By: Erica Aguilar
Pseudomonas pneumonia is an infection caused by the microbe known as Pseudomonas aeruginosa. It is an opportunistic pathogen because it is capable of attacking its host while its immune system is compromised. This pathogen belongs to the Gamma Proteobacteria bacterial class.  It is uncommon for healthy individuals to become infected with this organism and is usually a hospital-acquired bacterium. 
This microbe is found on the skin of humans or more commonly known as skin flora. The opportunist characteristics of this pathogen respond to a break down of the skin and enter the body of immunocompromised individuals.  Catheters inserted in patients, medical equipment, and central lines are common objects contaminated with P. aeruginosa and aid in passing this bacterium to patients.
Usual reservoirs for this pathogen are water, soil, agriculture plants, animals, and humans.  This microbe agent can survive in most conditions but is normally not a threat in most cases. 
This bacterium is an aerobic gram negative rod with single polar flagellum which allows it to be mobile.  Microscopic view measures approximately 0.5-0.8 micrometers by 1.5-3.0 micrometers.  P. aeruginosa is responsible for the majority of nosocomial infections. 
P. aeruginosa is obtained using sputum, blood, body fluids, feces, wounds, or lesions cultures. Many physicians will order multiple specimen sites to confirm P. aeruginosa. This bacterium produces a pyocyanin (blue-green pigment), fluorescein (yellow-green pigment), and/or a pyorubin color (brown-red pigment).  King, Ward, and Raney developed King A and King B agar media also referred to as Pseudomonas Agar P to increase pyocyanin production along with Pseudomonas Agar F to amplify fluorescein production.  In vitro, P. aeruginosa typically resembles a pearlescent color and is often foul-smelling. To confirm diagnostically, P. aeruginosa must present with pyocyanin production or fluorescein production as well as the ability to grow at 42°C.  This pathogen also is indentified by its gram-negative rod-like appearance, a positive oxidase reaction, and a lack to ferment lactose.  Another common test is the polymerase chain reaction (PCR) at the molecular cell level taken from the specimen culture.  The first step in this procedure is DNA extraction.  The next step is PCR amplification using various magnesium chloride concentrations, annealing temperature, primer solution, and a DNA template concentration.  After the DNA sample was heated at the appropriate temperature then the sample was subjected to varying thermal cycling parameters.  Next, 10 microliters of each reaction solution were subjected to gel electrophoresis.  Once the gel electrophoresis was completed, the gels were visualized under UV light.  It the band on the gel was seen at the correct estimated size for exoA or oprL loci, then the specimen was confirmed positive for P. aeruginosa. 
Signs and Symptoms:
Common signs and symptoms of pseudomonas pneumonia include shortness of breath, fever, chills, increased heart rate, decrease appetite, malaise, systemic inflammatory response, productive cough, increase sputum production that may have a yellow-green pigment, is thick, and usually foul smelling.  Symptoms vary depending on the site of infection.  Eye infections may present with inflammation, pus, pain, swelling, redness, and impaired vision.  Heart valve infections also known as endocarditis usually occur from intravenous drug users. These symptoms are similar to congestive heart failure.  Bacteremia from P. aeruginosa is commonly obtained by medical equipment and depends on the site of infection.  Ear infections will typically have pain, swelling, discharge, and itching. People more susceptible to infection are the immunosuppressed. For instance, people suffering from AIDS, COPD, cystic fibrosis, cancer, burn victims, intubated patients on a mechanical ventilator, or prolonged hospitalizations.
Gessard first isolated Pseudomonas aeruginosa in 1882 from soldier’s wound sites. The drainage from the wound stained their bandages with a blue-green discoloration.  In 1889, Charrin and Roger established evidence for acquired immunity in animals inoculated with P. aeruginosa and the mice were able to withhold further infection.  During that same year, Bouchard used cell-free filtrates from this organism to help create a vaccine that would stimulate non-specific immunity.  Hitschmann and Kreibich first reported in 1897 the skin manifestation leading to septicemia cause by this organism. 
P. aeruginosa has multiple virulence factors ranging from cell associated to extracellular factors that allows it to survive in many conditions as well as cause pathogenesis. The physical attributes include pilus, a single flagellum, alginate also referred to as biofilm, non-pilus adhesions, and lipopolysaccharide.  The extracellular virulence factors include multiple proteases such as LasB elastase, LasA elastase, and alkaline protease.  There are also hemolysins named phospolipase C and rhamnolipid, and then the exoenzyme S, exotoxin A, and pyocyanin.  Cell-associated virulence factors begin with the colonization of the impaired epithelium.  Almost half of hospitalized patients are susceptible to the colonization of P. aeruginosa. In healthy individuals, this organism is found in the oropharynx of about 6% and between 3% to 24% in fecal product of healthy individuals.  It is suspected that the flagella is not only responsible for movement but also may aid in adhesions to epithelial cells. After colonization and entry into the body, a signaling cascade produces a high amount of extracellular virulence factors in the acute phase.  Tissue damage caused by proteases and toxins invade blood vessels causing a systemic inflammatory response, dissemination to other organs that may lead to multiple organ failure and possibly death.  The two hemolysins produced by this bacterium may act together in breaking down lipids and lecins along with tissue damage caused by the cytotoxins. The next stage after the acute infection is the chronic phase but this stage can also happen directly after colonization. The chronic infection has selected alginate yielding mutants, protects from host immunity, has a low production of extracellular virulence factors, and the tissue damage is chiefly caused by the chronic inflammation process.
Current recommended drug therapies for P. aeruginosa include two antipseudomonal drug combinations.  For example a beta-lacam antibiotic along with an aminoglycoside is usually advised for acute infections and for patients who are immunocompromised.  Another aspect when initiating drug therapy for pseudomonas pneumonia will depend on the site of infection, how long the infection has been present as well as local resistance patterns.  Common antimicrobial medications include ceftazidime, cefepime, meropenem, imipenem, primaxin, zoysn, timentin, tobramycin, gentamicin, ciprofloxacin, aztreonam, streptomycin sulfate, tetracycline, and acetic acid.  Control of pseudomonas pneumonia involves consistent hand hygiene, and over-all hygiene of a patient, isolation precautions such as contact isolation, and modified equipment procedures.  Hospitals will often trend the different stains of P. aeruginosa in each unit for early detection. 
Currently, there is no vaccine available to prevent pseudomonas pneumonia.  Healthcare providers should consistently follow universal precautions and are sometimes monitored in every unit to reinforce this.  Hospital workers should also follow CDC recommendations for inserting catheters.  Starting antibiotic therapy prophylactically is not recommended due to the increase in multi-drug resistance organisms. 
Recently, a study was performed on mice consistenting of liposomal elements given intraperitoneally or intranasally.  The goal of this study was to trigger a systemic and airway humoral response to Pseudomonas aeruginosa.  The study resulted in the vaccines stimulating a production of the antibodies IgG and/or IgA against immunogenic peptide from this pathogen.  This experiment could not be validated but could be helpful in other research associated with a P. aeruginosa vaccine. Vaccine research is still under development at this time.
In 2006, University Hospital located in San Antonio, Texas saw an increase in P. aeruginosa infections in its neonatal intensive care unit, leading for a study to be conducted with data ranging from 2005 to 2007.  This unit generally has a low incidence of this pathogen and has seen fewer cases since revision of control measures.  The patients with this infection tended to be male and had received mechanical ventilation at one point.  During the study, 23 patients were confirmed with P. aeruginosa. Only 13% of patients were antibiotic resistance and 30% of the patients died.  In US hospitals, there are about 4 per 1000 discharges (0.4%) of P. aeruginosa infections.  Approximately 10.1% of nosocomial infections result due to this bacterium.  Also, this pathogen is responsible for about 16% of hospital acquired pneumonia, 12% of urinary tract nosocomial infections, 8% of surgical wound infections, and 10% of bacteremia infections. 
An outbreak in a Warsaw, Poland hospital saw 41 P. aeruginosa cases with PER-1 extended spectrum beta-lastamase. This clonal complex is normally seen in Turkey but has now been identified in the far eastern countries and Europe. In Greece, there was a hospital outbreak of multiple strains of this pathogen, which carried two metallo beta-lactamase gene variants.  Pseudomonas pneumonia is a common infection found in most hospitals throughout the world.
 Qarah, S., Cunha, B. A., Dua, P., & Lessnau, K. (2009, December 9). Pseudomonas aeruginosa infections. Retrieved March 13, 2010, from http://emedicine.medscape.com/article/226748-overview
 Van Delden, C., & Iglewski, B. H. (1998, October). Cell-to-cell signaling and pseudomonas aeruginosa infections . Retrieved March 12, 2010, from http://www.cdc.gov/ncidod/EID/vol4no4/vandelden.htm
 Todar, K. (2008). Pseudomonas aeruginosa . Retrieved March 14, 2010, from http://www.textbookofbacteriology.net/pseudomonas.html
 Quantification of pseudomonas aeruginosa. (n.d.). Retrieved March 11, 2010, from http://www.mdc-bt.com/pdf/Pseudomonas_aeruginosa-ST.pdf
 Rozwadowki, T., & Khachemoune, A. (2004, September). What caused these slightly tender papules and nodules?. Retrieved March 12, 2010, from http://www.skinandaging.com/article/3008
 Young, L. S. (1984, September). The clinical challenge of infections due to pseudomonas aeruginosa . Retrieved March 11, 2010, from http://www.jstor.org/pss/4453490
 Xu, J., Moore, J. E., Murphy, P. G., Millar, B. C., & Elborn, J. S. (2004, October 20). Early detection of pseudomonas aeruginosa – comparison of conventional versus molecular (PCR) detection directly from adult patients with cystic fibrosis (CF). Retrieved March 12, 2010, from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC529303/?log%24=activity
 Chen, S., & Rudoy, R. (2010, January 25). Pseudomonas infection: treatment & medication. Retrieved March 13, 2010, from http://emedicine.medscape.com/article/970904-treatment
 Obritsch, ., Fish, ., MacLaren, ., & Jung, . (2005). Multidrug-resistant pseudomonas aeruginosa: infection control. Retrieved March 14, 2010, from http://www.medscape.com/viewarticle/515330_6
 Heurtault, B., Gentine, P., Thomann, J., Baehr, C., Frisch, B., & Pons, F. (2008, September 10). Design of a liposomal candidate vaccine against pseudomonas aeruginosa and its evaluation in triggering systemic and lung mucosal immunity. Retrieved March 14, 2010, from http://www.springerlink.com/content/246262n75124l268/
 Madsen, T., Kostroun, L., Kelly, C., Patterson, J. E., Seidner, S., & Sreeramoju, P. (n.d.). Outbreaks and clusters . Retrieved March 13, 2010, from http://www.shea-online.org/Assets/files/08a_Outbreaks_and_Clusters.pdf
 J, E., K, F., A, M., W, H., DM, L., & M, G. (2008, July 18). Outbreak of pseudomonas aeruginosa infections with PER-1 extended-spectrum beta-lactamase in warsaw, poland: further evidence for an international clonal complex. Retrieved March 14, 2010, from http://www.ncbi.nlm.nih.gov/pubmed/17634312
 Pournaras, S., Maniati, M., Petinaki, E., Tzouvelekis, L. S., Tsakris, A., Legakis, N. J., & Maniatis, A. N. (2003, March 6). Hospital outbreak of multiple clones of pseudomonas aeruginosa carrying the unrelated metallo--lactamase gene variants blaVIM-2 and blaVIM-4. Retrieved March 14, 2010, from http://jac.oxfordjournals.org/cgi/content/abstract/dkg239v1