30-day mortality rate was 39%

Drugs of Choice The choices for treatment for P. aeruginosa infections include the following antimicrobial agents, with the fluroquinolones being the only oral options:                • Aminogylcosides (amikacin, tobramycin, gentamicin)                • Carbapenems (imipenem, meropenem, doripenem)                • Cephalosporins, third-generation (cefoperazone, cefsulodin, ceftazidime, but not cefotaxime or ceftriaxone)                • Cephalosporins, fourth-generation (cefepime, cefpirome, cefclidin)                • Fluoroquinolones (ciprofloxacin, levofloxacin)                • Monobactam (aztreonam)                • Extended-spectrum penicillins (ticarcillin and/or ticarcillin-clavulanate, piperacillin and/or piperacillin–tazobactam,azlocillin).                • Polymyxin B/Colistin

The aminoglycosides can be inactivated by acetylation of an amino group by acetyltransferases, by adenylation of a hydroxyl group by adenyltransferases, or by phosphorylation of a hydroxyl group by phosphotransferases

including first-, second-, and many third-generation cephalosporin, penicillins, and macrolide

cephalosporins (cefoperazone, cefsulodin and ceftazidime, but not cefotaxime or ceftriaxone), fourth generation cephalosporins (cefepime, cefpirome, cefclidin), extended spectrum penicillins (ticarcillin, piperacillin, azlocillin), monobactams (aztreonam); carbapenems (imipenem, meropenem), quinolones (ciprofloxacin, levofloxacin, gatifloxacin, moxifloxacin), and aminoglycocides (gentamycin, amikacin, tobramycin, colimycin).

 polar flagella, which are critical for motility in initial stages of pulmonary infection, activate IL-8 production by binding to toll-like receptor on the surface of airway epithelial cells, and facilitate adherence to epithelial and eukaryotic cells with pile/ non-piling adhesions (polar pili)

P. aeruginosa to be the second most common organism isolated in nosocomial pneumonia (17% of cases)

In gram-negative bacteria, relevance ratio of acinetobacter baumannii (AB) was the highest (18.4%) and followed by klebsiella pneumoniae (11.4%)

Pneumonia is the second leading reason for hospitalization of medicare beneficiaries and accounts for more than 600,000 medicare hospitalizations yearly [1,2]. It is common and potentially serious infected. The elderly are more susceptible to pneumonia and more likely to die from this infection than younger populations

biofilm which anchors the cells to their environment and in medical situations, it protects the bacteria from the host defenses such as lymphocytes, phagocytes, the ciliary action of the respiratory tract, antibodies and complement.

surface-bound exoenzyme S could serve as an adhesin for glycolipids on respiratory cells.

These adhesins appear to bind to specific galactose or mannose or sialic acid receptors on epithelial cells. Colonization of the respiratory tract by Pseudomonas requires pili adherence and may be aided by production of a protease enzyme that degrades fibronectin in order to expose the underlying pilus receptors on the epithelial cell surface

inability to ferment lactose, a positive oxidase reaction, its fruity odor, and its ability to grow at 42°C.

It grows well on most laboratory media and commonly is isolated on blood agar or eosin-methylthionine blue agar

including fluoroquinolones, gentamicin and imipenem

both R-factors and RTFs, and it is able to transfer these genes by means of the bacterial mechanisms of horizontal gene transfer (HGT), mainly transduction and conjugation.

Clinical samples, in general, yield one or another of two smooth colony types. One type has a fried-egg appearance which is large, smooth, with flat edges and an elevated appearance. Another type, frequently obtained from respiratory and urinary tract secretions, has a mucoid appearance, which is attributed to the production of alginate slime. The smooth and mucoid colonies are presumed to play a role in colonization and virulence

biofilm

According to the CDC, the overall incidence of P. aeruginosa infections in U.S. hospitals averages about 0.4 percent (4 per 1000 discharges), and the bacterium is the fourth most commonly-isolated nosocomial pathogen accounting for 10.1 percent of all hospital-acquired infections.

Pseudomonas aeruginosa infection is a serious problem in patients hospitalized with cancer, cystic fibrosis, and burns. The case fatality rate in these patients is near 50 percent.

opportunistic pathogen, meaning that it exploits some break in the host defenses to initiate an infection.

outer membrane protects it from antibiotics it has developed resistance because it lives among antibiotic producing bacteria and fungi in the soil

10% of all hospital-acquired infections

it is found mostly in hospitals; in food, sinks, toilets, mops, instruments such as respiratory equipment, or even transferred from the hands of healthy visitors or hospital staff

It uses pili with the aid of protease enzymes in attachment to epithelial cells, such as in the respiratory tract.  The bacterium has capsules or slime layers that protect it from antibodies, lymphocytes, and phagocytes.  In order to invade tissues, it produces extracellular enzymes such as elastase and alkaline protease.  There are also three soluble proteins involved in invasion, which are cytotoxin (mw 25 kDa) and two hemolysins.  It produces the extracellular toxins Exoenzyme S and Exotoxin A and also LPS, which is characteristic of Gram-negative bacteria.  All of these characteristics lead to a wide variety of diseases.

The bacterium is very low-maintenance when it comes nutrition.  It does not require organic growth factors, and can use over seventy-five organic compounds for growth.  In a lab setting, acetate and ammonium sulfate in a medium will satisfy it.  The optimum growth temperature is 37 degrees C, but it can grow in temperatures up to 42 degrees C.  Not only is it tolerant to temperature, but also to salts and dyes, weak antiseptics, and antibiotics.

Combination therapy with antipseudomonal antibiotics is used to ensure treatment of resistant strains and to prevent selection of resistant mutants.

In the present study, we did not find a significant association between age and CAP due to GNB or P aeruginosa, corroborating the view that age does not represent an independent risk factor for these pathogens.

CAP due to GNB has often been reported to be more frequent in the elderly population, especially by American authors in the 1970s.26- 28 A corresponding high incidence of 16% was found in a series of severe CAP in the elderly.

On the other hand, the value of sputum, tracheobronchial aspirates, and even bronchoscopically retrieved samples may be seriously questioned, especially in patients with structural lung disease such as COPD or bronchiectasis or even in patients with heavy cigarette use. Gram-negative bacteria may easily colonize the tracheobronchial tree in the presence of any alterations or damage of the respiratory epithelium

multidrug-resistant strains were isolated more frequently from ICU and nursing home patients.

20 to 35%

the overexpression of a multidrug resistance mechanism, i.e., an efflux pump

The highest prevalence of multidrug-resistant strains was observed among isolates from lower respiratory tract infections

. aeruginosa exhibits the highest rates of resistance for the fluoroquinolones

P. aeruginosa can develop resistance to antibacterials either through the acquisition of resistance genes on mobile genetic elements (i.e., plasmids) or through mutational processes that alter the expression and/or function of chromosomally encoded mechanisms.

Unfortunately, selection of the most appropriate antibiotic is complicated by the ability of P. aeruginosa to develop resistance to multiple classes of antibacterial agents, even during the course of treating an infection.

Patients with impaired immunity have higher risks for colonization by this organism

P. aeruginosa is seldom a member of the normal microbial flora in humans

can be isolated from various living sources, including plants, animals, and humans

by the CDC National Nosocomial Infections Surveillance System from 1986 to 1998 shows that P. aeruginosa was identified as the fifth most frequently isolated nosocomial pathogen, accounting for 9% of all hospital-acquired infections in the United States

Local Cases/Outbreaks:             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. [11] This unit generally has a low incidence of this pathogen and has seen fewer cases since revision of control measures. [11] The patients with this infection tended to be male and had received mechanical ventilation at one point. [11] During the study, 23 patients were confirmed with P. aeruginosa. Only 13% of patients were antibiotic resistance and 30% of the patients died. [11] In US hospitals, there are about 4 per 1000 discharges (0.4%) of P. aeruginosa infections. [3] Approximately 10.1% of nosocomial infections result due to this bacterium. [3] 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. [2]   Global Cases/Outbreaks:             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. [13] Pseudomonas pneumonia is a common infection found in most hospitals throughout the world.

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. [2] 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.  

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.

RESULTS: Twelve patients with a culture positive for P. aeruginosa with the unique susceptibility pattern were identified in June-July 2007. No cases were documented from March 1 through May 31, 2007. Culture specimens obtained from B1 after high-level disinfection revealed P. aeruginosa, prompting removal of B1 from service on July 23, 2007. No cases occurred after that date. Eleven (55%) of 20 patients who were exposed to B1 during the cluster period had a culture positive for P. aeruginosa, compared with 1 (2%) of 53 patients who were exposed to other bronchoscopes (P < .001). PFGE patterns for P. aeruginosa isolates obtained from case patients and from B1 were identical. An engineering evaluation of B1 documented several internal damages. Two (10.5%) of 19 patients exposed to B1 during the cluster period may have developed P. aeruginosa infection following exposure to B1.

These agents are bactericidal and exhibit synergy with other antimicrobials, most notably β-lactams, with which they are often administered for the treatment of Pseudomonas aeruginosa infections;

beta-lactam and aminoglycoside for 5 days and de-escalate to monotherapy based on organism culture sensitivity.

a positive catalase test.

Sputum Gram stain

Cultures grow best with aeration

P. aeruginosa grows well on LB broth

P. aeruginosa grows well at 37°C

the simplest medium for growth of Pseudomonas aeruginosa consists of acetate as a source of carbon and ammonium sulfate as a source of nitrogen.

combination of an antipseudomonal beta-lactam (eg, penicillin or cephalosporin) and an aminoglycoside. Carbapenems (eg, imipenem, meropenem) with antipseudomonal quinolones may be used in conjunction with an aminoglycoside.

It is not an active fermenter of carbohydrates and produces acid, but no gas, in glucose and is lactose-negative. The oxidase and catalase test for P.aeruginosa are positive.

These bacteria like moist environments, such as hot tubs and swimming pools, where they can cause a skin rash or swimmer's ear.

Pseudomonas can be spread on the hands of healthcare workers or by equipment that gets contaminated and is not properly cleaned.

Patients in hospitals, especially those on breathing machines, those with devices such as catheters, and patients with wounds from surgery or from burns are potentially at risk for serious, life-threatening infections.

Pseudomonas infections usually occur in people in the hospital and/or with weakened immune systems

P. aeruginosa is commonly found in the exoskeletons and droppings of the domestic cockroaches

low antibiotic susceptibility

Because it thrives on moist surfaces, this bacterium is also found on and in medical equipment, including catheters, causing cross-infections in hospitals and clinics. It

generally in the immunocompromised

Infected humans, animals, contaminated water, soil Footnote

carbenicillin, cephalosporins, ceftazidime, and ciprofloxacin

P. aeruginosa have been found to survive within droplet nuclei and can remain in aerosols for long periods of time, thus there is evidence of potential airborne transmission Footnote 20. Contact with contaminated water is also a major route, but since the oral infectious dose is thought to be very high, routes that pose the greatest health risk are skin exposure (for example, in contaminated hot tub water) and lung exposure from inhaling aerosols discharged from infected respiratory tracts Footnote 13. The bacterial can often enter the body through injuries and wounds Footnote 3. The use of contaminated mechanical respiratory ventilators in hospital settings is also a common source of nosocomial infections Footnote 12.

Humans, animals (wild, domestic, livestock), and plants (flora and fungi)

P. aeruginosa infections account for 20% of pneumonia and 16% of urinary tract infections Footnote 16. Prevalence in the community is less than in the hospital, and cases of severe community-acquired infection are rare

The common site of infection is the lower respiratory tract,

opportunistic pathogens,

P. aeruginosa can produce a large variety of extracellular toxins, including exotoxin A and enterotoxins

It is “opportunistic” because it seldom infects healthy individuals. Instead, it often colonizes immunocompromised patients, like those with cystic fibrosis, cancer, or AIDS

P.aeruginosa is an opportunistic human pathogen

P. aeruginosa is an obligate respirer, using aerobic respiration (with oxygen) as its optimal metabolism although can also respire anaerobically on nitrate or other alternative electron acceptors

rude prevalence of multidrug-resistant bloodstream P. aeruginosa isolates in our institution from 2005 to 2007 was 14%

Pneumonia can cause:Fever and chillsDifficulty breathingCough, sometimes with yellow, green, or bloody mucus

Bloodstream infections can cause various symptoms, including:Fever and chillsBody achesLight-headednessRapid pulse and breathingNausea and vomitingDiarrheaDecreased urination