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 Kathmandu Valley.

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

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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 Morbidity Mortality no.of
at risk samoles
22 16620 4250 369 44
First week
Second 14 15450 1235 232 28
week
Third 20 10260 848 157 40
week
Fourth 30 15700 2380 149 60
week
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

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both bacterial and mycological culture in respective media for culture and
identification laboratory findings of which is presented below.
Table: 2

Samples Bacterial Fungal Positi negative no

numbers spp spp.isolate ve no
isolated d
86 E.coli,Strep 59 27
tococcus,St
aphylococc
us spp.
86 Aspergillus 58 28
,Penicilliu
m,Candida
spp
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.

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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.

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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

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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

6
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.

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

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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