小麦是渑池县的一种主要粮食作物。在小麦腥黑穗病的发生上，渑池县20世纪50～60年代比较普遍，80年代以后大部分地区已基本绝迹。近年来，小麦腥黑穗病在部分地区开始暴发，而且发生面积逐年加大，有大面积漫延之势。在小麦腥黑穗病的发生上，开始大都为零星发生，病株率较低，加上大部分群众对该病害不具备识别能力，早期不易引起群众的足够重视。一般经过2～3年病菌的传播、扩散和病菌的积累后，随着发病面积不断扩大和田间病穗率的提高。小麦腥黑穗病病穗比正常小麦麦穗落黄时间晚3～5天。当正常小麦麦穗已变黄时，小麦腥黑穗病病穗略显暗绿色，颖壳和麦芒稍向外张开，露出部分病粒。病粒比好麦粒粗短，初为暗绿色，以后变为灰黑色或淡灰色，外面包着一层灰白色膜，里面充满鱼腥味的黑粉（病菌的厚垣抱子），所以俗称腥乌麦或臭黑疸。病株一般比健株矮小，分蘖增多。小麦腥黑穗病病原菌有两种，一种是Tilletia caries（DC.）Tul.（小麦网腥黑粉菌），另一种是Tilletia foetida（Wallr.）Liro（称小麦光腥黑粉菌）。有报道Tilletia ntraversa Kühn称小麦矮腥黑粉菌也能引起腥黑穗病发生。两种病原菌均属担子菌亚门真菌。小麦网腥黑粉菌孢子堆生在子房内，外包果皮，与种子同大，内部充满黑紫色粉状孢子，具腥味。孢子球形至近球形，浅灰褐色至深红褐色，大小14～20μm，具网状花纹，网眼宽2～4μm。小麦光腥黑粉菌孢子堆同上。孢子球形或椭圆形，有的长圆形至多角形，浅灰色至暗榄褐色，大小15～25μm，表面平滑，也具腥味。小麦矮腥黑粉菌成群的孢子为暗黄褐色，分散的孢子近球形，浅黄色至浅棕色，大小14～18μm，具网纹，网脊高2～3μm，网目直径3～4.5μm，有的可达9.5～10μm，外面包被厚1.5～5.5μm的透明胶质鞘。主要引致小麦矮腥黑穗病。小麦脱粒时，病粒破裂，病菌孢子飞散，粘附在种子表面，调运带有小麦腥黑穗病病菌的种子是造成小麦腥黑穗病远距离传播的主要途径。群众相互间的种子串换是造成小麦腥黑穗病在一定区域内大面积扩散的主要原因。混有病菌的麦糠、麦秸、淘麦水等沤粪或喂牲口，使粪肥中带有病菌，施入麦地，也可以传病；若多户群众共用一个麦场，在小麦脱粒或晾晒时也可以传病；在个别寒冷干燥的地区，落在土中的病菌孢子存活时间较长，也可传病。病菌以厚垣孢子附在种子外表或混入粪肥、土壤中越冬或越夏。小麦播种后，当种子发芽时，粘附在种子表面或粪肥、土壤中的病菌孢子发芽并侵入小麦幼芽，厚垣孢子也随即萌发，厚垣孢子先产生先菌丝，其顶端生6～8个线状担孢子，不同性别担孢子在先菌丝上呈“H”状结合，然后萌发为较细的双核侵染线。从芽鞘侵入麦苗并到达生长点，后病菌在麦株内以菌丝体形态随小麦而发育，到孕穗期，侵入子房，最后到达花部，破坏花器正常发育，抽穗时在麦粒内形成菌瘿即病原菌的厚垣孢子，即为病粒。小麦腥黑穗病菌的厚垣孢子能在水中萌发，有机肥浸出液对其萌发有刺激作用。萌发适温16～20℃。病菌侵入麦苗温度5～20℃，最适9～12℃。湿润土壤（土壤持水量40%以下）有利于孢子萌发和侵染。一般播种较深，不利于麦苗出土，但增加了病菌侵染机会，病害加重发生。病菌只能侵害未出土的幼芽，而不能侵害小麦的幼苗或植株，小麦一旦出苗后，病菌就不再侵染。所以小麦腥黑穗病防治必须抓好播种期这一关键时期。在小麦腥黑穗病的发生上，一般播种愈深愈晚，出土愈慢，发病愈重。土壤温度在5～12℃、土壤湿度中等时，最容易侵染。因此，冬麦迟播，春麦早播，发病较重。4.1 小麦腥黑穗病传播途径主要是种子传播。4.2 受小麦腥黑穗病侵染的小麦，从播种到抽穗前，田间基本没有明显的症状表现，只是到小麦落黄以后症状才表现出来。4.3 当种子发芽时，病菌孢子一旦侵入小麦幼芽使小麦感病，难以用药剂进行防治。4.4 带有小麦腥黑穗病病菌的小麦有毒，人一旦食用，轻者头晕恶心，重者引起中毒。5.1 违章调运是造成小麦腥黑穗病发生的重要原因。新的种子法实施后，随着种子市场的放开，私拉乱调现象十分严重，加上调种单位检疫意识淡薄，逃漏检现象突出，检疫不严是造成小麦腥黑穗病传播的一个主要途径。5.2 近年来群众对麦播药剂拌种重视不够，白种下地是造成小麦腥黑穗病连年发生的一个主要原因。5.3 群众更换新品种不及时，自留种现象普遍。一般是购买一次种子，连种3～5年，造成病菌积累，小麦腥黑穗病逐年加重。5.4 农户之间相互串换种子是造成小麦腥黑穗病在不同乡、村之间快速扩散和严重发生的一个重要原因。在小麦品种更换上，大部分群众为了节省成本，往往不到正规的种子门店购种，而是相互之间串换，造成小麦腥黑穗病在村、户之间或村、村之大面积传播发病，基本上发病一家，传遍全村。5.5 播种晚出苗时间长是部分年份发病严重的一个重要因素。由于气候原因，部分年份小麦播种期较晚，地温低，小麦在土壤中发芽出苗时间延长，使小麦腥黑穗病病菌侵染机会增加，来年发病就重。6.1.1 加强检疫执法力度，开展产地检疫和种子抽样室内检验，严把引种、调种和种子外调关。6.1.2 小麦腥黑穗病发病重的地区（病穗率超过0.6%，含0.6%）的小麦必须销毁处理，秸秆必须进行焚烧，严禁沤肥或喂牲口。发病轻的地区（病穗率小于0.6%），要及时拔除，毁灭病株，单打单收，禁止留作种用。6.1.3 广泛宣传，积极引导群众及时更换新品种，严禁群众间相互串种。小麦腥黑穗病主要是通过种子传播，实践证明及时更换品种，是防治小麦腥黑穗病的最有效措施。一般做到年年更换新品种，经过3～5年的品种连续更换，即可将小麦腥黑穗病完全根除；购种时必须到正规的种子部门，选购经过检疫部门检疫合格的种子。6.1.4 轮作倒茬、适时早播。发生小麦腥黑穗病的田块可改种其他作物，或与油料、蔬菜等非禾本科作物进行轮作；在小麦播种时，播种不易过迟、过深，覆土不易过厚，缩短小麦出苗时间。6.2.1 药剂种子处理。用种子重量0.15%的20%的粉锈宁乳油拌种，可防治此病，还可兼防治小麦秋苗期白粉病和锈病。也可用2.5%适乐时悬浮剂按种子量的0.15%拌种，防效均较好。6.2.2 也可用1%石灰水浸种。石灰1kg加水100kg浸小麦，种子60kg，以水淹过种子10～13cm为宜。气温20℃浸3～4天，25℃时浸2天，30℃时浸1天。种子入水后禁止搅动以防破坏水面石灰膜，浸后晒干待播。6.2.3 在粪肥或土壤传染地区，除用药剂拌种外，还需采用以下方法才能收到最好的效果：每亩用纯六氯代苯0.5kg（50%的用1kg）加干细土2.5～7.5kg，拌匀制成毒土，与种子混合均匀，用耧播下；用豆饼、花生饼、芝麻饼、菜籽饼等油饼磨成粉末，每亩园22.5kg，加入10～15倍细土或土粪拌匀，和麦种同时播下；在病粪中加入人粪尿、油饼、青草等有机质，经堆积腐熟，然后施用。适时早播。注意事项：一切参与小麦收割的农事工具及车辆在离开疫情发生地块前，使用50%粉锈宁可湿性粉剂200倍液消毒处理。

水稻条纹叶枯病由灰飞虱传播的发生严重的水稻病毒病。该病2004年在浙江长兴突然发生，全县发病面积为663.3hm2，发病较重的田块丛病率达50%以上，株病率达17.6%，一般丛病率在10%左右，株病率在1%～5%，其中产量损失10%～30%为21.7hm2，损失30%以上为2.79hm2，涉及15个乡镇，个别严重田块颗粒无收。2005年水稻条纹叶枯病以较快的速度蔓延，6月中旬在长兴夹浦、洪桥、虹星桥、雉城等乡镇的单晚秧田和早播直播稻相继发病，部分严重田块株病率超过25%，7月10日左右，出现第二个症状表现高峰，移（抛）栽稻、直播稻不同程度发病，发病面积达1万hm2，其中66.67hm2损失产量20%以上。针对水稻条纹叶枯病流行的严峻形势，为了有效地控制病害暴发流行，确保水稻生产安全，从2005年起，我们对水稻条纹叶枯病及传毒媒介灰飞虱发生动态进行较为系统的监测，开展了防治技术的研究。现将调查试验结果综述如下：在前一年发病较重的田畈，选取有代表性的田块对水稻条纹叶枯的发生情况进行定期跟踪调查，以观察水稻条纹叶枯病的田间消长规律。从田间调查来看，秧田从6月上旬后期开始发病，6月15日出现第一个症状表现高峰；移栽到大田后，6月23日调查，丛病率为6%，株病率为0.89%，病情指数为0.08，至7月10日左右出现第二个症状表现高峰；以后随着发病株的枯死和分蘖的增加，丛病率和株病率都呈下降趋势，株病率下降相对较快，8月20日左右出现第3个症状表现小高峰（见图1、图2）。从田间发病调查情况看，发病程度最重在7月底，见图3。图1 水稻条纹叶枯病丛发病率增长动态（浙江长兴）图2 水稻条纹叶枯病株病发病率增长动态（浙江长兴）图3 水稻条纹叶枯病病情指数增长动态（浙江长兴）2005年灯下监测，5月中旬成虫开始上升，6月中旬出现了第2代成虫高峰，诱虫量大，诱虫量为2936头，7、8月出现了3、4代成虫的小高峰，9月出现了5代成虫高峰，9月中旬和下旬分别诱到成虫1522头和1722头，10月还有大量的成虫出现，见图4。图4 灯下灰飞虱成虫消长情况（浙江长兴，2005）2006年灯下监测，5月上旬灯下始见，下旬成虫开始上升，迁入水稻秧田为害，6月上旬后期至中旬出现了第2代成虫高峰，为全年虫量最高，诱虫达6337头，7月上旬、8月上旬又出现了3、4代成虫的小高峰，8月底至9月初后灯下虫量上升，出现了5代成虫高峰，诱到成虫1520头；10月灯下诱虫量减少，见图5。图5 灯下灰飞虱成虫消长情况（浙江长兴，2006）2005年4月22日麦田调查，越冬代虫量为5.4万头/hm2，6月16日秧田虫量为13.05万头/hm2，6月21日平均卵量480万粒/hm2，6月28日秧田虫量为4.05万头/hm2，7月下旬虫量为1.05万头/hm2，8月上中旬虫量为0.45万头/hm2，9月上旬虫量为1.5万头/hm2，9月15日虫量为4.05万头/hm2，9月20日虫量为7.5万头/hm2，9月26日虫量为16.5万头/hm2，9月30日虫量为25.5万头/hm2，10月5日虫量为33万头/hm2，10月10日虫量为27万头/hm2，10月15日虫量为10.95万头/hm2。2006年4月上旬麦田调查，越冬代虫量为15.9万头/hm2，6月30日秧田虫量为16.95万头/hm2，7月3日秧田虫量为8.55万头/hm2，7月中下旬田间虫量下降，8月1日虫量为8.55万头/hm2，8月14日虫量为19.95万头/hm2，8月25日虫量为17.25万头/hm2，8月28日虫量为20.1万头/hm2，9月8日虫量为24万头/hm2，9月下旬虫量上升，9月25日为153.45万头/hm2，9月29日虫量为28.55万头/hm2，10月虫量还比较高，10月8日虫量为48万头/hm2，10月12日虫量为31.5万头/hm2，10月17日虫量为30万头/hm2。田间灰飞虱消长曲线见图6。图6 田间灰飞虱发生消长情况（浙江长兴，2006）灰飞虱的发生量和带毒率对水稻条纹叶枯病的发生有着密切的关系，近年来，随着灰飞虱发生量增加和带毒率的提高，水稻条纹叶枯病发生面积扩大，发生程度加重。据测定，2005年长兴县灰飞虱带毒率斑点免疫快速测定为11.27%，2007年达18%。水稻灰飞虱生物法测定传毒率，2006年为6.7%，2007年为7.4%。田间观察，5月中下旬的1代灰飞虱成虫传毒造成秧田和部分早播直播田（5月下旬播种）发病，至6月中旬左右出现了水稻条纹叶枯病的第一个显症高峰；6月上旬后期至中旬的2代灰飞虱成虫高峰造成了7月中旬左右的水稻条纹叶枯病的第2个显症高峰，由于6月上旬后期至中旬的灰飞虱成虫高峰量较大，因此，7月10日左右水稻条纹叶枯病表现高峰来势凶猛，发病面积大，发病程度重；8月中旬在病情发展上有一个小高峰，如2006年8月7日左右个别失治田块出现了第3个症状表现高峰，株病率达20%以上。以后随着水稻的生长，抗逆能力增强，田间虽有大量的灰飞虱成若虫，但基本不发病。水稻条纹叶枯病的防治应立足于预防，采取“抗、避、断、治”的综合防治措施。在目前水稻对条纹叶枯病防治还没有高抗品种的情况下，重点要切断灰飞虱的传毒途径。为此，我们围绕灰飞虱的防治开展一系列的农业防治措施和药剂防治试验，根据水稻条纹叶枯病的感病期，强化药剂浸种、拌种处理和秧苗期、大田前期灰飞虱的防治，配合使用病毒钝化剂，水稻条纹叶枯病得到了有效地控制。在条纹叶枯病重发区，推广秀水63、秀水09等抗病性好的品种，压缩武运粳7号、加育991等感病品种种植。浙江长兴1代灰飞虱成虫迁移高峰期在5月中下旬，推迟至6月上旬播种的直播稻可避开大部分1代灰飞虱的迁入传毒，减少发病机率。水稻条纹叶枯病的感病期主要在秧苗期，水稻秧田期的灰飞虱防治尤其重要。因此，要及时清除农田周边杂草，5月上旬前冬闲田提前翻耕，减少灰飞虱中间寄主，恶化灰飞虱生存环境，抓好麦田灰飞虱的防治，麦田收割后及时灌水翻耕，并抓好“四边”杂草中灰飞虱的防治。同时抓好药剂浸种、拌种处理的秧田期和大田前期的灰飞虱防治。坚持“治杂草和麦田保秧田、治秧田保大田、治大田前期保大田后期”的策略。经过几年来的试验示范，防治灰飞虱以5%锐劲特45～50ml/667m2、40%毒死蜱100～120ml/667m2、50%稻丰散100ml/667m2，加水50kg喷雾防治为佳。在浸种灵浸种的基础上，催芽露白后每千克种子用35%丁硫克百威（稻拌成、稻伴）种子处理干粉剂5g拌种，混拌均匀后播种，随拌随用。在水稻发病前和发病初期，配合使用病毒钝化剂2%菌克毒克100～150ml/667m2防治1～2次，减轻水稻发病程度，减少水稻产量损失。

核盘菌（Sclerotinia sclerotiorum）所致的油菜菌核病是毁灭性的。抗病性鉴定方法是抗病材料筛选和育种的关键。本研究探讨了一种有效的田间病害圃鉴定筛选的方法，该方法中维持适中的病害压力是鉴定区别油菜品系抗性的关键。病害圃中每年连作油菜，在播种前每行施两粒菌核。在开花期利用喷雾系统喷雾保湿。于成熟期按0～4级分级调查病害。在两年的试验中，90个品系发病率在3.3%～100%。发病率和病情指数在重复之间显著相关。小区的病情指数和相对抗性指数基本为正态分布。研究结果表明该方法是有效的、有用的和灵敏的。Sclerotinia sclerotiorum causes a highly destructive disease in oilseed rape(Brassica napus).Methods for identification of resistance to S.sclerotiorum are crucial to screening and selection of resistance materials.In the study,we described a field disease nursery method efficient for resistance screening of breeding lines or germplasm of oilseed rape where maintaining of a suitable disease pressure is considered to be most important in order to differentiate levels of resistance existed in different lines.In the disease nursery,S.sclerotiorum inoculum had been maintained by growing oilseed rape consecutively and by placing two sclerotia in each row before sowing in each of the previous four seasons.During the flowering time,all plants were sprayed with water using a spray system.At maturity,disease severity was assessed on a 0~4 scale and disease index was calculated.In tests of two years,percent diseased plants of 90 lines(3 replicates in each year)ranged from 3.3%~100%.The percent of diseased plants and disease indices were significantly correlated between replicates(P<0.05).The frequency distributions of both disease indices(each plot)and relative resistance indices were in a normal form while the frequency distribution of percent diseased plants was negatively skewed.These data indicated that the method is efficient and useful to differentiate resistance of oilseed rape varieties.

核盘菌是普遍存在的坏死性真菌病原，能够侵染75科408种植物。在寄主植物中尚未发现免疫种或单基因抗性，包括十字花科。然而在禾本科等非寄主植物中该病菌是不致病的或弱致病的。为研究非寄主抗性机制，我们用该病菌接种了竹子、小麦、玉米和油菜。接种后24 h，这些植物对病菌的反应是不同的，竹子和玉米上无病斑，小麦上有小的病斑，但不同品种有变化，而油菜上产生了大的病斑。扫描电子显微镜研究表明，接种的竹子叶表面形成了一层膜，但在光学镜下菌丝穿透进入了上表皮细胞。菌丝进入竹子和油菜叶表皮细胞的方式是不同的。在油菜上菌丝很快进入上表皮细胞和细胞间隙，但竹子中菌丝仅限于上表皮和叶肉细胞。我们推定禾本科植物叶表面物质和细胞壁成分可能是阻止菌丝进入细胞的重要障碍。需要进一步分析这些成分。Sclerotinia sclerotiorium(Lib.)de Bary is a ubiquitous necrotrophic fungal pathogen capable of infecting at least 408 plant species of 75 families.No highly resistant varieties or germplasm is found in hosts including Cruciferae plants.On non-host plants such as some Gramineae species,however,the pathogen is avirulent or weak virulent.To understand how these non-hosts resist the pathogen,we inoculated S.sclerotinia mycelium to the leaves of bamboo,wheat,maize and oilseed rape as well.There were different responses in these plants after 24 hpi(hours post inoculation).No lesion was found on bamboo and maize leaves.Small lesions were observed on wheat,but the lesion size varied among different cultivars.Larger lesions were observed on oilseed rape leaves than any other Gramineaes at earlier time after inoculation.The scanning electron microscope(SEM)study showed clearly that inoculated bamboo leaf formed a layer of membrane on the leaf surface,but the slides under a light microscope unveiled hyphae penetration into the epidermal cells.The modes that hyphae grew into the leaves were also different between bamboo and oilseed rape.The hyphal growthfast under the oilseed rape epidermal and in the intercellular space,but in bamboo the growth was limited in the epidermis and mesophyll cells.We assumed that surface substance and cell wall composition are important obstacles of the hyphal penetration in non-host Gramineae plants.Further work needs to be done to analyze these compounds in comparison with oilseed rape.

Rice stripe(RSV)has been known to distribute in rice areas all over the world,and it is very hard virus,transmitted by insect vectors,small brown planthopper(SBPH),Laodelphax striatellus,Fallen.Once the rice is infested,there is still no very effective measures to control,even the chemicals.The chemicals'effect is not ideal and more or less they could cause some environmental risks,so there is the common opinion in the IPM system that the rice varieties having resistance to rice stripe is one of the basic and effective measures to control this disease.In 2006 and 2007 for finding the resistant rice varieties that could be used for large scale in the field,the evaluation and screening of rice varieties were conducted in Jiaxing,Zhejiang Province.In 2006,there were 40 varieties provided for the experiement,just like Chunjiang 050,Xiushui 63,Y1,Zheda 510,Tai 03126,HZ586 and so on,and Jia 991 was set to be the control.Similar to 2006 studies,in 2007,there were 20 varieties used in 2006,and newly introduced into 17 varieties,just like Leyou 2,Jiaheyou 261,Bing 04～123,Jiashao 3.The control was still Jia 991.In 2006,the experiment was conducted in the yard of Shuangqiao Academic of Agricultural Science,Xiuzhou,Jiaxing.Last year in this plot rice was planted,and in winter no crop was planted.The water and fertilizer condition was good.The rice was seeded in 2th June,and transplanted to the field in 1st July.Randomed blocking design,and the size of every plot is 30m2,with three replications.The field management was as usual,except for no chemicals use for controlling the SBPH and RSV.In 2007,the experimental field was chose to north suburb of Jiaxing,where last year the RSV occurred hard.The experimental field condition and design were familiar with 2006,and total 111plots.Investigated Methods In 2006,after 5d from 1st July when the rice were transplanted,the investigation was conducted every 5d in field,till the diseases was stable,at that time the total rice tiller and the diseased tiller amount were recorded.Num.VarietiesDiseasepercentageinthefield(%)SSRP=0.05P=0.011Jiahe2156.03aA2Y25.33bB3Jiajing36485.24bB4Y33.9cC5Shaojing04-463.49dD6Jia991(CK)3.07eE7Yongjing04683.02efEF8Y62.88fgEFG9Tai04-42.83gFG10Xiushui032.73ghGH11Qianghu9142.73ghGH12Y102.59hiHI1336You7482.52ijHI14Xiushui092.51ijHI15ZH2512.42jkIJ16Xiushui1102.27klJK17Jingzhi202.27klJK18Y42.23lmJKL19Jia04-332.14lmnKLM20Jiahua12.11mnKLM21Xiushui632.04nLM22Jiahe2182nM23Zheda5101.99nM24Bing01-1131.74oN25R41011.69oN26Y51.59oN27Jingzhi270.94pO28Chunjiang0500.91pO29Chunjiang0510.91pO30Bing03-1230.88pO31Jiaheyou28880.87pO32Zheda5320.86pO33Y80.86pO34Y10.81pO35Ning04-450.45qP36Tai031260.44qP37HZ5860rR38Y70rR39Y90rR40JiaheyouTR0rRTable 1In 2007,after 15th May,when the seeds were seminated,the investigation was conducted periodically in seedling stage till 20th June,when the rice was transplanted,the total rice tiller and the diseased tiller amount were recorded.And in field,30th July,when the disease was stable,the same indexes were recorded.By the total rice tiller and the diseased tiller amount,the disease percentage could be got,and by DPS software the resistance of different rice varieties could be made with ANOVA method.From table 1,we could get that in 2006 the RSV occurred softly in the experimental field,the CK,Jia 991'disease percentage was just 3.07%.Shaonuo 04~46,Y3,Jiajing 3648,Y2,Jiahe 215's were higher than CK;but there were four varieties,Jiaheyou TR,Y9,Y7,HZ586,which no typical RSV was found.By ANOVA analysis,the resisstance of rice varieties were obviously different.Jiaheyou TR,Y9,Y7,HZ586,which no typical RSV was found,the resistance were the highest;the Yongjing 0468,Y6 and CK were in the same level and at P=0.01 there were no obvious difference;and Shaonuo 04～46,Y3,Jiajing 3648,Y2,Jiahe 215 resistance were weak.In 2007,in the field the RSV occurred seriously in the experimental field,the CK,Jia 991'disease percentage was 19.12%(Table 2).Disease percentage of Shi 1 and Yongjing 0468 were 27.8%and 25.65%,respectively;there were 16 varieties,for example Jia 991,the disease percentage were above 10%;and the disease percentage of HZ586,Chunjiang 051,Jiahe 218,Jiaheyou 555 and Y9 were below 2%.By ANOVA analysis,the resistance of these rice varieties were seriously different.Disease percentage of Shi 1 and Yongjing 0468 were obviously higher than CK,their resistance were weak;the disease percentage of HZ586,Chunjiang 051,Jiahe 218,Jiaheyou 555 and Y9 were far below from other variety,their resistance were high;and others resistance were in the middle level.In 2007,in the seedling field the disease percentage of Bing 04～132,Zheda532,Xiushui 09,Xiuishui 110 and Bing 05～15 were all above 5%;the disease percentage of was just 0.07%,and in the Chunjiang 051 there was no RSV found;Other varieties percentage of disease were in the middle of 5%and 0.07%(Table 2).Num.VarietiesDiseasepercentageinthefield(%)SSRP=0.05P=0.01VarietiesDiseasepercentageintheseedlingfield(%)SSRP=0.05P=0.011Shi127.8aABing04-1325.68aA2Yongjing046825.65aAZheda5325.6aA3Bing04-0819.62bBXiushui095.39aAB4Jia991(CK)19.12bBXiushui335.24abAB5Xiushui11018.5bBXiushui1104.85abcABCTable 2 Evaluation of rice varieties resistance to RSV (Jiaxing, 2007)Num.VarietiesDiseasepercentageinthefield（%）SSRP=0.05P=0.01VarietiesDiseasepercentageintheseedlingfield（%）SSRP=0.05P=0.016Bing05-1517.83bBCShi14.34abcdABCD7Bing01-11317.76bcBCJiahua14.34abcdABCD8Y517.33bcBCYongjing04684.24abcdABCDE9Jiahua116.5bcdBCBing05-154.15abcdeABCDEF10Xiushui3316.4bcdBCY53.78abcdefABCDEFG11Ning04-4516.26bcdBCBing04-083.66abcdefgABCDEFGH12Bing04-13215.75bcdBCJia991（CK）2.9bcdefghABCDEFGHI13Zheda53215.69bcdBCY22.88bcdefghABCDEFGHI14Y215.18bcdBCDBing01-1132.81bcdefghiABCDEFGHI15Shi215.06bcdBCDNing04-452.77cdefghijABCDEFGHI16Xiushui0914.99bcdBCDY12.66cdefghijABCDEFGHI17Y112.96cdeBCDEQianghu1712.52cdefghijkABCDEFGHI18Qianghu17112defCDEBing05-1142.48cdefghijkABCDEFGHI19Bing03-019.22efgDEFShi22.26defghijkBCDEFGHI20Bing04-1138.25fghEFGBing03-012.14defghijkBCDEFGHI21Jiaheyou6127.18ghiEFGHBing04-1131.69efghijkCDEFGHI22Bing03-1235.76ghijFGHJiaheyou2611.39fghijkDEFGHI23Leyou25.42ghijFGHJiaheyou6121.23ghijkDEFGHI24Jiaheyou2615.23ghijFGHBing03-1231.11hijkDEFGHI25Jiaheyou16204.76ghijFGHY71hijkEFGHI26Shaonuo04-464.36hijFGHChunjiang0500.99hijkEFGHI27Jiashao34.3hijFGHJiahe2180.94hijkFGHI28Chunjiang0503.22ijFGHLeyou20.9hijkFGHI29Y73.18ijFGHJiaheyou62230.72hijkGHI30Jiaheyou62233.1ijFGHJiaheyou5550.7hijkGHI31台031262.97ijFGHJiaheyou16200.5hijkGHI32Bing05-1142.9ijFGHY90.38hijkHI33HZ5861.83jGHHZ5860.32ijkI34Chunjiang0511.81jGHShaonuo04-460.24jkI35Jiahe2181.78jGHJiashao30.24jkI36Jiaheyou5551.53jHTai031260.07kI37Y90.94jHChunjiang0510kI续表2By ANOVA analysis,the different resistance of these rice varieties also existed.the disease percentage of Bing 04～132,Zheda532 and Xiushui 09 were higher,and their resistance were weak;the disease percentage of six varieties,Chunjiang 051,Tai 03126,HZ586,Shaonuo 04～46,Jiashao 3 and Y9,were lower,and they had comparatively high resistance.Through the rice varieties screening for resistance to rice stripe virus(RSV)in the seedlingstage and in the field in Jiaxing,in 2006 and 2007,the difference of rice varieties resistance to RSV could be found,and the resistance trends between different developmental stage and different year kept in the same trends.Chunjiang 051,Y9,Jiahe218,Jiaheyou 555,Tai 03126 and Bing 03~123,and so on,had the high resistance to RSV.Though most of the results showed that the varieties resistance behave the same in different developmental stage and different year,we also should notice that few varieties did not obey this trends,for example,Shaonuo04～46,in 2006 in the field it showed very weak resistance,but in 2007 in the seedling field it showed high resistance.This perhaps tell us that just use the index of disease percentage is not enough,and at the same time we could ignore that there is still no very clear criterion to evaluate the varieties resistance to RSV.These factors could influence our evaluation.In 2006 the RSV occurred softly in the experimental field,the CK,Jia 991 disease percentage was just 3.07%,but in 2007 the CK,Jia 991's disease percentage was 19.12%,far higher than that in 2006.That is because in 2007 we chose the field where in year before the RSV occurred seriously,and advanced the seeding date and transplanted date accordingly,which the two steps could make the optimal RSV occurring conditions.On other hands,in the same cultivated condition,the disease percentage different varieties could behave 10-folder difference,it could show us clearly that the varieties resistance could exert important role in the RSV IPM system.Research was funded by a grant from Zhejiang province Science and Technology Bureau.

Plant and fungal cells are surrounded by a cell wall rich in diverse polysaccharides and proteins.It has become apparent in recent years that the carbohydrates in the cell wall function not only to maintain cell shape and integrity,but also may serve as signals in plants(Mohnen et al.,1993).Oligogalacturonic acid(OGA),a well studied elicitor,is derived from plant cell walls(Nothnagel et al.,1983).When added to cultured plant cells,it induces an oxidative burst within minutes,releasing ROS via a pathway that involves receptor binding,activation of a G-protein,influx of Ca2+,stimulation of phospholipase C,and induction of a number of kinases(Apostol et al.,1989;Horn et al.,1989;Legendre et al.,1992;Chandra et al.,1995;Legendre et al.,1993).Purified OGAs 13 to at least 26 residues long stimulate pp34 thiophosphorylation in vitro(Philippe et al.,1995).OGAs are also involved in the induction of the jasmonate pathway during plant defense response to E.carotovora subsp.Carotovora attack(Cecilia et al.,1999).The first response observed after the addition of OGAs that is clearly involved in plant defense is the production of active oxygen species,including H2O2,and O2-.This response,termed the oxidative burst,occurs within a few minutes after the addition of OGAs to suspension-cultured soybean,tobacco,and tomato cells.Reactive oxygen species are thought to have direct(through cytotoxicity)and indirect(through signaling)roles in the plant cell death required for the HR.Reactive oxygen species induce the expression of defense related genes,and are implicated as second messengers that elicit other defense responses,including systemic acquired resistance(SAR)and the HR(Brent etal.,2001).Different elicitors are thought to activate different sets of second messengers.The two signaling events that appear to participate in the OGAs inducing plant defense include the oxidative burst and NO accumulation.Inhibitors of mammalian nitric oxide synthase reduced both OGA-induced NO ac-cumulation and NOS activity,suggesting that OGA-induced NO production occurs via a NOS-like enzyme(Hu et al.,2003). Nitric oxide(NO)is a highly reactive molecule that rapidly diffuses and permeates cell membranes.During the last few years NO has a significant role in plant resist-ance to pathogens by triggering resistance-associated cell death and by contributing to the local and systemic induction of defense genes.NO stimulates signal transduction pathways through protein ki-nases,cytosolic Ca2+mobilization and protein modification(María et al.,2004). Most of the ex-perimental data available on NO detection during plant-pathogen interactions come from studies of infections by biotrophic pathogens(María et al.,2004). Additionally,an increase in NOS activity correlated with the pathogen resistance response has been observed in resistant tobacco during TMV infection( Durner et al.,1998;Chandok et al.,2003).Here we report that OGAs induced a range of defense responses in tobacco,including oxidative burst,NO accumulation and stimulation of superoxide dismutase(SOD)activity and catalase(CAT)activity.Furthermore,we show that tobacco plant sprayed with OGAs developed a resistance against infection by tobacco mosaic virus.We also provide evidence that the defense response induced by OGAs was connected with H2O2 and NO pathway.Plants of tobacco(Nicotiana tabacum var.sam sun NN)were grown from seeds in a greenhouse and were used at the 4~6-leaf stage after 2 months in culture.The plants were kept in a growth chamber at(23±1)℃ with a photoperiod of 16 h and 70%~80%relative humidity for several days before treatments.Diphenylene iodonium(DPI),2-(N-morpholino)ethanesulfonic acid(MES),Sodium nitroprusside(SNP),catalase(CAT,from bovine liver),NG-nitro-L-arginine-methyl eater(L-NAME)and 4,5-diaminofluorescein diacetate(DAF-2 DA)were obtained from Sigma.2′,7′-dichlorofluorescin diacetate(H2DCF-DA)from Biotium.All other reagents were from Shanghai Chemical Reagent CO.,LTD,Tianjin Kermel Chemical Development Centre,or Beijing Chemical Plant.OGAs was prepared from enzymatic hydrolysis of pectin and separated with membrane according to the report(H Zhang et al.,1999).An aliquot of OGAs was dissolved in water and analyzed with a matrix-assisted laser desorption-ionization time-of-flight mass spectrometer(MALID-TOF-MS,Bruker,Germany).Tobacco mosaic virus(TMV)that came from our collection was multiplied in N.tabacum.TMV was extracted from systemic infected plants by homogenization of infected leaves in 0.05mol/LH3PO4 buffer(0.05mol/L KH2PO4,0.05 M Na2HPO4 pH 6.8)with subsequent clarification of the extract by centrifugation at 2000g for 6 min.The supernatant extract was used for mechanical inoculation.All leaves of plant were sprayed with 50μg/ml of OGAs,the control plants were sprayed with water.24h~25d after OGAs application,plants were inoculated mechanically with TMV.The lesion caused by TMV was investigated at 7d after inoculation.Results were analyzed using Duncan's multiple range test at P= 0.05.For measurements of SOD and CAT activities,tobacco leaves treated with OGAs were kept in liquid nitrogen.The enzymes in the frozen powders were extracted by adding 0.05g polyvinylpyrrolidone and 5ml 0.05mol/L sodium borate buffer at pH 8.8 and homogenized at 4℃.SOD activities were measured as described by Zhu Guanglian(Zhu Guanglian et al.,1990).CAT activity was determined using the method of Beers&Sizers(Beer et al.,1952).NO and H2O2 measurement was performed using their fluorescent indicator dye DAF-2 DA and H2DCF-DA as described previously by H.Kojima(H.Kojima et al.,1998)with slight modifications.The epidermis was peeled carefully from abaxial surface of the leaves and cut into 5-mm length.Epidermal strips were placed into Tris/KCl buffer(Tris 10 mmol/L and KCl 50mmol/L,pH 7.2)containing DAF-2 DA at a final concentration of 10μmol/L for 30min,or H2DCF-DA at 50μmol/L for 10min,at 26℃ in the dark.The epidermal sections were removed and transferred to a dish of fresh Tris/KCl buffer(without probe)to wash off excess fluorophore apart from light.Then the epidermal strips were placed in Tris/KCl buffer containing OGAs and inhibitors.Examination of peels was performed using laser scanning confocal microscopy(Leica,TCS SP2)with exciting wavelength 488 nm,emitting wavelength 505~530nm.Plants were sprayed with 0.01 and 0.1 mmol/L of sodium nitroprusside(SNP),50μg/ml of OGAs,1 mmol/L,10mmol/L and 100 mmol/L H2O2,H2O2 scavenger catalase(CAT,100unit/ml)and OGAs cotreatment,H2O2 scavenger ascorbic acid(0.1mmol/L)and OGAs cotreatment and NOS inhibitor L-NAME(1mmol/L)for 30min before OGAs respectively.The control plants were sprayed with water.In all cases,24h after OGAs and other materials applications,plants were inoculated with TMV.The lesion caused by TMV was investigated at 7d after inoculation.The effect of OGAs,SNP and H2O2 on local infection was calculated from the ratio of the number of local lesion produced on the treated leaves to that on the control leaves treated with water.The TOF-MS profiles of OGAs sample were showed in Figure 1.The mass spectrum indicated that peaks corresponding to the mass numbers of( M+ Na)+of trimer to enneamer were detected.So the sample was composed mainly of OGAs having degree of polymerization( DP)2-8.Figure 1 TOF-MS of oligochitosan sampleThe results of control effects on TMV with OGAs at different concentration(50～100μg/ml)showed that the best concentration was 50 μg/ml(data not shown).The effects of application of OGAs at different time were summarized in Table 1.It was found that tobacco leaves treated with OGAs were protected against TMV infection.When the inoculation occurred at 19d after spraying 50μg/ml OGAs on tobacco plants,the relative control effect was 53.42%.We concluded that the resistance induced by OGAs became better with the inducing time until 19d.The resistance was reduced after 19d.Dayof50μg/mlgalacturonideappliedNumberoflesioncausedbyTMVRelativecontroleffect(%)vcdsaw1d125±5814.40a?4d116±3920.55a?7d120±4217.81a10d84±3742.47ab13d97±4433.56ab16d90±3238.36ab19d68±3453.42b22d71±3451.37b25d89±3739.04bck146±51—Table 1We examined the effects of OGAs on the activity of plant resistance correlated enzymes.The results(Figure 2 and Figure 3.)indicated that OGAs increased activity of SOD and CAT compared with the H2O-treated ones.There are no distinct differences on the activity of POD and PPO of tobacco leaves treated with OGAs or water(data not shown).SOD and CAT are concerned with eliminating oxygen free radical.Within one hour,activities of CAT and SOD were induced to maximum.Figure 2 Time course of SOD activity in tobacco leaves treated by 50μg/ml OGAs or H2O as CKFigure 3 Time course of CAT activity in tobacco leaves treated by 50μg/ml OGAs or H2O as CKBecause of activity of SOD and CAT induced by OGAs and the two enzymes correlative with oxygen free radical,we examined the production of H2O2 induced by OGAs.To study the effects of OGAs on the production of H2O2 in tobacco cells,the H2O2-sensitive fluorophore H2DCF-DA were used.The results of production of H2O2 in epidermal cells of tobacco leaves induced by OGAs were shown in Figure 4.It was found that OGAs caused an increase of intracellular H2DCF-DA fluorescence in epidermal cells and guard cells of tobacco leaves,indicating the production of H2O2.Fluorescence became visible along the plasma membrane and in organelles in the epidermal cells of tobacco leaves treated with OGAs(Figure 4C),but the fluorescence was very faint in the epidermal cells only loaded with H2DCF-DA(Figure 4A).The Figure 4E and G showed that CAT and DPI could inhibit the level of H2DCF-DA fluorescence in the cells of tobacco leaves treated with OGAs.The results revealed that CAT and DPI could suppress the production of H2O2.Figure 4 Laser scanning confocal microscopy of OGA-induced production of H2O2 in epidermal cells of tobacco leaves. (A) The cells loaded with H2DCF-DA. (B) Bright field image of the cells loaded with H2DCF-DA. (C) The cells loaded with H2DCF-DA before treatment with OGA. (D)Bright field image of the cells loaded with H2DCF-DA before treatment with OGA. (E) The cells loaded with H2DCF-DA and elicited by OGA in the presence of the CAT. (F) Bright field image of the cells loaded with H2DCF-DA and elicited by OGA in the presence of the CAT. (G) The cells loaded with H2DCF-DA and elicited by OGA in the presence of the DPI. (H) Bright field image of the cells loaded with H2DCF-DA and elicited by OGA in the presence of the DPI.The NO-sensitive fluorophore DAF-2DA was used to observe NO accumulation.The observed LSCM results of OGAs-induced production of NO in epidermal cells of tobacco leaves were shown in Figure 5.It was found that OGAs could enhance the level of intracellular DAF-2DA fluorescence in epidermal cells of tobacco leaves,indicating massive production of NO.Production of NO and/or accumulation was observed in organelles and along the plasma membrane in the epidermal cells of tobacco leaves treated with OGAs(Figure 5C).However,the DAF-2DA fluorescence indicating production of NO was not observed in the epidermal cells only loaded with DAF-2DA(Figure 5A).The results also indicated that CPTIO and L-NAME could inhibit the level of H2DCF-DA fluorescence in the cells of tobacco leaves treated with OGAs(Figure 5E and G).The results representedthat CPTIO and L-NAME could suppress the production of NO.Figure 5 Laser scanning confocal microscopy of OGA-induced production of NO in epidermal cells of tobacco leaves. (A) The cells loaded with DAF-2 DA. (B) Bright field image of the cells loaded with DAF-2 DA. (C) The cells loaded with DAF-2 DA before treatment with OGA. (D) Bright field image of the cells loaded with DAF-2 DA before treatment with OGA. (E) The cells loaded with DAF-2DA and elicited by OGA in the presence of the CPTIO. (F) Bright field image of the cells loaded with DAF-2DA and elicited by OGA in the presence of the CPTIO. (G) The cells loaded with DAF-2DA and elicited by OGA in the presence of the L-NAME. (H) Bright field image of the cells loaded with DAF-2DA and elicited by OGA in the presence of the L-NAME.As H2O2 and NO appear to be a key factor associated with plant induced defense disease,it was interesting to test the effect of exogenous NO and H2O2.The effect of OGAs,NO donor SNP and H2O2 at different concentrations and some scavengers are summarized in Figure 6.It was found that treatment with OGAs,SNP and H2O2 protected tobacco leaves against TMV local infection.The least lesion was observed at the treatment of 50μg/ml OGAs among the all treatments.The inhibition effect of H2O2 showed dependence on the amount of H2O2.The lesion of co-treatment of OGAs and the H2O2 scavenger CAT or ascorbic acid on TMV infection was as high as CK.We also observed SNP inducing resistance was dose-dependent.When the tobacco plants were treated with L-NAME before OGAs,the induced resistance was depressed.Therefore,we can presume NO and H2O2 are important factors participating in OGAs inducing resistance to TMV.Figure 6 Effect of OGAs and exogenous NO and H2O2 on disease symptomPectic oligosaccharides,produced by microbial enzymes,are well-known oligosaccharins,eliciting defence responses in diseased plants(Dumville et al.,2000).A broad spectrum of OG-induced pathogenesis-related defense responses has been reported(M.T.Esquerré-Tugayé et al.,2000).Most defense and developmental responses are induced by OGAs with a degree of polymerization(DP)between 10 and 15 galacturonic acid residues.OGAs with a DP less than 8 can also trigger defense responses in plants:they induce accumulation of protease inhibitors(T.Moloshok et al.,1992),ethylene production(S.D.Simpson et al.,1998)and elicitation of genes involved in jasmonic acid metabolism in tomato(C.Norman et al.,1999).In this report,we observed the OGAs with a DP between 2~8 could induce tobacco resistance to TMV.The concentration of OGAs used was also discussed.OGAs-induced plant growth has been reported(LoSchiavo et al.,1991;Filippini et al.,1992),and the maximal effect to growth was about 10-4 M(Stephen et al.,1993).To elicit plant defense responses,OGAs concentration higher than those usually required for control developmental process.In our experiments,50μg/ml was the best concentration to induce resistance within 100μg/ml(data not shown).It showed the efficiency of the OGAs in inhibition of virus infection was not depended on the dose of OGAs.But the inhibition effect was dependent on the treatment time.We observed the inducing effect of resistance to TMV was gradually elevated before 19d,but the mechanism of this needed further study.Research showed that lag period of the induced resistance of glucohexaose was about 7days and the protection period was about 28 days(Li Hongxia et al.,2005).Furthermore,tobacco plants treated by sulfated fucan or linear β-1,3 glucan showed resistance to TMV or bacterium E.carotovora after 5 days(Olivier Klarzynski et al.,2003;2000).So far no oligosaccharides were reported to have so long time inducing effect.Therefore,OGAs have more predominance to be applied in agriculture.Experimental results also showed that NO and H2O2 played important roles in OGAs inducing tobacco resistance to TMV.NO and H2O2 as important signaling active molecules in pathogen defense reaction has been extensively studied(Levine et al.,1994;Mehdy et al.,1996;Baker et al.,1995;Jabs et al.,1996;Delledonne et al.,1998;Rout-Mayer et al.,1997?;Binet et al.,1998).First,we examine the activity of plant resistance correlated enzymes.Because the activity of PAL has been confirmed elevated by many reports(Messiaen et al.,1994;Lapous et al.,1998;Dixon et al.,1989;Tepper et al.,1990),we just mensurated the PPO,POD,SOD and CAT.This includes the activity of SOD and CAT elevated,so we estimated the extra H2O2 production.To evaluate the stimulatory effect of OGAs on tobacco cells,we measured the production of H2O2 and NO in tobacco cells.The data indicated that OGAs induced the production of H2O2 and NO in epidermal cells of tobacco within a short time.These results were in agreement with the reports by Xiangyang Hu,who claimed OGAs stimulated NO accumulation in the growth medium of ginseng suspension cultures(Hu et al.,2003).Rout-Mayer and Binet discovered respectively H2O2 production within a few minutes after the addition of OGAs to suspension-cultured tobacco cells(Rout-Mayer et al.,1997;Binet et al.,1998).Many reports show H2O2 and NO exist are correlated to plant defense.H2O2 is involved in the induction and/or execution of hypersensitive reaction(C.S.Bestwick et al.,1997).H2O2 is required for the cross-linking of plant cell wall components as a part of the structural defense response(C.Lamb et al.,1997).The production of H2O2 may also lead to the development of an antimicrobial environment within the apoplast(M.Peng et al.,1992).In many cases,H2O2 collaborate with NO to execute invading pathogens.H2O2 and NO production were induced almost at the same time by cryptogein,a fungal elicitor(Foissner et al.,2000).NOS inhibitors compromise the hypersensitive resistance response in Arabidposis and tobacco(Delledonne et al.,1998?;Huang et al.,1998).TMV infection could elevate NOS(nitric oxide synthase)activity,and NO could induce PR-1 expression(Durner et al.,1998).NO,as well as other ROS,have been shown to stimulate the accumulation of SA(Durner et al.,1999),which play a critical signaling role in the activation of plant defense responses after pathogen attack.Furthermore,to test whether OGAs functions on inducing resistance in tobacco via NO and H2O2 pathway,we examined the effects of OGAs,exogenous NO donor SNP and H2O2 on inducing resistance to TMV.It was found that all of these treatments reduced lesion caused by TMV.But co-treatment with OGAs and H2O2 scavenger CAT or ascorbic acid blocked the inducing resistance.The tobacco plants inhibited NOS activity by L-NAME were not induced resistance by OGAs.So the defense response induced by OGAs was connected with NO and H2O2 pathway.The study reported herein reveals that OGAs can induce the production of H2O2 and NO,and induce the defense response against TMV.Our understanding of OGAs induced resistance is sketchy.The mechanisms of OGAs eliciting defense responses of tobacco need further investigation.

川成都植物病害是由植物—病原—环境三者在一定适宜条件下，引起植物体发病，构成对植物正常生长发育和新陈代谢的干扰与破坏，最终造成植物的生物产量和经济产量减产，品质降低，给人类的农业、林业生产造成重大损失。植物病害的病原物是指能寄生于植物体并导致侵染性病害发生的生物。植物病害分成菌物（真菌）性病害、细菌性病害、病毒类病害、线虫类病害以及其他因素引起的植物病害。植物细菌性病害是植物病害中发生为害较重、发病规律比较难以掌握、防治技术要求高、防治效果很难凑效的一类病害。植物病原细菌是属于原核生物中的一个生物类群，它与真核生物在细胞结构及组成成分方面存在着较大的差异，正是这种细胞结构和组分上的差异，导致了细菌性病害比真菌性病害更难以防治。植物细菌性病害中比较著名的病害有：水稻细菌性条斑病、水稻白叶枯病、白菜软腐病、番茄青枯病、玉米细菌性枯萎病、柑橘溃疡病、梨火疫病、马铃薯环腐病。还有近年来被国际柑橘病毒学家确认的柑橘黄龙病等，这些植物细菌性病害给我国农业、林业生产带来了巨大的影响和危害。本文将对植物细菌性病害做了以下6个方面的初步探讨。早在2000多年前我国《诗经》中已经将生物划分成了植物、动物和蕈类三大类。1593年李时珍在《本草纲目》中将生物分成了植物、动物和人类三大类。在近代科学发展史上，以林奈为代表的生物分类学家将生物分成两界（即动物界Animaliae和植物界Plantae），这两界系统被人类科技界沿用了200多年。16～18世纪，随着显微镜发明和细胞学说的建立，人类才发现了单细胞生物——细菌。对于细菌在生物进化过程中，专家们普遍认为：细菌的出现应该是在植物和动物出现之前就已经存在了。1969年魏泰克将生物界分成五界系统，即：（1）以细菌为主的原核生物界；（2）以单细胞原生动物和藻类为主的原生生物界；（3）多细胞生物中以光合作用制造营养的植物界；（4）以多细胞为主吸收营养的真菌界；（5）多细胞生物中以摄取食物为营养来源的动物界。1974年黎德勒认为：取消原生生物界，将生物化分成四界系统，即：原核生物界、真菌界、植物界和动物界。1977年我国科学家陈世骧提出了生物学界的三总界构成六界系统，即：无细胞总界——（病毒界）；原核生物总界——（细菌界、蓝藻界）；真核生物总界——（真菌界、植物界、动物界）。1988～1989年（Cavalier-Smith），将生物学界划分成：两个总界组成的八界系统，即：一、细菌总界：①真细菌界；②古细菌界；二、真核总界：③古菌界；④原生动物界；⑤植物界；⑥动物界；⑦真菌界；⑧藻界。到2003年，他取消了古细菌界和古菌界，改为二总界六界学说。许志刚教授在2005年正式提出三域七界的最新分类体系，即无细胞生物域的病毒界；原核生物域的细菌界；真核生物域的原生生物界、真菌界、藻物界、植物界和动物界。反映了当前人们的认识水平。从上述分类系统可以看出，细菌的分类始终处于原核生物界内，它与真核生物在细胞结构及其组成成分上存在着许多本质上的差异。原核生物是以单位膜为界的，细胞核质无核膜包围，呈原核状态。含肽聚糖的细胞壁有或无；核糖体在细胞质内70S。染色体的数目为1。细菌的质粒DNA游离于细胞质中。细菌都是单细胞生物，它们的细胞膜外都有一层主要由肽聚糖（革兰氏阳性细菌）或脂多糖（革兰氏阴性细菌）构成的坚韧细胞壁。真核生物：具有以单位膜为界的细胞器，细胞壁不含肽聚糖。细胞核有核膜包围，呈真核状态，核糖体80S，在细胞器内的核糖体70S。细胞内有内质网、高尔基体、溶酶体、叶绿体有或无、有微管系统。染色体中有组蛋白；有核仁；要发生有丝分裂；细胞器有DNA（如线粒体）；配子能够融合；DNA不单向转移形成部分二倍体。最典型的是真核生物具有真正的细胞核以及其他细胞器组成成分。核是细胞的控制中心，它由核膜包着与核外的细胞质分开。核膜内有核仁和核质。植物病理学家们长期以来将植物细菌性病原种与对寄主的致病性作为一个非常重要的因素，同时要依据病原细菌的生理生化性状和血清学性状等指标来综合确定植物病原细菌的种。在《伯杰氏细菌学手册》第七版出版时已经命名的植物病原细菌种有200多种。根据生物学命名中优先命名权不能侵犯的原则，确定每一个新种必须查阅大量文献，以避免同物异名的出现。在《伯杰氏细菌学手册》第八版中将植物病原细菌种由原来的200多种削减为几十种，以保证所有种都可以用生化试验来进行鉴定并尽量保证能在实验室条件下可以重复实验，使之更具有科学性和重复性。1994年，根据《伯杰氏细菌学手册》第九版的系统分类：将细菌分成了四大类35个群。2000年以后，《伯杰氏细菌学手册》第二版分五卷陆续出版发行，该版本的最新分类体系中将细菌界包括了16门、26组、27纲、62目、163科、814属，共计4727种。植物病原细菌属于细菌界中普罗特斯门、放线菌门和厚壁菌门。普罗特斯门细菌细胞壁主要由脂多糖组成，肽聚糖含量较少，因而革兰氏染色阴性。放线菌门细菌的细胞壁中肽聚糖含量高，革兰氏染色阳性。厚壁菌门中的病原生物包括植原体（Phytoplasma）和螺原体（Spiroplasma）。已经描述的引起植物病害的原核生物有28个属。植物细菌性病害的病原菌主要分成五大类别。第一类：黄单胞菌属（Xanthomonas）。黄单胞菌属是细菌中的特殊类群，目前文献中描述的黄单胞菌属的种几乎都是植物病原细菌。它可以为害120多种单子叶植物和270多种双子叶植物。黄单胞菌引起许多重要植物病害，比较典型的病害有：（1）甘蓝黑腐黄单胞菌（X.campestris pv.campestris）；（2）水稻白叶枯病（X.oryzae pv.oryzae）；（3）水稻细菌性条斑病（X.oryzae pv.oryzicda）；（4）柑橘溃疡病（X.campestris pv.citri）。由黄单胞菌属细菌引起的植物病害大多数症状为叶枯、坏死、萎蔫等症状。第二类：假单胞菌属（Pseudomonas）。假单胞菌属细菌大多数都是土壤、水、其他基质上的腐生菌，有些是植物病原细菌。它的生态适应性广，表型差异大，是一个非常异质的组群。丁香假单胞菌（Pseudomonas syringae）是重要的植物病原细菌，能为害多种植物。在《伯杰氏细菌学手册》第九版中正式命名的植物病原细菌有7个种。第三类：欧文氏菌属（Erwinia）。欧氏菌属细菌是人类第一个发现的植物病原细菌。有史以来所发现的欧氏菌属细菌一部分是植物病原细菌，最常见的是各种植物的软腐病，也有萎蔫和坏死。典型的病害有：梨火疫病（E.amylovora）；玉米细菌性枯萎病（E.stewartii）；马铃薯和大白菜的软腐病等。由欧氏菌引起的细菌性软腐病在全世界均有发生分布。第四类：土壤杆菌属（Agrobacterium）。土壤杆菌属细菌是一类习居于土壤的细菌，在土壤中广泛的分布。常见的致病性细菌种有根癌土壤杆菌和发根土壤杆菌。根癌土壤杆菌（A.tumefaciens）能为害多种双子叶植物，在近土根茎部形成恶性肿癌。发根土壤杆菌（A.rhizogens），在侵染双子叶植物幼根后形成丛生的毛发状根群，称之为发根。第五类：棒形杆菌属（Clavibacter）。它是从棒状杆菌属（Corynebacterium）中分列出来的一个新属。国内发现的植物病原棒形杆菌属细菌中，最典型的病害有马铃薯环腐病菌（C.m.pv.sepeadonicum）在国内马铃薯产区均有分布。由于该病菌是以种薯传带的，所以在调运马铃薯种薯时必须要实施检疫。小麦蜜穗病菌（C.tritici）在国内华北冬麦区、山东、安徽、江苏、浙江、贵州等省已有发生。植物病原细菌从植物的气孔、皮孔、蜜腺等自然孔口以及伤口侵入寄主。植物细菌性病害主要见于高等被子植物和栽培植物上较多。植物病害的症状包括病状和病症两个方面。所谓病状：是指感病植物的外部特征，主要表现有：（1）变色：指整个植株、叶片或叶片部分变色。（2）坏死：指植物体局部细胞和组织的死亡。（3）腐烂：整个植物的组织和细胞被破坏和消解。（4）萎蔫：植物病害中的萎蔫是指植物的输导系统被病原物毒害或病组织的产物阻塞而造成不可逆转性的萎蔫。（5）畸形：感病植物组织和器官所发生的皱缩、卷曲、萎缩、丛枝、发根、肿瘤，花器和种子变态。所谓病症：是指病原物在病株发病部位上所表现的特征。主要表现有：（1）霉状物。（2）粉状物。（3）锈状物。（4）粒状物。（5）根状菌索。（6）菌脓。菌脓：是指发病部位产生的胶黏脓状物，干燥后形成白色的薄膜或黄褐色的胶粒。菌脓是细菌性病害在田间特有的病症。从多年田间病害症状诊断的实践环节看，植物细菌性病害田间症状诊断上着重注意几点：细菌性病害往往会出现局部坏死斑点，如柑橘溃疡病的病斑。腐烂：很多蔬菜类作物上出现的软腐病、马铃薯环腐病等。萎蔫：作物上出现的青枯病，全株性萎蔫。菌脓：如水稻细菌性条斑病病叶上出现的胶黏脓状物。细菌性病害往往不会出现整株变色、叶片上不会出现霉状物、粉状物、丛枝、萎缩等症状。细菌性病害会出现发根和肿瘤等症状。这个问题是一个非常复杂的问题，要回答好这个问题并非易事。从理论上探讨，所有植物病原细菌都可以通过种子传带。细菌附着在种子表面，也可以存活于种皮内，以及块茎组织内部。细菌在植物种子上一般存活1～2年。植物病原细菌一般产生胞外多糖，且一般具有鞭毛结构。因而，雨水的溅射和细菌自身在水中的游动可导致其传播。此外，随着灌溉水的流动，细菌可以在田块间传播。在20世纪60～70年代，水稻白叶枯病在四川省水稻产区流行蔓延，造成水稻产量严重减产，损失惨重。植物病原细菌可以通过苗木、接穗传播。嫁接工具、人为操作不当的行为均可以传播植物细菌性病害。柑橘溃疡病在我国柑橘主产省区均有不同程度地发生为害。狂风暴雨夹带雨滴是沿海岸线柑橘产区柑橘溃疡病蔓延猖獗的主要环境因素。通过媒介昆虫可以传带细菌性病害。柑橘黄龙病传毒主要媒介是柑橘木虱。要使柑橘黄龙病发生蔓延的几大因素是：一是要有柑橘黄龙病病树存在；二是要有传毒的媒介昆虫；三是要有感病的寄主。同时，昆虫的越冬寄主枳壳、九里香等存在为病菌的越冬和第二年的病菌的侵染循环创造了条件。如何掌握植物细菌性病害发病规律，作者认为应该注意以下几点：（1）植物的种子、苗木、接穗等一切繁殖材料均有可能携带植物细菌性病害的病原，并能在植物体表或表皮内较长时期的存活，是远距离传播植物细菌性病害的主要原因。（2）由于植物病原细菌的细胞有胞外多糖，在有水膜存在下可以加快细菌侵染速度，为害程度由点到片逐步加重。在雨季、大风、甚至飓风条件下加快了点片发生与为害的程度。（3）有灌溉水存在的条件下可以加快植物细菌性病害的流行蔓延，是大面积造成为害损失的主要诱因。（4）有媒介昆虫的发生、越冬寄主的存在，为植物细菌性病害的再次侵染循环奠定了基础和创造了条件。（5）嫁接工具、农事活动操作不当均可以造成寄主大量伤口，有利于病原细菌的侵入，导致田间植物细菌性病害近距离传播为害。（6）适宜的温湿度条件，加速了植物细菌性病害的侵染循环。根据植物细菌性病害发病的诱因和发病基本规律可以看出：种子、苗木可以带菌；细菌繁殖速度快、侵染途径多；远距离传播与近距离扩散相辅相成，加快了细菌性病害点、片发生，具有暴发成灾、损失严重的特点。植物细菌性病害很难防治，药剂防治效果很难奏效。四川省在防治水稻白叶枯病、水稻细菌性条斑病、柑橘溃疡病、柑橘黄龙病等细菌性病害中都不是单一地采用药剂防治。药剂防治只能作为综合治理植物细菌性病害技术环节中的一个重要环节，特别是柑橘溃疡病防治技术中，国内外至今尚未见到仅仅依靠药剂防治来完全控制其为害蔓延的成功范例。柑橘黄龙病的综合治理更是如此。（1）建立无病虫种子、苗木繁殖基地，生产健康无检疫性病虫的种子苗木。（2）种子苗木调运前实施田间产地检疫和抽样实验室检验相结合，保证调出种子苗木是无病的。（3）调入地尽量集中成片种植，播种前进行种子消毒处理，有利于生产管理和病虫害综合治理。（4）加强田间病虫害预测预报，发现细菌性病害点、片发生时，及时拔除病株销毁，并用药剂对周围植株进行保护性防治。（5）严格对发病田块的肥水管理，防止有病田块流水串灌或漫灌。（6）对较大面积发生细菌性病害的发病区要及时隔离，防止上游流水继续向下游流传，造成更大面积的细菌性病害流行。同时对发病区要进行较大规模的药剂防治。（7）及时换种、加强轮作换茬，防止细菌性病害在田间菌量的不断积累和再次暴发成灾。（8）注意嫁接工具的消毒，防止农事活动中人为的传播感染。

豆瓣菜（Nasturtium officinale R.Br.）又名西洋菜、水蔊菜、水田芥，属十字花科豆瓣菜属植物。枝叶柔嫩青翠，性喜冷凉，较耐霜冻，是深受人们喜爱的冬春上市的水生绿叶蔬菜。有关豆瓣菜菌核病国内尚未有专门报道。该病1999年在武汉旱地栽种的豆瓣菜田中仅见零星发生，到2001年春发病田中的发病面积可达1.61%，甚至到10%左右，表明病害有增重的趋势。豆瓣菜的茎、叶、叶柄均可受害。以中、下部贴近地面匍匐或半匍匐生长的枝叶受害最重。田间病害呈点片状发生，不规则分布。因豆瓣菜分枝多，生长繁茂，茎呈匍匐或半匍匐丛生，故发病初期常需拨开丛生状植株，才能发现感病枝叶，后期因植株枯死而呈现近圆形至不规则形病区。茎部受害，水渍状，淡褐色，边缘不清晰，从病处向两端扩展，空气湿度大时生茂密的绵毛状白霉，继而在植株表面及病茎的空腔中菌丝集结成近球形、扁球形、鼠粪状或不规则的菌核。菌核初白色，成熟后黑色，内部白色。罹病植株病部软腐，但无恶臭，最后失水干枯而呈枯草黄色。叶柄症状与茎部同。病叶受侵处灰褐色或浅黄褐色，湿度大时亦生较稀疏的绵毛状白霉，最后病叶腐烂或干枯。该病一般在12月上中旬出现病株，1月下旬至2月上中旬是大棚中豆瓣菜菌核病的盛发期，大棚和露地均在3月上旬病情趋于稳定。在近几年的调查观察中，一直未见浅水栽植的豆瓣菜有菌核病发生，而旱地栽植的豆瓣菜，不论大棚或露地种植的条件下均可受害，并且大棚中的病情有较露地重的趋势。病茎失水干枯后，菌核极易脱落，而病茎空腔内的菌核则随病株残体遗留在土中。该病的初侵染，来自遗留在土中的菌核产生的子囊孢子。子囊孢子不能侵染健壮的枝叶，而极易侵染中下部贴近地面匍匐或半匍匐生长的衰老叶片，此后才能侵染健壮的枝叶。再侵染主要通过病患组织接触，由病部长出的绵毛状菌丝体完成。豆瓣菜的匍匐或半匍匐生长及分枝多、生长繁茂、枝叶交错的植物学性状和病原菌侵染循环特点，决定了其有利于菌核病菌的接触蔓延，而不利于子囊孢子的气流较远距离的传播，因而造成了植株中、下部枝叶发病的现象，这样就使豆瓣菜菌核病具有一定的“隐蔽性”，也导致田间病害呈点片状发生及不规则分布的特点。菌丝管状、无色，有分枝具隔膜，田间自然情况下菌丝体白色绵毛状，在病茎表面及被害茎的空腔里均可形成菌核。在测量的87个菌核中，其大小（长径）为2.0～7.0mm。菌核无休眠期。将菌核置培养皿中双层浸湿的滤纸上，13.5～16.0℃，室内散射光下培养很易萌发。一个菌核可生出一至数个子囊盘，子囊盘高足杯状，初淡褐色，后为暗褐色。柄长短因环境而异，在黑暗无光条件下，柄长可达6.0 cm以上。子囊盘中生有大量子囊和侧丝，子囊无色棒状，内生8个排列一行的子囊孢子。子囊孢子椭圆形，无色单胞，大小8.7～13.7μm×4.9～8.1μm。子囊孢子成熟后稍受震动（如打开供菌核萌发的培养皿的盖），即可看到状如烟雾的子囊孢子放射现象。据上鉴定，认为豆瓣菜菌核的分离物为Sclerotonia sclerotiorum（Lib.）de Bary。这是我们首次在豆瓣菜上发现有由核盘菌引起的菌核病。进一步研究发现该菌菌丝生长温度范围很广，其中在4～5℃时，菌落在PDA平皿上扩展速度为8.3mm/天、33℃时为2.0 mm/天、当温度达到35℃时，菌落几乎停止生长。病菌菌丝生长最适温度是21℃，在此温度下，菌落扩展速度达32.2 mm/天。