P Gingivalis Synthesis

In the case of Bordetella perussis there are a few specific proteins which are known to be necessary for bacterial adhesion and infection (3). Pertussis toxin, adenylate cyclase, filamentous hemagglutinin, pertactin, and fimbriae are responsible for the adhesion of the bacterial cell to the extracellular matrix of the host cell (3). Pertussis toxin and adenylate cyclase also play a role in invading the cell, evading the host's immune system, and the actual infection process (3).

Clostridium tetani is a species of pathogenic bacteria which causes the disease tetanus in humans (World Health Organisation [WHO], 2008). Bacteria are prokaryotic microorganisms which contain various structural components. These components include a cell wall and outer membrane which is discovered by the gram stain procedure (Kratz, 2011). C. tetani are gram-positive bacteria therefore its cells have a thick wall however they do not possess an outer membrane ("Vaccines and immunisations," 2015). Other components include flagella which provide cell movement, pili which permit cell adhesion to surfaces such as host cells, and bacterial capsules also known as glycocalyx which prevents the cell from phagocytosis (Todar, 2012).

Hello, I am an Treponema Denticola, a gram-negative bacterium. I am from Spirochetes family. I am slim and curved; therefore, not to lose shape, I always move. My home is oral cavity because temperature and pH level in oral cavity is optimal for me. The normal temperature at which I can exist is ranged between 32-42°C, and pH level is ranged between 6.5-8.0. I love darkness where is no oxygen because I am an anaerobic microorganism, so I settle down deep to periodontium. If I have great conditions to grow and multiply in oral cavity, I can cause several periodontal diseases such as periodontitis, necrotizing ulcerative gingivitis, and acute pericoronitis.

Chronic periodontitis is common disease of the oral cavity, that can occur over a wide range of age. The major determinant of disease susceptibility is the host immune-inflammatory response to the sub-gingival biofilm. It is paradoxical that these defensive processes result in the majority of the tissue damage leading to the clinical manifestations of disease. The unique anatomy of the periodontium

Enterococcus cacae isolated from human stool differs because of its inability to produce acid from arabinose, lactose, and mannitol. Enterococcus camelliae was isolate from fermented tea leaves in Thailand; they are unable to produce acid from D-galactose and lactose. Enterococcus canis was isolated from rectal swabs and chronic otitis in dogs; they are unable to hydrolyse arginine or to grow on selective media that contain 0.04% azide. Enterococcus avium Enterococcus pseudoavium differs from their inability to produce acid from lactose. Enterococcus hermanniensis differ from the inability to produce acid from substrates. Enterococcus lactis are atypical and are isolated in raw milk Italian cheeses. Enterococcus quebecensis and Enterococcus termitis are negative for the Voges-Proskauer (VP) test, meaning that as a result of fermentation, acid is not produced. Enterococcus rivorum growth at 45ᵒC or in a 6.5% NaCl broth there is little or no growth. Enterococcus ureasiticus has a urease activity production. Some species found in water or on plants differ because they can produce pigments such as Enterococcus ureilyticus and Enterococcus rotai. The most common species seen in humans are Enterococcus facalis and Enterococcus faecium which through testing has shown a resistance to clindamycin and oxacillin but

Elderly institutionalized, chronic obstructive pulmonary disease, and ICU patients are at higher risk of periodontal colonization by nosocomial pathogens because of difficulties in oral hygiene, changes in salivary properties, and reduction of anaerobic flora.7, 8, 9 In ICU patients Oropharyngeal colonization by aerobic pathogens occurs very rapidly because of incumbent changes in antibacterial resistance, i.e., decreased immunoglobin (Ig)-A salivary content, reduced salivary secretion, mechanical injury induced by nasogastric and endotracheal tubes and mucosal desiccation. This in turn facilitates the mucosal adhesion of aerobic bacilli and allows bacterial multiplication and speedy growth on pharyngeal mucosa.10, 11 Oral Plaque harbors microorganisms in the sequence of initial colonization and represents an additional source of nosocomial colonization and infections in ICU patients. Plaque inside oral cavity is a dynamic and conglomerate system that associates microbes ingrained in an extracellular pattern. This mainly results from encampment and amplification of aerobic, anaerobic, and filamentous microorganisms on the surfaces of teeth, dental prostheses and soft tissues. Dental plaque is predominately located on the subgingival and supragingival surfaces of the teeth, but without

The human mouth is home to a complex biological environment in which a variety of microorganisms reside. With its composition of bone in the jaw, muscle in the cheeks and tongue, epithelium covering most structures, and teeth with a calcium enamel layer, organisms living in the mouth are selected that have structures built to withstand and utilize anything that passes through their environment. The mouth, or oral cavity, plays a major role in human respiration and digestion, making it a location in which various substances pass through and the environment can quickly change. In order to increase chance of survival, bacteria of the teeth form a biofilm, known more commonly as plaque, within which they can grow together in a more defensive manner. Biofilms form when planktonic bacteria attach to a surface and secrete an extracellular matrix of polysaccharide, and as more microorganisms group together they create a film on the surface. (7) In the case of dental plaque, bacteria become less vulnerable to the effects of antimicrobial agents that are often found in toothpastes and mouthwashes, as well as showing physiologic variations of structure compared to planktonic organisms that have not yet settled into a biofilm. (2) This formation also allows the bacteria to become more

Bacterium responsible for dental caries is Streptococcus mutants. It is a Gram positive, anaerobic bacterium that inhabitants oral cavity. This bacterium posses an enzyme glucansucrase, by which it converts sucrose to lactic acid. It uses Sucrose for cell wall formation, This is the reason that consumption of candies rich in sucrose most often by children results in dental caries as Sucrose helps these bacteria to flourish in oral cavity.

Studies show that half of Americans suffer from chronic gum disease. In today’s society, half of the issue with periodontal disease is learning how to address it. It has been proven that the same pathogens that are the root of periodontal disease can also contribute to other health factors that can affect the body. Many of the health factors that come with having periodontal disease consist of; diabetes mellitus,

This allows either gastric juice or the larval enzyme or both go to the underlying tissue as shown by Matthews (1982). ES products are capable of degrading the extracellular matrix. The biologically active ES products may also be capable to bind with a membrane receptor protein and cause intracellular changes which influence cell growth as shown by Raybourne (1986). By using the vitro scanning electron microscope, tunnels and burrows are found in the mucosa and submucosa of human stomach when the A. Simplex L3 penetrating the tissue layers as shown by Sakanari & McKerrow (1990). The hemorrhagic lesions, burrowing and tunnel formation result from tissue invasion cause abdominal pain, vomiting and nausea after few hours of ingestion of A.

Aggregaitbacter actinomycetemcomitans (A.a.)is a gram negative organism that is present in a large number of the populations mouths [2]. It also plays a key role in the formation of aggressive periodontitis, specifically the localized form (LAP). A. actinomycetemcomitans produces several products that contiribute to the destruction of the peridontium . It can cross the mucosal epithelial barrier, accessing the bloodstream and has been detected in atheroma plaques, periarditis, septicemia, pneumonia, and infection arthritis [4]. The fact that the bacterium is found elsewhere in the body is important in helping to develop a link between oral and systemic health.

The genetically determined capacity of the host to deal metabolically with chronically administered drugs, the responsiveness of gingival tissue to the drugs, and preexisting gingival condition, including inflammation may, differ among individuals.

We cannot ignore that we have identified H. pylori in 18 patients (20.63%) suffering from gastric and periodontal disease. Namiot DB et al. (10) detected it only in three cases among 157 patients. H. pylori was detected in dental plaque with a rate of 34.1% (16) and in 82.3% by Gao J et al. (24). Boyanova et al. (6) isolated oral strain from a child with both gingivitis and chronic gastritis. In the study of Anand et al., the occurrence of H. pylori in the dental plaque of patients with gastric H. pylori infection was higher than in controls (25). Sudhakar U et al.(1), identified five patients (10%) positive for H. pylori by culture. H. pylori was identified by culture in 2/208, and by PCR in 15/208 (7%) (26). This result demonstrates the

There are many techniques used to extract LPS include extraction with trichloroacetic acid (TCA), extraction with water at 80 "C, extraction with aqueous phenol and extraction with aqueous ether at 6-12"C, the extraction with aqueous phenol has obtained widespread popularity not only because it can be used to many groups of bacteria and is a relatively simple technique, but also because it represents one of the few techniques to extract LPS from R-mutant bacteria (63). Also there is EDTA-heat extraction method (64). Lipopolysaccharide able to eliciting an extensive variety of pathophysiological effect such as endotoxin shock , tissue injury and lethality in both human and animal (66). Upon infection with respiratory pathogens, the airway mucosal immune system rapidly develops a pro-inflammatory response

Their (outer) layers are formed of lipoproteins, lipopolysaccharides, lipid bilayer, and polysaccharides. The chance of occurrence of an infection through Proteus Mirabilis is determined by the presence of the bacteria and the host organism’s body defense mechanisms. These two factors determine the virulence behavior of Proteus Mirabilis. The size of inoculum for Proteus Mirabilis positively correlates with the chances of a host getting infected by the host.