Factors associated with mortality in Norwegian broiler flocks

Our aim in this longitudinal study (covering years from 1996 to 1999) was to use data regularly recorded in a production database, to identify farm- and flock-level factors associated with cumulative mortality in broiler flocks during: (a) the 1st week after housing and (b) the rest of the growout (2nd to 5th week). A total of 1664 broiler flocks kept in 132 broiler farms were included. The average weekly cumulative mortality was 1.54% (95% CI: 1.46, 1.62%) during the 1st week and 0.48% (95% CI: 0.47, 0.49%) during the rest of the growout.The final least-squares regression model of cumulative mortality during the 1st week identified the following significant factors: study year, flock size, stocking density, use of paper underlay for feeding during the 1st week, and the interaction terms between type of ventilation, drinking system and floor insulation. The final model for the 2nd to 5th week demonstrated that the factors age of the broiler house, heating system and control system for the air intake were associated with cumulative mortality, but the effects of the two latter variables were significantly modified by age of the broiler house. A significant difference in mortality between flocks delivered from various hatcheries was found in both analyses.Our results suggest that changes in several housing factors and management routines might reduce the mortality losses, but the relationship depends on the stage of production.     

The effect of 7,8-methylenedioxylycoctonine-type diterpenoid alkaloids on the toxicity of methyllycaconitine in mice

Larkspur plants contain numerous norditerpenoid alkaloids, which include the 7,8-methylenedioxylycoctonine (MDL)-type alkaloids and the N-(methylsuccinimido)anthranoyllycoctonine (MSAL)-type alkaloids. The MSAL-type alkaloids are generally much more toxic (typically >20 times). Toxicity of many tall larkspurs, such as Delphinium barbeyi, has been attributed to its large concentration of MSAL-type alkaloids, including methyllycaconitine (MLA). However, the norditerpenoid alkaloids found in the greatest concentrations in most D. barbeyi populations are either deltaline or 14-O-acetyldictyocarpine (14-OAD), both less toxic MDL-type alkaloids. Although the individual toxicities of MLA, 14-OAD, and deltaline have been determined, the impact (additive or antagonistic) that large concentrations of deltaline or 14-OAD in the plant have on the toxicity of MLA is unknown. Consequently, the effect of MDL-type alkaloids on the toxicity of MLA was compared by using median lethal dose (LD(50)) and toxicokinetic profiles of the brainand muscle from mice receiving i.v. administration of these alkaloids, individually or in combination, at ratios of 1:1, 1:5, and 1:25 MLA to MDL-type alkaloids. The LD(50) for MLA alone was 4.4 +/- 0.7 mg/kg of BW, whereas the coadministration of MLA and deltaline at 1:1, 1:5, and 1:25 resulted in an LD(50) of 2.7, 2.5, and 1.9 mg/kg of BW, respectively. Similarly, the coadministration of MLA and 14-OAD at 1:1, 1:5, and 1:25 resulted in an LD(50) of 3.1, 2.2, and 1.5 mg/kg of BW, respectively. Coadministration of mixtures did not result in increased MLA bioavailability or alterations in clearance from the brain and muscle. Consequently, the increased toxicity of the mixtures was not a result of increased MLA bioavailability (based on the maximum concentrations observed) or alterations in MLA clearance from the brain and muscle, because these were unchanged. These results demonstrate that MDL-type alkaloids have an additive effect on MLA toxicity in mice and may also play a role in the overall toxicity of tall larkspur plants in cattle.     

Purine metabolism in heterozygous carriers of hypoxanthine-guanine phosphoribosyltransferase deficiency

The urate pool and daily turnover of urate, together with the rate of incorporation of glycine into urate, were measured in three asymptomatic mothers who had sons with various degrees of deficiency of hypoxanthine-guanine phosphoribosyltransferase activity. Two of these mothers had abnormally increased values for the urate pool, urate turnover, and 24-hour urinary excretion of uric acid. These two mothers also had reduced hypoxanthine-guanine phosphoribosyltransferase activity and increased adenine phosphoribosyltransferase activity in erythrocyte lysates. All three mothers showed an abnormal increase in urate production, as judged by the rate of incorporation of glycinie into urate.     

Sedative, analgesic and cardiorespiratory effects of romifidine in cats

OBJECTIVE: To evaluate the sedative, analgesic, and cardiorespiratory effects of intramascular (IM) romifidine in cats. STUDY DESIGN: Prospective, randomized experimental trial. ANIMALS: Ten healthy adult cats. METHODS: Romifidine (100, 200, and 400 microg kg(-1)) or xylazine (1 mg kg(-1)) was given IM in a cross-over study design. Heart rate (HR), respiratory rate (RR), rectal temperature (RT), hemoglobin saturation, oscillometric arterial pressure, and scores for sedation, muscle relaxation, position, auditory response, and analgesia were determined before and after drug administration. Time to recumbency, duration of recumbency, and time to recover from sedation were determined. Subjective evaluation and cardiorespiratory variables were recorded before and at regular intervals for 60 minutes after drug administration. RESULTS: Bradycardia developed in all cats that were given romifidine or xylazine. No other significant differences in physiologic parameters were observed from baseline values or between treatments. Increasing the dose of romifidine did not result in increased sedation or muscle relaxation. Cats given xylazine showed higher sedation and muscle relaxation scores over time. Analgesia scores were significantly higher after administration of romifidine (400 microg kg(-1)) and xylazine (1 mg kg(-1)) than after romifidine at 100 or 200 microg kg(-1). Duration of lateral recumbency was not significantly different between treatments; however, cats took longer to recover after administration of 400 micro g kg(-1) romifidine. CONCLUSIONS AND CLINICAL RELEVANCE: Bradycardia is the most important adverse effect after IM administration of romifidine at doses ranging from 100 to 400 microg kg(-1) or 1 mg kg(-1) of xylazine in cats. The sedative effects of romifidine at 200 microg kg(-1) are comparable to those of 1 mg kg(-1) of xylazine, although muscle relaxation and analgesia were significantly less with romifidine than with xylazine.     

Cardiorespiratory effects of four alpha2-adrenoceptor agonist-ketamine combinations in captive red wolves

OBJECTIVE: To evaluate the cardiopulmonary effects of immobilizing doses of xylazine-ketamine (XK), medetomidine-ketamine (MK), medetomidine-ketamine-acepromazine (MKA), and medetomidine-butorphanol-ketamine (MBK) in captive red wolves. DESIGN: Prospective study. ANIMALS: 32 adult captive red wolves. PROCEDURE: Wolves were randomly assigned to 1 of 4 treatment groups: XK, MK, MKA, or MBK. Physiologic variables measured included heart rate, blood pressure, respiratory rate, tidal volume, oxygen-hemoglobin saturation (Spo2), end-tidal CO2, arterial blood gases, and rectal temperature. Induction time, muscle relaxation, and quality of recovery were assessed. RESULTS: Heart rates were lower in wolves in the MBK group than for the other groups. All 4 drug combinations induced considerable hypertension, with diastolic pressures exceeding 116 mm Hg. Blood pressure was lowest in wolves receiving the MBK combination. Respiratory rate was significantly higher in wolves receiving XK, MK, and MKA. Tidal volumes were similar for all groups. Wolves receiving XK, MK, and MKA were well-oxygenated throughout the procedure (SPo2 > 93%), whereas those receiving MBK were moderately hypoxemic (87% < Spo2 < 93%) during the first 20 minutes of the procedure. Hyperthermia was detected initially following induction in all groups. CONCLUSIONS AND CLINICAL RELEVANCE: The alpha2-adrenoceptor agonist-ketamine combinations provide rapid reversible anesthesia for red wolves but cause severe sustained hypertension. Such an adverse effect puts animals at risk for development of cerebral encephalopathy, retinal hemorrhage, pulmonary edema, and myocardial failure. Although the MBK combination offers some advantages over the others, it is advised that further protocol refinements be made to minimize risks associated with acute hypertension.     

Influence of the novel urease inhibitor N-(n-butyl) thiophosphoric triamide on ruminant nitrogen metabolism: I. In vitro urea kinetics and substrate digestion

Two in vitro digestion experiments were conducted to evaluate the influence of the novel urease inhibitor N-(n-butyl) thiophosphoric triamide (NBPT) on in vitro urea kinetics, substrate digestion, and fermentation characteristics. In Exp. 1, in vitro incubations were conducted in 50-mL test tubes containing .25 g of ground fescue hay to which 0, 6.5, 13, 26, or 52 mg of NBPT in a buffered ruminal fluid innoculum was added. Tubes were incubated in triplicate at 39 degrees C and replicated on consecutive days, with NH3 N and urea concentrations measured at 0, 10, 30, 60, 120, 240, and 360 min. Samples for VFA analysis were collected at 6 h, and incubations were continued through 48 h to estimate true digestibility (based on NDF analysis). Increasing the dose of NBPT tended (P < .12) to linearly depress the rate of urea hydrolysis and decreased (P < .0004) subsequent NH3 N formation. Although total VFA concentration at 6 h increased linearly (P < .03), acetate:propionate and estimated true digestibility decreased (P < .01) with increasing NBPT concentration. In Exp. 2, we compared in vitro urea kinetics and digestion of forage-only or mixed forage-grain substrates in response to addition of NBPT. In vitro incubations were conducted in 50-mL test tubes containing either .5 g of ground fescue hay or .5 g of a ground fescue hay and ground corn mixture (50:50, DM basis) to which 0, 6.5, 13, 26, or 52 mg of NBPT in a buffered ruminal fluid innoculum was added. Tubes were incubated in triplicate at 39 degrees C and replicated on consecutive days, with NH3 N and urea concentrations measured at 0, .5, 1, 2, 4, 8, 12, 24, and 48 h. At 48 h, samples for VFA analysis were collected and true digestibility (based on NDF analysis) was estimated. No (P > .10) NBPT dose x substrate interactions were detected. Increasing the dose of NBPT depressed (P < .003) the rate of urea hydrolysis and subsequent NH3 N formation, regardless of substrate. Although total VFA concentration was unaffected (P > .10), the acetate:propionate and estimated true digestibility decreased (P < .002) with higher NBPT addition. In both experiments, the rate of urea degradation was not different (P > .20) from zero for the 26 and 52 mg NBPT treatments, indicating that nearly complete inhibition of urease had been achieved. We conclude that NBPT can be used to reduce the rate of NH3 N release from dietary urea and, thereby, offers the potential to improve nonprotein nitrogen utilization in ruminants.     

Risk factors for Marek's disease and mortality in white Leghorns in Norway

A prospective longitudinal field study was conducted in the period from January 1994 to January 1996 to analyse the relationship between some selected risk factors in the growing and laying periods and (1) the flock-level occurrence of Marek’s disease (MD) during the period from 16 to 32 weeks of age and (2) the cumulative mortality during the same period. A total of 171 layer flocks in 102 egg-production farms were included in the statistical analyses.

A logistic regression (with strain of layer and vaccination program against MD as fixed effects) of flock-level MD-status during the first 16 weeks of the laying period was conducted. Of the risk factors investigated, “multi-age management” and “housing system” were significantly associated at the rearing farm, and “number of hens in each cage” at the egg-production farm. Flocks kept in single-age facilities had a lower risk of MD than flocks housed in farms with multi-age management. The odds of MD were larger for flocks housed on a litter floor in the rearing farms compared to flocks housed in battery cages. At the egg-production stage, flocks kept in battery cages housing more than three hens were at greater risk of MD than those held in cages for three hens or less.

A weighted least-squares regression (with strain of layer and flock-level MD-status as fixed effects) of cumulative mortality during the period from 16 to 32 weeks of age was also run. The same risk factors (with the same directions of effects) and “size of the rearing farm” were included in the final model of mortality. Chicks reared in medium-sized farms were at higher risk of dying than those coming from either small or large rearing farms. Our results confirm the importance of preventing chicks from being exposed to MD-virus during the rearing period, to reduce the risk of MD-outbreaks (and thereby, mortality losses) during the early stage of the egg-laying period.     

Vascular ultrastructure and DNA fragmentation in swine infected with Shiga toxin-producing Escherichia coli

Shiga toxins (Stx) produced by Escherichia coli cause systemic vascular damage that manifests as edema disease in swine and hemolytic uremic syndrome in humans. In vitro, Stx inhibit protein synthesis and, depending on circumstances, induce necrosis, apoptosis, or both. The mechanism of in vivo Stx-mediated vascular damage is not known. The ability of Stx to cause apoptosis of vasculature in vivo was studied in pigs with edema disease that was produced by oral inoculation with Stx-producing E. coli. Arterioles of ileum and brain were evaluated by terminal dUTP nick-end labeling (TUNEL) assay for DNA fragmentation in myocytes (10 infected pigs, 5 control pigs) and by transmission electron microscopy for ultrastructural changes characteristic of apoptosis (17 infected pigs, 8 control pigs). In comparison with controls, increased numbers of TUNEL-positive arterioles were detected in 6/10 (60%) subclinically affected pigs 14-15 days after inoculation. Ultrastructurally, lesions in myocytes consisted of lysis (necrosis), with cytoplasmic debris and nuclear fragments contained between intact basement membranes. Endothelial cell changes ranged from acute swelling to necrosis and detachment from basement membrane. Subclinically affected pigs (n = 14) tended to have changes predominantly in myocytes, whereas pigs with clinical illness (n = 3) more commonly had changes in endothelial cells. The arteriolar lesions and clinical signs of edema disease are attributed to the effects of Stx on vasculature. Therefore, our findings suggest that the Stx-induced arteriolar lesions seen in this study were primarily necrotic, not apoptotic. We suspect that necrosis was the principal cause of the DNA fragmentation detected.