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Year : 2014, Volume : 38, Issue : 1
First page : ( 49) Last page : ( 51)
Print ISSN : 0250-4758. Online ISSN : 0973-970X. Published online : 2014 March 1.
Article DOI : 10.5958/0973-970X.2014.01134.1

Pathological changes in induced acute fenvaleratetoxicity in broilers

Shriwas S.K.1, Mondal M.1,*, Ghosh R.C.1, Maity S.K.1, Koley K.M.1

1Department of Veterinary Pathology, College of Veterinary Science and Animal HusbandryIndira Gandhi Agricultural University, Anjora, Durg-491001, Chhattisgarh, India

*Corresponding author: email: drmondalmm@rediffmail.com

Received:  18  November,  2013; Accepted:  18  February,  2014.

Abstract

The present study on acute toxicity of fenvalerate was undertaken to find out its toxic effects and to know the approximate lethal dose (ALD) by oral route in broilers. Initially, different arbitrary doses (300, 450, 675, 1013 and 1519 mg/kg body weight) of fenvalerate were given to broilers of each group till the lowest lethal dose was achieved. The ALD of fenvalerate by oral administration in broilers was determined as 1519 mg/kg body weight. Intoxicated broilers exhibited depression, dullness, anorexia, yellowish diarrhoea, open mouth breathing, incoordination in movement and tremors followed by dyspnoea, tonic convulsion, coma and death. At necropsy, varying degree of congestion in most of the organs and severe haemorrhages in thymus were noticed in treated broilers. Microscopically, treated broilers had lesions suggestive of toxic hepatitis, nephritis and severe lymphocytolysis in the lymphoid organs. There was loss of striation with exudation and mild necrosis in cardiac muscles. Brain revealed congestion and degenerative to necrotic changes.

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Keywords

Acute toxicity, Broilers, Fenvalerate, Pathology.

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INTRODUCTION

Poultry industry in India has transformed itself from age old backyard farming into dynamic agri-based industry. Poultry industry is commonly chicken oriented in our country as more than 90% of Indian poultry birds are chicken1. In spite of rapid growth, the poultry industry suffered many setbacks in recent times due to rising cost of feed, emergence of new or re-emerging of existing diseases and fluctuating market price of broiler etc., which need to be addressed to make the poultry sector as a sustainable enterprise. Pesticide toxicity represents one of the most serious problems of poultry. In India, 90,000 MT of technical grade pesticides are used annually to control pests and plant diseases2. Pesticides are environmental pollutants and cause serious health hazards in livestock and poultry through contaminated soil and water3. Consumption of pesticide-treated crops may result in residual toxicity in animals and birds4.

Fenvalerate is a group II pyrethroid insecticide with moderate toxicity to mammals. It is used as spray for flies, fleas, leaf eaters, caterpillars scale and suckling insects and is preferred over organochlorine, organophosphorus and carbamates insecticides due to their high effectiveness, low toxicity to non targeted organisms and easy biodegradability5. The stability of fenvalerate in sunlight allows its application against a wide range of pests. So the present study was undertaken to estimate the acute toxic effects of fenvalerate in broiler.

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MATERIALS AND METHODS

Acute toxicity study of fenvalerate in broilers was determined by approximate lethal dose method as described by Hayes6. For this purpose 25 healthy broiler chicks aged two weeks having weight between 100-150g were taken. All the chicks were fasted overnight before dosing. Initially different arbitrary doses (300, 450, 675, 1013 and 1519 mg/kg body weight) of fenvalerate were administered orally to a set of five broilers until the lowest lethal dose was obtained. The broilers were kept under constant observations for acute manifestation of fenvalerate toxicity. The broilers died during the study period were thoroughly examined for detection of gross lesions. The representative tissue samples were collected in 10% buffered neutral formalin for histopathological study. Tissues were processed as per routine histological procedures. Paraffin sections of 5 μ thickness were cut and stained with haematoxylin and eosin for histopathological studies7.

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RESULTS

The approximate lethal dose of fenvalerate was determined as 1519 mg/kg body weight in broilers. The broilers fed with fenvalerate @ 300 mg/kg of body weight showed mild depression, dullness and anorexia. The broilers fed with fenvalerate @ 450 mg/kg body weight exhibited the symptoms of depression and incoordination. The broilers, which were administered fenvalerate orally @ 675 mg/kg body weight showed dullness, staggering gait and open mouth breathing. The broilers which received fenvalerate orally @ 1013 mg/kg body weight had symptoms consisting depression, incoordination in movement and mild convulsion within 20 minutes after administration. The broilers administered with fenvalerate @ 1519 mg/kg body weight exhibited depression within 10 minutes after dosing and manifested dullness, depression, anorexia and reluctant to move from 15 minutes onwards, followed by open mouth breathing, resting by keeping the head on support, twisting of neck and yellowish diarrhoea followed by tonic convulsion, coma and death.

Grossly, fenvalerate treated broilers showed varying degree of congestion in liver, kidneys, lungs, intestine and brain. Thymus was markedly enlarged and showed severe haemorrhages. Histopathological lesions in the liver consisted of severe degenerative to necrotic changes, congestion and serous exudation. Microscopically, lungs revealed severe congestion and hemorrhages around the pulmonary vessels and interstitial spaces (Fig. 1). Kidneys of treated broilers showed severe degenerative and necrotic changes of lining epithelium of proximal and distal convoluted tubules and severe congestion and haemorrhages in inter-tubular capillaries. There was congestion and severe depletion of lymphocyte population in the malpighian corpuscles of the spleen (Fig. 2). Treated broilers revealed severe lymphocytolysis in the bursal follicles (Fig. 3) and congestion, degeneration and depletion of lymphocytes in the thymic follicles. Microscopically, degenerative and necrotic changes along with haemorrhages, oedema and widening of muscle fibers due to accumulation of serous exudates were noticed in the cardiac muscles of broilers. Brain of treated broilers had mild neuronal degeneration, serous exudation and congestion in the cerebellum (Fig. 4).

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DISCUSSION

Majority of the clinical signs exhibited by fenvalerate administered broilers were in close conformity with earlier observations in broilers8. The gross pathological changes of the present study like varying degree of congestion in liver, kidneys, lungs, intestine and brain along with severe haemorrhages in thymus were in agreement with the earlier reports in broilers9. Mandal et al10 noticed sinusoidal congestion, accumulation of lysed RBCs and cellular debris in central vein, periportal fibrosis and connective tissue proliferation in liver of acute fenvalerate induced toxicity in male black Bengal goats. Similar findings were reported by Mohamed and Adam11 who observed fatty changes and necrosis in fenvalerate treated Nubian goats. Congestion and reduction in blood circulation might have caused anoxia leading to vacuolar degeneration12. The oral administration of toxicants like pyrethroids severely affect the liver, the primary organ involved in their activation and/or detoxification13.

Pesticide has been reported to cause immune dysfunction followed by depletion of lymphocytes in spleen of broilers14. Malpe et al15 observed microscopically severe congestion and hemorrhages in lungs of deltamethrin induced toxicity in rats. Similarly, Tamang et al16 observed congestion in lungs of black Bengal goats in acute cypermethrin toxicity. Present findings regarding histopathological lesions in kidneys were in agreement with the observations of earlier worker17 in cypermethrin intoxicated rats. However, Tapase et al18 noted hypertrophy and hyperplasia of the capillary endothelial cells of glomeruli leading to obliteration of capsular space in fenvalerate treated mice. Tamang19 suggested that the toxic irritant substance brought to the kidneys via blood circulation can exert direct toxic effect on tubular epithelium or may cause anoxia due to congestion and reduction in blood circulation. Thus, the changes in the kidneys could be the direct effect of fenvalerate and or result of anoxia due to congestion. Misri4 had reported similar findings of degeneration and necrosis of lymphoid follicles of bursa of Fabricius in acute toxicity of fenvalerate in broilers. The histopathological lesions of thymus were closely corroborated with the earlier reports in fenvalerate treated broilers9.

The present findings of degeneration, necrosis, haemorrhages and oedema in the cardiac muscles of broilers were in close conformity with the reports of earlier workers15 who have noticed severe congestion and haemorrhages in deltamethrin treated rats. Increased venous hydrostatic pressure in acute toxicity might be responsible for cardiac oedema20. In a previous study, cypermethrin intoxicated rats revealed mild neuronal degeneration, astrocytic proliferation and occasional necrosis of Purkinje cells17. The direct effect of pesticide coupled with interference of oxygen uptake and depression of brain cell respiration has been correlated to the damages observed in the brain tissues of malathion intoxicated rats21.

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Figures

Fig. 1.:

Section of lung showing congestion and hemorrhages. H&E ×400




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Fig. 2.:

Section of spleen showing mild depletion of lymphocytes in the Malpighian corpuscles. H&E ×400




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Fig. 3.:

Section of bursa showing depletion of lymphocytes in the follicles. H&E ×400




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Fig. 4.:

Section of cerebellum showing mild neuronal degeneration and congestion. H&E ×400



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