出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2013/12/20 01:26:44」(JST)
Helminths (/ˈhɛlmɪnθs/) are a polyphyletic group of eukaryotic parasites.[1] They are worm-like organisms living in and feeding on living hosts, receiving nourishment and protection while disrupting their hosts' nutrient absorption, causing weakness and disease. Those that live inside the digestive tract are called intestinal parasites. They can live inside humans and other animals.
Helminthology is the study of parasitic worms and their effects on their hosts. The word helminth comes from Greek hélmins, a kind of worm.
Helminths is a polyphyletic group of morphologically similar organisms, consisting of members of the following taxa: monogeneans, cestodes (tapeworms), nematodes (roundworms), and trematodes (flukes). The following table shows the principal morphological distinctions for each of these helminth families:
Cestodes (tapeworms) | Trematodes (flukes) | Nematodes (roundworms) | |
---|---|---|---|
Shape | Segmented plane | Unsegmented plane | Cylindrical |
Body cavity | No | No | Present |
Body covering | Tegument | Tegument | Cuticle |
Digestive tube | No | Ends in cecum | Ends in anus |
Sex | Hermaphroditic | Hermaphroditic, except schistosomes which are dioecious | Dioecious |
Attachment organs | Sucker or bothridia, and rostellum with hooks | Oral sucker and ventral sucker or acetabulum | Lips, teeth, filariform extremities, and dentary plates |
Example diseases in humans | Tapeworm infection | Schistosomiasis, swimmer's itch | Ascariasis, dracunculiasis, elephantiasis, enterobiasis (pinworm), filariasis, hookworm, onchocerciasis, trichinosis, trichuriasis (whipworm) |
Note: ringworm (dermatophytosis) is actually caused by various fungi and not by a parasitic worm.
Helminths often find their way into a host through contaminated food or water, soil, mosquito bites, and even sexual acts. Poorly washed vegetables eaten raw may contain eggs of nematodes such as Ascaris, Enterobius, Thichuris, and/or cestodes such as Taenia, Hymenolepis, and Echinococcus. Plants may also be contaminated with fluke metacercaria (e.g. Fasciola). Undercooked meats may transmit Taenia (pork, beef and venison), Trichinella (pork and bear), Diphyllobothrium (fish), Clonorchis (fish), and Paragonimus (crustaceans). Schistosomes and nematodes such as hookworms (Ancylostoma and Necator) and Strongyloides can penetrate the skin. Finally, Wuchereria, Onchocerca, and Dracunculus are transmitted by mosquitoes and flies.
Populations in the developing world are at particular risk for infestation with parasitic worms. Risk factors include inadequate water treatment,[2] use of contaminated water for drinking, cooking, irrigation and to wash food, undercooked food of animal origin, and walking barefoot. Simple measures can have strong impacts on prevention. These include use of shoes, soaking vegetables with 1.5% bleach, adequate cooking of foods, and sleeping under mosquito-proof nets.
Response to worm infection in humans is a Th2 response in the majority of cases. Inflammation of the gut may also occur, resulting in cyst-like structures forming around the egg deposits throughout the body. The host's lymphatic system is also increasingly taxed the longer helminths propagate, as they excrete toxins after feeding. These toxins are released into the intestines to be absorbed by the host's bloodstream. This phenomenon makes the host susceptible to more common diseases, such as viral and bacterial infections.
Intestinal helminths, a type of intestinal parasites, reside in the human gastrointestinal tract. They represent one of the most prevalent forms of parasitic disease. Scholars estimate over a quarter of the world’s population is infected with an intestinal worm of some sort, with roundworms, hookworms, and whipworms infecting 1.47 billion people, 1.05 billion people, and 1.30 billion people, respectively.[3] Furthermore, the World Bank estimates 100 million people may experience stunting or wasting as a result of infection.[4]
Because of their high mobility and lower standards of hygiene, school-age children are particularly vulnerable to these parasites.[5] Overall, an estimated 400 million, 170 million, and 300 million children are infected with roundworm, hookworm, and whipworm, respectively.[6] Children may also be particularly susceptible to the adverse effects of helminth infections due to their incomplete physical development and their greater immunological vulnerability.[5]
In patients with a heavy worm load, infection is frequently symptomatic. Conditions associated with intestinal helminth infection include intestinal obstruction, insomnia, vomiting, weakness, and stomach pains,[7] and the natural movement of worms and their attachment to the intestine may be generally uncomfortable for their hosts.[3] The migration of Ascaris larvae through the respiratory passageways can also lead to temporary asthma and other respiratory symptoms.[7]
In addition to the low-level costs of chronic infection, helminth infection may be punctuated by the need for more serious, urgent care; for example, the World Health Organization found worm infection is common reason for seeking medical help in a variety of countries, with up to 4.9% of hospital admissions in some areas resulting from the complications of intestinal worm infections and as many as 3% of hospitalizations attributable to ascariasis alone.[8]
Also, the immune response triggered by helminth infection may drain the body’s ability to fight other diseases, making affected individuals more prone to coinfection.[3] Reasonable evidence indicates helminthiasis is responsible for the unrelenting prevalence of AIDS and tuberculosis in developing, particularly African, countries.[9] A review of several data clearly revealed the effective treatment of helminth infection reduces HIV progression and viral load, most likely by improving helminth-induced immune suppression.[10]
One way in which intestinal helminths may impair the development of their human hosts is through their impact on nutrition. Intestinal helminth infection has been associated with problems such as vitamin deficiencies, stunting, anemia, and protein-energy malnutrition, which in turn affect cognitive ability and intellectual development.[8] This relationship is particularly alarming because it is gradual and often relatively asymptomatic.[11]
Parasite infection may affect nutrition in several ways. Some scholars argue worms may compete directly with their hosts for access to nutrients; both whipworms[6] and roundworms[4] are believed to impact their hosts in this way. Nonetheless, the magnitude of this effect is likely to be minimal; after all, the nutritional requirements of these intestinal worms is small when compared with that of their host organism.[3]
A more probable source of infection-induced malnutrition is the nutrient malabsorption associated with parasite presence in the body. For example, in both pigs and humans, Ascaris has been tied to temporarily induced lactose intolerance and vitamin A,[12] amino acid, and fat malabsorption.[8] Impaired nutrient uptake may result from direct damage to the intestines' mucosal walls as a result of the worms’ presence, but it may also be a consequence of more nuanced changes, such as chemical imbalances caused by the body’s reaction to the helminths.[13] Alternatively, the worms’ release of protease inhibitors to defend against the body’s digestive process may impair the breakdown of other nutritious substances, as well.[3][6] Finally, worm infections may also cause diarrhea and speed “transit time” through the intestinal system, further reducing the body’s opportunity to capture and retain the nutrients in food.[8]
Worms may also contribute to malnutrition by creating anorexia. A decline in appetite and food consumption due to helminthic infection is widely recognized by the literature,[4] with a recent study of 459 children in Zanzibar reporting even mothers noticed spontaneous increases in appetite after their children underwent a deworming regimen.[14] Although the exact cause of such anorexia is not known, researchers believe it may be a side effect of body’s immune response to the worm and the stress of combating infection.[3] Specifically, some of the cytokines released in the immune response have been tied to anorexic reactions in animals.[6]
Helminths may also affect nutrition by inducing iron-deficiency anemia. This is most severe in heavy hookworm infections, as N. americanus and A. duodenale feed directly on the blood of their hosts. Although the impact of individual worms is limited (each consumes about .02-.07 ml and .14-.26 ml of blood daily, respectively), this may nonetheless add up in individuals with heavy infections, since they may carry hundreds of worms at a given time.[8] One scholar went so far as to predict, “the blood loss caused by hookworm was equivalent to the daily exsanguination of 1.5 million people”,[3] while a study in Zanzibar showed a 15¢ triannual application of mebendazole could avert 0.25 l of blood loss per child per year. Although whipworm is milder in its effects, it may also induce anemia as a result of the bleeding caused by its damage to the small intestine.[3][8]
The connection between worm burden and malnutrition is further supported by studies indicating deworming programs lead to sharp increases in growth; the presence of this result even in older children has led some scholars to conclude, “it may be easier to reverse stunting in older children than was previously believed.”[4]
Once the links between helminth infection and various forms of malnutrition are established, a number of pathways of parasite burden may affect cognition. For example, poor performance on normal growth indicators appears to be correlated with lower school achievement and enrollment, worse results on some forms of testing, and a decreased ability to focus; iron deficiency may result in “mild growth retardation”, difficulty with abstract cognitive tasks, and “lower scores...on tests of mental and motor development...[as well as] increased fearfulness, inattentiveness, and decreased social responsiveness” among very young children.[6] Anemia has also been associated with reduced stamina for physical labor, a decline in the ability to learn new information, and “apathy, irritability, and fatigue”.[8]
These connections are supported by a number of deworming studies. For example, using 47 students from the Democratic Republic of the Congo, iron supplements acted as a complement to deworming medication, producing better effects on mental cognition when they were applied in conjunction than when they were individually administered.[15] This result may be because iron supplements may “improve [students’] physical well-being to the point of enhancing attentional or arousal mechanisms influential in learning and cognitive performance”, with deworming medication only acting to extend these benefits by further reducing the tendency to anemia.[15]
A number of papers take the study of intestinal helminth beyond the malnutrition-cognition link to focus on the connections between worm infections and memory formation. For example, interventions to reduce whipworm infection in 159 Jamaican schoolchildren led to better “auditory short-term memory” and “scanning and retrieval of long-term memory;” particularly fascinating was his discovery that a nine-week period was all that was necessary for dewormed students to “catch up” to their worm-free peers in test performance.[16] Nokes’ optimistic conclusion that “whipworm infection['s]...adverse effect on certain cognitive functions...is reversible by therapy” is particularly significant because it suggests the effects of worms on intellectual performance may not be restricted to the mechanism of long-term malnutrition, since the physical and developmental effects of such malnutrition would theoretically be irreversible.[16]
The studies of Ezeamama et al. (2005) and Sakti et al. (1999) studied worm burden in the Philippines and Indonesia, respectively. Both authors found significant negative impacts of helminthic infection on memory and fluency, findings that are particularly meaningful because they included controls for socioeconomic status, hemoglobin levels, and proxies of nutrition (nutritional status and stunting, respectively). As Ezeamama observes, these studies suggest “undernutrition is not the primary mediator of the observed relationships”[17] between worm infection and intellectual performance, particularly because their findings were significant in aspects of intellect that went beyond mere cognition and reaction time.[18]
Finally, much as physical activity is “nutritionally mediated” as patients with heavy worm burden struggle to preserve energy and fight malnutrition, so too could “the poorly nourished mind similarly adapt...by reducing mental effort in the form of arousal and sustained attention.”[3] While they find little evidence this adaptation would provide benefits in the form of energy conservation, the active course of ongoing parasitic disease clearly could impose other, more direct limitations on an individual’s attention span.
The day-to-day costs of illness provide a strong explanation for yet another negative consequence of helminth infection, or the observation that it acts as “a very real barrier to children’s progress in school” as quantified by “outcome measures such as absenteeism, under-enrollment, and attrition.”[6] Parasite-heavy students may be too weak to attend classes, or their families may be too indebted by medical bills and low worker productivity to pay for school enrollment fees. This effect may be conceptually distinct from previous findings about the impact of parasitism on cognition and learning; for example, deworming programs improve school attendance by 25% without affecting test outcomes at all.[19] Nonetheless, these effects may also be related; school attendance and enrollment grew significantly in the school-age populations that benefited most from the Rockefeller Foundation’s deworming programs, leading to a long-term increase in income, as well as a rise in literacy rates.[20]
Public health campaigns to reduce helminth infections in the US may be traced as far back as 1910, when the Rockefeller Foundation began the fight against hookworm – the so-called “germ of laziness” – in the American South.[3] This campaign was enthusiastically received by educators throughout the region; as one Virginian school observed: “children who were listless and dull are now active and alert; children who could not study a year ago are not only studying now, but are finding joy in learning...for the first time in their lives their cheeks show the glow of health.”[20] From Louisiana, a grateful school board added: "As a result of your treatment...their lessons are not so hard for them, they pay better attention in class and they have more energy...In short, we have here in our school-rooms today about 120 bright, rosy-faced children, whereas had you not been sent here to treat them we would have had that many pale-faced, stupid children."[20]
Similar (albeit somewhat more imperialist) reports emerged from various other regions of the developing world at the time; for example, two scholars in Puerto Rico found that: "Over all the varied symptoms with which the unfortunate jibaro [peasant], infected by uncinaria [hookworm], is plagued, hangs the pall of a drowsy intellect, of a mind that has received a stunning blow...There is a hypochondriacal, melancholy, hopeless expression, which in severe cases deepens to apparent dense stupidity, with indifference to surroundings and lack of all ambition.’[3]
Such observations made an intuitive connection between worm burden and intellectual performance, but even today this link is anything but well-established. While it seems that worms may impair cognition in some way, the mechanisms driving this relationship are still hotly debated.
One popular approach to intestinal helminth control is school deworming programs. These programs have a number of advantages. They allow health policymakers to take advantage of existing infrastructure and institutions for the dispensation of medical treatment. Furthermore, students already plan to attend school on a somewhat regular basis, and can be educated about the importance of deworming.
School deworming programs have also been shown to have strong positive externalities. A difference-in-difference model proved the deworming programs in some schools reduced the burden of disease in neighboring, untreated schools; deworming children also has strong benefits for adult infection rates, since children are a significant source of transmission.[21]
The nature of the intestinal helminths and the medications available to treat them also favor universal deworming programs. Infection is generally diffuse, so it is worth treating a wide sample of the population; furthermore, a drug such as albendazole is a cheap, safe intervention that is not particularly specific, so can be used fairly effectively against all three of the main intestinal helminths (or any coinfection of them).[4] Finally, because these worms cannot replicate inside their hosts, reducing transmission may be the best way to reduce prevalence, and mass interventions on an annual or biannual basis may in fact be a reasonable means of achieving this goal.[21]
Parasitic worms have been used as a medical treatment for various diseases, particularly those involving an overactive immune response.[22] As humans have evolved with parasitic worms, proponents argue they are needed for a healthy immune system.[22] Scientists are looking for a connection between the prevention and control of parasitic worms and the increase in allergies such as hay-fever in developed countries.[22] Parasitic worms may be able to damp down the immune system of their host, making it easier for them to live in the intestine without coming under attack.[22] This may be one mechanism for their proposed medicinal effect.
One study suggests a link between the rising rates of metabolic syndrome in the developed worlds and the largely successful efforts of Westerners to eliminate intestinal parasites. The work suggests eosinophils (a type of white blood cell) in fat tissue play an important role in preventing insulin resistance by secreting interleukin 4, which in turn switches macrophages into "alternative activation". Alternatively-activated macrophages are important to maintaining glucose homeostasis (i.e., blood sugar regulation). Helminth infection causes an increase in eosinophils. In the study, the authors fed rodents a high-fat diet to induce metabolic syndrome, and then injected them with helminths. Helminth infestation improved the rodents' metabolism.[23] The authors concluded:
Although sparse in blood of persons in developed countries, eosinophils are often elevated in individuals in rural developing countries where intestinal parasitism is prevalent and metabolic syndrome rare. We speculate that eosinophils may have evolved to optimize metabolic homeostasis during chronic infections by ubiquitous intestinal parasites….[23]
Notes
|
|
全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.
リンク元 | 「蠕虫」「微生物学」「Nematomorpha」「parasitic worm」「Aschelminthes」 |
拡張検索 | 「Trochelminthes」「helminthiasis」 |
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) |
.