An ultrastructural study of an ascitic syndrome in young broilers reared at high altitude

Maxwell, M.H.; Dolan, T.T.; Mbugua, H C

doi:10.1080/03079458908418620

Cited by 18 publications

(5 citation statements)

References 15 publications

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“…Maxwell et al (1986b) and Domiguez et al, (1990) describe thickening of the respiratory membrane and marked swelling of the capillary endothelial cells in broilers with ascites. Similar ultrastructural changes are described in broilers at high altitude and in hypoxic conditions (Maxwell et al, 1989;Maxwell, 1990c). Some of these broilers had ascites from RVF.…”

Section: Pathological Lesionssupporting

confidence: 58%

“…The mitochondrial hyperplasia described by Maxwell (1990c) in the heart of 7-day-old broilers was probably pressure-induced. The other myocardial changes described by Maxwell et al, (1989) and Maxwell (1990c) and others might be pressure-induced or they could result from hypoxia following RVF.…”

Section: Signs and Lesions Caused By Pulmonary Hypertensionmentioning

confidence: 99%

“…Other changes observed include necrosis and mineralization of scattered renal cortical tubules, dilation of collecting tubules, atrophy of skeletal muscle fibres, and an increase in the amount of zymogen in pancreatic acinar cells. Maxwell et al (1986bMaxwell et al ( , 1989, Maxwell (1990c) and Dominguez et al (1990) described ultrastructural lesions in ascites secondary to RVF. Many of the changes are the result of rather than the cause of PH and the myocardial changes described are similar to those in spontaneous turkey cardiomyopathy and NaClinduced cardiomyopathy (Gough et al, 1981;Onderka & Bhatnagar, 1982).…”

Section: Pathological Lesionsmentioning

confidence: 99%

“…Stretch-induced muscle hypertrophy occurs because of increased intracardiac and intravascular pressure and is the result of DNA ploidy (Owens & Schwartz, 1982;Maxwell et al, 1989;Maxwell, 1990c;DeVol, 1991). RVH results from increased volume and/or pressure work-load causing stretching of muscle fibres, and RVH reflects PH (Cueva et al, 1974;Sillau et al, 1980;Guthrie et al, 1987).…”

Section: Pathogenesis Of Pulmonary Hypertensionmentioning

confidence: 99%

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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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Section: Pathological Lesionssupporting

confidence: 58%

Section: Signs and Lesions Caused By Pulmonary Hypertensionmentioning

confidence: 99%

Section: Pathological Lesionsmentioning

confidence: 99%

Section: Pathogenesis Of Pulmonary Hypertensionmentioning

confidence: 99%

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Ascites in poultry

1993

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“…These tissue lesions together with the haematological profile closely resembled changes seen in young broilers with an ascitic syndrome (Maxwell et al, 1986a,b). Although these abnormalities were never as severe as those identified in ascitic birds at low (Maxwell et al 1986a.b) or high altitude (Maxwell et al 1989), the reduced oxygen tensions of the present study may be important in the development of these lesions. The evidence of parabronchial congestion and dilation, which was completely absent from the lungs of the control birds, may signify the onset of chronic pulmonary hypertension which in turn led to the myocardial changes and right-sided enlargement.…”

Section: Discussionmentioning

confidence: 42%

Haematological and morphological responses of broiler chicks to hypoxia

Maxwell¹,

Spence²,

Robertson³

et al. 1990

Avian Pathology

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Broiler chicks were subjected to experimentally-induced hypoxia and the haematology, together with the histopathology and ultrastructure of heart, liver, lung and kidney and the ultracytochemistry of heart tissues were examined. The haemoglobin concentration, packed cell volume and red blood cell counts were significantly increased compared with controls. The results resembled the haematology of similar aged broilers with an ascitic syndrome and also 1-day-old chicks after induced hypoxia. The morphological changes were also similar in all organs examined and compared with those described in ascitic syndromes. Lactate dehydrogenase was increased in the hearts of hypoxic and ascitic birds indicating reduced oxygen utilisation. It was suggested that hypoxia may be an important factor in the aetiology ascitic syndromes of flocks kept at low altitude.

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Developmental, Metabolic, and Other Noninfectious Disorders

Crespo¹

2019

Diseases of Poultry

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An ultrastructural study of an ascitic syndrome in young broilers reared at high altitude

Cited by 18 publications

References 15 publications

Ascites in poultry

Ascites in poultry

Haematological and morphological responses of broiler chicks to hypoxia

Developmental, Metabolic, and Other Noninfectious Disorders

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