Novel Staged Free-Fall Reactor for the (Catalytic) Pyrolysis of Lignocellulosic Biomass and Waste Plastics.

Pyrolysis of lignocellulosic biomass and waste plastics has been intensely studied in the last few decades to obtain renewable fuels and chemicals. Various pyrolysis devices have been developed for use in a laboratory setting, operated either in batch or continuously at scales ranging from milligrams per hour to tenths of g per hour. We report here the design and operation of a novel staged free-fall (catalytic) pyrolysis unit and demonstrate that the concept works very well for the (catalytic) pyrolysis of pinewood sawdust, paper sludge, and polypropylene as representative feeds. The unit consists of a vertical tube with a pretreatment section, a pyrolysis section, a solid residue collection section, a gas-liquid separation/collection section, and a catalytic reaction section to optionally perform ex situ catalytic upgrading of the pyrolysis vapor. The sample is placed in a tube, which is transported by gravity through various sections of the unit. It allows for rapid testing with semicontinuous feeding (e.g., 50 g h-1) and the opportunity to perform reactions under an (inert) gas (e.g., N2) at atmospheric as well as elevated pressure (e.g., 50 bar). Liquid yields for noncatalytic sawdust pyrolysis at optimized conditions (475 °C and atmospheric pressure) were 63 wt % on biomass intake. A lower yield of 51 wt % (on a biomass basis) was obtained for the noncatalytic pyrolysis of paper sludge, likely due to the presence of minerals (e.g., CaCO3) in the feed. The possibility of using the unit for ex situ catalytic pyrolysis (pyrolysis at 475 °C and catalytic upgrading at 550 °C) was also successfully demonstrated using paper sludge as the feed and H-ZSM-5 as the catalyst (21 wt % catalyst on biomass). This resulted in a biphasic liquid product with 25.6 wt % of an aqueous phase and 11 wt % of an oil phase. The yield of benzene, toluene, and xylenes was 1.9 wt % (on a biomass basis). Finally, the concept was also proven for a representative polyolefin (polypropylene), both noncatalytic as well as in situ catalytic pyrolysis using H-ZSM-5 as the catalyst at 500 °C. The liquid yield of thermal, noncatalytic plastic pyrolysis was as high as 77 wt % on plastic intake, while in situ catalytic pyrolysis gave a combined 7.8 wt % yield of benzene, toluene, and xylenes on plastic intake.

A Central Bioactive Region of LTBP-2 Stimulates the Expression of TGF-ß1 in Fibroblasts via Akt and p38 Signalling Pathways.

Latent transforming growth factor-ß-1 binding protein-2 (LTBP-2) belongs to the LTBP-fibrillin superfamily of extracellular proteins. Unlike other LTBPs, LTBP-2 does not covalently bind transforming growth factor-ß1 (TGF-ß1) but appears to be implicated in the regulation of TGF-ß1 bioactivity, although the mechanisms are largely unknown. In experiments originally designed to study the displacement of latent TGF-ß1 complexes from matrix storage, we found that the addition of exogenous LTBP-2 to cultured human MSU-1.1 fibroblasts caused an increase in TGF-ß1 levels in the medium. However, the TGF-ß1 increase was due to an upregulation of TGF-ß1 expression and secretion rather than a displacement of matrix-stored TGF-ß1. The secreted TGF-ß1 was mainly in an inactive form, and its concentration peaked around 15 h after addition of LTBP-2. Using a series of recombinant LTBP-2 fragments, the bioactivity was identified to a small region of LTBP-2 consisting of an 8-Cys motif flanked by four epidermal growth factor (EGF)-like repeats. The LTBP-2 stimulation of TGF-ß expression involved the phosphorylation of both Akt and p38 mitogen-activated protein kinase (MAPK) signalling proteins, and specific inactivation of each protein individually blocked TGF-ß1 increase. The search for the cell surface receptor mediating this LTBP-2 activity proved inconclusive. Inhibitory antibodies to integrins ß1 and αVß5 showed no reduction of LTBP-2 stimulation of TGF-ß1. However, TGF-ß1 upregulation was partially inhibited by anti-αVß3 integrin antibodies, suggestive of a direct or indirect role for this integrin. Overall, the study indicates that LTBP-2 can directly upregulate cellular TGF-ß1 expression and secretion by interaction with cells via a short central bioactive region. This may be significant in connective tissue disorders involving aberrant TGF-ß1 signalling.

LTBP-2 Has a Single High-Affinity Binding Site for FGF-2 and Blocks FGF-2-Induced Cell Proliferation.

Latent transforming growth factor-beta-1 binding protein-2 (LTBP-2) belongs to the fibrillin-LTBP superfamily of extracellular matrix proteins. LTBPs and fibrillins are involved in the sequestration and storage of latent growth factors, particularly transforming growth factor ß (TGF-ß), in tissues. Unlike other LTBPs, LTBP-2 does not covalently bind TGF-ß, and its molecular functions remain unclear. We are screening LTBP-2 for binding to other growth factors and have found very strong saturable binding to fibroblast growth factor-2 (FGF-2) (Kd = 1.1 nM). Using a series of recombinant LTBP-2 fragments a single binding site for FGF-2 was identified in a central region of LTBP-2 consisting of six tandem epidermal growth factor-like (EGF-like) motifs (EGFs 9-14). This region was also shown to contain a heparin/heparan sulphate-binding site. FGF-2 stimulation of fibroblast proliferation was completely negated by the addition of 5-fold molar excess of LTBP-2 to the assay. Confocal microscopy showed strong co-localisation of LTBP-2 and FGF-2 in fibrotic keloid tissue suggesting that the two proteins may interact in vivo. Overall the study indicates that LTBP-2 is a potent inhibitor of FGF-2 that may influence FGF-2 bioactivity during wound repair particularly in fibrotic tissues.

Targeting Pim kinases for cancer treatment: opportunities and challenges.

Pim oncogenes are highly expressed in many types of hematological and solid cancers. Pim kinases regulate the network of signaling pathways that are critical for tumorigenesis and development, making Pim kinases the attractive drug targets. Currently, two approaches have been employed in designing Pim kinase inhibitors: ATP-mimetics and non-ATP mimetics; but all target the ATP-binding pocket and are ATP-competitive. In this review, we summarize the current progress in understanding the Pim-related structure and biology, and provide insights into the binding modes of some prototypical Pim-1 inhibitors. The challenges as well as opportunities are highlighted for development of Pim kinase inhibitors as potential anticancer agents.

LTBP-2 has multiple heparin/heparan sulfate binding sites.

Latent transforming growth factor-beta-1 binding protein-2 (LTBP-2) is a protein of poorly understood function associated with fibrillin-1-containing microfibrils during elastinogenesis. In this study we investigated the molecular interactions of LTBP-2 with heparin and heparan sulfate proteoglycans (HSPGs) since unidentified cell surface HSPGs are critical for normal fiber assembly. In solid phase assays, heparin conjugated to albumin (HAC) bound strongly to recombinant full-length human LTBP-2. This interaction was completely blocked by addition of excess heparin, but not chondroitin sulfate, confirming specificity. Analysis of binding to LTBP-2 fragments showed that HAC bound strongly to N-terminal fragment LTBP-2 NT(H) and more weakly to central fragment LTBP-2 C(H). No binding was detected to C-terminal fragment LTBP-2 CT(H). Kds for heparin binding were calculated for full-length LTBP-2, LTBP-2 NT(H) and LTBP-2 C(H) as 0.9 nM, 0.7 nM and 80 nM respectively. HAC interaction with fragment LTBP-2 NT(H) was not sensitive to EDTA or EGTA indicating that binding had no requirement for Ca(2+) ions whereas HAC binding to fragment LTBP-2 C(H) was markedly reduced by these chelating agents indicating a degree of Ca(2+) dependence. Inhibition studies with synthetic peptides identified three major heparin binding sequences in fragment LTBP-2 NT(H), including sequence LTEKIKKIKIV in the first large cysteine-free domain of LTBP-2, adjacent to the previously identified fibulin-5 binding site. LTBP-2 was found to interact strongly in a heparin-inhibitable manner with cell surface HSPG syndecan-4, but showed no interaction with recombinant syndecan-2. LTBP-2 also showed strong interaction with the heparan sulfate chains of basement membrane HSPG, perlecan. The potential importance of HSPG-LTBP-2 interactions in elastic fiber assembly and microfibril attachment to basement membranes is discussed.

The response of the heart and pulmonary arteries to hypoxia, pressure, and volume. A short review.

The pulmonary arterioles react to hypoxia by contraction and to increased pressure and volume by hypertrophy of the muscular wall, referred to as pulmonary vascular remodeling, both of which increase vascular resistance and result in increased pulmonary arterial pressure. Heart muscle reacts to increased pressure by hypertrophy of cardiac myocytes and thickening of the muscular wall. The heart responds to increased volume by dilation of the chamber that may result in physiologic or pathologic hypertrophy of the muscle wall. Heart muscle cells are very sensitive to hypoxia or other insults, and this may result in death of individual cardiac myocytes with lengthening and thinning of the remaining heart muscle cells and dilation of the chamber in a process called dilated cardiomyopathy.

Heritability of sudden death syndrome and its associated correlations to ascites and body weight in broilers.

(1) Genetic parameters for the sudden death syndrome (SDS) were estimated in meat-type chickens. Data were collected over 11 generations of selection for body weight within two distinct breeds (Cornish and White Rock). (2) The animal model was used exclusively with linear methods (LM) to estimate genetic parameters. Heritability (h2) of SDS on the liability scale was 0.30 +/- 0.002 and 0.25 +/- 0.002 in the Cornish and White Rock breeds, respectively. (3) A positive genetic correlation (r(g)) with ascites (AS) was determined (approximately 0.3 +/- 0.006). However, it was not possible to estimate the rg of SDS with body weight because of the low prevalence of the defect trait studied (1.8% in the Cornish and 1-5% in the White Rock). (4) Heritability of SDS calculated using male records only was 0.45 +/- 0.009 and 0.35 +/- 0.009, and r(g) with body weight was 0.30 +/- 0.010 and 0.27 +/- 0.009, in the Cornish and White Rock breeds, respectively. (5) In conclusion, the heart defect investigated was heritable with a positive genetic correlation with AS and body weight.

Molecular characterization and analysis of the acrB gene of Aspergillus nidulans: a gene identified by genetic interaction as a component of the regulatory network that includes the CreB deubiquitination enzyme.

Mutations in the acrB gene, which were originally selected through their resistance to acriflavine, also result in reduced growth on a range of sole carbon sources, including fructose, cellobiose, raffinose, and starch, and reduced utilization of omega-amino acids, including GABA and beta-alanine, as sole carbon and nitrogen sources. The acrB2 mutation suppresses the phenotypic effects of mutations in the creB gene that encodes a regulatory deubiquitinating enzyme, and in the creC gene that encodes a WD40-repeat-containing protein. Thus AcrB interacts with a regulatory network controlling carbon source utilization that involves ubiquitination and deubiquitination. The acrB gene was cloned and physically analyzed, and it encodes a novel protein that contains three putative transmembrane domains and a coiled-coil region. AcrB may play a role in the ubiquitination aspect of this regulatory network.

Estimation of genetic parameters for ascites syndrome in broiler chickens.

Genetic parameters for the ascites syndrome (AS) were estimated for meat-type chickens. Data had been collected over 11 generations of selection for body weight and other traits within two distinct breeds (Cornish and White Rock). Linear methods (LM) were used to estimate genetic parameters and also to analyze a binary measure of survival. Survival analyses (SA) were also conducted to estimate the effects of various factors influencing the incidence of AS by evaluating the number of days that the birds survived. The animal model was used exclusively with linear methods. Heritabilities (h2) on the liability scale were 0.12 +/- 0.02 and 0.22 +/- 0.01 in the White Rock and Cornish breeds, respectively; however, the genetic correlation (r(g)) with body weight was not possible to estimate due to the low prevalence of the defect trait studied (1.5% in the Cornish and 1.1% in the White Rock). Because males are more prone to AS, the h2 using the male records only were 0.22 +/- 0.017 and 0.41 +/- 0.009, and the r(g) were 0.35 +/- 0.007 and 0.22 +/- 0.009 in the dam and sire populations, respectively. In conclusion, the heart defect investigated was heritable and had a positive genetic correlation with body weight.

The effect of dietary chloride and bicarbonate on blood pH, haematological variables, pulmonary hypertension and ascites in broiler chickens.

1. The effect of supplementing grower diets with bicarbonate or chloride on haematological variables, pulmonary hypertension syndrome and ascites in broilers exposed to cold temperature was investigated. 2. High concentrations of dietary chloride had no effect on the pH of the venous blood but a low chloride/high bicarbonate diet significantly increased blood pH. There was no consistent effect of dietary chloride or bicarbonate concentrations on growth performance, although in 1 experiment birds given a low chloride/high bicarbonate diet consumed less food and gained less weight than controls. 3. Birds fed on high-chloride diets tended to have a higher incidence of ascites and pulmonary hypertension than controls. Birds fed on low-chloride and high-bicarbonate diets had significantly lower pulmonary hypertension and lower heart weights, which may have indicated a decrease in pulmonary and systemic blood pressure. 4. We conclude that increasing dietary bicarbonate and reducing dietary chloride has potential as a low cost and effective method to reduce the pulmonary hypertension which leads to ascites in broiler chickens.

The effects of dietary flax oil and antioxidants on ascites and pulmonary hypertension in broilers using a low temperature model.

1. Three experiments were conducted using a low temperature model to induce pulmonary hypertension (PH) and ascites in broiler chickens. Diets containing 25 g or 50 g flax oil/kg food and control diets with an equivalent amount of animal/vegetable (A/V) blend oil, with and without supplemental antioxidants (vitamin C and vitamin E) were used. The amount of PH was assessed by the ratio of right ventricle weight to total ventricle weight (RV/TV ratio). Birds were considered to suffer from pulmonary hypertension syndrome (PHS) if the RV/TV ratio was greater than 0.299. 2. In experiment 1, the test diets contained 50 g oil/kg food and were given during the grower period only. Birds fed on the flax oil diet tended to have a lower incidence of PHS, ascites and lower RV/TV ratios than birds fed on the control diet. However, when the flax oil diet was supplemented with antioxidants, the incidence of ascites, PHS, haematocrit and whole blood and plasma viscosity increased compared with birds fed on the flax oil diet without antioxidants. These effects were not seen in experiment 2, when the test diets containing 30 g oil/kg food (25 g flax oil plus 5 g A/V blend oil/kg food compared to 30 g A/V blend oil/kg food) were given during the grower period. However, in experiment 3, when the test diets containing 30 g oil/kg food were given from day 1 to week 8, birds fed on the control diet supplemented with antioxidants had a higher incidence of PHS than those fed on the control diet alone. 3. In all 3 experiments, there was no significant effect of dietary fat source or supplemental antioxidants on total food intake or food conversion. 4. We conclude that diets containing 50 g flax oil/kg food tend to reduce the incidence of PHS and ascites in broilers using a low temperature model but the results were not statistically significant. In some cases, supplementing diets with a combination of vitamin E and vitamin C increased the incidence of ascites and PHS.

Experimental Escherichia coli respiratory infection in broilers.

This study determined optimal conditions for experimental reproduction of colibacillosis by aerosol administration of avian pathogenic Escherichia coli to 2-to-4-wk-old broiler chickens. The basic model for reproducing disease was intranasal administration of approximately 10(4) mean embryo infectious dose of infectious bronchitis virus (IBV) followed by aerosol administration of an 02 or an 078 strain of E. coli in a Horsfall unit (100 ml of a suspension of 10(9) colony-forming units/ml over 40 min). Scores were assigned to groups of infected chickens on the basis of deaths; frequency and severity of lesions in the air sacs, liver and heart; and recovery of the challenge E. coli 6 days post-E. coli infection. An interval of 4 days between the IBV and E. coli challenges was best whether the chickens received the IBV at 8 or 20 days of age. Typically, 50%-80% of the chickens developed airsacculitis and 0 to 29% of the chickens developed pericarditis or perihepatitis, with little or no mortality. Escherichia coli alone resulted in no deaths and 0 to 20% airsacculitis, but these percentages increased to 0 to 5% and 52%-60% when the E. coli aerosol was administered through a cone-shaped chamber. Administration of IBV alone failed to induce lesions. Recovery of the challenge E. coli from chickens did not correlate well with lesions. On the basis of these data, administration of IBV to 20-day-old chickens followed 4 days later by exposure to an avian pathogenic E. coli reproduces avian colibacillosis with the low mortality, high percentage of airsacculitis, and low percentage of septicemic lesions characteristic of the conditions seen in the natural disease.

Physiological, management and environmental triggers of the ascites syndrome: a review.

In meat-type chickens, an inadequacy of vascular capacity for blood flow through the lung to provide the tissues with the oxygen needed for rapid growth is the primary cause of pulmonary hypertensioninduced ascites. There are a variety of other factors that can trigger the ascites syndrome. These factors may cause increased blood flow because of a higher metabolic rate (cold, heat, certain nutrients, chemicals, etc.) or they may cause pulmonary hypertension-induced ascites in rapidly growing chickens because of greater resistance to blood flow in the lung by: (i) increased blood viscosity or red blood cell rigidity; or (ii) reduced vascular capacity in the lung. Some secondary factors, such as high sodium from salt in feed or water, may cause both increased flow and increased resistance to flow. Measures to reduce the ascites syndrome must address the primary genetic cause of insufficient vascular flow capacity in the lung and oxygen delivery to tissues, and the secondary factors that increase oxygen requirement, blood flow and the resistance to blood flow in the lung.

The use of selected plasma enzyme activities for the diagnosis of fatty liver-hemorrhagic syndrome in laying hens.

Profiles of plasma enzymes were compared in two strains of single comb white leghorn laying hens, a normal commercial strain and strain UCD-003, which is highly susceptible to fatty liver-hemorrhagic syndrome. Plasma activity of lactate dehydrogenase (LDH), glutamate dehydrogenase (GDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatine kinase (CK) averaged 194 +/- 27, 4.0 +/- 2.8, 146 +/- 20, 1.0 +/- 1.0, and 1041 +/- 268 U/liter, respectively in normal birds. Activities of LDH, GDH, AST, and ALT, but not CK, were significantly higher in UCD-003 than in normal hens. A bimodal distribution of activities of all enzymes was found in the UCD-003 hens, with some birds showing activities comparable with those of the normal hens and others with values that were 2-10 times greater than those found in normal hens. These results are consistent with the extensive hepatic lesions observed in the UCD-003 strain of birds. Average gross hemorrhagic scores from visual inspection (scale of 0-3) were 0.28 +/- 0.45 in normal birds and 1.63 +/- 0.94 in the UCD-003 birds. Even though no clear relationship was found between plasma enzyme activities and the extent of liver hemorrhage in individual birds, the UCD-003 hens consistently had average values significantly higher for plasma enzymes that indicate liver damage. The results suggest that measurement of enzyme activities indicative of liver damage in birds, particularly AST, LDH, and GDH, is a valuable tool in the diagnosis of fatty liver-hemorrhagic syndrome in a flock of layers.

Effect of dietary flax oil and hypobaric hypoxia on pulmonary hypertension and haematological variables in broiler chickens.

1. Three experiments were conducted with broiler chickens using hypobaric chambers and control pens, feeding diets containing 25 or 50 g flax oil/kg food or control diets with equivalent amounts of animal/vegetable (A/V) blend oil for 4 weeks. The effect of these diets on haematological variables and the extent of right ventricular hypertrophy (RVH) leading to ascites was determined. 2. Overall growth rate was not consistently affected by dietary treatment, although feeding the 25 g flax oil/kg diet reduced weight gain in week 4 of one experiment. Feeding the 50 g flax oil/kg diet but not the 25 g flax oil/kg diet reduced RVH in birds exposed to hypobaric conditions compared to feeding control diets. 3. Feeding the 50 g flax oil/kg diet under hypobaric conditions reduced the haematocrit and haemoglobin content, increased the erythrocyte deformability and the proportion of unsaturated fatty acids in the erythrocyte membranes, and reduced the whole blood viscosity compared to feeding control diets. These effects were not seen when the 25 g flax oil/kg diet was fed. The ratio of n-3 to n-6 fatty acids in erythrocyte membranes was increased in the 50 g flax oil/kg treatment group compared to controls. 4. Including 50 g flax oil/kg broiler diet reduces RVH in broiler chickens. This may be attributable in part to an increase in erythrocyte deformability from an increased proportion of unsaturated fatty acids in the erythrocyte membranes.

Rapid growth problems: ascites and skeletal deformities in broilers.

Over the last 40 yr, genetic selection for rapid growth and improved feed efficiency has been very effective in meat-type poultry. Combined with changes in the feed that have increased both the nutritional and physical density to encourage a high nutrient intake, growth rate has more than doubled. The effect of genetic selection for high muscle to bone ratio and high calorie intake of a ration that supplies all nutritional requirements causes significant mortality from cardiovascular disease. In the chicken, sudden death syndrome (flip-over) and pulmonary hypertension syndrome resulting in ascites are the most important. Ruptured aorta, spontaneous turkey cardiomyopathy (round heart), and cardiomyopathy causing sudden death produce high mortality in turkeys. Rapid growth induced by high nutrient intake alone can cause severe lameness, bone defects, and deformity, as these problems are seen in animals that have not been selected for rapid growth: dogs, horses, pigs, ratites and wild birds kept in zoologic gardens. In meat-type poultry, growth-related disease can be reduced or eliminated by reducing feed intake without affecting final body weight. Rapid growth alone may not be the pathogenic mechanism that results in cardiovascular or musculoskeletal defects. Metabolic imbalance induced by high nutrient intake may cause some of the conditions. These metabolic problems might be corrected without reducing growth rate.

Effect of dietary flax oil and hypobaric hypoxia on right ventricular hypertrophy and ascites in broiler chickens.

1. The effect of dietary flax oil on growth rate, blood haemoglobin content, mortality and incidence of pulmonary hypertension and ascites in broilers at ambient pressure and at reduced atmospheric pressure was examined. 2. Birds were housed either in hypobaric chambers simulating 1000, 1500 or 2200 m altitude or in pens at ambient atmospheric pressure and fed on diets containing 100 g/kg added fat as either an animal/vegetable (A/V) blend or flax oil. 3. Birds raised under hypobaric conditions had a decreased growth rate and increased mortality, blood haemoglobin content, and incidence of pulmonary hypertension and ascites compared to the groups at normal atmospheric pressure. 4. Broilers fed on the diet containing flax oil showed no difference in growth rate or blood haemoglobin content compared to birds fed on the A/V fat diet raised at the same altitude. 5. Inclusion of flax oil in the diet decreased mortality and the incidence of ascites at 2200 m and pulmonary hypertension at 1500 m. 6. Flax oil may be an effective method of reducing ascites and pulmonary hypertension in broilers without affecting performance.

Description of cellulitis lesions and associations between cellulitis and other categories of condemnation.

A total of 110 broiler flocks processed in a single processing plant in southern Ontario were studied for purposes of describing the cellulitis lesions and investigating possible associations between cellulitis and other categories of condemnation at the processing plant. Two hundred and ninety-five carcasses condemned for cellulitis were examined. They came from 65 of the 110 flocks. The lesions tended to be unilateral with most carcasses (87%) having one lesion. The majority of the lesions (92%) were located on the abdomen. Almost 65% of the lesions were large (> or = 8.1 cm2), and 27% were medium (2.1-8.0 cm2). On the basis of gross appearance, 69% of the lesions were classified as severe, 26% moderate, and 5% mild. Of 149 lesions examined histologically, 74% were classified as chronic, 21% ongoing, and 5% mild-acute. Condemnation data from the 110 broiler flocks were analyzed using Poisson regression. Simple relationships were examined between a count outcome (number of cellulitis-condemned carcasses per flock) and other categories of condemnation and average bird weight. Cellulitis was significantly associated with average bird weight (P = 0.0018), Escherichia coli-related conditions (SEROSITIS; P < or = 0.0001), ascites (P = 0.0004), cyanosis (P < or = 0.0001), valgus varus deformity (P < or = 0.0001), REJECT (combined carcass condemnations for bruising, mutilation, and contamination; P = 0.0003), and the interaction terms "average bird weight and ascites" (AVWT*ASCIT; P < or = 0.0001) and "average bird weight and cyanosis" (AVWT*CYAN; P < or = 0.0001). Average bird weight, SEROSITIS, ascites, cyanosis, valgus varus deformity, and AVWT*ASCIT were the only significant factors after adjusting for clustering. No association was observed between cellulitis and emaciation and dead on arrival. Variables significantly associated with cellulitis in the multivariate analysis could be considered as potential predictors. These predictors may share common risk factors predisposing broiler chickens to cellulitis.

Effect of graded levels of dietary nitrite on pulmonary hypertension in broiler chickens and dilatory cardiomyopathy in turkey poults.

In two separate trials, day-old broiler chicks and turkey poults were fed graded levels of dietary sodium nitrite in order to investigate the possible role of nitrite-induced methaemoglobinaemia on the incidence of chicken pulmonary hypertension and spontaneous turkey cardiomyopathy (STC). A transient low level of methaemoglobinaemia was observed after 7 days of exposure to dietary nitrite, but the levels returned to normal afterwards in spite of the presence of nitrite in the diet throughout the experiment. No effect on pulmonary hypertension, as measured by the right ventricle weight to total ventricle weight ratio, was observed in chickens exposed to dietary nitrite. The group of turkey poults receiving 1200 mg/kg nitrite in the diet had a higher incidence of STC than controls (20 v. 5%), although the difference was not statistically significant. The levels of nitrite-induced methaemoglobinaemia were probably too low to be considered as the aetiology of increased STC incidence.

Escherichia coli cellulitis: experimental infections in broiler chickens.

The objectives of this study were to evaluate the role of trauma to the skin in development of Escherichia coli cellulitis and to compare the abilities of three cellulitis isolates (O78, O115, O21,83), one airsacculitis isolate (untypable) and one fecal isolate (O86) of E. coli to induce cellulitis in broiler chickens. Forty-eight 4-week-old commercial broiler chickens were housed in groups of six in eight battery cages. For five groups, the skin on the left side of the abdominal region of chickens was traumatized by scratching with a 22-gauge needle, then contaminated with a swab dipped in a broth culture of one of the five E. coli isolates. For chickens in the remaining three groups, an avian cellulitis culture (O115, O21,83) or sterile broth was applied to intact skin. The experiment was duplicated. All birds were euthanatized 10-13 days postinoculation. No lesion developed in chickens in which the skin had not been traumatized. Among the traumatized birds, cellulitis isolates induced characteristic lesions of cellulitis in 86% of the birds, whereas airsacculitis and fecal isolates induced lesions in 42% and 8% of birds, respectively. Severe or moderate gross pathologic changes were found in 86% and microscopic pathologic changes were found in 88% of birds inoculated with cellulitis isolates; the corresponding percentages for the airsacculitis isolate were 25% and 17%. This study demonstrated that trauma to the skin is necessary for initiating disease and that strains of E. coli of serotypes epidemiologically associated with cellulitis are highly virulent in experimental infection.