Clinical Laboratory Investigation of Involvement of Systematic Mycosis in Outbreak of Sudden Death Syndrome in Broiler Chicken in Kathmandu Valley Nep
Clinical Laboratory Investigation of involvement of Systematic mycosis in Outbreak of Sudden Death Syndrome in Broiler Chicken in Kathmandu Valley Nepal
Dr.Kedar Karki , Central Veterinary Laboratory in Kathmandu Tripureshwor, Nepal
Dr Esmeraldo M. Cabana, Veterinary Pathologist, Animal Health Laboratories, Diagnostic Services Branch Department of Primary Industries and Water, Tasmania, Australia,
ABSTRACT:
The incidence of sudden death of broiler birds above 40 days suddenly increased in the month of August 2008 in Kathmandu valley. Birds that were presented for post-mortem examination in Central Veterinary Laboratory Tripureswor Kathmandu were usually found dead on their backs with wings out-stretched. Incidence rate was recorded between 1.5 to 2.5% of the flock. The mean mortality due to sudden death syndrome was 1.3 – 9.6% and mortality usually occurs after 6 week of age. Postmortem examination of birds that died of sudden death syndrome revealed following major outstanding gross pathology. All birds were well fleshed, with muscle oedema and general pulmonary congestion and oedema. Feed was present along the entire digestive tract and the gall bladders of birds were usually filled with bile. The liver was pale to yellow enlarged molted appearance and kidneys were usually slightly congested and have patchy subcapsular haemorrhage. Usually, the proventriculus contains a milky fluid with hemorrhagic patches and intact food particles are present in gizzard. Crop in some bird was full with liquid intact food particles. Intestine was ballooning in appearance with thick mucous filled ingesta was present .Congestive splenomegaly was observed in almost all birds. Bursa was almost normal to atrophid.
Penicillium spp., Aspergillus spp., Candida spp, E.coli, Streptococcus spp. and Staphylococcus spp. were the usual organisms isolated from culture samples of liver, lung, spleen and proventriculus. Reduction of mortality was achieved by feed restriction, supplementation of glucose containing electrolyte, liquid toxin binder, Immunomodulaters, acidifier and antibiotic therapy. The condition seems to be related to fast growth rate. A practical approach seems to use diets with 5-7% reduction in nutrient density. The provision of more space and supportive treatment with anti-stress medicine may also be beneficial.
Key word:
Sudden death syndrome , broiler birds, Kathmandu Valley, Nepal
Background of outbreak of Sudden Death Syndrome in KathmanduValley.
From the first week of August 2008 there sudden increase in mortality of broilers above 6 week age (Table 1). There are no premonitory signs. Just before death, birds appear normal and it is common to observe the birds feeding, drinking or walking normally. Then suddenly, affected birds exhibit clinical signs such as extending their neck, squawk and start wing beating as well as leg extension before falling back on their back and die suddenly.
Table: 1. Epidemiology of Affected flock in KathmanduValley 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
Postmortem finding of SDS birds:
Postmortem examination of birds that died of sudden death syndrome revealed showed no outstanding gross pathology. All birds were well fleshed, with muscle oedema and general pulmonary congestion and oedema. Feed was present along the entire digestive tract and the gall bladders of birds were usually filled with bile. The liver was pale to yellow enlarged molted appearance and kidneys were usually slightly congested and have patchy subcapsular haemorrhage. Usually, the proventriculus contains a milky fluid with hemorrhagic patches and intact food particles are present in gizzard. Crop in some bird was full with liquid intact food particles. Intestine was ballooning in appearance with thick mucous filled ingesta was present .Congestive splenomegaly was observed in almost all birds. Bursa was almost normal to atrophid.All these post mortem observations conform to the descriptions of the syndrom made by Ononiwu et. al. (1979).
Laboratory Finding of Mycobiota and Microbiota of Postmortem Tissue samples:
A total 86 tissue samples of lung, iver, speen, peoventriculus 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
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.Antibiotics like tylosin,inroxin,cholertin,anticoccicidal drugs and 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). 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). 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. Due to the effect of chronic mycosis Proventriculi lose their normal flusiform shape and normal constriction at the junction with gizzard are diffusely enlarged and have a thickened and turgidwall. Thickening of the wall is more marked upon incising the proventriculus.The proventricular glands protrude irregularly from the mucosal surface, lose their normal pattern and contain milky fluid that could be expressed with slight pressure. The gizzard is often smaller than normal and flabby. The gizzard peels off easily with haemorrhagic ulceration of the gizzard wall(Dr. Avinash Dhawale) 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). The SDS seems to be worse when biotin is marginal and other Vitamin B are in excess. Among many drugs used in poultry the role of anticoccidial drugs perhaps have received more attention than other drugs. There is some evidence of higher SDS mortality when anticoccidial drugs are used. (Dr.H.A.Upendra.www.vetcareindia.com/halchal_Sudden death Syndrome.htm 2008).
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 is indicated by the presence of feed and fluid filled crop,pale yellowish coloration of liver hepatomegaly and full distended gall bladder,milky fluid with hemorrhagic patches in muscular junction of gizzard and proventriculus yellowish tinge color of gizzard surface and intact feed in gizzard seems to be exaggerated the syndrome which has not been reported by any previous worker. This incidence of sudden death syndrome in birds in Kathmandu Valley was reported for the first time and needs to be investigated further.
Dr.Kedar Karki M.V.St. Preventive Veterinary Medicine
Senior Veterinary Officer
Central VETERINARY lABORATORY
Tripureshwor Kathmandu
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Clinical Laboratory Outbreak of Sudden Death Syndrome in Broiler Chicken in Kathmandu Valley Nepal
Clinical Laboratory Outbreak of Sudden Death Syndrome in Broiler Chicken in Kathmandu Valley Nepal
1: Dr.Kedar Karki Senior Veterinary Officer
Central Veterinary Laboratory in Kathmandu Tripureshwor, Nepal
2: Dr Esmeraldo M. Cabana, Veterinary Pathologist,
Animal Health Laboratories, Diagnostic Services Branch Department of Primary Industries and Water, Tasmania, Australia,
ABSTRACT:
The incidence of sudden death of broiler birds above 40 days suddenly increased in the month of August 2008 in Kathmandu valley. Birds that were presented for post-mortem examination in Central Veterinary Laboratory Tripureshwor Kathmandu were usually found dead on their backs with wings out-stretched. Incidence rate was recorded between 1.5 to 2.5% of the flock. The mean mortality due to sudden death syndrome was 1.3 – 9.6% and mortality usually occurs after 6 week of age. There are no outstanding gross lesions on post mortem examinations, except for muscle oedema, pulmonary, renal and liver congestion, and congestive spleenomegally.
Penicillium spp., Aspergillus spp., Candida spp, E.coli, Streptococcus spp. and Staphylococcus spp. were the usual organisms isolated from culture samples of liver, lung, spleen and proventriculus. Reduction of mortality was achieved by feed restriction, supplementation of glucose containing electrolyte, liquid toxin binder, Immunomodulater, acidifier and antibiotic therapy. The condition seems to be related to fast growth rate. A practical approach seems to use diets with 5-7% reduction in nutrient density. The provision of more space and supportive treatment with anti-stress medicine may also be beneficial.
Key word:
Sudden death syndrome, broiler birds, Kathmandu Valley, Nepal
Background of outbreak of Sudden Death Syndrome in KathmanduValley.
During the first week of August 2008 there sudden increase in mortality of broilers above 6 week age (Table 1). There are no premonitory signs. Just before death, birds appear normal and it is common to observe the birds feeding, drinking or walking normally. Then suddenly, affected birds exhibit clinical signs such as extending their neck, squawk and start wing beating as well as leg extension before falling back on their back and die suddenly.
Table: 1. Epidemiology of Affected flock 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
Total
86
58030
8713
(15.01%)
907
(1.56%)
172
Postmortem finding of SDS birds:
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 are usually empty. The liver and kidneys were usually slightly congested and have patchy sub capsular hemorrhage. Usually, the proventriculus contains a milky fluid, and intact food particles are present in gizzard. Congestive spleenomegally was observed in almost all birds. All these post mortem observations conform to the descriptions of the syndrome made by Ononiwu et. al. (1979).
Laboratory Finding of Mycobiota and Micro biota of Postmortem Tissue samples:
A total 86 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
86
E.coli,
Streptococcus,
Staphylococcus
59
27
86
Aspergillus,
Penicillium,
Candida
58
28
172
117
55
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, Immunomodulater, 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.
Result and 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). 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). 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. 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).
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.
References.
Bowes VA, R.J. Julian, S. Leeson and T. Stirtzinger (1988). Effect of feed restriction on feed efficiency and incidence of sudden death syndrome in broiler chickens. Poultry Science 67(7):1102-4
Mollison B., W. Guenter,and B.R. Boycott (1984). Abdominal fat deposition and sudden death syndrome in broilers: the effects of restricted intake, early life caloric (fat) restriction, and calorie: protein ratio. Poultry Science 63(6):1190-200
Nain S, B. Laarveld B, C. Wojnarowicz C, and A.A. Olkowski (2007). Excessive dietary vitamin D supplementation as a risk factor for sudden death syndrome in fast growing commercial broilers. Comparative biochemistry and physiology. Part A, Molecular & Integrative Physiology 148(4):828-33
Olkowski, A.A., C. Wojnarowicz, S. Nain, B. Ling, J. M. Alcorn, and B. Laarveld (2008). A study on pathogenesis of sudden death syndrome in broiler chickens. Research in Veterinary Science 2008 Aug;85(1):131-40
Ononiwu, J.C., R.G. Thomson, H.C. Carlson, and R.J. Julian. (1979). Pathological Studies of “Sudden Death Syndrome” in Broiler Chickens. Canadian Veterinary Journal 20(3): 70–73
Ononiwu, J.C., R.G. Thomson, H.C. Carlson, and R.J. Julian. (1979b). Studies on effect of lighting on “Sudden death syndrome” in broiler chickens. . Canadian Veterinary Journal 20(3):74-7
Olkowski A.A. and H.L. Classen (1998). High incidence of cardiac arrhythmias in broiler chickens. Zentralblatt für Veterinärmedizin. Reihe A 45(2):83-91
Olkowski A.A. and H.L. Classen (1997). Malignant ventricular dysrhythmia in broiler chickens dying of sudden death syndrome. Veterinary Record. 15;140(7):177-9
Proudfoot FG, H.W. Hulan, K.B. McRae (1982). The effect of crumbled and pelleted feed on the incidence of sudden death syndrome among male chicken broilers. Poultry Science 61(8):1766-8
Reams R.Y, H.L. Thacker, D.D. Harrington, M.N. Novilla, G.E. Rottinghaus, G.A. Bennett , and J. Horn (1997). A sudden death syndrome induced in poults and chicks fed diets containing Fusarium fujikuroi with known concentrations of moniliformin. Avian Disease 41(1):20-35
Rotter B, W. Guenter, and B.R. Boycott (1985). Sudden death syndrome in broilers: dietary fat supplementation and its effect on tissue composition. Poultry Science 64(6):1128-36
Scheideler SE, D.V. Rives, J.D. Garlich, and P.R. Ferket (1995). Dietary calcium and phosphorus effects on broiler performance and the incidence of sudden death syndrome mortality. Poultry Science 74(12):2011-8
Acknowledgment:
We would like to thank Dr. Dev Raj Adhikari SVO and incharge of Central Veterinary Hospital Tripureshwor, Kathmandu for providining early indication of problem. Thanks are due to Dr.Pragya Koirala Veterinary Officer Mr.Bal Bahadur Kunwar Srnior Vet.Technician and Mr.Bhimsen Adhikari Vet.Technician of Microbioly Unit of Central Veterinary Laboratory for doing the microbiology works, Dr. Lin Tsang Long, Avian Pathologist, and Dr. Stephen B. Hooser, Stephen, Head, Toxicology Section and Assistant Director, Animal Disease Diagnostic Laboratory Purdue University U.S.A for their critique of the manuscript. Dr.Poornima Manandhar, Chief of CVL Tripureshwor deserves special thanks from this investigation team.
Dr.Kedar Karki.M.V.St. Preventive Veterinary Medicine CLSU Philippines
Life would be much easier if any problem would have only one cause. We would have a lot less problems finding a solution. In the case of acne, we could easily locate the source of the condition and find an effective cure to get rid of it. Unfortunately the causes for sudden acne breakouts are various and cannot be associated with any particular instance. The fact that this disease or condition varies from one person to another makes it rather unclear about what causes sudden acne breakouts.
The Underlying Process
Although the actual cause of acne is quite unclear, the underlying process behind sudden acne breakouts is getting clearer everyday. Doctors and researchers are working everyday to better understand the real reasons behind sudden acne breakouts. The process is the following, the skin of most acne sufferer often produce an excess of oil by the sebaceous gland. This excess will then mix with the dead skin blocking the pores of the skin at the level of the hair follicles and thus giving rise to pimples.
When studying the cause of acne we may have to look at hormones as another possible factor responsible for sudden acne breakouts. This is not the case for everybody, but for some especially during the puberty, the body increases is hormones production and causes the glands to get over stimulated leading to acne in some cases.
There is no doubt that hormones are, in some cases, are a contributing factor to what causes acne. This is especially true for teenagers and pregnant women. There are also other factors that are contributing to sudden acne Breakouts like stress, heredity and even medication.
So the causes for sudden acne breakouts are different from person to person. This is what makes it so difficult to pinpoint the exact causes for sudden acne breakouts, and thus finding the proper cures for it. There many myth about this condition that are believed to be the causes of sudden acne breakouts. Things such as:
- Eating chocolate
- Greasy Food
- Other dietary foods
You should know that although food can play a role in your acne problem, it is not the causes for sudden acne breakouts. Of course, you will certainly have a lot more problem eliminating your acne problem if you eat French fries everyday. Other mythical causes would include such things as:
- Dirt
- Touching of the skin
- And makeup
The simple fact is this: The causes for sudden acne breakout cannot be one particular thing or habit in each and every person who suffers from this condition.
Clinical-laboratory Investigation of Involvement of Systemic Fungus in Outbreak of Sudden Death Syndrome in Broiler Chicken in Kathmandu Valley Nepal
Clinical-Laboratory Investigation of Involvement of Systemic Fungus in Outbreak of Sudden Death Syndrome in Broiler Chicken in Kathmandu Valley Nepal
Dr.Kedar Karki
Central Veterinary Laboratory in Kathmandu Tripureshwor, Nepal
1: Introduction
2: Material and Methods.
3: Result and Discussion.
4: Conclusion:
Introduction:
The incidence of sudden death of broiler birds above 40 days suddenly increased in the month of August-September 2008 in Kathmandu valley. Birds that were presented for post-mortem examination in Central Veterinary Laboratory Tripureswor Kathmandu were usually found dead on their backs with wings out-stretched. Incidence rate was recorded between 1.5 to 2.5% of the flock. The mean mortality due to sudden death syndrome was 1.3 – 9.6% and mortality usually occurs after 6 week of age. There are no outstanding gross lesions on post mortem examinations, except for muscle oedema, pulmonary, renal and liver congestion, and congestive spleenomegaly.
ABSTRACT:
Penicillium spp., Aspergillus spp., Candida spp, E.coli, Streptococcus spp. and Staphylococcus spp. were the usual organisms isolated from culture samples of liver, lung, spleen and Proventriculus. Reduction of mortality was achieved by feed restriction, supplementation of glucose containing electrolyte, liquid toxin binder, Immunomodulaters, acidifier and antibiotic therapy. The condition seems to be related to fast growth rate. A practical approach seems to use diets with 5-7% reduction in nutrient density. The provision of more space and supportive treatment with anti-stress medicine may also be beneficial.
Key word:
Sudden Death Syndrome, broiler birds, Penicillium spp., Aspergillus spp., Candida spp, Kathmandu Valley, Nepal,
Material and Methods: Background of outbreak of Sudden Death Syndrome in Kathmandu Valley.
During the first week of August 2008 there sudden increase in mortality of broilers above 3-6 week age (Table 1). There are no premonitory signs. Just before death, birds appear normal and it is common to observe the birds feeding, drinking or walking normally. Then suddenly, affected birds exhibit clinical signs such as extending their neck, squawk and start wing beating as well as leg extension before falling back on their back and use to die suddenly. Most of birds in flock were diagnosed as suffering from diseases like C.R.D,Coccidiosis,Gout,Lichchi heart disease, and were treated with using drugslikeTylosine,Cholestin,Enroxin,Gentamycine,Anticoccidiostates,MultivitaminBcomplex and liver tonics alternately but there was no improvement of flock health rather there was continuous but death of birds were recorded in every flock .
Table: 1. Epidemiology of Affected flock 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
Total
86
58030
8713
(15.01%)
907
(1.56%)
172
Postmortem finding of SDS birds:
Postmortem examination of birds that died of sudden death syndrome revealed showed no outstanding gross pathology. All birds were well fleshed, with muscle oedema and general pulmonary congestion and oedema. Feed was present along the entire digestive tract and the gall bladders of birds are usually empty. The liver and kidneys were usually slightly congested and have patchy subcapsular haemorrhage. Usually, the proventriculus contains a milky fluid, and intact food particles are present in gizzard. Congestive splenomegaly was observed in almost all birds. All these post mortem observations conform to the descriptions of the syndrom made by Ononiwu et. al. (1979).
Laboratory Finding of Mycobiota and Microbiota of Postmortem Tissue samples:
A total 86 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
86
E.coli,
Streptococcus,
Staphylococcus
59
27
86
Aspergillus,
Penicillium,
Candida
58
28
172
117
55
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, Immunomodulaters, 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). 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). 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. 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).
Conclusion and Recommendation:
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.
References.
Bowes VA, R.J. Julian, S. Leeson and T. Stirtzinger (1988). Effect of feed restriction on feed efficiency and incidence of sudden death syndrome in broiler chickens. Poultry Science 67(7):1102-4
Mollison B., W. Guenter,and B.R. Boycott (1984). Abdominal fat deposition and sudden death syndrome in broilers: the effects of restricted intake, early life caloric (fat) restriction, and calorie: protein ratio. Poultry Science 63(6):1190-200
Nain S, B. Laarveld B, C. Wojnarowicz C, and A.A. Olkowski (2007). Excessive dietary vitamin D supplementation as a risk factor for sudden death syndrome in fast growing commercial broilers. Comparative biochemistry and physiology. Part A, Molecular & Integrative Physiology 148(4):828-33
Olkowski, A.A., C. Wojnarowicz, S. Nain, B. Ling, J. M. Alcorn, and B. Laarveld (2008). A study on pathogenesis of sudden death syndrome in broiler chickens. Research in Veterinary Science 2008 Aug;85(1):131-40
Ononiwu, J.C., R.G. Thomson, H.C. Carlson, and R.J. Julian. (1979). Pathological Studies of “Sudden Death Syndrome” in Broiler Chickens. Canadian Veterinary Journal 20(3): 70–73
Ononiwu, J.C., R.G. Thomson, H.C. Carlson, and R.J. Julian. (1979b). Studies on effect of lighting on “Sudden death syndrome” in broiler chickens. . Canadian Veterinary Journal 20(3):74-7
Olkowski A.A. and H.L. Classen (1998). High incidence of cardiac arrhythmias in broiler chickens. Zentralblatt für Veterinärmedizin. Reihe A 45(2):83-91
Olkowski A.A. and H.L. Classen (1997). Malignant ventricular dysrhythmia in broiler chickens dying of sudden death syndrome. Veterinary Record. 15;140(7):177-9
Proudfoot FG, H.W. Hulan, K.B. McRae (1982). The effect of crumbled and pelleted feed on the incidence of sudden death syndrome among male chicken broilers. Poultry Science 61(8):1766-8
Reams R.Y, H.L. Thacker, D.D. Harrington, M.N. Novilla, G.E. Rottinghaus, G.A. Bennett , and J. Horn (1997). A sudden death syndrome induced in poults and chicks fed diets containing Fusarium fujikuroi with known concentrations of moniliformin. Avian Disease 41(1):20-35
Rotter B, W. Guenter, and B.R. Boycott (1985). Sudden death syndrome in broilers: dietary fat supplementation and its effect on tissue composition. Poultry Science 64(6):1128-36
Scheideler SE, D.V. Rives, J.D. Garlich, and P.R. Ferket (1995). Dietary calcium and phosphorus effects on broiler performance and the incidence of sudden death syndrome mortality. Poultry Science 74(12):2011-8
Acknowledgment:
We would like to thank Dr. Dev Raj Adhikari SVO and incharge of Central Veterinary Hospital Tripureshwor, Kathmandu for providining early indication of problem. Thanks are due to Dr.Praggya Koirala V.O.,Dr. Banshi Sharma S.V.O. Dr. Salina Manandhar V.O, Mr.Bal Bahadur Kunwar Srnior Vet.Technician and Mr.Bhimsen Adhikari Vet.Technician of Microbioly Unit of Central Veterinary Laboratory for doing the microbiology works, Dr Esmeraldo M. Cabana, Veterinary Pathologist, Animal Health Laboratories, Diagnostic Services Branch Department of Primary Industries and Water, Tasmania, Australia, and Dr. Lin Tsang Long, Avian Pathologist, and Dr. Stephen B. Hooser, Stephen, Head, Toxicology Section and Assistant Director, Animal Disease Diagnostic Laboratory Purdue University U.S.A for their critique of the manuscript. Dr.Poornima Manandhar, Chief of CVL Tripureshwor deserve special thanks from this investigation team.
Dr.Kedar Karki M.V.St. Preventive Veterinary Medicine
A Review on Clinical Laboratory Outbreak of Sudden Death Syndrome in Broiler Chicken in Kathmandu Valley Nepal
A Review on Clinical Laboratory Outbreak of Sudden Death Syndrome in Broiler Chicken in Kathmandu Valley Nepal
Kedar Karki ; Pragya Koirala
Central Veterinary Laboratory in Kathmandu Tripureshwor Nepal
ABSTRACT:
Sudden death of broiler birds of above 40 days was suddenly increased in the month of August 2008 in Kathmandu valley. Birds which were presented for post-mortem examination in Central Veterinary Laboratory Tripureswor Kathmandu were usually found dead on their backs with wings out-stretched. Incidence of this condition recorded was between 1.5 to 2.5% of the flock. The mean mortality due to sudden death syndrome was 1.3 – 9.6% and mortality was peak after 6 week of age. Post-mortem necropsies of birds affected by Sudden Death Syndrome were well-fleshed with edema and general pulmonary congestion. Feed was present along the entire digestive tract and the gall bladder was empty. The liver and kidneys were slightly congested and have patchy subcapsular hemorrhage. The heart was containing clotted blood in the atria and the ventricles are most often empty. Microbial and Mycobial culture of tissue samples of liver, lung, spleen, Proventriculus revealed in majority of samples the growth of Penicillium and Aspergillus spp of fungus and E.coli and Staphylococcus spp of bacteria. On feed restriction, supplementation of glucose containing electrolyte, liquid toxin binder, Immunomodulaters, acidifier and antibiotic reduced the mortality. The condition seems to be related to fast growth rate . In extreme situations, feed restriction need to be practiced which will virtually eliminate sudden death syndrome. A practical approach seems to use diets with 5-7% reduction in nutrient density. Giving more space and supportive treatment with anti-stress medicine may be beneficial.
Key word:
Sudden death syndrome , broiler birds, Microbial and Mycobial culture, Penicillium and Aspergillus spp of fungus, feed restriction, glucose containing electrolyte, liquid toxin binder, Immunomodulaters, acidifier,
Background of outbreak of Sudden Death Syndrome in KathmanduValley.
During the first week of August 2008 there sudden increase in mortality of broilers of above 6 week age. Just before death birds appear normal and it is common to observe that these birds will be feeding, drinking or walking normally. Birds exhibit clinical signs such as extending their neck, squawk and start wing beating as well as leg extension before fall back on their back and birds used to die suddenly. Post-mortem necropsies of birds affected by Sudden Death Syndrome were well-fleshed with edema and general pulmonary congestion. Feed was present along the entire digestive tract and the gall bladder was empty. The liver and kidneys were slightly congested and have patchy subcapsular hemorrhage. The heart was containing clotted blood in the atria and the ventricles are most often empty.
Material and Methods:
1:Clinical Epidemiological observation of affected flocks.
2: Post-mortem examination and Microbial and Mycobial evaluation of tissue samples.
3: Evaluation of possible treatment and preventive measure
Epidemiology of Affected flock with sudden Death Syndrome in Month of August 2008:
Table: 1
Duration
no.of farm
Population at risk
Morbidity
Mortality
no.of samoles
First week
22
16620
4250
369
44
Second week
14
15450
1235
232
28
Third week
20
10260
848
157
40
Fourth week
30
15700
2380
149
60
Total
86
58030
8713
907
172
Postmortem finding of SDS birds:
Postmortem finding of birds which died of sudden death syndrome revealed all birds were well-fleshed with edema and general pulmonary congestion. Feed was present along the entire digestive tract and the gall bladder was empty. The liver and kidneys were slightly congested and have patchy subcapsular hemorrhage. The heart with containing clotted blood in the atria and the ventricles were most often empty. The edematous lung was observed. There was milky fluid in proventricular gland and intact food particles were present in gizzard, spleenomegally to spleeno atrophy was observed in almost all birds which were examined.
Laboratory Finding of Mycobiota and Micro biota of Postmortem Tissue samples:A total 86 tissue samples of lung,liver,speen,peoventriculus gizzard,were collected during postmortem examination and were subjected for both bacterial and mycological culture in respective media for culture and identification laboratory findings of which is presented below.
Table: 2
Samples numbers
Bacterial spp isolated
Fungal spp.isolated
Positive no
negative no
86
E.coli,Streptococcus,Staphylococcus spp.
59
27
86
Aspergillus,Penicillium,Candida spp
58
28
172
117
55
Treatment and Preventive measure advised to rest of birds in flock:
All birds remaining in flocks were advised two restrict the feed up to 8-10% and feed to twice daily only. Along with this it was advised to supplement glucose containing electrolyte liquid toxin binders like toxolivum ,toxol, kokonil, immunomodulater like immunocare,and and simple broad-spectrum antibiotics were advised to provide in water while supplementation of multivitamin B complex was totally withdrawn .
Review of literatures:
Sudden Death Syndrome is an acute heart failure disease that affects mainly male fast growing chickens that seem to be in good condition. The birds suddenly start to flap their wings, lose their balance, sometimes cry out, and then fall on their backs or sides and die; usually all within a minute (Satya 1).Sudden Death Syndrome kills 0.1% to 3% of broilers in European Countries. UK survey of broiler ascites and sudden death syndrome in 1993(The Welfare of Broiler Chicken 2). H.A. Upandra reported that Broilers that die of sudden death syndrome show no specific abnormalities. Birds usually male, appear healthy and are often above average flock body weight. Just before death birds appear normal and it is common to observe that these birds will be feeding, drinking or walking normally. Birds exhibit clinical signs such as extending their neck, squawk and start wing beating as well as leg extension before fall back on their back. Hence some farmers call this condition as cases of heart attack. Death occurs within minutes. Post mortem examination fails to exhibit any specific lesion. Hence it is also considered as a Behavioral Disease. However many workers who recorded behavioral pattern of birds concluded that there is no single behavior pattern can be attributed to this condition.
Pathology of sudden death syndrome is studied many workers and they found that birds affected by sudden death syndrome are always well-fleshed with edema 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 congested and have patchy subcapsular hemorrhage. The heart may contain clotted blood in the atria and the ventricles are most often empty. The edematous lung observed in cases of SDS was thought to be the contributing factor of death but in all probabilities it is a normal observation in birds that on their back for some time.
A number of studies have been aimed at correlating changes in tissue mineral, electrolyte and fat content as it relates to Sudden Death Syndrome. Sudden Death Syndrome affected birds showed elevated levels of liver calcium and reduced iron in lungs and kidneys. A small but statistically significant reduction in the potassium content and an increase in sodium content of heart tissue are also reported in Sudden Death Syndrome birds. However it is not known if these changes are causative or the consequence of Sudden Death Syndrome.
Because female broilers have a much lower incidence of Sudden Death Syndrome and Leghorns of either sex rarely show the condition, a comparative study was made in male broiler birds using either female broilers or Leghorn birds as control in studying the blood parameters. Male birds consistently exhibited elevated levels of blood glucose, Blood uric acid and lactate dehydrogenase as compared to females birds. As far as blood electrolyte study is considered, Sudden Death Syndrome birds had higher levels of blood potassium. These data again pose the question of how to interpret biochemical profiles of Sudden Death Syndrome birds, because in most instances, birds have been dead for some time prior to blood sampling.
Other factors such as diet texture and restriction programs have been studied with a view to isolating causative agents in Sudden Death Syndrome . It is reported that feed restriction can reduce mortality due to Sudden Death Syndrome in broiler chicks but feed restriction can reduce the body weight of these birds. It is concluded that Sudden Death Syndrome can be prevented by growing birds at a slower rate.
Diet protein per se seems to have little effect on Sudden Death Syndrome . Relatively little research aimed at investigating the role of dietary aminoacids on incidence of SDS is taken up. Taurine is considered to be a non-essential amino-acids for poultry. While avian species are assumed to synthesize sufficient taurine, reduced cardiac taurine levels have been associated with heart tissue degeneration in turkeys. Furazolidone is known to cause heart muscle degeneration in turkeys and this is accompanied by reduction in tissue taurine levels. Feeding up to 0.2% taurine to broilers resulted in a small reduction in incidence of Sudden Death Syndrome.
Use of various sources of energy in the diet has also been suspected in affecting the occurrence of Sudden Death Syndrome. The replacement of carbohydrate by fat is suspected to be a factor. The occurrence of Sudden Death Syndrome seems to be increased by feeding hydrogenated fat such as coconut oil as compared to birds fed comparable levels of unsaturated sunflower oil.
Biotin has been singled out most frequently among vitamins as a possible factor in Sudden Death Syndrome. It is suggested that biotin may be an important factor in increasing the occurrence of Sudden Death Syndrome if it is complicated by the incidence of fatty liver and kidney syndrome. The Sudden Death Syndrome seems to be worse when biotin is marginal and other Vitamin B are in excess.
Among many drugs used in poultry the role of anticoccidial drugs perhaps have received more attention than other drugs. There is some evidence of higher Sudden Death Syndrome mortality when anticoccidial drugs are used. Historically the occurrence of Sudden Death Syndrome does coincide with the introduction of the ionophore anticoccidials. However the involvement of ionophores in Sudden Death Syndrome is far from clear and typical pathological lesion of ionophore toxicity have not been reported in Sudden Death Syndrome diagnosed birds.
It is obvious that there is no one treatment or preventive system for the control of SDS in broilers. The condition is undoubtedly related to fast growth rate and as such management techniques to reduce the early maximum genetic potential for growth after the best preventive measure. One of the most successful techniques used to hamper early growth rate is a step-down lighting programme. Broilers are subjected to reduced day light between 5-18 day of growth. This effectively reduces feed intake and so hampers early growth rate. In extreme situations, feed restriction can also be practiced and this will virtually eliminate Sudden Death Syndrome. A practical approach is to use diets with 5-7% reduction in nutrient density. Giving more space and supportive treatment with anti-stress medicine may be beneficial (H.A. Upandra). Sudden death syndrome in fast growing broiler chickens has been recognized as a patho-physiological entity for four decades, but its pathogenesis still remains unknown. More recent investigations provided evidence that link SDS to cardiac arrhythmia, but the mechanism triggering arrhythmogenesis and factors responsible for fatal outcome are poorly understood. In order to understand the chain of events leading to Sudden Death Syndrome in broilers, the present study focused on putative mechanisms that trigger arrhythmia and mechanisms that predispose the myocardium to fatal arrhythmia. Susceptibility of broilers to cardiac arrhythmia under stress conditions was evaluated using a simulated stress test with epinephrine. Detailed histopathological evaluation of the broiler heart was undertaken to identify structural features that may predispose the myocardium to fatal arrhythmia. The simulated stress challenge revealed that many broilers are highly susceptible to stress induced cardiac arrhythmia. In some broilers the stress challenge induced severe ventricular arrhythmia, and the life threatening nature of this arrhythmia was evidenced by the fact that several birds showing the most severe arrhythmic responses, died suddenly within several days after the stress challenge. Examination of hearts of broilers that died of Sudden Death Syndrome revealed microscopic lesions in the cardiomyocytes, and widespread changes in the sub-endocardial and mural His-Purkinje system (HPS). Immune staining for Caspase-3 confirmed that numerous Purkinje cells in the left ventricular myocardium from broiler chickens that died of SDS were undergoing apoptosis. The observed lesions suggest that the electrical stability of the myocardium was compromised. Taken together, our findings indicate that stress is a most likely trigger of cardiac arrhythmia in broilers, whereas the pathological changes seen in the myocardium and in the HPS in fast growing broilers provide a very conducive milieu for sustained ventricular arrhythmia. In cases where the electrical stability of the myocardium is compromised, even an episodic arrhythmic event may readily degenerate to catastrophic ventricular fibrillation and sudden death. We conclude that the combination of stress and changes in the cardiomyocytes and HPS are the key requisite features in the pathogenesis of SDS (4 A A Olkowski, C Wojnarowicz, S Nain, B Ling, J M Alcorn, B Laarveld). A condition of broiler chickens of unknown cause, possibly metabolic. It can be induced by lactic acidosis and about 70% of birds affected are males(5 www.thepoultrysite.com/diseaseinfo/146/sudden-death-syndrome-flipover ). Sudden death syndrome usually occurs in heavy, fast-growing and healthy-looking broilers. Most of the affected birds are males. The characteristic necropsy changes are seen in well-fleshed broilers with edema and generalized pulmonary congestion, recently ingested feed in the crop and gizzard, distended intestine with creamy content and empty gall bladder. The liver and kidneys are slightly enlarged and the latter have patchy areas of subcapsular hemorrhage. The heart contains clotted blood in the atria but the ventricles are often empty and the left ventricle in particular assumes a hypertrophied appearance (6 J.C. Ononiwu, R.G. Thomson, H.C. Carlson, and R.J. Julian). A syndrome specifically associated with broiler breeders. Clinical signs – Mortality ranging from 0.5 to 8% per week with most of the birds dying at feeding time. No evidence of respiratory infection. Commences as flock reaches about 5% production and being worst about 20-30% production. It is believed that this is most likely to be due to a mineral imbalance associated with low potassium as the flock comes into lay. Treatment including 3.5Kg/tonne of potassium carbonate has reduced the incidence (7 members.tripod.com/poultryworld/dis_dir.htm).
Result and Discussion:
All the birds remaining in all affected flocks responded to the above treatment management and there was marked improvement in controlling of the syndrome.As todays broiler birds are genetically so engineered that they are suppose to achieve maximum body weight gain during the schedule period of 45days there is trend of using feed additives which also exerts some health problem in broiler as well they causes the problem like tibial dyschondroplacia in heavey weight broiler has been reported by many workers in Europe and elesewhere.As today universally a total of 30-35 grains are being contaminated with one or other toxigenic fungus whose deleterious effect on livestock and poultry health has been well documented were it causes sudden death also coincides with finding of this observation. Further more especially during hot humid season whish increases stress to birds as well as there is a conducive environment for the growth of mold and fungus also provides higher risk to the birds for the deleterious effect of mycotoxin in broiler health.Still today so far in the management of mycotoxin and mycosis only there is practice of using toxinbinders only during feed formulation process in feed mills.Which alone is not suffient to minimize effect to fungal contamination during storage if poultry especially broilers of finisher age have to protected some management pattern need to be changed.
Conclusion and recommendation:
All clinical laboratory and epidemiological patterns observed in this investigation indicates that broilers in good body weight condition when not harvested timely and remain in poultry shade for prolong time due to the congestion of space enhances a stress factor. Along with this with increase in humidity and hot season favors the growth of mold and fungus in stored feeds there was increasing the risk of birds to mycosis. Under such circumstances birds are in danger to be affected by mycotoxicosis under such situation if a proper preventive measure to prevent the deleterious effect of mycotoxin is not under taken any time an unexpected syndrome may appear in poultry establishment. As this was a sudden mortality in broiler has been reported for first time finding of this invested need to be looked into.
.
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Reference:
1: Satya Feb 06: The Real Cost of Cheap Chicken by Joyce D’Silva www.satyamag.com/feb06/dsilva.html – Retrieved on 8 August 2008
2:The Welfare of Broiler Chicken ciwf.org.uk/publications/…/the_welfare_of_broiler_chickens_2000.pdf – Retrieved on 8 August 2008
3: SUDDEN DEATH SYNDROME:Dr. H.A. Upandra, Associate Professor, Dept. of Clinical Veterinary Medicine, Veterinary College, UAS, Bangalore: www.vetcareindia.com/halchal_sudden%20syndrome.htm – 15k – Retrieved on 8 August 2008
4: Res Vet Sci. 2007 Sep 26; : 17904171 (P,S,E,B,D) A study on pathogenesis of sudden death syndrome in broiler chickens. A A Olkowski, C Wojnarowicz, S Nain, B Ling, J M Alcorn, B Laarveld : lib.bioinfo.pl/pmid:17904171 – 62k. Retrieved on 8 August 2008
5: Sudden Death Syndrome, ‘Flipover’ ThePoultrySite Quick Disease Guide www.thepoultrysite.com/diseaseinfo/146/sudden-death-syndrome-flipover- Retrieved on 8 August 2008
6 : Pathological Studies of “Sudden Death Syndrome” in Broiler Chickens
J.C. Ononiwu, R.G. Thomson, H.C. Carlson, and R.J. Julian
:www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1789498- Retrieved on 8 August 2008
7: THE A-Z POULTRY DISEASE INDEX: members.tripod.com/poultryworld/dis_dir.htm- Retrieved on 8 August 2008
Acknowledgement:
We would like to extend our sincier thanks to Dr.Dev Raj Adhikari SVO and incharge of Central Veterinary Hospital Tripureshwor, Kathmandu for providining early indication of problem. Our gratitude goes to the all broiler farmers of Kathmandu Valley for cooperating with this investigation team through out the observation period. Mr.Bal Bahadur Kunwar Srnior Vet.Technician and Mr.Bhimsen Adhikari Vet.Technician of Microbioly Unit of Central Veterinary Laboratory for their tedious work in lab for cultureing and processing of all samples deserves a special thanks. We would like to extend our heartfelt gratitude to Dr Esmeraldo M. Cabana, DVSM, MVSt (VPath) Veterinary Pathologist Animal Health Laboratories
Diagnostic Services Branch Department of Primary Industries and Water, Australian Government service Tasmania.and Dr.Lin, Tsang Long,Avian Pathologist and Dr.Hooser, Stephen B Head, Toxicology Sect. & Asst. Director,Animal Disease Diagnostic Laboratory Purdue University U.S.A for their continuous guidance through Email for this investigation and its documentation.Last but not least Dr.Poornima Manandhar chief of CVL Tripureshwor deserve a special thanks from this investigation team for her continuous inspiration
Dr.Kedar Karki.M.V.St. Preventive Veterinary Medicine CLSU Philippines
Senior Veterinary Officer
Central Veterinary Laboratory
Tripureshwor
Kathmandu Nepal
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