Hydropericardium and Ascites in Chicks Fed a Chlorinated Hydrocarbon

McCune, E. L.; Savage, J. E.; O’Dell, Boyd L.

doi:10.3382/ps.0410295

Cited by 63 publications

(22 citation statements)

References 2 publications

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“…Prompted by the observation of tubular dilatation in the kidneys in previous studies after PCB ingestion (McCune et al, 1962;, measurements were made on random samples of capsules of Bowman and glomeruli in 2-p kidney sections. Measurements of one axis of the greatest diameter of both capsule and glomerulus were made of 25 renal corpuscles in a straight traverse across the cortex of each kidney.…”

Section: Methodsmentioning

confidence: 99%

Dermal toxicity studies of technical polychlorinated biphenyls and fractions thereof in rabbits

Vos

Beems

1971

Toxicology and Applied Pharmacology

115

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A significant difference in toxicity between 3 polychlorinated biphenyl (PCB) preparations was found in a prior study: Clophen A 60 and Phenoclor DP6 showing the highest, Aroclor 1260 the lowest, toxicity . A subsequent study revealed the presence of tetra-and pentachlorodibenzofuran in Phenoclor and Clophen . In the present study, application of 118 mg of the 3 PCB's (5 times per wk, for 38 days) on the back skin of rabbits also resulted in differences in toxicity.PCB-induced skin lesions were hyperplasia and hyperkeratosis of the epidermal and follicular epithelium. Histopathology of the liver included centrolobular degeneration, centrolobular liver cell atrophy, focal necrosis, and cytoplasmic hyalin degeneration. Definite hyperplasia and hyperkeratosis of the follicular epithelium of the ear skin were seen after the topical application of fractions of Phenoclor and Clophen eluted from chromatographic columns with 25 ",/, diethylether in hexane. The fraction from Aroclor caused a minimal hyperplasia and hyperkeratosis of the follicular epithelium. PCB-induced kidney lesions were hydropic degeneration of the convoluted tubules and tubular dilatation with the presence of casts. This dilatation was demonstrated also by a significantly increased relative percentage of the diameter which corresponds to the space of Bowman. Moreover, thymus atrophy and lymphopenia were found. Fecal coproporphyrin and protoporphyrin excretion was increased.

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Section: Methodsmentioning

confidence: 99%

Dermal toxicity studies of technical polychlorinated biphenyls and fractions thereof in rabbits

Vos

Beems

1971

Toxicology and Applied Pharmacology

115

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“…Endothelial damage has been suggested as the cause of the fluid leakage in ascites caused by some phenolic compounds and coal-tar derivatives (creolin, carbolineum, etc. ), dioxin (toxic fat syndrome) (Bressler et al, 1951;Flick et al, 1973;Lekkas et al, 1986;, pentachlorophenol (Prescott et al, 1982) and chlorinated hydrocarbons (McCune et al, 1962). When large quantities of fluid are found in the coelomic spaces in the toxic fat syndrome (dioxin toxicity) or viral myocarditis such as Angara disease (Anjum et al, 1989a), both endothelial damage and increased hydraulic pressure from myocardial or liver damage are probably involved (Allen, 1964;.…”

Section: Ascites Associated With Increased Vascular Permeabilitymentioning

confidence: 99%

Ascites in poultry

1993

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SUMMARYResearch on ascites occurring in meat-type chickens reared at moderate and low altitude has shown that the pathogenesis is similar to that of the high altitude disease. Pulmonary hypertension (PH) caused by increased blood flow or increased resistance to flow in the lung results in right ventricular hypertrophy (RVH), valvular insufficiency, increased venous pressure and ascites. The structure of the avian heart, with its thin-walled right ventricle and muscular right atrioventricular valve, allows PH to induce heart failure quickly. The sudden increase in pulmonary hypertension syndrome (PHS) in meat-type chickens in the 1980s was associated with a rapid increase in growth rate and feed conversion. This was a result of a combination of genetic selection for fast-growing, heavy broilers with low feed conversion and a more dense, high caloric, pelleted food that supplied all the nutrients required for rapid growth and encouraged a high nutrient intake. PHS in meat-type chickens is usually primary pulmonary hypertension, that is, PH that occurs without evidence of prior heart or lung disease that could account for the increase in blood flow or resistance to flow that results in the increased pressure in the pulmonary arteries. The lungs of birds are firm and fixed in the thoracic cavity and they do not expand to draw air into the lung. The blood and air capillaries form a rigid network that allows only minimal expansion of the blood capillaries when more blood flow is required. Air is moved through the lung by abdominal movement which draws air in and out of the air sacs. The anatomy and physiology of the avian respiratory system are important in the susceptibility of meat-type chickens to PHS. The small stature of the modern meat-type chicken, the large, heavy breast mass, the pressure from abdominal contents on air sacs, and the small lung volume compared to body weight, may all be involved in the increased incidence of PHS. There is limited space for blood flow in the avian lung. Factors that increase blood flow or increase resistance to flow are additive. Increased blood viscosity caused by the polycythaemia of hypoxia, or increased erythrocyte rigidity of high Na + , are more likely to produce PH in fast-growing than in slow-growing birds. Increased flow due to cold exposure is also additive. Ascites caused by PH is a production-related disease at low altitude. It can be prevented easily by restricting growth rate. It is possible that some meat-type chickens of the phenotype we have created have reached the limit of blood flow through their lungs and that future improvements in growth rate will only be possible if the lung and abdominal cavity capacities are enlarged.

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“…These include, alimentary toxaemia (Sanger et al, 1958), myocarditis (Hall and Machicao, 1968), chick oedema disease, endotheliosis, hydropericardial disease, oedema, toxopathic hepatitis, water belly (Hungerford, 1969), ascites, avian oedema, congestive heart failure, toxic heart disease, toxic lipidiosis (Agudelo, 1983) and altitude disease (Huchzermeyer, 1984). Some haematological parameters have been examined in spontaneously-or experimentally-induced ascites in chicks (Flick et al, 1965;Hall and Machicao, 1968;Cueva et al, 1974;Lohr, 1975;Sillau et al, 1980;Agudelo, 1983) and there have been many pathological studies (Sanger et al, 1958;Simpson et al, 1959;McCune et al, 1962;Allen, 1964;Olander et al, 1967;Hall and Machicao, 1968;Teuscher et al, 1971;Cueva et al, 1974;Lohr, 1975Lohr, ,1977Bergmann et al, 1979).…”

Section: Introductionmentioning

confidence: 99%

Studies on an ascitic syndrome in young broilers 1. haematology and pathology

1986

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SUMMARYIn the present investigation, the haematology and pathology of young broiler chicks with an ascitic syndrome were examined. Gross changes included cardiomegaly, ascites, congested lungs, shrunken livers, enlarged kidneys, dark breast muscle and congested intestines. Many blood parameters were significantly raised including the packed cell volume (PCV), haemoglobin (Hb), red (Rbc) and white blood cell (Wbc) counts. The heterophils and monocytes were also increased at the expense of the lymphocytes compared with control birds. The histopathology revealed degenerative changes in all organs examined which resembled lesions reported elsewhere in birds maintained at high altitude. In addition, large numbers of infiltrating leukocytes, in particular heterophils, were also present in the tissues. In many cases the syndrome was characterised by congestive heart failure.

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Hydropericardium and Ascites in Chicks Fed a Chlorinated Hydrocarbon

Cited by 63 publications

References 2 publications

Dermal toxicity studies of technical polychlorinated biphenyls and fractions thereof in rabbits

Dermal toxicity studies of technical polychlorinated biphenyls and fractions thereof in rabbits

Ascites in poultry

Studies on an ascitic syndrome in young broilers 1. haematology and pathology

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