Treatment

P. aeruginosa is frequently isolated from non-sterile sites (mouth swabs, sputum, and so forth), and, under these circumstances, it often represents colonisation and not infection. The isolation of P. aeruginosa from non-sterile specimens should, therefore, be interpreted cautiously, and the advice of a microbiologist or infectious diseases physician should be sought prior to starting treatment. Often no treatment is needed.

When P. aeruginosa is isolated from a sterile site (blood, bone, deep collections), it should be taken seriously, and almost always requires treatment.

P. aeruginosa is naturally resistant to a large range of antibiotics and may demonstrate additional resistance after unsuccessful treatment, particularly through modification of a porin. It should usually be possible to guide treatment according to laboratory sensitivities, rather than choosing an antibiotic empirically. If antibiotics are started empirically, then every effort should be made to obtain cultures, and the choice of antibiotic used should be reviewed when the culture results are available.

Antibiotics that have activity against P. aeruginosa include:

* aminoglycosides (gentamicin, amikacin, tobramycin);
* quinolones (ciprofloxacin and levofloxacin but not moxifloxacin)
* cephalosporins (ceftazidime, cefepime, cefpirome, but not cefuroxime, ceftriaxone, cefotaxime)
* ureidopenicillins (piperacillin, ticarcillin: P. aeruginosa is intrinsically resistant to all other penicillins)
* carbapenems (meropenem, imipenem, but not ertapenem)
* polymyxins (polymyxin B and colistin)[25]
* monobactams (aztreonam)

These antibiotics must all be given by injection, with the exception of fluoroquinolones and of aerosolized tobramycin. For this reason, in some hospitals, fluoroquinolone use is severely restricted in order to avoid the development of resistant strains of P. aeruginosa. In the rare occasions where infection is superficial and limited (for example, ear infections or nail infections), topical gentamicin or colistin may be used.

[edit] Antibiotic resistance

Pseudomonas aeruginosa is a highly relevant opportunistic pathogen. One of the most worrisome characteristics of P. aeruginosa is its low antibiotic susceptibility. This low susceptibility is attributable to a concerted action of multidrug efflux pumps with chromosomally-encoded antibiotic resistance genes and the low permeability of the bacterial cellular envelopes. In addition to this intrinsic resistance, P. aeruginosa easily develops acquired resistance either by mutation in chromosomally-encoded genes or by the horizontal gene transfer of antibiotic resistance determinants. Development of multidrug resistance by P. aeruginosa isolates requires several different genetic events that include acquisition of different mutations and/or horizontal transfer of antibiotic resistance genes. Hypermutation favours the selection of mutation-driven antibiotic resistance in P. aeruginosa strains producing chronic infections, whereas the clustering of several different antibiotic resistance genes in integrons favors the concerted acquisition of antibiotic resistance determinants. Some recent studies have shown that phenotypic resistance associated to biofilm formation or to the emergence of small-colony variants may be important in the response of P. aeruginosa populations to antibiotics treatment.[12]

[edit] Prevention

Medical-Grade honey (i.e., containing Unique Manuka Factor) may reduce colonization of many pathogens including Pseudomonas aeruginosa.[26] Probiotic prophylaxis may prevent colonization and delay onset of pseudomonas infection in an ICU setting.[27] Immunoprophylaxis against pseudomonas is being investigated. [28]

In January 2009, a Brazilian model named Mariana Bridi da Costa had her hands and feet both amputated due to Pseudomonas aeruginosa that presented itself as a urinary tract infection. In early January, she went into septic shock due to the infection, and later had both hands and feet amputated in an effort to save her life. Bridi lived only a few days after the amputations and died on January 24, 2009 at 2:30 am. The doctors that treated Bridi attribute her death to complications with the generalized infection and the subsequent surgery. She was 20 years old at the time of her death.[29]



They really screwed up by mis diagnosing her infection this led to wasting time instead of taking a blood sample and starting the above treatment there is only 1 type of penecillin that could work against it btw according the above article... sux.