WHAT IMPACT DOES IT HAVE?
Youngstock which have yet to develop immunity can be at serious risk from clinical disease (parasitic gastroenteritis/PGE). This is associated with large numbers of gutworms in the abomasum and intestines.
Ostertagiosis is associated with poor weight gain, poor body condition, scour and potentially death if very heavy worm burdens are present. There are two forms of ostertagiosis depending on the time of year; type 1, which is by far the more common, and type 2.
Type 1 ostertagiosis infection occurs when first grazing season calves become infected with overwintered larvae on pastures. Once these cattle develop adult worm burdens they begin to shed eggs onto pasture, contributing to pasture contamination. As these eggs develop to infective larvae, animals go through cycles of re-infection, rapidly amplifying pasture contamination. A similar pattern can occur in autumn-born beef calves turned out the following spring. It is possible to see disease as early as 4 to 6 weeks after turnout if pastures are heavily ontaminated from cattle grazing in previous years. The number of calves affected within the group is generally high but deaths are less common, especially if treatment is given early.
Type 2 ostertagiosis occurs in late winter or spring in cattle that were housed carrying high numbers of encysted Ostertagia larvae, ingested from the pasture in the autumn. Larval development becomes arrested within the host but when it resumes, large numbers of the parasite can mature at the same time, causing significant damage to the abomasal wall as they emerge. Usually only a small number of animals within a group are affected but death is not uncommon in those cases. Treating cattle at housing with a wormer that has efficacy against larval stages will prevent type 2 ostertagiosis.
Adult cattle, although resilient to the clinical disease associated with gutworm infection such as scour, have been found to carry worms numbering into the hundreds of thousands. These animals do suffer from sub-clinical disease, which leads to poor performance through decreased milk yield, poor appetite and reduced fertility.
Growing cattle take longer to reach target weight, which can increase age at first service and lead to overall reduced fertility throughout the animal’s life. A delay in reaching target weights for fattening animals will also eat into profits. Research has shown that even immune cows, when exposed to a significant gutworm challenge, have a reduced appetite. Many studies have proven that even immune cattle carry a worm burden; being immune means the risk of developing clinical disease is extremely small. In adult dairy cows, eating less as a result of infection can have a direct effect on milk yield and reduce lactation by as much as 2.6 litres per cow per day.1
This effect on appetite can be particularly significant for newly calved cows, where maximising feed intake is important to reduce the ‘energy gap’. If appetite is reduced at this critical time and food intake is compromised, the negative energy gap will increase, causing the cow to milk off her back and lose significant body condition.
A recent study demonstrated that cows treated around the time of calving produced an average of 1 litre more milk each day for the entire lactation than those that were untreated.2
Studies have also shown that worming dairy cows can improve fertility, with treated animals demonstrating a 13-day shorter calving to conception interval and a 20% higher conception rate at first service.3
