瘧疾

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瘧疾
分類系統及外部資源

人體血液中的惡性瘧原蟲環狀體和配子母細胞
ICD-10 B50
ICD-9 084
OMIM 248310
DiseasesDB 7728
MedlinePlus 000621
eMedicine med/1385 emerg/305 ped/1357
MeSH C03.752.250.552


瘧疾英語Malaria)是一種蚊媒病,由寄生性的原生生物界(一種單細胞 微生物瘧原蟲[1]引起,人類及其他動物的全球性急性寄生蟲傳染病。瘧疾引起的典型症狀有發燒倦怠不適英語Malaise嘔吐以及 頭痛。在嚴重的病例中會引起黃疸癲癇發作英語Epileptic_seizure昏迷死亡[2]。這些症狀通常在被蚊子叮咬後十到十五天內開始出現,沒有受到適當治療的病人(但症狀緩解)可能於數個月後會再次出現這些症狀[1]。而在瘧疾倖存者中,再次感染通常引起的症狀通常較輕微。如果沒有持續暴露在瘧疾環境中,這種少量的抵抗力英語Immunity會在數月至數年間消失[3]

一般來說,瘧疾是透過受感染的雌性瘧蚊叮咬來傳播的。寄生蟲瘧原蟲會透過瘧蚊叮咬從蚊子的唾液中傳入至人類的血液[1],接著瘧原蟲會隨血液移動至肝臟,在肝臟細胞中發育成熟及繁殖。瘧原蟲屬中有五種是可藉由感染人類進行散播[2],多數死亡案例由惡性瘧P. falciparum)、間日瘧英語Plasmodium vivaxP. vivax)及卵形瘧英語Plasmodium_ovaleP. ovale)所造成,而三日瘧英語Plasmodium_malariaeP. malariae)則產生較輕微的瘧疾症狀[1][2]。另外,猴瘧蟲英語Plasmodium_knowlesiP. knowlesi,又稱諾氏瘧蟲)較少在人類身上造成疾病[1]。診斷瘧疾主要透過顯微鏡檢驗血液抹片英語Blood_film或是加上快速瘧疾抗原診斷測試英語Malaria_antigen_detection_tests[2]。近年發展聚合酶鏈式反應來偵測瘧原蟲的DNA,但目前因為成本及複雜性,而沒有廣泛地應用在瘧疾盛行地區[4]

避免瘧蚊叮咬能夠降低感染瘧疾的風險,透過使用蚊帳以及驅蟲劑 或其他控制蚊蟲生長英語Mosquito contro的方法,像是噴灑殺蟲劑以及清除積水[2]。前往瘧疾盛行區的旅客可以使用幾種藥物來預防瘧疾英語Malaria_prophylaxis,而瘧疾好發地區的嬰兒及過了懷孕初期第一妊娠期孕婦也建議適量使用周效磺胺/比利美胺英語Sulfadoxine/pyrimethamine。20世紀中期以後也出現了一些新的藥物,中國科學家研製的 青蒿素 有很好的抗瘧疾效果。儘管有所需求,但瘧疾尚無疫苗,目前相關研究正在進行中[1]。瘧疾的建議治療是併用青蒿素及另一種抗瘧疾藥物[1][2],包括甲氟喹英語Mefloquine苯芴醇英語Lumefantrine周效磺胺/比利美胺英語Sulfadoxine/pyrimethamine[5]。如果青蒿素無法取得,則可使用奎寧加上去氧羥四環素[5]。由於擔心抗藥性的增加,建議在瘧疾盛行地區儘可能確診為瘧疾後再開始治療。目前瘧疾逐漸對於幾種藥物發展出抗藥性,例如:具有氯化奎寧英語chloroquine(氯喹)抗藥性的惡性瘧已經散布到多數的瘧疾地區,另外青蒿素抗藥性問題在部分東南亞地區日益嚴重[1]

瘧疾普遍存在於熱帶亞熱帶地區,位於赤道周圍的寬大帶狀區域[2]。主要流行地區是 非洲中部南亞東南亞南美北部的熱帶地區,這其中又以 非洲 的疫情最甚。就中國而言,瘧疾主要的流行地帶為華中華南的叢林多山地區,但疫情遠較非洲為輕。世界衛生組織預估2012年,將會有二億七百萬例瘧疾案例,同時也預估該年因患瘧疾死亡人數介於四十七萬三千人至七十八萬九千人之間,多數為非洲的孩童[1]。瘧疾與貧困息息相關,造成經濟發展相當大的負面影響[6][7]。非洲預估每年損失一百二十億美元,因為健康照護的花費增加,勞動力減少,以及瘧疾對觀光旅遊業造成的影響[8]。根據世界衛生組織的統計,2013年全世界的瘧疾病例共有1.98億例。[9][10]造成584,000至855,000人死亡,當中有90%是在非洲發生[11][9]

主要病徵[編輯]

瘧疾主要症狀[12]

感染瘧原蟲後8-25天會發病[12],但如果有先服用預防性藥物的人可能會在之後才發生[4]。病人可能會有如下流感樣症狀[13]:忽冷忽熱、頭痛發熱顫栗關節痛嘔吐溶血反應、瘧原性貧血、黃疸血尿視網膜損害、抽搐[14]。最典型的症狀為忽冷忽熱循環——先發冷、打冷顫,然後發熱、出汗。這是因為瘧原蟲生活周期具有明顯的生理節奏(circadian rhythm),如間日瘧原蟲(Plasmodium vivax)導致的瘧疾發熱周期為48小時,因而病患的發燒症狀也呈現周期性。如果瘧原蟲侵入腦部血管,則會導致最為嚴重的腦部瘧疾,這通常會造成病者昏迷。由於早期跡象與流行性感冒有相似之處,許多對該疾病不熟悉的外來旅遊者容易將瘧疾誤認為感冒,從而因為沒有得到及時的藥物治療而使得病情惡化。

按照瘧疾病徵的嚴重程度不同,瘧疾可以分為非重症瘧疾(uncomplicated malaria)和重症瘧疾(complicated / severe malaria),能有效治療這兩類瘧疾的藥物不太相同。重症瘧疾通常是由惡性瘧原蟲所導致,因此又稱為惡性瘧疾,通常在感染後9至30天發病[13],得到腦瘧疾的患者常產生神經系統疾病,包括姿態異常英語abnormal posturing眼球震顫共軛凝視麻痺英語conjugate gaze palsy(眼球無法朝同一方向轉動)、角弓反張抽搐,或昏迷[13]


併發症[編輯]

瘧疾常常導致一些嚴重的併發症。其中一個症狀是呼吸困難,在惡性瘧疾的患者當中,多達25%的成人和40%的幼童會有此症狀。可能病因為代謝性酸中毒造成的呼吸代償、非心源性肺水腫、併發肺炎,和貧血

如果瘧疾患者同時感染上HIV,死亡風險則會提高。[15]腎臟損傷會導致黑水熱英語blackwater fever,原因是瘧原蟲會造成溶血,使血紅素進入尿液當中,造成尿液呈暗紅色至黑色[13]

惡性瘧疾會導致腦瘧疾,會導致視網膜白化,此為臨床上重要判斷依據。[16]其他症狀包括脾腫大、嚴重頭痛、肝腫大低血糖,以及腎衰竭[13]。腎衰竭則可能導致血紅蛋白尿、自發性出血和凝血功能障礙。[17] 得到瘧疾的孕婦英語Pregnancy-associated malaria可能會造成死胎流產,胎兒體重過輕[18]。特別是在惡性瘧疾,和部分間日瘧原蟲瘧疾上[19]

病原[編輯]

瘧疾疫區,2006年。[20]
    氯喹及多重耐藥性瘧疾高發區     氯喹抗藥性瘧疾發生區     無抗藥性瘧疾發生區     無瘧疾

瘧疾的致病源是瘧原蟲(瘧原蟲屬,Plasmodium spp.),這是一類單細胞真核生物,屬於細胞內寄生蟲,它們以瘧蚊蚊子的其中一個屬,瘧蚊屬的部分種類)作為傳病媒介,通過雌蚊叮咬吸血來傳播病原體。

瘧原蟲屬生物是頂復合器門(Apicomplexa)的原生生物,這一門的生物幾乎都是寄生蟲。大部分脊椎動物都可以作為瘧原蟲的主要宿主,比如齧齒動物,蝙蝠,蜥蜴,鳥等等。這也使得生物學家可以通過建立生物模型(比方說,用老鼠做瘧疾病理研究)的方式來研究人類瘧疾。

只有四種瘧原蟲能夠感染人類[21][22],包括:

  • 惡性瘧原蟲Plasmodium falciparum):世界最主要的感染性瘧原蟲(75%),亦是造成患者死亡率最高的瘧原蟲。[4]


非洲最主要的患者為惡性瘧原蟲,但非洲之外的國家間日瘧原蟲的比例則較高。[23]。雖然曾經有文獻指出人類可能會被一些人猿類傳染瘧疾,但除了諾氏瘧原蟲[22]之外,其餘都沒有什麼公共衛生重要性。[24]


中國以間日瘧與惡性瘧最為常見,三日瘧少見,卵形瘧極少發生。惡性瘧主要發生在西南與海南。間日瘧發生在東北、華北、西北。

全球暖化增加了瘧蚊的活動範圍,但對於瘧疾的傳播影響,至今仍不明確[25][26]

生活史[編輯]

瘧原蟲的生活史。首先,蚊子藉由叮咬造成瘧原蟲的子孢子(sporozoites)進入體內,隨血液運移到肝臟,侵入肝細胞。子孢子在肝細胞內部吸收營養,長大成熟後分裂生殖形成很多小的裂殖子(merozoites)。裂殖子成熟後,破壞肝細胞進入體液、血液中,一部分再侵入肝細胞重複上述循環,一部分侵入紅細胞,成為像個戒指的環狀體(ring forms)。環狀體進一步長大,向四周伸出偽足,稱為阿米巴樣體或大滋養體(trophozoites)。大滋養體進一步發育形成裂殖體(schizonts),裂殖體成熟後放出很多裂殖子,破壞紅細胞後進入血液,繼續感染其他紅細胞。同時瘧原蟲也會進行有性生殖,此時患者可能又被瘧蚊叮咬,攜入其他健康者身上,延續下一個生活史。

瘧原蟲的生命周期很複雜。在瘧原蟲的生活始中,雌性瘧蚊(最終宿主)扮演的是一個媒介的角色。雌按蚊叮咬人時,唾液中的瘧原蟲的長梭形的子孢子(sporozoite)進入人體內,隨血液運移到肝臟,侵入肝細胞。子孢子在肝細胞內部吸收營養,長大成熟後分裂生殖形成很多小的裂殖子(merozoites)。裂殖子成熟後,破壞肝細胞進入體液、血液中,一部分再侵入肝細胞重複上述循環,一部分侵入紅細胞

在紅細胞內,裂殖子逐漸吸收血紅蛋白作為營養長大,成為像個戒指的環狀體。環狀體進一步長大,向四周伸出偽足,稱為阿米巴樣體或大滋養體(trophozoites)。大滋養體進一步發育形成裂殖體(schizonts),裂殖體成熟後放出很多裂殖子,破壞紅細胞後進入血液,繼續感染其他紅細胞。由於人體內的瘧原蟲的裂殖子同時破壞大量紅細胞進入血液,人體會產生瘧疾的典型症狀,如發冷發熱。如果宿主環境不利,一些裂殖子進入紅細胞後可形成大、小配子母細胞。這些配子母細胞在人體中不再進一步發育,如果不能被蚊子吸血時吸走,配子母細胞在人體內可存活60天。

當蚊子吸取受感染人體的血液後,雄、雌配子母細胞(gametocytes)進入蚊子中腸內,進入有性繁殖世代。雌雄配子母細胞會在蚊子的中腸成熟並結合為卵動子英語ookinete,並在腸壁下形成卵囊(oocyte)。卵囊中瘧原蟲進行無性繁殖,最終形成子孢子。成熟後,卵囊破裂,子孢子進入蚊子體腔,穿透各種組織,進入蚊子唾液腺。蚊子唾液腺中的子孢子可達20萬,子孢子在蚊子體內存活70天,準備感染新的脊椎動物宿主[27][28]

除了蚊蟲感染之外,瘧原蟲也有可能藉由輸血感染,但此情況相當罕見。[29]2006年,台北榮民總醫院發生了一起嚴重的院內感染案例,造成4名病患感染惡性瘧疾死亡,即因輸血方式不當。[30]

瘧疾的復發[編輯]

瘧疾的患者可能會在一段無症狀期後復發,此種復發現象可因原因不同而分為「再發作英語recrudescence」(recrudescence)、「復發英語relapse」(relapse),和「重複感染」(reinfection)三種。

再發作(recrudescence)是指說病人體在經歷無症狀期後又再次復發瘧疾。無症狀期中,體內雖仍有瘧原蟲存在,但卻沒有任何症狀發生,為治療不完全所致。[31]


復發(relapse)的意思是說血液中的瘧原蟲雖染已經清除乾淨,但肝細胞中仍有瘧原蟲休眠體(hypnozoites)存在。此類的病人無症狀期約有8-24週左右,通常是在間日瘧原蟲和卵形瘧原蟲感染上見到。[4]溫帶地區的間日瘧休眠體會有「越冬英語overwintering」的現象,意即患者在被蚊子叮咬後到隔年年初才復發。[32]


重複感染(reinfection)指的是患者體內的病原體已經清除完畢後,又在遭受新的病原體感染,臨床上很難與再發作區分。[33]但通常如果痊癒後的患者仍時常遭受感染,身體會產生一定免疫力,症狀不會如初次感染那樣嚴重。

病理生理學[編輯]

因母體染瘧疾而造成的死胎胎盤H&E染色。無核的反紅色圓形顆粒為紅血球,而紅血球中的藍色或黑色構造則為瘧原蟲所致。

瘧疾感染有兩分兩階段:

  1. 紅血球外發育期(exoerythrocytic phase):病原體在肝臟內發育。
  2. 紅血球內發育期(erythrocytic phase):病原體在紅血球內發育。

當人被受感染的瘧蚊叮咬,瘧原蟲子孢子會隨蚊子的唾腺進入血流,並流動至肝臟,感染肝細胞,以無性方式大量增殖。這段時間沒有症狀,為期約8至30天。[34]此時的病原體受到肝細胞膜保護,難以被免疫系統偵測[35]。 經過一段休眠期之後,瘧原蟲會產生數以千計的裂殖子,他們會打破肝細胞,逸入血漿中。這些裂殖子會感染紅血球,進入紅血球內發育期[34]

在紅血球內,病原體大量無性繁殖,並週期性地爆破紅血球,並入侵更多紅血球。也由於此週期性,造成病患會出現忽冷忽熱的症狀。[34]


治療[編輯]

治療瘧疾的藥物稱為抗瘧藥,會依瘧疾的種類及嚴重程度選用不同的藥物。和解熱劑英語Antipyretic一起服用的效果還不是很明確[77]

抗瘧疾最著名的藥物是奎寧。口服和肌肉注射都有效。1969年-1972年間,屠呦呦領導的523課題組發現並從黃花蒿中提取了青蒿素[78],是由菊科植物黃花蒿[79]所提煉出來的倍半萜內酯化合物,是治療惡性瘧原蟲所引發的瘧疾的特效藥。

非重症的瘧疾可以用口服藥物治療,最有效的療法是青蒿素配合其他抗瘧藥一起服用(稱為青蒿素聯合療法,簡稱ACT),可以減輕對單一藥物的抗藥性[80]。其他的抗瘧藥包括阿莫地喹英語amodiaquine本芴醇英語lumefantrine、甲氟喹(mefloquine)或磺胺多辛/乙胺嘧啶英語sulfadoxine/pyrimethamine[81]。另一建議的聯合療法是雙氫青蒿素喹哌英語piperaquine[82][83]。若用在非重症瘧疾,青蒿素聯合療法有效的比率約有90%[57] 。若是治療孕婦的瘧疾,世界衛生組織建議在懷孕初期(前三個月)用奎寧克林黴素,在中後期則用青蒿素聯合療法[84]。在2000年左右,在東南亞已經出現對青蒿素有抗藥性的瘧疾[85][86]

若是感染間日瘧、卵形瘧,或三日瘧,則通常不住院治療。間日瘧的治療通常需要同時清除血液和肝臟中的病原體,血液通常使用氯喹或ACT,肝臟則以伯氨喹英語primaquine治療。[87]

重症瘧疾則建議使用靜脈注射抗瘧藥。不論是成人或孩童,重症瘧疾的優先使用藥物為青蒿琥酯[88]。治療方式包括支持療法(尤其是於重症加護病房),包含控制高燒、低血糖,和低血鉀[89]

抗藥性[編輯]

預測[編輯]

歷史[編輯]

社會與文化[編輯]

研究[編輯]

疫苗[編輯]

藥物治療[編輯]


其他[編輯]

其他動物[編輯]


預防與治療[編輯]

人體免疫反應[編輯]

瘧原蟲生活史

人體對瘧原蟲有一定的免疫反應。先天免疫系統可以發現病原體和受感染的細胞並加以殺死。人體還可以產生抗體來對抗瘧原蟲和受感染細胞,這些免疫反應是造成病人病理反應的部分原因。實際上,人體對瘧疾的抵抗能力是有一定效果的,瘧疾死者多為10歲以下免疫功能並不完善的兒童。然而,瘧原蟲具有一套非常複雜的遺傳系統,在宿主的免疫反應壓力下,瘧原蟲可以通過基因重組的方式迅速改變它們及所寄生細胞的表面抗原,從而使得寄生蟲在血液內不容易被根除。許多病人在病理特徵減輕後進入寄生蟲血症(Parasitaemia)階段,此時免疫系統很難完全消滅瘧原蟲,病情進入慢性期。

疫苗[編輯]

研究瘧疾疫苗的難度很高,現時有一些試驗中的疫苗。

傳播途徑[編輯]

一種甘比亞按蚊,是瘧原蟲的最終宿主

雌按蚊叮人傳播瘧疾,但並非所有蚊都能傳播瘧疾,大部分蚊抗瘧原蟲,只有按蚊屬(Anopheles spp.)下的部分種類,易受瘧原蟲。

預防方法[編輯]

填平濕地及破壞原始森林是一種預防方法,但是此種破壞生態的方法會造成更多問題,在這些地區的瘧蚊(按蚊)是難以根治的,人類避免受瘧疾感染,主要是避免受蚊子的叮咬。

  • 避免在原始森林和河澗逗留。
  • 使用DDT等殺蟲劑,但是要小心破壞生態及蚊蟲抗藥性等問題。
  • 到瘧疾肆虐地區之前應該先做好防疫措施,例如請醫師開立奎寧類藥物服用預防。
  • 若需要到郊外或森林,盡量避免在晨早或黃昏時按蚊活躍期間。
  • 穿著淺色長袖衣服、長褲、帽子,減少皮膚外露。
  • 使用蚊帳、蚊香等滅蚊措施;浸泡過殺蟲劑的蚊帳效果更好。
  • 使用含DEET水劑的防蚊液,塗在外露皮膚上,出汗後需要再次塗上。
  • 在滅絕按蚊的幼蟲孑孓方面,可以將河道的雜草清除,和將部份河道的障礙物如石頭移走,令河道的流量加快。
  • 在室內可將滅蚊劑噴在房間的牆壁。因為蚊習性於叮人血後依附在牆上休息消化,殘留在牆壁上的滅蚊劑可以殺掉蚊子。
  • 若到外地旅遊,應詳盡紀錄所到地方,以防當自己懷疑染疾時可向醫護人員提供可靠資料。
  • 東南亞雖然是仍然存在瘧疾的地理區域,但疫情主要集中在中南半島內陸山區和馬來群島偏遠島嶼,新加坡曼谷吉隆坡清邁等大都市以及巴厘島普吉島吳哥窟等熱門旅遊景點並無瘧疾疫情,若不是進行叢林探險的背包客則不必在出發前接種疫苗。
  • 南亞次大陸撒哈拉以南的非洲大陸為最易感染瘧疾的地理區域,即便是前往孟買拉各斯金夏沙等大城市也有必要在出發前接種瘧疾疫苗。
  • 南美洲的瘧疾疫情主要集中在緯度和海拔較低的蓋亞那蘇利南和巴西東北部,庫斯科馬丘比丘里約熱內盧科隆群島等熱門旅遊景點均無瘧疾疫情,無須在行前接種疫苗。
  • 多米尼加共和國的貧民區及海地共和國外,其餘的加勒比島國均無瘧疾疫情。

參見[編輯]

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