Ascites Syndrome In Meat-Type Chickens

Introduction

Ascites is an accumulation of non-inflammatory fluid in one or more of the abdominal spaces. There may be clots of yellow material in the fluid.

Ascites caused by right ventricular failure (RVF) has been an important cause of illness and death in meat-type (broiler) chickens worldwide. The number of cases in the U.K., Canada and the U.S. increased during the past decade, and coincided with broilers’ continuing genetic and nutritional improvement in feed efficiency and rate of growth.

The incidence of ascites ranged from 1% to 2% in 1995 in Western Canada, and from 0% to 30% in 2002 in U.S. broiler flocks. Ascites syndrome has both economic and welfare implications for the broiler industry due to bird suffering, increased late mortality and condemnation (Kalmar et al., 2013).

Causes and Predisposing Factors of Ascites

The primary cause of ascites in meat-type chickens is right ventricular failure (RVF) as a result of increased pulmonary (lung) arterial pressure.

Increased pulmonary arterial pressure can be produced in birds by lack of oxygen. When the oxygen supply is insufficient, the heart must circulate blood more rapidly to provide the same amount of oxygen to the body.

In meat-type chickens, the lack of oxygen causes a marked increase in the number of red blood cells that makes the blood more viscid and difficult to pump through the lung, causing pulmonary hypertension (PH). The right side of the heart enlarges in response to the increased workload, and, if the heart has to continue working harder than normal, the result is right ventricular valve insufficiency, volume overload, right ventricular dilatation and RVF. As a result, venous blood pressure increases, and fluid leaks out of the veins and accumulates in peritoneal cavities, resulting in ascites.

The causes of insufficient oxygen supply and subsequent development of ascites in broilers are complex. Predisposing factors that increase the amount of oxygen required, reduce oxygen-carrying capacity of the blood, increase blood volume or interfere with blood flow through the lung may result in flock outbreaks of ascites.

The most important cause of increased work for the heart at low altitude appears to be the high oxygen requirement of rapid growth in modern broilers, combined with restricted space for blood flow through the small blood vessels of the lung.

The lungs of chickens are rigid and moulded into the thoracic cavity and they cannot expand like mammalian lungs. The capillaries can expand only a little to allow for increased blood flow. The lungs of chickens grow less rapidly than the rest of the body, and lung capacity does not keep up with the very rapid growth of muscle in fast-growing broiler chickens. In addition to high oxygen demands associated with their fast growth rate, the fast metabolism of the modern broiler chicken increases the production of reactive oxygen types that increase oxidative stress, causing damages to pulmonary vessels (Kalmar et al., 2013).

Ascites caused by RVF has also been produced by rickets, poor air quality (high levels of ammonia, carbon monoxide and carbon dioxide) and pneumonia (lung infection). This makes breathing difficult and decreases oxygen supply, which increases the number of red blood cells in the blood.

Cold is also a common cause of outbreaks of ascites in backyard flocks because of enhanced blood flow through the lungs of birds in an effort to produce endogenous heat (Kalmar et al., 2013).

Another environmental cause of ascites is salt intoxication, when drinking water contains excessive levels of sodium, which increases blood volume and constricts arterioles, increasing pulmonary pressure.

Aside from environmental causes, genetics can predispose birds to pulmonary hypertension-induced ascites, as genes associated with the syndrome have moderate to high hereditability (Kalmar et al., 2013). Research suggests only a few major genes are involved in ascites hereditability (Wideman et al., 2012). Ascites in broilers demonstrates a significant role of atypical innate and adaptive immune responses (Wideman et al., 2012).

Other causes of ascites include liver damage (caused by Clostridium perfringens), inflammatory or degenerative disease of the myocardium and/or valves, and congenital heart disease (Kahn, 2005).

Clinical Signs

Mortality from ascites is greatest in birds at the end of their rearing period. Occasionally, young broilers will develop ascites, particularly in poor nutritional and environmental conditions.

Since growth stops as RVF develops, affected broilers may be smaller than their pen mates. Their abdomen is distended with fluid (hence “water-belly”), and the pressure results in an increased respiratory rate and reduced exercise tolerance. Clinically affected broilers might show open beak breathing, cyanosis of the comb and wattles, dullness and/or depression, abnormally slow heart rate and/or red abdominal skin with congested blood vessels.

Post-Mortem Examination and Diagnosis

At post-mortem, there is a large or small quantity of clear yellow fluid and clots of fibrin in the abdomen. The liver may be swollen and congested, or firm and irregular with edema (fluid), and have fibrin adherent to the surface. It may be nodular or shrunken; it may be white with edema under the capsule or have large or small blebs of edema in the sacs around the liver. There is a mild-to-marked increase in fluid in the sac around the heart and occasionally there is inflammation of the outer surface of the heart. There is enlargement of the right side of the heart and thickening of the muscle of the right side (hypertrophy) or dilatation with thinning of the left side of the heart. The right atrium and vena cava are very dilated. The lungs are extremely congested and edematous.

Not all broilers that die from RVF have ascites. Death may occur before clinical signs are observed, and affected broilers frequently die on their back. At necropsy, there may be a swollen liver, venous congestion, a dilated right atrium and vena cava, and thickening of the right heart, as well as marked lung congestion and edema (death is likely from respiratory failure). The intestine may or may not be empty, but the heart changes will differentiate RVF from flip-over.

Prevention

Slowing growth to reduce the oxygen required after 30-35 days of age can prevent ascites caused by primary pulmonary hypertension. Restricting feed, feeding a mash diet, using a less energy-dense diet or decreasing daylight hours in the barn could accomplish this.

Control environmental temperature, litter moisture, humidity and air quality to prevent excessive body heat loss and to maintain bird health. Monitor sodium levels in feed and water to prevent salt intoxication. Altitudes above 900 m are inadequate for meat-type chickens, and growth must be slowed to prevent mortality (Kahn, 2005).

References

Julian, R.J. The effect of increased sodium in the drinking water on right ventricular hypertrophy, right ventricular failure and ascites in broiler chickens. Avian Pathology 16: 61-71, 1987.

Kalmar, I.D., et al. Broiler ascites syndrome: Collateral damage from efficient feed to meat conversion. The Veterinary Journal (2013). http://dx.doi.org/10.1016/j.tvjl.2013.03.011

Kahn, C.M., S. Line, ed. The Merck Veterinary Manual (9th ed.). (2005). Ascites syndrome. p. 2,269-2,270 Philadelphia, PA: Merck & Co., Inc.

Wideman, R., D. Rhoads, G. Erf, and N. Anthony. (2012). Pulmonary arterial hypertension (ascites syndrome) in broilers: A review. Poultry Science, 92, 64-83.