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Causes of Acute Community-Acquired Pneumonia
Usual causes of acute community-acquired pneumonia are S. pneumonia, H. influenza, M. catarrhalis, S. aureus, and Klebsiella pneumonia. The Gram-stained smear for S. pneumonia indicates Gram–positive and lancet-shaped pairs of cocci. For H. influenza, the Gram-stained smear shows Gram–negative small rod-shaped and pleomorphic coccobacilli. M. catarrhalis is characterized by the presence of Gram–negative diplococci (Mahon, Lehman, and Manuselis 388-402). For S. aureus, the smear shows Gram–positive cocci that are often presented in clusters like the grape. The test for Klebsiella pneumonia indicates the presence of Gram-negative encapsulated and rod-shaped bacilli that can be observed as single bacilli or pairs and chains of bacilli (Parija 262).
Complications of Staphylococcal Pneumonia
The complications of Staphylococcal pneumonia can include empyema, the active formation of abscesses, and pleural effusions caused by toxins with the following spread of S. aureus not only in lungs but also in the whole organism (Schaechter 149). The invasion of S. aureus and the formation of colonies in the body are the results of the work of such toxin as Panton-Valentine Leukocidin (PVL). The pathogenesis depends on the colonization of S. aureus caused by the PVL factor (Eisele and Anderson 7).
Pneumococcal Surface Protein A (PspA) is the first virulence factor to mention as important to influence S. pneumonia virulence. PspA works to protect pneumococci. The electronegative components of PspA add to the anticomplementary quality of this factor concerning S. pneumonia (Jedrzejas 189). Hyaluronate lyase (Hyl) is the second factor that contributes to the invasion and spread of S. pneumonia by affecting the hyaluronan (Jedrzejas 192). The final factor to mention is Neuraminidase that is effective to influence glycosylation and provoke the active colonization of S. pneumonia.
Development of Bacterial Pneumonia
Bacterial pneumonia develops as a reaction to the invasion of pathogens that disrupt the epithelium with the help of toxins. They can survive during a long period because of intracellular life cycles, and their invasion is possible because of certain virulence factors. In the epithelium, pathogens can replicate and cause the further destruction of epithelial cells. Thus, Francisella tularensis can resist β-defensins, and this aspect promotes its invasion in the epithelium. Staphylococcus aureus is characterized as the antibiotic-resistant strain. In its turn, Yersinia pestis can invade because of changing the LPS structure to adapt to the host (Eisele and Anderson 5-9).
It is hypothesized that possible reasons for the decline in pulmonary function of Cystic Fibrosis (CF) patients can be Pseudomonas aeruginosa and Burkholderia cepacia complex (BCC) organisms. In this case, the reference to Pseudomonas aeruginosa is frequent in the evidence-based literature and studies (Hauser et al. 30). Another frequently mentioned cause is S. aureus. The researchers also mentioned M. abscessus as the possible cause of the discussed problems. (Hauser et al. 35-38)
Infections in CF Patients
The hypermutable phenotype related to H. influenza is significant in terms of guaranteeing the long-term persistence of hypermutable strains. As a result, in CF patients, H. influenza can develop more actively (Hauser et al. 35). The significance of the hypermutable phenotype concerning P. aeruginosa is in the increased adaptation of pathogens, and it can also cause increased resistance to antibiotics (Hauser et al. 45).
Susceptibility to S. Aureus
Mice deficient in Myd88 can be more susceptible to S. aureus because the deficiency in Myd88 is associated with the deficiency in TLR2 that is responsible for recognizing the bacteria. As a result, receptors cannot determine pathogens, and MyD88 serves as an important molecule necessary for this process (Eisele and Anderson 6). The lack of Myd88 indicates the possibly higher susceptibility to S. aureus in people.
Eisele, Nicholas, and Deborah Anderson. “Host Defense and the Airway Epithelium: Frontline Responses That Protect against Bacterial Invasion and Pneumonia.” Journal of Pathogens 2011.1(2011): 1-16. Print.
Hauser, Alan, Manu Jain, Maskit Bar-Meir, and Susanna McColley. “Clinical Significance of Microbial Infection and Adaptation in Cystic Fibrosis.” Clinical Microbiology Reviews 24.1 (2011): 29-70. Print.
Jedrzejas, Mark. “Pneumococcal Virulence Factors: Structure and Function.” Microbiology and Molecular Biology Reviews 65.2 (2001): 187-207. Print.
Mahon, Connie, Donald Lehman, and George Manuselis. Textbook of Diagnostic Microbiology. New York: Elsevier Health Sciences, 2014. Print.
Parija, Subhash Chandra. Textbook of Microbiology and Immunology. New York: Elsevier Health Sciences, 2014. Print.
Schaechter, Moselio. Schaechter’s Mechanisms of Microbial Disease. New York: Lippincott Williams & Wilkins, 2012. Print.