I found my hen alone and in a corner of the coop. I thought maybe egg bound but I feel no egg, only kinda squishy, like filled with liquid. I have taken in the house and place her in a warm towel in a box sitting in near a heater. She was shaking a little when I found her. She will not drink or eat, however her crop is full. Wondering if anyone here may be able to tell me what is wrong and what to do for her. Please help
Might be ascities. From:http://www1.agric.gov.ab.ca/$department/deptdocs.nsf/all/pou3546 Ascites Sign up for our E-Newsletter Definition | Recent trends | Diagnosis | Contributing factors | Etiology | Preventative management | Related articles | References | Glossary Definition Ascites is not a disease, it is a condition in which excess amounts of ascitic fluids (a combination of lymph and blood plasma which has leaked from the liver) accumulate in the body cavity (Figure 1). In broiler chickens, the condition often leads to death. If the bird survives until the time of processing, the carcass would most often be condemned. The ascites syndrome is associated with abnormally high blood pressure between the heart and lungs (pulmonary hypertension) leading to right heart failure, increased blood pressure in the veins, and excessive buildup of fluid in the liver (passive liver congestion) which leaks into the body cavity. Figure 1 An ascitic broiler carcass with excessive accumulation of fluid in the body cavity. Recent Trends The incidence of ascites has increased worldwide over the past several years. This increase coincides with ongoing genetic and nutritional improvements in the areas of growth rate and feed efficiency (Julian et al., 1986). In the World Broiler Ascites Survey (Maxwell and Robertson, 1996), information on 18 countries from four continents showed that ascites affects 4.7% of live broilers worldwide. In Canada, ascites related condemnation of chicken carcasses at processing increased from 3.5% in 1986 to 19% of total condemns in 1994. From 1996 that number has decreased from 16% of total condemnations due to ascites to 8.5% in 2004 (Agriculture and Agri-Food Canada, 1996,2005). The cost to the Canadian broiler industry in 2003 was $2.25 million dollars (Chicken Farmers of Canada 2004, Agriculture and Agrifood Canada, 2004). The cost to the worldwide broiler chicken industry due to ascites related mortality has been estimated to be in excess of $500 billion per year. Meat-type chickens are selected for growth rate and muscle mass. Due to very successful genetic selection techniques, growth rate has increased at a rate of 4 to 5% per year over the past 30 years. Broiler performance (average of both sexes) has improved so much that the growing period to produce broilers of the same weight has decreased by 30% in just 15 years. A 2 kg bird took 56 days to produce in 1976; it can now be produced in less than 40 days. Selection for rapid growth and efficient feed conversion has resulted in a broiler with such a high rate of metabolism that its heart and lungs are barely capable of providing enough oxygen to sustain the body (Julian, 1990). Diagnosis Ascites is most commonly diagnosed at 4 - 5 weeks of age, although signs of ascites have been recorded in day-old birds (Muirhead, 1987). Low oxygen status of embryos during incubation may be related to the onset of ascites (Maxwell et al., 1987). Panting is often observed in ascitic birds even in the absence of apparent heat stress. This panting in ascitic birds is due to physical restriction of the large abdominal air sacs. The excessive abdominal fluid accumulation results in a reduction in the volume of air that is exchanged per respiration. Gurgling sounds often accompany panting. Julian (1993) observed that the abdomen of ascitic birds is often dilated (enlarged) because of ascitic fluid in chickens that have an increased respiration rate and reduced exercise tolerance. Older birds which are mildly ascitic may show signs of cyanosis (a blue discolouration of the skin) especially around the comb and wattles. Cyanosis is also a condition for which birds are condemned at the time of processing, and it is often an indication of early stages of ascites. Cyanotic birds have been observed to die spontaneously, especially when excited. Post mortem analyses of ascitic birds indicate that the skin and tissues are congested and they are often a dark red colour (Figure 2). Figure 2 The upper breast muscle (pectoralis major and pectoralis minor) is from an ascitic broiler. The lower breast muscle is from a normal broiler. Opening the abdominal cavity of an ascitic bird reveals an amber or clear fluid (lymph) that resembles blood plasma (Figure 3). This abdominal fluid is called ascitic fluid. The heart of ascitic birds is enlarged and there is fluid in the pericardium (the sac surrounding the heart). The liver may be edematous (swollen and congested) and may have fibrin (blood clotting protein which is soluble in the blood) adhering to the surface. Blood plasma builds up in the low-pressure liver venous system because it is unable to return to the heart in sufficient volume. Figure 3 Opened abdominal cavity of an ascitic broiler chicken. Note the enlarged heart and the abundance of ascitic fluid. Classically, the right ventricle (RV) is grossly dilated, and can make up as much as 40% of total ventricle weight, compared with the normal 20%. Varying degrees of lung damage are seen. Lungs of ascitic birds often appear pale or grayish (Leeson et al., 1995). The lungs are extremely congested and edematous (Julian, 1993). Contributing Factors Ascites is a metabolic disorder. Several factors are known to influence the occurrence of ascites in broilers. These include: the housing environment temperature respirable dust (small particle size of 0.5 to 10 µ m) carbon dioxide / oxygen levels rapid growth rates high basal metabolic rate high energy rations (Scheele et al., 1991; Julian, 1993). Typically, the series of events that lead to the development of the ascites syndrome begin when broilers first start to gain body weight or muscle mass. Etiology Rapid growth rate requires a high basal metabolic rate (Figure 4). Sustaining a high metabolic rate requires oxygen. The broiler chicken has more genetic potential for growth than it has potential to provide oxygen to sustain that growth. Witzel and associates (1990) indicated that the demand for oxygen may exceed the cardiopulmonary capacity to supply sufficient oxygen . This ultimately leads to an oxygen deficit. The heart responds by increasing its output of (deoxygenated) blood to the lungs for oxygenation. Figure 4. Factors which contribute to the onset of the ascites syndrome. Figure 5 Diagram of the heart showing the direction of blood flow through the heart. The right ventricle (which pumps blood to the lung) responds to the increased demand for oxygen by increasing heart rate and blood volume (Figure 5). The thin right ventricle is prone to becoming distended in response to its increased workload (Figure 6). Increased pulmonary arterial pressure (blood pressure between the heart and the lungs) is due to both an increase in blood flow and increased resistance to blood flow. Figure 6 A cross sectional slice through the ventricles of two hearts. The section on the left is the heart of a healthy broiler at 42 days of age. The heart section on the right is from a broiler with the ascites syndrome. In an attempt to increase the blood's oxygen carrying capacity, red blood cell production is increased. This causes a 'thickening' of the blood, and further resistance to blood flow, compounding the lung congestion problem. As the right ventricle dilates, the valves become increasingly inefficient and allow some blood to flow back into the atrium. This leads to right ventricular failure. The increase in back flow causes liver congestion (edema) because the capillaries cannot exchange the fluid and the high pressure causes the plasma to leak from the liver and capillary beds into the body cavity. Management Practices to Prevent Ascites Feed restriction Reducing the feed intake of broilers decreases the growth performance. Feed restriction is only of economic benefit when the incidence of ascites is very severe. From a metabolic point of view, the first three weeks of life are an especially stressful period for a broiler. Muscle and bone growth, as a percentage of body weight, is greatest during this time. Slower growing birds have reduced oxygen needs. Feed restriction slows body growth, allowing the cardiopulmonary organs (heart and lungs) to keep up with the oxygen demands of the birds. Feed restriction during the finishing period is less important because the weight gain relative to frame size is less. Birds which are feed restricted early may be able to enter the grower and finisher periods with stronger cardiopulmonary systems (Arce et al., 1992). With moderate feed restriction, the birds may be able to achieve similar weights to non-restricted birds. With a smaller frame size, there is less feed required for maintenance, and overall feed conversion efficiency is improved through compensatory growth. Improved feed efficiency increases the oxygen requirements of the bird. Methods of feed restriction 1. Feed form (Mash v.s. Pellets) Reducing the intake of nutrients can reduce the incidence of ascites. Pelleted feed is more nutrient dense, and allows birds to increase nutrient intake. Mash feed can be fed during the starter period (from day 0 to 21 or 28 days of age) to reduce ascites (Shlosberg et al., 1991). When fed in the first 4 wk., mash feed reduced mortality without downgrading market parameters (Shlosberg et al., 1991). 2. Composition of the feed (nutrient reduction programs) Qualitative feed restriction can be achieved by lowering the energy content of the diet. If this is done early in life, when feed intake per unit of metabolic weight is at its highest (Albers et al., 1990), oxygen requirements are reduced and therefore susceptibility to ascites is also reduced. It has also been suggested that dietary compositions that improve feed conversion ratio also increase the incidence of ascites. These factors include high energy density, a high protein:energy ratio, and pelleted diets (Schelle, 1993). 3. Limited access to feed (meal feeding) Lighting programs are a method of restricting feed intake by restricting access to feed. Lighting programs have been used to reduce the incidence of leg problems, sudden death syndrome (SDS) and ascites. Sudden death syndrome in broilers may be related to ascites, and can occur secondarily to right ventricular failure (Classen et al., 1991). It is possible that the step-up lighting program reduces the level of activity (which also increases oxygen demand) compared with continuous lighting. 4. Skip a day feeding Skip a day feeding programs are not recommended except where mortality due to ascites is very severe. This is because the compensatory growth of the broilers following severe feed restriction is not sufficient to compensate for the reduction in early growth rate. Skip-a-day programs used early in the starting period reduce negative effects on subsequent body weight gain (Arce et al., 1992). The most effective treatment reported for the control of ascites was a skip-a-day feed restriction program used in Kenya. The skip-a-day program was applied during the starter period (no feed on days 7, 9, 11, and 13) in association with a low protein starter capon mash. This program has been used successfully for the past two years and consequently has dramatically reduced the annual incidence at altitude (Nirobi - 5 600m) from >30% to 5% (Maxwell and Robertson, 1997). Feed restriction can be an effective means of reducing the incidence of ascites, but it must be used in conjunction with good management. Once optimal management practices have been insured, restricted feeding can be highly effective in further reducing the incidence of ascites in commercial broiler flocks (Arce et al., 1992). Environmental factors Temperature - Careful attention to brooding temperatures is critical in the prevention of ascites. Low temperature brooding forces the birds to use energy (which requires oxygen) in order to maintain body temperature. This predisposes a flock of broilers to ascites, although the signs of ascites show up later in production. Air temperature is also important later in production, but it is especially critical early. Air Quality - Any further challenges to the bird's ability to exchange oxygen with its environment predispose it to ascites. Dust - Dusty environments can contribute to the onset of ascites. McGovern (1998) found that the right ventricle area of the heart ascites score was reduced when dust levels were controlled in broilers that were not feed restricted. Dust can be controlled by spraying canola oil on the litter at 0.8 liters / m2 over the six week growing period. Disease causing microorganisms can also attatch themselves to dust particles, and be respired, causing irritation or infection in the lungs. This further reduces oxygen transfer between the bird and the environment. Ammonia - High levels of ammonia in the broiler house can irritate the lungs, resulting in decreased oxygen transfer between the bird and the environment. Oxygen - Natural gas open-flame brooders contribute to oxygen depletion in broiler houses. This burning of oxygen is in direct competition with the birds. Ventilation rates must supply enough air to replenish the oxygen consumed. The volume of air coming in the air intakes should be uniformly distributed to the birds. In cold weather, air must be preheated before it comes into contact with the birds. When CO2 levels are maintained at 2500 ppm, the air quality should be acceptable. Proper levels of oxygen typically coincide with low levels of ammonia and respirable dust. Adequate air exchange must be provided to broilers as a preventative method for ascites. Because broilers have rapid growth rates, adequate oxygen levels are essential to prevent increased stress on the respiratory system and consequently the heart. Related Articles Growth performance and the incidence of ascites in broilers in response to carbon dioxide concentrations (I. Edeogu) Environmental factors can affect ascites in broiler chickens (M. J. Zuidhof) References Agriculture and Agri-food Canada 1996. Poultry Marketplace:Chicken Condemnations 2004 January Condemnation Report. English.(Note: 2003 data is summarized in the monthly reports for 2004) http://www.agr.gc.ca/misb/aisd/poultry/documents/C0401CHI.pdf Agriculture and Agri-food Canada 1996. Poultry Marketplace:Chicken Condemnations 1996 Annual Report. English. http://www.agr.gc.ca/misb/aisd/poultry/c96chi_e.htm Arce, J., M. Berger, and C. L. Coello, 1992. Control of ascites by feed restriction techniques. J. Appl. Poultry Research. 1:1-5. Chicken Farmers . of Canada 2004. Chicken Data Guide 2004. http://www.chicken.ca/app/DocRepository/1/Data_Handbook/2004_Data_Booklet.pdf Classen, H. L., C. Riddell, and F. E. Robinson, 1991. Effects of increasing photoperiod length on performance and health of broilers Br. Poultry Sci. 32:21-29. Julian, R. J., 1990. Pulmonary hypertension: a cause of right heart failure, ascites in meat-type chickens. Feedstuffs: Jan 20, 1990. Julian, R. J., 1993. Ascites in Poultry. Avian Pathology. 22:419-454. Julian, R. J., J. Summers, and J. B. Wilson, 1986. Right ventricular failure and ascites in broiler chickens caused by phosphorous-deficient diets. Avian Dis. 30:453-459. Julian, R. J., G. W. Friars, H. French, and M. Quinton, 1987. The relationship of right ventricular hypertrophy, right ventricular failure, and ascites to weight gain in broiler and roaster chickens. Avian Dis. Vol. 31, No. 1:130-135. Leeson, S., G. Diaz, and J. D. Summers, 1995. Poultry Metabolic Disorders and Mycotoxins. University Books, Guelph, Ontario, Canada, 29-50. Maxwell, M. H. and G. W. Robertson, 1997. World broiler ascites survey 1996. Poultry Int. http:\\www.wattnet.com\library\. Maxwell, M. H., S. G. Tullett, and F. G. Burton, 1987. Haematology and morphological changes in young broiler chicks with experimentally induced hypoxia. Res. Vet. Sci. 43:331-338. McGovern, R. H., 1998. Growth performance, carcass characteristics, and the incidence of ascites in broilers in response to feed restriction and litter oiling. (In Preparation for Submission) Muirhead, S., 1987. Research defines events leading to the accumulation of fluid in broilers. Feed stuffs. Jan. 19, 1987. Schelle, C. W., 1993. Effects of nutritional factors on the occurrence of ascites and heart failure syndrome. Pages 149-162 in : Proceedings of the 9th European Symposium on Poultry Nutrition, September 5-9, 1993. Jelling Gore, Poland. Shlosberg, A., E. Berman, U. Bendheim, and I. Plavnik, 1991. Controlled early feed restriction as a potential means of reducing the incidence of ascites in broilers. Avian Dis. 35:681-684. Witzel, D. A., W. E. Huff, L. F. Kubena, R. B. Harvey, and M. H. Elissalde, 1990. Ascites in growing broilers: A research model. Poultry Sci. 69:741-745. Glossary Ascitic fluid - a combination of lymph fluid and blood plasma that leaks from the liver Cardiopulmonary system - the heart and lungs and associated blood vessels Cardiopulmonary capacity - the maximum amount of blood the heart can pump to the lungs for oxygenation condemnation - birds that are removed from food line for food safety and quality reasons (e.g. for contamination, ascites, cyanosis, emaciaiton) central venous pressure - blood pressure in the veins cyanosis - blue discoloration of the skin due to the presence of de-oxygenated blood dilated - widened or enlarged edema - presence of abnormally large amounts of fluid in tissues fibrin - insoluble protein formed in blood-clotting from the soluble blood-plasma protein liver congestion - an excessive amount of blood and fluid in the liver lymph - colorless fluid from tissues or organs of the body, like blood but without red corpuscles necropsy - postmortem examination protein accrual - increase in muscle mass, deposition of protein on the muscles pulmonary arterial pressure - pressure of the blood in the arteries that send blood from heart to lungs pulmonary hypertension - abnormally high blood pressure in the lung respirable dust - dust particles between 10 µ and 0.5 µ, not trapped in the upper respiratory tract, able to penetrate to the terminal air sacs of the lungs blocking the alveoli serous - having properties of a watery fluid valvular insufficiency - inablity of the valves within the heart to close and prevent back flow of the blood For more information about the content of this document, contact Brenda Schneider. This information published to the web on January 29, 1999. Last Reviewed/Revised on July 15, 2008.
Thank you Casportpony, the article was very interesting. It could have very well have been this ascites. However, unfortunately my hen has passed. I went to check on her and she was gone.
I'm sorry for your loss, I also lost one today. It's also possible that she had peritonitis, both present the same way, I believe. I don't want to sound insensitive, but you could do your own necropsy, or send her off for one, I'm sending mine tomorrow.
i also have a problem i need help with, today i went outside to check on my silkies who up the three days ago i had kept in the house because of the weather. anyhow, i noticed one was missing and i found her alone under their box. she was very slow and lathargic, i picked her up and she had a HUGE deer tick attached right next to her eye. i removed, alcoholed and neosporin, has anyone else ever heard of this and are there any other precautions i can take?
