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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 Kathmandu Valley.

 

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 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





 

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

Dr.Kedar Karki M.V.St. Preventive Veterinary Medicine
Senior Veterinary Officer
Central VETERINARY lABORATORY
Tripureshwor Kathmandu

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