出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2013/12/06 04:48:49」(JST)
Chlamydophila pneumoniae | |
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Scientific classification | |
Kingdom: | Bacteria |
Phylum: | Chlamydiae |
Order: | Chlamydiales |
Family: | Chlamydiaceae |
Genus: | Chlamydophila |
Species: | C. pneumoniae[1] |
Chlamydophila pneumoniae is a species of Chlamydophila, an obligate intracellular bacterium[2] that infects humans and is a major cause of pneumonia. It was known as the Taiwan acute respiratory agent (TWAR) from the names of the two original isolates – Taiwan (TW-183) and an acute respiratory isolate designated AR-39.[3] Until recently, it was known as Chlamydia pneumoniae, and that name is used as an alternate in some sources.[4] In some cases, to avoid confusion, both names are given.[5]
C. pneumoniae has a complex life cycle and must infect another cell to reproduce; thus, it is classified as an obligate intracellular pathogen. The full genome sequence for C. pneumoniae was published in 1999. It also infects and causes disease in koalas, emerald tree boas (Corallus caninus), iguanas, chameleons, frogs, and turtles.
The first known case of infection with C. pneumoniae was a case of sinusitis in Taiwan. This atypical bacterium commonly causes pharyngitis, bronchitis and atypical pneumonia,[6] mainly in elderly and debilitated patients, but in healthy adults, also.[7]
Chlamydophila pneumoniae is a small gram negative bacterium (0.2 to 1 μm) that undergoes several transformations during its life cycle. It exists as an elementary body (EB) between hosts. The EB is not biologically active, but is resistant to environmental stresses and can survive outside a host for a limited time. The EB travels from an infected person to the lungs of an uninfected person in small droplets and is responsible for infection. Once in the lungs, the EB is taken up by cells in a pouch called an endosome by a process called phagocytosis. However, the EB is not destroyed by fusion with lysosomes, as is typical for phagocytosed material. Instead, it transforms into a reticulate body (RB) and begins to replicate within the endosome. The reticulate bodies must use some of the host's cellular metabolism to complete its replication. The reticulate bodies then convert back to elementary bodies and are released back into the lung, often after causing the death of the host cell. The EBs are thereafter able to infect new cells, either in the same organism or in a new host. Thus, the life cycle of C. pneumoniae is divided between the elementary body, which is able to infect new hosts but can not replicate, and the reticulate body, which replicates but is not able to cause new infection.
C. pneumoniae is a common cause of pneumonia around the world; it is typically acquired by otherwise healthy people and is a form of community-acquired pneumonia. Because its treatment and diagnosis are different from historically recognized causes, such as Streptococcus pneumoniae, pneumonia caused by C. pneumoniae is categorized as an "atypical pneumonia" .[8]
In addition to pneumonia, C. pneumoniae less commonly causes several other illnesses. Among these are meningoencephalitis (infection and inflammation of the brain and meninges), arthritis, myocarditis (inflammation of the heart), and Guillain-Barré syndrome.[who?][citation needed]
Multiple studies have evaluated prior C. pneumoniae infection and a possible connection to lung cancer. One meta-analysis of serological data comparing prior C. pneumoniae infection in patients with and without lung cancer found results suggesting prior infection was associated with a slightly increased risk of developing lung cancer.[9]
In research into the association between C. pneumoniae infection and atherosclerosis and coronary artery disease, serological testing, direct pathologic analysis of plaques and in vitro testing suggest chronic infection with C. pneumoniae may be a risk factor for development of atherosclerotic plaques. C. pneumoniae infection increases adherence of macrophages to endothelial cells in vitro and aortas ex vivo.[10] However, the current data do not define how often C. pneumoniae is found in atherosclerotic or normal vascular tissue, nor does it allow for determining whether C. pneumoniae infection has a causative effect on atheroma formation or is merely an "innocent passenger" in these plaques. The largest trials that studied the use of antibiotics as a prevention for diseases associated with atherosclerosis, such as heart attacks and strokes, did not show any significant difference between antibiotics and placebo.[11]
C. pneumoniae has been found in the cerebrospinal fluid of some patients diagnosed with multiple sclerosis.[12]
Serological evidence for possible chronic C. pneumoniae infection was first associated with wheezing, asthmatic bronchitis and adult-onset asthma in 1991.[13] Subsequent studies of bronchoalveolar lavage fluid from pediatric patients with severe chronic respiratory illnesses including asthma have demonstrated that over half had evidence of C. pneumoniae by direct organism identification.[14][15] The only prospective study of new-onset adult asthma carried out in a primary care clinic diagnosed acute C. pneumoniae infection serologically in 5/5 patients with acute wheezing that became chronic and that was later diagnosed as asthma, and in another patient who developed new-onset chronic bronchitis who had the organism cultured from his sputum 6 months after illness onset.[16] These observations suggest that acute C. pneumoniae infection is capable of causing protean manifestations of chronic respiratory illness, some of which is diagnosed as asthma.
That these associations are clinically relevant in the primary care setting is suggested by the results of two observational trials[17][18] and two randomized controlled trials[19][20] of azithromycin treatment for asthma. One of these RCTs[20] and another macrolide trial[21] suggest that the treatment effect may be greatest in patients with severe, refractory asthma. These clinical results correlate with epidemiological evidence that C. pneumoniae is positively associated with asthma severity[22] and laboratory evidence that C. pneumoniae infection creates steroid-resistance.[23] Currently available asthma guidelines do not address this evidence.
There is no vaccine to protect against Chlamydophila pneumoniae. Research is on-going. Identification of highly immunogenic antigens is critical for the construction of an efficacious subunit vaccine against C. pneumoniae infections.
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国試過去問 | 「105A051」 |
リンク元 | 「特殊な細菌」「クラミドフィラ・ニューモニエ肺炎」「急性咽頭炎」「クラミドフィラ属」「C. pneumoniae」 |
拡張検索 | 「Chlamydophila pneumoniae肺炎」 |
関連記事 | 「pneumoniae」 |
BE
※国試ナビ4※ [105A050]←[国試_105]→[105A052]
科 | 寄生性 | 大きさ | グラム染色性 | 細胞壁 | LPS | ペプチド グリカン |
封入体 | 免疫原性 | 感染経路 | 無効抗菌薬 |
マイコプラズマ科 | 直径0.3μm | なし | なし | なし | なし | 飛沫感染 | βラクタム薬 | |||
リケッチア科 | 偏性細胞寄生性 | (0.3-0.5)x(0.8-2.0)μm | 陰性 | あり | あり | あり | なし | 媒介動物 | βラクタム薬 | |
クラミジア科 | 偏性細胞寄生性 | 陰性 | あり | あり | なし | あり | なし | 飛沫感染/接触感染/性行為 | βラクタム薬、アミノ配糖体系 |
科 | 属 | 病原体名 | 疾患名 | 潜伏期 | 感染経路 | 診断 | 症状 | 治療 | |
マイコプラズマ科 | マイコプラズマ属 | Mycoplasma pneumoniae | 肺炎マイコプラズマ | マイコプラズマ肺炎 | 飛沫感染 | マクロライド系・テトラサイクリン系 | |||
リケッチア科 | オリエンチア属 | Orientia tsutsugamushi | ツツガムシ病 | 4-18日 | ツツガムシ | Weil-Felix反応/蛍光抗体法/免疫ペルオキシダーゼ法/ペア血清 | テトラサイクリン系 ニューロキノロン系 | ||
リケッチア科 | リケッチア属 | Rickettsia japonica | 日本紅斑熱 | 2-8日 | マダニ | Weil-Felix反応 | |||
リケッチア科 | エールリキア属 | Ehrlichia sennetsu | 腺熱 | 10-17日 | 不明 | ||||
リケッチア科 | コクシエラ属 | Coxiella burnetii | Q熱 | 14-26日 | 経気道的、経口的、経皮的。人獣共通感染症 | テトラサイクリン系・ニューキノロン系・リファンピシン併用 | |||
リケッチア科 | バルトネラ属 | Bartonella henselae | Bartonella henselae感染症 (ネコひっかき病/細菌性血管腫症) |
マクロライド系・テトラサイクリン系 | |||||
クラミジア科 | クラミジア属 | Chlamydia psittaci | オウム病クラミジア | 7-10日 | テトラサイクリン系、マクロライド系。 βラクタム、アミノ配糖体無効。 基本小体に作用しない | ||||
クラミジア科 | クラミジア属 | Chlamydia trachomatis | トラコーマクラミジア | 1-5週 | 性行為 | ||||
クラミジア科 | クラミドフィラ属 | Chlamydophila pneumoniae | 肺炎クラミジア | 3-4週 |
[★] Streptococcus pneumoniae、Klebsiella pneumoniae、Mycoplasma pneumoniae、Chlamydia pneumoniae、Chlamydophila pneumoniae
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