Pseudomonas Aeruginosa Research Paper

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Psuedomonas Aeruginosa

Pseudomonas aeruginosa

Epidemiology

The Gram-negative, motile, rod-shaped bacterium Pseudomonas aeruginosa is an opportunistic killer that takes advantage of people suffering from medical problems (Van Delden and Iglewski, 1998).For this reason, P. aeruginosa is one of the most common nosocomial infection that occurs in hospitals. P. aeruginosa is responsible for causing 16% of pneumonia cases, 12% of urinary tract infections, 10% of bloodstream infections, and 8% of surgical infections due to hospital care. Patients who are immune-compromised are also susceptible to P. aeruginosa infections, such as patients undergoing chemotherapy, suffering from HIV / AIDS, recovering in burn units, and suffering from cystic fibrosis. With death rates ranging from 30 to 60% for these patients, P. aeruginosa is considered to be a significant threat to patient health.

Ecology

P. aeruginosa can switch between a free-swimming planktonic form and colonies enclosed within slime-protected biofilms attached to surfaces (Baltch and Smith, 1994, p. 1). The planktonic form is susceptible to all forms of bactericidal agents, including antibiotics, but when encased within the biofilm (mucoid form) the bacterium can survive many of these agents, in addition to environmental predators.

P. aeruginosa is almost ubiquitous in the environment, but pathogenic concentrations can be found wherever humans and livestock are found (Botzenhart and Doring, 1993, p. 3-6). Water sources are particularly susceptible to contamination, including plumbing fixtures, swimming pools, and saunas. It can be found in bodies of water contaminated with human waste, including ocean bays, rivers, and lakes. Nursing homes, hospitals, intensive care units, medical clinics, and dental clinics are frequently found to be reservoirs of P. aeruginosa.

Surprisingly though, healthy humans are not considered to be a natural habitat for P. aeruginosa. When the fecal matter from healthy people was examined, only 1.2% to 2.3% contained this bacterium. In contrast, P. aeruginosa is able to grow on stainless steel or in highly pure water. This suggests P. aeruginosa cannot withstand an assault from a healthy immune system.

Pathogenesis

For P. aeruginosa to cause disease, the normal barriers to entry must be compromised (Van Delden and Iglewski, 1998). A compromised immune system, a break in an epithelial barrier due to trauma, disease, or surgery, or the insertion of a medical device like a catheter, can create an opportunity for colonization by P. aeruginosa.

Once colonized, the bacterium will attach to surfaces through adhesion molecules (Van Delden and Iglewski, 1998). This can happen through type 4 pili, through non-pilus mechanisms which are not well-known, or through the adhesin properties of the flagella structure. The attachment to epithelia surfaces is considered irreversible.

The planktonic form of P. aeruginosa is generally susceptible to first line antibiotic treatments, so this course of disease, though acute, is curable once diagnosed (Hurley, Camara, and Smyth, 2012). The disease course will vary depending on the health condition of the person exposed and the concentration of bacteria, since healthy individuals are almost invariably immune to the planktonic form of P. aeruginosa and biofilms cannot form. However, established biofilms are generally considered resistant to all antibiotics and even hydrogen peroxide. When biofilms are found to be contaminating inserted medical devices, such as catheters, they must be scraped off.

Once attached to an epithelial surface, the bacterium begins to produce small signaling molecules (Hurley, Camara, and Smyth, 2012). If enough bacteria have attached in the same location, the concentration of these molecules become sufficient to turn on genes producing virulence factors. This sensing process is called quorum sensing. The virulence factors are responsible for causing the disease and the most common are exotoxin A, exoenzyme S, phospholipas C, rhamnolipid, and a number of proteases. The result is the local destruction of tissue and immune suppression (Van Delden and Iglewski, 1998).

There is also considerable phenotypic variation between P. aeruginosa strains, resulting in considerable variability in susceptibility to medical interventions (Hurley, Camara, and Smyth, 2012). P. aeruginosa is also capable of rapid adaptation, including the development antibiotic resistance within the same individual. When encased in a biofilm, the metabolic activity can slow to the point that even if antibiotics penetrate, a viable inner core of bacteria remain that can resume normal metabolic activity once the antibiotic treatment has ceased. In other words, P. aeruginosa is capable of entering a state equivalent to mammalian hibernation in the presence of bactericidal agents and reemerging once the threat has passed.

Signs and Symptoms

The development of an acute P. aeruginosa infection results in signs and symptoms similar to infections with other gram negative bacteria (Baltch and…[continue]

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