Diagnosis, Treatment and Control: Dealing with Coccidiosis in Cattle

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Diagnosis, treatment and control: dealing with coccidiosis in cattle

Author : Adam Martin

Categories : Vets

Date : January 17, 2011

Adam Martin discusses the causes of bovine coccidiosis and the financial costs of an outbreak as well as providing advice on preventive measures

THERE are two genera of coccidia associated with disease in farmed mammals – Eimeria and Isospora.

Generally, the parasites are species specific, meaning it is unlikely the coccidia that cause disease in lambs will cause disease in calves. However, there are a few incidences when the absolute nature of species specificity has been questioned.

Coccidia in the genus Isospora are associated with disease in piglets, while Eimeria species have been associated with disease in poultry, rabbit and ruminant production. More than 20 species have been found in cattle and the vast majority are regarded as harmless. However, E bovis and E zuernii are known to be major causes of enteritis and disease in calves.

E alabamensis is described as an infrequent cause of coccidiosis in cattle at pasture, although the author is aware of a significant outbreak in housed suckler cattle. In addition, other members of the genera have been associated with clinical disease.

Financial cost

While there is a consensus that the losses associated with bovine coccidiosis are huge, there is

1 / 5 sparse information on how much the disease is costing the industry. Costs include treatment and mortality, and reduced growth rates, but also subtler costs, such as longer term reduced feed conversion efficiency and increased opportunity costs per kilo of beef sold because calves take longer to reach service/ slaughter weights. It has been postulated that animals that have suffered severe coccidiosis are unlikely ever to be profitable (Fox, 1985).

It is likely there are hidden costs associated with reduced production and increased susceptibility to disease later in life. It is also thought the costs associated with sub-clinical disease are greater than those associated with clinical disease. However, by definition this disease is subclinical and therefore extremely difficult to measure and quantify in terms of actual costs. In 1980 the worldwide costs associated with bovine coccidiosis were believed to be US$700m (Fitzgerald, 1980). Accounting for an annual inflation rate of four per cent across 30 years, the estimated cost would be more than US$2.2b.

Eimeria are ubiquitous unicellular apicomplexan parasites. The life cycle of all Eimeria species is similar. Infection occurs by the faeco-oral route; once the infective sporulated oocysts have been ingested, the host’s digestive enzymes digest its protective coat and activate the sporozoites. The sporozoites infect the epithelial cells of the lower duodenum and jejunum. On entering these cells, the parasites undergo a period of asexual fission – called merogony.

The number of merozoites in the epithelial cell increase until the cell ruptures and the merozoites are released into the intestinal lumen. This process is repeated twice before the next phase of development begins – gametogony.

Gametogony occurs in the cells of the distal intestinal tract, typically the lower ileum, colon or caecum. This sexual reproductive process involves the fusion of macrogametes and flagellated microgametes to produce a zygote. An impermeable membrane forges around the zygote, to form an oocyst. The oocysts are then shed from host cells into the lumen of the gastrointestinal tract and are passed in the faeces.

Once shed from host cells, the parasite undergoes a maturation process known as sporogony. During sporogony, the immature (or unsporulated) oocyst, incapable of infecting animals, develops into the infective form – a sporulated oocyst, which has a life cycle of two to three weeks, dependent on the species involved and environmental ambient temperature. An exception to this is E alabamensis, which has a life cycle of six days. Patency following Eimeria species infection will last for a number of days, but it has been reported to last as long as two weeks.

Diagnosis

Coccidiosis diagnosis is generally by examining faecal samples after flotation for oocysts. The process is made more difficult by the large number of coccidia species present. Differentiation of species is important as many coccidia are not considered pathogenic. It can be performed under

2 / 5 microscopy; however, the differences between the species are small and require a trained eye.

Largely speaking, a total oocyst count in eggs per gram of faeces is reported and used as the basis for diagnosis. This technique has three main problems. Firstly, if species identification has not been performed, are the coccidia present pathogenic or not? Secondly, there is poor agreement on what the diagnostic cut-off value is for disease-causing levels of infection. Thirdly, signs of disease do not always correlate with levels of oocyst excretion.

Normally, the disease’s clinical signs – such as reduced voluntary feed intake and diarrhoea – will begin before the animal starts shedding large numbers of oocysts. This can be problematic in acute diarrhoea outbreaks, as the pathogen cannot always be found. However, this makes sense as diarrhoea, and particularly bloody diarrhoea, is the sign we often associate with coccidiosis. This occurs because of the damage caused to the cells of the gastrointestinal tract. The cell damage begins during merogony, as epithelial cells rupture, destroying the integrity of the gastrointestinal tract and reducing its surface area, resulting in less efficient food digestion and fluid absorption.

Diarrhoea is often seen from day four after infection while the peak of oocyst excretion occurs 10 to 12 days after the ingestion of the sporulated oocyst. Conversely, animals that were infected more than two weeks before sampling will often have relatively low levels of oocyst excretion despite having had severe and prolonged diarrhoea. The reason is that while the immune system has managed to overcome the infection, the intestines have not had sufficient time to regenerate to stop the diarrhoea. Unfortunately, a number of animals never seem to overcome the infection and remain chronic “poor doers”.

Coccidiosis is described as a self-limiting disease. Following a primary infection, protective immunity is usually established meaning future infections are generally disease free. This immunity does not prevent the shedding of oocysts, although when it occurs the numbers are considerably lower than in immune-naive animals.

If an effective level of immunity is to be achieved, primary exposure needs to be great enough to stimulate an effective antigenic challenge. Protective immunity is usually specific to a particular coccidial species and cross immunity among Eimeria species is rare. The ubiquitous distribution of coccidia means animals are constantly exposed to low level infection resulting in boosted immunity. The protective immunity received via natural challenge is mostly cellular immunity; however, maternally derived antibodies are important in preventing disease in young animals.

The passive immunity acquired from colostrum is important considering oocyst excretion from the dam increases around calving. The increase is the presumed result of immunosuppression related to calving, although the mechanism has yet to be fully elucidated.

Infection level is closely related to clinical disease – even immune animals can contract clinical disease if subjected to high enough infective doses. Therefore, it is vital calves are born and

3 / 5 housed in a clean environment.

Prevention

To this end, snatch calving can be beneficial. Housing calves in older buildings has been shown to increase the risk of disease compared to housing them in new calf buildings. It is likely that newer calf buildings allow for adequate cleaning and disinfection to be performed without too much effort.

Interestingly, herds with spread calving patterns also have higher disease levels than those with concentrated calving patterns. This is probably because those with concentrated calving patterns can prevent a build-up of pathogens by operating all in, all out systems.

Irrespective of the calving pattern, calf pens should be regularly cleaned and disinfected. The majority of commercially available disinfectants are ineffective against coccidial cysts due to their protective cell wall. It is important the disinfectants used can destroy coccidial oocysts and that they are used at the appropriate concentrations and contact times to do so. Cresolbased disinfectants are capable of destroying oocysts.

It is unsurprising that basic calf husbandry is important in both preventing disease and controlling it. Calves can shed millions of oocysts per day, so isolating calves that have begun to scour is a simple, but critically important, control measure once disease has appeared.

Otherwise the calf’s environment should not place it under any stress. Animals should be warm and free from draughts, but not hot. Social stresses should not be ignored – overcrowding increases the incidence of coccidiosis. It is also known that providing adequate nutrition helps prevent disease.

Interestingly, there has been little research into the effects of concurrent disease on the incidence of coccidiosis, but it seems intuitive that concurrent disease is likely to predispose the calves to coccidiosis infection. However, there is little relationship between coccidiosis and either cryptosporidiosis or giardiasis.

Several pharmaceutical products are available to use therapeutically, metaphylactically and prophylactically against coccidiosis. These products are generally coccidiostatic drugs used strategically at risk times in an animal’s life to prevent excessive challenge. It is important to note that therapy may be disappointing. This is because the majority of the damage has been caused by the time the disease has peaked. In fact, the goal of therapy should be to limit the excretion of oocysts into the environment.

Generic fluid therapy is perhaps the most useful therapy and applicable to all cases of calf diarrhoea. In the case of coccidiosis, treatment is better than cure and prophylactic actions should be taken to prevent clinical coccidiosis occurring. However, before resorting to pharmaceutical

4 / 5 methods of control, an assessment of calf housing and husbandry procedures should be made to ensure significant management deficiencies do not lie in the calf rearing system.

References

Fitzgerald P R, (1980). The economic impact of coccidiosis in domestic animals, Adv Vet Sci Comp Med 24: 121-143. Fox J E, (1985). Coccidiosis in cattle, Mod Vet Pract 66: 113-116.

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