• Urease:
The highly acidic peptic environment make it almost impossible for any organism to exist, but thanks to the ability of H.Pylori to produce the enzyme Urease, H.Pylori can thrive in the stomach. Urease has the ability raises the surrounding pH throughout converts urea to ammonia plus carbon dioxide, raising the pH of the surrounding area. Which can lead to mild protection against gastric acid.
• Shape and flagella:
Gastric pH still high for the bacteria to survive for a long time, comes the helical shape of H. pylori that enhances its polar flagella to propel over the mucus epithelial lining. In addition to the chemotaxis systems that guide H.Pylori into some amino acids, bicarbonate, and cholesterol. This will leave the bacteria
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pylori infection. H. pylori infects the gastric mucosa, making intimate contact with gastric epithelial cells through molecules such as the adhesin BabA. Adhesion to epithelial cells allows secretion of virulence factors, such as CagA and VacA, into the cells, where their activity can modify host cell function. H. pylori establish a chronic infection despite strong induction of host immune responses. Inadequate innate immune recognition, through mechanisms such as the inability of H. pylori lipopolysaccharide to be recognized by Toll-like receptor 4 (TLR4) as well as the inability of FlaA to activate TLR5, might contribute to the failure of the adaptive immune response to clear the infection. In terms of the adaptive immune response, dendritic cells have emerged as an important cell population responding to H. pylori infection by preferentially producing IL-12 (typical of a Th1 response) and a moderate IL-10 induction (more typical of a Th2 response) that might be important for the activation of T regulatory cells. H. pylori –specific T regulatory cells can suppress the memory T-cell response to H. pylori in infected individuals, contributing to the inability of the host to clear the infection. Furthermore, other cells of the immune system are also affected by H. pylori products: For example, VacA has been reported to modify T-cell proliferation and S.cagPAI products, in addition to inducing IL-8 secretion by epithelial cells (responsible for the infiltration of neutrophils in the H.pylori –infected gastric mucosa), have recently been implicated in the induction of monocyte apoptosis. Apoptosis of macrophages is also induced by H. pylori, an activity that requires the enzyme arginase II. A role for arginase in impairment of macrophage activity and T-cell proliferation has also been
Making H. pylori a vital microorganism to research in order to expand the study of microbiology and its interaction with humans. According to Blaser, the H. pylori “is a group of extremely varied strains cooperating and competing with one another. They compete for nutrients, niches in the stomach and protection from stresses.” There can be a variety of strains found in a single stomach, and even though they appear identical, their genes are very different.
The effects of low pH, in guinea-pigs digestive tract, showed a similar effect to that of human lactase in a low pH environment. The pH levels tested in the guinea-pigs experiment were 2.5, 3.0, 3.5, and the control was 6.5. As the pH became
The helicobacter pylori bacterium also commonly known as H. pylori is a spiral shaped bacterium that is often found growing in the digestive tract. H. pylori bacteria are found in more than half of the world’s population. The bacteria normally attack the lining of the stomach and the small intestines. Although they are present in many people the H. pylori bacteria is usually harmless. The bacteria are adapted to live and survive in the acidic environment of the digestive tract. Furthermore, H. pylori reduces the acidity of the environment around it to survive and will penetrate the lining of the stomach and small intestines where the mucus lining protects it from the body’s immune cells. H. pylori sometimes can interfere with the body’s immune response to ensure their survival and this causes stomach problems (Flemin & Alcamo, 2007).
The SMART goal for the patient’s diagnosis of diarrhea is that the patient will defecate formed, soft stool every 1 to 3 days and will express relief of cramping with little or no diarrhea. The intervention to meet this smart goal is the administration of fidaxomicin, a narrow spectrum antibiotic, to treat the infection of Clostridium difficile (Sears, 2013). Another nursing intervention for the treatment of diarrhea is assessing the patient for sodium and potassium loss, as well as explaining the prevention methods to avoid the spread of excessive diarrhea (Mitchell, 2014). The nurse must also provide proper skin integrity care to the peritoneal are and make the environment safe and easy for access to the bathroom. The SMART goal for the patient’s diagnosis of acute pain is that the patient will state relief of pain in abdominal area after treatment with opioids in a 24hr period. The nursing intervention for acute pain is the administration of opioids as well as positioning to keep patient in as much comfort as possible and take pressure off of the abdominal area. The nurse must also assess the patient’s vital signs and pain level
The stomach naturally produces acid, which is mainly responsible for food digestion and the destruction of any foreign pathogen or bacteria ingested with food. Acid is secreted by stimulating the partial
bottom edges are not tightly shut, and acid moves form the stomach up into the
In addition to its traditional clinical manifestations, GAS can also cause serious invasive disease such as necrotizing fasciitis, colloquially known as the flesh-eating disease. First broadly reported during the Civil War, when it was known as gangrene, necrotizing fasciitis occurs when an individual’s subcutaneous fat and superficial fascia become rapidly necrotic. Though incidence data is limited, one study estimated that, worldwide, there are approximately 660,000 cases of invasive GAS disease per year, with 97% of those cases occurring in low-income populations (4). Many microorganisms other than GAS have been linked with necrotizing fasciitis, including Staphyloccocus aureus, Escherichica coli, and Klebsiella pneumoniae, and the disease is often caused by a polymicrobial infection. However, the most well known causative agent in necrotizing fasciitis cases is usually Group A streptococci (6). Although risk factors for necrotizing fasciitis include diabetes, old age, and immunosuppression, nearly half of all infections occur i...
Gut bacteria keep humans healthy by stimulating the digestive process within the large intestines. In order for nutrients to be successfully absorbed in the colon, non-digestible carbohydrates are degraded by beneficial gut microbial. One example of an anaerobically respiring bacterium which dominates the large intestine is bacteroide thetaiotaomicron. This bacteri...
To understand the human gut health and aetiology, the first step is to understand the gastrointestinal (GI) microflora and its distribution through the digestive system [2]. The human GI tract is inhabited by trillions of microorganisms, which together is known as the microbiota [5]. These microorganisms come from both archeal and bacterial domains. Bacteria are the predominant kingdom of organisms and it is composed mainly by five bacterial phyla: Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria and Verrucomicrobia [3]. The great majority of mammalian gut microbiota belongs to the three phyla: the Gram-negative anaerobe Bacteroidetes, the Gram-positive Actinobacteria and Firmicutes [5].
Acid is produced naturally in your stomach to help you digest food and to kill bacteria. This acid irritates the stomach lining so our body produces a natural mucus barrier which protects it. Sometimes this barrier may be damaged thus allowing the acid to damage the stomach causing inflammation, ulcers and other conditions. Other times, there may be a problem with the muscular band at the top of the stomach that keeps the stomach tightly closed and this allows the acid to escape and irritate the oesophagus. This is called 'acid reflux' and can cause heartburn and/or oesophagitis. Proton pump inhibitors such as omeprazole stop cells in the lining of the stomach from producing too much acid. This can help prevent ulcers from forming or assist the healing process. By decreasing the amount of acid, they can also help to reduce acid reflux related symptoms such as heartburn.
Once in the stomach, the glands that are there begin to secrete enzymes and a mucous that help to protect the stomach from its own acids. While this is being done, the muscles of the stomach are contracting. This causes the food to be turned and moved all throughout the stomach. This process turns the food into chyme, which is just a liquefied version of the food that was first taken...
The inflammatory response is a nonspecific response to cellular injury and bacterial invasion. Inflammation is the primary defense in early gingivitis. Biofilm can initiate an inflammatory response if it is left undisturbed for as little as seventy two hours. Redness and swelling are two of the cardinal signs of inflammation and can be observed clinically in gingivitis. Histamine is released by mast cells and responsible for the redness and swelling of tissues. Histamine causes both an increase in vascularity and permeability of blood vessels at the site of injury. Swelling may occur in response to the accumulation of fluid at a specific site. The inflammatory response includes cellular components of the immune system polymorphonuclear leukocytes and macrophages. Polymorphonuclear leukocytes are crucial to the cellular immune response. Polyporphonuclear leukocytes are the first cells that arrive at an inflammatory site. Polymorphonuclear leukocytes arrive at the site via chemotaxis, and begin to phagocytize bacteria. As the disease continues and the inflammatory reaction is not strong enough to subside the bacterial infection the immune response is further
Adaptive immune system happens much quicker to the presence of an “infection creating potent mechanisms for neutralizing or eliminating the microbes. There are two types of adaptive immune responses: humeral immunity, mediated by antibodies produced by B lymphocytes, and cell-mediated immunity, mediated by T lymphocytes.”
ix. citric acid increases the acidity of foods and makes it harder for bacteria to
Food borne illnesses are caused by consuming contaminated foods or beverages. There are many different disease-causing microbes, or pathogens. In addition, poisonous chemicals, or other harmful substances can cause food borne illnesses if they are present in food. More than two hundred and fifty different food borne illnesses have been described; almost all of these illnesses are infections. They are caused by a variety of bacteria, viruses, and parasites that can be food borne. (Center 1)