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Biomedical subjects

N B Anthony

Publications and source records attributed to N B Anthony.

At least 19 recordsLinked to original sources

Stress-induced colibacillosis and turkey osteomyelitis complex in turkeys selected for increased body weight.

Two stress models were used to induce colibacillosis and turkey osteomyelitis complex (TOC): Escherichia coli challenge following dexamethasone injection (Dex) and E. coli challenge preceding transport stress (Transport). A total of 160 birds from 3 lines of turkeys: a slow-growing line selected for egg production (Egg), a line selected for 16-wk BW (F line), and a Commercial line (Comm), were studied in a 3 x 3 x 2 (line x treatment x sex) factorial design. At 14 wk, the Dex group was treated with 3 injections of 2 mg of Dex/kg of BW followed by airsac challenge with 100 cfu of E. coli. The Transport group was given 5,000 cfu of the same E. coli and 8 d later was transported for 3 h and held for an additional 9 h in the transport vehicle. Controls of each line were neither stressed nor challenged with E. coli. Birds were necropsied 2 wk postchallenge. All birds were sexed, scored for airsacculitis (AS) and TOC, and knee synovia were cultured for E. coli. Percent mortality was unaffected by sex, was increased by the Dex treatment, and was higher in Dex-treated male Comm-line birds and Dex-treated female F-line birds compared with their respective nonchallenged controls. Both treatments increased AS scores, and scores of Dex-treated male Comm-line birds and female F-line birds were also higher compared with their respective controls. Male Comm birds under Transport had higher AS scores as compared with nonchallenged males and challenged females. The TOC incidence was increased by Dex only. There was no TOC in Egg-line birds, whereas TOC incidence approached significance in both Comm and F lines compared with the Egg line (P = 0.06). Males had twice as much TOC as females, and this approached significance in the F line (P = 0.06). There was a low level of TOC in male Transport birds of both large-bodied lines, whereas no female Transport birds had TOC lesions. Dex-treated male birds of both the F line and Comm line had significantly higher incidence of TOC compared with their respective nonchallenged controls. The challenge strain of E. coli was isolated from more knee cultures of both large lines compared with the Egg line. Isolation was increased by Dex and was higher in male Comm-line birds and both male and female F-line birds relative to their controls. The difference in disease resistance between these lines suggests that selection for fast growth of turkeys may affect the stress response, resulting in increased chronic bacterial disease such as TOC.

Animals↗

Pulmonary hypertension triggered by lipopolysaccharide in ascites-susceptible and -resistant broilers is not amplified by aminoguanidine, a specific inhibitor of inducible nitric oxide synthase.

Nitric oxide (NO) is a potent pulmonary vasodilator that modulates the pulmonary vasoconstriction and pulmonary hypertension (PH) triggered by bacterial lipopolysaccharide (LPS) in broilers. The amplitude and duration of the LPS-induced PH are markedly enhanced following pretreatment with N(omega)-nitro-L-arginine methyl ester (L-NAME), which inhibits NO synthesis by both the constitutive (endothelial) and inducible (inflammatory) forms of nitric oxide synthase (eNOS and iNOS, respectively). In the present study L-NAME and the selective iNOS inhibitor aminoguanidine (AG) were administered to differentiate between iNOS and eNOS as the primary source of NO that attenuates the pulmonary vascular response to LPS. Clinically healthy male progeny from ascites-susceptible and ascites-resistant lines were anesthetized, and their pulmonary artery was cannulated. The initial pulmonary arterial pressure (PAP) was recorded, then the broilers either remained untreated (control group) or were injected i.v. with AG. Ten minutes later all birds received an i.v. injection of LPS, followed 40 min later by an i.v. injection of L-NAME. When compared with untreated controls, AG neither increased the baseline PAP nor did it increase or prolong the PH response to LPS. The ascites-susceptible broilers maintained a higher PAP than the ascites-resistant broilers throughout the experiment, and the ascites-resistant broilers exhibited greater relative increases in PAP in response to LPS than did the ascites-susceptible broilers. Within 40 min after the LPS injection, PAP subsided to a level that did not differ from the respective preinjection value for each line. Injecting L-NAME reversed the decline in PAP, and within 5 min PAP returned to hypertensive levels approaching the maximum peak PH response to LPS. The absence of any impact of AG coupled with the profound response to L-NAME indicates that NO synthesized by eNOS rather than iNOS likely modulated the acute (within 1 h) PH elicited by LPS. Evidently eNOS is activated by the increased shear stress exerted on the endothelium during the PH response to LPS, whereas LPS-mediated up-regulation of iNOS expression may take longer than 1 h before biologically effective quantities of NO are produced.

Animals↗

Variation in the pulmonary hypertensive responsiveness of broilers to lipopolysaccharide and innate variation in nitric oxide production by mononuclear cells.

Variability among broilers in their pulmonary hypertensive (PH) responsiveness to lipopolysaccharide (LPS) appears to reflect innate variation in the types or proportions of vasodilators and vasoconstrictors released by leukocytes and endothelial cells. Two experiments were designed to evaluate possible correlations between the PH responsiveness to LPS in vivo and the quantities of nitric oxide (NO; a potent pulmonary vasodilator) produced by mononuclear cells in vitro. In Experiment 1, blood samples were collected from male broilers from a base population (control group) and from survivors of a 60% lethal dose i.v. injection of cellulose microparticles (MP survivor group). In Experiment 2, blood samples were collected from male broilers from a relaxed line and from lines known to be susceptible or resistant to pulmonary hypertension syndrome. Peripheral mononuclear cells (PMNC) from each blood sample were cultured at 2 million cells per well, remained unstimulated, or were stimulated with LPS to elicit the expression of inducible NO synthase, and the 24-h production of NO was measured. In both experiments, unstimulated PMNC cultures did not produce consistently detectable levels of NO, whereas LPS-stimulated cultures produced quantities of NO that varied widely among individuals. Nitric oxide production by cultured PMNC also was evaluated by flow cytometry, demonstrating that LPS-stimulated PMNC produced substantially more NO than did unstimulated cells in all of the groups evaluated. Moreover, NO-producing PMNC were identified to be monocytes. The same broilers from which PMNC had been isolated were catheterized subsequently to record pulmonary arterial pressure, LPS was injected i.v. to assess the amplitudes of peak and postpeak PH responses, then N(omega)-nitro-L-arginine methyl ester was injected to inhibit ongoing NO production. In Experiment 1, the amplitude of the peak and postpeak PH responses to LPS were correlated with the quantity of NO produced by LPS-stimulated cultured PMNC from broilers in the control group but not for MP survivors. In Experiment 2, the postpeak PH response to LPS was correlated with the quantity of NO produced by LPS-stimulated PMNC from broilers in the relaxed line, but not in the susceptible or resistant lines. In all groups, N(omega)-nitro-L-arginine methyl ester injections triggered substantial increases in pulmonary arterial pressure (> or = 8 mm Hg), thereby revealing a significant ongoing modulation by NO of the PH response to LPS. We concluded that most of the modulatory NO generated in vivo during the acute PH response to LPS (within 60 min postinjection) likely is produced by constitutive NO synthase in the vascular endothelium. In addition, the NO produced by inducible NO synthase in PMNC appeared to have modulated the LPS-stimulated PH responses of unselected broilers having the broadest range of pulmonary vascular capacities (control broilers and relaxed line), but not in broilers whose pulmonary vascular capacities had been selected to represent the higher (MP survivors, resistant line) or lower (susceptible line) extremes of the population.

Animals↗

Differential expression of cardiac muscle mitochondrial matrix proteins in broilers from ascites-resistant and susceptible lines.

Ascites is a metabolic disorder of modern broilers that is distinguished by cardiopulmonary insufficiency in the face of intense oxygen demands of rapidly growing tissues. Broilers with ascites exhibit sustained elevation of pulmonary arterial pressure and right ventricular hypertrophy, the end result of which is heart failure. It has been shown that mitochondrial function is impaired in broilers with ascites. In the current study, mitochondrial matrix protein levels were compared between ascites-resistant line broilers and ascites-susceptible line broilers with and without ascites using two-dimensional (2-D) gel electrophoresis. One hundred seventy-two protein spots were detected on the gels, and 9 of the spots were present at different levels in the 4 groups of broilers. These 9 protein spots were selected for identification by mass spectrometry. Two of the spots were found to contain single mitochondrial matrix proteins. Both mitochondrial matrix proteins, the dihydrolipoamide succinyltransferase component of the 2-oxoglutarate dehydrogenase complex and the alpha-subunit of mitochondrial trifunctional enzyme, were present at higher levels in ascites-resistant line broilers with ascites in the present study. The elevated levels of 2 key proteins in aerobic metabolism in ascites-resistant line broilers with ascites observed in the present study suggests that the mitochondria of broilers with this disease may respond inappropriately to hypoxia.

Animals↗

Stress response differences and disease susceptibility reflected by heterophil to lymphocyte ratio in turkeys selected for increased body weight.

Three genetic lines of turkeys were compared for their responses to Escherichia coli challenge following dexamethasone injection (Dex) or E. coli challenge preceding transport stress (TS). The turkey lines were a slow growing line selected for increased egg production (Egg line), a fast growing line selected for increased 16-wk BW (F line), and a commercial line (Comm line). At 14 wk of age, the Dex group was treated with 3 injections of 2 mg of Dex/kg of BW followed by airsac challenge with 100 cfu of E. coli. The TS group was given the same E. coli challenge at 1 x 10(4) cfu/bird without Dex treatment, and was subjected to transport stress, including 12 h of holding time in a transport vehicle, 8 d after the challenge. All treated birds and untreated control birds were bled at the same time, which was 1 d after transport and 9 d after challenge with E. coli. The main effect mean (MEM) total leukocyte counts (WBC) and the percentages of eosinophils (Eos) and basophils (Baso) were the same for all 3 lines; however, the MEM percentages of heterophils (Het) and monocytes (Mono) and the heterophil/lymphocyte ratio (H/L) were lower and the percentage of lymphocytes (Lym) was higher in the Egg line compared with the 2 fast-growing lines. Both stress treatments increased WBC, Het, and H/L and decreased Lym in all 3 lines; however, these effects were significantly greater in both fast growing lines compared with the Egg line. Sixteen-week BW was unaffected by either treatment in the Egg line and was decreased by both treatments in the Comm line and by the Dex treatment in the F line. Main effect mean airsacculitis score (AS) was not affected by line and was significantly increased by TS and Dex treatments. Neither treatment affected AS of the Egg line birds, whereas Dex treatment increased AS of the F line, and both Dex and TS increased AS of the Comm line. Mortality was significantly higher in the Comm line compared with the Egg line and was intermediate in the F line. The differences between these lines in their disease resistance and physiological response to stress in 2 stress models suggests that increasing selection for BW of turkeys is accompanied by changes in the stress response resulting in increased susceptibility to opportunistic bacterial infection.

Animals↗

Effect of prebiotic on gut development and ascites incidence of broilers reared in a hypoxic environment.

Modern broilers have been genetically selected for an increased growth rate and improved feed conversion, but they are also more susceptible to ascites. Ascites occurs when there is an imbalance between available oxygen and the oxygen demand of the broiler. We hypothesized that promoting neonatal gut development with a prebiotic, such as Aspergillus meal (Prebiotic-AM), would enhance gut efficiency, decrease the oxygen demand of the gut, and reduce ascites incidence. In this study, we compared the effect of Prebiotic-AM on ascites incidence and gut development in commercial broilers reared at a local altitude (390 m above sea level) and a simulated high altitude (2,900 m above sea level). Half of the birds received a National Research Council recommended corn-soybean ration, and the other half received the same ration supplemented with 0.2% Prebiotic-AM. These 2 groups were further divided into a local altitude group and a simulated high altitude group for a total of 4 treatment combinations. Tissues were collected on d 1, 3, 7, 14, and 21 from the duodenum and lower ileum and placed in 10% buffered formalin for morphometric analysis. At a simulated high altitude, ascites incidence was 68% for birds fed the Prebiotic-AM supplement compared with 92% ascites incidence in birds given the control feed. The simulated high altitude decreased (P < 0.05) gut development, but prebiotic-treated birds reared in hypoxic conditions had similar gut development to control birds reared at local altitude. These data suggest that a feed ration supplemented with Prebiotic-AM may reduce the effect of hypoxia on broiler gut development and ascites incidence.

Altitude↗

Hypobaric hypoxia in ascites resistant and susceptible broiler genetic lines influences gut morphology.

Genetic selection based on rapid growth rates, improved feed conversion, and increased body weights has led to a predisposition to ascites in broiler populations. Sire-family selection was applied to a commercial elite line to produce divergent lines of ascites-resistant (RES) and ascites-susceptible (SUS) broilers by the 8th generation. One objective of this research was to determine the effects of hypobaric hypoxia on gut morphology in these genetic lines. In two separate trials, pedigree broiler chickens were randomly assigned to cages in a hypobaric chamber (simulated 2,900 m above sea level) or a matching local altitude chamber (390 m above sea level). Ascites incidence was characterized by heart enlargement and fluid accumulation in the abdominal cavity. At the end of the study on d 42, all surviving birds were killed and evaluated for the presence of ascites and 2-cm sections from the duodenum and lower ileum were collected from 5 chickens per line, per altitude for each trial for morphometric analysis. At a high altitude, ascites incidence was lower in the RES line (20.9 and 3.7%) than in the SUS line (86.4 and 66.9%, Trials 1 and 2, respectively). No ascites was observed at a local altitude. Under hypoxic conditions, duodenum villus surface area was higher (P < 0.05) in the RES line (181.3 +/- 16.8 and 219 +/- 10.9 microm) compared with the SUS line (130.1 +/- 10.5 and 134.3 +/- 9.3 microm; Trials 1 and 2, respectively). No differences in ileum villus morphology were observed for any of the parameters measured. The reduced surface area in the duodenum of birds selected for ascites susceptibility suggests reduced enteric function and may provide clues as to why these birds have increased incidence of ascites.

Altitude↗

Effect of strain, feed allocation program, and age at photostimulation on reproductive development and carcass characteristics of broiler breeder hens.

A study was conducted with broiler breeder pullets to investigate the effects of strain, age at photostimulation (PS), and release from feed restriction at PS on age, BW, ovarian morphology, and carcass characteristics at sexual maturity (point of initiation of lay). Sixty birds of each of 4 strains were used. The 4 types represented a classic strain (A), 2 high-yield strains (B, C), and a roaster strain (D). Photostimulation (8L:16D to 14L:10D) was applied at 2 different ages (21 and 24 wk) to 30 birds of each strain type. Within each of the PS periods, 15 birds of each strain were fed ad libitum (F), and the remaining 15 were feed-restricted (R) following a common feeding schedule. On the day that each bird had its first oviposition, its feed was withdrawn. It was euthanized the following morning by cervical dislocation and organs were collected. Of the 3 main effects, feeding program had the greatest effect on all the parameters measured. Within the 21-wk PS treatment group, R birds reached onset of sexual maturity later than F birds (50.2+/-1.64 vs. 36.6+/-1.01 d, respectively). There were no differences in the age at sexual maturity between R and F birds for the 24-wk PS treatment (28.9+/-0.95 vs. 26.9+/-0.85 for R and F, respectively). These results suggest that by 24 wk, all strains had reached a threshold BW and responded uniformly to PS regardless of feeding program. Feed restriction reduced the number of large yellow follicles (LYF) (diameter >10 mm) (8.43+/-0.23 vs. 9.65+/-0.33 for R and F birds, respectively). Follicle number was not different between birds photostimulated at 21 or 24 wk (9.6+/-0.33 vs. 8.45+/-0.23, respectively). Feed restriction affects sexual development that can be modulated by the PS program.

Age Factors↗

Differential expression of mitochondrial electron transport chain proteins in cardiac tissues of broilers from pulmonary hypertension syndrome-resistant and -susceptible lines.

Pulmonary hypertension syndrome (PHS) is a metabolic disease associated with the rapid growth rate of modern broilers. Broilers susceptible to PHS experience sustained elevation of pulmonary arterial pressure leading to right ventricular hypertrophy and ultimately heart failure. Previous studies have shown that mitochondrial function is defective in broilers with PHS; they use oxygen less efficiently than broilers without PHS. In this study mitochondrial electron transport chain (ETC) protein levels were compared in cardiac tissues from PHS resistant and susceptible line broilers using quantitative immunoblots. Seven of 9 anti-mammalian mitochondrial ETC protein antibodies tested exhibited cross-species reactivity. Six ETC proteins were differentially expressed in the right ventricles of broilers raised under simulated high altitude conditions (2,900 m above sea level). Four ETC proteins were present at higher levels in resistant line birds without PHS than in resistant line birds with PHS or in susceptible line birds with or without PHS. One ETC protein was present at higher levels in broilers without PHS than in broilers with PHS in both lines, and one ETC protein was present at lower levels in susceptible line birds without PHS than in susceptible line birds with PHS or in resistant line birds with or without PHS. Interestingly, differential expression of mitochondrial ETC proteins was not observed in the right ventricles of broilers raised at local altitude (390 m above sea level) nor was it observed in the left ventricles of broilers exposed to simulated high altitude. These results suggest that higher levels of mitochondrial ETC proteins in right ventricle cardiac muscle may be correlated with resistance to PHS in broilers.

Animals↗

Sequence analysis of bone morphogenetic protein receptor type II mRNA from ascitic and nonascitic commercial broilers.

Ascites syndrome, also known as pulmonary hypertension syndrome (PHS), is a common metabolic disorder in rapidly growing meat-type chickens. Environmental factors, such as cold, altitude, and diet, play significant roles in development of the disease, but there is also an important genetic component to PHS susceptibility. The human disease familial primary pulmonary hypertension (FPPH) is similar to PHS in broilers both genetically and physiologically. Several recent studies have shown that mutations in the bone morphogenetic protein receptor type II (BMPR2) gene are a cause of FPPH in humans. To determine whether mutations in the chicken BMPR2 gene play a similar role in PHS susceptibility, BMPR-II mRNA from ascitic and nonascitic commercial broilers were sequenced and compared with the published Leghorn chicken BMPR-II mRNA sequence. Fourteen single nucleotide polymorphisms (SNP) were identified in the commercial broiler BMPR-II mRNA. No mutations unique to ascites-susceptible broilers were present in the coding, 5' untranslated or 3' untranslated regions of BMPR-II mRNA. The twelve SNP present within the coding region of BMPR-II mRNA were synonymous substitutions and did not alter the BMPR-II protein sequence. In addition, analysis of BMPR2 gene expression by reverse transcriptase-PCR indicated that there were no differences in BMPR-II mRNA levels in ascitic and nonascitic birds. Therefore, it appears unlikely that mutations in the BMPR2 gene were responsible for susceptibility to PHS in these commercial broilers.

Animals↗

Effect of cold stress on broilers selected for resistance or susceptibility to ascites syndrome.

Genetic selection for an ascites-resistant line of broilers is seen as a permanent solution to the ascites problem. Ascites-resistant and ascites-susceptible lines have been developed using sire family selection based on mortality data taken from siblings reared in a hypobaric chamber (simulated 2,900 m above sea level). The relaxed line is representative of the original commercial pureline stock randomly mated with no artificial selection pressure. The objectives of this study were to evaluate the differences between the lines when reared in floor pens and subjected to an ascites-inducing cold stress. Seven hundred eighty three straight run broilers were reared in floor pens at local elevation (390 m above sea level). Feed and water were available ad libitum. Birds were brooded at 32 C during the first week. The second week birds were maintained at 30 degrees C. Cold stress was applied for the remaining 4 wk at 14 degrees C. Mortalities were necropsied daily to determine cause of death. Birds and feed were weighed weekly. At 6 wk, five birds per pen were bled, and half the survivors in each pen (8 to 15 birds) were killed, necropsied, and scored for ascites. Blood gases, clinical chemistries, and blood cell counts were taken. Liver, spleen, split heart, and lung weights were recorded. Body weights were not different among the resistant, susceptible, and relaxed lines (P < 0.05). Feed conversion was better in the resistant line when compared to the susceptible and relaxed lines (P < 0.05). Ascites incidence, as measured by mortality and lesion score at necropsy, was higher in the susceptible and relaxed lines when compared to the resistant line; 18.8, 12.7, and 1.6% respectively (P < 0.001). Susceptible and relaxed lines showed more right ventricular hypertrophy when compared with the resistant line (P < 0.05). The results show that under severe cold stress at local altitude (390 m above sea level), the ascites-resistant line was growing as rapidly as the other lines and was as resistant to ascites as it had been under hypobaric conditions.

Animal Feed↗

Use of ultrasonography to characterize ovarian status in chicken.

Much research has been conducted to investigate the effects of environmental and nutritional treatments on ovarian development in poultry. However, to investigate the ovary, the hen must be killed, and thus, lifelong egg production can only be inferred. To date, the ability to noninvasively determine ovarian status has not been available. Improvements in ultrasound technology now make it possible to observe ovarian condition in vivo, thereby allowing for repeated sampling of the same bird over an entire egg production cycle. In the current study, large yellow follicles (LYF; diameter greater than 10 mm) were characterized in broiler breeder hens using Aloka ultrasound diagnostic equipment. Ultrasound images were used to determine the number and diameter of the LYF as well as the presence of an egg in the oviduct. Immediately following ultrasonography, hens were killed and dissected to determine the number and diameter of LYF. From the ultrasound images, the number of LYF +/- 1 was predicted with 96.3% accuracy in Experiment 1 and 93.3% accuracy in Experiment 2. Diameter measurements were used to classify follicles hierarchically. Of the birds determined via dissection to have multiple hierarchies, 77.8% were identified with ultrasound. All regressing or regressed ovaries were correctly identified with ultrasound.

Animal Husbandry↗

Intravenous micro-particle injections and pulmonary hypertension in broiler chickens: acute post-injection mortality and ascites susceptibility.

Intravenously injected micro-particles become trapped within the pulmonary vasculature where they increase the resistance to blood flow and trigger pulmonary hypertension. We tested the hypothesis that i.v. micro-particle injections can be used to trigger acute (24 to 48 h) post-injection mortality in broilers having the most limited pulmonary vascular capacity, or ascites in broilers whose marginal cardiopulmonary capacity renders them susceptible to pulmonary hypertension syndrome (PHS). Progressive inflammation-associated responses were initiated within the lung parenchyma by 10 to 80 microm diameter dextran polymer (Sephadex) and 30 microm diameter cellulose micro-particles, leading to the scavenging of Sephadex micro-particles from the pulmonary vasculature by <5 d post-injection, whereas the cellulose micro-particles persisted for >7 d post-injection. The persistency and size of the cellulose apparently facilitated chronic occlusion of blood flow through precapillary arterioles, thereby triggering appreciable post-injection mortality and PHS at relatively low injection volumes (0.3 to 0.6 mL at 0.02 g/mL). In contrast, the small size of the polystyrene microspheres (15 microm), and the lack of persistency of the Sephadex micro-particles, apparently precluded the reliable occurrence of post-injection mortality or PHS until higher volumes (>0.8 mL at 0.02 g/mL) were injected. Values for the total susceptibility index (TSI: 24 to 48 h post-injection mortality + PHS mortality) following cellulose injections were higher for broilers reared at cool temperatures than at thermoneutral temperatures. The incidences of PHS induced by exposing broilers from different genetic lines to constant cool temperatures qualitatively paralleled the respective post-injection mortalities elicited by injecting the cellulose micro-particle suspension into the same lines. These observations indicate the micro-particle injection methodology potentially can replace unilateral pulmonary artery occlusion as the technique of choice for genetically selecting broilers that have a sufficiently robust pulmonary vascular capacity to resist the onset of pulmonary hypertension and PHS. The functional importance of the relative antigenicity of different micro-particle types, and the extent to which key immune-mediated responses, either beneficial or detrimental, might be co-selected by the micro-particle injection technology, remain to be clarified.

Animals↗

Ascites syndrome and related pathologies in feed restricted broilers raised in a hypobaric chamber.

It has been demonstrated that the incidence of ascites can be significantly reduced through feed restriction. This method is thought to have an effect by slowing the growth rate of the birds. Interestingly, when birds are grown in a hypobaric chamber, ascites incidence increases while the overall growth rate of the birds is decreased. Unfortunately, the restriction programs practiced also have a detrimental effect on growth characteristics. An experiment was conducted to determine if the timing and duration of feed restriction can be used to reduce the incidence of ascites for broilers reared under high altitude and local elevation without having a negative impact on growth. A total of 600 commercial broiler males were used. Birds were divided, placing 360 birds in the hypobaric chamber at a simulated 2900 m (9,500 ft) above sea level, and 240 birds were placed at local elevation [390 m (1,300 ft) above sea level]. At each altitude there were four treatments: 1) fully fed controls; 2) feed available for 8 h/d for 6 wk (the duration of the study); 3) feed available for 8 h/d during the first 3 wk, then full feed for the remaining 3 wk; and 4) full feed for the first wk, then 3 wk of 8 h of feed availability, then 2 wk of full feed. Birds and feed were weighed weekly, and mortalities were necropsied to determine the cause of death. At the end of 6 wk, blood samples were taken, and the birds were weighed, necropsied, and scored for ascites, and organ weights were recorded. All feed restriction treatments significantly reduced ascites incidence, when compared with the fully fed controls. Treatment 2 birds were significantly lighter than any other group at both altitudes. The fully fed controls at local elevation were heavier than the fully fed controls at simulated high altitude, as seen in past experiments.

Animals↗

Electrocardiographic and genetic evaluation of giant jungle fowl, broilers, and their reciprocal crosses following unilateral bronchus occlusion.

Electrocardiography is useful as a noninvasive technique for detecting right ventricular hypertrophy in birds developing pulmonary hypertension (PH) and pulmonary hypertension syndrome (PHS, ascites). The objective of this study was to identify every aspect of the Lead II ECG wave form (amplitude or duration) that can be correlated with right ventricular hypertrophy [increased right:total ventricular weight ratios (RV:TV)] indicative of PH across a broad genetic background. Sham operations were conducted, or PH was induced by occluding one extrapulmonary primary bronchus in 14-d-old chicks produced from matings of broilers (B x B), Giant Jungle Fowl (J x J), and their reciprocal crosses (B x J and J x B). Standard three-lead electrocardiograms (ECG) were recorded on Days 28 and 42, and final necropsies were conducted to evaluate the incidence of ascites, confirm sex, and obtain ventricular weights for calculating RV:TV. Ascites did not develop in the J x J, and one each of the B x J and J x B chicks developed ascites; consequently, only data from birds that did not develop ascites were compared. Heart rate was recorded, and the following amplitudes and durations were measured or calculated for three consecutive wave cycles of the Lead II ECG: base of R to the peak of R (RbR), peak of R to base of S (RS), base of S to peak of R' (SR'), S, peak of R' to base of R' (R'R'b), and base of S to peak of T (ST). Differences between the ECG of sham and bronchus clamp groups were more prominent in B x B and B x J than in J x B, and bronchus occlusion did not affect the ECG, growth, or RV:TV ratios of J x J. In contrast, sex influences were more prominent in J x J and J x B than in B x J and B x B. These observations suggest a paternal pattern of inheritance for Lead II ECG wave forms, with crosses sired by broilers (B x B, B x J) exhibiting susceptibility to PH and few ECG differences related to sex, whereas crosses sired by Giant Jungle Fowl U x J, J x B) exhibited resistance to PH and numerous ECG differences related to sex.

Animals↗

Electrocardiographic evaluation of broilers following unilateral occlusion of an extrapulmonary primary bronchus.

This study was conducted to provide a comprehensive evaluation of both the amplitudes and durations of the Lead II electrocardiogram (ECG) in nonascitic and ascitic broilers. At 14 d of age, male and female broiler chicks were sham-operated (SHAM, n = 27), or pulmonary hypertension was initiated by occluding one extrapulmonary primary bronchus (BRONCHUS CLAMP, n = 57). Lead II ECG and BW were recorded on Days 28 (ECG1) and 42 (ECG2), necropsies were conducted on all birds dying after Day 28, and final necropsies were conducted on Day 49. Data collected at necropsy included the presence (ASCITIC) or absence (NONASCITIC) of ascites, sex, and ventricular weights for calculating the right:total ventricular weight ratio (RV:TV), which serves as a reliable index of pulmonary hypertension. In each bird, three consecutive ECG1 and ECG2 wave cycles were quantified for both amplitude and duration of the following wave segments: Rb-R, R-S, S-R', R'-R'b, and S-T. The S wave amplitude was calculated by subtracting R-S from Rb-R and heart rate (HR) was measured from the peak of one T wave to the peak of the next. In the majority of comparisons, ASCITIC and BRONCHUS CLAMP broilers had larger S, R'-R'b, and S-T amplitudes, longer R-S, R'-R'b, and S-T durations, and a slower HR than NONASCITIC and SHAM broilers, regardless of sex. The differences in ECG wave forms and durations between ASCITIC and NONASCITIC broilers were greater on Day 42 (ECG2) than on Day 28 (ECG1), but when both ECG were used to develop a regression equation to estimate RV:TV, the R2 was 0.79. The most important Lead II ECG parameters associated with the development of ascites were an increasingly negative S wave amplitude and greater amplitudes and durations for R'-R'b and S-T as well as a decrease in the HR.

Airway Obstruction↗

Effect of feed withdrawal or challenge with Pasteurella multocida on growth, blood metabolites, circulating growth hormone, and insulin-like growth factor-I concentrations in eight-week-old turkeys.

The daily effects of feed withdrawal or a bacterial disease (Pasteurella multocida; PM) challenge was studied in a slow-growing line of turkeys. The following groups (n = 6 birds/group) were sampled for up to 13 d: untreated control (CON), 4-d feed withdrawal followed by refeeding (FAST), a group that succumbed within the first 2 to 3 d after PM challenge (E-DEAD), a group that succumbed 8 to 9 d after PM challenge (L-DEAD), a group that survived the PM challenge (SUR), and a group treated with both PM challenge and 4-d feed withdrawal followed by refeeding (FAST/CHAL). Daily feed intake and BW gains were markedly reduced in the E-DEAD and L-DEAD groups immediately and 3 d after PM challenge, respectively. Feed intake and BW gain between CON and SUR groups of turkeys were not different throughout the trial. The turkeys in the FAST group followed the expected feed withdrawal and refeeding patterns for feed intake and BW loss or gain. The FAST/CHAL turkeys consumed the minimal amount of feed to maintain BW after refeeding. Plasma uric acid sharply increased 1 d prior to death in both E-DEAD and L-DEAD groups of turkeys. Plasma uric acid also increased each consecutive day during fasting in the FAST and FAST/CHAL groups of turkeys. Plasma growth hormone was measured in only the CON and FAST groups and increased from about 40 to 85 ng/mL in the FAST group during fasting but returned to control levels within 1 d of refeeding. Circulating plasma insulin-like growth factor-I (IGF-I) decreased from about 17 to 5 ng/mL in the PM-challenged (E-DEAD, L-DEAD, and FAST/CHAL groups) and FAST groups. The concentration of IGF-I returned to prefeed withdrawal levels within 3 d of refeeding the FAST group of turkeys. It was concluded that 1) turkey poults that were not susceptible to the PM challenge generally maintained physiological functions at control bird levels, 2) susceptible turkey poults generally exhibited depressed feed intake and BW gains, and 3) poults challenged with both feed withdrawal and PM treatment responded differently than poults challenged with either feed withdrawal or challenge with PM. The depletion of energy intake and mobilization of energy stores in susceptible poults might have contributed to the rate at which PM caused the poults to die.

Animals↗