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Poultry farming is a complex endeavor that requires careful attention to the health and well-being of the flock. Several common health conditions can affect poultry, including visceral gout, fatty liver syndrome, cloacal prolapse, osteomalacia, vitamin E deficiency, and ascites syndrome. Understanding these conditions and implementing appropriate management strategies can help prevent and treat them effectively.
(a) Visceral Gout (Urolithiasis):
Visceral gout, characterized by the accumulation of uric acid crystals in organs such as the kidney, heart, lungs, and gut, is a frequent condition observed in older layer flocks. It is often associated with kidney failure and can contribute to flock mortality.
The causes of kidney damage include low phosphorus diets, water deprivation, excessive calcium consumption before sexual maturity, and high levels of vitamin D3. Gout-related losses in poultry are usually chronic, and affected birds may show no symptoms before death or appear thin.
Studying Gout (Pathology):
The lesions of gout are linked to the buildup of urates on the surfaces of internal organs (visceral gout) and within joint spaces and synovial membranes (articular gout). These urates have a gritty and white appearance, which distinguishes them from the inflammatory exudate seen in bacterial infections. In cases of gout, the kidney may appear atrophic or absent in some areas while appearing swollen (compensatory hypertrophy) in others.
Visceral Gout Treatment in Poultry:
Birds affected by gout can be treated with varying degrees of success by adding ammonium sulfate or ammonium chloride to their diet. However, these treatments may lead to wet droppings and a decrease in eggshell quality.
To prevent gout, it is essential to provide balanced nutrition with appropriate levels of calcium and phosphorus throughout the growth period. Calcium supplementation for layer birds is particularly crucial before their first egg, and water deprivation should be avoided.
(b) Fatty Liver Syndrome:
The fatty liver syndrome occurs due to an imbalance in energy and protein intake, resulting in excessive fat accumulation in the liver. This condition is commonly observed in caged laying hens and occasionally in breeder turkey hens. The sedentary lifestyle of caged hens, coupled with high-calorie diets, makes them more susceptible to this syndrome.
Lesions:
In fatty liver syndrome, the liver becomes enlarged and appears pale orange, soft, and friable, easily breaking upon pressure. The rupture of a fatty liver can lead to hemorrhage into the abdominal cavity, causing death in laying hens.
Treatment and Prevention:
Treatment involves adding choline chloride, vitamin K, biotin, and vitamin E to the feed for two weeks, with varying results. Prevention of fatty liver syndrome requires maintaining a balanced diet with appropriate levels of energy and protein.
(c) Cloacal Prolapse:
Cloacal prolapse occurs when the cloaca (vent) of laying hens becomes permanently everted and inflamed, usually due to trauma from pecking, cannibalism, or large egg size. The strain of the bird, beak trimming quality, ration quality, space availability, light intensity, and egg size can affect the severity and incidence of this condition.
Prevention:
Preventing cloacal prolapse involves using low light intensity in layer housing, providing appropriate beak trimming, ensuring adequate floor, drinker, and feeder space, and offering perches and obstacles in floor-raised systems. A hen ratio of 1 nest to 4 hens can help decrease fighting for nest space.
(d). Osteomalacia (Softening of Bones):
This is also known as cage layer fatigue in laying hens. This nutritional disease is characterized by low minerals in the bones, resulting in soft, pliable bone, including the beak, curved keel bone, and beading of the ribs at the costochondral junction.
High-producing hens maintained in cages can show paralysis during the period of peak egg production. The birds carry approximately 200 grams of calcium in their skeletal system and use 2 grams per day to produce an eggshell. The condition is caused by impaired calcium flux related to the high output of calcium into the shell.
Calcium depletion in the long and medullary bones is usually seen in caged birds, and this mainly suggests that there is reduced activity/exercise as a predisposing factor.
At the time of initial paralysis, birds can appear healthy and will have a shelled egg in the oviduct. Death occurs from starvation or dehydration, a failure of the birds to reach the feed or water.
A high incidence of cage layer fatigue can be prevented if pullets receive a high calcium diet (minimum of 3.5% calcium) at least two weeks before the first oviposition. Older caged layers are also quite susceptible to bone breakage, most especially during the transportation process.
When young birds have soft bones, it is referred to as rickets. This disorder is usually caused by abnormal Calcium/Phosphorus ratios in the ration, low vitamin D3 levels, or intestinal malabsorption associated with enteric diseases. The birds are often recumbent, but bright and alert, with extremely pliable beaks and long bones.
(e). Vitamin E (Alpha-Tocopherol) Deficiency:
This is also known as crazy chick disease or cherry brain. This disease is caused by a deficiency of vitamin E.
This deficiency is usually diagnosed in young chicks and turkey poults, but it can affect a wide variety of birds. Vitamin E is a natural antioxidant, and it is needed for the maintenance of brain tissue and embryo development, especially in growing birds.
Selenium is needed for vitamin E metabolism. The three diseases associated with vitamin E deficiency are the below;
1. Encephalomalacia: ataxia, loss of balance, falling over backward, prostration with legs outstretched. Gross lesion of swollen cerebellum that has a variable size and hemorrhagic to necrotic areas (“cherry brain”).
2. Exudative diathesis: Blue-green staining and edema of the subcutis of the ventral abdomen and thighs. Birds may have difficulty walking and standing with legs far apart. The pericardial sac may be distended with clear fluid.
3. Muscular dystrophy: Often no signs in the live bird. At necropsy, one can see white to yellow regions within the breast, legs, gizzard, and heart muscles. Gizzard (left photo) and heart (right photo) of a White Pekin duck with Vitamin E-Selenium deficiency.
Note: The white regions of the walls of both organs (heart and gizzard) is where the degeneration of muscle fibers occurs.
Prevention of these disorders requires the use of fresh feeds with minimal storage times or using antioxidants (synoquin or ethoxyquin)in the feeds, and always avoiding prolonged storage of the feeds.
(f). Ascites Syndrome and Right Ventricular Failure in Broilers:
Ascites syndrome is a noninfectious metabolic disease of broiler chickens and ducklings characterized by pulmonary hypertension, right-sided heart failure, and accumulation of excessive fluid (transudate) in the abdomen.
This is a form of congestive heart failure in chickens. Birds are predisposed to right-sided heart failure because of a muscular flap that forms part of the right atrioventricular valve.
Study and analysis of ascites (Epidemiology)
Ascites in broiler chickens can be caused by several factors, including genetics, high altitude, respiratory infections, and poor ventilation. In some flocks, the mortality rate can reach up to 1-2% or more.
Feed restriction can be used to reduce the ascites caused by genetics, but this can also slow down the growth rate and performance of the birds. It is important to address the underlying cause of ascites and improve the living conditions for the broiler chickens to prevent this condition and improve the overall health of the flock.
Clinical Signs:
Gross lesions
Predisposing factors
Broiler chickens are bred for high feed efficiency with a rapid rate of growth and muscle development. Broiler chickens have a lower ratio of total lung volume and body weight compared to their ancestor (Red Jungle Fowl) or white leghorn chicken.
Continuous availability of high-energy and high-quality feeds typically contributes to a high growth ratio.
Pathogenesis of ascites
Cornish breeds have a high rate of gain and consume high-energy feeds, which leads to rapid muscle mass increase and a high oxygen demand for muscle growth. This leads to increased oxygen consumption and a lower growth rate of the heart and lungs compared to skeletal muscle. This can result in hypoxia or low levels of oxygen in the body tissues.
This leads to increased cardiac output, with a greater amount of blood pumped by the heart, increased blood flow to the lungs, an increased number of circulating red blood cells (polycythemia), and increased hemoglobin inside red blood cells. This can lead to pulmonary hypertension, or increased pulmonary blood pressure, which results in an increased workload on the right ventricle to pump blood to the lungs, causing it to dilate with a thickened wall.
If the right ventricle becomes overworked, it can result in right-sided heart failure and systemic hypertension. This, in turn, can lead to fluid loss across the liver capsule into the body cavity and fluid accumulation in the air sacs and lungs, causing suffocation.
Prevention
Decrease the amount of energy levels put in feeds to slow down the growth rate; however, this is not practical in commercial broiler operations. Restricted feeding programs, such as reduced lighting during the growing period, can also be a remedy.
NOTE: If mortality is greater than 1-2% from ascites look for other complicating factors such as high sodium levels in feed or water, vitamin E or selenium deficiency, respiratory infection, furazolidone, or coal tar toxicity. Maintain good air quality with adequate ventilation, especially during winter.
Conclusion
In conclusion, maintaining the health and well-being of poultry in farming operations is crucial for successful and sustainable production. This requires understanding and addressing common health conditions such as visceral gout, fatty liver syndrome, cloacal prolapse, osteomalacia, vitamin E deficiency, and ascites syndrome. By implementing appropriate management strategies, including balanced nutrition, preventive measures, and timely treatment, these conditions can be effectively prevented and treated.
Visceral gout, characterized by uric acid crystal accumulation in organs, can be managed through balanced nutrition and avoiding factors that contribute to kidney damage. Fatty liver syndrome, caused by an energy and protein imbalance, can be prevented through a balanced diet and treated by supplementing specific nutrients.
Cloacal prolapse can be minimized by optimizing housing conditions and ensuring adequate space and resources for the flock. Osteomalacia, a nutritional disease resulting in soft bones, can be prevented by providing a high-calcium diet and avoiding cage confinement.
Vitamin E deficiency can be addressed through the use of fresh feeds and antioxidants to maintain brain tissue health and embryo development. Ascites syndrome, a metabolic disease in broilers, can be reduced by addressing genetic factors, improving ventilation, and considering feed restriction.
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