登革熱 (dengue )
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登革熱 (dengue )
• 又名骨痛病或天狗熱,為一種流行性熱病,主要分佈於熱帶、亞熱帶地區,溫帶亦常有發現。本病之病原為一種節肢動物傳染之 B 群濾過性病 (Group B Arbovirus) ,有四個明顯之血清型 (Dl , D2 , D3 , D4) ,主要由蚊蟲在人與人之間傳播,病媒蚊以斑蚊屬 (Aedes) 為主。在台灣此屬則有十種之多。
埃及斑蚊及白線斑蚊• 在台灣地區,媒介登革熟之病媒蚊主要為埃及斑蚊及白線
斑蚊,前者分佈於北緯 24“50‘ 以南之地區及澎湖,主要在嘉義縣布袋鎮以南,尤其是沿海地帶及大河流之流域;後者則在普遍發生,主要為 1,000 公尺以下地區。
• 埃及斑蚊之主要發生地為家屋內外盛水之各種容器,屋內貯存井水之水缸為最易發生之場所。此種蚊蟲之飛翔距離不大,至多為 25 公尺左右。白天在屋內或野外蔭暗處吸血。
• 白線斑蚊其幼蟲之發生場所主要是在防火用水甕、水桶,水槽,而附有蓋子之裝水容器內發生最多。其它尚有建築物內外之瓶類、空罐、水盤、墓地插花處,防空壕及避難所內之積水等亦會發生。此外,遠離住屋之樹穴,竹林中之竹筒及癈棄之輸胎等亦為主要發生場所。
• 二種斑蚊均為白天活動的種類,一般在上午九時及下午四時各有一活動高峰。
症狀• 初覺惡寒,身體疲勞倦怠,體溫急劇上升至 39-4
1℃ 。發熱時,前頭劇痛,眼睛充血,膝部及其它關節激痛,淋巴腫大,腰部及脊椎等處之筋肉同時疼痛,二、三日後,熱度下降,過二、三日而有第二次熱症出現。發病後二、三日同時有米粒大小之斑疹出現於顏面、耳及頸部,然後漸漸擴至手掌、足蹠、前胸等處。體溫下降後斑疹會消失,發疹時,全身感到搔癢異常。
• 登革熱之病毒在人體之潛伏期約 3-15 天,一般則為 5-6 天。
登革出血熱(dengue hemorrhagic fever, DHF)
• 本病盛行於夏季,患病後之死亡率甚低,且能獲得免痠。登革出血熱 (dengue hemorrhagic fever, DHF) 則可造成嚴重之死亡率,尤以 3-6歲之幼童。DHF 在菲律賓、泰國、越南、印尼、新加坡及印度等地均曾流行。在泰國, 1972年時有 23,000病例, 1975年時有 17,000 病例,死亡率達 7% 。
• 登革出血熱 , 一般相信係同時或連續感染一種以上之血清型病毒所引起之過敏反應之結果,目前,僅知與埃及斑蚊之傳播有關。
登革熱流行病歷史(一)• 1870年以來,台灣便有登革熱之記載,本地醫生常以“
PANSUA”( 斑痧,意即發疹之熱病 )稱之。• 約在 1902-1903年間,一度流行但範圍不大; 1915-1916年,此病復發流行,影響遍及全島,病例超過一百萬人;1922-1927年間,此病一度流行於南部地區及澎湖群島;1931-1932年,又有一次流行,亦以南部地區。 1942年時,由於菲律賓群島於該年三月及四月發生登革熱流行,正逢日軍攻打巴丹半島 (Bataan peninsula) ,因此,此病可能在當時隨日軍蔓延,由高雄開始,七月下旬已蔓延至台北州,尤以台北巿為甚;八月澎湖、台中州、新竹州、花蓮港廳;九月下旬,台東廳等處。當時日本總督府將九月廿八日至十月四日訂為「登革熱強調週間」,全島一起實施防治措施,透過大規模之衛生教育宣導,演講、標語及電影之宣傳。
登革熱流行病歷史(二)• 光復後,雖然沒有明顯之流行跡象,但是根據 Clarke 於 1966年在台南以血清法調查結果,推測該地區在五年之前可能曾有小規模之流行。民國 70年 7月時,屏東縣琉球鄉開始出現登革熱病例,自七月上旬開始病例增加,至八月底與九月上旬達最高峰。
登革熱流行病歷史(三)• 民國七十六年十月底,登革熱再度由屏東東港、
高雄市陸續發生,且有向北蔓延之趨勢,在經過約四十年之沈寂,登革熱仍然再度臨降本省。七十七年確定病例達 4389 人,爾後幾乎年年有病例發生。八十四年,台中東海大學及台北縣中和市同時發生本土性登革熱流行,也證明了白線斑蚊也是重要病媒。八十五年台北市六張黎亦發生局部流行,自此,全台灣均籠罩在登革熱之陰影下。
東海大學的登革熱• 一九九五年九月,東海大學忽然發生登革熱。第一
個病例是生物系林俊義老師,此後陸續有幾位老師、眷屬及學生均有類似症狀,亦一一採送衛生署預防醫學研究所檢驗。總計確定病例共十名,均為第二型病毒。其中教師四人 (男、女各二,中、外各二 ) ,眷屬二人 ( 均女性 ) ,學生二人 (男、女各一 ) 及校外人士二人 ( 均曾在校園工作 ) 。這些病例中,學生一人住女生宿舍,另一人住別墅區,其餘東海校園內之病例均在教職員宿舍區,且約在範圍 500 公尺內,證明有地緣關係。亦與白線斑蚊在戶外活動之特性相符。此與南部地區許多全家一起感染之情形不同,蓋南部之病媒埃及斑蚊,主要棲息於室內之故也。
• 傳染登革熱之病媒白線斑蚊,在本校為常見之蚊種,主要於白天活動,其幼蟲孳生於人工容器,此外,某些天然的孳生源如 : 樹洞、竹筒等亦可孳生。這些孳生源在東海校園,特別是教職員宿舍區最為常見。此蚊白日活動吸血,夜晚則通常停於樹叢棲息。每日活動高峰期為上五 9-10 時,下午 4-5 時,但並非絕對。日落後往往不活動,因此,補蚊燈對其並無功效。
• 卵浸水後,幼蟲孵化,約一週即可成蚊。若遇乾旱,蟲卵亦可耐乾燥六個月以上。
• 環保、衛生單位,上自中央大員,下至基層人員均到東海視察關心,各式媒體記者或報導,或專欄,甚至中廣及全國廣播亦有「叩應」節目捧場。
• 本次之登革熱流行有幾個特別意義 : 一、台中市首次流行;二、首次發現新的第二型病毒;三、與台北中和同時證明白線斑蚊亦可傳播登革熱;四、流行範圍最小,流行期間最短。
• 斑蚊幼蟲分佈之調查,以縣市為單位,每月作定期調查,另外,國際港區、機場則需由衛生署各檢疫所加強辦理。幼蟲之調查,以下述計算方法估計其分佈密度。l. 家屋指數 (House Index , HI):指調查之家屋內或附近,至少有一容器內有斑蚊幼蟲者之家屋數佔全調 查之百分率。
2. 容器指數 (Container Index , CI ):指內有斑蚊幼蟲孳生之容器數與全部調查容器總數之百分比。3. 布氏指數 (Breteau Index , BI):指每 100 間住屋所含有幼蟲孳生之容器總數。4. 幼蟲密度區分 (Density figure):據WHO 之標準,以前述三種指數,區分為九個等級, 以判斷幼蟲之密度。二以下才較安全。
Three Lines of Defense
• Barriers at body surfaces
• Nonspecific responses
• Immune responses
Barriers at Body Surface
• Intact skin and mucous membranes
• Lysozyme 分解酶
• Normal bacterial flora
• Flushing effect and low pH of urine
Nonspecific Responses
• Lymph nodes trap and kill
pathogens
• Natural killer cells attack a
range of targets
• Inflammation 發炎
Acute Inflammation 發炎反應
• Nonspecific response to foreign invasion,
tissue damage, or both
• Destroys invaders, removes debris, and
prepares area for healing
• Characterized by redness 紅 , swelling
腫 , warmth 熱 , and pain 痛
Inflammation
• Mast cells release histamine• Capillaries dilate and leak• Complement proteins attack bacteria• White cells attack invaders and clean up
Features of Immune System
• Immunological specificity(專一性)– B and T cells zero in (瞄準) on certain
kinds of pathogens; response is pathogen specific
• Immunological memory(記憶性)– Immune system recognizes and reacts
swiftly to a pathogen it has “seen”
Key Component of Immune Response
• MHC markers(分子標記)• Antigen-presenting cells• Helper T cells(幫助型 T細胞)
• Effector cytoxic T cells(細胞殺手)
• Natural killer cells(自然殺手)• B cells
Overview of Interactions
Naive helper T cell
Naive B cell
Antigen-presenting cell
Activated helper T cell
Effector B cell
Naive cytotoxic T cell
Effector cytotoxic T cell
Antibody - mediated response
Cell - mediated response
Immunological Memory
• Memory cells specific for an antigen are quickly activated to divide upon subsequent exposure to that antigen
effector cells memory cells
naive T or B cell
effector cells memory cells
Antibody-Mediated Response抗體免疫反應
• Carried out by B cells
• Targets are intracellular pathogens and
toxins
• Antibodies bind to target and mark it for
destruction by phagocytes吞食 and
complement補體
Antibody Structure
• Antibody consists of four polypeptide chains
• Certain parts of each chain are variable; impart antigen specificity
variable regionof heavy chain
antigen-binding site antigen-binding site
hinge region(flexible)
variable region of light chain
constant region of light chain
Antibody- Mediated Response
Naive B cell
Antigen-presentingB cell
Helper T cell
Interleukins
Memory B cell
Effector B cellsecretes antibodies
• Virgin B cell becomes antigen-presenting B cell
• Helper T cell binds to antigen-MHC complex on the B cell
• Interleukins stimulate B cell division and differentiation
• Effector cells secrete antibodies
5 Classes of Immunoglobulins
• IgM are secreted first; trigger complement reactions, agglutination
• IgD function is not understood
• IgG activates complement; can cross placenta
• IgA associates with mucus-coated surfaces
• IgE triggers inflammation
Cell-Mediated Response細胞媒介
One macrophage
Another macrophage
interleukins
interleukins Helper T cell
Cytotoxic T cell
Infected body cell
• Carried out by T cells
• Stimulated by antigen-
presenting macrophages
• Main target is antigen-
presenting body cells
(cells with intracellular
pathogens) or tumor cells
B and T Cell Interactions
Types of T Cells
• Helper T (TH) cells release cytokines to stimulate B cells to make antibodies and present antigens
• Cytotoxic T cells (Tc) kill cells by poking holes in membrane or triggering cell suicide (apoptosis)
疾 病 名 稱 統計數字紅斑性狼瘡 22
B型肝炎 20
糖尿病 17
帕金森氏症 16
唐氏症(喜憨兒) 12
地中海行貧血 11
蜂窩性組織炎 10
愛滋病 7
氣喘 7
腸胃炎 6
帶狀泡疹 5
腎結石 5
老人癡呆症 5
骨癌 5
類風濕關節炎 5
心臟病 5
鼻竇炎 5
Dr. Carlo Urbani• Doctors Without Bord
ers working in Hanoi, Vietnam
• The first people alters WHO about the dangers of the SARS (severe acute respiratory syndrome; atypical pneumonia) epidemic
• 10% mortality
The SARS coronavirus
Primary and Secondary Immune Responses
Vaccines
• Antigen that stimulates B cells to make memory cells, but doesn’t actually make us ill– Heat-killed polio virus 脊髓灰質炎病毒 has co
at proteins to stimulate B cells– Attenuated viruses are weakened, don’t make
us sick, but stimulate B cells
Monoclonal Antibodies單株抗體
• Manufactured antibodies against tumor-
specific antigens
• First created by fusing antigen-producing
B cells from mice with cells from B cell
tumors
• Now made in genetically engineered cells
Allergies
• Triggers inflammatory response
• IgE antibodies stimulate mast cells to release histamine when they recognize antigen
Autoimmune Disorders1. Immune system makes
antibodies against self
antigens
2. Grave’s disease 甲狀腺素過多
• Myasthenia gravis 肌肉無力• Rheumatoid arthritis 類風濕
性關節炎
AIDS
• Combination of disorders that follows
infection with HIV
• Includes
– Yeast (Candida) infections
–Pneumocystis pneumonia
– Karposi’s sarcoma
HIV Replication (1)
• RNA retrovirus
• A protein (gp120) at virus surface binds to host cells with CD4 receptors
• These receptors occur on helper T cells
• Once bound, RNA and viral enzymes enter the host cell
HIV Replication (2)
• Viral RNA is reverse transcribed to DNA
• HIV DNA is called provirus; it inserts into
host DNA
• The host cell makes copies of viral DNA
and viral proteins that assemble to form
new virus particles
• The loss of helper T cells– Results from infection by the human
immunodeficiency virus (HIV)
1µmFigure 43.22
T Cell Decline
• Release of new viral particles kills the host T cell
• The body is constantly making new T cells, but cannot outpace the rate of destruction
• As infection proceeds, T cell numbers inevitably decline
Effect of T Cell Decline
• CD4 helper T cells play a vital role in immune function
• They are required for both cell-mediated and antibody-mediated immunity
• Infected individual becomes vulnerable to other infections, which eventually result in death
Years after infection
Hel
per
T-c
ell c
on
cen
trat
ion
in b
loo
d (
cells
/mm
3 ) Initial infection Few symptoms
Obvious decrease in immune function,characteristic diseases such as yeast infections
AIDS:Loss of cellular
immunity
Antibody concentration
HIV virusconcentration
T-cell concentration
Transmission of HIV
• HIV does not live long outside human
body
• Most often spread by exchange of bodily
fluids with an infected person
• In the U.S., anal intercourse and needle
sharing are main modes of transmission
Transmission of HIV
• Less commonly transmitted by vaginal intercourse and oral sex
• Can travel from mothers to offspring during pregnancy, birth, or breast-feeding
• Not known to be transmitted by food, air, water, casual contact, or insect bites
Treatment
• No cure
• Once HIV genes are incorporated, no way to get them out
• AZT, and other drugs slow the course of the disease and increase life span
• Researchers continue to develop drugs and to work toward an AIDS vaccine
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