How Are Microorganisms Affect Bacterial Growth?

The conditions needed for the growth of micro-organisms are: Micro - organisms need food to survive. They like high protein food to survive, eg. Poultry & fish. Most micro - organisms need warmth & grow best at 20-40c. They need moisture to multiply. They need air to multiply, though some can without. A single Micro-organism becomes two every twenty minutes.

Background information: In this lab you will be looking at the growth of bacteria under different conditions to see the how populations of bacteria grow. Read about cells in the text or e-text. For everyone, in your e-text read chapter 13, sections 13.3 and 13.4 to learn more about bacteria. Then answer the questions below.

When testing this certain type of bacteria the warm temperature caused it to grow exceptionally fast comparted to the room temperature. Bacteria are single celled microbes. The cell structure is simpler than that of other organisms as there is no nucleus or membrane

The history of Helicobacter pylori goes back to 1875 when German scientists found the spiral shaped bacteria in the stomach linings of patients (“Helicobacter Pylori,” Wikipedia). However, Helicobacter pylori, also known as H. pylori, was officially discovered in 1982 by Barry Marshall and Robin Warren when they ended up leaving petri dishes incubating over Easter weekend (“Helicobacter pylori,” Wikipedia). After returning to the petri dishes after five days they discovered they had unintentionally successfully cultured the bacteria and were finally able to visualize it (“Helicobacter pylori,” Wikipedia). Until 1989, Helicobacter pylori was called Campylobacter pylori (“Helicobacter pylori,” Wikipedia). However further research done in 1989

Helicobacter pylori, also known as H. pylori, is a spiral bacterium that lives inside the human stomach. H. pylori likes the acidic environment that the stomach provides and evidence has linked it to a variety of minor gastrointestinal illnesses. H. pylori causes inflammation in the lining of the stomach and is involved in 90% of stomach and intestinal ulcers. H. pylori also has an apparent cause to the development of adenocarcinoma, a common stomach cancer. J. Robin Warren first detected H. pylori in the stomachs of ulcer patients in 1979. Warren then isolated the microbe in a culture and tested it effects by swallowing some of the inoculum. A short-term case of gastritis (inflammation of the lining of the

Helicobacter Pylori is a gram negative bacteria that is found in the stomach. Helicobacter Pylori is referred to as H. Pylori. This type of bacteria lives in your bodies digestive tract. H. Pylori is a common bacterial infection, and can cause ulcers in the lining of your stomach. Once H. pylori gets into your stomach, it attacks the lining of your stomach. After the bacteria damages the lining of the stomach, acid gets through the lining of your stomach which is what causes the ulcers to occur. The ulcers can bleed and keep food from going through to digestive tract. The symptoms of an ulcer caused by H. Pylori are, dull burning pain in your belly, bloating, burping, not feeling hungry, nausea, vomiting, weight loss for no clear reason. And

Helicobacter pylori is structurally small, gram negative rods which is microaerophilic in nature and has capability of colonizing regularly in human stomach (Strausbaugh et al., 2002). Due to such colonizing capability, it is regarded as one of the most common bacterial pathogen present in almost 50% of the world’s population (Zhao et al., 2014) and the reason behind such well adaptation or enduring of H.pylori in the Human’s stomach is due to the combined effects of several factors that addresses different challenges or obstacles presented by the nasty environment inside the stomach (Montecucco and Rappuoli, 2001). Helicobacter pylori produce the urease that neutralize the gastric acid or shows the buffering effect around the surroundings within the stomach. Moreover, it has a capacity of crossing the thick mucus lining of the stomach easily and binding itself to the antigen known as Lewis antigen that are basically present in gastric cells and whose function is to secrete different factors associated with stimulating and attracting the inflammatory cells and Toxin VacA that performs the multiple functions and such activities of H.pylori is possible due to its helicoidal shape the mode of action of flagella present. Mainly, the presence of the cag pathogenicity island (Cag-PAI) which is a 40-kb DNA insertion elements containing 32 genes and encoding a type IV secretion system helps in the optimal fitness of the bacteria in the stomach and appearance of pathogenic traits.

A few different factors that affect bacterial growth are the availability of resources and nutrients, temperature and pH. (Act For Libraries) stated in the above paragraph, once the resources and nutrients are

Gastric cancer is one of the deadliest cancers in the world. Most stomach cancers are adenocarcinomas and according to Lauren classifications divide to intestinal and diffuse types. It's caused by many factors such as genetic, environmental, age, gender, race, ethnicity factors. H. pylori infection is the most important factor. The bacteria is a carcinogen type A. Helicobacter pylori is a gram negative and spiral bacteria. And its urease activity neutralizes the stomach acid. The bacteria cause stomach inflammation that could eventually lead to stomach cancer. In this review, we consider the role of Helicobacter pylori in gastric

Helicobacter pylori is found commonly in the mucosal lining of the stomach and the duodenum without penetrating epithelium because its adaptability to the highly acidic and low pH environment. However, occasional or persistent presence has been suggested, (Figure 2) H.pylori DNA was successfully isolated from other locations in the body, such as atherosclerotic plaques and oral cavity, which is not surely confirmed whether its presence due to true colonization for those sites or due to traveling of H.pylori to distant sites as a result of body pathophysiological mechanism. For instance, the phagocytized H.pylori from stomach being transported on macrophages through blood to the atherosclerotic plaques and oral presence as a result of gastric reflux. Other evidences suggesting the presence of Evidence of H. pylori colonization has also been found in the gallbladder, ears, nose, skin, and even eyes.

Explanations for the fast rise in occurrence of EAC involve the increasing prevalence of gastroesophageal reflux and obesity as well as the declining incidence of Helicobacter pylori infection. Helicobacter pylori infection is correlated with hypergastrinemia, the excess of gastrin in the blood. Gastrin is a hormone that is secreted by G cells situated in the gastric antrum and works on the parietal cells to trigger the production of hydrochloric acid. Constant hypergastrinemia due to daily PPI therapy contributes to the raised gastric acid-secretory capacity that is not obvious throughout PPI therapy, but that emerges quickly when the drug is stopped. Increased acid production due to hypergastrinemia poses a risk factor for development of

Classification of the causative agent: H. Pylori is a gram – spiral shaped bacterium History: Helicobacter pylori is the first formally recognized bacterial carcinogen. Virulence factors of the causative agent: The H. pylori adhesion protein BabA2 is thought to play a crucial role in bacterial colonization and in induction of severe gastric inflammation, particularly in combination with expression of CagA and VacA. Mode of transmission: The exact route of transmission is unknown, but acquisition is likely to occur during childhood through faecal–oral or oral–oral contact or during gastrointestinal tract transit disorders. Transmission may also occur through food-borne,

Helicobacter Pylori or H. Pylori is a type of bacteria that invades the body and infects the digestive tract. It was discovered around 1983 by Warren, a biologist and Marshall, a clinician. It is named because of the spiral shape that allows the bacterium to burrow itself deep within the mucosal layer of the stomach wall. This penetration of the stomach lining enables to the bacteria to protect itself against immune cells that would recognize the organism as an invader. In order to survive the natural acidity of the stomach and its contents H. Pylori secretes an enzyme called urease. Although this enzyme helps protect the H. Pylori bacterium against the acidity of the stomach, it does not provide any protection for the depressions or holes in the stomach wall caused by the bacteria. This damage to the stomach wall can lead to ulcers that may bleed, cause other infections, or keep food from passing through the digestive tract. If these ulcers are left untreated, they can more severe diagnoses such as GERD, gastric cancer or gastric mucosa-associated lymphoid tissue lymphoma if left untreated.

He does have a history of Gastritis and takes omeprazole 40mg po daily. He does have bowel movement every day and doesn’t take any stool softners. There is no change in stool color or consistency. He complaints of occasional “gas trouble” and he takes gelucil from over the counter as needed. No complaints of hemorrhoid or rectal

But first, let us talk about the discovery of cells and the cell theory. Robert Hooke, an english scientist, was the man who first discovered the cell in 1665, proof being a book he released at that time called Micrographia. In this book, Hooke gave 60 observations of random objects under a compound microscope with a magnification of 30x. Because of this, he was not able to see the internal structures in the cell, like nuclei and vacuoles, and what he proclaimed to be cells were just empty cell walls of plant tissues. He shared his observations with The English Royal Society, until they started receiving letters from a scientist named Anton van Leeuwenhoek. The letters stated that Anton made use of a microscope containing improved lenses that magnified objects up to 275x, enough to identify the living parts of a cell. He kept on sending