Sudden death syndrome

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Sudden death syndrome; morte subita; acute death syndrome; dead in good condition; heart attack; flip-over disease Dr.Kedar. Karki M.V.St Preventive Veterinary Medicine Post-Mortem /Parasitology Unit Central Veterinary Laboratory Tripureshwor

Transcript of Sudden death syndrome

Sudden death syndrome; morte subita; acute deathsyndrome; dead in good condition; heart attack; flip-overdisease

Dr.Kedar. KarkiM.V.St Preventive Veterinary Medicine

Post-Mortem /Parasitology UnitCentral Veterinary Laboratory

Tripureshwor

Introduction

Flip-over disease has been reported in most areas of the world that intensively raise broilers. Young, healthy, fast-growing broiler chickens die suddenly with a short, terminal, wing-beating convulsion. Many affected broilers just “flip-over” and die on their backs; 60-80% are males. The condition is uncommon or unrecognized when low-density feed is used and the ratio of feed intake to weight gain is >2.5 at 6 wk, or when broilers take 8 wk to reach 2 kg.

Etiology and Epidemiology:

The cause is unknown but probably is a metabolic disease related to carbohydrate metabolism, cell membrane integrity, and intracellular electrolyte balance. Death likely results from ventricular fibrillation. The modern broiler tends to overeat and continues to grow rapidly while maintaining a low feed-to-gain ratio. Flip-over appears to be related to high carbohydrate intake. It is not known whether a genetic predisposition exists.

Etiology and Epidemiology:

Incidence has been increasing since the condition was first recognized, likely at least in part because of continuing improved growth rate of ~5% in broilers. Mortality may now average 2% in North America; in some all-male flocks, mortality is >4%. In flocks with good management and disease control, it may be the most important cause of death, responsible for up to 70% of the flock mortality.

Table: 1. Epidemiology of Affected flock in Kathmandu Valley with sudden Death Syndrome in Month of August 2008 :

Duration no.of farm Population at risk

Morbidity(%)

Mortality(%)

No. of samples examined

First week 22 16620 4250 (25.57%)

369(2.22%)

44

Second week

14 15450 1235(7.99%)

232(1.50%)

28

Third week

20 10260 848(8.26%)

157(1.53%)

40

Fourth week

30 15700 2380(15.16%)

149(0.94%)

60

Fifth week 13 16450 4750(30%)

1650(0.3%)

26

Sixth week 12 18850 4550(25%)

876(0.19%)

24

Total 111 93330 18013(17.01%)

3436 (1.56%)

222

Clinical Findings:

Broilers show no premonitory signs. They appear healthy and may be feeding, sparring, walking, or resting, but suddenly extend their necks, gasp or squawk, and die rapidly with a short period of wing beating and leg movement, during which they frequently flip onto their backs. They also may be found dead on their sides or breasts.

Clinical Findings:

Flip-over may occur as early as day 3 and may continue until 10-12 wk in roaster flocks. The time of peak mortality varies but usually is between days 12 and 28, although it can be as early as day 9. It may occur after day 28, particularly if growth is restricted in young broilers. Mortality of 0.25%-0.5% per day can occur for 1-3 days.

Post-mortem Lesions:

. Postmortem examination of birds that died of sudden death syndrome revealed showed no outstanding gross pathology. All birds were well fleshed, with muscle edema and general pulmonary congestion and edema. Feed was present along the entire digestive tract and the gall bladders of birds were distended usually filled with bile.

Post-mortem Lesions:

The liver was pale to yellow enlarged molted appearance and kidneys were usually slightly congested and have patchy sub capsular hemorrhage. Usually, the proventriculus contains a milky fluid with hemorrhagic patches and intact food particles are present in gizzard.

Post-mortem Lesions:

Crop in some bird was full with liquid intact food particles. Intestine was ballooning in appearance with thick mucous filled ingesta was present .Congestive spleenomegally was observed in almost all birds. Bursa was almost normal to atrophid.

Post-mortem Lesions:

The ventricles of the heart are contracted (but not hypertrophied), and the atria are dilated and blood filled. The lungs are congested and frequently edematous;

Laboratory Finding of Mycobiota and Microbiota of Postmortem Tissue samples:

A total 222 tissue samples of lung, liver, spleen, proventriculus and gizzard, were collected during postmortem examination and were subjected for both bacterial and mycological culture. Results of microbiological examination done are given in Table 2.

Table: 2.

No. of samples

Bacterial isolated

Fungi isolated Positive no

negative no

111 E.coli,Streptococcus,Staphylococcus

70 41

111 Aspergillus,Penicillium,Candida

80 31

222 150 72

Diagnosis:

Good broilers found dead on their backs may be assumed to have died of flip-over because that position is rare in death from other causes except cardiac tamponade, asphyxia, and ascites syndrome ( Ascites Syndrome). Good birds on their sides or breasts, scattered in a random fashion in the pen also usually are considered to be dead from flip-over. Diagnosis is supported by the full GI tract (particularly the full intestine); the large, pale liver; the large, normal bursa; the contracted ventricles and dilated, blood-filled atria; the lung congestion and edema; and the lack of pathological lesions.

DDX

Sudden death in turkeys can be caused by choke, aortic rupture ( Dissecting Aneurysm), focal (obstructive) granulomatous pneumonia, or by hypertrophic cardiomyopathy ( Round Heart Disease Of Turkeys) with lung congestion and edema, splenomegaly, and perirenal hemorrhage ( Perirenal Hemorrhage Syndrome Of Turkeys: Introduction).

Prevention and Control:

Activity caused by bright light (particularly sunlight), noise, and other disturbances may increase the incidence. After the first 3-4 days, low-intensity or low-intensity intermittent lighting should be used, and broilers should be disturbed as little as possible. Long, dark periods (18 hr dark for 3-4 wk) after the first 3-4 days reduce flip-over. Slowing growth rate by feeding a less dense or lower protein ration or by reducing feed intake by 15-20% may prevent the condition.

Treatment and Preventive measure given to the rest of birds in flock:

All birds remaining in flocks were subjected to restricted feed up to 8-10%, and feed to twice daily only. Supplementation with glucose containing electrolyte, liquid toxin binders, immunomodulator, and simple broad-spectrum antibiotics were provided in water. Vitamin B complex supplementation was totally withdrawn. All birds remaining in all affected farms responded well to the above management and there were marked improvement in the overall condition of the flock.

Discussion.

Sudden Death Syndrome (SDS) is an acute heart failure disease that affects mainly male fast growing chickens that seem to be in good condition. Although a common condition in fast growing birds, the pathogenesis remains unclear (Ononiwu et. al. 1979). Cardiac arrhythmias are involved in the pathogenesis of SDS with ventricular arrhythmias (VA) being the most common observation representing premature ventricular contractions and fibrillation (Olkowski and Classen, 1997; 1998).

Discussion.

It has been reported that broilers fed with high vitamin D3 diet above the recommended levels in an attempt to prevent commonly occurring leg problems were 2.5 fold more likely to succumb to acute heart failure and die of SDS (Nain et. Al. 2007).

Discussion.

SDS was also experimentally induced by feeding diets containing the mycotoxin moniliformin that resulted to cardiac injury with subsequent alterations in cardiac electrical conductance (Reams et al, 1997) suggesting the possible role of chronic mycotoxicosis to the causation of SDS.

Discussion.

Other implicated causes of SDS include continuous artificial lighting (Ononiwu et al, 1979b), deviations in dietary calcium and phosphorus (Scheideler et al, 1995), feeding crumble-pellet diets (Proudfoot et al, 1982), dietary fat content (Rotter et al, 1985) and feeding frequency Bowes et al, 1988). The latter recommendation of restricted feeding supports well the previous observation that abdominal fat deposition increases the risk of SDS such that restrictions on calorie:protein ratio decreases the incidence of SDS (Mollison et al, 1984).

Discussion.

SDS seems to worse when Vitamin B complex are in excess.

Among many drugs used in poultry anticoccidial drugs are in question?

There are evidence of higher SDS mortality when these drugs are being used

Recomendetion

The present investigation indicates that broilers in good body weight condition when not harvested timely and remain in poultry shade for prolonged periods suffer stressful events and even sudden death. Also, it is possible that the increased humidity and hot season favors the growth of mold and fungus in stored feeds increasing the risk of birds to mycotoxicosis. This incidence of sudden death syndrome in birds in Kathmandu Valley was reported for the first time and needs to be investigated further.

Review of literature

Sudden death syndrome (SDS) is the name given todeath in healthy, fast-growing, commercial broilers thatdie suddenly. It has been recognized as a specific

conditionsince the 1950s when broiler chickens began to begrown commercially in large numbers. SDS occurs in allcountries where broilers are grown rapidly under

intensiveconditions (Jackson et al., 1972; Volk et al.,1974; Julian,

1996a). In healthy flocks it is the most frequent cause of death with up to 4% mortality in some all-male flocks (Julian and Bowes, 1984; Julian, 1986).

Review of literature

Young, healthy, fast-growing boiler chickens die suddenly while standing, walking, sparring or feeding.They die with a short terminal wing-beating convulsion

and frequently are found on their back. SDS can start as

early as day 3, and continues for 8–12 weeks with the

highest losses between days 9–22. The faster-growing

males make up approximately two-thirds of affected

birds (Julian, 1986; Newberry et al., 1987).

Review of literature

There are no diagnostic lesions in broilers that have

died from SDS, but the sudden death in a previously healthy broiler (Bowes and Julian, 1986, 1988) would suggest that death is the result of ventricular fibrillation (Julian and Bowes, 1987; Greenlees et al., 1989; Olkowski and Classen, 1997a; Blanchard et al., 2002).

Review of literature

There is a specific association with feed intake. SDS can be prevented completely by restricting feed intake to 75% of what would be eaten free-choice (Bowes et al.,1988). There is some evidence that carbohydrate availability and type, rather than protein or fat are part of the pathogenesis (Julian and Bowes, 1984).

Review of literature

Much of the published literature on SDS relates to feeding trials to try to induce or prevent SDS (Rotter et al., 1988; Olkowski and Classen, 1997b). Except for the use of mash feed or other methods that reduce feed intake or growth rate there is little evidence that feedstuffs or vitamins have an effect on the incidence of SDS in commercial broilers on the farm.

Review of literature

The confirmation of SDS at necropsy is difficult sincethere are no lesions that are pathognomonic. The

condition was first reported as being caused by lung oedema

(Hemsley, 1965) and the lungs are oedematous, except in

freshly dead birds (Julian, 1996a). The bursa is large and

normal, which again suggests that the bird was healthy

immediately prior to death. Heart ventricles are contracted,and atria are dilated and filled with blood, a

significant observation.

Review of literature

There are no specific gross or histopathological lesions that would distinguish broilers that have died from SDS from a healthy broiler that had been euthanased. Changes that have been described(Ononuwu et al., 1979a; Riddell and Orr, 1980; Greenleeset al., 1989; Riddell, 1993; Grashorn, 1994; Crespo and Shivaprasad, 2003) are artifact,

Review of literature

post-mortem change or incidental findings (congestion, haemorrhage, lymphoid and myeloid foci) that might be present in any normal healthy broiler that has been euthanased or that dies suddenly from hypoxia or hyperthermia (Julian 1996b). It is unlikely that broilers that are ‘found dead on arrival’ at the processing plant have died from SDS. SDS is probably a metabolic disease, in which an imbalance of metabolites or electrolytes results in ventricular fibrillation.

Review of literature

Lowering energy intake by changing feed texture or density (mash), or management methods such as feed restriction or long dark periods (Classen and Riddell, 1989) will reduce mortality from SDS. Increased mortality is associated with crowding, unusual activity or bright light (Ononuwu et al., 1979b), particularly sunlight, so low-intensity light is recommended and the flock should be disturbed as little as possible

Review of literature

Sudden death syndrome in broiler breeders, reported from Australia, is a different condition occurring in hens at the commencement of production. It is associatedwith low dietary potassium and hypokalaemia (Hopkinson, 1991).

Reference

Production and growth related disorders and other metabolic diseases of poultry – A review Richard J. Julian *Department of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, Ont., Canada N1G 2W1Accepted 28 April 2004TheVeterinary Journal www.elsevier.com/locate/tvjlThe Veterinary Journal 169 (2005) 350–369