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Broiler chickens selected for rapid growth are highly susceptible to dilated cardiomyopathy (DCM). In order to elucidate the pathophysiology of DCM, the present study examines the fundamental features of pathological remodelling associated with DCM in broiler chickens using light microscopy, transmission electron microscopy (TEM), and synchrotron Fourier Transform Infrared (FTIR) micro-spectroscopy. The morphological features and FTIR spectra of the left ventricular myocardium were compared among broiler chickens affected by DCM with clinical signs of heart pump failure, apparently normal fast-growing broiler chickens showing signs of subclinical DCM (high risk of heart failure), slow-growing broiler chickens (low risk of heart failure) and Leghorn chickens (resistant to heart failure, used here as physiological reference). The findings indicate that DCM and heart pump failure in fast-growing broiler chickens are a result of a complex metabolic syndrome involving multiple catabolic pathways. Our data indicate that a good deal of DCM pathophysiology in chickens selected for rapid growth is associated with conformational changes of cardiac proteins, and pathological changes indicative of accumulation of misfolded and aggregated proteins in the affected cardiomyocytes. From TEM image analysis it is evident that the affected cardiomyocytes demonstrate significant difficulty in the disposal of damaged proteins and maintenance of proteostasis, which leads to pathological remodelling of the heart and contractile dysfunction. It appears that the underlying causes of accumulation of damaged proteins are associated with dysregulated auto phagosome and proteasome systems, which, in susceptible individuals, create a milieu conducive for the development of DCM and heart failure. RESEARCH HIGHLIGHTS The light and electron microscopy image analyses revealed degenerative changes and protein aggregates in the cardiomyocytes of chickens affected by DCM. The analyses of FTIR spectra of the myocardium revealed that DCM and heart pump failure in broiler chickens are associated with conformational changes of myocardial proteins. The morphological changes in cardiomyocytes and conformational changes in myocardial proteins architecture are integral constituents of pathophysiology of DCM in fast-growing broiler chickens.

Femoral bone degeneration has been recognized as an important cause of lameness in broiler chickens for many years, but the pathogenesis of this condition has not been completely elucidated. The current work presents comprehensive analyses of changes associated with femoral bone degeneration based on findings from gross pathology, histopathology, biochemistry, and synchrotron-based imaging techniques. Gross lesions were predominantly seen in epiphysis and metaphysis of the proximal femur, and infrequently in distal femur, but we did not observe gross lesions in the diaphysis. Bone fractures were observed occasionally, but the most common lesions involved separation of articular cartilage of the femoral bone head, with progressive erosions of the subchondral bone. In advanced cases, on histopathological examination, changes in femoral bone were indicative of chondronecrosis and osteonecrosis. Computed tomography revealed that the degenerative process involves loss of trabecular bone. The course of the lesion development in the mineralized matrix appears to be coupled with increased bone resorption associated with excessive proliferation of pathologically altered osteoclasts. Light microscopy, Fourier transform infrared spectroscopy, and biochemical analysis provided consistent evidence that lowered protein content of the bone organic matrix is an integral component of femoral bone pathology, but these changes do not appear to be associated with excessive activity of matrix metalloproteinases. Taken together, our findings indicate that femoral bone degeneration is associated with structural changes occurring in both inorganic and organic matrix of the bone, but insufficiency in protein metabolism is most probably a primary aetiological factor in the natural history of femoral bone degeneration. However, it is important to stress that our findings do not negate the importance of bacterial infection in the evolution of this condition. Pathogens play a critical role in the progressive pathogenesis of this condition, which ultimately is manifested, in most instances, as femoral head necrosis.

The present work describes specific congenital intestinal accidents found in commercial broiler chickens where the affected individuals have their intestinal loops translocated outside the abdomen. These anomalies have been observed in many embryos that failed to hatch, in newly hatched chicks, as well as in broilers at various stages of growth. It appears that these lesions stem from incomplete closure of the abdominal cavity during the last stages of embryonic development.

Thermal processing of meat products generates cardiotoxic compounds capable of inducing heart failure in both humans and laboratory animals. Such compounds may be present in broiler diets because supplements such as meat meal (MM), which are commonly used in broiler rations, are rendered at high temperature. Our objective was to evaluate whether putative cardiotoxic compounds in MM increase the risk of heart failure in broilers. The treatment and control diets were prepared by mixing the condensed MM extract (equivalent to dietary MM inclusion of 25%) or placebo (condensed extraction medium) with commercial broiler feed, and the respective diets were offered to commercial male broilers randomly allocated to either treatment or control groups. Broilers fed a diet spiked with MM extract showed a higher incidence (P<0.05) of chronic heart failure (65.5%) in comparison with the control group (55.4%). Postmortem examination upon termination of the experiment revealed that, in comparison with control broilers, broilers fed diet containing MM extract showed higher incidence of lesions indicative of subclinical heart disease evidenced grossly by ventricular dilation and pericardial effusions, microscopically by changes characteristic of cardiomyocyte degeneration, and ultrastructurally by changes in contractile elements and in mitochondria. Measurements of cardiac high-energy phosphates revealed that broilers fed the diet containing MM extract had lower (P<0.05) levels of cardiac energy reserve as compared with birds fed control diet. We conclude that cardiotoxic factors that can induce patho-physiological changes in the heart are present in MM.

The present study examined the possible role of reactive oxygen species in the pathogenesis of heart failure in broilers. Data were collected from three groups of birds at various risk of heart failure: Leghorn chickens (resistant to heart failure), slow-growing feed-restricted broilers (low risk of heart failure), fast-growing ad libitum fed broilers (high risk of heart failure), and broilers with congestive heart failure (CHF). In the first part of the study, basic clinical parameters and ultrastructural changes were examined in the context of lipid peroxidation of the ventricular myocardium. This was followed by the study of in vitro changes in the activity of selected cytosolic enzymes (creatine kinase and lactate dehydrogenase) and mitochondrial enzymes (pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase) in the presence of oxidants (hydrogen peroxide or tertiary butyl hydroperoxide). The distinctive clinical feature in the fast-growing broilers and in the broilers with CHF as compared with slow-growing broilers or Leghorn chickens was a significantly lower heart rate (P <0.05). Electron microscopy revealed marked morphological changes in myocardial mitochondria in these broilers (i.e. fast-growing broilers and broilers with CHF). The level of malondialdehyde equivalents, an indicator of lipid peroxidation subsequent to generated oxidative stress, was significantly higher (P <0.05) in ad libitum fed broilers and was highest (P <0.01) in broilers with CHF. In vitro, the presence of oxidants had a detrimental effect on creatine kinase and alpha-ketoglutarate dehydrogenase activity, while lactate dehydrogenase activity increased. The activity of pyruvate dehydrogenase was not altered by oxidants. Our results indicate that the deterioration of heart function in fast-growing commercial broilers in our experimental model is associated with oxidative stress leading to lipid peroxidation of cellular and mitochondrial membranes, and decreased activity of myocardial creatine kinase and alpha-ketoglutarate dehydrogenase enzymes critical for energy synthesis and transformation pathways.

The present study examines the differences in blood gas parameters, cardiac output, cardiac index, oxygen delivery and tissue oxygen extraction in slow growing chickens (leghorn and feed restricted broilers), fast growing chickens (broilers fed ad libitum) and chickens with fulminant heart failure and ascites. In comparison to leghorns, broiler chickens had lower pO2 and O2 saturation levels in venous blood (P < 0.001). At the age of 35 days, broilers had arterial and venous pO2 significantly lower than 7-day-old broilers (P < 0.05). Overall, blood pO2 and O2 saturation tended to decline, and CO2 content tended to increase with age. Chickens developing ascites had lower blood pO2 and O2 saturation levels, and higher blood CO2 content in comparison to normal chickens (P < 0.05). In comparison to other chickens, ascitic chickens had the lowest pO2 and O2 saturation, and highest CO2 content in both venous and arterial blood (all P < 0.001). Broilers at 35 days of age had higher arterial O2 content than leghorn chicks, and there were only minor differences between normal and ascitic chickens. However, ascitic chickens had the lowest venous O2 content (P < 0.001), but the highest tissue O2 extraction index (P < 0.001). Cardiac index was higher in leghorn chicks than in broilers (P 0.001). Ascitic birds had the lowest cardiac index (P < 0.001). Oxygen delivery was higher in leghorns than in broilers (P < 0.001). Ascitic birds had the lowest oxygen delivery index. The present study has identified significant differences in previously unexamined performance indicators of the cardiovascular system between slow growing chickens, fast growing chickens and chickens with heart failure. Low cardiac index in broiler chickens appears to be the key haemodynamic problem leading to hypoxaemia and ultimately cardiovascular failure in fast growing broilers.

The results presented here are based on a collection of heart necropsy data obtained from a large population of ascitic and normal broiler chickens raised at low altitude. The hearts were subjected to gross postmortem evaluation. Generally, gross changes in the cardiac muscle predominantly consisted of various degrees of right and left ventricular enlargement and atrial enlargement, and were observed in all hearts from birds that developed ascites and in some apparently normal chickens. These hearts appeared flaccid, had a thin ventricular muscle wall, and lacked the normal tone of healthy heart muscle. Ventricular enlargement (mostly dilation) and AV valve degeneration (endocardiosis) were observed as early as 7 to 10 days of age and throughout the remaining growth period in broilers with or without ascites. The hearts from 264 ascitic and 255 apparently normal commercial broilers were used for quantitative analysis, with emphasis on dilatory changes of the ventriculi and detailed evaluation of the atrio-ventricular (AV) valves. The lesions of the AV apparatus and the degree of dilation of the ventriculi were graded according to a priori established standards, and categorized as mild, moderate or severe. Severe or moderate dilation of both the right and left ventricle were observed more frequently (P < 0.001) in ascitic birds than in normal birds. Of hearts from apparently normal birds, 34 and 61% had grossly normal right and left ventricle, respectively. Overall, 30% of ascitic birds had a grossly normal left ventricle, but some degree of right ventricular dilation was found in all ascitic birds. Prominent endocardiosis was a common feature in a majority of hearts from ascitic birds and in some apparently normal birds. Endocardiosis of the left AV valves was observed considerably more frequently (P < 0.001) than of right AV valves. Most severe lesions were found on left AV valves, and consisted of nodules or coalescing formations associated with annulus, valve cusps, chordae tendineae, and sometimes spread to the mural endocardium in the vicinity of the valve apparatus. Frequently the cusps appeared thickened and rigid, and had rolled edges. Chordae tendineae were frequently thickened, and sometimes ruptured. These severe left AV valve lesions were found most frequently (P < 0.001) in the hearts from ascitic birds (52%) in comparison to apparently normal birds (18%). The right AV valve lesions were mainly in the form of small nodules found around the orifice, and less frequently seen on the muscular leaflets of the right valve. Only in a few instances the nodules were larger, ranging from 1 to 3 mm in diameter. The severity of gross lesions on the left AV valve were indicative of stenosis and/or insufficiency of the valve apparatus. A hypothesis that left atrio-ventricular valve degeneration and left ventricular dilation should be considered as a possible aetiologic association with pulmonary hypertension, right ventricular failure, and ascites in broiler chickens is presented and discussed.