PGE in Cattle

Introduction

Parasitic gastroenteritis is a significant cost to the UK cattle sector primarily through reduced growth rates. It usually affects first and second year grazers but can cause disease in any age if immunity has not developed. Clinical signs are weight loss and green diarrhoea in summer or severe, watery diarrhoea in winter. Disease can be prevented through reducing exposure to high risk pasture and by effective treatment with anthelmintics. 

Cause

The two most significant roundworm types causing parasitic gastroenteritis (PGE) in cattle are Ostertagia ostertagi and Cooperia species, both of which only infect cattle. Larvae are ingested from forage and initially enter digestive glands of either the abomasum (stomach; Ostertagia), or small intestine (Cooperia) where they develop over a period of around 18-21 days before re-emerging and maturing into adult worms, producing eggs from three weeks post-infection. Over the grazing season accumulation of adult worm burdens can lead to large numbers of eggs being shed in faeces onto pastures. These hatch and develop to their infective larval stages in 1-6 weeks depending on the environment, with mild and moist conditions being the most favourable. They can then remain viable on pastures for the remainder of the grazing season and the subsequent winter. Typically, this pattern results in a animals initially becoming infected through ingestion of overwintered larvae early in the season, with subsequent increasing pasture burdens as the season progresses, peaking in late-summer coinciding with peak risk period for PGE, or type-1 ostertagiosis, in at-risk animals.

Cooperia is generally only an issue for youngstock in their first full grazing season. These animals will develop immunity over the course of this season under normal conditions, whilst immunity against Ostertagia may take two grazing seasons to fully develop. Healthy, adult cattle generally have good immunity to both parasites, provided they had adequate exposure as youngstock and in each subsequent grazing season as adults.

Importantly, both of these roundworms have the ability to arrest their development (termed hypobiosis) when in the abomasal or intestinal wall. This may occur when animals continue to acquire infection into the autumn. These arrested larval stages then undergo a triggered mass emergence in the late-winter or early-spring. In large numbers this can cause extensive gut damage and what is commonly termed “type-2” disease.

 

 

Figure 1. Faecal worm egg counts can indicate the presence of adult worms in individuals or groups

Welfare and Economics

Weight loss and lack of appetite account for most of the production and economic effects even in the absence of diarrhoea because damage to the abomasum releases chemicals which suppress feeding. Animals with ostertagiosis have significant growth suppression, meaning growth rate monitoring is a sensitive early marker for problems. 

In severe clinical disease there is a marked loss of body condition (up to 10% body weight). Recovery takes a long time and may extend the time to slaughter or breeding weights by up to three months.

Severe diarrhoea caused by PGE in young animals and adults can be lethal, and may occur alongside other pathogens. Type-2 disease in winter and early spring may also cause sudden death, sometimes before diarrhoea is even observed.

 

 Figure 2. Severe diarrhoea caused by Type-2 Ostertagiosis in early spring

Clinical Signs and diagnosis

Clinical type-1 ostertagiosis in the grazing season causes a loss of appetite with sudden and profuse green diarrhoea. It usually affects most animals in the group at a similar time and is most common from August onwards. Calves and young stock are most at risk, particularly autumn and winter-born weaned calves entering their first grazing season and spring-born beef suckler calves entering their second grazing season.

 

 Figure 3. Type 1 Ostertagiosis causes loose green faeces usually from late summer

Type-2 disease usually occurs from late winter to earl;y spring and causes a severe, very sudden and profuse, watery diarrhoea. Sudden death can occur. Disease from Cooperia alone is usually milder but in combination with Ostertagia can cause more severe disease than either parasite alone.

 

Figure 4. Cooperia is seen in first year grazers and is more serious when present in combination with Ostertagia.

Aside from time of year and clinical signs, faecal worm egg counts can be used to confirm the presence of eggs from both Cooperia and Ostertagia through the grazing season. This gives an indication as to the level of pasture contamination and egg shedding, either in individuals or groups of animals through pooled faecal samples. However, egg counts do not indicate the number of parasites present in an individual and cannot be used to diagnose type-2 disease.

Diagnosis of acute ostertagiosis can be aided by blood sampling to measure levels of pepsinogen, an enzyme released by damaged abomasal glands into the blood. This test can also help to confirm type-2 disease in the live animal which occurs before the parasites are mature enough to lay eggs. 

An antibody test is also available for detecting Ostertagia antibodies in blood and milk samples.

Prevention and control

Pasture management can have a significant role in avoiding PGE and significantly reducing the need for anthelmintics. Grazing the most vulnerable groups on the lowest risk pastures reduces larvae intakes and overall risk from early in the season.  

 

 Table 1. Pasture Risk for PGE

Where strategic dosing is not being practiced (see treatment), rotational grazing rather than set stocking prevents build up of pasture larval burdens by reducing re-infection. Low stocking rates for youngstock and grazing practices to leave higher forage residuals (sward height or density) also reduce exposure to parasites usually present closer to the ground. Follow-on grazing practices are also useful in this context, with pastures initially grazed by youngstock followed by immune adults which then graze the lower residual grass height where infective larvae are likely to have accumulated. This also has nutritional benefits as young cattle take the nutrient rich top of the plants and older cattle eat the fibrous stems.

Co-grazing or mixed grazing, where sheep, goats or horses share or rotate through the grassland allows one species to clean up the parasite larvae from the other species. This reduces PGE risk but does not reduce the risk of liver fluke.

 

 Figure 6. Co-grazing cattle and sheep reduces the roundworm risk but not the liver fluke risk

As with all diseases, healthy, well fed animals have greater resilience to the effects of roundworms on the gut. Production and clinical impacts are greater in animals lacking in energy or other nutrients, or those suffering from other concurrent diseases.

Treatment

Ostertagia and Cooperia can be treated with group 1-BZ, 2-LV and 3-ML anthelmintics (white, yellow and clear drenches). These are available in a range of formulations and presentations with varying lengths of activity from zero days up to several weeks in the case of pulse-release boluses and long-acting injectables.

It should be noted that group 3-ML resistant Cooperia have been detected in the UK. Resistance of Ostertagia to this class is reported but not considered widespread currently.

The COWS group currently advise one of two treatment approaches to control PGE in at-risk groups of cattle over the grazing period:

1. With a strategic approach, anthelmintics are used at fixed times to minimise egg shedding through the early part of the grazing season to prevent build up of infective larvae later in the season. Useful products for this approach include long acting or pulse release boluses given prior to or within 3 weeks of turnout. Alternatively, long acting injections, or application of group 3-ML products at set intervals may be applied from three and eight weeks after turnout depending upon the product used. To be effective, this approach requires set-stocking in the early part of the season, although animals can be moved over to safe pastures such as hay or silage aftermath later in the season as these become available. Minimal handling is required with this approach, nor is extensive diagnostic testing, although performance testing through weight gain and worm egg counts (including post-treatment efficacy testing) are a useful way to check your parasite control plan is working as expected. This is important, as repeated and/or prolonged dosing with anthelmintics increases selection for drug resistant parasites. Furthermore, where lungworm infection is present on farms, strategic dosing may not allow first season animals to develop a fully protective immunity and should therefore be considered a risk in animals which are strategically dosed the previous year. Consequently, these control programmes should be planned carefully with veterinary input. 
2. The alternative approach is a therapeutic strategy where anthelmintics are used only when growth rate monitoring and / or faecal egg counts identify a rising problem. It is not appropriate to wait until clinical signs of parasitism appear before treating e.g. loose faeces. At this stage there has already been a negative impact on appetites and growth. Therapeutic dosing with anthelmintics work well with lower risk system. Pasture rotation, strip grazing and extensive grazing can all help reduce exposure and subsequent use of anthelmintics (and selection for drug resistance) considerably. However, this approach is much more labour intensive and requires detailed, consistent and accurate recording to be successful.

To prevent type-2 disease, treatment at housing can be given. Risk assessments based on grazing history and herd health plans can help identify where there is a need to do this. It is essential anthelmintics used for this purpose are licenced as effective against arrested stage larvae. This includes most group 3-MLs and some group 1-BZ products.

In general adult cattle over two years of age do not require anthelmintic treatment, although dairy heifers may benefit from treatment during their first lactation following testing for Ostertagia antibodies by ELISA.

Spring born suckler calves do not usually require treatment in their first grazing season. Their limited grass intake early in the season combined with co-grazing with dams which shed very few eggs on to pastures means their exposure to worms is low and gradual. These animals may still be at risk of PGE in their second grazing season, however.

 

Figure 5. Spring born suckler calves do not usually require anthelmintic treatment in the grazing season. Image credit: Lowertown Farm

Artificially reared calves and spring born suckler calves are at high risk of PGE in their first grazing season because they typically consume large quantities of grass from early in the season, and as a group will shed larger numbers of eggs on to pastures before immunity develops. 

Treatment requirements for second year grazers should be risk assessed with a vet or medicines advisor and monitored through weighing and / or FECs.