Search

Monitoring antimicrobial resistance of foodborne pathogens in poultry is critical for food safety. We aimed to compare antimicrobial resistance phenotypes in Salmonella isolated from poultry samples as influenced by isolation and antimicrobial susceptibility testing methods. Salmonella isolates were cultured from a convenience sample of commercial broiler ceca with and without selective broth enrichment, and resistance phenotypes were determined for 14 antimicrobials using the Sensititre® platform and a qualitative broth breakpoint assay. The broth breakpoint method reported higher resistance to chloramphenicol, sulfisoxazole, and the combination of trimethoprim and sulfamethoxazole, and lower resistance to streptomycin as compared to the Sensititre® assay in trial one. Selective enrichment of samples containing Salmonella in Rappaport-Vassiliadis broth reported lowered detectable resistance to amoxicillin/clavulanic acid, ampicillin, azithromycin, cefoxitin, ceftriaxone, nalidixic acid, and meropenem, and increased resistance to streptomycin and tetracycline than direct-plating samples in trial one. Using matched isolates in trial two, the Sensititre® assay reported higher resistance to chloramphenicol and gentamicin, and lower resistance to nalidixic acid as compared to the broth breakpoint method. These results suggest methodology is a critical consideration in the detection and surveillance of antimicrobial resistance phenotypes in Salmonella isolates from poultry samples and could affect the accuracy of population or industry surveillance insights and intervention strategies.

Salmonellosis is a zoonotic infection caused by Salmonella enterica serotypes contracted from contaminated products. We hypothesized that competitive exclusion between Salmonella serotypes in neonatal broilers would reduce colonization and affect the host immune response. Day of hatch broilers were randomly allocated to one of six treatment groups: (1) control, which received saline, (2) Salmonella Kentucky (SK) only on day 1 (D1), (3) Salmonella Typhimurium (ST) or Salmonella Enteritidis (SE) only on D1, (4) SK on D1 then ST or SE on day 2 (D2), (5) ST or SE on D1 then SK on D2, and (6) SK and ST or SE concurrently on D1. Salmonella gut colonization and incidence were measured from cecal contents. Livers and spleens were combined and macerated to determine systemic translocation. Relative mRNA levels of interleukin-1β (IL-1β), IL-6, IL-10, IL-18, and gamma interferon (IFN-γ) were measured in cecal tonsils and liver to investigate local and systemic immune responses. When a serotype was administered first, it was able to significantly reduce colonization of the following serotype. Significant changes were found in mRNA expression of cytokines. These results suggest competitive exclusion by Salmonella enterica serotypes affect local and systemic immune responses.

Simple Summary Livers from meat geese are popular in China for different kinds of dishes. High-frequency electrical stunning (ES) was suggested to improve chicken meat quality in previous studies. Limited research has been performed on the effect of ES on liver quality of the meat goose. This study was performed to evaluate the effects of different current intensities on lipid oxidative stability and antioxidant capacity in the liver of Yangzhou goose (a typical meat goose) based on a typical high-frequency level (500 Hz). Stunning each goose with the current intensity at 60 V/40 mA improved lipid oxidative stability and antioxidant capacity from day 0 to day 4 and the lightness at day 0 in the liver of meat geese during cold storage. A combination of 60 V/40 mA/ 500 Hz/ 10 s per bird could be applied in the ES of Yangzhou geese in order to improve the lipid oxidative stability and antioxidant capacity in the livers. Abstract Limited research has been performed to evaluate the effects of high-frequency electrical stunning (ES) methods on the lipid oxidative stability of the meat goose livers. This study was conducted to evaluate the effects of high-frequency-ES current intensities on lipid oxidative stability and antioxidant capacity in the liver of Yangzhou goose (Anser cygnoides domesticus). Forty 92-day-old male Yangzhou geese were randomly divided into five treatments (n = 8). Geese were not stunned (control) or exposed to ES for 10 s with alternating current (AC) at 500 Hz in a water bath. Current intensities were set at 30 V/20 mA (E30V), 60 V/40 mA (E60V), 90 V/70 mA (E90V), or 120 V/100 mA (E120V), respectively. The malondialdehyde level at day 0 was the highest in 120 V (p < 0.05). Antioxidant enzymes’ activity on day 2 was the highest in E60V. The 1, 1-diphenyl-2-picrylhydrazyl free radical (DPPH·) elimination ability was lower in the E120V than that in the E60V at two days and four days postmortem (p < 0.05). A combination of 60 V/40 mA/ 500 Hz/ 10 s per bird could be applied in the ES of Yangzhou geese to improve the lipid oxidative stability and antioxidant capacity in the livers.

Simple Summary Male layer chicks do not have economic value and are humanely killed after hatching. The layer industry is seeking alternative methods to humanely kill recently hatched male chicks. This study evaluated the use of gases or negative air pressure as a means of humane and viable alternatives to maceration. The treatments included carbon dioxide, nitrogen, reduced air pressure, and a negative control. The study showed that chicks exposed to treatments, gases or negative air pressure, did not differ significantly in terms of the physiological stress response. The use of carbon dioxide resulted in a faster onset of unconsciousness and ultimately death as compared to nitrogen or negative air pressure treatments. Abstract Hatched male layer chicks are currently euthanized by maceration in the United States. Public concerns on the use of maceration have led to the search for alternative methods. We hypothesized that gas inhalation and low atmospheric pressure stunning (LAPS) are viable and humane alternatives to instantaneous mechanical destruction. The objective of this study was to evaluate the physiological and behavioral responses of recently hatched male layer chicks when subjected to carbon dioxide, nitrogen inhalation, or LAPS. The study consisted of seven treatments: breathing air (NEG), 25% carbon dioxide (CO2), 50% CO2, 75% CO2, 90% CO2, 100% nitrogen (N2), or LAPS. Ten day-of-hatch, male layer chicks were randomly assigned to each treatment, and each treatment was replicated on ten different days. A custom-made vacuum system was used to reduce air pressure inside the chamber from 100.12 kPa to 15.3 kPa for the LAPS treatment. Serum corticosterone and serotonin levels were measured using commercially available competitive enzyme linked immunosorbent assay (ELISA). Latencies to loss of posture and motionlessness were determined from video recordings. The 25% and 50% CO2 treatments were discontinued after the first replication, as the majority of the chicks recovered. The chicks in the negative (NEG) group had significantly higher levels of corticosterone than the other four euthanasia treatments. On the other hand, the serotonin levels of chicks in the NEG group was significantly lower when compared to the other four euthanasia treatments. The latencies to loss of posture and motionlessness of chicks exposed to 75% and 90% CO2 were significantly shorter than those in the LAPS and N2 inhalation treatments. These data suggest that the stress responses of chicks to the CO2, N2, and LAPS treatments do not differ among each other. However, the CO2 inhalation method was faster in inducing loss of posture and motionlessness in chicks than the LAPS and N2 inhalation treatments.

Simple Summary Compressed air, detergent, and water make up compressed air foam. Our laboratory has previously reported that compressed air foam may be an effective method for mass depopulation of caged layer hens. Gases, such as carbon dioxide and nitrogen, have also been used for poultry euthanasia and depopulation. The objective of this study was to produce compressed air foam infused with carbon dioxide or nitrogen to compare its efficacy against foam with air and gas inhalation methods (carbon dioxide or nitrogen) for depopulation of caged laying hens. The study showed that a carbon dioxide-air mixture or 100% nitrogen can replace air to make compressed air foam. However, the foam with carbon dioxide had poor foam quality compared to the foam with air or nitrogen. The physiological stress response of hens subjected to foam treatments with and without gas infusion did not differ significantly. Hens exposed to foam with nitrogen died earlier as compared to methods such as foam with air and carbon dioxide. The authors conclude that infusion of nitrogen into compressed air foam results in better foam quality and shortened time to death as compared to the addition of carbon dioxide. Abstract Depopulation of infected poultry flocks is a key strategy to control and contain reportable diseases. Water-based foam, carbon dioxide inhalation, and ventilation shutdown are depopulation methods available to the poultry industry. Unfortunately, these methods have limited usage in caged layer hen operations. Personnel safety and welfare of birds are equally important factors to consider during emergency depopulation procedures. We have previously reported that compressed air foam (CAF) is an alternative method for depopulation of caged layer hens. We hypothesized that infusion of gases, such as carbon dioxide (CO2) and nitrogen (N2), into the CAF would reduce physiological stress and shorten time to cessation of movement. The study had six treatments, namely a negative control, CO2 inhalation, N2 inhalation, CAF with air (CAF Air), CAF with 50% CO2 (CAF CO2), and CAF with 100% N2 (CAF N2). Four spent hens were randomly assigned to one of these treatments on each of the eight replication days. A total of 192 spent hens were used in this study. Serum corticosterone and serotonin levels were measured and compared between treatments. Time to cessation of movement of spent hens was determined using accelerometers. The addition of CO2 in CAF significantly reduced the foam quality while the addition of N2 did not. The corticosterone and serotonin levels of spent hens subjected to foam (CAF, CAF CO2, CAF N2) and gas inhalation (CO2, N2) treatments did not differ significantly. The time to cessation of movement of spent hens in the CAF N2 treatment was significantly shorter than CAF and CAF CO2 treatments but longer than the gas inhalation treatments. These data suggest that the addition of N2 is advantageous in terms of shortening time to death and improved foam quality as compared to the CAF CO2 treatment.

Simple Summary Reportable diseases, such as avian influenza, spread rapidly among poultry, resulting in the death of a large number of birds. Once such a disease has been diagnosed at a farm, infected and susceptible birds are rapidly killed to prevent the spread of the disease. The methods to eliminate infected caged laying hens are limited. An experiment was conducted to study the effectiveness of foam made from compressed air, water, and soap to kill laying hens in cages. The study found that stress levels of the hens killed using compressed air foam in cages to be similar to the hens killed by carbon dioxide or the negative control. Hens exposed to carbon dioxide died earlier as compared to the foam methods. The authors conclude that application of compressed air foam in cages is an alternative to methods such as gas inhalation and ventilation shutdown to rapidly and humanely kill laying hens during epidemics. Abstract During the 2014–2015 US highly pathogenic avian influenza (HPAI) outbreak, 50.4 million commercial layers and turkeys were affected, resulting in economic losses of $3.3 billion. Rapid depopulation of infected poultry is vital to contain and eradicate reportable diseases like HPAI. The hypothesis of the experiment was that a compressed air foam (CAF) system may be used as an alternative to carbon dioxide (CO2) inhalation for depopulating caged layer hens. The objective of this study was to evaluate corticosterone (CORT) and time to cessation of movement (COM) of hens subjected to CAF, CO2 inhalation, and negative control (NEG) treatments. In Experiment 1, two independent trials were conducted using young and spent hens. Experiment 1 consisted of five treatments: NEG, CO2 added to a chamber, a CO2 pre-charged chamber, CAF in cages, and CAF in a chamber. In Experiment 2, only spent hens were randomly assigned to three treatments: CAF in cages, CO2 added to a chamber, and aspirated foam. Serum CORT levels of young hens were not significantly different among the CAF in cages, CAF in a chamber, NEG control, and CO2 inhalation treatments. However, spent hens subjected to the CAF in a chamber had significantly higher CORT levels than birds in the rest of the treatments. Times to COM of spent hens subjected to CAF in cages and aspirated foam were significantly greater than of birds exposed to the CO2 in a chamber treatment. These data suggest that applying CAF in cages is a viable alternative for layer hen depopulation during a reportable disease outbreak.

Neonatal alcohol exposure produces long-term changes in the suprachiasmatic nucleus (SCN) that are presumably responsible for disturbances in the light–dark regulation of circadian behavior in adult rats, including the pattern of photoentrainment, rate of re-entrainment to shifted light–dark cycles, and phase-shifting responses to light. Because SCN neurons containing vasoactive intestinal polypeptide (VIP) receive direct photic input via the retinohypothalamic tract and thus play an important role in the circadian regulation of the SCN clock mechanism by light, the present study examined the long-term effects of neonatal alcohol exposure on VIP neuronal populations within the SCN of adult rats. Male Sprague-Dawley rat pups were exposed to alcohol (EtOH; 3.0, 4.5, or 6.0 g/kg/day) or isocaloric milk formula (gastrostomy control; GC) on postnatal days 4–9 using artificial-rearing methods. At 2–3 months of age, animals from the suckle control (SC), GC, and EtOH groups were exposed to constant darkness (DD) and SCN tissue was harvested for subsequent analysis of either VIP mRNA expression by quantitative polymerase chain reaction (PCR) and in situ hybridization or of VIP-immunoreactive (ir) neurons using stereological methods. Neonatal alcohol exposure had no impact on VIP mRNA expression but dramatically altered immunostaining of neurons containing this peptide within the SCN of adult rats. The relative abundance of VIP mRNA and anatomical distribution of neurons expressing this transcript were similar among all control- and EtOH-treated groups. However, the total number and density of VIP-ir neurons within the SCN were significantly decreased by about 35% in rats exposed to alcohol at a dose of 6.0 g/kg/day relative to that observed in both control groups. These results demonstrate that VIP neuronal populations in the SCN are vulnerable to EtOH-induced insult during brain development. The observed alterations in SCN neurons containing VIP may have an impact upon clock responses to light input and thus contribute to the long-term effects of neonatal alcohol exposure on the photic regulation of circadian behavior.

In humans, prenatal alcohol exposure produces long-term changes in the neural regulation of behavior including learning difficulties, attention deficits, sleep–wake disturbances, bipolar affective disorder and depression (Roebuck et al., 1999). Animal studies have yielded further details on the neurobehavioral consequences of alcohol (EtOH) exposure during critical stages of brain development. In rats, exposure to alcohol during the neonatal period, which corresponds to the third trimester equivalent in human brain development (Dobbing and Sands, 1979), induces chronic deficits on learning /memory and motor performance tasks and these behavioral manifestations are associated with alcohol-induced damage to the hippocampus and cerebellum (Goodlett et al., 1987, 1988; Kelly et al., 1988; Thomas et al., 1996, 1998). Recent applications of this animal model have revealed that circadian or 24-hour behavioral rhythmicity is also vulnerable to alcohol-induced insult during CNS development. Specifically, neonatal alcohol exposure alters fundamental properties of the activity rhythm in adult rats including its free-running period, phase-shifting responses to light and entrainment to light–dark cycles (Allen et al., 2005a,b; Farnell et al., 2004). At present, the molecular or cellular basis for these alcohol-induced disturbances in the neural regulation of rat circadian behavior is unknown. Because modifications in the molecular “gears” of the circadian clockworks produce tangible changes in the circadian regulation of behavior (Reppert and Weaver, 2002), it is possible that neonatal alcohol exposure may permanently modulate circadian properties of the rat activity rhythm by disrupting the clock mechanism perhaps through altered expression or temporal configuration of its molecular components. In mammals, the internal biological clock mediating the generation of circadian rhythms and their entrainment or synchronization to light–dark cycles is located in the suprachiasmatic nuclei (SCN) of the anterior hypothalamus. The “gears” of the molecular clockworks in the SCN consist of interlocked transcription–translation feedback loops in which the gene products of core components rhythmically regulate their own transcription or the expression of other clock genes. Clock, Period1 (Per1), Per2, Cryptochrome1 (Cry1), Cry2, and Bmal1 (Mop3) have been identified as core molecular elements of the circadian clock mechanism in the SCN based on studies demonstrating that targeted disruption or knockout of these genes in mice alters or abolishes circadian behavior (Reppert and Weaver, 2002). For example, Per1-, Per2- and Cry1-deficient mice show activity rhythms in which the free-running period is shorter than that observed in wild type animals (Bae et al., 2001; van der Horst et al., 1999; Vitaterna et al., 1999; Zheng et al., 2001). Although the SCN are essential for the generation of mammalian circadian rhythms in many biochemical, physiological, and behavioral processes, the expression and rhythmic regulation of these core clock genes are not spatially confined to the SCN. Instead, rhythmic fluctuations in the same clock genes comprising the molecular core of the SCN clockworks occur widely in other brain regions and many peripheral tissues, including the liver, heart, kidney, endocrine organs, and skeletal muscles (Shearman et al., 1997; Yamazaki et al., 2000; Zylka et al., 1998). These clock gene oscillations in other tissues are currently thought to provide for their “local” organization in time through a hierarchical system in which the SCN functions as a pacemaker linking periodic environmental cues with the internal circadian timekeeping mechanism in peripheral oscillators throughout the body. Consequently, the effects of neonatal alcohol exposure on the regulation of adult circadian behavior may be coupled with alcohol-induced changes in molecular components of the clockworks not only in the SCN pacemaker but also in peripheral oscillators. To determine whether the molecular mechanism for circadian timekeeping is vulnerable to alcohol-induced insult during the brain growth spurt, we examined the long-term impact of neonatal alcohol treatment on the temporal regulation of core clock genes in the SCN pacemaker and other brain or peripheral tissue oscillators. In this study, rats were exposed to alcohol during the neonatal period and the clock genes Per1, Per2, Cry1, Bmal1, and Rev-erbα were assessed for evidence of alcohol-induced changes in their circadian expression within the SCN, cerebellum, and liver. Because alterations in specific genetic components of the circadian clockworks have been linked to abnormal regulation of human sleep–wake cycles (Toh et al., 2001), which is a known neurobehavioral correlate of prenatal alcohol exposure in humans (Sher, 2004), information from this study may have important implications in understanding how alcohol-induced injury during rapid brain growth produces pathologies in the circadian regulation of sleep and other body processes.

In rats, neonatal alcohol (EtOH) exposure coinciding with the period of rapid brain growth produces structural damage in some brain regions that often persists into adulthood and thus may have long-term consequences in the neural regulation of behavior. Because recent findings indicate that the circadian clock located in the rat suprachiasmatic nucleus is vulnerable to alcohol-induced insults during development, the present study examined the long-term effects of neonatal alcohol exposure on the photic regulation of circadian behavior in adult rats. Rat pups were exposed to alcohol (3.0, 4.5, or 6.0g·kg −1 ·day −1 ) or isocaloric milk formula on postnatal days 4–9 using artificial-rearing methods. At 2 months of age, animals were housed individually and circadian wheel-running behavior was continuously analyzed to determine the effects of neonatal alcohol treatment on the rate of reentrainment to a 6-h advance in the 12-h light:12-h dark photoperiod and the phase-shifting properties of free-running rhythms in response to discrete light pulses on a background of constant darkness. For all doses, neonatal alcohol exposure had a significant effect in reducing the time for reentrainment such that EtOH-treated rats required four to five fewer days than control animals for stable realignment of the activity rhythm to the shifted light–dark cycle. Coupled with the accelerated rate of reentrainment, the amplitude of light-evoked phase delays at circadian time 14 and advances at circadian time 22 in the 4.5 and 6.0g·kg −1 ·day −1 EtOH groups was almost twofold greater than that observed in control animals. The present observations indicate that the mechanisms by which photic signals regulate circadian behavior are permanently altered following alcohol exposure during the period of rapid brain development. These long-term alterations in the photic regulation of circadian rhythms may account, at least partially, for some neurobehavioral consequences of prenatal alcohol exposure in humans such as depression.

IN HUMANS, THE central nervous system is susceptible to structural damage from alcohol (EtOH) exposure during critical stages of brain development (Clarren et al., 1978; Jones and Smith, 1973; Mattson et al., 1996; Sowell et al., 1996). Detailed animal studies have revealed that developmental EtOH exposure similarly disrupts the structural organization of different brain regions. In rats, EtOH exposure during the brain growth spurt (early postnatal period), which corresponds to the equivalent period of human brain development during the third trimester of gestation (Dobbing and Sands, 1979), has been shown to retard brain growth; produce microencephaly; cause neuronal loss in the hippocampus, cerebellum, and olfactory bulb; and alter neuronal circuitry (Bonthius et al., 1992; Bonthius and West, 1990; Chen et al., 1998; Goodlett et al., 1998; Goodlett and Johnson, 1999; Kelly et al., 1988; Maier et al., 1996; West et al., 1981). Furthermore, hippocampal and cerebellar cell loss in rats exposed to EtOH during the early postnatal period have been observed in association with behavioral deficits in learning/memory and motor performance tasks (Goodlett et al., 1987, 1988; Kelly et al., 1988; Thomas et al., 1996, 1998). However, further analysis is necessary to fully determine the scope of the developmental EtOH-induced damage to the brain and whether the resulting neuroanatomical changes have long-term neurobehavioral consequences. The circadian clock and its regulation of circadian behavior have recently emerged as a significant area of interest in the analysis of specific neurobehavioral disturbances associated with developmental EtOH exposure. The internal biological clock responsible for the generation of mammalian circadian rhythms is located in the suprachiasmatic nuclei (SCN) of the anterior hypothalamus. The endogenous timekeeping function of the SCN is complemented by its role in mediating the entrainment or synchronization of mammalian circadian rhythms to light/dark cycles. Entraining light/dark signals are transduced by the retina and conveyed to the SCN via the retinohypothalamic tract (RHT), a monosynaptic projection from a subpopulation of retinal ganglion cells that terminates bilaterally within the ventrolateral subfield of each nucleus (Moore, 1983; Pickard, 1982). In rodents, complete ablation of the SCN abolishes circadian rhythmicity in various physiologic and behavioral processes (Moore, 1983; Turek, 1985), whereas destruction of the RHT eliminates entrainment of the activity rhythm to light/dark cycles without affecting other visual functions (Johnson et al., 1988). Initial evidence for EtOH-induced disturbances of circadian clock function has emanated from rodent studies indicating that prenatal EtOH exposure alters the light/dark regulation of circadian rhythms (Sei et al., 2003). Consistent with these effects of developmental EtOH on the SCN clock, our preliminary findings demonstrate that postnatal EtOH treatment disrupts endogenous neurochemical rhythmicity in the SCN and alters the free-running period and light/dark entrainment of circadian rhythms (Earnest et al., 1997; Marchette et al., 2003). On the basis of the effects of developmental EtOH exposure on circadian entrainment to light/dark cycles, this study was conducted to determine whether early postnatal EtOH exposure permanently alters other aspects of the photic regulation of circadian behavior. Photoentrainment of circadian rhythms requires daily adjustment of the SCN circadian clock by an amount equal to the difference between its circadian period and the length (usually 24 hr) of the entraining light/dark cycle. Light is thought to mediate these adjustments by inducing time-dependent phase shifts of the SCN clock mechanism. Circadian rhythms freerunning in constant darkness (DD) are phase-delayed or reset to a later time in response to a brief light exposure during the early subjective night (i.e., coinciding with a previous dark phase or the animal’s active period) but are phase-advanced or displaced to an earlier time when light pulses are administered during the late subjective night. Because phase-shifting responses to light are directly correlated with circadian period (Daan and Pittendrigh, 1976, Pittendrigh and Daan, 1976), it is anticipated that light-induced phase shifts of the activity rhythm in adult rats will be altered in association with the long-term changes in free-running period caused by early postnatal EtOH exposure. Consequently, the circadian rhythm of wheel-running behavior was assessed in adult rats for evidence of developmental EtOH-related alterations in phase-shifting responses to light pulses administered at either 2 or 10 hr after the onset of activity [i.e., during the early subjective night at circadian time (CT) 14 or during the late subjective night at CT 22, respectively], because light exposure at these times induces maximal phase delays or advances of the rat activity rhythm. Because partial damage to the SCN alters circadian clock properties (e.g., period) that influence phase-shifting responses to light (Davis and Gorski, 1984; Pickard and Turek, 1982, 1985), this study also examined whether long-term changes in the photic regulation of circadian behavior are accompanied by developmental EtOH-induced insults on SCN integrity. Specifically, neuronal number and density in the SCN were analyzed for evidence of cell loss in adult rats exposed to EtOH during the early neonatal period.