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Technically Speaking

Combating Coccidiosis in Broiler Breeders

Charles L. Hofacre, DVM, MAM, PhD The University of Georgia

How many times have you heard someone in the poultry industry say, “We’ve been doing it this way for 25 years”?

Even if some things have remained the same, 25 years has meant a lot of change in the broiler industry, especially regarding genetic progress. Consider broilers in 1976. It took about 65 days to reach 4.4 lbs (2 kg) body weight. Today, broilers reach that weight in only 35 days (Figure 1). Broilers today are also more feed efficient: 1.70 now vs. 2.50 in 1976 (Figure 2).

Improvements in efficiency due to genetic progress have a price, however. It’s more difficult to manage breeders now because they grow so fast and are so feed-efficient. If anything limits their early growth, such as poor chick quality, poor brooding conditions or disease, the result is a flock with poor body weight and uniformity of frame size.

Impact on growth

Coccidiosis is one disease that can greatly affect growth at its most critical stage for frame size development.

In today’s highly competitive broiler industry, we strive to capitalize our pullets by feeding the least amount necessary, which places emphasis on frame size. The majority of skeletal growth in broiler breeders occurs in the first 5 to 6 weeks of life.1 If birds experience either clinical or subclinical coccidiosis during this period, their frame size — and thus flock uniformity — will be greatly affected (see photo).

In a flock with poor uniformity, hens that are smaller become timid and fall even farther behind. It is easy for us to see the impact on egg production, but we often don’t realize that roosters in the same house with pullets are also experiencing coccidiosis.

Coccidiosis can become an even greater problem in male chicks since they usually are smaller than females; if they don’t surpass female weight by 50% by 5 weeks of age, we risk having poor hatchability for the life of the flock.

The biology of coccidia

In general, the life cycle of all coccidia are similar. The bird eats a sporulated oocyst, then sporozoites are released by the grinding activity of the gizzard and penetrate the cells of the intestinal mucosa. This begins the asexual cycle of development called schizogony. Next comes the sexual phase, resulting in the release of oocysts in the bird’s feces. The entire process takes approximately 7 days.2 By day 14, after initial infection, the production of oocysts usually is diminishing and ceases around 18 to 20 days. Most damage to the intestine occurs early in the parasite’s life cycle, during schizogony.

Eimeria species

The Eimeria species that affect chickens are E. acervulina, E. maxima, E. tenella and E. necatrix as well as E. brunetti, E. praecox and E. mivati. Those of particular importance to breeder pullets and roosters are E. acervulina, E. maxima, E. tenella and E. necatrix.

The two species that cause intestinal hemorrhage and pullet death are E. tenella and E. necatrix. E. tenella is also the species that causes bloody droppings, along with mortality; it is often the easiest for flock supervisors to recognize due to the characteristic bloodfilled ceca of dead pullets.

E. necatrix usually does not cause many problems until after 6 weeks of age because it does not compete as well against other coccidia. This means that mortality caused by E. necatrix usually begins around 7 to 9 weeks of age; necropsy signs of white/red or white/black (salt and pepper) are seen in the mid intestine. It is also important to know that E. necatrix is the least immunogenic of the chicken coccidia. This will become more important when we discuss control and immune response.

Perhaps the more economically important coccidia species the world over for pullet and rooster frame size and body uniformity are those that do not cause death but have an impact on the bird’s ability to absorb nutrients from feed. The most commonly recognized are E. acervulina and E. maxima. The signs of these two species are not as obvious, so their effects are often overlooked until it is too late. Therefore, it is important to necropsy a few birds during the first 3 to 4 weeks of a pullet flock’s life to determine levels of these two types of coccidia. E. acervulina will cause white stripes in the duodenum, while E. maxima may cause a ballooning of the intestine with orange mucus in the lumen.2

There are three species of coccidia that are difficult to identify in pullets when performing a routine necropsy. These are E. mitis, E. praecox, and E. brunetti.

E. mitis is normally found in the lower small intestine and produces rather indistinct lesions. E. praecox also does not have prominent lesions and is also often missed at necropsy. Most of the infection by E. praecox is in the duodenum and may result in pinpoint hemorrhages. E. brunetti can also affect the lower small intestine, usually around the yolk stalk. It does not produce any recognizable gross lesions. All three of these species are generally only diagnosed by microscopy.2

Coccidiosis control

Control of coccidiosis in breeder pullets and roosters can be summarized in just one word: immunity. It does not matter if we are using a drug or vaccine: in both instances, the goal is to allow hens to develop life-long, lasting immunity to coccidia by 12 weeks of age.3 To accomplish this goal, we must look for ways to maximize the immune response without causing a negative impact on the birds’ frame size and uniformity.

Factors that affect the development of immunity are management conditions such as litter moisture, partial vs. full-house brooding and a feed restriction regimen (skip-a-day feeding). We also need to be aware of other disease or live vaccine challenges, particularly those that directly impact the immune response, such as infectious bursal disease virus, Marek’s disease, chicken anemia virus and exposure to mycotoxins in feed.

Chemotherapy.

A variety of drugs will allow enough coccidia to complete their life cycle for development of an adequate immune response in the pullet/ rooster. We often refer to this partial suppression as “leakage.”

Anticoccidal drugs are broken into two broad classes: chemicals and ionophores. Chemical anticoccidial drugs that can be used to allow immunity to develop (leakage) in replacement breeders are amprolium, amproli- um with ethopabate, zoalene and clopidol in the US. However, in Europe, many of these products are no longer available.

Amprolium has been used on many pullet farms for about 40 years, so there is a significant level of coccidia that have become resistant to this drug. Amprolium is very good against the hemorrhage-producing coccidia E. tenella and E. necatrix and it has some activity against E. maxima. When you add ethopabate, you broaden effectiveness to include control of E. acervulina.4

Clopidol and zoalene are very safe for use in pullets, but resistance develops quickly. Neither of these drugs has been used extensively so they may be a good choice for control of coccidiosis in replacement breeders.

The ionophore anticoccidial drugs, such as monensin and salinomycin, are effective against all of the Eimeria species of concern in replacement pullets/ roosters. Because they are coccidiocidal, they are used at lower doses than in broilers to allow immunity to develop.

Vaccination.

Resistance to any anticoccidial drug develops on a farm with continuous use of the drug, which selects for those Eimeria that can survive. Over time, the proportion of coccidia that are resistant to the drugs increases and the result is the development of more severe lesions, which can lead to poor uniformity and adversely affect frame size. The alternative is to rotate from the anticoccidial drug to a live vaccine containing drug-sensitive strains.

Coccidiosis vaccines have two advantages. Over time, the farm’s population of coccidia reverts back to being sensitive to the anticoccidial drug while the birds are vaccinated.5 The vaccine also provides a “controlled exposure.” This means you know exactly when the birds should experience the greatest amount of coccidia lesions, which produce immunity. In other words, you know when to keep a close watch and provide support to the birds if needed. This can be especially important in pullet flocks that are reared in concrete floored houses or on new litter, because exposure may be delayed for these birds. The key to vaccination is that it provides all the coccidia species earlier in the bird’s life than is seen with natural exposure and results in a more uniform development of immunity.

There are two types of live coccidia vaccines available worldwide: attenuated vaccines and controlled exposure vaccines. In the United States, only controlled exposure vaccines are available. This means that the coccidia vaccine given at one day of age are nonattenuated sporulated oocysts and the birds, when vaccinated at 1 day of age, will experience peak oocyst production at about 7 to 10 days of age until about 28 days.6 Outside the US, there are two attenuated strains available for use in pullets. Both products produce a good immune response and may also produce fewer lesions.

It should be remembered that pullets will experience a reaction to E. necatrix later (6-12 weeks of age) than is seen with the other coccidia because E. necatrix is less immunogenic. This more predictable reaction to E. necatrix is another advantage to using coccidial vaccines because the reaction also normally occurs very uniformly and earlier than is seen with anticoccidial drug programs.

Keep in mind that death and bloody droppings are not the only signs to watch for during this period of “vaccine reaction.” Reaction to E. acervulina and E. maxima can affect the pullet’s ability to absorb vitamins, especially fat-soluble A, D, E and K. This is one reason that rickets may develop and that an increase may be seen in leg problems at around 4 weeks of age. One solution is to routinely add vitamins to the pullets drinking water during the vaccine reaction period.

Treatment

Treatment may be necessary for various reasons. One such scenario occurs when the anticoccidial drug program begins to fail due to an increase in the number of resistant oocysts. Another scenario occurs when there is an extreme challenge before immunity has had time to develop as might occur if the litter becomes wet or there is a delay in the development of immunity after vaccination. Remember, the choice to treat may slow or even stop the development of the immune response, so the flock must be watched closely in the future for further coccidiosis. It should be noted that routine administration of anticoccidial medication to vaccinated flocks can slow or stop the development of immunity. Therefore, good flock supervision, routine necropsy of mortality and treatment only when necessary is advisable.

In the US, our choice of drugs to treat in the drinking water is limited to amprolium and the sulfa drugs such as sulfaquinoxoline or sulfadimethoxine. In addition to these drugs, toltrazuril, available in several countries outside the United States, has been a very effective medication. It is important to identify the Eimeria species most affecting pullets/roosters, because amprolium is more effective against E. tenella and E. necatrix (hemorrhage producers) and sulfa drugs work best against E. acervulina and E. maxima.4

Summary

Today’s replacement breeders are far more feed-efficient and grow more rapidly than they did 25 years ago. Consequently, we must do a better job managing the development of immunity to coccidia if we are to minimize the impact on skeletal frame size and body weight uniformity. There are several options available to help birds develop lifelong immunity, ranging from anticoccidial drugs to vaccines.

Whichever method is used, birds must still be closely monitored for signs of excessive coccidial damage. If we don’t do a good job managing our “cocci program,” we may significantly affect both egg production in hens and fertility in roosters.

References

1 Boren B. Does frame size matter? In: Proceedings of the Arkansas Poultry Symposium, Springdale, AR. April 9-10:15-22, 2002.

2 McDougald LR and Reid WM. Coccidiosis. In: Diseases of Poultry, 10th edition, B.W. Calnek, ed. Iowa State Press, Ames, Iowa. pp. 865-883, 1997.

3 Bafundo KW. Managing coccidiosis in broiler breeder replacements. World Poultry, Vol. 7, No. 9:30, 1991.

4 Gill G. Anticoccidials versus Eimeria: Managing drug resistance. Feed Management, Vol. 49, No. 7:12-17, 1998.

5 Chapman HD, Cherry TE, and Quiroz MA. Sensitivity of field isolates of Eimeria to anticoccidial drugs following the use of Coccivac in broilers. In: Proceedings of the Forty-fifth Western Poultry Disease Conference, Cancun, Mexico. May 1-5:107- 108, 1996.

6 Stiff MI and Bafundo KW. Development of immunity in broilers continuously exposed to Eimeria sp. Avian Diseases. 37:295-301, 1993.





Source: CocciForum Issue No.6, Schering-Plough Animal Health.

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