Bacterial cells in a curved shape. According to the degree of bending and hardness of the cell, and often will be divided into three types. Vibrio species first, short cells, only one bend, arc shape, such as cholera; 2 species pylori cell is twice or more curved spiral than tough, such as small Azospirillum; 3 burgdorferi species, more than 2 times the cell spirally curved, flexible cells. It was also advocated the separation of these three types are independent of each type. Moreover, in some species with flagella spirochetes, some do not have flagella. Helicobacter pylori is humanity's oldest, is also one of the most intimate partners, the German anatomist discovered as early as 1875 human gastric mucosa layer there lived a spirochete, but because they can not cultivate a pure line strains, the The result was neglected and forgotten. Until 1982, doctors in Australia Marshall and Warren was isolated from the bacteria. Higher risk in the next 10 years, researchers found that people with this microorganism in the stomach, suffering from peptic ulcer (stomach or intestinal wall 12 refers to the damage); while H. pylori may also lead to one of the most common gastric . Due to the widespread use of antibiotics and the improvement of public health, hindering the spread of bacteria, making the past 100 years, Helicobacter pylori in developed countries is gradually disappeared. When H. pylori retreat, peptic ulcers and gastric cancer incidence also followed lower; same time, however, esophageal disorders (including acid reflux and a particularly vulnerable to deadly esophageal cancer) there is a surge phenomenon, there is a wide range of and sufficient evidence to show that these diseases increases with the disappearance of Helicobacter pylori. The bacteria may actually protect people suffering from gastrointestinal disease free, which is of great significance. For example, currently used for the eradication of H. pylori in the stomach of antibiotic therapy should be re-evaluated in order to avoid the damage is greater than the benefits. In order to fully understand the impact of H. pylori on health, researchers are further explore the complex interactions between the microbe and host. Diversification of Helicobacter pylori After scientists started studying H. pylori, and soon discovered that different from strains isolated from humans, with a high degree of inconsistency between (just in the same person's stomach, it is possible to find a variety of strains). Although the appearance of the same strains, they have great differences in the genetic code. Researchers have located the genome sequences of two strains of dna: Both have a small chromosome, the nucleic acids of nearly 1.7 million, about 1,550 genes. Which Helicobacter pylori strains with caga genes, will result in more serious stomach inflammation and tissue damage, so the genetic strain of human infection caga higher morbidity. H. pylori strains, the laboratory will epithelial cells form a large hole (vacuoles). This phenomenon is caused by a toxin substance called "bubble toxin" (vaca), it is called a gene vaca. Vacuole formation of toxins in addition to make the cell vacuole, it makes the white blood cells fight infection stomach loss of vitality, diminished immune response to H. pylori. Caga different and are all H. pylori strains have va-ca genes, but there is a big difference to each other in the sequence, only some strains can produce toxins fully functional. vaca has four main variants: m1, m2, s1 and s2. Mechanism of H. pylori and gastric parietal cells is to use a configuration similar to the hypodermic needle, the protein was injected into the stomach wall caga epithelial cells. Helicobacter pylori while also releasing toxins vacuole, let epithelial cells formed hollow inside. With m1 and s1 Helicobacter pylori genotypes most lethal toxins produced vacuole. Therefore, if the body is m1 genotype strains vaca or s1, plus caga gene, who suffer the highest probability of gastric cancer. Make things even more complicated, some people will contribute their genes inflammation caused by bacteria, more susceptible to stomach cancer. The worst case is that a person with a pro-inflammatory genes, and the stranger the stomach with Helicobacter pylori and s1/m1vaca caga genotypes. Most cases of stomach cancer are this high risk group of hosts, and just hit particularly strong aggressive strains. The other side of Helicobacter pylori extinction Humans are the only host of Helicobacter pylori, the bacteria by mouth to mouth or mouth to spread on the face. Infection rate is much lower than in developed countries in other regions, such as geographic differences may be partly due to improve over the past century in Europe and America and other developed countries for public health. But the widespread use of antibiotics is caused by the gradual disappearance of H. pylori; Even short-term use of antibiotics for any reason, will destroy bacteria in the body. In the more developed countries infrequent use of antibiotics in children older than 10 years from 70% to 100% have H. pylori in the stomach, most people have their lives stomach bacterium; contrast, the American-born now Children less than 10% of the body have this organism, this difference shows a significant change in human microbiology. Moreover, the disappearance of H. pylori may be a warning, the display may also have other microbes are also facing extinction fate. Helicobacter pylori is the only bacteria can survive in the acidic environment of the human stomach, it's there or not, you can easily through the blood, feces, respiratory or gastric tissue samples test out; But other parts of our body, such as the mouth, colon, skin and vagina, and there are also complex protist populations, if there is another common bacteria disappeared, we can not even detect whether it reduces diagnostic tools are not. Disappearance of H. pylori will be affected? Peptic ulcer developed countries (apart from ulcers due to aspirin or ibuprofen sort of non-steroidal anti-inflammatory drug-induced) and a significantly lower incidence of gastric cancer. Because these diseases take years before development, especially gastric cancer, thus reducing morbidity phenomenon actually lower than that of H. pylori infection delayed for decades, but the current situation is quite alarming decline. When in 1900 the United States of gastric cancer is still a major killer, to 2000 when the gastric cancer incidence and mortality rates have been reduced by more than 80%, it is now after the colon, prostate, breast and lung cancer lagging. And there is ample evidence to show that the continued extinction of Helicobacter pylori in gastric cancer reduced the incidence of the phenomenon plays an important role, which is good news. At the same time, however, there is another aspect of a new class of diseases of the esophagus, and morbidity unexpectedly surged. Since 1970, the United States, Britain, Sweden, Australia, epidemiologists have noted a steep rise of esophageal adenocarcinoma, which is a place in the inner wall of the upper esophagus, stomach, a very aggressive cancer. In the United States, the incidence of esophageal adenocarcinoma increased by 7% to 9% a year, making it America's fastest-growing major cancers. After patients diagnosed with esophageal cancer, the survival rate after five years is less than 10%. These horrible cancer came out from where? We know that the most important risk factors causing this cancer is "gastroesophageal reflux disease": the influx of stomach acids back to the esophagus and cause chronic inflammatory disease, and is often referred to as "acid reflux." Such symptoms until 1930 only appeared in the medical literature, however, since then, it steadily increased incidence of acid reflux, and now this disease in the United States and other Western European countries are quite common. Acid reflux may lead to Barrett's esophagus, a precancerous lesion of this phenomenon in 1950 by a British surgeon Barrett first proposed. Barrett's esophagus increase of just echoes and increase acid reflux, and the risk of patients with these symptoms of esophageal adenocarcinoma was higher. We now know about acid reflux will start a course of 20 to 50 years: In some cases, the symptoms will gradually evolve into Barrett's esophagus, and then progressed to cancer, and other epithelial tissues gradually similar to the case of cancer development. However, acid reflux disease and its follow-up, why is it becoming more common? Emergence of these diseases, Helicobacter pylori is just disappearing in the occasion, can not help but wonder if there is correlation between the two, but in recent years, a growing number of studies support the stranger actually Helicobacter pylori stomach theory can be avoided to protect the esophagus from acid reflux. Furthermore, strains with caga (that is the most toxic, can cause ulcers and stomach cancer strains) seems to protect the esophagus is relatively strong. In 1998, the U.S. National Cancer Institute researchers found that people infected with H. pylori strains with caga lower esophagus and stomach closest to the esophagus site developed significantly lower risk of adenocarcinoma. Then the United States and the Netherlands, the researchers confirmed that acid reflux and Barrett's esophagus, Helicobacter pylori infection and also had a similar association; Other independent studies from the UK, Brazil and Sweden, and also get the same conclusion. However, perhaps because researchers used different methods, not all researchers have found that this effect, however, the available scientific evidence has a considerable persuasive. [Treatment] Helicobacter pylori in vitro are very sensitive to a variety of antimicrobial agents, but the body of a drug alone, several full invalid. Clinical often metronidazole, tetracycline, ampicillin, amoxicillin and other drugs for two to three combined.
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No. 2
螺旋菌
English name: Helicobacter pylori (H. pylori or H. pylori) Bacterial cells in a curved shape. According to the degree of bending and hardness of the cell, and often will be divided into three types. The first one kind of Vibrio cells is short, less than a lap only once bent, rounded in such Desulfovibrio (Vibrio desulfuricans), was shaped like a comma: comma vibrio (Vibrio comma), is one of Vibrio cholerae one kind, may be connected to each other Vibrio spiral; 2 species pylori cell is twice or more curved spiral than tough, such as small Azospirillum; 3 burgdorferi species, more than two bends into the cells spiral cell soft. It was also advocated the separation of these three types are independent of each type. Moreover, in some species with flagella spirochetes, some do not have flagella. Pylori in anaerobic sludge purple sulfur pylori (Thiospirillum violaceum), Rhodospirillum genus (Rhodospirillum) and green snail species. Helicobacter pylori is humanity's oldest, is also one of the most intimate partners, the German anatomist discovered as early as 1875 human gastric mucosa layer there lived a spirochete, but because they can not cultivate a pure line strains, the The result was neglected and forgotten. Until 1982, doctors in Australia Marshall and Warren was isolated from the bacteria. Higher risk in the next 10 years, researchers found that people with this microorganism in the stomach, suffering from peptic ulcer (stomach or intestinal wall 12 refers to the damage); while H. pylori may also lead to one of the most common gastric . Due to the widespread use of antibiotics and the improvement of public health, hindering the spread of bacteria, making the past 100 years, Helicobacter pylori in developed countries is gradually disappeared. When H. pylori retreat, peptic ulcers and gastric cancer incidence also followed lower; same time, however, esophageal disorders (including acid reflux and a particularly vulnerable to deadly esophageal cancer) there is a surge phenomenon, there is a wide range of and sufficient evidence to show that these diseases increases with the disappearance of Helicobacter pylori. The bacteria may actually protect people suffering from gastrointestinal disease free, which is of great significance. For example, currently used for the eradication of H. pylori in the stomach of antibiotic therapy should be re-evaluated in order to avoid the damage is greater than the benefits. In order to fully understand the impact of H. pylori on health, researchers are further explore the complex interactions between the microbe and host. Diversification of Helicobacter pylori After scientists started studying H. pylori, and soon discovered that different from strains isolated from humans, with a high degree of inconsistency between (just in the same person's stomach, it is possible to find a variety of strains). Although the appearance of the same strains, they have great differences in the genetic code. Researchers have located the genomic DNA sequences of two strains: both have a small chromosomes, the nucleic acids of nearly 1.7 million, about 1,550 genes. Which Helicobacter pylori strains with the cagA gene, will result in more serious stomach inflammation and tissue damage, so people infected with cagA gene strains morbidity is higher. H. pylori strains, the laboratory will epithelial cells form a large hole (vacuoles). This phenomenon is caused by a toxin substance called "bubble toxin" (vaca), it is called a gene vacA. Vacuole formation of toxins in addition to make the cell vacuole, it makes the white blood cells fight infection stomach loss of vitality, diminished immune response to H. pylori. CagA and different, all strains of H. pylori have va-cA genes, but there is a big difference to each other in the sequence, only some strains can produce toxins fully functional. There are four major vacA variants: m1, m2, s1 and s2. Mechanism of H. pylori and gastric parietal cells is to use a configuration similar to the hypodermic needle, the CagA protein was injected into the stomach epithelial cells. Helicobacter pylori while also releasing toxins vacuole, let epithelial cells formed hollow inside. With m1 and s1 Helicobacter pylori genotypes most lethal toxins produced vacuole. Therefore, if the body vacA genotype strains is m1 or s1, coupled with cagA gene, who suffer the highest probability of gastric cancer. Make things even more complicated, some people will contribute their genes inflammation caused by bacteria, more susceptible to stomach cancer. The worst case is that a person with a pro-inflammatory genes, and the stranger the stomach with Helicobacter pylori cagA and s1/m1vacA genotypes. Most cases of stomach cancer are this high risk group of hosts, and just hit particularly strong aggressive strains. The other side of Helicobacter pylori extinction Humans are the only host of Helicobacter pylori, the bacteria by mouth to mouth or mouth to spread on the face. Infection rate is much lower than in developed countries in other regions, such as geographic differences may be partly due to improve over the past century in Europe and America and other developed countries for public health. But the widespread use of antibiotics is caused by the gradual disappearance of H. pylori; Even short-term use of antibiotics for any reason, will destroy bacteria in the body. In the more developed countries infrequent use of antibiotics in children older than 10 years from 70% to 100% have H. pylori in the stomach, most people have their lives stomach bacterium; contrast, the American-born now Children less than 10% of the body have this organism, this difference shows a significant change in human microbiology. Moreover, the disappearance of H. pylori may be a warning, the display may also have other microbes are also facing extinction fate. Helicobacter pylori is the only bacteria can survive in the acidic environment of the human stomach, it's there or not, you can easily through the blood, feces, respiratory or gastric tissue samples test out; But other parts of our body, such as the mouth, colon, skin and vagina, and there are also complex protist populations, if there is another common bacteria disappeared, we can not even detect whether it reduces diagnostic tools are not. Disappearance of H. pylori will be affected? Peptic ulcer developed countries (apart from ulcers due to aspirin or ibuprofen sort of non-steroidal anti-inflammatory drug-induced) and a significantly lower incidence of gastric cancer. Because these diseases take years before development, especially gastric cancer, thus reducing morbidity phenomenon actually lower than that of H. pylori infection delayed for decades, but the current situation is quite alarming decline. When in 1900 the United States of gastric cancer is still a major killer, to 2000 when the gastric cancer incidence and mortality rates have been reduced by more than 80%, it is now after the colon, prostate, breast and lung cancer lagging. And there is ample evidence to show that the continued extinction of Helicobacter pylori in gastric cancer reduced the incidence of the phenomenon plays an important role, which is good news. At the same time, however, there is another aspect of a new class of diseases of the esophagus, and morbidity unexpectedly surged. Since 1970, the United States, Britain, Sweden, Australia, epidemiologists have noted a steep rise of esophageal adenocarcinoma, which is a place in the inner wall of the upper esophagus, stomach, a very aggressive cancer. In the United States, the incidence of esophageal adenocarcinoma increased by 7% to 9% a year, making it America's fastest-growing major cancers. After patients diagnosed with esophageal cancer, the survival rate after five years is less than 10%. These horrible cancer came out from where? We know that the most important risk factors causing this cancer is "gastroesophageal reflux disease": the influx of stomach acids back to the esophagus and cause chronic inflammatory disease, and is often referred to as "acid reflux." Such symptoms until 1930 only appeared in the medical literature, however, since then, it steadily increased incidence of acid reflux, and now this disease in the United States and other Western European countries are quite common. Acid reflux may lead to Barrett's esophagus, a precancerous lesion of this phenomenon in 1950 by a British surgeon Barrett first proposed. Barrett's esophagus increase of just echoes and increase acid reflux, and the risk of patients with these symptoms of esophageal adenocarcinoma was higher. We now know about acid reflux will start a course of 20 to 50 years: In some cases, the symptoms will gradually evolve into Barrett's esophagus, and then progressed to cancer, and other epithelial tissues gradually similar to the case of cancer development. However, acid reflux disease and its follow-up, why is it becoming more common? Emergence of these diseases, Helicobacter pylori is just disappearing in the occasion, can not help but wonder if there is correlation between the two, but in recent years, a growing number of studies support the stranger actually Helicobacter pylori stomach theory can be avoided to protect the esophagus from acid reflux. Furthermore, strains with cagA (that is the most toxic, can cause ulcers and stomach cancer strains) seems to protect the esophagus is relatively strong. In 1998, the U.S. National Cancer Institute researchers found that people infected with H. pylori cagA strains, lower esophagus and stomach closest to the esophagus site developed significantly lower risk of adenocarcinoma. Then the United States and the Netherlands, the researchers confirmed that acid reflux and Barrett's esophagus, Helicobacter pylori infection and also had a similar association; Other independent studies from the UK, Brazil and Sweden, and also get the same conclusion. However, perhaps because researchers used different methods, not all researchers have found that this effect, however, the available scientific evidence has a considerable persuasive. [Treatment] Helicobacter pylori in vitro are very sensitive to a variety of antimicrobial agents, but the body of a drug alone, several full invalid. Clinical often metronidazole, tetracycline, ampicillin, amoxicillin and other drugs for two to three combined.
