Multi Drug Resistant Psuedomonas
A Microbial Biorealm page on the genus Multi Drug Resistant Psuedomonas
Classification
Higher order taxa
Domain-Bacteria
Phylum-Proteobacteria
Class-Gamma proeobacteria
Order-Pseudomonadales
Family-Pseudomonadaceae
Genus-Pseudomonas
Species Group-Pseudomonas aeruginosa group
Species
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NCBI: Taxonomy |
Pseudomonas aeruginosa
Description and significance
Pseudomonas aeruginosa is a gram negative, rod shaped bacteria with polar flagella. Respiratory is its preferred mechanism of metabolism, but can grow in the absence of oxygen if nitrate is present as a respiratory electron acceptor (textbookofbacteriology.net). This bacterium has minimal nutritional requirements and can survive under a variety of conditions. Its optimum temperature for growth is 37 degrees Celsius, but can survive in cooler temperatures (textbookofbacteriology.net). Characteristics of P. aeruginos include producing a blue-green pigment pyocyanin and emitting a sweet odor (emedicine.com).
Genome structure
P. aeruginosa measures 0.5 to 0.8 um by 1.5 to 3.0 um (textbookofbacteriology.net). According to Psuedomonasgenomedatabase.com it contains 6264404 bp and a 66.6% guanine-cytosine content. Genes include CDS, ncRNA, pseudogene, rRNA, regRNA, sRNA, tRNA, and tm RNA. This bacteria divides through horizontal gene transfer mainly using transduction and conjugation (textbookofbacteriology.net). According to pseudomonas.com, genome sequencing for pseudomonas was completed in 2000. It was noted for its large size and diverse metabolic capacities. This sequencing has lead to further studies in regards to cystic fibrosis patients. The large genome of pseudomonads also codes for several very efficient efflux pump systems that eject antibiotics from the cell before they can function (Tortora, Funke, & Case 2010). These pump systems work to block the antibiotic, inactivate the enzymes, alter the target molecule, and efflux the antibiotic.
Cell structure and metabolism
P. aeruginosa is a facultative aerobe, prefers oxidative metabolism through a glucose substrate and gains energy through the electron-transport chain. The bacteria are capsulated, porous and are able to form a biofilm which protects it from opsonization, complement deposition, and phagocyte engulfment (textbookofbacteriology.net). The pili and flagella help the bacteria attach to the epithelial cells. Next, there are adhesins released to help colonize the bacteria and form a biofilm. The biofilm helps protect the bacteria from lymphocytes, phagocytes, antibodies and complement. The pyocyanin impairs the normal function of human nasal cilia, disrupts the respiratory epithelium, and exerts a proinflammatory effect on phagocytes (textbookofbacteriology.net).
Ecology
P. aeruginosa is commonly found in soil, water and can survive on the surface of plants and animals. In addition, in the hospital it can be found in reservoirs such as sink taps, disinfectants, respiratory equipment, food, toilets, showers and mops (textbookofbacteriology.net). In the aquatic environment it is known to be one of the fastest swimmers and is found as a biofilm on rocks and marine life. Since its natural habitat is the soil, living in association with the bacilli, actinomycetes and molds, it has developed resistance to a variety of their naturally-occurring antibiotics (textbookofbacteriology.net).
Pathology
As mentioned above, P. aeruginosa is an opportunistic infection that commonly invades immune-compromised patients. These patients include those who have cystic fibrosis, HIV, diabetics, burn victims, and those in the ICU. Most Pseudomonas infections are both invasive and toxinogenic. The ultimate Pseudomonas infection may be seen as composed of three distinct stages: (1) bacterial attachment and colonization; (2) local invasion; (3) disseminated systemic disease. However, the disease process may stop at any stage. Particular bacterial determinants of virulence mediate each of these stages and are ultimately responsible for the characteristic syndromes that accompany the disease (emedicine.com). P. aeruginosa has intrinsic resistance and external mechanisms of resistance. These mechanisms include phagocytosis, exotoxins, adhesins, invasins, motility and chemotaxis, toxins, and immune and bacterial defenses. Antibiotics that are effective at treating P. aeruginosa are floroquinolones, gentamicin and imipenem (textbookofbacteriology.net). Additionally, a combination therapy has proven to be most effective at treating P. aeruginosa. Some of the ways the bacteria has been known to spread is through patient to patient contact through staff, direct contact with contaminated reservoirs and/or instruments, and by ingestion (textbookofbacteriology.net). Diseases caused are endocarditis, respiratory infections, bacteremia, septicemia, CNS infections, ear infections, eye infections, bone and joint infections, urinary tract infections, gastrointestinal infections and wound infections. The invasion of this bacteria can be reduced in the hospital setting if staff is properly using aseptic technique, isolation precautions, and proper cleaning of respirators, catheters and other instruments (textbookofbacteriology.net).
Current Research and or Application to Biotechnology
Since the completion of the genome sequencing there have been advances in regards to cystic fibrosis patients who contract pseudomonas. Studies are able to understand more behind the epidemiology between CF patients, how the genes are transferred, and what types of antibiotics can be taken. The genome sequencing project was important especially to these patients since the mortality rate is so high. Another current research application is in regards to the chronic respiratory complications in cystic fibrosis. Scientists are studying the bacteria to try and understand the genetics behind the biofilm formation. Lastly, according to CFF.org, The FDA approves Cayston® (aztreonam for inhalation solution), the first inhaled antibiotic for the treatment of CF approved in more than a decade. Cayston treats Pseudomonas aeruginosa and was made possible by significant support from the Cystic Fibrosis Foundation.
References
Classification, By Function. "Pseudomonas Aeruginosa PAO1 Summary." Pseudomonas Genome Database and PseudoCAP. 17 Sept. 2001. Web. 06 Oct. 2010. <http://www.pseudomonas.com/genomeMenu.do?organism=Pseudomonas aeruginosa PAO1&submit=Submit>. "Cystic Fibrosis Foundation - Research Milestones." Cystic Fibrosis Foundation - Home. 1 Mar. 2010. Web. 06 Oct. 2010. <http://www.cff.org/research/ResearchMilestones/>. Deretic, V., D. W. Martin, M. J. Schurr, M. H. Mudd, N. S. Hibler, R. Curcic, and J. C. Boucher. "Access : Conversion to Mucoidy in Pseudomonas Aeruginosa : Nature Biotechnology." Nature Publishing Group : Science Journals, Jobs, and Information. 1993. Web. 06 Oct. 2010. <http://www.nature.com/nbt/journal/v11/n10/pdf/nbt1093-1133.pdf>. Matthew, Levison E. "Pseudomonas Infections: Bacterial Infections: Merck Manual Home Edition." Merck & Co., Inc. - We Believe the Most Important Condition Is the Human One. Sept. 2008. Web. 05 Oct. 2010. <http://www.merck.com/mmhe/sec17/ch190/ch190q.html>. Qarah, Samer, Burke A. Cunha, Pratibha Dua, and Klaus-Dieter Lessnau. "Pseudomonas Aeruginosa Infections: [Print] - EMedicine Infectious Diseases." EMedicine - Medical Reference. 9 Dec. 2009. Web. 05 Oct. 2010. <http://emedicine.medscape.com/article/226748-print>. Roy, P. H., S. G. Tetu, and A. Larouche. "Complete Genome Sequence of the Multiresistant Taxonomic Outlier Pseudomonas Aeruginosa PA7." PubMed.com. 22 Jan. 2010. Web. 06 Oct. 2010. <http://www.ncbi.nlm.nih.gov/sites/entrez?db=genomeprj&cmd=Link&LinkName=genomeprj_pubmed&from_uid=16720>. Todar, Kenneth. "Pseudomonas." Online Textbook of Bacteriology. 2008. Web. 06 Oct. 2010. <http://www.textbookofbacteriology.net/pseudomonas_2.html>. Tortora, Gerard J., Berdell R. Funke, and Christine L. Case. Microbiology: an Introduction. San Francisco, CA: Pearson Benjamin Cummings, 2010. Print.
Edited by student of Dr. Nighat P Kokan, Cardinal Stritch University http://www.stritch.edu
