Attribution of human infections with Shiga toxin‐producing Escherichia coli (STEC) to livestock sources and identification of source‐specific risk factors,The Netherlands (2010–2014)

Shiga toxin‐producing Escherichia coli (STEC) is a zoonotic pathogen of public health concern whose sources and transmission routes are difficult to trace. Using a combined source attribution and case–control analysis, we determined the relative contributions of four putative livestock sources (cattle, small ruminants, pigs, poultry) to human STEC infections and their associated dietary, animal contact, temporal and socio‐econo‐demographic risk factors in the Netherlands in 2010/2011–2014. Dutch source data were supplemented with those from other European countries with similar STEC epidemiology. Human STEC infections were attributed to sources using both the modified Dutch model (mDM) and the modified Hald model (mHM) supplied with the same O‐serotyping data. Cattle accounted for 48.6% (mDM) and 53.1% (mHM) of the 1,183 human cases attributed, followed by small ruminants (mDM: 23.5%; mHM: 25.4%), pigs (mDM: 12.5%; mHM: 5.7%) and poultry (mDM: 2.7%; mHM: 3.1%), whereas the sources of the remaining 12.8% of cases could not be attributed. Of the top five O‐serotypes infecting humans, O157, O26, O91 and O103 were mainly attributed to cattle (61%–75%) and O146 to small ruminants (71%–77%). Significant risk factors for human STEC infection as a whole were the consumption of beef, raw/undercooked meat or cured meat/cold cuts. For cattle‐attributed STEC infections, specific risk factors were consuming raw meat spreads and beef. Consuming raw/undercooked or minced meat were risk factors for STEC infections attributed to small ruminants. For STEC infections attributed to pigs, only consuming raw/undercooked meat was significant. Consuming minced meat, raw/undercooked meat or cured meat/cold cuts were associated with poultry‐attributed STEC infections. Consuming raw vegetables was protective for all STEC infections. We concluded that domestic ruminants account for approximately three‐quarters of reported human STEC infections, whereas pigs and poultry play a minor role and that risk factors for human STEC infection vary according to the attributed source.     

Ammonia dynamics in relation to hatching in Atlantic halibut (Hippoglossus hippoglossus L.)

Total ammonia content (T_Amm) and excretion (J_Amm), and ionic content (K⁺, Na⁺, Cl_-) have been studied in embryos and yolk-sac larvae of Atlantic halibut (Hippoglossus hippoglossus L.) maintained in darkness (6 °C and 34% S) or in light (light-arrested, nonon-hatching embryos). The T_Amm of the eggs increased from 250-300 nmol ind^-1 during the first 5-10 days post fertilization (dPF) to 400-500 nmol ind^-1 at the time of natural hatching in darkness. T_Amm did not start to decrease before 2-5 days after hatch, and yolk-sac larvae had a higher T_Amm compared to the light-arrested embryos of the same age and batch. J_Amm increased exponentially rom about 0.05 nmol ind^-1 h^-1 at 10 dPF to about 3 nmol ind^-1 h^-1 at hatch. Embryos undergoing hatching showed a significantly higher J_Amm than non-hatching, light-arrested embryos of the same age. The content of K+ in distilled water rinsed eggs declined from about 0.85 µmol ind^-1 at 2-4 dPF to about 0.15 µmol ind^-1 at hatch, while that of Cl^- remained constant at about t 0.85 µmol in^-1, and that of Na⁺ increased slowly from 0.10 to 0.20 µmol ind^-1 . Based on the measured ions, there was an anionic deficit in the egg, especially during the first week of development. When exposed to increased ambient total ammonia (0-27 mM NH4Cl), no mortality occurred, and no significant increase was found in the T_Amm of the Atlantic halibut egg before 9.2 dPF despite an estimated large inward diffusion gradient for the un-ionized ammonia species (NH₃). The delayed release of T_Amm comp ared to embryos and yolk-sac larvae of other marine teleosts, may relate to the deep-water spawning of the Atlantic halibut, and the buoyancy regulation of the yolk-sac larvae.     

氨氮胁迫对中国明对虾血淋巴氨氮、尿素氮含量和抗氧化能力的影响

将600尾体重为(5.0±1.2)g的健康中国明对虾(Fenneropenaeus chinensis)随机分为5组,每组6个重复,每个重复20尾虾,分别暴露于不同氨氮质量浓度(0 mg/L、2 mg/L、4 mg/L、6 mg/L和8 mg/L)海水中,于胁迫后6 h、24 h、48 h、72 h和96 h测定血淋巴氨氮、尿素氮含量、总抗氧化能力(T-AOC)、抗超氧阴离子活力和血淋巴细胞过氧化氢酶(CAT)基因、过氧化物还原酶(Prx)基因和含半胱氨酸的天冬氨酸蛋白水解酶(caspase)基因的相对表达量,以0 mg/L氨氮组作为对照。结果显示,随着氨氮胁迫时间的延长,中国明对虾血淋巴氨氮含量逐渐积累,以8 mg/L组对虾血淋巴氨氮含量最高,是对照组的5.85倍。氨氮胁迫6 h,胁迫组中国明对虾血淋巴尿素氮含量显著高于对照组(P0.05),其中6 mg/L组对虾血淋巴尿素氮含量最高,是对照组的2.22倍。氨氮胁迫下中国明对虾血淋巴T-AOC、Prx mRNA相对表达量随着取样时间推移先升高后降低,而血淋巴抗超氧阴离子活力、CAT和caspase mRNA相对表达量随时间增加呈现先上升后下降再上升的变化过程。氨氮胁迫下中国明对虾血淋巴抗氧化能力被显著诱导,这可能破坏机体的氧化-抗氧化系统的平衡,从而导致caspase mRNA相对表达量的上调。     

干露胁迫对鼠尾藻生理生化影响的研究

鼠尾藻(Sargassum thunbergii)集生于中潮带和低潮带岩石上,在高、中潮带的水陆或石沼中,有的甚至在低潮时较长时间暴露于日光下。低潮露空下的干露胁迫是影响鼠尾藻生存的关键因子。本研究采集野生鼠尾藻为实验材料,在培养箱中分别失水干露0、1、3、6 h,并在海水中恢复培养,测定不同胁迫时间下藻体的失水率、叶绿素荧光参数和生化参数。结果显示,不同大小的鼠尾藻干露胁迫不同时间后的失水率显著不同,胁迫时间越短,藻体越大,失水率越低,大藻体鼠尾藻的保水能力高于小藻体;干露胁迫使鼠尾藻的叶绿素荧光值显著降低,同株鼠尾藻不同部位对干露胁迫的耐受程度显著不同,梢部耐受能力较差,基部耐受能力较强,小藻体和大藻体的梢部伤害较大,不能恢复,鼠尾藻基部可恢复正常生理状态,干露胁迫时,鼠尾藻以非调节性能量耗散机制为主;干露胁迫时,藻体梢部通过抗氧化酶类[(抗超氧阴离子自由基(ASAFR)、超氧化物歧化酶(SOD))和非抗氧化物质(可溶性糖、脯氨酸)共同作用来应对胁迫,藻体基部主要是通过上调蛋白、可溶性糖和脯氨酸等含量抵抗胁迫。高中潮带的鼠尾藻较易处于高温、强光和干露失水叠加的胁迫状态,同时,又因外部形态和生活环境的不同,藻体各部分的生理生化特性也有一定的差异。本研究探讨了鼠尾藻干露胁迫下的生理生化状态,对研究鼠尾藻抵抗环境胁迫的生态适应性具有重要的指导意义。     

干露胁迫对脊尾白虾(Exopalaemon carinicauda)呼吸代谢相关酶的影响

为了研究离水干露对脊尾白虾(Exopalaemon carinicauda)呼吸代谢能力的影响,以常温干露(22-24℃)、低温干露(4℃)2个实验组和1个对照组进行脊尾白虾干露胁迫实验,于胁迫后60、90、120、180 min取组织,测定琥珀酸脱氢酶(SDH)、细胞色素氧化酶(CCO)、延胡索酸还原酶(FRD)、乳酸脱氢酶(LDH)4种呼吸代谢酶活力和乳酸含量.结果显示,常温干露组肝胰腺、鳃、肌肉SDH和CCO活力随干露时间的延长而降低,且显著低于对照组(P＜0.05);FRD、LDH活力和肌肉乳酸含量随胁迫时间的延长呈先升高后降低趋势,且显著高于对照组(P＜0.05).低温干露组在胁迫60 min时,各组织呼吸代谢酶活力和肌肉乳酸含量与对照组无显著差异(P＞0.05),之后的变化趋势和常温干露组相同.常温干露组和低温干露组中肝胰腺和鳃SDH/FRD比值的变化幅度大于肌肉.研究表明,脊尾白虾通过提高无氧代谢来应对干露胁迫;低温干露下的脊尾白虾在胁迫早期可以维持有氧呼吸,肝胰腺和鳃比肌肉对干露胁迫更加敏感.     

Marine protected areas and ocean basin management

1. All reserve designs must be guided by an understanding of natural history and habitat variability. 2. Differences in scale and predictability set aside highly dynamic pelagic systems from terrestrial and nearshore ecosystems, where wildlife reserves were first implemented. Yet, as in static systems, many pelagic species use predictable habitats to breed and forage. Marine protected areas (MPAs) could be designed to protect these foraging and breeding aggregations. 3. Understanding the physical mechanisms that influence the formation and persistence of these aggregations is essential in order to define and implement pelagic protected areas. We classify pelagic habitats according to their dynamics and predictability into three categories: static, persistent and ephemeral features. 4. While traditional designs are effective in static habitats, many important pelagic habitats are neither fixed nor predictable. Thus, pelagic protected areas will require dynamic boundaries and extensive buffers. 5. In addition, the protection of far‐ranging pelagic vertebrates will require dynamic MPAs defined by the extent and location of large‐scale oceanographic features. 6. Recent technological advances and our ability to implement large‐scale conservation actions will facilitate the implementation of pelagic protected areas. 7. The establishment of pelagic MPAs should include enforcement, research and monitoring programmes to evaluate design effectiveness. 8. Ultimately, society will need a holistic management scheme for entire ocean basins. Such overarching management will rely on many innovative tools, including the judicious use of pelagic MPAs. Copyright © 2000 John Wiley & Sons, Ltd.     

2-硝基-4'-羟基二苯胺(HC Orange No.1)在鲫鱼肝脏中的富集及其对肝脏抗氧化指标的影响

采用室内模拟方法研究了2-硝基-4'-羟基二苯胺(HCOrangeNo.1)在鲫鱼(Carassiusauratus)肝脏中的富集规律及不同暴露时间对鲫鱼肝脏抗氧化指标的影响。结果表明,10d左右鲫鱼肝脏对HCOrangeNo.1的富集达到最大值,肝脏过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、谷胱甘肽硫转移酶(GST)及还原型谷胱甘肽(GSH)对HCOrangeNo.1都非常敏感,其中GST活性和GSH含量总体上被诱导增加;SOD和CAT活性基本上都是先升高后受到抑制。上述抗氧化指标可考虑作为水生生态系统中HCOrangeNo.1污染的生物监测指标。     

Tolerance of Atlantic salmon (Salmo salar) to dietborne endosulfan assessed by haematology,biochemistry, histology and growth

The inclusion of plant‐based ingredients in commercial fish feeds may pose a challenge because of the presence of undesirable substances, such as the pesticide endosulfan. Waterborne endosulfan is highly toxic to fish, whereas dietborne exposure has varied toxicity in different species. To investigate the systemic effects of endosulfan exposure, quadruplicate groups of Atlantic salmon (Salmo salar) were fed either 0 (control), 0.005 mg kg^?1; the European Union's maximum limit, or 10 or 20 times this level (0.05 and 0.1 mg kg^?1 respectively) for 95 days. There were no significant differences (P > 0.05) in liver somatic index, spleen somatic index, condition factor or growth among treatments. There were no indications of liver damage in fish from any of the groups in the biomarkers measured: plasma aspartate aminotransferase, plasma alanine aminotransferase and histopathology. Similarly, there were no apparent treatment‐related effects on the haematological parameters Hct, Hb, mean corpuscular volume, mean corpuscular haemoglobin concentration and mean corpuscular haemoglobin, and blood sodium, potassium, calcium and chloride levels were not significantly (P > 0.05) different among groups. Lipid digestibility, but not energy, protein, or glycogen digestibility, was significantly (P < 0.05) reduced at the highest exposure concentration. However, no significant differences were observed in lipid production value or lipid efficiency ratio. In contrast to previous studies, clinical histological abnormalities were not observed in the intestine, liver or spleen of endosulfan‐treated fish.     

Dietary α‐Ketoglutarate supplementation alleviates harmful effects of high environmental ammonia on grass carp,Ctenopharyngodon idella

Current intensive fish farming usually causes high environmental ammonia (HEA) in ponds that is toxic to fish. α‐Ketoglutarate (α‐KG) can be rapidly transaminated to glutamic acid and further aminated to glutamine. Therefore, we hypothesized that dietary α‐KG supplementation would alleviate HEA toxicity to fish. To test the hypothesis, 270 healthy grass carp (Ctenopharyngodon idella) juveniles were randomly assigned to control, HEA (18.37 mg/L ammonia) and HEA + α‐KG (0.75% of α‐KG) groups. Ammonia and free amino acid content in plasma and brain, liver glutamic pyruvic transaminase and glutamic oxaloacetic transaminase activity, and urea and glycogen content were measured on the first, seventh and 42nd days. Our results showed short‐term HEA exposure (1 day) led to a significant ammonia accumulation in the brain and plasma and significantly decreased glutamic and aspartic acid content in the brain and increased glutamine content in the brain and plasma. The long‐term HEA exposure (42 days) caused significant reductions in glycine and arginine content in the brain tissue. In most cases, dietary α‐KG supplementation alleviated the fluctuations in FAA content in the brain and plasma. Our results suggested dietary α‐KG alleviated HEA toxicity to grass carp.     

Exposure assessment of professional pesticide users during treatment of potato fields

In this study four different mixing/loading and application practices in potato fields were monitored for exposure of operators to pesticides. Each operation – mixing, loading, and application – was measured individually in order to assess its relative contribution to the total exposure value. Inhalation exposure was measured by trapping the pesticides with a sorbent tube while sampling the air around the operator's face. Dermal deposition, which was measured by means of cotton gloves on the hands and by attaching patches to the operator's clothing, was the main contributor to the total exposure. Dermal deposition on the hands during mixing and loading exceeded all other dermal values. The experimental results are compared with the results obtained by the exposure assessment model PHED V1.1. This model gives an underestimation of the levels of operator exposure during mixing, loading and application. © 1999 Society of Chemical Industry