SUDDEN DEATH SYNDROME IN POULTRY

SUDDEN DEATH SYNDROME IN POULTRY

ETIOLOGY

The cause is unknown, but it is thought to be a metabolic disease related to carbohydrate metabolism, lactic acidosis, loss of cell membrane integrity, and intracellular electrolyte imbalance. Recent studies link this disease to cardiac arrhythmias. Stress is the most likely trigger of cardiac arrhythmias in broilers, which predisposes the bird to death from ventricular fibrillation.

OCCURRENCE

Sudden death syndrome may occur as early as day 3 and may continue until 10–12 week in roaster flocks. Mortality usually peaks between days 12 and 28, although it may peak as early as day 9. If growth is restricted early, it may peak only after day 28. Males are more affected than female. It is common in healthy broiler with high growth rate and high calorie in feed.

PATHOGENESIS

Broilers are fast growing birds having a large proportion of muscles compared to visceral organs which are not proportionally developed leading to inadequate supply of oxygen resulting in hypoxia and lack of aerobic metabolism. Production of lactate in high amount causes increase in lactic acid resulting into systemic acidosis, change in blood pH, cardio-vascular system disturbances leading to cardiac arrhythmia. Overload to heart cause cardiac hypertrophy and lead to cardiac arrhythmias and then death due to ventricular fibrillation if high amount of feed is continued.

CLINICAL SIGN

There are no specific gross lesions. Dead birds are well fleshed, have an empty or partially filled crop, and feed in the gizzard. The abdomen is distended because the bird is fat and the intestines are filled with ingest, indicating per acute death. The muscles are mottled red and white as a result of focal congestion, and the organs are moderately to severely congested. There may be small hemorrhages in the liver and kidney. Although the ventricles of the heart are contracted, there is no sign of hypertrophy, and the atria are dilated and blood filled. The lungs are congested and frequently edematous; however, pulmonary edema increases with time after death and is not prominent in broilers that are examined within a few minutes of death. The gallbladder may be small or empty, because feed intake is normal up until the time of death.

DIAGNOSIS

Diagnosis is supported by necropsy findings if there is a lack of obvious pathology (a digestive tract filled with ingesta, contracted ventricles, dilated and blood-filled atria, lung congestion, and edema). The presence of characteristic microscopic lesions in cardiomyocytes and subendocardial Purkinje cells is helpful in confirming the diagnosis.

PREVENTION

The incidence of sudden death syndrome can be minimized by slowing the growth rate of broilers, particularly during the first 3 wk of life. Growth rate can be moderated by controlling nutrient intake. This can be accomplished by reducing the number of hours of light per day, reducing the energy and protein level in the diet, or limiting the amount of feed provided.

DIFFERENTIAL DIAGNOSIS

Cardiac tapenade

Asphyxia

Ascites

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