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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 Kathmandu Valley.

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.

About the Author

Dr.Kedar Karki.M.V.St. Preventive Veterinary Medicine CLSU Philippines
Senior Veterinary Officer
Central Veterinary Laboratory
Tripureshwor
Kathmandu Nepal

Do we have a proof of evolution in any animal?

sorry for my english, but i was wondering if we have any proof of evolution in animals.
I know evolution in laboratories is possible in the "micro" world and i know also in the plants, if im not mistaken, but i haven't read anywhere that we have proof of evolution in animals or humans.
thanks
please enlight me with simple words.
thank u for your answers, but still there is this small petite chance that dna doesn't necerrerily means evidence of evolution in species.
Well im not a scientist and i would be pleased when we will have indenial evidence and proofs about evolution in humans and animals.
Thank u

First, we do not speak of "proof" in science. We speak of *EVIDENCE*.

What's the difference? "Proof" is absolute (something "proved" by logic alone). Evidence is *cumulative* (it accumulates, but is never considered "proved".)

We use the word "proof" in mathematics, not in science.

So with that said, do we have *evidence* of evolution in any animal?

Absolutely! Yes. We have *evidence* of evolution in every animal we know about.

The strongest evidence is in DNA. Take *any* two species ... (chimps and humans, chimps and squirrels, chimps and eagles, chimps and orchids) ... and when we examine their DNA we find sequences that match, letter-for-letter. These aren't just explained by common features, because a lot of these sequences in common *do not code for anything* ... the only explanation for them is that they are *inherited* from a common ancestor.

It is really important to understand two things about this DNA evidence.
(1) This works for *ANY* two species ... so it is not just a matter of saying "similarities between species A and B is not 'proof' of evolution" but that the similarity is a small piece of evidence, and so is the similarity between B and C, and A and C ... and so on, throughout every living organism on the planet.
(2) Where it really compelling is recognizing *patterns* ... A is *more* related to B than it is to C. Those patterns are absolutely consistent with a long long history of *BRANCHING* evolution. Species splitting, and splitting again.

So even without a single fossil ever being discovered, we already have massive *evidence* that any two living species on the planet share a common ancestor.

So then we start adding the fossil evidence. The fossils tell us a lot about what those earlier ancestors *looked* like. (Again, fossils are not necessary to know that those ancestors existed ... but it sure adds to the evidence.) They tell us *when* they lived (by the depth in the soil), and *where* (by where on the planet they are discovered), and what kind of environment they lived in (by the other fossils in the same layers), and what *structures* were developing (e.g. a sequence of primates in shallower and shallower layers of soil that had a slowly increasing braincase, upright posture, etc.) etc.

Then there's the way that all living things *develop* as embryos. The *sequence* of development follows the sequence in which features got added (e.g. in humans, the spinal cord develops first, then the lower brain stem, then the upper, and finally the huge cerebral cortex for which humans are known ... if human embryos developed in the opposite sequence, this would be evidence *against* evolution). Some features develop and then disappear that are throwbacks to genes inherited from ancestors who needed those features ... like gill folds, tails, and webbed fingers in human embryos). Sometimes individuals are born with these features still intact (like babies born with short tails or webbed fingers, or dolphins born with small legs). (These are called atavisms.)

And there's more. A lot more. Vestigial features (a feature that is useless in species A, but useful in species B that point to inheritance from a common ancestor ... such as the useless muscle in your calf called the Plantaris muscle that is used in other primates for grasping with the feet, or your appendix, or the muscles for moving your ears). Homologous features (structures or proteins shared between two species that have the same *structure* but different *function* ... like the common bone structure in the human hand and the bat's wing ... same basic bone-for-bone structure, radically different function.

So that's just an overview of the *evidence*.

Revisiting chicxulub: A broad look at the evidence for a dinosaur-killing impact
One factor that is not in dispute: the end of the Cretaceous 65.5 million years ago was marked by one of the most devastating extinctions our planet has faced.

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