Also known as Campylobacter pylori
species of bacteria
Helicobacter pylori is a species of bacteria that lives in the stomach and can infect humans. It matters because it can cause serious digestive problems, including ulcers and inflammation of the stomach lining.
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Helicobacter pylori
SPECIES
感染之胃粘膜上皮組織圖像(Warthin-Starry染色) 幽門桿菌對胃黏膜造成的傷害① 胃内幽門桿菌的鞭毛在胃粘液層内部移動、並附著於上皮細胞的表面。 ② 尿素酶遇上黏液中的尿素而產生氨,中和了胃酸。 ③ 沒被胃酸殺死的幽門桿菌在黏液層進行增殖。此外,趨化因子將週圍的其他幽門螺桿菌引來。 ④ 幽門桿菌產生的各種分解酵素破壞了黏液層,讓失去黏膜保護的上皮細胞發炎(參考圖中央)。此外細菌分泌出的VacA等毒素(右)、透過IV型分泌装置注入上皮細胞的反應器(effector)分子(左)對上皮細胞產生傷害,讓發炎的症狀惡化。 幽門桿菌或幽門螺旋桿菌、幽門螺旋菌、 胃幽門桿菌(學名:Helicobacter pylori,发音为/ˌhɛlɪkɵˈbæktər pɪˈlɔəraɪ/)是革蘭氏陰性、微需氧的細菌,生存於胃部及十二指腸的各區域內。它會引起胃黏膜輕微的慢性發炎,甚或導致胃及十二指腸潰瘍與胃癌。超過80%的帶原者並不會表露病徵。 幽門桿菌最初被命名為幽門彎曲菌(Campylobacter pyloridis),後為修正拉丁語語法錯誤而變為C. pylori。1989年,16S rRNA基因定序等研究顯示其並不屬於彎曲菌屬,幽門螺桿菌便被獨立歸類至螺桿菌屬。螺桿菌屬(Helicobacter)源自古希臘的詞彙「hělix/ἕλιξ」(意為螺旋或纏繞)。屬名加詞「pylōri」則是指「幽門的」或幽門閥(從胃部通往十二指腸的圓狀開口),源自古希臘詞彙「πυλωρός」,意為守門人。 一旦家庭中成年人被發現有「胃幽門螺旋桿菌」的感染時,共同生活的孩童亦會有相同的感染現象。 這也是一般病患在門診診治中經常提到的實際問題。根據流行病學的統計研究,發現胃幽門螺旋桿菌在人群中的感染率與社會經濟、家庭衛生環境、教育水準或者個人衛生習慣有極大的關係;換句話說,人口雜處、家庭衛生較差、教育水準較低或者個人飲食衛生習慣較差的地區,會有較高的胃幽門螺旋桿菌感染率。根據台灣地區消化內科醫學會的初步研究報告發現[來源請求],在台灣地區居住民眾的胃幽門螺旋桿菌感染情形如下:十歲以下的孩童感染率約為20%;二十歲以下的青少年感染率約為40%;而年齡在三十歲左右者,其感染率則高達50%;四十歲以上則超過75%。對於年齡較小的幼童亦可以經由抽血檢查血清偵測其是否具有胃幽門螺旋桿菌的抗體而得知是否受感染。香港中文大學研究團隊審閱近200份醫學文章及報告,估計現時全港約有30%人口屬帶菌者。病菌能刺激胃酸分泌損害胃壁,引致潰瘍,患者或會長期感到胃痛和受胃酸倒流之苦。 世界超過50%人口在消化系統上部带有幽門螺桿菌。感染較盛行於发展中國家,而西方國家的影響範圍也逐漸縮小。幽門螺桿菌的傳染途徑為口口或粪口傳播,但個體通常是於幼時被感染。一般认为幽門螺桿菌的螺旋狀(其亦是屬名的由來)进化是为了能够使其通過
via GBIF
Helicobacter pylori, previously known as Campylobacter pylori, is a gram-negative bacterium best known for its role in causing gastric ulcers in the human stomach. Its helical body (from which the genus name Helicobacter derives) is thought to have evolved to penetrate the mucous lining of the stomach, helped by its flagella, and thereby establish infection. Mutants can have a rod or curved rod shape that exhibits less virulence. While many earlier reports of an association between bacteria and the ulcers had existed, such as the works of John Lykoudis, it was only in 1983 when the bacterium was formally described for the first time in the English-language literature as the causal agent of gastric ulcers by Australian physician-scientists Barry Marshall and Robin Warren. In 2005, the pair was awarded the Nobel Prize in Physiology or Medicine for their discovery.
Infection of the stomach with H. pylori does not necessarily cause illness: over half of the global population is infected, but most individuals are asymptomatic. Persistent colonization with more virulent strains can induce a number of gastric and non-gastric disorders. Gastric disorders due to infection begin with gastritis, or inflammation of the stomach lining. When infection is persistent, the prolonged inflammation will become chronic gastritis. Initially, this will be non-atrophic gastritis, but the damage caused to the stomach lining can bring about the development of atrophic gastritis and ulcers within the stomach itself or the duodenum (the nearest part of the intestine). At this stage, the risk of developing gastric cancer is high. However, the development of a duodenal ulcer confers a comparatively lower risk of cancer. Helicobacter pylori are class 1 carcinogenic bacteria, and potential cancers include gastric MALT lymphoma and gastric cancer. Infection with H. pylori is responsible for an estimated 89% of all gastric cancers and is linked to the development of 5.5% of all cases of cancers worldwide. H. pylori is the only bacterium known to cause cancer.
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Discovered by embedding cosine similarity (sentence-transformers MiniLM, 384-dim).