出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2015/02/23 23:55:29」(JST)
Taenia solium | |
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Scolex (head) of Taenia solium | |
Scientific classification | |
Kingdom: | Animalia |
Phylum: | Platyhelminthes |
Class: | Cestoda |
Order: | Cyclophyllidea |
Family: | Taeniidae |
Genus: | Taenia |
Species: | T. solium |
Binomial name | |
Taenia solium Linnaeus, 1758 |
Taenia solium is the pork tapeworm belonging to cyclophyllid cestodes in the family Taeniidae. It is an intestinal zoonotic parasite found throughout the world, and is most prevalent in countries where pork is eaten. The adult worm is found in humans and has a flat, ribbon-like body, which is white in color and measures 2 to 3 m in length. Its distinct head, the scolex, contains suckers and a rostellum as organs of attachment. The main body, the strobila, consists of a chain of segments known as proglottids. Each proglottid is a complete reproductive unit; hence, the tapeworm is a hermaphrodite. It completes its life cycle in humans as the definitive host and pigs as intermediate host. It is transmitted to pigs through human faeces or contaminated fodder, and to humans through uncooked or undercooked pork. Pigs ingest embryonated eggs, morula, which develop into larvae, the oncospheres, and ultimately into infective larvae, cysticerci. A cysticercus grows into an adult worm in human small intestines. Infection is generally harmless and asymptomatic. However, accidental infection in humans by the larval stage causes cysticercosis. The most severe form is neurocysticercosis, which affects the brain and is a major cause of epilepsy.
Human infection is diagnosed by the parasite eggs in the faeces. For complicated cysticercosis, imaging techniques such as computed tomography and nuclear magnetic resonance are employed. Blood samples can also be tested using antibody reaction of enzyme-linked immunosorbent assay. Broad-spectrum anthelmintics such as praziquantel and albendazole are the most effective medications.
Adult T. solium is a triploblastic acoelomate, having no body cavity. It is normally 2 to 3 m in length, but can become much larger, sometimes over 8 m long. It is white in colour and flattened into a ribbon-like body. The anterior end is a knob-like head called a scolex, which is 1 mm in diameter. The scolex bears four radially arranged suckers (acetabula) that surround the rostellum. These are the organs of attachment to the intestinal wall of the host. The rostellum is armed with two rows of spiny hooks, which are chitinous in nature. The 22 to 32 rotelllar hooks can be differentiated into short (130-µm) and long (180-µm) types. The elongated body is called the strobila, which is connected to the scolex through a short neck. The entire body is covered by a special covering called tegument, which is an absorptive layer consisting of a mat of minute hair-like microtriches. The strobila is divided into segments called proglottids, 800 to 900 in number. Body growth starts from the neck region, so the oldest proglottids are at the posterior end. Thus, the three distinct proglottids are immature proglottids towards the neck, mature proglottids in the middle, and gravid proglottids at the posterior end. A monoecious species, each mature proglottid contains a set of male and female reproductive systems. The numerous testes and a bilobed ovary open into a common genital pore. The oldest gravid proglottids are full of fertilised eggs,[1][2][3][4]
The infective larave, cysticerci, in humans, have three morphologically distinct types.[5] The common one is the ordinary "cellulose" cysticercus, which has a fluid-filled bladder 0.5 to 1.5 cm in length and an invaginated scolex. The intermediate form has a scolex, while the "racemose" has no evident scolex, but is believed to be larger and much more dangerous. They are 20 cm in length and have 60 ml of fluid, and 13% of patients can have all three types in the brain.
The life cycle of T. solium is indirect. It passes through pigs, as intermediate hosts, into humans, as definive hosts. From humans, the eggs are released in the environment where they await ingestion by another host. Humans as the definitive hosts are directly infected from contaminated meat.
Humans are infected by the larval stage, the cysticercus (Cysticercus cellulosae), from measly pork. A cysticercus is oval in shape, containing an inverted scolex (specifically "protoscolex"), which pops out externally once inside the small intestine. This process of evagination is stimulated by bile juice and digestive enzymes of the host. Using the scolex, it anchors to the intestinal wall. It grows in size using nutrients from the surroundings. Its strobila lengthens as new proglottids are formed at the neck. In 10–12 weeks after initial infection, it becomes adult worm. As a hermaphrodite, it reproduces by self-fertilisation, or cross-fertilisation if gametes are exchanged between two different proglottids. Spermatozoa fuse with the ova in the fertilisation duct, where the zygotes are produced. The zygote undergoes holoblastic and unequal cleavage resulting in three cell types, small micromeres, medium mesomeres, and large megameres. Megameres develop into syncytial layer called outer embryonic membrane. Mesomeres develop into radially striated inner embryonic membrane or embryophore. Micromeres become the morula. The morula transforms into a six-hooked embryo known as oncosphere, or sometimes hexacanth ("six hooked") larva. A single gravid proglottid can contain more than 50,000 embryonated eggs. Gravid proglottids often rupture in the intestine, liberating the eggs in faeces. The intact gravid proglottids are shed off in groups of four or five. The free eggs and detached proglottids are released into the environment through peristalsis. Eggs can survive in the environment for up to two months.[2][6]
Pigs ingest the eggs from human faeces or vegetation contaminated with human excreta. The embryonated eggs enter the intestine where they hatch into motile oncospheres. The embryonic and basement membranes are removed by the host's digestive enzymes (particularly pepsin). Then the free oncospheres get attached on the intestinal wall using their hooks. With the help of digestive enzymes from the penetration glands, they penetrate the intestinal mucosa to enter blood and lymphatic vessels. They move along the general circulatory system to various organs, and large numbers are cleared in the liver. The surviving oncospheres preferentially migrate to striated muscles, as well as the brain, liver, and other tissues, where they settle to form cysts called cysticerci. A single cysticercus is spherical, measuring 1–2 cm in diameter, and contains an invaginated protoscolex. The central space is filled with fluid like a bladder, hence it is also called bladder worm. Cysticerci are usually formed within 70 days and may continue to grow for a year.[7]
Humans are also accidental primary hosts when they are infected by embryonated eggs, either by autoinfection or ingestion of contaminated food. As in pigs, the oncospheres hatch, enter blood circulation, and have a predilection for brain tissue and other soft muscle tissues. When they settle to form cysts, clinical symptoms of cysticercosis appear. The cysticercus is often called the metacestode. If they localize in the brain, serious neurocysticercosis follows.[8][9]
Intestinal infection of T. solium is called taeniasis which is quite asymptomatic. Only in severe cases, conditions of intestinal irritation, anaemia, and indigestion occur, which can lead to loss of appetite and emaciation. Cysticercus is clinically pathogenic. Ingestion of T. solium eggs or proglottids which rupture within the host intestines can cause larvae to migrate into host tissue to cause cysticercosis. This is the most frequent and severe disease caused by T. solium. In symptomatic cases, a wide spectrum of symptoms may be expressed, including headaches, dizziness, and occasional seizures. In more severe cases, dementia or hypertension can occur due to perturbation of the normal circulation of cerebrospinal fluid. (Any increase in intracranial pressure will result in a corresponding increase in arterial blood pressure, as the body seeks to maintain circulation to the brain.) The severity of cysticercosis depends on location, size and number of parasite larvae in tissues, as well as the host immune response. Other symptoms include sensory deficits, involuntary movements, and brain system dysfunction. In children, ocular location of cysts is more common than cystation in other locations of the body.[8]
In many cases, cysticercosis in the brain can lead to epilepsy, seizures, lesions in the brain, blindness, tumor-like growths, and low eosinophil levels. It is the cause of major neurological problems, such as hydrocephalus, paraplegy, meningitis, convulsions, and even death.[10]
The best way to avoid getting tapeworms is to not eat undercooked pork. Moreover, a high level of sanitation and prevention of faecal contamination of pig feeds also plays a major role in prevention. Infection can be prevented with proper disposal of human faeces around pigs, cooking meat thoroughly and/or freezing the meat at −10°C for 5 days. For human cysticercosis, dirty hands are attributed to be the primary cause, and especially common among food handlers.[7] Therefore, personal hygiene such as washing one's hands before eating is an effective measure.
T. solium is found worldwide, but is more common in cosmopolitan areas. Because pigs are intermediate hosts of the parasite, completion of the life cycle occurs in regions where humans live in close contact with pigs and eat undercooked pork. Therefore, high prevalences are reported in Mexico, Latin America, West Africa, Russia, India, Pakistan, Manchuria, and Southeast Asia.[11] In Europe it is most widespread among Slavic people.[3][12] Cysticercosis is often seen in areas where poor hygiene allows for contamination of food, soil, or water supplies. Prevalence rates in the United States have shown immigrants from Mexico, Central and South America, and Southeast Asia account for most of the domestic cases of cysticercosis.[13] Taeniasis and cysticercosis are very rare in predominantly Muslim countries, as Islam forbids the consumption of pork. Human cysticercosis is acquired by ingesting T. solium eggs shed in the feces of a human tapeworm carrier by gravid proglottids, so can occur in populations that neither eat pork nor share environments with pigs, although the completion of the life cycle can occur only where humans live in close contact with pigs and eat pork.
In 1990 and 1991, four unrelated members of an Orthodox Jewish community in New York City developed recurrent seizures and brain lesions, which were found to have been caused by T. solium. All of the families had housekeepers from Latin American countries and were suspected to be source of the infections.[14][15]
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リンク元 | 「蠕虫」「有鉤条虫」 |
関連記事 | 「Taenia」 |
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) |
.