Sudden Death in Broilers

Sudden death syndrome (SDS) is a condition in which fast growing broiler chicks die suddenly with no apparent causes. It has developed in to a major problem for broiler industry in many parts of the world. Broiler chicken of all ages are affected starting as early as 2 days of age and continues up to marketable age. Peak mortality usually occurs between 3^rd and 4^th week of age with more affect being observed in male birds than the females. There is usually a short wing beating, convulsions prior to death. Majority of affected broilers are found dead lying on their backs. This condition is often referred to as "flip-over disease." Lung oedema is a prominent PM lesion. There is no proper treatment and preventive measures to control SDS.

The major factors include faulty management, nutrition, metabolic disorders and fast growth.

Sudden death syndrome (SDS) is a condition affecting fast growing broiler chicken especially males. The normal incidence is 1.5-2 % of the flock affecting birds from 21-28 days of age. Affected birds appear healthy, well fleshed and invariably have feed in their digestive tract. Death occurs within 1-2 minutes with birds most frequently being found dead on their backs. There are few changes in gross pathology. The heart may contain blood clots that are likely post-mortem in origin and ventricles are usually empty. Diagnosis is usually by exclusion of other diseases. Lungs are often oedematous. There are no specific changes in the tissues or blood profile. The condition is precipitated by fast growth rate and so conversely it can be prevented when ionophore anticoccidials are used or if the diet contains a readily available carbohydrate source such as glucose.

The condition can best be prevented or reduced in incidence by inducing a period of initial slow growth rate. This can be achieved by reducing day length, physical feed restriction and/or the use of low nutrient dense diets. However there is no proper treatment and preventive measures for control of SDS but incidence can be reduced by proper management techniques.

Sudden death syndrome is a cause of mortality in apparently normal fast growing broiler chicken. Birds often males are usually found dead on their backs with wings outstretched. The condition rarely occurs in layer birds although there have been reports of similar type deaths in adult meat breeders. The disease is basically of a metabolic origin but genetic, environmental and nutritional factors also play an important role.

Broilers that die of SDS show no specific abnormalities. Birds usually healthy males an above average body weight are mostly affected. Immediately prior to death, they appear normal and are often seen feeding, drinking and walking. Birds extend their neck, squawk and due to wing beating and leg extension quickly work themselves onto their backs. Most poultry bird farmers describe the condition as a heart attack. Death occurs within minutes although birds can be revived with limited long-term success if they are vigorously massaged during the early stages of the attack.

Dead birds are always well fleshed with oedema and general pulmonary congestion. Feed is present along the entire digestive tract and the gall bladder is usually empty. The liver and kidneys may be slightly enlarged and have patchy sub capsular haemorrhage. The heart may contain clotted blood especially in the atria, although the ventricles may appear slightly hypertrophied. The pathological lesions seen in SDS are associated with some type of vascular disturbance. The process likely starts with circulatory lesions manifested by increased capillary permeability followed by the congestion of many tissues. There seems to be some discrepancy regarding the occurrence of enlarged and/or haemorrhagic livers. Hypertrophied livers may relate to fatty liver and kidney syndrome showing pale fatty liver and in their birds. This suggests that the fatty liver syndrome may predispose to SDS, although a common diagnosis with an empty intestine since affected birds rarely eats as the condition progresses.

A number of studies have been aimed at correlating changes in tissue mineral, electrolyte and fat extent. There is a small but statistically significant reduction in the K content and an increase in the Na+ content of heart tissue in the affected birds. SDS birds show elevated levels of liver Ca and reduced Fe in lungs and kidneys. The heart, lungs and especially the liver also exhibit reduced levels of dry matter. The elevated levels of liver Ca is of interest in relation to SDS condition occurring in broilers.

Affected male birds consistency exhibit elevated blood glucose compared to female birds. Similarly there is increase in the blood uric acid and lactate dehydrogenase levels. Conversely the higher level of this enzyme suggests higher concentrations of substrate and so perhaps elevated lactate levels.

A number of factors have been studied with a view to isolate causative agents in SDS. When reviewing these factors, it must be remembered that SDS is a condition exclusively seen in very fast growing birds. Most studies have investigated diet texture and composition as there are numerous nutritional and physiological factors which may lead to SDS. The level and type of fat in the diet has a significant influence on the incidence of SDS. Similarly sudden noising and high intensity lighting appears to increase the incidence of SDS. The possible factors which may be responsible for the occurrence of sudden death syndrome are as follows:

Since SDS occurs only in fast growing birds that are assumed to be eating to near physical capacity. Physical feed restriction reduces the rate of mortality by 75% than the birds maintain on free choice feeding programme.

In broilers pelleted feed is extremely used. It has significantly higher digestibility when compared to mash type feed. Thus there is fast growth among these birds. Hence incidence of sudden death syndrome is increased when birds are fed with pelleted diets. It has been observed that certain toxic substances by pelleting protein ingredients which predispose to SDS.

The fast growing birds that are to be assumed to be eating to near physical capacity are prone to sudden death syndrome. Mortality  due  SDS is more than doubled when glucose is the predominant energy source compared to 2.1% mortality when fat is a major contributor or 2.5% when corn starch is used. A diet which is marginally deficient in the vitamin biotin may cause sudden unexpected death of young broiler chicken when exposed to stress.

Dietary protein seems to have little effect on SDS. It has been observed that the meat meal supplies some unidentified factor that provides protection against SDS.

Sudden death syndrome may relate in some way to mineral availability suggesting a potential hypomagnesaemia tetany caused by nutrient interaction.

Sudden death syndrome incidence is increased when biotin pyridoxic acid and thiamine are marginally present in the diet. Biotin has perhaps been singled out most frequently as a possible factor in sudden death syndrome. Similarly SDS/fatty liver kidney syndrome seems to worse when biotin is marginal while as the other B-complex vitamins are in excess.

Lactate accumulates when there is inadequate oxygen for normal aerobic metabolism. Production of lactate rather than pyruvate due to anoxia leads to acidosis. Broilers receiving diet high in glucose flip within 30 minutes of dosing with lactic acid while birds receiving a diet high in corn-starch take over 1.5 hours to flip.

A period of short day length during early growth has recently been shown to be benefited in reducing SDS in broilers. There is about 30-60% reduction in incidence of SDS when broilers are subjected to 6 hours light from 3-4 days or various incremental programmes of 6 hour increasing to 23 hour over the 35 day period. Early growth rate is reduced because birds have less time to eat thus reducing the incidence of SDS.

Boiler chickens are generally reared at a considerably higher stocking density. Such rearing conditions may act on the birds as a stress causing functional disorders in their organs including the heart.

Since heart function is obviously implicated in SDS a number of pharmaceutical products have been tested. Among them anticoccidial drugs when added to the diet cause more mortality due to SDS. It has been observed that SDS was substantially higher when birds are fed diets containing ionophores namely monensin and maduramicin ammonium. Generally ionophore compounds increase the movement of metal ions across the cell membranes.

Stress is the main contribute towards the pathogenesis of SDS. When the course of disease is acute there is vascular disturbance which starts with circulatory lesions manifested by increased permeability of the peripheral circulatory system. This physiological permeability caused by short term increase in blood pressure is usually reversible. However when the stimulus surpasses the tolerance level, irreversible changes occur not only in the wall of the blood vessel but also in the tissue which they supply. In SDS death appears to be caused by heart damage which leads to lung oedema, so that the chicks are unable to breath sufficient fluid is lost from the circulatory system into the lung tissue spaces causing peripheral circulatory failure. The histological changes of intense congestion and oedema in the lungs result in the tissue parenchyma becoming separated from fresh blood supply leading to hypoxia. Vascular congestion is a constant feature of most of the tissue examined microscopically particularly the lungs where much of the effective air spaces are lost because of engorgement of pulmonary capillaries. Lymphocytic infiltration and inflammation involving the secondary bronchi and the presence of oedema in the alveoli considerably reduce gaseous exchange thus enhancing respiratory distress.

Diagnosis is based on the history of sudden death, gross and microscopic pathology and no evidence of other disease. Blood profile and tissue analysis has little role in confirmative diagnosis.

E)  Prevention and control:

There is no single treatment or preventive measure to control the sudden death syndrome. The condition is undoubtedly related to fast growth rate and as such managemental technique to reduce the early maximum genetic potential for growth offer the best preventive scenario.

1)  Broiler are most commonly fed diets in pelleted form to maximise feed consumption but if same diet in crumble form consume less to reduce early growth in chicks.

2)   Use diets with 5-7% less nutrient density diet, thereby tampering early fast growth rate up to 18-120 days.

3)   Feed a low protein/low energy diet during first 14 days to reduce the oxygen demand.

4)   Protein supplements with soya bean meal, canola meal and fish meal which are not pelleted decrease the incidence of SDS.

5)   All birds can be subjected to restricted feed up to 8-10% and fed twice daily only.

6)   Supplement the birds with glucose containing electrolytes.

7)   Feed liquid toxin binders and immunomodulators.

8)   Provide only simples broad spectrum antibiotics through water.

9)    Follow a step down lighting programme from 5-18 day period of growth.