2011年11月30日 星期三

給 "台灣的女兒" 解謎;對美國商會說明的經濟政策



「台灣的女兒」和非典型的「政治人」 小英後援會現場




彭明敏




日前參加一場「白色恐怖被害者(前政治犯)小英後援會」。許多被害人已悄然去世,殘存者都已高齡,有的抱病由子女陪同,拖著不自由的身體,辛苦參加。這些長輩受盡國民黨的殘忍迫害,犧牲一生,還是擔憂台灣前途,其悲情使人欷歔不捨。




當小英上台時,一老先生,拄著枴杖步履蹣跚,走到台前,一言不發,將一小紅包塞進小英手裡,轉身慢慢走回。不久,又有一老婦人,衣著樸素,彎腰駝背,緩步到了台前,也不發一語,把一紅包塞給小英,一步步走回原位。這個光景,使得不少會眾感動流淚,當張炎憲教授說「在這些老輩的眼中,小英好像自己的女兒」時,腦裡湧出一個「台灣的女兒」的映像。




走過複雜痛苦的歷史,台灣人民終於產生了能夠在世界的舞台上驕傲地代表「真正台灣」的一位女性。她土生土長,身藏河洛、客家、原住民的基因,受過最高的教育,競選總統則與過去不同,不咆哮、不怒罵、不誇張、不做作、不悲憤激昂,一口流利的台語、華語和英語(在台美商會演講,馬氏盯著原稿照唸,蔡則無稿,以優雅的英語,滔滔講了半小時)。




她所以有獨特的魅力,因為不是強悍辛辣的女暴君,而是代表台灣女性傳統的溫和柔情,對於支持者,諄諄講理,對於反對者,冷靜辯駁。她之認同台灣,與人民命運相同,自自然然,理所當然,無需用「燒成灰也是台灣人」一類血腥虛勢來掩飾「終極統一」的陰謀。由老輩看來,好像愛女即將冒險遠行,以紅包祈願一路順風;由同輩看來,好像親密的姊妹即將開始艱難的巨大事業;由後輩看來,好像敬愛的學姊即將接受嚴峻的考驗;大家衷心祝福她。




她與對方外來的巨富權貴傲慢虛偽,呈現何等強烈的對照。她若當選,也必須承擔對方所留下龐大惡質重荷。真實的改革,不一蹴而成,需要長期的能耐奮鬥。「較好的台灣」能否出現,要看台灣人民當「真實的台灣總統」為要解決「真實的台灣問題」而苦鬥時,能否覺悟並了解現實,隱忍難免的長期辛苦,真誠合作,支持她到底。(作者為前總統府資政)






















《林保華專欄》 小英解謎 12/1/2011


[轉載自:自由時報]










台灣政壇選舉到目前階段,馬總統陷入困境,只能以罵街來轉移政策焦點

來打混仗。有的幫閒也還在做蔡英文是謎一樣人物的舊調調,以此製造不

信任感,打擊小英越來越高的人氣。

有幸小英最近出版了《洋蔥炒蛋到小英便當》的自傳,可以從中了解小英

的治國能力與人格特質,只是因為她是一個非典型的政治人物,過去行事

低調,也沒有行銷自己,才被某些人誤解為謎一樣人物

看了這本書以後,我有三點過去被人們忽略的認識:第一,她是鄰家女孩

式普通人物,不是什麼一生出來就一路走來準備坐上總統大位的人;第二

是她的談判技巧;第三是協調能力。由於她參與競選總統,所以後兩條尤

其重要。

小英這方面的表現,見於她參與加入WTO談判,十幾年中,從翻譯做到首

席顧問,顯然是對她工作的肯定。看了她在書中講述的許多談判技巧,從

中獲益許多。

這些包括領導人的決心,幕後團隊的組成及前置、後置作業,臨場折衝,

對談判對手文化背景的了解,以及任何情況下的不動聲色等。小英尤其強

調,絕對不要在壓力下倉促做決定,否則代價可能是嚴重,甚至致

命的。反觀馬英九上台後立即放棄總統稱號、外交休兵、國際場合全面

退守到中華台北等,還沒談判就投降

加入WTO,會損害台灣農業,政府必須以津貼農戶來保護,這點小英對台

灣農業的認識,遠比馬英九靠long
stay
作秀,不知深刻多少倍。這是權

貴出身的馬英九所沒有的感情與認知,所以馬只能在何不早說與搞不

清流通領域裡多種價格而付諸情緒性發洩。

小英的協調能力,從談判中開始嶄露頭角,後來出任陸委會主委,因為跨

部會的工作性質得到提高,出任行政院副院長期間召開台灣經濟永續發展

會議,於惡劣的政治環境中,面對兩岸關係的敏感問題,甚至是在她父喪

期間,可以在一七五位各界菁英中取得五一六條共識,再次考驗了她的理

性與包容。

我們看到比較多的,則是她出任民進黨主席後協調派系的能力,以及如何

面對社會情緒。有人擔心她被派系綁架,但她開玩笑的說,也許反而是她

綁架了派系。

小英對談判的深刻認識,與協調各界的能力,是未來台灣如何團結內部、

凝聚共識,面對與中國談判,並且走向世界所不可或缺的,對照金馬體制

分裂藍營,以及惡化藍綠惡鬥,哪一個人更適任台灣總統職務也是不言而

喻也。

   


 




蔡英文出席美國商會 2011年度會員大會

TWIMI | 獨立媒體 http://www.twimi.net
(
轉貼請保留此連結)


民進黨主席暨總統參選人今(11/22)日出席「美國商會 2011年度會員大會」並發表演說,蔡英文致詞時表示,過去 60年來,台灣得到美國多方的協助,台美合作不只是台灣國家安全和經濟發展的重要基礎,也是美國政府和企業全球戰略的重要支柱及最佳夥伴。



蔡英文說,台灣將在明年 1月進行總統大選,雖然我的競爭對手馬總統和我一樣,都強調高度重視台美關係,也重視台、美、中國三者間的平衡關係,但我必須指出,自 2008年台灣 2次政黨輪替迄今,台灣和中國關係的發展速度遠超過台美關係,這種不平衡的發展必須有力及有效地調整,這也是若我當選總統首要的對外工作目標。



蔡英文認為,從世界局勢變化來看,問題的解答愈來愈清楚,亞太地區的加速發展與擴大合作,是引導全球經濟脫離泥沼、展現生機的最有力憑藉。歐巴馬政府的全球戰略正朝向這個-方向快速前進,台灣也正在全球新情勢下尋找新的定位。在這個關鍵時刻,我強烈主張台美之間應建立新的策略夥伴關係,我的主張是基於以下三大因素:



第一,台美在亞太區域安全及穩定上具有共同責任與共同利益。尤其,面對中國的崛起,台灣和美國更須緊密合作,共同維護台海的和平穩定及促進區域的共榮發展。



第二,長期以來,台美間對自由貿易的共同信念和堅持。台灣在建立世界貿易規則上,一直和美國的步調一致,讓雙方在建立亞太貿易新秩序上有更大的合作空間。



第三,台美在拓展新興市場尤其亞太市場方面具有高度互補性。台美在全球IT產業供應鏈上有密不可分的長期策略聯盟關係;在綠色產業、生技、新能源、新興產業方面,也有很大-的互補及合作空間。台美這樣緊密的產業關係有助於共同拓展新興市場,尤其是亞太地區的中國、東南亞、印度及中南美洲,透過雙方企業的通力合作,台美企業將能為亞太乃至世界-經濟復興作出重要貢獻。

台美間的新策略夥伴關係需建立在以下幾個努力方向上。



蔡英文說,我們瞭解兩岸關係的重要性,但在這場選舉中,還有其他議題,如貧富差距、就業、經濟等,也是一樣重要。為了台灣的長遠利益,在大選中以及選後,我對兩岸政策的作-法,就是建立共識,而不是以黨派之見分化台灣。我們絕不會將兩岸議題當作選戰工具。在選戰中,兩黨政策上的差異主要在於國內議題。雖然大選期間,我們和中國方面的對話受到-限縮;勝選之後,從政權轉移期間開始,我們即會積極尋求對話,以維持兩岸關係穩定。



其次,在台美經貿關係方面,致力推動並實踐自由貿易的理念與目標,應是台美雙方共同的意願。我必須指出,馬政府上任以來,積極發展和中國的經貿關係,去(2010)年
6
月進一步和中國簽署 ECFA,但是,過去三年來,台灣和美國的經貿關係卻相對停滯不前。



我也很感慨,台灣貿易最大的競爭對手國韓國,與歐盟及美國的 FTA已陸續生效,但台灣和美國及主要國家的 FTA卻毫無進展。我充分認同美國商會不斷強調台灣「平衡發展經貿關係」的重要性,因此,台美間的經貿合作協定,不應該、也不能再停滯不前。



民進黨多年前透過多種管道,希望美國推動以 APEC為基礎的亞太自由貿易區協定,並將台灣包含在內,所以,我們很高興看到美國正在積極推動 TPP。我
9
月間赴美訪問時,也和許多美國朋友談到,TPP要求的標準很高,台灣必須要有決心做好加入TPP的準備。如今馬政府雖然也把加入TPP當成目標,但我們完全看不到進行準-備的決心與具體做法。



在民進黨執政時期,台美之間透過溝通互相理解、解決問題,是很愉快的經驗。我保證,未來民進黨執政後,仍然會是一個充分溝通的團隊。我也有自信,民進黨政府和美國政府及美-國商會之間的溝通,會勝過現在的馬政府;貴會的白皮書對於政府效能的抱怨,一定也會大幅度減少。



最後蔡英文說,我對於贏得明年初的總統選舉充滿信心,也因此我相信,台美關係的前景,特別是在建立新的策略夥伴關係上,將會有充滿期待的發展空間與願景,創造台美的「雙贏-」及亞太地區的「多贏」。





 


選蔡英文當總統,好處多多

台人2011/10/16 (鯨魚網站)

1.蔡英文有精心規劃的「十年政綱」,也有執行政綱的人才,選她可以促進台灣經濟、文化、環境、農工的轉型,增加台灣的競爭力。

2.蔡英文鼓勵「在地經濟」,以我土、我財、我民三合一,創造就業機會;選她,比較容易找到工作。

3.蔡英文主張老農津貼增加一千元,基本工資提高到二萬元以上,選他,大家都可以加薪。

4,蔡英文很會持家,民進黨在她領導下,解決數億負債,選她,會讓台灣的財政減少赤字,下一代不必背負沈重的負債。

5.蔡英文讓民進黨谷底翻身,支持度超越國民黨,可見能力超強,勇於負責任事,選她,就像選個好媳婦,認真打拚,可以讓國家富強。

6.民進黨的人才比國民黨多了太多,蘇貞昌、謝長廷、游錫堃、陳菊、賴清德...等等,每個都有改造台灣之能。選蔡英文,就是讓這些人才能為大家做事。[KMT貪汙人才技術是超多、超級的!]

7.蔡英文父親是客家人,母親是鶴佬人,祖母是原住民,選她一人,代表原民、鶴佬、客家人都當了總統。

8.蔡英文以理性著稱,她不激情,不訴求階級仇恨,是個「講道理」的政治領袖;選她,台灣政治可以提昇到政策論辯的層次,減少無謂的口水鬥爭。

9.蔡英文關心中下階層的生活,她沒有身段,很自然地與人民融合起來。選她,你受苦的聲音會被重視,你的生活問題會得到解決。

10.蔡英文有國際談判的豐富經驗,選她,你會有一個最具國際觀,並受外國友人尊崇的總統。

11.蔡英文學者出身,思考嚴密,論述很有內涵。選她,你會有一個學識淵博,很有水準,堪為兒女榜樣的總統。

12.蔡英文一旦當選台灣第一女總統,可見我國性別平等,民主成熟,已達到先進國家的水平。選她,你可以出國時走路有風。

13.蔡英文主張台灣是一個國家,她不會為了討好中國,而偷偷把主權出賣掉。選她,你不會在台灣受中國官僚的鳥氣,不用怕拿國旗會被警察取締。

14.蔡英文的英文很好,她可以和國際人士充份溝通,民主理念也容易獲得對方的肯定。選她,你就有一個可以在國際出頭的總統。

15.蔡英文與美國、日本關係良好,上回出訪,深受友邦重視。選了她,要買想要的武器就有望了,美日安保系統也會義無反顧協防台灣。

16.蔡英文理性優先,態度溫和,中國沒理由找她的碴。而且她是女性,中國如果對她惡形惡狀,必然遭到國際的反感。選她,台海兩國絕不會發生衝突,依然和平。

17.蔡英文長相可愛,待人和藹可親,笑容自然,態度誠懇。選了她,你一看到就輕鬆愉快。不會像看到某個賣米酒的小丑和他的黃臉婆,整天感到苦悶。

18.蔡英文沒有結婚,也沒有操弄權柄又作威作福的密友,選了她,你不用擔心總統配偶的干政和觀感,也不用煩惱要不要巴結所謂的總統密友。

19.蔡英文家境富有,對金錢不看重。陸委會主委任內,特別費不夠用時,還叫爸爸拿錢來贊助。選她,你不用擔心她會貪污,更不會像馬英九那樣巧立名目為自己加薪。

20.蔡英文當民進黨主席將近四年,沒領半毛薪水,反而常找家人捐款。選了她,萬一政見沒如期實踐,你叫她捐薪水,絕對比馬英九阿莎力
      








 





 














2011年11月28日 星期一

KMT議員陳明義的誠信、人格

[KMT中常委陳明義議員在電視節目上竟信口開河,無人性! 原來他也不守誠信,和馬先生如出一轍! 難怪他能當上國民黨中常委! ]


 


國民黨籍的議員陳明義在年代新聞面對面節目中說:蔡英文在登記參選記者會上所講述探望花蓮年輕的彌留黨員一事是假的杜撰的,是在講故事,陳明義還用品德教育來污衊蔡英文是-在捏造故事。民進黨議員劉曉玫隨即在臉書上公布一段影片,請大家看看蔡英文主席前往探望這位黨員的畫面。 http://www.taiwanus.net/news/press/2011/201111281100291877.htm

原本是私密令人感傷的畫面,卻因為中國國民黨為了選舉不擇手段,滿口胡言而不得不公布。陳明義作為一個民意代表,卻公開在媒體上胡言亂語,這對家屬根本就是二度傷害,對死-者更是大不敬,讓家屬情何以堪。

陳明義也曾經衝著一名匿名投書報社拒領
18%的退休老師說,只要這名老師敢出面,自己就下跪改姓,結果老師出面了陳明義卻不認帳,沒下跪也不改姓,這樣沒誠信滿口胡說八道的人,現在連往生的人都可以污衊為在捏-造故事,陳明義還有資格為民喉舌嗎?20111128


 


 


蔡探視彌留黨員 陳明義影射捏造?



家屬哭訴抗議 促靈前道歉



〔記者林恕暉、曾德峰、陳慧貞/綜合報導〕國民黨文傳會發言人、新北市議員陳明義十一月二十四日在政論節目中,指稱民進黨主席蔡英文探視彌留民進黨員林龍成,是「捏造一個虛實的故事」。林龍成妻子沈淑惠昨天哭訴,指她先生在小英主席探視後不久往生,陳明義怎能說是捏造?要求陳明義到林龍成靈前道歉。


陳稱被扭曲 將向家屬致意



陳明義則指控,三立新聞跳接他在年代新聞台「新聞面對面」的發言畫面,製作假新聞引發往生民進黨員家屬誤解。他說,感佩這位民進黨員臨終前的堅持,雖分屬不同政黨,在取得家屬同意下,今天會搭機前往花蓮向家屬致意。



陳明義在政論節目影射蔡英文「捏造一個虛實的故事來教人家品德,捏造這過程就沒有好的品德了」,引發林龍成家屬強烈反彈。



沈淑惠昨天哽咽說,蔡英文探視時,林龍成血壓只有六十、二十,林龍成只希望蔡能當選;蔡英文離開後,她先生就離開醫院返家,回家一小時後就往生了,陳明義怎能說這是捏造?她要求國民黨、陳明義到林龍成靈前道歉。



民進黨昨天也公布蔡英文探視林龍成臥病在床的影片。花蓮縣議員劉曉玫說,陳明義事前可以打聽,卻沒有求證,家屬也不希望這是事實,但陳明義的指控讓家屬不能接受,陳明義必須道歉。



三立:陳所稱皆非事實



陳明義則表示,其論述被刻意抹黑、扭曲、栽贓,揚言委請律師對三立電視公司及延伸評論辱罵他沒人性的大話新聞主持人鄭弘儀、來賓鍾年晃、徐永明及民進黨總部發言人徐佳青等人,提出刑事與民事告訴,以維護個人聲譽。三立新聞部則表示,陳明義所稱皆非事實,不予回應。



陳明義強調,當時引用自由時報十一月二十三日頭版新聞「品德教育賽,得獎故事是編的」,裡頭敘述品德教育虛構故事,是要評論民進黨虛構監察院分案調查三胞胎及三隻小豬事件,卻被其他來賓打斷,指控他影射蔡英文訪視彌留黨員的故事是虛構。


 


林龍成家屬 苦等道歉/陳明義未到靈前上香 綠斥戲弄家屬


〔記者林欣漢、曾德峰、李欣芳/綜合報導〕國民黨文傳會發言人、新北市議員陳明義日前質疑民進黨主席蔡英文探視彌留黨員林龍成是「捏造一個虛實的故事」,前天在記者會上表示會向林龍成上香致敬,但昨訂了機票卻未現身花蓮。


民進黨昨痛批陳明義,在林龍成家屬要求陳道歉後,陳明義竟以「不寒而慄」形容蔡英文探視林龍成的影片。民進黨發言人康裕成質問陳明義「到底有沒有人性」,說要向家屬致意卻戲弄家屬,要求國民黨主席馬英九也應出來道歉。




口出「不寒而慄」 很沒人性


林龍成遺孀沈淑惠表示,已完全無法接受陳明義的道歉,「陳明義說我們放林龍成的影片,是在消費他,其實是陳明義在消費,還說我老公影片令人毛骨悚然,對家屬的傷害太大了,之前是在我傷口灑鹽,現在是在傷口灑鹽酸。」


花蓮縣議員劉曉玫說,該段影片是由林龍成弟弟林龍興所拍攝,打算留做永恆紀念,因陳明義指這件事是捏造,家屬為了讓陳了解這件事是真的,才把影片放上臉書,陳卻仍不斷發表傷害家屬的言論,「很沒有人性!」


陳明義昨天表示,是三立電視台將他的記者會「掐頭去尾扭曲本意的播出」、「杜撰我已上飛機,其心可議」,為避免媒體誤導及造成家屬困擾,已改請民進黨花蓮縣議員劉曉玫代他轉達節哀之意,並要對三立提告。


陳明義說,死者家屬的意見,他都尊重,至於民進黨對這起事件的發言與批評,一律不予回應,他也強調此事無關選舉。


劉曉玫昨天說,陳明義前晚致電她說要到靈堂上香,並要求家屬先看過他政論節目的影片,但訂了機票卻沒來,還指家屬拍攝的畫面是「不寒而慄、毛骨悚然」。她認為,陳明義不斷發表傷害家屬的言論,是在打烏賊戰,準備今天提出告訴。


陳明義前天開記者會,指他是遭三立扭曲抹黑,但允諾昨天會搭機到花蓮上香致意。昨天上午,眾人等候多時,陳明義沒出現,他傳簡訊給劉曉玫說:「三立電視昨日又再次將我的記者會掐頭去尾扭曲本意的播出,其心可議!早上又杜撰說我已上飛機,十點會去靈前道歉,必定會誤導媒體去喪宅,造成家屬困擾,對於亡靈實在不敬,請您轉達家屬節哀!」


民進黨副總統參選人蘇嘉全昨日走訪花蓮時也前往林龍成靈堂上香。


2011-12-1 自由電子報



 



2011年11月25日 星期五

漢語考「 季姬擊雞記」



[四聲是北京漢語很重要的一部分。漢文的羅馬字拼音應該顯示漢語四聲,例如: "fei-chang2-hau3-kan4",有四聲的顯示,就可知道(起碼猜得出) 其漢字應該是 "非常好看"。


漢語四聲會因為中國地區鄉音而不同;下列的例子如果用羅馬字拼音,就算有四聲也無法猜出原來的字句。可是,標準中文羅馬字拼音不顯示四聲,是很大的錯誤。參看: http://tw.myblog.yahoo.com/ccshsu-clement/article?mid=2932&next=2928&l=f&fid=55 ]




最近網路上出現一段影片「漢語六級考」,要考外國人的聽力,文章名為「季姬擊雞記」,真的是考倒人了!整篇文章80個字都用「ㄐ一」這個讀音寫成,只有音調上有四個聲調的變化!
網友質疑連母語是中文的我們都不懂這是什麼意思,怎麼期待老外聽得懂






中文才能寫出只能看不能讀的文章!!




《季姬擊雞記》--這篇作者季姬,他是誰網路上查不到,唸唸看吧,一堆的雞雞..





季姬寂,集雞,雞即棘雞。棘雞飢嘰,季姬及箕稷濟雞。雞既濟,躋姬笈,季姬忌,急咭雞,雞急,繼圾幾,季姬急,即籍箕擊雞,箕疾擊幾伎,伎即齏,雞嘰集幾基,季姬急極屐擊雞,雞既殛,季姬激,即記《季姬擊雞記》。




注釋




季姬感到寂寞,羅集了一些雞來養,是那種出自荊棘叢中的野雞。野雞餓了叫嘰嘰,季姬就拿竹箕中的小米餵牠們。雞吃飽了,跳到季姬的書箱上,季姬怕髒,忙叱趕雞,雞嚇急了,就接著跳到幾桌上,季姬更著急了,就借竹箕為趕雞的工具,投擊野雞,竹箕的投速很快,卻打中了幾桌上的陶伎俑,那陶伎俑掉到地下,竟粉碎了。季姬爭眼一瞧,雞躲在幾桌下亂叫,季姬一怒之下,脫下木屐鞋來打雞,把雞打死了。想著養雞的經過,季姬激動起來,就寫了這篇《
記》。




《飢雞集磯記》述幾隻飢餓的雞,要藉水車和自己的伎倆吃鯽魚,終沒有吃到的故事,其作者已不可考。




唧唧雞,雞唧唧。
几鸡挤挤集矶脊。幾雞擠擠集磯脊。
机极疾,鸡饥极,鸡冀己技击及鲫。機極疾,雞飢極,雞冀己技擊及鯽。 机既济蓟畿,鸡计疾机激几鲫。機既濟薊畿,雞計疾機激幾鯽。 机疾极,鲫极悸,急急挤集矶级际。機疾極,鯽極悸,急急擠集磯級際。 继即鲫迹极寂寂,继即几鸡既饥,即唧唧




译文: 叫着的鸡,鸡不停的叫,几只鸡在拥挤的笼里找吃的,运鸡的车子走得极快,鸡也饿极了,它们的翅膀已经如同拼死一搏般坚硬如鱼鳞。终于,运鸡的车子到达了蓟。終於,運雞的車子到達了薊。 突然,有几只鸡撞开了笼子,所有的鸡都极快地想要冲下车来。突然,有幾隻雞撞開了籠子,所有的雞都極快地想要衝下車來。 可是车子还在极快的走着,那几只翅膀已经硬朗的鸡看见飞驰的轮子便害怕了,赶忙退了回去,也不顾笼子里有多么拥挤。可是車子還在極快的走著,那幾隻翅膀已經硬朗的雞看見飛馳的輪子便害怕了,趕忙退了回去,也不顧籠子裡有多麼擁擠。 最后,笼子里安静了下来,鸡即使再饿,也只敢唧唧的叫。最後,籠子里安靜了下來,雞即使再餓,也只敢唧唧的叫。




《侄治痔》




芝之稚侄郅,至智,知制纸,知织帜,芝痔炙痔,侄至芝址,知之知芷汁治痔,至芷址,执芷枝,蜘至,踯侄,执直枝掷之,蜘止,侄执芷枝至芝,芝执芷治痔,痔止。




譯文: 阿芝有個年幼的侄子叫大郅,人很聰明,會造紙,會織布。 有一天,阿芝长了痔疮,用火燎烧了一下,结果反而越来越严重了,大郅到阿芝家里去,知道了这件事情,大郅知道芷的汁液可以治痔疮,就到长着芷的地方去采摘。有一天,阿芝長了痔瘡,用火燎燒了一下,結果反而越來越嚴重了,大郅到阿芝家裡去,知道了這件事情,大郅知道芷的汁液可以治痔瘡,就到長著芷的地方去採摘。 突然来了一只疯狗,疯狗绕着大郅来回走,大郅拿起一根笔直的枝条扔了过去,砸到了疯狗的脚,疯狗停住不敢上前。突然來了一隻瘋狗,瘋狗繞著大郅來回走,大郅拿起一根筆直的枝條扔了過去,砸到了瘋狗的腳,瘋狗停住不敢上前。 大郅拿着芷的枝条给阿芝,阿芝用芷的汁液治好了痔疮。大郅拿著芷的枝條給阿芝,阿芝用芷的汁液治好了痔瘡。 阿芝为了感谢大郅,给了他肥肥的烧鸡腿。阿芝為了感謝大郅,給了他肥肥的燒雞腿。




《易姨醫胰》 --江濤 [曾任都柏林天文臺副台長的華人天文學]




易姨悒悒,依議詣夷醫。醫疑胰疫,遺意易姨倚椅,以異儀移姨胰,弋異蟻一億,胰液溢,蟻殪,胰以醫。易姨怡怡,貽醫一夷衣。醫衣夷衣,怡怡奕奕。噫!以蟻醫胰,異矣!以夷衣貽夷醫亦宜矣!




注釋




易阿姨悶悶不樂,大家叫她去看洋人醫生。醫生懷疑她胰臟有毛病,叫她靠在椅子上,用特殊的儀器移動他的胰臟,並設法取來一億隻特殊的螞蟻配合治療。結果胰髒的液汁流出來,螞蟻死去,胰病得到醫治。易阿姨非常高興,送給醫生一套洋裝。醫生穿上洋裝,十分高興,非常精神。啊!用螞蟻來醫治胰髒的疾病,多麼奇特呵!把洋裝送給洋醫生,又多麼適宜啊!




《施氏食獅史》 趙元任




石室詩士施氏,嗜獅,誓食十獅。施氏時時適市視獅。十時,適十獅適市。是時,適施氏適市。氏視是十獅,恃矢勢,使是十獅逝世。氏拾是十獅屍,適石室。石室濕,氏使侍拭石室。石室拭,氏始試食是十獅。食時,始識是十獅,實十石獅屍。試釋是事。




 




注釋




石室裏住着一位詩人姓施,愛吃獅子,決心要吃十隻獅子。他常常去市場看獅子。十點鐘,剛好有十隻獅子到了市場。那時候,剛好施氏也到了市場。他看見那十隻獅子,便放箭,把那十隻獅子殺死了。他拾起那十隻獅子的屍體,帶到石室。石室濕氣重,施氏叫侍從把石室擦乾。石室擦乾了,他才試試吃那十隻獅子。吃的時候,才發現那十隻獅子,原來是十隻石頭的獅子。試試解釋這件事吧。




這是趙元任的另一篇短文:《遺鎰疑醫》




伊姨殪,遺億鎰。伊詣邑,意醫姨疫,一醫醫伊姨。翌,億鎰遺,疑醫,以議醫。醫以伊疑,縊,以移伊疑。伊倚椅以憶,憶以億鎰遺,以議伊醫,亦縊。噫!亦異矣。




注釋




他的姨媽過世, 留下億元財產. 他曾通告全城,
希望能醫治他姨媽的病, 於是有一位醫師前來醫治他姨媽. 第二天,
億元財產竟不翼而飛, 他懷疑是那醫師幹的, 並以此非議醫師.
醫師由於他的懷疑, 竟上吊自殺來去除他的懷疑. 他倚靠在椅子上來回想此事,
想到自己因億元財產失蹤而非議他的醫師, 竟也想不開而上吊身亡了. ,
也是太奇怪了!




趙元任趙元任先生還曾寫過一篇《熙戲犀》




西溪犀,喜嬉戲。
席熙夕夕携犀徙,席熙细细习洗犀。席熙夕夕攜犀徙,席熙細細習洗犀。 犀吸溪,戏袭熙。犀吸溪,戲襲熙。 席熙嘻嘻希息戏。席熙嘻嘻希息戲。 惜犀嘶嘶喜袭熙。惜犀嘶嘶喜襲熙。




譯文: 西溪的犀牛,喜歡玩耍,席熙每天帶犀出去,席熙忙著細心幫犀牛洗澡,犀牛吸著溪水噴向席熙逗他,席熙笑嘻嘻讓犀牛不要鬧,可是犀牛樂此不疲,就愛嬉戲。




《於瑜與餘欲漁遇雨》——作者:楊富森




於瑜欲漁,遇餘於寓。
语余:余欲渔于渝淤,与余渔渝欤?余语于瑜:余欲鬻玉,俞禹欲玉,余欲遇俞于俞寓。余与于瑜遇俞禹于俞寓,逾俞隅,欲鬻玉与俞,遇雨,雨逾俞宇。語餘:餘欲漁於渝淤,與餘漁渝歟?餘語於瑜:餘欲鬻玉,俞禹欲玉,餘欲遇俞於俞寓。餘與於瑜遇俞禹於俞寓,逾俞隅,欲鬻玉與俞,遇雨,雨逾俞宇。 余语于瑜:余欲渔于渝淤,遇雨俞寓,雨逾俞宇,欲渔欤?鬻玉欤?于瑜与余御雨于俞寓,余鬻玉与俞禹,雨愈,余与于瑜踽踽逾俞宇,渔于渝淤。餘語於瑜:餘欲漁於渝淤,遇雨俞寓,雨逾俞宇,欲漁歟?鬻玉歟?於瑜與餘禦雨於俞寓,餘鬻玉與俞禹,雨愈,餘與於瑜踽踽逾俞宇,漁於渝淤。




譯文: 於瑜想打漁,在我住處見到我,對我說:我想到那個叫''的大水塘里打魚,您願和我一起去麼?我對他說: 我想賣掉一塊玉,有個叫俞禹的想要,我想到他的寓所去找他。說著我就和於瑜一起到俞禹的住所去拜訪他,剛走過俞禹住處的牆角,想賣玉給俞禹,正巧天下雨了,這雨水很快漫過了俞禹的住所。 我就对于瑜说:我也想到渝淤去打鱼,不巧在俞禹这里遇到雨,而雨水又漫过了俞禹的家,你看我是去打鱼呢,还是去卖玉?于瑜同意先在这儿避雨。我就對於瑜說:我也想到渝淤去打魚,不巧在俞禹這裡遇到雨,而雨水又漫過了俞禹的家,你看我是去打魚呢,還是去賣玉?於瑜同意先在這兒避雨。 接着我把玉卖给了俞禹,这时雨停了,我和于瑜慢慢地走过俞禹的住处,到渝淤去打鱼了。接著我把玉賣給了俞禹,這時雨停了,我和於瑜慢慢地走過俞禹的住處,到渝淤去打魚了。




 





2011年11月24日 星期四

在美中國人客觀的觀察: "海外台灣人" 的藍與綠



[有個小故事: "有一群人佔了你的家、用鐵鍊鎖住你的手腳、從你的口袋拿走你的錢、天天侮辱你是次等人、你出聲就賞耳光、割你一刀。有一天,這群人的首腦決定這個家要改建,又決定不打了,放開限制你手腳的鐵鍊。你好高興! 向他跪下去,立他的銅像,稱他為偉人"。


這個小故事,聽來很怪吧? 被欺侮的人是否還無法擺脫奴才心態? 這不就是目前台灣人對蔣經國的評語嗎? 每次聽到台灣人稱讚蔣經國多偉大,我心中哀嘆!!


海外的國民黨員對蔣經國開放台灣人應有的自由,還不滿呢!!!]


 


前人民日報記者程凱:海外台灣人的藍與綠




http://www.taiwanus.net/news/press/2011/201111200922101452.htm




海外台灣人的藍與綠




程凱






美國舊金山唐人街有一幢屋頂飄揚著中華民國青天白日滿地紅旗的建築,那是國民黨美國總支部所在地。進出這幢建築物的都是海外國民黨人和以國民黨為主的海外泛藍陣營人士,他們之間都講國語而從不講台灣話。



在舊金山灣區南灣的二三七高速公路旁,有一幢寫著「台灣會館」的建築,進出的都是民進黨和海外泛綠陣營人士,這幢建築物裡的人都講台灣話而沒有人講國語,也從來不懸掛中華民國國旗。




來自台灣的兩個「族群」




海外台灣人都來自台灣,由於分成藍與綠,就變成了截然不同的兩個族群。去年美國進行人口普查,泛藍台灣人在表格中的「原居住國」一欄填寫「中華民國」,而泛綠人士則填寫「台灣」。



美國的舊金山灣區,對於台灣的藍、綠兩大陣營,都是海外的重要地盤。每逢台灣有總統大選或者五都市長選舉之類的重要政治活動,這裡的藍、綠陣營人士為各自的候選人助選的熱情,不亞於台灣本土。



不久前,台灣2012年總統大選民進黨候選人蔡英文到美國造勢和籌款,尾追而來的是以馬英九總統競選連任辦公室總裁金溥聰、國民黨副主席黃慧敏率領的一個團隊。到達舊金山後,泛藍泛綠在相距僅十分鐘車程的兩間賓館、同一時間舉行造勢大會。「互別苗頭」竟至於此。



那一次,也顯示了藍與綠的不同:國民黨的造勢大會以餐會形式進行,席開一百多桌,參與者們一邊大嚼牛扒一邊高喊「馬英九再幹四年」。而民進黨的造勢大會,不但沒有牛扒可吃,參加者還都餓著肚子帶著支票捐款給蔡英文,助她「凍蒜(當選)」。




李登輝在執行蔣經國的遺願




作為生活在舊金山的大陸人,我對國民黨的好感是從2000年李登輝和平交權開始的。在民進黨的陳水扁當選為台灣總統就職典禮那一刻,我覺得真正偉大的,不是走上總統寶座的陳水扁,而是走下總統寶座的李登輝,和他領導的從執政黨成為在野黨的國民黨。僅此一條,李登輝就應與他的前任蔣經國一樣名垂千古。



但我與海外泛藍人士交談,發現他們卻無不對李登輝恨之入骨:是李登輝讓國民黨失掉了政權,是十惡不赦的罪人。其實李登輝是在執行蔣經國的遺願而已,蔣經國開放黨禁報禁,李登輝開創了政黨輪替,以極大的勇氣把蔣經國的遺願付諸實踐。我知道海外國民黨人對蔣經國也是怨恨的,這從他們開口閉口「老總統蔣公」而極少以同樣充滿感情的語調談論「先總統經國先生」就可以看出,只不過他們都是跟隨蔣家兩位總統走過來的,有怨恨也難以啟齒。



我曾見識海外國民黨人失掉政權後的痛苦。2004年台灣總統大選前夕,海外泛藍人士舉行回台灣投票奪回政權的誓師大會,與會者大多七老八十,他們曾是台灣顯赫的黨政軍官員,因忍受失掉政權四年的痛苦而在會場上表現失態以致歇斯底里。我終於明白,他們對政權的觀念與共產黨完全一樣,有了就等於有了一切,失掉了就等於失掉一切。



海外泛藍陣營人士,從來認為自己是中國人而不是台灣人。他們每年舉辦「祭孔大典」,開辦向自己的下一代教授中國語言文字和中國文化知識的中文學校,僅舊金山灣區,就辦了八十多間。卻從來不舉辦任何弘揚台灣本土文化的活動。



1949
年以後,國民黨對中華民族的貢獻:一是保住了台灣未被中共侵吞,二是在台灣實現了自由、民主、人權下的政黨輪替。國民黨也由一個專制的政黨轉型為民主政黨。但專制政黨的基因仍在民主政黨的肌體內起作用,這就形成如今的國民黨人士和海外泛藍陣營人士的精神和行為特質




泛綠沒有權貴氣息和中國氣息




接著談海外泛綠陣營。我首先要介紹舊金山的一位民進黨人士張國鑫。張國鑫二十年前由台灣來美國留學,獲博士學位,在舊金山灣區的矽谷有一份高薪工作。他連任民進黨舊金山支黨部主任委員。今年五月他應民進黨中央的徵召,回台灣老家南投縣競選台灣立法委員。為此他必須放棄在美國的一切,包括工作、家庭和美國公民的身份。而放棄了這一切後,卻並無競選必勝的把握。人們都覺得他腦子壞了。但他說:台灣的政黨輪替是他學生時代就孜孜以求的夢想。政黨輪替後,他還沒有參與實踐,他願意回台灣,為民主化的落實和鞏固,貢獻自己的心力。



這樣的事情必然發生在海外泛綠人士身上而不是泛藍人士之中。在台灣威權統治時期,就有許多民進黨人士受國民黨迫害流亡海外,而後又為台灣的自由和民主,前赴後繼闖關回台灣。這是海外民進黨人士與生俱來的奉獻犧牲精神,張國鑫是民進黨前輩的後繼者。



與海外泛藍陣營人士相比,泛綠人士沒有國民黨的權貴氣息和中國氣息。這裡的泛綠陣營人士的政治活動,充滿底層民眾的悲情氣氛,因為他們面對的是一個富有的、被他們認為是外來統治者的國民黨,和海峽對岸強大而野蠻專制的中國共產黨。



他們認為自己是台灣人,或者是華人,絕不是中國人。他們不會去舉辦和參加諸如「祭孔大典」之類的活動,而是每年舉辦「台灣文化節」、「宜蘭童玩節」,把十足台灣味道的媽祖、三太子、布袋戲、民歌小調《草螟弄雞公》、夜市小吃蚵仔煎,搬來舊金山。「宜蘭童玩節」是民進黨舊金山支黨部首席顧問洪順五全資贊助的,而這樣為台灣奉獻的精神在泛藍陣營裡甚為鮮見



民進黨的誕生是因為國民黨的威權統治,民進黨的台獨主張是因為海峽對岸有一個獨裁專制的共產黨。海外泛綠陣營的存在,向國際社會宣示一種理念:只要中國由集權專制的共產黨統治,台獨就是一項偉大正義而且悲壯的事業。民族主義下的國家統一、領土完整,對於自由、民主、人權和人民的福祉來講,無足輕重。泛綠陣營的存在和奮鬥,是台灣民進黨人對華人世界思想和精神進步的一大貢獻




海外華人也分「海峽兩岸」




海外的大陸人,凡親共的人士和團體,都贊同和支持海外泛藍陣營,但國民黨卻與他們保持距離,因為親共的紅色標籤令他們吃不消。八九「六四」以後,海外國民黨曾在精神上和財力上支持海外中國民主運動,後來這種支持一年一年減少。近年來海外民運甚至成為他們避之唯恐不及的麻煩,原因當然是國民黨對共產黨的恐懼,同時因為他們自己的基因作怪。



海外大陸人中的民運人士,一般都認同泛綠陣營人士的理念,但鮮少與民進黨交流與合作,生怕被貼上支持台獨、分裂國家的標籤,民進黨人士也甚少與大陸民運人士交流與合作。



--原載香港《動向》雜誌201111月號




 




曹長青網站編者按




程凱先生為中國資深新聞工作者,曾為《人民日報》駐深圳首席記者、《海南日報》總編輯兼黨委書記。




1989年北京天安門事件時,程凱領導的《海南日報》旗幟鮮明地站在學生一邊。據後來該報的「社史」,在李鵬發表講話要戒嚴時,「在程凱親自拍板下」,《海南日報》刊出「趙紫陽,您好!!!」、「反對暴力」等巨幅照片。




六四屠殺後,中共國務院發言人袁木稱天安門沒死一個人,《海南日報》在頭版刊出中國統計會議消息時,以大標題「謊報數字要繩之以法」嘲諷袁木的謊言。




據八九學生領袖、海南高自聯主席林大軍的回憶:「『六四』運動遭血腥鎮壓後,全國萬馬齊喑,但《海南日報》卻於當年七月勇敢地在頭版右上角刊出民運新聞,報導了『六四』流亡民運人士在法國成立民運組織的活動,此壯舉堪稱驚世駭俗。」




結果《海南日報》遭整肅,程凱被撤銷黨內外一切職務,後又被開除黨籍和公職。




他逃亡到美國,在洛杉磯出任中國旅美新聞工作者主辦的宗旨為「揭露六四真相、傳播中國真實」的報紙《新聞自由導報》總編輯。




目前程凱為總部在華盛頓的「自由亞洲電台」(RFA)北加州記者。)




 





2011年11月23日 星期三

1988年新發現的致病菌Coagulase negative Staphylococcus lugdunensis


[http://www.medscape.com/viewarticle/751649?src=mp&spon=3 ]


 


Staphylococcus lugdunensis1988年才被報導的細菌,以它原先被發現的法國都市Lyon的拉丁名字命名。它和Coagulase negative (CoN) Staphylococcus epidermidis一樣,是皮膚表面的正常菌之一,在腋下、會陰部、腳趾頭常見到。它不像Staph. aureus,沒有enterotoxinexfoliatintoxic shock syndrome toxin (TSST)等毒素,它不會產生coagulaseoxidase,但會產生catalase,有幾種抑制宿主免疫功能的機制,而會引起各種嚴重感染症。它的抗藥性不大,對oxacillinpenicillin等都有藥敏性。



 



同樣CoNStaph. epidermidis致病性不大,但是S. lugdunensis卻常常引起心內膜炎、骨關節、人工關節、皮膚、眼睛、中樞神經系統、血液等嚴重感染,也會引起septic shockTSS。這種致病的毒性來自下述細菌特性。(使用TEE= trans-esophageal echocardiogrpahy診斷心內膜炎vegetation的存在,精準性達96%,而普通TTE= transthoracic echocardiography只有30%)(人工關節的感染可以手術後六星期到四年之間發生)



此細菌有和S. aureus相似的heat-stable delta-toxin,是一種hemolysin,可以使此菌避免吞噬細胞的消化;它有稱為OatA (O-acetyltransferase)peptidoglycan在細菌表面,可以避免吞噬細胞內lysozyme的附著,逃避lysozyme的破壞。它又有adhesin (黏著素)而可以和宿主組織的蛋白質附著。它能夠分泌von Willebrand factor-binding protein (此蛋白質在有血管傷害、有血小板附著時,會黏附在這些蛋白質),而這被認為是引起心內膜炎的原因。這些特性使這個細菌能引起人工關節等合成物質表面的感染。它又會產生biofilm (一種glycocalyx,會刺激prostaglandin E2的分泌,此PG E2可以抑制性T細胞的產生),在其內繁殖,避免吞噬細胞免疫細胞的攻擊。



此細菌有bound coagulase (又稱為clumping factor),因而常被誤認為S. aureus在自動辨認儀器沒有特殊認出此菌的ornithine decarboxylase之類的功能時,常會被誤認;最常被誤認為是 S. haemolyticus。如果用ribotypingPCR就可以很快辨識。



此菌會有hemolysis,會有positive catalase, pyrrolidonyl arylamidases ornithine decarboxylase tests。在培養劑表面,它會有smooth and glossy, rough and dull等不同型態,稱為colony variation;這會使人誤解為有contamination。血液中培養出只一次的這種CoNS,也要當做是可能有嚴重感染治療。



治療用batalactam應該可以,不過,已經知道有高達24-40%(US)mecA gene,產生betalactamases而會有這些藥物的抗藥性。最近也發現有mecA-negative而有對betalactams都有抗藥性者。Clinical Laboratory and Standards Institute建議分離出此菌時,要用PCR檢查mecA-gene,以及用latex agglutination檢查penicillin-binding protein 2A (PBP2a)2005年規定此菌oxacillin 藥敏性的MICs 2 µg/mL 為藥敏;MICs 4 µg/mL為有抗藥性。Vancomycin抗藥性迄今還未有過。最新的glycopeptidetelavancin,是很有效。使用cipro + rifampin治療人工關節失敗,可用linezolid



 [回想起來,以前似乎有過幾次血液培養出 "Staph. epidermidis"、應該是"汙染菌",卻似有感染症狀,可能就是S. lugdunensis感染。不過可能因為對各種抗生素有藥敏性,所以投藥後都沒導致嚴重的問題。] 



 



Staphylococcus lugdunensis: The Coagulase-negative Staphylococcus You Don't Want to Ignore



Elizabeth Babu; John Oropello



Department of Surgery, Division of Critical Care Medicine, The Mount Sinai School of Medicine, New York, NY 10029, USA.

† Author for correspondence
john.oropello@mountsinai.org



Posted: 11/14/2011; Expert Rev Anti Infect Ther. 2011;9(10):901-907. © 2011 Expert Reviews Ltd.




Abstract and Introduction



Abstract



Staphylococcus lugdunensis is a virulent coagulase-negative staphylococcus (CoNS) that behaves like Staphylococcus aureus. Toxic shock syndrome, osteomyelitis, septic arthritis and postoperative endopthalmitis have been observed. Endocarditis complicated by heart failure, periannular abscess formation and embolic phenomenon have brought particular attention to this CoNS. Mortality rates for endocarditis appear higher when compared with other CoNS. Owing to the laboratory methods used, identification may be misleading. β-lactam antimicrobials are recommended pending sensitivities. Evaluation for endocarditis should be pursued in bacteremic patients due to its pathogenic potential.




Epidemiology



According to the most recent SENTRY Antimicrobial Surveillance Program,[1] which monitors predominant pathogens and antimicrobial resistance in the USA, Canada, Latin America and Europe, Staphylococcus lugdunensis was the seventh most common coagulase-negative staphylococcus (CoNS) species isolated in bloodstream infections during the 12-month study period in 1997.



To date, the frequency of isolation of S. lugdunensis among CoNS from clinical specimens has been reported in a few isolated studies. Rates range from less than 1% in Denmark[2] and Korea,[3,4] approximately 3% in Japan,[5] 6% in Argentina[6] and from 3 to as high as 7% in the USA.[7,8]



S. lugdunensis is normally found as part of human skin flora and has been identified in cultures from the entire body.[9] Studies carried out to look into specific areas of colonization have not been very thorough. The most comprehensive study obtained 525 cultures from eight sites in 75 healthy subjects.[10] Swabs from the groin, toes and axilla yielded S. lugdunensis most frequently. Further studies need to be performed to clarify if the organism has a preferred site of colonization, if the site is different in hospitalized patients and if these sites are a permanent or transient habitat.




History



In 1988, the first description of two new species of Staphylococcus, S. lugdunensis and Staphlococcus schleiferi, was published by Freney et al..[11] These two species were obtained from a collection of unidentified Staphylococcal strains at The French National Reference Center for Staphylococci. In total, 11 strains were identified as the new genomic species described formally as Staphylococcus lugdunensis. It assumed the Latin name of Lyon, the French city where the organism was first identified. Of the 11 strains, five were obtained from blood, and one each from an intrauterine device, thoracic drain, umbilicus, axillary lymph node, abscess drain and an unknown site. The 11 strains studied were variable depending on the culture medium and the time of incubation. All strains were Gram-positive cocci, 0.8–1.0 µm in diameter, occurring singly, in pairs, small clusters or chains. All strains produced catalase and did not produce coagulase or oxidase. Enterotoxins A, B and C, toxic shock syndrome toxin (TSST) and exfoliative toxin production were not described with this pathogen. All strains were susceptible to oxacillin and penicillin.




Clinical Features



S. lugdunensis has been associated with a wide variety of infections, including cardiovascular infections, osteomyelitis and prosthetic joint infections, bloodstream infections, skin and soft-tissue infections, central nervous infections, peritonitis, endopthalmitis and urinary tract infections.



S. lugdunensis has been described as the etiology of cardiovascular infections including severe native and prosthetic valve endocarditis, device-related endocarditis, myocarditis[12] and infected cardiac myxoma.[13] In general, CoNS are unusual causes of native valve endocarditis but are one of the leading causes of prosthetic material-associated endocarditis. The clinical course is subtle, subacute or even chronic without fulminant signs of infection.[14] Infections with CoNS are typically not associated with abscess formation, heart failure or embolic phenomenon. Furthermore, compared with Staphylococcus aureus, CoNS are more amendable to medical and/or surgical therapy and typically have shorter courses with better clinical outcomes.[15] The reports of S. lugdunensis are quite different. S. lugdunensis has been reported as the cause of endocarditis in 67 cases since 1988.[16] Reported cases have been mostly community acquired but not associated with injection drug use. This reporting may represent a significant bias since cases with complicated courses and poor outcomes tend to be published. However, the cases provide a spectrum of complications including acute onset, heart failure,[17] periannular abscess formation,[18] peripheral embolism[19] and shock, which typically is not described in CoNS. In addition, clinical outcomes mimic cases involving S. aureus native and prosthetic valve endocarditis.



A prospective cohort study of two centers described their experience with ten cases of S. lugdunensis endocarditis and, in addition, performed a combined analysis of 59 cases in a literature review.[20] Their findings noted that in native valve endocarditis the mitral valve is involved the majority of the time, surgery was required in 51% of the cases and the mortality rate reached as high as 42%. In prosthetic valve endocarditis the aortic valve was most frequently affected, also required surgical intervention, and the mortality rate was 78%.



Pacemaker/defibrillator lead endocarditis caused by S. lugdunensis was associated with better prognosis when antibiotic treatment was combined with a surgical removal of the device. Therefore, lead extraction should be performed without delay as recommended by the American Heart Association scientific statement on nonvalvular cardiovascular device-related infections.[21]



Native valve endocarditis has been a consequence of infection originating at other sites, including skin and soft-tissue infections,[9] hemodialysis,[22] vascular catheters,[23,24] coronary angioplasty, vasectomy,[25] kidney transplantation[26] and prosthetic joint infections.[27]



Transesophageal echocardiogram (TEE) is the gold standard for identification of intracardiac vegetations with a sensitivity of 96% compared with transthoracic echocardiogram (TTE) of only 30%.[28] TTE can lead to false-negative results and a delay in appropriate therapy. TEE should be considered as the initial imaging modality in endocarditis.[21] Although uncommon, S. lugdunensis is very destructive and plays a major role in infective endocarditis. Echocardiographic evaluation can change medical and surgical management and may improve clinical outcome in individuals with S. lugdunensis endocarditis. Therefore, evaluation with echocardiography should be pursued.



The next most common serious infections are bone and joint infections, both native and prosthetic. Reports have included vertebral osteomyelitis,[29] disk space infection,[30] spondylodiscitis[31] and septic arthritis.[32] Following surgical procedures, both temporal bone osteomyelitis[33] and septic arthritis[34] have been described. Prosthetic joint infections[35,36] have been reported to manifest as early as 6 weeks to as late as 4 years after implantation.



In a study looking at S. lugdunensis bacteremia in 63 patients, 15 (23.8%) had clinically significant bacteremia defined as positive blood cultures and systemic inflammatory response syndrome without an alternative explanation.[4] Of those with clinically significant bacteremia, the source was unknown in eight (53%) and associated with central venous catheters in five (33%) patients. In addition, in this subset of patients, endocarditis was seen in four (26%) patients, two of whom had underlying valvular heart disease.



Among the reports of S. lugdunensis, sepsis,[37] septic shock[38] and toxic shock syndrome have been described. A report described septic shock in a 71-year-old man after receiving platelet[39] and red cell transfusions for pancytopenia secondary to myelodysplasia. Blood cultures and cultures of the platelets yielded S. lugdunensis. The transfused blood was sterile and there was no evidence of allergic reaction to the blood products or any other source of infection.



Toxic shock syndrome was described in a 33-year-old healthy woman 48 h after a tooth extraction with Gelfoam packing.[40] Blood and purulent maxillary sinus cultures were identified as S. lugdunensis. Tests for coagulase, TSST-1, staphylococcal enterotoxins A–E and exfoliatin toxin A were negative. Neither S. aureus nor S. pyogenes were isolated from any samples of blood, urine, sputum, sinus or vaginal specimens from this patient.



Fadel et al. examined the outcomes of 29 patients with a single S. lugdunensis positive blood culture.[41] From the chart review, the primary treating physician considered nine (31%) cases clinically significant, did not acknowledge the culture in 14 (48%), and disregarded the culture as a contaminant in six (21%) cases. Fadel et al. reclassified the cases based on defined criteria and found that 13 (45%) patients with a single positive blood culture had clinically significant bacteremia. Therefore, they concluded that all blood cultures for CoNS should be screened for S. lugdunensis and isolation of this organism from one blood culture should not be assumed to be contamination.



Skin and soft-tissue infection account for the majority of infections caused by S. lugdunensis. When isolated from a superficial infection it is more likely to be significant compared with S. epidermidis.[42] S. lugdunensis is well known to cause suppurative skin and soft-tissue infections including furuncles, cellulitis and abscesses.[43] Abscesses have mostly been reported to affect the perineal and inguinal area[44,45] and have usually been associated with surgical procedures. However, abscesses have also been described in nonlactating women.[46,47] One case of a severe acute necrotizing sinusitis complicated by periorbital cellulitis and ulceration through the maxillary sinus through the hard palate has been reported.[48] Pyomyoma after a cesarean section[49] and endometritis[50] has also been described.



Infections of the CNS have included abscesses from dental infections, septic emboli from native valve endocarditis, multiple mycotic cerebral aneurysms[51] and meningitis from ventriculostomy and ventriculoperitoneal shunt infections.[52] The ventriculoperitoneal shunt infections occur both with an early and late onset.[53,54]



Peritonitis has been described in a patient after cesarean section[55] and in a patient undergoing continuous peritoneal dialysis.[56]



In a 4-year multicenter study looking at the species distribution of CoNS in patients with endopthalmitis, S. lugdunensis was the second most common CoNS after S. epidermidis.[57] In a series of postoperative endopthalmitis caused by S. lugdunensis, endopthalmitis was characterized by severe visual loss (hand motion or less) that occurred a mean 7.6 days after cataract surgery and necessitated pars plana viterectomy in three of the five cases.[58] The authors stated that compared with other CoNS, patients infected with S. lugdunensis were characterized by a worse final functional prognosis at 6 months and a higher frequency of viterectomy retinal detachment (60 vs 3%).




Pathogenesis



The toxins produced by S. aureus such as enterotoxins, exfoliatin and TSST have not been identified in any S. lugdunensis isolates despite the syndrome of toxic shock that has been reported. However, various virulence factors have been identified that may explain the similar pathogenic potential to S. aureus. Regions of homology to the S. aureus accessory gene regulator (agr) locus, the regulator of virulence factors, have been identified. This includes heat-stable δ-like hemolysin, which is similar to δ toxin in S. aureus. δ toxin enables the staphylococci to escape killing and digestion by the phagosomes.[59] Another similarity to S. aureus is S. lugdunensis' resistance to lysozyme. Lysozymes, abundant in the cytoplasmic granules of polymorphonuclear neutrophils, are enzymes created by the immune system that damage cell walls. S. lugdunensis possesses in its genome a homologous region to S. aureus that functions in lysozyme resistance. Known as OatA (O-acetyltransferase), this membrane-bound peptidoglycan prevents the binding of lysozyme to the cell wall, thereby averting the immune system.[60]



In addition to averting the immune system, S. lugdunensis has been found to have properties that promote tissue interaction. These properties include adhesins that promote binding to proteins found in host tissue. An investigation to identify these cell surface factors revealed that S. lugdunensis binds to collagen type I found primarily in scar tissue and collagen type IV found on the basal lamina – the extracellular matrix on which the epithelial cell sits.[61] Binding to fibronectin, fibrinogen, laminin, vitronectin and plasminogen, key factors in cell adhesion and wound healing, has also been described. The production of von Willebrand factor-binding protein by this organism has been thought to be a contributing factor in the pathogenesis of endocarditis. This protein primarily functions to bind other proteins particularly involved in platelet adhesion following vascular injury.[62] These various adherence factors enable attachment to, and infection of, host tissue as well as synthetic surfaces.



S. lugdunensis is also able to protect itself from the immune system via the production of biofilm.[63] Even though organisms may demonstrate susceptibility to an array of antimicrobials, infections can be very difficult to treat if organisms form and proliferate within biofilms. A biofilm is a polymeric matrix of cells, adherence proteins and polysaccharides in which microorganisms can replicate and thrive. This extracellular slime embeds onto host tissues or indwelling medical devices and is difficult to eradicate due to the high level of resistance to antimicrobial therapies as well as the production of factors that interfere with innate immune defenses. One mechanism of this glycocalyx is the ability to stimulate monocyte prostaglandin E2. Prostaglandin E2 modulates the immune system by inhibiting T-cell proliferation.[64]




Diagnosis



In contrast to S. aureus, S. lugdunensis is coagulase negative. Caution should be taken with the latex agglutination test since around 58% of strains of S. lugdunensis produce a bound coagulase.[11,61] Also known as clumping factor, on slide it can suggest that the organism produces coagulase and the technician can falsely identify the organism as S. aureus. S. lugdunensis does not produce coagulase and therefore in the test tube will always be coagulase negative. In addition, some automated identification systems fail to identify S. lugdunensis if the database lacks insufficient discriminatory biochemical reactions, such as ornithine decarboxylase.[65,66] Mateo et al. studied 17 isolates and S. lugdunensis was misidentified most frequently as S. haemolyticus.[67] Species misidentification rates were 5.9, 23.5 and 29.4% with the Crystal (Becton Dickinson, MD, USA), Vitek 2 (bioMérieux, Marcy l'Etoile, France) and Wider (Soria Melguizo SA, Madrid, Spain) systems, respectively. The ATB32-Staph system (bioMérieux) correctly identified all isolates. The Manual of Clinical Microbiology provides the list of systems that have S. lugdunensis in their database.[68] Molecular identification with ribotyping[69] and PCR amplification[70,71] is a rapid and effective alternative to conventional identification strategies.



Morphologically, S. aureus and S. lugdunensis have a slight yellow pigmentation and on blood agar plates demonstrate hemolysis. Manual identification demonstrates positive catalase, pyrrolidonyl arylamidases and ornithine decarboxylase tests. Another feature of this organism is that it demonstrates colony variation.[72] Colony variation essentially means that isolates demonstrate mixed morphotypes. Strains can appear both smooth and glossy or rough and dull. In the laboratory this feature may suggest that there exists a mixed population of organisms such as you find in a contamination.



Coagulase-negative staphylococci are among the most frequently isolated bacteria in the clinical microbiology laboratory. These bacteria are normal inhabitants of human skin and mucous membranes and therefore one of the major challenges of daily diagnostic work is to distinguish clinically significant CoNS from contaminant strains. One should have a high degree of suspicion if the clinical course does not correlate with a CoNS organism on culture, especially from a sterile site. Fadel et al. found that 45% of cases with a single positive blood culture for S. lugdunensis were clinically significant.[41] This was defined as having prolonged fever, hypotension, leukocytosis, neutropenia or disseminated intravascular coagulopathy.[2] Many laboratories do not routinely identify CoNS to the species level and presume contamination unless requested. Being aware of these characteristics, including the increased probability of laboratory misidentification, is helpful in earlier recognition and appropriate management of S. lugdunensis infection.




Treatment



Most isolates of S. lugdunensis described have been sensitive to an array of antimicrobial therapy. However, there have been isolated case reports of resistance to erythromycin,[73] streptomycin,[73] tetracycline,[4] penicillin,[74,75] gentamicin,[55] ceftazidime,[55] aminoglycosides[20] and macrolides.[27] Development of resistance to ciprofloxacin[67] and rifampin in a patient on chronic treatment for septic arthritis, vertebral osteomyelitis and aortic and mitral valve endocarditis has been described.[76] β-lactamase, the enzyme that confers resistance to β-lactam antimicrobials such as penicillin, has been reported in the USA as well as in Europe.[55,77] The frequency of β-lactamase in S. lugdunensis is between 7 and 24% in France,[78] 12% in Spain,[9] 15% in Sweden[79] and 24–40% in the USA.[80,81] The mecA gene is part of the staphylococcal cassette chromosome that confers resistance to oxacillin and generally all β-lactams. The mecA gene has been reported in several reports to date;[82–84] the first in a neonate[80] with S. lugdunensis bacteremia associated with an intravascular catheter and the second isolate from a nasal swab.[81] Currently, the Clinical Laboratory and Standards Institute has recommended that S. lugdunensis isolates should be screened for the mecA gene by PCR or penicillin-binding protein 2A (PBP2a) by latex agglutination. Recently, a mecA-negative S. lugdunensis isolate resistant to all β-lactams has been described.[85] In 2005, the breakpoints for oxacillin sensitivity were revised to follow the breakpoints for S. aureus: MICs of 2 µg/ml are considered susceptible and MICs 4 µg/ml are classified resistant.[86] Reports of vancomycin (a glycopeptide antimicrobial agent) resistance have not been documented to date. In a recent in vitro study based on MIC50/90 values, the newest glycopeptide telavancin demonstrated potent activity against S. lugdunensis.[87] The successful eradication of S. lugdunensis prosthetic joint infection with linezolid after failure of ciprofloxacin and rifampin has been reported.[88]



In their prospective study of ten patients with S. lugdunensis endocarditis, Anguera et al. observed no difference in mortality between monotherapy (β-lactam or vancomycin) and combination therapy (β-lactam with an aminoglycoside or rifampin or cephalosporin and vancomycin with an aminoglycoside or rifampin or cephalosporin or carbapenem).[20]



There is a lack of randomized controlled data on the efficacy of antimicrobial agents for S. lugdunensis infections. The Infectious Diseases Society of America guidelines for endocarditis recommends treatment based on in vitro susceptibility profiles and follow-up monitoring of the development of periannular extension or extracardiac spread of infection.[89] Empiric treatment with a β-lactam agent should be appropriate. For patients with penicillin allergies, vancomycin is an alternative. Source control with drainage of abscesses, early surgical intervention for valvular compromise and removal of intravascular catheters and pacemaker leads should be pursued. In addition, transesophageal echocardiograms to assess valvular involvement and CT scans to evaluate for embolic phenomena should be strongly considered.




Prognosis



S. lugdunensis, unlike other CoNS, is associated with a high rate of complications.




Expert Commentary & Five-year View



S. lugdunensis is a Gram-positive CoNS species normally found as part of human skin flora. Owing to an increased effort to identify all staphylococcus isolates, the number of S. lugdunensis isolates has increased. Depending on methods used, the laboratory can incorrectly identify S. lugdunensis as S. aureus or more problematic, simply not further speciate a CoNS isolate, assuming contamination.



Unlike other CoNS species, S. lugdunensis is unusually virulent and capable of the spectrum of infection as that of S. aureus. This includes skin and soft tissue, bone, joint, cardiovascular and CNS infections. The toxins typically associated with S. aureus have not been identified; however, various virulence factors are shared that may explain the similar pathogenic potential to S. aureus.



S. lugdunensis is more aggressive than other CoNS and despite being sensitive to many antibiotics, carries a high mortality rate in patients with endocarditis compared with other CoNS.[16,20,25] If the clinical situation does not correlate with CoNS, prompt identification to the species level should be performed for identification of S. lugdunensis. Treatment with a β-lactam and removal of any infected foreign material should be pursued. For penicillin-allergic patients, vancomycin is an alternative. Based on the virulence of this organism, if S. lugdunensis is isolated, a TEE to evaluate for infective endocarditis should be pursued.




Sidebar



Key Issues




  • Staphylococcus lugdunensisbehaves likes Staphylococcus aureusand should not be considered a typical coagulase-negative staphylococcus.
  • Infections may be underdiagnosed owing to identification methods.
  • Cardiovascular infections including native and prosthetic valve endocarditis, pacemaker-related endocarditis and myocarditis have been described.
  • Endocarditis, secondary to other coagulase-negative staphylococci, tends to be indolent. However, the spectrum of infective endocarditis including valve dehiscence, abscess formation and vegetation with embolic phenomenon is seen with S. lugdunensis.
  • In the CNS, brain abscess, meningitis and ventriculoperitoneal shunt infections have been observed.
  • Skin and soft-tissue infection, bacteremia, septic shock, toxic shock syndrome, peritonitis, osteomyelitis, prosthetic joint infections and ocular infections have been reported.
  • Infective endocarditis should be ruled out in patients with S. lugdunensisbacteremia.
  • Obtaining a S. lugdunensisisolate from clinical specimens should prompt an approach similar to the approach considered for etiology, management and treatment of S. aureus.

[ CLOSE WINDOW ]



References




  1. Pfaller MA, Jones RN, Doern GV, Sader HS, Kugler KC, Beach ML. Survey of blood stream infections attributable to Gram-positive cocci: frequency of occurrence and antimicrobial susceptibility of isolates collected in 1997 in the United States, Canada, and Latin America from the SENTRY Antimicrobial Surveillance Program. SENTRY Participants Group. Diagn. Microbiol. Infect. Dis. 33(4), 283–297 (1999).
  2. Jarlov JO, Hojbjerg T, Busch-Sorensen C et al. Coagulase-negative staphylococci in Danish blood cultures: species distribution and antibiotic susceptibility. J. Hosp. Infect. 32(3), 217–227 (1996).
  3. Shin JH, Jung HJ, Lee HR, Kim JH, Kim HR, Lee JN. Prevalence, identification, and antimicrobial susceptibility of Staphylococcus lugdunensis from various clinical specimens in Korea. Jpn J. Infect. Dis. 60(5), 312–313 (2007).
  4. Choi SH, Chung JW, Lee EJ et al. Incidence, characteristics, and outcomes of Staphylococcus lugdunensis bacteremia. J. Clin. Microbiol. 48(9), 3346–3349 (2010).
  5. Kawamura Y, Hou XG, Sultana F et al. Distribution of Staphylococcus species among human clinical specimens and emended description of Staphylococcus caprae. J. Clin. Microbiol. 36(7), 2038–2042 (1998).
  6. De Paulis AN, Predari SC, Chazarreta CD, Santoianni JE. Five-test simple scheme for species-level identification of clinically significant coagulase-negative staphylococci. J. Clin. Microbiol. 41(3), 1219–1224 (2003).
  7. Kleeman KT, Bannerman TL, Kloos WE. Species distribution of coagulase-negative staphylococcal isolates at a community hospital and implications for selection of staphylococcal identification procedures. J. Clin. Microbiol. 31(5), 1318–1321 (1993).
  8. Kleiner E, Monk AB, Archer GL, Forbes BA. Clinical significance of Staphylococcus lugdunensis isolated from routine cultures. Clin. Infect. Dis. 51(7), 801–803 (2010).
  9. Herchline TE, Ayers LW. Occurrence of Staphylococcus lugdunensis in consecutive clinical cultures and relationship of isolation to infection. J. Clin. Microbiol. 29(3), 419–421 (1991).
  10. Bieber L, Kahlmeter G. Staphylococcus lugdunensis in several niches of the normal skin flora. Clin. Microbiol. Infect. 16(4), 385–388 (2010).
  11. Freney J. Staphylococcus lugdunensis sp. nov. and Staphylococcus schleiferi sp. nov., two species from human clinical specimens. Int. J. Syst. Bacteriol. 38(2), 168–172 (1988).
  12. Pirila L, Soderstrom KO, Hietarinta M, Jalava J, Kyto V, Toivanen A. Fatal myocardial necrosis caused by Staphylococcus lugdunensis and cytomegalovirus in a patient with scleroderma. J. Clin. Microbiol. 44(6), 2295–2297 (2006).
  13. Bhanot N, Sahud AG, Bhat S, Lane S, Manyam H, Chan-Tompkins NH. Fever of unknown origin: a case of cardiac myxoma infected with Staphylococcus lugdunensis. South. Med. J. 103(7), 697–700 (2010).
  14. Patil R, Patil T, Hussain KM. Staphylococcus lugdunensis native tricuspid valve endocarditis: a case report and review of literature. J. Gen. Intern. Med. DOI: 10.1007/s11606-011-1718-5 (2011) (Epub ahead of print).
  15. Longauerova A. Coagulase negative staphylococci and their participation in pathogenesis of human infections. Bratisl. Lek. Listy 107(11–12), 448–452 (2006).
  16. Liu PY, Huang YF, Tang CW et al. Staphylococcus lugdunensis infective endocarditis: a literature review and analysis of risk factors. J. Microbiol. Immunol. Infect. 43(6), 478–484 (2010).
  17. Van Hoovels L, De Munter P, Colaert J et al. Three cases of destructive native valve endocarditis caused by Staphylococcus lugdunensis. Eur. J. Clin. Microbiol. Infect. Dis. 24(2), 149–152 (2005).
  18. De Hondt G, Ieven M, Vandermersch C, Colaert J. Destructive endocarditis caused by Staphylococcus lugdunensis. Case report and review of the literature. Acta. Clin. Belg. 52(1), 27–30 (1997).
  19. Koh TW, Brecker SJ, Layton CA. Successful treatment of Staphylococcus lugdunensis endocarditis complicated by multiple emboli: a case report and review of the literature. Int. J. Cardiol. 55(2), 193–197 (1996).
  20. Anguera I, Del Rio A, Miro JM et al. Staphylococcus lugdunensis infective endocarditis: description of 10 cases and analysis of native valve, prosthetic valve, and pacemaker lead endocarditis clinical profiles. Heart 91(2), e10 (2005).
  21. Baddour LM, Bettmann MA, Bolger AF et al. Nonvalvular cardiovascular device-related infections. Clin. Infect. Dis. 38(8), 1128–1130 (2004).
  22. Kamaraju S, Nelson K, Williams DN, Ayenew W, Modi KS. Staphylococcus lugdunensis pulmonary valve endocarditis in a patient on chronic hemodialysis. Am. J. Nephrol. 19(5), 605–608 (1999).
  23. Matthews PC, Missouris CG, Jordaan J, Lessing MP. Staphylococcus lugdunensis endocarditis following cardiac catheterisation. Int. J. Cardiol. 130(1), 87–88 (2008).
  24. Polenakovik H, Herchline T, Bacheller C, Bernstein J. Staphylococcus lugdunensis endocarditis after angiography. Mayo Clin. Proc. 75(6), 656–657 (2000).
  25. Fervenza FC, Contreras GE, Garratt KN, Steckelberg JM. Staphylococcus lugdunensis endocarditis: a complication of vasectomy? Mayo Clin. Proc. 74(12), 1227–1230 (1999).
  26. Patel R, Piper KE, Rouse MS, Uhl JR, Cockerill FR 3rd, Steckelberg JM. Frequency of isolation of Staphylococcus lugdunensis among staphylococcal isolates causing endocarditis: a 20-year experience. J. Clin. Microbiol. 38(11), 4262–4263 (2000).
  27. Kragsbjerg P, Bomfim-Loogna J, Tornqvist E, Soderquist B. Development of antimicrobial resistance in Staphylococcus lugdunensis during treatment-report of a case of bacterial arthritis, vertebral osteomyelitis and infective endocarditis. Clin. Microbiol. Infect. 6(9), 496–499 (2000).
  28. Karchmer AW, Longworth DL. Infections of intracardiac devices. Cardiol. Clin. 21(2), 253–271, vii (2003).
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