出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2012/08/29 21:34:43」(JST)
Brugia malayi | |
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B. malayi, blood smear, Giemsa stain. | |
Scientific classification | |
Kingdom: | Animalia |
Phylum: | Nematoda |
Class: | Secernentea |
Order: | Spirurida |
Family: | Onchocercidae |
Genus: | Brugia |
Species: | B. malayi |
Binomial name | |
Brugia malayi Brug 1927 |
Brugia malayi | |
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Classification and external resources | |
ICD-10 | B74.1 |
ICD-9 | 125.1 |
Brugia malayi is a nematode (roundworm), one of the three causative agents of lymphatic filariasis in humans. Lymphatic filariasis, also known as elephantiasis, is a condition characterized by swelling of the lower limbs. The two other filarial causes of lymphatic filariasis are Wuchereria bancrofti and Brugia timori, which differ from B. malayi morphologically, symptomatically, and in geographical extent.[1]
B. malayi is transmitted by mosquitoes and is restricted to South and South East Asia. It is one of the tropical diseases targeted for elimination by the year 2020 by the World Health Organization, which has spurred vaccine and drug development, as well as new methods of vector control.
Contents
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Lichentenstein and Brug first recognized B. malayi as a distinct pathogen in 1927. They reported the occurrence of a species of human filariae in North Sumatra that was both physiologically and morphologically distinct from the W. bancrofti microfilariae commonly found in Jakarta and named the pathogen Filaria malayi.[2] However, despite epidemiological studies identifying Filaria malayi in India, Sri Lanka, China, North Vietnam, and Malaysia in the 1930s, Lichentenstein and Brug’s hypothesis was not accepted until the 1940s, when Rao and Mapelstone identified two adult worms in India.[3]
Based on the similarities with W. bancrofti, Rao and Mapelstone proposed to call the parasite Wuchereria malayi [2] In 1960, however, Buckley proposed to divide the old genus Wuchereria, into two genera, Wuchereria and Brugia and renamed Filaria malayi as Brugia malayi. Wuchereria contains W. bancrofti, which so far has only been found to infect humans, and the Brugia genus contains B. malayi, which infects humans and animals, as well as other zoonotic species.[4]
In 1957, two subspecies of human infecting B. malayi were discovered by Turner and Edeson in Malaysia based on the observation of different patterns of microfilaria periodicity.[5] Periodicity refers to a pronounced peak in microfilariae count during a 24 hour interval when microfilariae are present and detectable in the circulating blood.[4] The basis for this phenomenon remains largely unknown.[6]
B. malayi is transmitted by a mosquito vector. The principal mosquito vectors include Mansonia, Anopheles, and Aedes mosquitoes.[7] The mosquito serves as a biological vector – it is required for the developmental cycle of the parasite (see Life Cycle).[6] The geographical distribution of the disease is thus dependent on suitable mosquito breeding habitat.
The accumulation of many infective mosquito bites—several hundreds to thousands—is required to establish infection. This is because a competent mosquito usually transmits only a few infective L3 larvae (see Life Cycle), and less than 10% of those larvae progress through all the necessary molting steps and develop into adult worms.[8] Thus those at greatest risk for infection are individuals living in endemic areas—short term tourists are unlikely to develop lymphatic filariasis.[9]
Development and replication of B. malayi occurs in two discrete phases: in the mosquito vector and in the human. Both stages are essential to the life cycle of the parasite.
Mosquito: The mosquito serves as a biological vector and intermediate host – it is required for the developmental cycle and transmission of B. malayi.
4. The mosquito takes a human blood meal and ingests microfilariae (worm-like sheathed eggs) that circulate in the human blood stream.
5-7 In the mosquito, the microfilariae shed sheaths, penetrate the midgut, and migrate to the thoracic muscles were the microfilariae increase in size, molt, and develop into infective larvae (L1 and L3) over a span of 7–21 days. No multiplication or sexual reproduction of microfilariae occurs in the mosquito.
8-1 The infective larvae (L3) migrate to the salivary glands, enter the proboscis and escape onto human skin when the mosquito takes another blood meal.[10]
Human: B. malayi undergoes further development in the human as well as sexual reproduction and egg production.
1-2 The infective larvae (L3) actively penetrate the skin through the bite hole and develop into adults in the lymphatic system over a span of 6 months. Adult worms can survive in the lymphatic system for 5–15 years [11]
3. The male and female adult worms mate and the females produce an average of 10,000 sheathed eggs (microfilaria) daily [11] The microfilariae enter the blood stream and exhibit the classic nocturnal periodicity and subperiodicity.
4. Another mosquito takes a blood meal and ingests the microfilariae. Infection depends on the mosquito taking a blood meal during a periodic episode – when microfilariae are present in the bloodstream.[6][10]
Adult worms resemble the classic nematode roundworm. Long and threadlike, B. malayi and other nematode possess only longitudinal muscles and move in an S-shape motion.[12] Adults are typically smaller than adult W. bancrofti, though few adults have been isolated. Female adult worms (50 mm) are larger than male worms (25 mm).[13]
B. malayi microfilariae are 200-275 um in length and have a round anterior end and a pointed posterior end. The microfilariae are sheathed, which stains heavily with Giemsa. The sheath is actually the egg shell, a thin layer that surrounds the egg shell as the microfilariae circulates in the bloodstream. The microfilariae retain the sheath until it is digested in the mosquito midgut.[6]
B. malayi microfilariae resemble W. bancrofti and Loa loa microfilariae with minor differences that can aid in laboratory diagnosis. B. malayi microfilariae can be distinguished by the noncontinuous row of nuclei found in the tip of the tail. There are two terminal nuclei that are distinctly separated from the other nuclei in the tail, whereas the tail of W. bancrofti contains no nuclei and Loa loa microfilariae nuclei form a continuous row in the tail. B. malayi microfilariae also have a characteristic cephalic space ratio of 2:1.[6][14]
B. malayi is one of the causative agents of lymphatic filariasis, a condition marked by infection and swelling of the lymphatic system. The disease is primarily caused by the presence of worms in the lymphatic vessels and the resulting host response. Signs of infection are typically consistent with those seen in bancroftian filariasis—fever, lymphadenitis, lymphangitis, lymphedema, and secondary bacterial infection—with a few exceptions.
Lymphadenitis, the swelling of the lymph nodes, is a commonly recognized symptom of many diseases. An early manifestation of filariasis, lymphadenitis more frequently occurs in the inguinal area during B. malayi infection and can occur before the worms mature.[6]
Lymphangitis is the inflammation of the lymphatic vessels in response to infection. It occurs early in the course of infection in response to worm development, molting, death, or bacterial and fungal infection. The affected lymphatic vessel becomes distended and tender, and the overlying skin becomes erythemous and hot. Abscess formation and ulceration of the affected lymph node occasionally occurs during B. malayi infection, more readily than in Bancroftian filariasis. Remnants of adult worms can sometimes be found in the ulcer drainage.[6]
The most obvious sign of infection, elephantiasis, is the enlargement of the limbs. A late complication of infection, elephantiasis is a form of lymphedema and is caused by repeated inflammation of the lymphatic vessels. Repeated inflammatory reactions causes vessel dilation and thickening of the affected lymphatic vessels, which can compromise function. The lymphatic system normally functions to maintain fluid balance between tissues and the blood and serves as an integral part of the immune system. Blockage of these vessels due to inflammatory induced fibrosis, dead worms, or granulomatous reactions can interfere with normal fluid balance, thus leading to swelling in the extremities.[15] Elephantiasis resulting from B. malayi infection typically affects the distal portions of the extremities. Unlike bancroftian filariasis, B. malayi rarely affects genitalia and does not cause funiculitis, orchitis, epididymitis, hydrocele, or chyuria, conditions more readily observed with bancroftian infection.[6]
Secondary bacterial infection is common among patients with filariasis. Compromised immune function due to lymphatic damage in addition to lymph node ulcerations and abscesses exposure and impaired circulation due to elephantiasis can cause secondary bacterial or fungal infection. Elephantiasis, in addition to the physical burden of a swollen limb, can be a severely dehabilitating condition given bacterial infection. Part of the WHO’s "Strategy to Eliminate Lymphatic Filariasis" targets hygiene promotion programs in order to alleviate the suffering of affected individuals (see Prevention Strategies).[6][16]
However, clinical manifestations of infection are variable and depend on several factors, including host immune system, infectious dose, and parasite strain differences. Most infections appear asymptomatic, yet vary from individual to individual. Individuals living in endemic areas with microfilaremia may never present with overt symptoms, whereas in other cases, only a few worms can exacerbate a severe inflammatory response.[6]
The development of the disease in humans, however, is not well understood. Adults typically develop worse symptoms, given the long exposure time required for infection. Infection may occur during childhood, but the disease appears to take many years to manifest. The incubation period for infection ranges from 1 month to 2 years and typically microfilariae appear before overt symptoms. Lymphedema can develop within six months and development of elephantiasis has been reported within a year of infection among refugees, who are more immunologically naive. Men tend to develop worse symptoms than women.[16]
Tender or enlarged inguinal lymph nodes or swelling in the extremities can alert physicians or public health officials to infection.
With appropriate laboratory equipment, microscopic examination of differential morphological features of microfilariae in stained blood films can aid diagnosis—in particular the examination of the tail portion, the presence of a sheath, and the size of the cephalic space.[6] Giemsa staining will uniquely stain B. malayi sheath pink.[14] However, blood films can prove difficult given the nocturnal periodicity of some forms of B. malayi.
PCR based assays are highly sensitive and can be used to monitor infections both in the human and the mosquito vector. However, PCR assays are time-consuming, labor intensive and require laboratory equipment. Lymphatic filariasis mainly affects the poor, who live in areas without such resources.[17]
The ICT antigen card test is widely used in the diagnosis of W. bancrofti, but commercial antigens of B. malayi have not been historically widely available. However, new research developments have identified a recombinant antigen (BmR1) that is both specific and sensitive in the detection of IgG4 antibodies against B. malayi and B. timori in ELISA and immunochromatographic rapid dipstick (Brugia Rapid) test. However, it appears that immunoreactivity to this antigen is variable in individuals infected with other filarial nematodes.[18] This research has led to the development of two new rapid immunochromatographic IgG4 cassette tests—WB rapid and panLF rapid—which detect bancroftian filariasis and all three species of lymphatic filariasis, respectively, with high sensitivity and selectivity.[17]
The ["Global Alliance to Eliminate Lymphatic Filariasis"] was launched by the World Health Organization in 2000 with two primary goals: 1) to interrupt transmission and 2) to alleviate the suffering of affected individuals. Mass drug treatment programs are the main strategy for interrupting parasite transmission, and morbidity management, focusing on hygiene, improves the quality of life of infected individuals.[19]
A goal of community base efforts is to eliminate microfilariae from the blood of infected individuals in order to prevent transmission to the mosquito. This is primarily accomplished through the use of drugs. The treatment for B. malayi infection is the same as for bancroftian filariasis. Diethylcarbamazine (DEC) has been used in mass treatment programs in the form of DEC-medicated salt, as an effective microfilaricidal drug in several locations, including India.[20] While DEC tends to cause adverse reactions like immediate fever and weakness, it is not known to cause any long-term adverse drug effects. DEC has been shown to kill both adult worms and microfilariae. In Malaysia, DEC dosages (6 mg/kg weekly for 6 weeks; 6 mg/kg daily for 9 days) reduced microfilariae by 80% for 18–24 months after treatment in the absence of mosquito control.[6] Microfilariae numbers slowly return many months after treatment, thus requiring multiple drug doses over time in order to achieve long-term control. However, it is not known how many years of mass drug administration is required to eliminate transmission. But currently, there have been no confirmed cases of DEC resistance.[20]
Single doses of two drugs (albendazole-DEC and albendazole-ivermectin) have been shown to remove 99% of microfilariae for a year after treatment and help to improve elephantiasis during early stages of the disease.[19] Ivermectin does not appear to kill adult worms but serves as a less toxic microfilaricide.[6]
Since the discovery of the importance of Wolbachia in the lifecycle of B. malayi and other nematodes, novel drug efforts have targeted the endobacterium. Tetracyclines, rifampicin, and chloramphenicol have been effective in vitro by interfering with larvae molting and microfilariae development. Tetracyclines have been shown to cause reproductive and embryogenesis abnormalities in the adult worms, resulting in worm sterility. Clinical trials have demonstrated the successful reduction of Wolbachia and microfilariae in onchocerciasis and W. bancrofti infected patients. These antibiotics, while acting through a slightly more indirect route, are promising antifilarial drugs.[21]
Secondary bacterial infection is often observed with lymphatic filariasis. Rigorous hygiene practices, including washing with soap and water daily and disinfecting wounds can help heal infected surfaces, and slow and potentially reverse existing tissue damage. Promoting hygiene is essential for lymphatic filariasis patients given the compromised immune and damaged lymphatic systems and can help prevent suffering and disability.[9][19]
There is currently no licensed vaccine to prevent lymphatic filariasis. However, recent research has produced vaccine candidates with good results in experimental animals. A glutathione-S-transferase, a detoxification enzyme in parasites isolated from Setaria cervi, a bovine filarial parasite, reduced B. malayi adult parasite burden by more than 82% 90 days post parasite.[22]
Vector control has been effective in virtually eliminating lymphatic filariasis in some regions, but vector control combined with chemotherapy produces the best results. It is suggested that 11–12 years of effective vector control may eliminate lymphatic filariasis.[23] Successful methods of B. malayi vector control include residual house spraying using DDT and insecticide treated bednets. Mansonia larvae attach their breathing tubes to underwater roots and plants in order to survive. While chemical larvicides have only provided partial control, plant removal would prevent vector development, but would have potential adverse effects on the aquatic environment. Lymphatic filariasis vector control is neglected in comparison to the far more established efforts to control malaria and Dengue vectors. Integrated vector control methods should be applied in areas where the same mosquito species is responsible for transmitting multiple pathogens.[24]
B. malayi infects 13 million people in south and southeast Asia and is responsible for nearly 10% of the world’s total cases of lymphatic filariasis.[23][24] B. malayi infection is endemic or potentially endemic in 16 countries, where it is most common in southern China and India, but also occurs in Indonesia, Thailand, Vietnam, Malaysia, the Philippines, and South Korea.[6][7] The distribution of B. malayi overlaps with W. bancrofti in these regions, but does not coexist with B. timori.[6] Regional foci of endemicity are determined in part by the mosquito vectors (see Transmission).
On September 20, 2007, scientists sequenced the genome of Brugia malayi in the paper "Draft Genome for the Filarial Nematode Parasite Brugia malayi" by Elodie Ghedin, et al. Science 317, 1756 (2007); doi:10.1126/science.1145406. Identifying the genes of this organism might lead to development of new drugs and vaccines.[25]
To decipher the genome, "Whole Genome Shotgun Sequencing" was performed. The genome was found to be approximately 90-95 mega bases in size. The results of the sequencing was then compared to that of the C. elegans, along with its prototype C. briggsae. These other organisms were incorporated in the study and proved to be important for several reasons:
Sequence comparisons between the two genomes allow us to map C. elegans orthologs to B. malayi genes. Using these orthology mappings (between C. elegans and B.malayi) and by incorporating the extensive genomic and functional genomic data, including genome-wide RNAi screens, that already exist for C. elegans, we identify potentially essential genes in B. malayi. Scientists are hoping to be able to use these genes as potential new drug targets for new drug treatments. The longevity of this parasite complicates treatment because existing drugs target the larvae and, thus, do not completely kill the worms. The drugs often must be taken periodically for years, and the worm can cause a massive immune reaction when it dies and releases foreign molecules in the body. Drug treatments for filariasis have not changed significantly in over 20 years, and with the risk of resistance rising, there is an urgent need for the development of new anti-filarial drug therapies. From the genome sequence, Dr. Ghedin and her co-investigators identified several metabolic pathways containing dozens of gene products that they believe are likely to be helpful for the discovery of more targeted and effective drug therapies.
These potential new targets for drugs or vaccines should provide new opportunities for understanding, treating and preventing elephantiasis.
The relationship between the bacteria Wolbachia and B. malayi is not fully understood. Some theories based on research done with Wuchereria bancrofti, another worm that causes filariasis, believe that Wolbachia may: aid in embryogenesis of the worm, be responsible for potent inflammatory responses from macrophages and filarial disease, and may be linked to the onset of lyphodema and blindness sometimes associated with B. malayi infections. According to a study done by University of Bonn in Ghana, doxycycline was effective in depleting Wolbachia from W. bancrofti. It is likely that the mechanism of doxycycline is similar to that in other filarial species, i.e., a predominant blockade of embryogenesis, leading to a decline of microfilariae according to their half-life. This could render doxycycline treatment an additional tool for the treatment of microfilaria-associated diseases in bancroftian filariasis, along with B. malayi fiariasis. The doxycycline course of treatment would be much shorter as it would be able to target the adult worm rather than the larvae current treatments kill, and there would be fewer side effects for the infected individual.
Another hopeful use for the research is in the area of transplant research. Because the B. malayi genome is the first parasitic genome to have been sequenced, the implications on the mechanism of parasitism in humans are crucial to understand. According to Alan L. Scott, Ph.D., a collaborator at Johns Hopkins University, it is this understanding of how a particular parasite, such as B. malayi, which can adapt to humans, that may yield medical benefits far beyond treating elephantiasis. According to the author, "This worm can reside in the host for years and not necessarily cause disease, in fact the less disease the individual has, the more worms there are in circulation. Now that we know those genes don't exist in humans we can target them to control disease." Some of the predicted proteins for these new genes appear to be similar to known immuno-modulator proteins, regulators of the immune system, suggesting that they are involved in deactivating the host's immune system to ensure the parasite remains undetected. Knowledge of these previously unknown immune suppressors could also be of use in organ transplants and to help treat autoimmune disease.
A specific gene of interest is the Brugia malayi MIF (macrophage migration inhibition factor) gene. Results suggest that B. malayi MIF may interact with the human immune system during the course of infection by altering the function of macrophages in the infected individual, and studies are currently testing the hypothesis that MIF may be involved in reducing the host’s immune response to the filarial parasite.
According to the Filarial Genome Project being done by The Special Programme for Research and Training in Tropical Diseases (TDR), the Brugia malayi MIF gene is expressed in all life-cycle stages of the parasite, and results suggest that B. malayi MIF may interact with the human immune system during the course of infection by altering the function of macrophages in the infected individual. TDR also states that studies are currently testing the hypothesis that MIF may be involved in reducing the host’s immune response to the filarial parasite. Understanding how this particular parasite has adapted to humans may help organ transplant researchers by figuring out how to prevent the immune system from attacking the transplanted tissue.
The genomic information gives us a better understanding of what genes are important for different processes in the parasite’s life cycle. So, it will now be possible to target these genes more specifically and interrupt its life cycle. And, understanding how this particular parasite has adapted to humans may yield medical benefits far beyond treating elephantiasis, says collaborator Alan L. Scott, Ph.D., of the Bloomberg School of Public Health at Johns Hopkins University. "Parasitic worms are a lot like foreign tissue that has been transplanted into the human body. But unlike baboon hearts or pig kidneys, which the immune system quickly recognizes as foreign and rejects, worms can survive for years in the body. Discovering how they do so may someday benefit transplant surgery," explained Dr. Scott.
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リンク元 | 「蠕虫」「糸状虫症」「マレー糸状虫」 |
関連記事 | 「Brugia」 |
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 |
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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) |
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