After ingestion the larvae develop in the lumen of an abomasal gland before they emerge from the gland to become mature on the mucosal surface.

The entire parasitic life cycle usually takes three weeks but under certain circumstances many of the ingested larvae become inhibited in development for periods of up to six months.

The presence of O.ostertagi in the abomasum in sufficient numbers gives rise to extensive pathological and biochemical changes and severe clinical signs. These changes are maximal about 18 days after infection but it 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 and to denature proteins. There is also a loss of bacteriostatic effect in the abomasum. Secondly, there is an enhanced permeability of the abomasal epithelium to macromolecules such as pepsinogen and plasma proteins. The results of these changes are a leakage of pepsinogen into the circulation leading to elevated plasma pepsinogen levels and the loss of plasma proteins into the gut lumen eventually leading to low blood protein levels. Clinically these consequences are reflected as inappetance, weight loss and diarrhoea and precise cause of the latter being unknown.

In lighter infections the main effects are sub-optimal weight gains.

CLINICAL SIGNS

Bovine ostertagiosis is known to occur in two clinical forms. In temperate climates with cold winters the seasonal occurrence of these is as follows.

The Type I disease is usually seen in calves grazed intensively during their first grazing season as the result of large numbers of larvae ingested 3-4 weeks previously; this normally occurs from mid-July onwards.

The 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 inhibited in their development.

The main clinical sign in both Type I and Type II disease is a profuse diarrhoea and in Type I, where calves are at grass, this is usually persistent, watery 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. The coats of affected animals in both syndromes are dull and the hind quarters heavily soiled with faeces.

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. Carcass quality may also be affected since there is a reduction in total body solids relative to total body water.

EPIDEMIOLOGY

Dairy Herds

From epidemiological studies the following important facts have emerged:

1. A considerable number of larvae can survive the winter on pasture and in soil. Sometimes the numbers are sufficient to precipitate Type I disease in calves 3-4 weeks after they are turned out to graze in the spring. However, this is unusual, and the role of the surviving larvae is rather to infect calves at a level which produces patent sub-clinical infection which ensures contamination of the pasture for the rest of the grazing season.

2. A high mortality of overwintered larvae on the pasture occurs in spring and only negligible numbers can usually be detected by June. This mortality combined with the dilution effect of the rapidly growing herbage renders most pastures, not grazed in the spring, safe for grazing after mid-summer.

However, despite the mortality of larvae on the pasture it now appears that some can survive in the soil for at least another year and on occasion appear to migrate on to the herbage. Whether this is a common occurrence and whether the larvae migrate or are transported by terrestrial populations of earthworms or beetles is not definitely known but the occurrence of this apparent reservoir of larvae in soil may be important in relation to certain systems of control based on grazing management.

3. The eggs deposited in the spring develop slowly to larvae; this rate of development becomes more rapid towards mid-summer as temperatures increase, and as a result, the majority of eggs deposited during April, May and June all reach the infective stage from mid-July onwards. If sufficient numbers of these larvae are ingested the Type I disease occurs any time from July until October. Development from egg to larvae slows during the autumn and it is doubtful if many of the eggs deposited after September ever develop to larvae.

4. As autumn progresses and temperatures fall an increasing proportion (up to 80%) of the larvae ingested do not mature but become inhibited. In late autumn, calves can therefore harbour many thousands of larvae but few developing forms or adults. These infections are generally asymptomatic until maturation takes place during winter and early spring and if large numbers of these larvae develop synchronously, Type II disease occurs. Where maturation is not synchronous clinical signs may not occur but the adult worm burdens which develop can contribute to pasture contamination in the spring.

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

Secondly, in dry summers the larvae are retained within the crusted faecal pat and cannot migrate on to the pasture until sufficient rainfall occurs to moisten the pat. If rainfall is delayed until late autumn many larvae liberated on to pasture will become inhibited following ingestion and so increase the chance of Type II disease. Indeed, epidemics of Type II ostertagiosis are typically preceded by dry summers.

Although primarily a disease of young dairy cattle, ostertagiosis can affect groups of older cattle, particularly if these have had no previous exposure to the parasite since there is no significant age immunity to infection. Also, acquired immunity in ostertagiosis is slow to develop and calves do not acquire a significant level of immunity until the end of their first grazing season. If they are then housed for thewinter and acquired immunity has waned by the following spring and yearlings turned out at that time are partially susceptible to reinfection and can contaminate the pasture with small numbers of eggs. However, immunity is rapidly reestablished and any clinical signs which occur are usually of a transient nature. During the second and third year of grazing a strong acquired immunity develops and adult stock in endemic areas are generally highly immune to reinfection. An exception to this rule occurs around the periparturient period when immunity wanes, particularly in heifers, and there are reports of clinical disease following calving. The reason is unknown but may be due to the development of larvae which were arrested in their development as a result of host immunity.

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 larvae occurs prior to the suckling calves ingesting significant quantities of grass. Consequently only low numbers of larvae 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 after they are weaned. The epidemiology is then similar to that seen in dairy calves. Whether Type I or Type II disease subsequently occurs depends on the grazing management of the calves following weaning.

In older animals the clinical signs and history are similar but laboratory diagnosis is more difficult. A useful technique to employ in such situations is to carry out a pasture larval count on the field on which the animals had been grazing. Where the level of infection is more than 1,000 larvae per kg of dried herbage the daily larval intake of grazing cows is in excess of 10,000 larvae. This level is probably sufficient to cause clinical disease in susceptible adult animals or to upset the normal functioning of the gastric mucosa in immune cows.

TREATMENT

Type I disease responds well to treatment at the standard dosage rates with any of the modem benzimidazoles (albendazole, fenbendazole or oxfendazole), the probenzimidazoles, levamisole, or ivermectin. 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. The field where the outbreak has originated may be grazed by sheep or rested until the following June.

For the successful treatment of Type II disease it is necessary to use drugs which are effective against inhibited larvae as well as developing larvae and adult stages. Only the modem benzimidazoles listed above or ivermectin are useful in the treatment of Type II disease when used at standard dosage levels although the probenzimidazoles are also effective at higher dose rates.

In young animals this decision is based on:

• The clinical signs of inappetance, weight loss and diarrhoea

• The season. For example, Type I occurs from July until September and Type II from March to May

• The grazing history. In Type I disease, the calves have usually been set-stocked in one area for several months, in contrast, Type II disease often has a typical history of calves being grazed on a field from spring to mid-summer, before being moved and then brought back to the original field in the autumn. Affected farms usually also have a history of ostertagiosis in previous years.

• Faecal egg counts. In Type I disease these can be more than 1,000 eggs per gram and are a useful aid to diagnosis; in Type II counts are highly variable, may even be negative and are of limited value.

• Plasma pepsinogen levels. In clinically affected animals up to two years old these are usually raised. 

• Post-mortem examination

This may be done by grazing calves on new grass leys although it is doubtful if this should be recommended for replacement dairy heifers, as it would result in a pool of susceptible adult animals. A better policy is to permit 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:

First, by using anthelmintics to limit pasture contamination with eggs during periods when the climate is optimal for development of the free-living larval stages i.e. spring and summer.

Alternatively by resting pasture or grazing it with another host, such as sheep, which are not susceptible to O.ostertagi, until most of the existing larvae on the pasture have died out.

Sometimes a combination of these methods is employed.

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 turnout 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, three and seven weeks later are used, whereas calves turned out in April require three treatments. With some anthelmintics which have a persistent effect and prevent infection for several weeks after administration, various regimens are recommended. For example ivermectin at 3, 8 and 13 weeks post turnout or doramectin at turnout and 8 weeks later.

Several rumen boluses have been developed which release in a sustained fashion or as programmed single ‘pulse* doses. When these boluses are administered to calves just prior to turn-out they prevent the development of infections acquired from overwintered larvae and so prevents the deposition of eggs during the spring. This in turn prevents the development of high levels of pasture contamination with larvae which are responsible for disease.

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 is usually referred to as the ‘dose and move" system and is based on the knowledge that the annual increase of larvae 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 larvae which 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.

Alternate grazing of cattle and sheep

This system ideally utilises a three year rotation of cattle, sheep and crops. Since the effective life-span of most O.ostertagi larvae is under one year and cross infection between cattle and sheep in temperate areas is largely limited to Trichostrongylus axei, 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 and less so for marginal or upland areas, but in these areas good control has been reported using an annual rotation of beef cattle and sheep.