If youngstock at grass look thin or have scour, it is easy to assume worms are at fault.
However, on an increasing number of occasions, coccidiosis is the cause.
Coccidiosis is caused by a protozoa parasite infection. The lifecycle involves damage to the gut wall, as the various stages develop and reproduce, eventually resulting in shedding of “oocysyts”, the highly resistant eggs, in massive quantities in faeces. These oocysts are the source of new infection, and can survive many months in the correct conditions, and even over-winter on pasture.
There are three main pathogenic species of coccidiosis (Eimeria) in cattle: E zuernii, E bovis and E alabamensis, each with slightly different life cycles.
Generally, the lifecycle is around 3 weeks (slight shorter for E alabamensis) which means that calves are most likely to show disease from 3-4 weeks onwards, but disease occurs commonly up to yearling stage, and occasionally in older cattle.
Classic coccidiosis symptoms include weight loss with dark diarrhoea, straining and streaks of blood, typically in calves 6-12 weeks of age. Whilst this might be the “classic” form, there is a very wide range of degrees of disease. It is fair to say that all farms will have some coccidiosis – the protozoa is found virtually everywhere.
In around half of farms, the infection is self-limiting, with low doses of infection stimulating immunity and calves becoming immune before disease develops: the calf wins. In the other half of farms, the parasite wins. In most cases, this means the calves fail to grow as well, they lose their appetite, and some might scour. Although they eventually recover, large economic losses will occur.
In the minority of cases, the scour is severe, the calves constantly strain, and blood is passed in the faeces. In these cases, the calves can die without treatment as the parasite definitely has the upper hand, and the calves no longer have the ability to fight off the infection and gain immunity.
So, coccidiosis immunity, infection and disease is always a balance, with the “classic” signs being the tip of the ice-berg representing the scenario when the parasite has clearly won.
Fig 1: Balance between infection and immunity:
Coccidiosis at pasture:
Usually, E alabamensis is involved as this can over-winter. Relatively small numbers of over-wintered oocysts can be multiplied up in infected calves to cause heavy pasture contamination, and disease which can be confused with gut worms.
Perhaps the most common scenario occurs with spring block calving herds, where large mobs of calves are grazing, particularly if calves are turned onto the same pasture as the previous year.
Sometimes a trigger factor seems to be involved, such as a change in weather, or reduction of concentrate feed. The first symptom is calf growth rates slowing, followed by progressively more calves developing diarrhoea.
A wide gap can soon develop between the biggest and smallest calves in the group, with more severely affected calves falling behind. This can be very significant for block-calving herds in particular, where growth rates must be maintained so heifers can be served to calve in the block.
As sheep farmers will confirm, differentiating coccidiosis from worm infestation is not always straight forward. Laboratory diagnosis using faeces samples is the most usual method to use, via the vet.
Detecting coccidiosis eggs in faeces does not always confirm the diagnosis, as some coccidial species do not cause disease, so always involve your vet in interpretation of results too. There other potential causes of ill-thrift and scour which your vet can help rule out.
Once a diagnosis has been established, treat the affected calves, but just importantly, plan ahead for future batches or years, as prevention is always better than cure. It is important to have in mind that once the calves have started scouring, anticoccidial therapy has a limited effect on avoiding the consequences of the disease.
The setback suffered is virtually impossible to compensate for later.
A good preventive strategy will keep the balance of infection in the calves’ favour, allowing immunity to develop. Reducing environmental build up of oocytes and keeping calves otherwise fit and healthy are the two cornerstones of prevention.
Preventive strategies include:
1: Reducing stress – e.g. avoid sudden diet changes and keep well fed to avoid nutritional stress.
2: Reduce infection risk – e.g. keep feed and water troughs clean, and raised to avoid dung contamination. Rotate pastures – avoid set-stocking. Turn out onto clean pasture from previous year. Keep stocking density low. Maintain youngstock in even age-groups.
3: Strategic use of Deccox in feed. This requires a veterinary prescription, and is added in either a preventive dose or a higher treatment dose. Accurate daily feed intakes must be known, so the inclusion rate used can be correctly calculated by your vet: under-dosing is common, especially when feed is withdrawn to encourage grazing. There is no residual activity, so once feeding stops, protection stops, until immunity has developed.
4: Strategic oral dosing with a coccidiostat. Vecoxan and Baycox Bovis are the two licensed products. Neither have residual activity, so targeted dosing is necessary, timed to coincide with likely infection – usually approximately 14 days after exposure. Once sufficient exposure has occurred, immunity develops. Vecoxan does not treat Eimeria alabamensis, which is the species most often present at pasture.
- Be vigilant for the possibility of coccidiosis in calves at pasture: it is not only a disease of housed calves.
- Coccidiosis parasites are found everywhere: problems occur only when the balance of challenge and immunity is upset, but classic coccidiosis scour symptoms should be seen as the tip of the ice-berg.
- Develop a control strategy using your vet and your agricultural merchant, so that clinical disease does not occur, and growth rates are maintained. If treatment is required, the control strategy has failed.
Written by Owen Atkinson