All commercial poultry, at some time in their life, will become infected with coccidia. That’s some 8,882,000,000 coccidia infected chickens each year in the USA alone not counting layers, breeders and turkeys. Coccidia are protozoan (Eimeria spp) parasites that infect the intestine or ceca of poultry. The level and species of coccidia will vary with anticoccidial programs, management, and bird age.
Several factors enable coccidia to spread rapidly and infect large numbers of confinement reared birds. All of the Eimeria spp infecting poultry have a rapid, approximately 7-day life cycle and a high reproductive capacity. One Eimeria oocyst (external infective stage) can produce 10’s of thousands of coccidial oocysts. In a poultry house where millions of oocysts are present it is easy to understand how quickly a clinical parasitic problem can occur. An oocyst is highly resilient to environmental conditions, including normal disinfectants that have no deleterious effect. Removing used litter, litter amendments, and fire flame treatment of floors can reduce oocyst level. However, due to a high reproductive capacity, the house will become contaminated again before the end of the bird’s production period. The differences in timing and severity of coccidiosis in built-up litter and clean-out of houses will be discussed later.
Another important characteristic of Eimeria is very limited cross species immunogenic protection. An example is immunity developed against E. acervulina will not provide any protection against E. maxima or E. tenella, two of the major species that infect chickens.
Prevalence of species
Polymerase Chain Reaction (PCR) technology uses the amplification of species-specific DNA sequences to determine the species of Eimeria present in poultry litter. Jenkins, USDA, ARS, using PCR technology examined over 100 field litter samples and found E. acervulina and E. maxima in all samples. At least 50 percent of the farms had E. praecox. The occurrence of the other species dropped off from there, with E. tenella (~ 5-10 percent) occasionally seen, and E. brunetti and E. mitis infrequently (< 5 percent) seen. This technology is being applied to tracking not only species but strains of Eimeria on poultry farms. The traditional method of using field necropsy to diagnose coccidiosis has shown a similar prevalence of species. Fitz-Coy, using necropsy and microscopic examination, found the average prevalence of E. acervulina, E. maxima and E. tenella from 3 complexes to be 26 percent, 44 percent and 6 percent, respectively.
Ingestion of sufficient numbers of coccidial oocysts that produce clinical signs of the disease is referred to as coccidiosis. Intestinal tissue damage occurs during the growth of the parasite within the cells. The amount of damage is related to the species, amount and frequency of exposure. Coccidiosis, even mild cases, has had a negative impact on production with losses in feed conversion, weight gain, uniformity, pigmentation, and increased mortality. Teeter examined the effects of coccidiosis along several points in the growth of broilers using a calorimetric chamber. He found the detrimental effects of coccidiosis to be more pronounced as birds mature, especially during the major growth period which occurs in the later phase of the grow-out. Because coccidiosis can not be totally avoided, it is better to have a controlled level of coccidiosis early, so the birds can develop an adequate immunity and to allow compensatory performance gain to reach its fullest potential. With that said, it is also important to not overly challenge birds during the first weeks of life. Some of the high yield breeds are easily set back if extreme stresses are encountered during the brooder phase. Using anticoccidial vaccines improperly (example; overdosing) or keeping birds confined in the brooder area too long can greatly increase the challenge to young chicks. Proper vaccine application, anticoccidial drug use, and proper farm management can prevent early damage.
With all vaccines there is a small oocyst shedding peak around Day 7 followed by a major peak at Days 18 to 24 and then a steady downward progression. Because coccidia are multiplying within the birds, some degree of intestinal damage will occur especially during the peak period at Days 18-24. Clostridium perfringens proliferates where there is intestinal damage and allows for Necrotic Enteritis to develop. Feed additive antibiotic growth promoters (AGPs) have traditionally been used to control Necrotic Enteritis. Due to many factors the use of APGs has decreased. Various natural products have been examined to replace the APGs. Duffy and Mathis have demonstrated that feed additive functional carbohydrates such as mannanoligosaccharides alone and in combination with botanical extracts may improve broiler performance and reduce Necrotic Enteritis levels in coccidial vaccinated birds.
Coccidiosis control programs rely on immunity
Eimeria are very immunogenic. With each cycle of coccidia in the host, immunological protection increases. The development of self-limiting immunity, which eventually protects a flock, is a very critical objective for a coccidiosis control program, whether vaccination or an anticoccidial drug program. Today poultry coccidiosis is controlled by the use of prophylactic feeding of anticoccidial drugs or vaccinating with live coccidial vaccines. Both types of programs rely on immunity development.
Anticoccidial drugs have been successfully used for over 50 years. Anticoccidials are broadly divided into synthetic (or chemical) and ionophores. Chemical anticoccidials generally have a broad spectrum of activity, high efficacy, a potential for rapid resistance development, and generally allow only limited immunity development. The ionophores have a broad spectrum of anticoccidial activity. The use of chemical and ionophore anticoccidials in shuttle programs and rotating drugs with each production cycle have extended the life of many of these drugs. A chemical that has continued to be effective is Nicarbazin (developed around 1955). Combinations of Nicarbazin and ionophores provide a synergistic anticoccidial advantage and have been widely used. Bafundo ascertained that there is a concern for more rapid resistance development to both drugs by excessively using this combination.
Many of these drugs are still successfully used. However, numerous reports have shown a reduced sensitivity to some degree to all in-feed anticoccidial drugs used in the poultry industry. It was hoped that the ionophores would be spared this fate. However, through very extensive usage, there is not the same level of control as when first introduced. There is a level of sensitivity of an isolate that has never been exposed to any drugs (laboratory strain) compared to a 2008 commercial field isolate. Clearly, effectiveness of control has diminished. Does this mean that these ionophores are no longer useful? No, even with decreased sensitivity they still exert some degree of effectiveness. The parasites that do survive and develop stimulate the immunological protection of the bird to coccidia. This drug efficacy coupled with immunity development provides a program that continues to be extremely utilized and successful.
Newman and Mathis demonstrated, using oocyst shedding patterns, that levels of coccidiosis were higher and later on in an anticoccidial ionophore program when birds were reared in clean litter houses compared to heavily used litter houses or vaccinated birds. The clean litter did not supply enough oocysts for adequate early oocyst cycling and proper immunity development. Used litter and/or vaccination did provide oocysts in sufficient levels. The delayed onset of an adequate immunity can result in coccidiosis related losses during the major growth and feed consumption period of production, immediately prior to slaughter.
Due to the increasing demand for drug-free birds and concerns of resistance issues with anticoccidials, the use of coccidiosis vaccination has grown tremendously in the last few years. The only method to produce a truly drug-free bird is through the use of vaccination. Vaccination programs use live oocysts which are administered using a hatchery spray or gel, a gel puck placed into hatchery box, or in-ovo dosing. These methods provide a prescribed amount of oocysts at an early age enabling immunity development to progress rapidly but still at a desired rate. A significant amount of immunological protection develops by 14 days of age, allowing birds to withstand a substantial challenge by 21 to 28 days of age. Coccidial vaccines are of two types; non-attenuated (not altered) and attenuated. All vaccines contain at least E. acervulina, E. maxima, and E. tenella. Some contain E. mivati, E. necatrix, E. brunetti, and or E. mitis, and possibly more than one strain of E. maxima. Non-attenuated vaccines contain strains that are generally milder than field strains while maintaining their reproductive and immune stimulating characteristics.
Attenuated vaccine strains have been selected for reduced pathogenicity by shorting the life cycle. This is accomplished by collecting the first oocysts passed (13-27 hours earlier). This selection has produced stable strains that have one less asexual development stage or just have faster development. Passage of E. tenella through eggs also reduces pathogenicity. This reduced pathogenicity is the major selling point for the attenuated vaccines. The down side of attenuated vaccines is that the strains have less reproductive and immunological capacity compared to field strains. Thus proper administration is even more critical than with a non-attenuated vaccine.
Even though coccidiosis always occurs it can be controlled. Using anticoccidial sensitivity tests to determine level of resistance will provide information on which drug has the best potential for usefulness. Vaccination programs can equal effectiveness and performance to a drug program. Key factors of vaccination are application, vaccine storage, and farm management. Using the most effective drug program, including utilizing immunity and vaccination programs will provide successful coccidiosis control.