Pathogenesis

According to the patient’s condition it can be suggested that he might be suffering from an atypical pneumonia due to the presence of a pulmonary pathogen named //Legionella Pneumophilia// (Newton H.J. //et al//, 2010). Therefore, //L. pneumophilia// have been shown to enter into monocytes through not only coiling phagocytosis but also through conventional phagocytic mechanisms, such as direct inhalation, aspiration of oropharyngeal contents, direct spread from the mucosal membrane and hematogenous spread (Ganong //et al.//, 2006; Cirillo //et al//, 2001). The bacteria //L. pneumophilia// has micro dimensions (Fig. 1), which allows it to be engulfed by the alveoli easily and grow within it as an intracellular parasite. Although this pathogen activity could be demobilized by mucociliary action, the deterioration of this defense at a certain level will compromise mucociliary clearance (unclear), therefore allowing the hazard progression of the pneumonia (Madigan //et al//, 2009). avoid using text books

** Figure 1: The Legionella Pneumophila. (Primewater) **

 The primary host defence is usually characterized by cell-mediated immunity response against //Legionella// infection where the activation of further macrophages will allow the production of cytokines that will control antimicrobial activity against this pathogen (Cirillo //et al//, 2001).During infection, //L. pneumophilia// generates a reproduction vacuole within eukaryotic cells which will then affiliate with mitochondria and then obtain components of the endoplasmic reticulum. (not clear) This will therefore not only lead to the encoding of a Type IVb secretion system (T4bSS) through Icm/Dot genes (which is important because?), but will also bring the aid of antibodies and complements, until cellular endocytic physiology is completely compromised, therefore, permitting the pathogen to have entree to an atypical rough ER-bounded phagosome (Cirillo //et al//, 2001)(Fig.2 does not show antibodies, complement etc.. ). The capability of survival and the intracellular trafficking of this pathogen inside the host depend on the early activity of Icm/Dot genes, which will therefore involve effector proteins, such as Ank proteins, enhancing the host endosomes destruction (Pan X //et al//, 2008). According to Allen L.-A.H. (2003), with the progression of the infection, Icm/Dot proteins become vital, and phagosomes incorporated with amplified bacteria, will therefore obtain lysosomal properties (?). Once the infection is stabilized, this pathogen will not only promote fibrinopurulent pneumonia but will also affect other organs such as kidney, liver, brain, lymph nodes as it can be observed by this patients clinical background (i.e. multisystem failure, abnormal liver and renal function)(Rathore M.H. //et al//, 2009). However, Legionella activity could be is? quickly defeated by PMNs (polymorphonuclearleukocyte) or completely annulled by the action of MPO-derived oxidants (myeloperoxidases), in cell-free systems ( Allen L.-A.H., 2003). Why is this last part important?

** Figure 2: Infection Cycle of //L. pneumophilia//. (Machner M.P., 2011) **

 ** References ** Allen L.-A.H. (2003), //Mechanisms of pathogenesis: evasion of killing by polymorphonuclear leukocytes//, Microbes and Infection 5, Elsevier, 1329-1335.

====Cirillo //et al// (2001), //Legionella pneumophilia Entry Gene rtx A is involved in virulence//. Papers in Vetereinary and Biomedical Science. Paper 73, Vol 69, No.1, Infection and Immunity, January 2001, p.508-517. ====

Ganong W.F. //et al// (2006), //Pathophysiology of Disease – An introduction to Clinical Medicine//, 5th Edition, McGraw-Hill Companies, Medical Publishing Division, 76-78. **ISBN-13:** 978-0071441599

<span style="color: black; font-family: 'Times New Roman',Times,serif; font-size: 120%;">Machner M.P. (2011), //The Machner Lab: Unit on Microbial Pathogenesis//. Eunice Kennedy Shriver National Institute of Child Health and Human Development. Last accessed on December 2011, at URL: [] [online]

====<span style="color: black; font-family: 'Times New Roman',Times,serif; font-size: 120%;">Madigan //et al// (2009//), Biology of Microorganisms//, 12th Edition, Brock, Pearson International Edition, 1038-39. **ISBN-13:** 978-0321536150 ====

<span style="color: black; font-family: 'Times New Roman',Times,serif; font-size: 120%;">Newton H.J. //et al// (2010), //Molecular Pathogenesis of Infections Caused by Legionella pneumophila,// Clinical Microbiology Reviews, April 2010, 23(2):274.

====<span style="color: black; font-family: 'Times New Roman',Times,serif; font-size: 120%;">Pan X //et al// (2008), //Ankyrin repeat proteins comprise a diverse family of bacterial type IV effectors//. Science 320 (5883): 1651-4. ====

<span style="color: black; font-family: 'Times New Roman',Times,serif; font-size: 120%;">Rathore M.H. //et al// (2009), //Legionella Infection//, Medscape, last updated on October 2011, at URL: [|http://emedicine.medscape.com] [online]

====<span style="color: black; font-family: 'Times New Roman',Times,serif; font-size: 120%;">Scharstuhl E. (2011), //Contamination in water//, Prime Water, last accessed on December 2011, at [|URL:http://www.primewater.com/verontreiniging-water-3] [online] ====

<span style="color: #ff0000; font-family: 'Times New Roman',Times,serif; font-size: 120%;">Good list of reference, good attempt at an in-depth analysis but you fail to clarify your comments and it is not clear either what point you are trying to make or why that point is important and relevant.