptomatically. In calves, foot stamping and signs of itching may accompany skin penetration by the larvae.

Diagnosis: The clinical signs of anaemia and perhaps diarrhoea in calves 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 adhered. 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 sub-tropics and in some areas, such as Nigeria, the highest worm burdens are found at the end of the dry season, apparently due to the maturation of hypobiotic larvae. Young livestock are most susceptible. B. phlebotomum is often a serious pathogen in many regions such as the southern and mid-western USA, Australia and parts of Africa. In temperate countries, high worm burdens are usually uncommon. The prophylactic dosing regimes, adopted for the control of trichostrongyles, have contributed to the low prevalence of Bunostomum.

Treatment: Anthelmintics listed for O. ostertagi are effective.

Control: A combination of strategic dosing with anthelmintics and pasture management is used in the control of larvae as they 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. Stabled cattle 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.

Agriostomum vryburgi

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Ancylostomatoidea

Description, gross: Worms are stout and greyish white in colour. Males are around 9–11 mm and females 13–16 mm in length. Spicules are equal in length and a gubernaculum is present.

Description, microscopic: The shallow bucal capsule contains four pairs of large teeth on its margin and has a rudimentary leaf-crown. The large oesophageal opening houses two small subventral lancets. Eggs measure about 130–190 × 60–90 μm.

Hosts: Cattle, buffalo, ox and zebu

Life cycle: The life cycle is probably direct.

Geographical distribution: Asia and South America

Pathogenesis: The hookworms attach to the mucosa of the anterior small intestine. The pathogenicity, although unknown, presumably depends on its haematophagic habits, inducing anaemia.

Notes: Agriostomum vryburgi is a common hookworm of the large intestine throughout its distribution range.

Details on the diagnosis, treatment and control are likely to be similar to B. phlebotomum.

Strongyloides papillosus

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Rhabditoidea

For more details see Chapter 3 (Sheep and goats).

Toxocara vitulorum

Synonym: Neoascaris vitulorum

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Ascaridoidea

Description, gross: This is a very large whitish nematode, the adult male is up to 25 cm and the female 30 cm.

Description, microscopic: The cuticle is less thick than other ascarids and somewhat soft and translucent. There are three lips, broad at the base and narrowing anteriorly. The oesophagus is 3–4.5 mm long and has a posterior, granular ventriculus. The tail of the male usually forms a small spike-like appendage. There are about five pairs of post-cloacal papillae; the anterior pair is large and double. Pre-cloacal papillae are variable in number. The vulva is situated about one eighth of the body length from the anterior end. The egg of T. vitulorum is subglobular, with a thick finely pitted shell, and is almost colourless (75–95 × 60–74 μm) (Fig. 2.11).

Fig. 2.11 Egg of Toxocara vitulorum.

Hosts: Cattle, buffalo and zebu, rarely sheep and goats

Life cycle: The life cycle is direct. The most important source of infection is the milk of the dam in which larvae are present for up to 3–4 weeks after parturition. There is no tissue migration in the calf following milk-borne infection and the prepatent period is 3–4 weeks. The ingestion of larvated eggs by calves over 6 months old seldom results in patency, the larvae migrating to various tissues where they remain dormant; in female animals, resumption of development in late pregnancy allows further transmammary transmission.

Geographical distribution: Africa, India, Asia

Pathogenesis: The main effects of T. vitulorum infection appear to be caused by the adult worms in the intestines of calves up to 6 months old. Heavy infections are often associated with unthriftyness, catarrhal enteritis and intermittent diarrhoea, and in buffalo calves particularly, fatalities may occur. Heavy burdens can be associated with intestinal obstruction and occasionally perforation may occur leading to peritonitis and death.

Clinical signs: Diarrhoea, poor condition

Diagnosis: In some instances heavily infected calves may exhale an acetone-like odour. The sub-globular eggs, with thick, pitted shells, are characteristic in bovine faeces. Egg output in young calves can be very high (>50 000 epg) but patency is short and by around 4–6 months of age, calves have expelled most of their adult worm population.

Pathology: The pathological effects of adult worms in the intestine are poorly defined. Heavy infections may obstruct the gut and lead to gut perforation. Migration up the bile or pancreatic duct may lead to biliary obstruction and cholangitis.

Epidemiology: The most important feature is the reservoir of larvae in the tissues of the cow, with subsequent milk-borne transmission ensuring that calves are exposed to infection from the first day of life. The majority of patent infections occur in calves of less than 6 months of age.

Treatment: The adult worms are susceptible to a wide range of anthelmintics, including piperazine, levamisole, macrocyclic lactones and the benzimidazoles. Many of these drugs are also effective against developing stages in the intestine.

Control: The prevalence of infection can be dramatically reduced by treatment of calves at 3 and 6 weeks of age, preventing developing worms reaching patency.

Capillaria bovis

Synonym: Capillaria brevipes

Predilection site: Small intestine

Parasite class: Nematoda

Superfamily: Trichuroidea

Description, gross: These are very fine filamentous worms, the narrow stichosome oesophagus occupying about one third to half the body length. Males measure around 8–9 mm and females up to 12 mm.

Description, microscopic: The males have a long thin single spicule about 0.9 mm long and often possess a primitive bursa-like structure. The eggs are barrelshaped (similar to Trichuris), 45–50 × 22–25 μm, are colourless and have thick shells that are slightly striated with bipolar plugs.

Hosts: Cattle, sheep, goat

Life cycle: The life cycle is direct. The infective L₁ develops within the egg in about 3–4 weeks. Infection of the final host is through ingestion of this embryonated infective stage and development to adult worms occurs without a migration phase. The prepatent period is 3–4 weeks.

Geographical distribution: Worldwide

Pathogenesis: Considered to be of low pathogenicity and of little veterinary significance.

Clinical signs: No clinical signs have been attributed to infection with this parasite.

Diagnosis: Because of the non-specific nature of the clinical signs and the fact that, in heavy infections, these may appear before eggs are present in the faeces, diagnosis depends on necropsy and careful examination of the small intestine for the presence of the worms. This may be carried out by microscopic examination of mucosal scrapings squeezed between two glass slides; alternatively the contents should be gently washed through a fine sieve and the retained material resuspended in water and examined against a black background.

Pathology: No associated pathology

Epidemiology: Infection is by ingestion of the larvated eggs. Infection is common in sheep though not significant.

Treatment: Not usually required

Control: Not required

Moniezia benedeni

Predilection site: Small intestine

Parasite class: Cestoda

Family: Anoplocephalidae

Description, gross: These are long tapeworms, 2 metres or more, which are unarmed, possessing prominent suckers.

Description, microscopic: Segments are broader than they are long (up to 2.5 cm wide) and contain two sets of genital organs grossly visible along the lateral margin of each segment (Fig. 2.12). There is a row of inter-proglottidal glands at the posterior border of each segment, which may be used in species differentiation; in M. benedeni they are confined to a short row close to the middle of the segment. The irregularly quadrangular eggs have a well defined pyriform apparatus and vary from 55–75 μm in diameter.

Final host: Cattle

Intermediate hosts: Forage mites, mainly of the family Oribatidae.

Life cycle: Mature proglottids or eggs are passed in the faeces and on to pasture where the oncospheres are ingested by forage mites. The embryos migrate into the body cavity of the mite where they develop to cysticercoids in 1–4 months and infection of the final host is by ingestion of infected mites during grazing. The prepatent period is approximately 6 weeks, but the adult worms appear to be short lived, patent infections persisting for only 3 months.

Geographical distribution: Worldwide

Fig. 2.12 Proglottids of Moniezia benedeni.

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