Ascites refers to an accumulation of abnormal fluid in the abdomen, which is secondary to right heart failure. The problem of ascites or congestive heart failure gets much worse as you near the end of the growing out period.
Condemnation in the commercial killing plants due to ascites has risen from 0.062 in 1986 to 0.42 in 1998. There is no denying that there has been a dramatic outbreak of ascites in the last decade.
The modern day broiler, due to its rapid growth rate has a hard time pumping enough blood through its relatively small lungs. This gives us two different results: a build up of pressure in the right side of the heart, leading to pulmonary hypertension and heart failure causing leakage of fluid into the abdomen. Secondly, heart failure can also result in a back up of blood in the skin muscles creating a dark bluish carcass.
The four major things to help control ascites are:
The higher the altitude the higher the demand for oxygen. Alberta has the highest rate of ascites in the country, probably due to this fact.
Cold exposure also raises the need for oxygen to keep the bird warm. Trying to maintain a consistent temperature is the only way to combat this particular problem.
Controlling the level of sodium intake is important. If you are in an area prone to high sodium content in the water, you may have to adjust the sodium in their feed accordingly.
At the start it is good to decide what you want out of your broilers. If you sell your broilers commercially and time is a factor in how many flocks you produce in a year, restricting their feed consumption may not be an option. For the small flock farmers this is not the case though. By restricting the bird's feed intake from days 4 to 25 you can cut your chances of an outbreak in ascites dramatically. We recommend two feedings - one in the morning and again around suppertime. This is a sufficient amount of feed while they are on the chick starter. When your birds switch to grower, we recommend letting them eat whenever they want and you can just watch them grow.
There is good news on the horizon. Primary breeders have selectively used breeders that show greater resistance to attacks of ascites. This will help reduce ascites in their progeny in the future.
We at Miller Hatcheries feel extremely confident that the use of this information along with your own knowledge of poultry will make raising your flock of broilers a worry free enterprise for the whole family.
For a more detailed report about Ascites - see Alberta Agriculture's report.
Ascites refers to an accumulation of abnormal fluid in the abdomen, which is secondary to right heart failure. The problem of ascites or congestive heart failure gets much worse as you near the end of the growing out period.
Condemnation in the commercial killing plants due to ascites has risen from 0.062 in 1986 to 0.42 in 1998. There is no denying that there has been a dramatic outbreak of ascites in the last decade.
The modern day broiler, due to its rapid growth rate has a hard time pumping enough blood through its relatively small lungs. This gives us two different results: a build up of pressure in the right side of the heart, leading to pulmonary hypertension and heart failure causing leakage of fluid into the abdomen. Secondly, heart failure can also result in a back up of blood in the skin muscles creating a dark bluish carcass.
The four major things to help control ascites are:
The higher the altitude the higher the demand for oxygen. Alberta has the highest rate of ascites in the country, probably due to this fact.
Cold exposure also raises the need for oxygen to keep the bird warm. Trying to maintain a consistent temperature is the only way to combat this particular problem.
Controlling the level of sodium intake is important. If you are in an area prone to high sodium content in the water, you may have to adjust the sodium in their feed accordingly.
At the start it is good to decide what you want out of your broilers. If you sell your broilers commercially and time is a factor in how many flocks you produce in a year, restricting their feed consumption may not be an option. For the small flock farmers this is not the case though. By restricting the bird's feed intake from days 4 to 25 you can cut your chances of an outbreak in ascites dramatically. We recommend two feedings - one in the morning and again around suppertime. This is a sufficient amount of feed while they are on the chick starter. When your birds switch to grower, we recommend letting them eat whenever they want and you can just watch them grow.
There is good news on the horizon. Primary breeders have selectively used breeders that show greater resistance to attacks of ascites. This will help reduce ascites in their progeny in the future.
We at Miller Hatcheries feel extremely confident that the use of this information along with your own knowledge of poultry will make raising your flock of broilers a worry free enterprise for the whole family.
For a more detailed report about Ascites - see Alberta Agriculture's report.
Blackhead disease, or more correctly, histomoniasis, is primarily a disease of young turkeys. Chickens are more resistant to the effects of the infection but may act as carriers of the disease-causing organism. Histomoniasis is caused by a microscopic protozoan called Histomonas Meleagridis. The name blackhead is a poor descriptive term because the heads of the birds infected with this parasite are not dark. The protozoan causes considerable damage to the liver and ceca of infected turkeys, and the untreated birds usually die.
Histomoniasis can cause considerable losses in farm turkey flocks. It is a disease commonly seen in these birds at veterinary diagnostic labs in Alberta. It is less common in commercial turkeys because their rations contain low levels of histomoniasis preventing agents.
Histomonas meleagridis is most often transmitted to turkeys in the eggs of a second parasite, the cecal worm, commonly found in both chickens and turkeys. The eggs of the cecal worm may remain infective in the soil for three years of longer and could transmit the blackhead-causing protozoan during this period.
H. meleagridis may also be transmitted by earthworms that accidentally eat the cecal worm eggs. The cecal worm larva released from the egg and the blackhead parasite within that larva may remain in the earthworm for a year of more. When chickens or turkeys eat infected earthworms, the cecal worm larvae containing the blackhead parasites are released and a blackhead infection may result.
Turkeys may acquire the blackhead organism directly from the droppings of infected birds. However, meleagridis found free in the droppings and not protected by a namatode egg die quickly, particularly during warm dry weather.
SignsA decrease in feed consumption and loss of weight may be the first signs observed. Sick birds appear dull and depressed, and often stand by themselves with dropping trails, ruffled feathers, and a sleepy appearance. Sulphur colored yellow droppings may be observed. If birds are not treated, or if treatment is delayed, mortality may be very high. Birds dying of histomoniasis have characteristic enlarged livers with circular depressed areas and enlarged ceca containing a rather dry cheesy material (Figures 1 and 2). Recovered birds may show swollen hard and scarred livers at the time of slaughter.
TreatmentThe drug Dimetridazole can be used in the drinking water or feed to control outbreaks oh histomoniasis. Other drugs occasionally are used for treatment but are better used as preventatives. Sick birds should be isolated from the main flock and treated separately. Dead birds should be burned or buried deeply. All equipment used by an infected flock should be thoroughly cleaned and disinfected.
Prevention and ControlThe protozoa-causing blackhead may remain infective within the eggs of the cecal worms in the soil for nearly three years; therefore each flock of new turkeys should be raised on new uncontaminated ground. Young turkeys should never be reared near older turkeys or with chickens that may carry the infection. In addition to domestic chickens, various wild birds such as pheasant and grouse may serve as reservoirs of infection for domestic turkeys.
The periodic moving of feeders, waterers, and roosts will help prevent the local buildup of infective organisms. Good sanitation and litter management will help prevent transmission of the cecal worm as well as the blackhead organism. Many histiostats or preventative drugs are available and they are commonly included in commercial turkey rations. Because of the very serious nature of blackhead in turkeys, it is advisable to develop a regular program of preventative drug treatment.
Information prepared by:Chickens, turkeys, pheasants and quail will literally pick each other to death at times. This problem can be very expensive for the producer and can make life for the flock very uncomfortable. Once cannibalism starts, it readily becomes a habit that must be stopped.
For our purposes, cannibalism includes feather pulling, toe pecking and head, wing, and tail picking. Prevention is much easier for man and bird than is treatment.
CauseIt is usually impossible to pinpoint any one reason for the start of this behavioral problem in birds. There are many management conditions that are known to be involved with or related to an outbreak. Some of these are:
A combination of these factors is usually involved in any outbreak. Some cannot be corrected even though you know they are involved. Birds usually do need to be moved from the brooder house to growing facilities, and in some cases, moved a third time into laying quarters. If a nervous breed is purchased, you have to live with the problem, at least until the birds are marketed. Temperature control is expensive and sometimes impossible. A nutritional deficiency or a disease is sometimes very difficult to detect and, at best, considerable time is required to make these kinds of determinations. In the meantime, the birds may have devoured each other.
To make matters worse, if an outbreak occurs and one or more corrections are made, the outbreak may continue. Once the habit is started, it is often too late for effective management changed with the affected flock. Perhaps the most frustrating thing about cannibalism is that management may be near perfect and outbreaks still occur. This makes prevention through "bird care" alone virtually impossible.
Stopping an Outbreak
This habit must be stopped quickly. A variety of methods are talked about and have been tried to accomplish this objective. Some of them are:
All of these techniques, singly and in combination, have been shown to be effective on some flocks. However, the only one that is consistently effective in stopping an outbreak is beak trimming. The others work sometimes, and sometimes they don't. You never know beforehand whether they will work on your flock.
"Goggles" and "bits" are probably second to beak trimming in effectiveness. These devices are not readily available and do not always fit young birds. When cost, labor, inconvenience and bird comfort are considered, trimming is usually a better approach.
It is a good idea to apply "anti-pick" compounds to injured birds even though the flock has been trimmed to stop the outbreak.
PreventionEven though outbreaks sometimes occur in the best-managed flock, it is well documented that the better the management, the less often problems arise. Therefore, the first step in a cannibalism control program is to give the birds the best care possible. Correct management conditions that may contribute to an outbreak before one occurs.
Raising birds in continuous dim light does discourage picking. However, they must be reared in a windowless mechanically ventilated house to be able to control all light and still keep the birds comfortable. Even with total light control some outbreaks of cannibalism have been reported. Dim lights are sometimes used in combination with beak trimming to prevent cannibalism.
A combination of good management, correct lighting and beak trimming will prevent the problem. Beak trimming can be used to control the malady even when management is not good. However, trimming alone does not correct poor management and can serve to temporarily "cover-up" management problems that may result in poor performance from the flock, so good management is essential.
Coccidiosis causes the poultry industry to suffer a considerable economic loss, especially in the production of broiler chickens. Chickens are susceptible to at least 11 species of coccidia. The most common species in Alberta are Eimeria tenella, which causes the cecal or bloody type of coccidiosis, and E. acervulina and E. maxima, which cause chronic intestinal coccidiosis.
The broiler industry in Alberta produces about 35 million birds each year. To control coccidiosis, yearly expenditures on anticoccidial drugs total approximately $650,000. For poultry producers, this is probably the largest expenditure for medication.
General life cycle of coccidiaStages of coccidia in chickens appear both within the host as well as outside. The developmental stages in the chicken give rise to a microscopic egg (called an oocyst) which is passed out in the droppings. Under proper conditions of temperature and moisture the oocyst develops within one to two days to form a sporulated oocyst which is capable of infecting other chickens. At this stage the ooycst contains eight bodies (called sporozoites), each of which is capable of entering a cell in the chicken's intestine after the oocyst is eaten. When sporozoites enter the cells, they divide many times producing either a few or many offspring (merozoites). The numbers produced depend on the species of coccidia involved. Each merozoite in turn may enter another intestinal cell. This cycle may be repeated several times. Because of this cyclic multiplication, large numbers of intestinal cells are destroyed. Eventually, the cycle stops and sex cells (male and female) are produced. The male fertilizes the female to produce and oocyst which ruptures from the intestinal cell and passes in the droppings. Thousands of oocysts may be passed in the droppings of an infected chicken. Therefore, poultry raised in crowded or unsanitary conditions are at great risk of becoming infected.
Special features of the life cycleEimeria tenella This parasite develops in the cells of the cecca which are the two blind sacs near the end of the intestine. It is one of the most pathogenic (disease producing) coccidia to infect chickens.
E. necatrix - E. necatrix develops in the small intestine (early stages) and later in the cecum (sexual stages). Like E. tenella, it develops within deeper tissues of the small intestine and is a major pathogen of poultry.
E. accervulina and E. maxima - Both species develop in epithelial cells, primarily in the upper part of the small intestine.
How do birds become infected?Normally, most birds pass small numbers of oocysts in their droppings without apparent ill effects. Coccidiosis becomes important as a disease when animals live, or are reared, under conditions that permit the build-up of infective oocysts in the environment. The intensive rearing of domestic chickens may provide these conditions.
Young chickens pick up the infection from contaminated premises (soil, houses, utensils, etc.). These may have been contaminated previously by other young infected birds or by adult birds that have recovered from the condition. Wet areas around water fountains are a source of infection. Oocysts remain viable in litter for many months. In this way they can contaminate a farm from year to year. Oocysts are killed by freezing, extreme dryness and high temperatures.
How do coccidia harm chickens?Several factors influence the severity of infection. Some of these are:
Coccidiosis in chickens is generally classified as either intestinal or cecal. Most serious cases of intestinal coccidiosis in Alberta are caused by E. necatrix. Cecal coccidiosis is due to E. tenella. Coccidiosis occurs most frequently in young birds. Old birds are generally immune as a result of prior infection. Severe damage to the ceca and small intestine accompany the development of the coccidia. Broilers and layers are more commonly infected, but broiler breeders and turkey and pheasant poults are also affected. Coccidiosis generally occurs more frequently during warmer (May to September) than colder months (October to April) of the year. E. acervulina and E. maxima develop in epithelial cells within the small intestine and generally cause chronic intestinal coccidiosis.
How will I know when my chickens are infected?The most easily recognized clinical sign of severe cecal coccidiosis is the presence of bloody droppings. Dehydration may accompany cecal coccidiosis. Coccidiosis caused by E. tenella first becomes noticeable at about three days after infection. Chickens droop, stop feeding, huddle together and by the fourth day blood begins to appear in the droppings. The greatest amount of blood appears by day five or six and by the eighth or ninth day the bird is either dead or on the way to recovery. Mortality is highest between the fourth and sixth days. Death may occur unexpectedly, owing to excessive blood loss. Birds that recover may develop a chronic illness as a result of a persistent cecal core. However, the core usually detaches itself by eight to ten days and is shed in the droppings.
E. necatrix causes a more chronic disease than E. tenella and does not produce as many oocysts. Therefore, a longer time is usually required for high levels of environmental contamination. Birds heavily infected with E. necatrix may die before any marked change is noticed in weight or before blood is found in the feces.
E. acervulina is less pathogenic than E. tenella or E. necatrix. E. acervulina is responsible for subacute or chronic intestinal coccidiosis in broilers, older birds and chickens at the point of lay. The clinical signs consist of weight loss and a watery, whitish diarrhea. At postmortem, greyish-white, pin-point foci or transversely elongated areas are visible from the outer (or serous) surface of the upper intestine. The foci consist of dense areas of oocysts and gamete (male and female sex cells) production.
E. maxima produces few marked changes in the small intestine until the fifth day after infection. After which, in severe infections, numerous small hemorrhages occur along with a marked production of thick mucus. The intestine loses tine and becomes flaccid and dilated. The inner surface is inflamed and the intestinal content consists of a pinkish mucoid secretion. How can I prevent my chickens from getting coccidiosis?
A few good management practices are listed that will help control coccidiosis. Contact your veterinarian for full details.
Diagnosis is best accomplished by postmortem examination of a representative number of birds from the flock. The location of the major lesions gives a good indication of the species of coccidia concerned. For example, hemorrhagic lesions in the central part of the small intestine suggest E. necatrix, those in the cecum, E. tenella. Microscopic examination of the affected areas along with measuring oocysts will confirm the identification.
How do I treat infected birds?Losses to the flock can be minimized by prompt chemotherapeutic treatment. Amprolium or one of the sulpha-based drugs is usually recommended. If sulfas are used, overdosing may lead to toxicity. The emergence of drug-resistant strains of coccidia may present a major problem. Methods used to avoid the development of drug resistance include switching classes of drugs and the "shuttle program" which is a planned switch of drug in the middle of the bird's growing period.
Information prepared by:
Murray J. Kennedy, Ph.D. and J.A. Hanson, B.Sc., D.V.M.
Animal Health Division
Flip-over disease, or acute death syndrome, can cause a serious mortality rate in broiler chickens.
Flip-over disease usually affects the larger, and rapidly growing, broilers that are between 2 and 12 weeks old. Most cases occur when the birds are between 3 and 5 weeks old. Although the percentage of birds affected is usually low, perhaps about one percent, in some instances it may be as high as 5 percent. The condition can also affect small farm flocks.
Small farm broiler flocks may be affected by the disease, but it is not usually a problem in these situations because the rations are often not conducive to rapid growth.
SignsBirds that succumb to flip-over disease are often found dead on their stomachs with their legs stretched out behind them and their necks extended forward. Occasionally, a dead bird is fount on its back. There is rarely any sign of sickness prior to such deaths, but some people have observed a bird, which appeared to be perfectly normal, suddenly squawk, and make a small jump into the air and land on its back. The wings flutter, there are some convulsive movements and the bird is dead.
CauseThe cause of flip-over disease is still obscure. Heart attacks and enterotoxemia have both been suggested as causes, but neither theory has been substantiated.
PreventionDecreasing the light intensity in commercial broiler barns, thereby slowing down the activity of the birds, appears to reduce the incidence of flip-over disease. Inhibiting the growth of the birds has also been reported to reduce the problem, but this is obviously not a practical approach. Apart from keeping the birds as calm as possible, there is very little that can be done to prevent flip-over in flock of broilers, or to prevent it from occurring in other flocks, until the cause of the condition has been determined.
In an economic loss, Marek's disease is a most important malady of chickens. It often causes severe death loss in pullet flocks and has been a major cause of condemnations at the broiler processing plant. Generally, chickens under 16 weeks of age are most often affected.
CauseCaused by a herpesvirus, the disease is often characterized by abnormal cell growth in the peripheral nerves and central nervous system. Hence, the common name for one form of Marek's: fowl paralysis. In addition to the nerves, however, the disease also may cause lesions on visceral organs and other tissues, including feather follicles of the skin. The most prominent lesions may be tumors on the liver, kidneys, testes, ova, spleen and lungs. In such cases, nerve swelling may not be involved.
How Marek's Disease is SpreadChicken "dander" from feather follicles spreads the disease. The virus also is excreted in the saliva, and the virus probably enters the body through the respiratory system. Transmission via the egg is not significant.
SignsSome chickens die without any clinical signs of Marek's disease. Most of the affected birds will have some degree of paralysis, although chickens with the acute form may not show this condition. Those with paralysis may die because they are unable to reach feed and water. The first indication of infection is a variation in the growth rate and degree of feathering.
LesionsSwelling of the peripheral nerves, particularly of the nerves of the leg and wing, is often noticeable. The visceral organs may contain tumors ranging from microscopic size to fairly large. Such tumor lesions may be confused with those of lymphoid leukosis without a qualified laboratory diagnosis.
PreventionTumor formation from Marek's disease can be prevented through vaccination. Salsbury MD-Vac, a vaccine of chick-embryo tissue culture, is recommended. Vaccination at one day of age usually protects birds through their lifetime. There is no treatment for Marek's disease.
Piling, which can affect all types of poultry, is most commonly caused by too low of a brooding temperature, birds getting excessively wet or by sudden and unexpected movements and noises. Birds that are chilled or frightened tend to huddle on top of each other, smothering the birds underneath. Maintain dry litter, adequate watering equipment and proper temperatures, especially during the night.
Power failures may also cause birds to panic when continuous lighting is given. If possible, give at least 1 hour of darkness per 24 hours.
One of the most frustrating things about prolapse is that it takes its toll form the best birds in the house - - those in lay. Now that marek's is out of fashion, prolapse can account for a very substantial proportion of laying house mortality. The problem frequently fades in retrospect, however, because the flock that passes through the "prolapse syndrome" usually goes on to a good performance record once it settles down. This may account in part for the fact that comparatively little attention is given to the condition, and to its prevention and cure.
Prolapse, in lay language, is the eversion of the oviduct and rectal organs through the vent to the extent that they don't retract again. It is a condition that almost invariable results in death. Even if the prolapse is discovered in time, and the organs replaced in position, the bird will seldom make a recovery. What happens more often than not, is that she quickly becomes a "pickout".
The foundations for prolapse are laid down in the rearing stage, and faulty feeding and light programs during that period contribute to the condition.
The overly fat pullet at point of lay is a prime target for prolapse. The use of a rearing program that allows her to eat ad lib, when she should be slightly restricted, or one that encourages over consumption of protein is asking for trouble because of the association of high levels of protein and egg size.
Equally at fault is the mistimed light program that brings immature pullets to point of lay before the oviduct muscles have developed elasticity and strength. Worse still, perhaps, is the too-sudden increase in day length that results in erratic ovulation - - many double-yolked eggs which, by size alone, can cause prolapse or blowouts.
The laying of an egg is invariable accompanied by some eversion of the oviduct. This is out. The tissues around the vent are wonderfully elastic, even in young pullets at the point of lay and after the egg is produced, and everything returns to its original position with no harm done. Nor harm done, that is, if we haven't set the stage for trouble by faulty feeding and lighting.
If we have allowed the bird to build up too much abdominal fat, this reduces the elasticity of the oviduct and vent muscles, often to the point where they cannot return to their normal position - - hence, prolapse, or blowout. If the light program has encouraged too early egg production or oversized eggs, before the muscles can cope with the situation, we find ourselves with the same problem.
Management DetailsOther causes of prolapse
The entire blame for prolapse cannot be placed at the door of light and feed. There are other causes: over crowding, enteritis, hormone imbalance, and one of the most common - - physical damage inflicted on the oviduct tissues. In this latter case, picking at the slightly exposed oviduct, as it is laid, can sometimes inflict sufficient bruising and irritation upon the tissues that they prolapse after the next egg is produced.
Good management is the key to preventing prolapse, and good management, promptly applied, can help to minimize the seriousness of blowouts if the "syndrome" begins to appear. The incidence of "pickouts", for example, can be drastically reduced by attention to two relatively simple details - - beak retrimming and light intensity.
A good percentage of the mortality that is generally ascribed to prolapse is not true prolapse, as we know the term. It is actually cannibalism triggered by pullets picking at the slightly inverted vent of another during egg laying, until she becomes a victim of pickout. And it can generally be either prevented or brought under control by reducing the intensity of light to 1.5 foot-candles at feed trough level, and or by retrimming the beaks of those pullets that require this treatment at housing.
Checking the pullet for enteritis, worms or any other health hazard that could cause prolapse.
So, too, will a watchful eye on flock density. C. E. Ostrander, of Cornell University's poultry husbandry department, reports on a cage density test using no beak trimmed birds. No cannibalism showed in two and three-bird cages, but it did occur in those housing four and five birds.
Occasionally, a producer will pin his prolapse problems onto the strain of bird he is handling at the moment. Actually, of all competitive stocks on the market today, none has the prolapse tendency as a recognizable fault; breeders have long ago eliminated families showing the characteristic.
Four key details in growing pulletsIn the prevention of prolapse, the pullet replacement grower should concentrate on four key details.
In the control of prolapse, the laying house operator has four important areas to watch.
Keep in mind that outbreaks of prolapse and pickouts are nearly always triggered by something we mismanaged somewhere back along the line. These problems can be prevented and they can be controlled.
Young chicks, as early as 1-week-old, exhibit curling of the toes, inability to walk and sometimes diarrhoea.
Treatment and ControlAdministering vitamin B preparations brings a rapid cure. Only in advanced cases will birds be dehydrated and emaciated, requiring further treatment.
It is important to ensure adequate vitamin B levels not only in starter and grower diets, but also in the diet of parent breeders.
