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出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2016/03/18 22:16:03」(JST)
Wuchereria bancrofti | |
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Microfilar of W. bancrofti, from a patient seen in Haiti - the thick blood smears are stained with hematoxylin | |
Scientific classification | |
Kingdom: | Animalia |
Phylum: | Nematoda |
Class: | Secernentea |
Order: | Spirurida |
Suborder: | Spirurina |
Family: | Onchocercidae |
Genus: | Wuchereria |
Species: | W. bancrofti |
Binomial name | |
Wuchereria bancrofti (Cobbold, 1877) Seurat, 1921 |
Wuchereria bancrofti is a human parasitic roundworm that is the major cause of lymphatic filariasis. It is one of the three parasitic worms, besides Brugia malayi and B. timori, that infect lymphatic system to cause lymphatic filariasis. These filarial worms are spread by a mosquito vector. W. bancrofti is the most prevalent among the three and affects over 120 million people, primarily in Central Africa and the Nile delta, South and Central America, and the tropical regions of Asia including southern China and the Pacific.[1] If the infection is left untreated, it can develop into a chronic disease called elephantiasis.[2] In rare conditions it also causes tropical eosinophilia, an asthmatic disease. Limited treatment modalities exist and no vaccines have been developed.
The effects of W. bancrofti were documented early in ancient text. Ancient Greek and Roman writers noted the similarities between the enlarged limbs and cracked skin of infected individuals to that of elephants. Since then, this condition has been commonly known as elephantiasis. However, this is a misnomer, since elephantiasis literally translates to “a disease caused by elephants”.
W. bancrofti was named after physician Otto Wucherer and parasitologist Joseph Bancroft, both of whom extensively studied filarial infections.
W. bancrofti is speculated to have been brought to the New World by the slave trade.[3] Once it was introduced to the New World, this filarial worm disease persisted throughout the areas surrounding Charleston, South Carolina until its sudden disappearance in the 1920s.[4]
As dioecious worm, W. bancrofti exhibits sexual dimorphism. The adult worm is long, cylindrical, slender, and smooth with rounded ends. It is white in colour and almost transparent. The body is quite delicate making it difficult to remove from tissues. It has a short cephalic or head region connected to the main body by a short neck which appears as a constriction. There are dark spots which are dispersed nuclei throughout the body cavity, with no nuclei at the tail tip. Male and female can be differentiated by size and structure of tail tip. The male worm is smaller, 40 millimetres (1.6 in) long and 100 micrometres (0.0039 in) wide, and features a ventrally curved tail. The tip of the tail has 15 pairs of minute caudal papillae, the sensory organs. The anal region is an elaborate structure consisting of 12 pairs of papillae, of which 8 are in front and 4 are behind the anus. In contrast, the female is 60 millimetres (2.4 in) to 100 millimetres (3.9 in) long and 300 micrometres (0.012 in) wide, nearly three times larger in diameter than the male. Its tail gradually tapers and rounded at the tip. There are no additional sensory structures. Its vulva lies towards the anterior region, about 0.25 mm from the head. Adult male and female are most often coiled together and are difficult to separate. Females are ovoviviparous and can produce thousands of juveniles known as microfilariae.[5]
The microfilaria is a miniature adult and retains the egg membrane as a sheath and are often considered advanced embryos. It measures 280 μm long and 25 μm wide. It is quite structureless in living condition. However by histological staining it is shown to have primitive gut, nerve ring and muscles.[6]
W. bancrofti carry out their life cycle in two hosts. Human beings serve as the definitive host and mosquitoes as their intermediate hosts. The adult parasites reside in the lymphatics of the human host. They are found mostly in the afferent lymphatic channels of the lymph glands in the lower part of the body. The first-stage larvae, known as microfilariae, are present in the circulation. The microfilariae have a membrane "sheath". This sheath, along with the area in which the worms reside, makes identification of the species of microfilariae in humans easier to determine. The microfilariae are found mainly in the peripheral blood and can be found at peak amounts from 10 p.m. to 4 a.m. They migrate between the deep and the peripheral circulation exhibiting unique diurnal periodicity. During the day, they are present in the deep veins, and during the night, they migrate to the peripheral circulation. The cause of this periodicity remains unknown, but the advantages of the microfilariae being in the peripheral blood during these hours may ensure the vector, the nighttime mosquito, will have a higher chance of transmitting them elsewhere. Physiological changes also are associated with sleeping, such as lowered body temperature, oxygen tension and adrenal activity, and an increased carbon dioxide tension, among other physical alterations, any of which could be the signals for the rhythmic behavior of microfilarial parasites. If the hosts sleep by day and are awake at night, their periodicity is reversed. In the South Pacific, where W. bancrofti shows diurnal periodicity, it is known as periodic.
The microfilariae are transferred into a vector, which are most commonly mosquito species of the genera Culex, Anopheles, Mansonia, and Aedes. Inside the mosquito, the microfilariae mature into motile larvae called juveniles. When the infected mosquito has its next blood meal, W. bancrofti is egested via the mosquito’s proboscis into the blood stream of the new human host. The larvae move through the lymphatic system to regional lymph nodes, predominantly in the legs and genital area. The larvae develop into adult worms over the course of a year, and reach sexual maturity in the afferent lymphatic vessels. After mating, the adult female worm can produce thousands of microfilariae that migrate into the bloodstream. A mosquito vector can bite the infected human host, ingest the microfilariae, and thus repeat the life cycle.[6][7][8]
W. bancrofti is responsible for 90% of lymphatic filariasis. Recently, 120 million worldwide cases of lymphatic filariasis were estimated. W. bancrofti largely affects areas across the broad equatorial belt (Africa, the Nile Delta, Turkey, India, the East Indies, Southeast Asia, Philippines, Oceanic Islands, and parts of South America.)
The mosquito vectors of W. bancrofti have a preference for human blood; humans are apparently the only animals naturally infected with W. bancrofti. There is no reservoir host,[9] and the disease could therefore potentially be eradicated.
The pathogenesis of W. bancrofti infection is dependent on the immune system and inflammatory responses of the host. After infection, the worms will mature within 6–8 months, male and female worms will mate and then release the microfilariae. These microfilariae can be released for up to ten years.
Wuchereria bancrofti | |
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Classification and external resources | |
Specialty | Infectious disease |
ICD-10 | B74.0 |
ICD-9-CM | 125.0 |
DiseasesDB | 29234 |
[edit on Wikidata]
|
A blood smear is a simple and fairly accurate diagnostic tool, provided the blood sample is taken during the period in the day when the juveniles are in the peripheral circulation.[10] Technicians analyzing the blood smear must be able to distinguish between W. bancrofti and other parasites potentially present.
A polymerase chain reaction test can also be performed to detect a minute fraction, as little as 1 pg, of filarial DNA.[11]
Some infected people do not have microfilariae in their blood. As a result, tests aimed to detect antigens from adult worms can be used.
Ultrasonography can also be used to detect the movements and noises caused by the movement of adult worms.[12]
Dead, calcified worms can be detected by X-ray examinations.
The severe symptoms caused by the parasite can be avoided by cleansing the skin, surgery, or the use of therapeutic drugs, such as diethylcarbamazine (DEC), ivermectin, or albendazole. The drug of choice, however, is DEC, which can eliminate the microfilariae from the blood and also kill the adult worms with a dosage of 6 mg/kg semiannually or annually.[13] A polytherapy treatment that includes ivermectin with DEC or albendazole is more effective than each drug alone.[14] Protection is similar to that of other mosquito-spread illnesses; one can use barriers both physical (a mosquito net), chemical (insect repellent), or mass chemotherapy as a method to control the spread of the disease.
Mass chemotherapy should cover the entire endemic area at the same time. This will significantly decrease the overall microfilarial titer in blood in mass, hence decreasing the transmission through mosquitoes during their subsequent bites.
Antibiotic active against the Wolbachia symbionts of the worm have been experimented with as treatment.[15]
Prevention focuses on protecting against mosquito bites in endemic regions. Insect repellents and mosquito nets are useful to protect against mosquito bites. Public education efforts must also be made within the endemic areas of the world to successfully lower the prevalence of W. bancrofti infections.
The WHO is coordinating an effort to eradicate filarisis. The mainstay of this programme is the mass use of antifilarial drugs on a regular basis for at least five years.
In April 2011, Sri Lanka was certified by the WHO as having eradicated this disease.
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リンク元 | 「蠕虫」「糸状虫症」「バンクロフト糸状虫症」「W. bancrofti」 |
関連記事 | 「Wuchereria」 |
蠕虫類 | 病原体名 | 病名 | 感染経路 | 寄生部位 | 症状 | 診断 | 治療 | |
線虫類 | Ancylostoma duodenale | ズビニ鉤虫 | 鈎虫症/十二指腸虫症 | F型幼虫経口感染、経皮 | 空腸上部 | 皮膚炎、若菜病、貧血 | 飽和食塩水浮遊法、遠心沈降法 | pyrantel pamoate、鉄剤 |
Necator americanus | アメリカ鉤虫 | |||||||
Strongyloides stercoralis | 糞線虫 | 糞線虫症 | F型幼虫経皮感染 | 小腸上部 | Loffler症候群 | 糞便塗沫、普通寒天平板培養による R型、F型幼虫の検出 |
thiabendazole, ivermectin | |
Enterobius vermicularis | 蟯虫 | 蟯虫症 | 虫卵経口感染 | 盲腸~大腸 | 夜間の掻痒、不眠、情緒不安定 | 肛囲検査法「柿の種」 | pyrantel pamoate | |
Ascaris lumbricoides | 回虫 | 回虫症 | 虫卵経口感染 | 小腸孵化→門脈→ 肺発育→食道嚥下→小腸 |
Loffler症候群。急性腹痛 | 糞便虫の虫卵の証明 | pyrantel pamoate | |
Toxocara canis | イヌ回虫 | 幼虫移行症 | 生後1-2ヶ月の感染犬の 糞から経口感染 |
なし | 幼虫移行症→失明 | 免疫診断 | 治療法無し? | |
Wuchereria bancrofti | バンクロフト糸状虫 | フィラリア症/糸状虫症 | アカイエカ | リンパ系 | 急性期:リンパ肝炎、リンパ腺炎を伴う熱発作(filarial fever) 慢性期:乳糜尿、リンパ管瘤、陰嚢水腫、象皮病 |
急性期:夜間のmicrofilariaの検出 慢性期:特有の症状を考慮 |
diethylcarbamazine & ivermectin | |
Brugia malayi | マレー糸状虫 | |||||||
Dirofilaria immitis | イヌ糸状虫 | アカイエカ | なし | 幼虫移行症→肺血管閉塞→胸部X線画像銭形陰影 | ||||
Gnathostoma spinigerum | 有棘顎口虫 | 顎口虫症 | ドジョウ、雷魚、ヘビの生食 | 消化管壁貫通→皮下移動による腫瘤や線状皮膚炎 | 移動性腫瘤、皮膚爬行疹 雷魚やドジョウの生殖の問診 免疫血清診断 |
なし | ||
Gnathostoma hispidum | 剛棘顎口虫 | |||||||
Gnathostoma doloresi | ドロレス顎口虫 | |||||||
Gnathostoma nipponicum | 日本顎口虫 | |||||||
Anisakis simplex, larva | アニキサス幼虫 | アニサキス症 (1)胃アニサキス症、 (2)腸アニサキス症、 (3)異所性アニサキス症 |
経口感染 終宿主:クジラ、イルカ。 中間宿主:オキアミ。 待機宿主:サバ、ニシン、アジ、タラなど |
胃や腸 | (1)急激な上腹部痛"胃けいれん" (2)腹痛、急性虫垂炎、イレウス様。劇症型と緩和型がある (3)腹腔内の炎症性肉芽腫 |
胃内視鏡検査 | 内視鏡による虫体摘出 | |
Pseudoterranova decipiens | ||||||||
Trichinella spiralis | 旋毛虫 | 旋毛虫症 | 経口感染 豚肉、クマ肉の生食 |
(1)成虫侵襲期:下痢、腹痛 (2)幼虫筋肉移行期:顔面浮腫、心筋障害など (3)幼虫被嚢期:全身浮腫、衰弱 |
急性期:ステロイド 殺虫:mebendazole | |||
鞭虫症 | 盲腸 | 慢性下痢、腹痛、異食症、貧血 | セロファン重層塗沫法、 ホルマリンエーテル法 |
mebendazole | ||||
Spirurin nematode larva | 旋尾線虫 | 旋尾線虫幼虫 | ホタルイカの生食 | なし | 皮膚爬行疹、イレウス様症状 | 予防:-30℃24時間。 生食には-30℃4日間以上 |
摘出 | |
吸虫類 | Shistosoma japonicum | 日本住血吸虫 | 日本住血吸虫症 | 糞便虫の虫卵→ミラシジウム→ ミヤイリガイ体内でセルカリア→ 人畜の皮膚より浸入→循環系→ 門脈に寄生 |
門脈 | (1)潜伏期:侵入部の掻痒性皮膚炎。肺移行期:咳、発熱 (2)急性期:虫卵の門脈系寄生、産卵。住血吸虫性赤痢。 (3)慢性期:虫卵の肝、脳などの塞栓。肝硬変。脾腫、腹水 |
糞便虫の虫卵の検出。 直腸粘膜層掻爬法、 肝穿刺による組織内虫卵の検出。 補助診断として免疫血清学的検査。 |
praziquantel |
Paragonimus westermani | ウェステルマン肺吸虫 | 肺吸虫症/肺ジストマ症 | 経口感染 淡水産のカニ、イノシシ肉の生食 |
肺 | 痰、咳、胸痛、時に喀血 | 痰や便の虫卵検査、 胸部写真、 断層写真で明らかな虫嚢。 免疫学血清検査 |
||
Paragonimus miyazakii | 宮崎肺吸虫 | 肺 | 気胸、胸水貯留、膿胸、好酸球増加 | praziquantel | ||||
Clonorchis sinensis | 肝吸虫 | 肝吸虫症/肝ジストマ症 | 経口感染 虫卵→(マメタニシ:セルカリア)→ セルカリア→(魚:メタセルカリア)→ 摂取→(ヒト:成虫)→虫卵 |
胆管 | 胆汁流出障害による肝障害→肝硬変 | 糞便、胆汁(十二指腸ゾンデ法)。 肝吸虫卵の検出。CT像。エコー検査。 |
praziquantel | |
横川吸虫症 | 淡水魚(アユ、フナ、ウグイ、シラウオ)の生食 | 小腸粘膜 | 下痢、腹痛 | 糞便虫の虫卵 | praziquantel | |||
条虫類 | Taeniarhynchus saginatus | 無鉤条虫 | 腸管条虫症 | 経口感染。中間宿主:ウシ | 小腸 | 無症状。下痢。 広節裂頭条虫感染では悪性貧血。 |
糞便虫の虫卵と体節により診断 | praziquantel。 有鉤条虫の場合はガストログラフィン。 有鉤条虫の駆虫の際、 虫体を破壊しない →虫体の融解による嚢虫症 |
Taenia solium | 有鉤条虫 | 経口感染。中間宿主:ブタ | ||||||
Diphyllobothrium latum | 広節裂頭条虫 | 経口感染。中間宿主:サケ、マス | ||||||
日本海裂頭条虫 | 経口感染。中間宿主:サケ | |||||||
腸管外条虫症 | ||||||||
有鉤嚢虫症 | 有鉤条虫の虫卵の経口摂取 | 皮下、筋肉内 脳、脊髄、眼球 |
皮下、筋肉内:小指頭大の無症状腫瘤 脳、脊髄、眼球:Jacksonてんかん。痙性麻痺など |
皮下の虫嚢 | 外科的摘出。 成虫寄生がなければ、praziquantel, albendazole + ステロイド | |||
Echinococcus granulosus | 単包虫 | 包虫症/ エキノコックス症 (単包虫症) |
終宿主:イヌ、キツネなど。 中間宿主:ヒト、ブタ、野ネズミなど。 終宿主の糞便虫の虫卵を中間宿主が接種して発症 |
肝、肺、まれに脳、腎、筋肉 | 肝寄生:肝部疼痛、満腹、時に黄疸、下肢浮腫 肺寄生:胸部圧迫感、胸痛、咳、血痰、時に喀血 |
肝や肺の嚢胞形成から疑う。 早期に診断に皮内反応→ CT、エコー→ 生検。免疫血清学的診断法 |
外科的切除。 albendazoleの長期投与 | |
Echinococcus multilocularis | 多包虫 | 包虫症/ エキノコックス症 (多包虫症) |
[★] バンクロフト糸状虫 Wuchereria bancrofti
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