Pathophysiology and pathological remodelling associated with dilated cardiomyopathy in broiler chickens predisposed to heart pump failure.

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.

Changes in eggshell structure and predisposition of broilers to health problems: is there a common pathophysiology?

A study of broiler breeder eggs differing in eggshell matrix optical density was conducted to determine the association of eggshell structural quality and the risk of disease in broilers. A total of 10 000 eggs from a broiler breeder flock were examined according to the pre-established criteria, and allocated to groups classified as having a high or low density shell matrix. The eggs from respective groups were incubated and hatched in a commercial hatchery. Samples of unhatched eggs from each group were subjected to detailed examination to establish the cause of reproductive failure. First, quality chicks from each group were raised as separate flocks in a commercial broiler barn. Group performance, morbidity, and mortality were monitored throughout the growth period. All birds were processed in a commercial plant, and condemnation data were compiled. There were significantly more unhatched eggs, and fewer quality chicks in the group classified as having a low density eggshell matrix, in comparison to the high-density group. Embryo pathology accounted for a large proportion of the overall reproductive failure in both groups, with a large proportion of embryos showing anatomical anomalies. The eggs and embryos from the low-density eggshell matrix group were three times more likely to be infected. Significantly higher production losses associated with mortality/morbidity, and condemnations of carcasses at processing were observed in broilers from the low-density eggshell group compared with the high-density eggshell group. It is concluded that common metabolic/physiological changes in breeder hens associated with eggshell pathology may be also risk factors linked with predisposition of broiler chicks to some health problems.

Biochemical and physiological weaknesses associated with the pathogenesis of femoral bone degeneration in 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.

Congenital intestinal incarceration in broiler chickens.

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.

Vascular remodeling and its role in the pathogenesis of ascites in fast growing commercial broilers.

This study examined the putative role of blood vessel pathology in the development of ascites in broilers. Major blood vessels (aorta, brachiocephalic arteries, pulmonary arteries, and vena cava) from normal commercial male broiler chickens, and broilers that developed congestive heart failure (CHF) with or without ascites were subjected to gross and microscopic examination. On cross-section, grossly, the arteries from normal broilers and those showing dilated cardiomyopathy without ascites appeared circular, with firm wall tone characteristic of the normal artery. In contrast, the arteries from ascitic broilers appeared flaccid and lacked elasticity, which was evidenced by collapsing, ellipsoid cross-sectional arterial lumen owing to the structural weakness of the arterial walls. Microscopically, ascitic broilers showed thinning or occasionally total loss of elastic elements in the arterial wall, and reduced network density of the structural matrix of the vascular wall, as well as increased thickness of fibers in vena cava. The structural changes seen in the major arteries from ascitic broilers are maladaptive, and as such would definitively impose an increased hemodynamic burden on the already failing heart pump. The changes in veins are indicative of pathological remodeling conducive to increased permeability of the vascular wall, particularly in the situation when a poorly distensible structure is further subjected to wall stress associated with increased pressure and volume overload. Taken together, increased hemodynamic burden and reduced structural density of the venous wall constitute conditions conducive for seepage and accumulation of ascitic fluid.

Effects of dietary vitamin E and C supplementation on heart failure in fast growing commercial broiler chickens.

1. It has recently been shown that oxidative stress is involved in the pathogenesis of congestive heart failure (CHF) in broiler chickens. Vitamins E and C, common antioxidants, have been advocated for the prevention of heart failure in humans. The present study examines the effects of supplementation of these vitamins on incidence of CHF and prevention of oxidative stress in the myocardium. 2. Commercial male broilers were randomly allocated to three experimental groups and, respectively, offered commercial broiler diet (control), commercial diets fortified with vitamin E (960 IU/kg) or vitamin C (400 mg/kg). The broilers were monitored daily for overt signs of heart failure and clinical data including ECG and blood gas analysis were collected periodically. Lipid peroxidation was measured in cardiac tissues from apparently normal broilers and broilers developing CHF in each group using thiobarbituric acid reactive substances (TBARS) assay. 3. Overall, the incidence of CHF in broilers given diets fortified with vitamin E or vitamin C was not significantly different as compared to the control group. The incidence of overt signs of hypoxaemia was lower in the vitamin C group than in the control group. Lipid peroxidation was highest in broilers that developed CHF as compared to apparently normal broilers fed either vitamin E or C fortified diets. Neither vitamin E nor vitamin C was effective in preventing oxidative damage in broilers that developed CHF. 4. In conclusion, the present study confirmed that oxidative stress is involved in the pathogenesis of heart failure in broilers, but dietary supplementation of antioxidant vitamins did not prevent oxidative damage in broilers that developed CHF. Beneficial effects of vitamin C supplementation were evidenced by lower incidence of hypoxaemia, and the tendency to reduce the susceptibility of broilers to heart failure. However, vitamin E did not have any impact on clinical status or the incidence of CHF.

Putative cardiotoxic compounds extracted from meat meal as a potential risk factor for the development of heart failure in fast-growing commercial broilers.

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 role of oxidative stress in the development of congestive heart failure in a chicken genotype selected for rapid growth.

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.

Sub-clinical necrotic enteritis in broiler chickens: novel etiological consideration based on ultra-structural and molecular changes in the intestinal tissue.

The present study revealed several previously not recognized etiological details in the development of necrotic enteritis (NE) in broilers. We provide evidence that the pathological process leading to mucosal epithelium necrosis follows morphologically distinct phases commencing at the basal domain of the mucosal epithelium and then progressively invading the entire lamina propria. Initially mucosal epithelium appears normal, but as the pathological changes progress throughout the lamina propria, the adjacent enterocytes begin to show features of necrotic cell death and the necrotic process of the epithelium progresses from being focal to locally extensive. Ultra-structural examination showed that primary changes occur at the level of basal and lateral domains of the enterocytes, whereas the apical domain of enterocytes remains intact even in the face of advanced necrotic changes. This indicates that the mucosal necrosis does not result from direct damage to the mucosal epithelium. Rather, the necrotic death of enterocytes is a consequential effect of the destruction of lamina propria, the extra-cellular matrix, and intercellular junctions. The nature of these morphological changes indicates that initiation of the pathological process leading to NE involves proteolytic factors affecting the extra-cellular matrix and cellular junctions. Further studies revealed that, indeed, the elevated activity of collagenolytic enzymes in the mucosal milieu and in intestinal tissue represents an integral component of the pathological process leading to NE. In the first instance we discovered that Clostridium perfringens strains isolated from field cases of NE secrete several potent collagenolytic enzymes. In the second instance we observed that, in comparison to controls, broilers challenged with C. perfringens isolated from field cases of NE show high levels of several collagenolytic enzymes in the intestinal tissue. A major component of the overall collagenolytic activity detected in the intestinal tissue was identified by zymography as matrix metalloproteinases (MMPs). Dominant activity was associated with MMP-2. We confirmed using immuno-histochemistry that this enzyme is expressed at high levels in mucosal tissue showing signs of NE. The high levels of collagenolytic activities, in particular associated with MMP-2, demonstrated in our studies are consistent with the nature of morphological changes observed primarily in extra-cellular matrix (ECM) at the basal domain of enterocytes, as well lateral domains of enterocytes. The lack of changes at the level of apical domain of mucosal epithelium indicates that the lipolytic aspect of alpha toxin in NE is not an essential factor in primary lesions development. Taken together, our findings indicate that the early lesions leading to NE are associated with virulence factors that induce proteolytic activity, rather than lipolytic activity.

A study on pathogenesis of sudden death syndrome in broiler chickens.

Sudden death syndrome (SDS) in fast growing broiler chickens has been recognized as a patho-physiological entity for four decades, but its pathogenesis still remains unknown. More recent investigations provided evidence that link SDS to cardiac arrhythmia, but the mechanism triggering arrhythmogenesis and factors responsible for fatal outcome are poorly understood. In order to understand the chain of events leading to SDS in broilers, the present study focused on putative mechanisms that trigger arrhythmia and mechanisms that predispose the myocardium to fatal arrhythmia. Susceptibility of broilers to cardiac arrhythmia under stress conditions was evaluated using a simulated stress test with epinephrine. Detailed histopathological evaluation of the broiler heart was undertaken to identify structural features that may predispose the myocardium to fatal arrhythmia. The simulated stress challenge revealed that many broilers are highly susceptible to stress induced cardiac arrhythmia. In some broilers the stress challenge induced severe ventricular arrhythmia, and the life threatening nature of this arrhythmia was evidenced by the fact that several birds showing the most severe arrhythmic responses, died suddenly within several days after the stress challenge. Examination of hearts of broilers that died of SDS revealed microscopic lesions in the cardiomyocytes, and widespread changes in the sub-endocardial and mural His-Purkinje system (HPS). Immune staining for Caspase-3 confirmed that numerous Purkinje cells in the left ventricular myocardium from broiler chickens that died of SDS were undergoing apoptosis. The observed lesions suggest that the electrical stability of the myocardium was compromised. Taken together, our findings indicate that stress is a most likely trigger of cardiac arrhythmia in broilers, whereas the pathological changes seen in the myocardium and in the HPS in fast growing broilers provide a very conducive milieu for sustained ventricular arrhythmia. In cases where the electrical stability of the myocardium is compromised, even an episodic arrhythmic event may readily degenerate to catastrophic ventricular fibrillation and sudden death. We conclude that the combination of stress and changes in the cardiomyocytes and HPS are the key requisite features in the pathogenesis of SDS.

Biochemical factors limiting myocardial energy in a chicken genotype selected for rapid growth.

Broiler chickens (Gallus gallus) genetically selected for rapid growth are inherently predisposed to heart failure. In order to understand the biochemical mechanisms associated with the deterioration of heart function and development of congestive heart failure (CHF) in fast-growing chickens, this study examined several factors critical for myocardial energy metabolism. Measured variables included cardiac energy substrates [creatine phosphate (CrP), adenosine triphosphate (ATP), l-carnitine], activity of selected cytosolic enzymes [creatine kinase (CK; EC 2.7.3.2), lactate dehydrogenase (LDH; EC 1.1.1.27)] and mitochondrial enzymes [pyruvate dehydrogenase (PDH; EC 1.2.4.1), alpha-ketoglutarate dehydrogenase (alpha-KGDH; EC 1.2.4.2)]. The CK activities were higher in fast-growing and CHF broilers as compared to slow-growing broilers (p<0.05). Cardiac LDH and alpha-KGDH activities were not changed (p>0.05), whereas PDH activity was highest (p<0.05) in broilers with CHF. Deterioration of heart function is correlated with lowered cardiac ATP, CrP, and l-carnitine levels (all p<0.05). Depletion of high energy phosphate substrates, ATP and CrP, is evident in fast-growing chickens and those that developed CHF. Increased activity of CK suggests that cardiac energy management in fast-growing broilers and those with CHF largely depends on contribution of this pathway to regeneration of ATP from CrP. In this scenario, inadequate level of CrP is a direct cause of ATP insufficiency, whereas low cardiac l-carnitine, because of its role in fatty acid transport, is most likely an important factor contributing to shortage of key substrate required for synthesis of cardiac ATP. The insufficiencies in cardiac energy substrate synthesis provide metabolic basis of myocardial dysfunction in chickens predisposed to heart failure.

Excessive dietary vitamin D supplementation as a risk factor for sudden death syndrome in fast growing commercial broilers.

Broiler diets are frequently fortified with vitamin D (D3) above the recommended levels in an attempt to prevent commonly occurring leg problems. Since the basal levels of dietary D3 are rarely known, there is a risk of over-supplementation. Over-supplementation of D3 has been shown to have detrimental effects on the heart. Sudden death syndrome (SDS) is a condition commonly observed in broiler flocks and is associated with acute heart failure. The present study examines the effects of excessive levels of vitamin D3 on cardiac health in fast growing broiler chickens. Commercial male broilers (Gallus gallus) were exposed to either a commercial diet or a commercial diet supplemented with D3. Throughout the trial all birds were monitored several times daily for overt signs of heart disease, and periodically electrocardiographic measurements were obtained. Morbidity and mortality data were collected daily. On day 32 a simulated stress challenge consisting of a single injection of epinephrine (100 microg/kg BW) was administered under continuous ECG monitoring. Broilers fed the high D3 diet were 2.5 fold more likely to succumb to acute heart failure and die of SDS (p<0.05). Electrocardiographic examination showed a higher rate of cardiac arrhythmia in birds fed the high D3 diet (22.6%), in comparison to those fed the control diet (11.8%). The stress challenge test revealed that broilers exposed to high dietary D3 were more susceptible to ventricular arrhythmia. Our findings indicate that over-supplementation of vitamin D increases the risk of SDS in broilers, and that the most likely mechanism is associated with increased susceptibility of the ventricular myocardium to arrhythmia.

Comparative study of myocardial high energy phosphate substrate content in slow and fast growing chicken and in chickens with heart failure and ascites.

In order to explain the biochemical mechanisms associated with deteriorating heart function in broiler chickens, this study compared myocardial high energy phosphate substrates in leghorns, feed restricted (Broilers-Res) broilers, ad libitum fed broilers (Broilers-AL), and in broilers that developed heart failure and ascites. The profile of adenine nucleotide content in the heart tissue did not differ between leghorns and Broilers-Res, but there were significant differences among Broilers-Res, Broilers-AL, and broilers with ascites. During intensive growth periods, leghorns and Broilers-Res showed increasing trends in heart ATP levels, whereas in fast growing broilers the heart ATP declined (p<0.021). ATP:ADP and ATP:CrP ratios increased with age in both leghorn and Broilers-Res, declined in fast growing broilers, and were the lowest in broilers that developed heart failure. The changes in heart high energy phosphate profile in broilers suggest that the energy demand of the heart during a rapid growth phase may exceed the bird's metabolic capacity to supply adequate levels of high energy phosphate substrate. The insufficiency of energy substrate likely contributes to the declining heart rate. In some individuals this may lead to impaired heart pump function, and in more severe cases may progress to heart pump failure.

Responses of broiler chickens orally challenged with Clostridium perfringens isolated from field cases of necrotic enteritis.

The present study examines the responses of broiler chickens to oral administration of Clostridium perfringens freshly isolated from field cases of necrotic enteritis (NE). The challenge studies included long-term exposure and short-term exposure, factored in with dietary and management variables including high levels of dietary components such as fish meal, meat meal, abrupt change of feed, and fasting. In the long-term exposure trials, the birds were orally inoculated daily, with 1 ml (1.0 or 2 x 10(8) CFU/ml) of an overnight culture of C. perfringens for 7 days. Short-term exposure trials involved challenge with 1 ml (3 x 10(10) CFU/ml) administered as a single dose. The responses of broilers to orally administered C. perfingens under laboratory controlled conditions are presented and discussed in the context of authentic field cases of necrotic enteritis. None of the challenge trials produced overt clinical signs of NE and there were no mortalities associated with oral exposure to high doses of C. perfringens. However, many of the challenged birds showed distinctly pronounced pathological changes in the intestinal tissue. On gross examination the responses in birds challenged orally with C. perfringens could be placed into two categories: (1) no apparent pathological changes in the intestinal tissue and (2) sub-clinical inflammatory responses with focal, multi-focal, locally extensive, or disseminated distribution throughout various sections of duodenum, jejunum, ileum, and ceca. In birds that responded with intestinal lesions, hyperemia and occasional hemorrhages were the main gross changes. In some birds, the mucosa was covered with a brownish material, but typically, the mucosa was lined by yellow or greenish, loosely adherent material. Mild gross changes were seen in some control birds, but both qualitatively and quantitatively, the lesions were distinctly more pronounced in the challenged birds. Upon histological examination, none of the experimentally exposed birds showed overt mucosal necrosis typical of field cases of NE, but typically the lamina propria was hyperemic and infiltrated with numerous inflammatory cells. Most significant changes were seen at the interface of the basal domain of enterocytes and lamina propria. Multifocally, these areas were extensively edematous, allowing for the substantial disturbance of the structural integrity between the lamina propria and the enterocytes. The lesions observed in the present study were consistently reproduced in all of our challenge trials, hence these responses may signify newly emerging patterns of sub-clinical enteric disorders in contemporary strains of poultry. The pathological changes observed in broilers challenged orally with C. perfringens in the present study, differ significantly from those reported previously, and must be clearly differentiated from those described in cases of NE or ulcerative enteritis. Although no overt necrosis of the intestinal mucosa typical of field cases of NE were observed in the present study, the birds challenged with C. perfringens showed strong inflammatory reaction to the introduced pathogens. The distinct features of the microscopic lesions were changes involving apparently normal enterocytes at the interface of the basal domain of villar epithelia and lamina propria. Although the pathological changes in the intestinal tissues observed in our trials appear to be rather subtle when compared to field cases of NE, the nature of these lesions suggest a significant negative effect on the digestive physiology of intestinal mucosa.

The role of first line of defence mechanisms in the pathogenesis of cellulitis in broiler chickens: skin structural, physiological and cellular response factors.

The present study examined several basic attributes of first-line defence mechanisms in the skin as potential factors that may explain the susceptibility of broiler chickens to cellulitis. The variables including structural characteristics of the skin, physicochemical properties and cellular responses to the challenge with pathogens were compared between two categories of chickens, a strain of fast-growing commercial broiler chickens (susceptible to cellulitis) and leghorn chickens (resistant to cellulitis). There were substantial differences between leghorns and broilers with regard to physiological characteristics of the skin. Broiler skin was more amenable to injury and the wound-healing process was slow. Compared with leghorns, the lesions resulting from sub-dermal challenge in broilers were more severe and disseminated over a larger area. Mobilization of phagocytic cells (heterophils and macrophages) in leghorns was brisk even in the areas distant from the site of infection, whereas only few heterophils were recruited in the skin of broilers. The functional competence of heterophils in broilers was inferior when compared with leghorns. Based on the present finding, the predisposition of broilers to cellulitis appears to be primarily associated with the inferior first line of defence of their skin. Broilers in commercial situations may be at higher risk to succumb to even minor infection and eventually develop cellulitis because: (1) structural weaknesses of the skin may predispose broilers to skin injury and thus the risk of skin infection by pathogens is increased; (2) broiler skin surface is more likely to provide a conducive environment for colonization of Escherichia coli; (3) in the event of infection, poor recruitment of phagocytic cells to the site of infection may readily lead to widespread colonization of the tissue by pathogens causing cellulitis and (4) poor functional quality of the phagocytic cells that are mobilized compromise the ability of the host to contain the spread of infection.

The aetiology of hypoxaemia in chickens selected for rapid growth.

In comparison to other classes of chickens, broilers selected for rapid growth tend to be hypoxaemic, and many develop congestive heart failure (CHF). In order to explain the physiological mechanisms associated with hypoxaemia in fast-growing broiler chickens (Gallus gallus), this study examined several basic physiological parameters including the blood gas profile in arterial [left atrial (LA)] and mixed venous [right atrial (RA)] blood, systemic oxygen extraction ratio, and intrapulmonary shunt fraction. These parameters were further studied in the context of blood flow in the pulmonary circulation, structural characteristics of the lungs, and cardiac function [measured as cardiac index (CI)]. Overall, broilers had lower arterial and mixed venous blood pO(2) levels and higher pCO(2) levels compared to leghorns. The cardiac index was lower in fast-growing and CHF broilers compared to leghorn chickens or feed-restricted broilers. Systemic oxygen extraction ratio (ER) and intrapulmonary shunt fraction were significantly higher in fast-growing broilers and birds with CHF (all P<0.01). Lungs of all broilers, but not leghorns, contained ectopic, irregular nodular formations located within air spaces. Broilers with clinical signs of hypoxaemia revealed the highest number of these formations in their lung. Taken together, the present findings indicate that key factors associated with the development of hypoxaemia in fast-growing broilers include: (1) high demand for oxygen as evidenced by high oxygen ER; (2) inadequate cardiac output (CO) to fulfill the higher oxygen demands, leading to severe depletion of O(2) in mixed venous blood; and (3) elevated intrapulmonary shunt fraction and possibly dead space associated with specific pathological and anatomical characteristics within the lung.

Feeding high levels of lupine seeds to broiler chickens: plasma micronutrient status in the context of digesta viscosity and morphometric and ultrastructural changes in the gastrointestinal tract.

This work examines the effects of lupine-based diets on the status of the host's riboflavin and zinc. Test diets contained 35% soybean meal (control) or raw (40%) or dehulled (35%) lupine seed meal and were isocaloric (13.4 MJ of AME/kg) and isonitrogenous (23% crude protein). Each diet was offered ad libitum to a group of 16 male commercial broiler chicks for 21 d, starting at 1 d of age. Broilers fed lupine diets had lower feed intakes and growth rates. All sections of the intestinal tract were significantly enlarged (P < 0.01) in all groups fed lupine-based diets in comparison with broilers fed the soybean meal diet, but there were no differences in the morphologies of the mucosa, submucosa, muscularis, or serosa. Increased size of the duodenum, jejunum, and ileum was predominantly attributed to the increase in length rather than intestinal tissue mass. Hence, the enlargement of the intestinal tract was consistent with physiological hyperplasia and not pathological remodeling and hypertrophy. Overall, broilers fed lupine-based diets had more viscous digesta than those fed the soybean meal diet, but the differences were statistically not significant. Blood plasma Zn concentration did not differ between broilers fed lupine-based diets and those fed soybean-meal-based diets, and all broilers fed lupine-based diets had significantly higher (P < 0.001) riboflavin concentrations. In this context, it is apparent that the bioavailability of these micronutrients from lupine diets is not compromised. Intestinal tissue hyperplasia may be interpreted as physiological adaptation to increase absorptive capacity and thus maximize absorption of essential nutrients in the face of antinutritional factors in the diet.

Lesions of the pericardium and their significance in the aetiology of heart failure in broiler chickens.

The present study focuses on lesions of the pericardium commonly observed in fast growing broilers. These lesions are examined in the context of electrophysiological and functional changes associated with cardiac performance and patho-physiology in broilers succumbing to acute or chronic heart failure. Typical lesions involving the pericardium in fast growing broiler chickens included: (1) excessive pericardial effusion, (2) locally extensive or focal adhesions between parietal and visceral components of the pericardium, (3) fibrous deposits on visceral pericardium, and (4) thickened pericardium. Echocardiographic evidence indicated that severe pericardial effusion and/or adhesions may have a restrictive effect on heart pump function, where both diastolic and systolic function of the heart may be affected. Electrocardiographic data showed a strong trend indicating that pericardial adhesions may be associated with ventricular arrhythmia and increased risk of sudden death in fast growing broilers. Relatively high levels of matrix metalloproteinase MMP-2 activity have been found in pericardial effusions from affected chickens, suggesting a possible involvement of this enzyme in the aetiology of pericardial lesions. The present results indicate that pericardial lesions may be associated with biochemical, morphological, electrophysiological, and functional changes occurring in the hearts of broilers succumbing to acute or chronic heart failure and ascites.