A resistant bacteria is responsible for so-called hospital-acquired pneumonia that inevitably results to death. Patients with hospital-acquired pneumonia caused by highly resistant bacteria are twice as likely to die as patients infected with other, less-resistant bacteria, according to a new Brazilian study. The study is the first to show that this form of bacteria, called metallo-beta-lactamase-producing Pseudomonas aeruginosa, which is highly resistant to virtually all antibiotics, is associated with a much higher death rate than other types of bacteria that cause hospital-acquired pneumonia.The higher death rate may be due to the use of inappropriate antimicrobial treatments for metallo-beta-lactamase-producing P. aeruginosa infections, the study authors wrote. They suggested that hospitals with high rates of infection with this bacterium should review their therapeutic approaches.It included 150 patients with hospital-acquired pneumonia at two hospitals in Porto Alegre, Brazil. Of those patients, 42 were infected with the resistant bacteria. The 30-day death rate for these patients was 57.1 percent, compared with 29.6 percent for patients infected with other strains of P. aeruginosa.The researchers also found that only half the patients infected with the highly resistant bacteria were treated with right antibiotics. However, the death rate among these patients was still high even when they received appropriate treatment. This suggests that the optimal treatment for this strain of bacteria has yet to be found.The word Pseudomonas means ‘false unit’, from the Greek pseudo meaning false and monas that means single unit. The word was used in the history of microbiology to refer to germs. Aeruginosa is the Latin word for verdigris or copper rust. This describes the blue-green bacterial pigment seen in laboratory cultures of P. aeruginosa. Pyocyanin biosynthesis is regulated by quorum sensing as in the biofilms associated with P. aeruginosa’s colonization of the lungs of cystic fibrosis patients.An opportunistic pathogen of immunocompromised individuals, P. aeruginosa typically infects the pulmonary tract, urinary tract, burns, wounds, and also causes other blood infections. Pseudomonas can in rare circumstances cause community acquired pneumonias, as well as ventilator-associated pneumonias, being one of the most common agents isolated in several studies. Pyocyanin is a virulence factor of the bacteria and has been known to cause death in C. elegans by oxidative stress. Still, research indicates that salicylic acid can inhibit pyocyanin production. One in ten hospital-acquired infections are from Pseudomonas. Cystic fibrosis patients are also predisposed to P. aeruginosa infection of the lungs. P. aeruginosa may also be a common cause of hot-tub rash, dermatitis, caused by lack of proper, periodic attention to water quality. The most common cause of burn infections is P. aeruginosa.P. aeruginosa uses the virulence factor exotoxin A to ADP-ribosylate eukaryotic elongation factor 2 in the host cell, much as the diphtheria toxin does. Without elongation factor 2, eukaryotic cells cannot synthesize proteins and necrose. The release of intracellular contents induces an immunologic response in immunocompetent patients.P. aeruginosa is frequently isolated from non-sterile sites like 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 such as blood, bone, deep collections, it should be taken seriously and almost always requires treatment.P. aeruginosa is naturally resistant to a great 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.
It is important to know antibiotics that have activity against P. aeruginosa include minoglycosides, quinolones, cephalosporins, ureidopenicillins, carbapenems, polymyxins and monobactams. These antibiotics must all be given by injection, with the exception of fluoroquinolones. 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
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