Actinomycetemcomitans Essay

Lipopolysaccharide (LPS, endotoxin) is a component of the membrane of Gram-negative bacteria that causes sepsis [20]. Bacterial toxins play a pivotal role in the pathophysiology of sepsis and mechanisms of multiple organ system dysfunction. However, the literature illustrates that no single mediator/system/pathway/pathogen drives the pathophysiology of sepsis [21]. Current knowledge on sepsis pathogenesis [1, 22-26] includes infection development and interaction with the host before bacteria enter the bloodstream. Actually, the mechanisms of host defense in extravasal compartment (local immunity) is different from the mechanisms of intravasal (bloodstream) defenense because extravasal defense is provided mainly by leukocytes whereas intravasal cellular defense is fulfilled by erythrocytes. The humoral immunity events of pre-septic stage affect bacteremic (septic) stage and interfere with the study of sepsis “per se.” As a result, the pathogenesis and pathophysiology of some pivotal aspects of sepsis remain

Neutrophils and wandering macrophages (originating form monocytes) were most likely the WBCs that phagocytized the tissues and pathogens early in Ed's infection. They gather at sites of infection or inflammation by means of emigration. They are

Bacteria are ubiquitous; they can be found on the skin, in the soil, and inside the body. Because of the very nature of this ubiquity, it is important to be able to determine between different strains of bacteria. An example of this is determining the causative agent for a disease so that the patient will be treated with the appropriate antibiotics. It may be important to determine the bacteria in a certain region, because like with enteric bacteria, it is normal to find them in the digestive tract as they are in a symbiotic relationship with our bodies in this area; however, they also cause opportunistic infections in places outside of the digestive tract to our detriment, such as with a urinary tract infection. Some strains of bacteria are common to nosocomial infections, and identifying these bacteria as such helps create the guidelines for healthcare workers in antiseptic technique. All of the morphology and characteristics of each strain of bacteria help us to better understand the role of bacteria in the body as well as helps us understand how they can cause illness, and what treatment regimen to set in place. In lab this semester, a sample of unknown

When an inflammatory response happens white blood cells release endotoxins and exotoxins that destroy the bacteria causing infection. However, these toxins also cause damage to the surrounding blood vessels and therefore leak into the

We will isolate the bacteria by plating out the root nodule extract on enriched media and typing unique colonies using 16S rRNA sequencing. Additionally, to understand how these bacterial isolates behave in the presence of other actinobacteria, we will test all isolates arising from these purity streaks against an actinomycete known as C3BA. We will observe the interaction between the C3BA companion strain and the test strain and screen for morphology, color, and the ability to inhibit or affect the growth or behavior of either strain. Finally, we will use mass spectrometry to analyze interactions that produce a visible effect, and we will search for unique natural products that may be responsible for the physiological changes observed. If the mass spectrum yields any unique compounds, we will subsequently isolate these compounds and then analyze the compound by NMR to determine the structure of the molecule. This project ties into the larger theme of identifying novel compounds produced by actinobacteria in the environment, with the ultimate goal of potentially identifying a new molecule that may have useful therapeutic

Cytokinines are the one of the primary mediators that signal other cells to release additional mediators such as tumour necrosis factor-a (TNF-a) interleukin (IL)-1, IL-6, IL-8, interferon, leukotrienes, histamine, bradykinin, prostaglandins, thromboxane A2, serotonin, nitric oxide, arachidonic acid, platelet-activating factor (PAF), oxygen free radicals and myocardial depressant factor (Munford, 2001:67). If the invading organism is a gram negative bacterium, endotoxins are also released, which further stimulate the production of these inflammatory mediators (Jones & Bucher, 1999:134).

Swartz et al (1987) demonstrated coaggregation and cohesion with dental plaque bacteria, where Actinomyces viscosus foster the biofilm establishment of Bacteroides gingivalis on teeth by enhancing its adherence. Similarly, the present study finding showed that the contact lens case isolates, Micrococcus spp and Acinetobacter spp can influenced the adherence of Staphylococcus spp in the contact case surface. Staphylococcus spp. identified as the most commonly from the contact lens cases in asymptomatic wearers, also reported as the most commonly found as a part of the normal ocular flora (eye lid, conjunctiva) or extra-ocular microbiota (facial) and elsewhere on human body8,14 Along

The total number of leukocytes (20-30 million in peripheral blood) is not enough for bacteria clearing. Leukocytes are less than 0.1% of the blood cells, besides, only 68% of peripheral blood leukocytes are “professional” phagocytic cells [59]. As a result, bactericidal leukocytes are 0.068% of all blood cells and they have 1200-1500 times fewer chances to contact bacteria than other cells, particularly, erythrocytes [51, 52]. Neutrophils die after engulfing a few pathogens, their life span is form 13 hours to 5.4 days [60-62], whereas erythrocytes, circulating for 100–120 days, live 18-22 times longer than neutrophils [44, 45]. Bacteria are able to kill phagocytes [63-66] and for many pathogens, phagocytosis is indispensable for proliferation and dissemination [67-70]. These data demonstrate that phagocytosis have no bactericidal role in the blood and leukocytes do not provide bloodstream clearance from

BACKGROUND: Aggressive periodontitis (AgP) by definition is a group of rare, very destructive forms of periodontitis, usually manifests itself at an early age and shows a marked tendency to aggregate in families. A variety of factors, such as microbial, environmental and behavioral have been suggested as risk factors of Aggressive periodontitis.

faecalis is the most dominant post-treatment microbe isolated in apical periodontitis and has often been isolated from the root canal in pure cultures. Prevalence of this bacterial infection ranges from 24% to 77% in asymptomatic persistent endodontic infections. E. faecalis are frequently isolated from obturated root canals of teeth that exhibit chronic periapical pathology. E.faecalis, intrinsically or via acquisition, may be resistant to a wide range of antibiotics which, if used may shift the micro biota in favor of E.faecalis.4 Over the past decade oral microbiota have shown resistance to some the commonly used antibiotics which in turn increases the need for monitoring susceptibility patterns periodically by using susceptibility tests and various efficacy

— Interleukin-2- These are part of the body’s natural response to microbial infection by discriminating between foreign non-self-cells and self-cells. This protein regulates the body’s wbc, leukocytes and lymphocytes that are responsible

Actinomycosis is a rare, chronic, and slowly progressive granulomatous disease caused by filamentous Gram positive anaerobic bacteria from the Actinomycetaceae family. Actinomyces israelii is the most common etiologic organism of actinomycosis [1]. Less common species include A naeslundii, A odontolyticus, A viscosus, A meyeri, A turicensis, and A radingae [9.10]. Actinomyces are commensals of the humanoropharynx, gastrointestinal tract and urogenital tract. When tissue integrity is breached through a mucosal lesion they can incade local structures and organs and become pathogenic. Actinomycosis is therefore mainly an endogenous infection [9]. The incidence of actinomycosis infection is rare. In the 1970s the incidence in Cleveland, USA, was reported to be one per 300 000, compared with Germany and the Netherlands in the 1960s where it was estimated to be one per million [11]. The Department of Health in the United Kingdom reported that 0.0006% of hospital consultations (71 in total) were for actinomycosis in England between 2002 and 2003[12]. In recent, abdominopelvic actinomycosis of 23 patients for 15 years and 22 patients for 7 years were reported in respective single center in Korea [13-14]. In present study, we reported 13 patients of abdominoplevic actinomycosis for 20 years.

Enterococci are gram positive cocci that can occur singly, in pairs or as short chains. They are facultative anaerobes, possessing the ability to grow in the presence or absence of oxygen. Enterococci can withstand harsh environmental conditions. There are currently 23 enterococci species and they are divided into five groups based on their interaction with mannitol, sorbose and arginine 5 .E. faecalis can survive extreme challenges. Its pathogenicity ranges from life-threatening diseases in compromised individuals such as bacteremia, septicemia, endocarditis, and urinary tract infections to less severe conditions, such as infection of obturated root canals with chronic apical periodontitis.The persistence of E.faecalis might be due to the

Virulence Factors: The most important virulence factor of S. aureus is the specific surface proteins that allow the organism to attach to host proteins. The surface proteins of this bacterium allow it to attach to host proteins such as laminin and fibronectin, which form the extracellular matrix of epithelial and endothelial cells. S. aureus also produces a number of membrane damaging toxins that allow the organism to further invade and harm the host, of which the alpha- toxin is the most well studied and is the protein responsible for septic shock. The alpha- toxin is a protein that binds to a specific receptor in platelets and monocytes in humans, forming pores that eventually destroy the cell.

Pathogenic L. monocytogenes go through an intracellular life cycle involving early escape from the phagocytic vacuole, rapid intracytoplasmic multiplication, bacterially induced actin-based motility, and direct spread to neighboring cells, in which they reinitiate the cycle. The bacterium is first phagocytosed by these cells and secretes a pore-forming toxin called listeriolysin, which allows the bacterium to escape from the phagosome. All virulent strains of L. monocytogenes synthesize and secrete listeriolysin. Phospholipase A and B are other virulence factors that facilitate escape of L. monocytogenes from the phagosome. Once out of the phagosome L. monocytogenes is capable of rapid division in the cytoplasm, evading the immune response and moving throughout the cytoplasm from cell to cell. L. monocytogenes is well known for its ability to propel itself like a rocket through the cell cytoplasm. This is the result of the bacterium’s ability to polymerize actin filaments at its tail end. Actin is arranged in subunits to form microfilaments that are capable of directing cell movement. L. monocytogenes accomplishes cell motility through a virulence factor called ActA that takes advantage of normal actin polymerization going on in the cell. The ActA protein shares sequence homology with a protein called WASP that is found in virtually all eukaryotic cells. WASP is responsible for recognizing and