Many<unk>  isolates are resistant to a large range of antibiotics and may demonstrate additional resistance after unsuccessful treatment. 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 (before administering the first dose of antibiotic), and the choice of antibiotic used should be reviewed when the culture results are available. The antibiogram of<unk>  on Mueller–Hinton agar Due to widespread resistance to many common first-line antibiotics, carbapenems, polymyxins, and more recently tigecycline were considered to be the drugs of choice; however, resistance to these drugs has also been reported. Despite this, they are still being used in areas where resistance has not yet been reported. Use of β-lactamase inhibitors such as sulbactam has been advised in combination with antibiotics to enhance antimicrobial action even in the presence of a certain level of resistance. Combination therapy after rigorous antimicrobial susceptibility testing has been found to be the best course of action in the treatment of multidrug-resistant<unk> . Some next-generation antibiotics that are reported as being active against<unk>  include doripenem, ceftobiprole, and ceftaroline. However, these require more clinical trials for standardization. Therefore, research for the discovery of new antibiotics and drugs against<unk>  is very much needed. Antibiotics that may have activity against<unk>  include: *aminoglycosides (gentamicin, amikacin, tobramycin, but not kanamycin) *quinolones (ciprofloxacin, levofloxacin, but not moxifloxacin) *Examples of antibiotic susceptibility testing of<unk> . The disk diffusion test (A) and the MIC test (B).<unk>  is intrinsically resistant to ampicillin/sulbactam, tigecycline and trimethoprim/sulfamethoxazole (no breakpoints in Img. B).cephalosporins (ceftazidime, cefepime, cefoperazone, cefpirome, ceftobiprole, but not cefuroxime, cefotaxime, or ceftriaxone) *antipseudomonal penicillins: carboxypenicillins (carbenicillin and ticarcillin), and ureidopenicillins (mezlocillin, azlocillin, and piperacillin).<unk>  is intrinsically resistant to all other penicillins. *carbapenems (meropenem, imipenem, doripenem, but not ertapenem) *polymyxins (polymyxin B and colistin) *monobactams (aztreonam) As fluoroquinolones are one of the few antibiotic classes widely effective against<unk> , in some hospitals, their use is severely restricted to avoid the development of resistant strains. On the rare occasions where infection is superficial and limited (for example, ear infections or nail infections), topical gentamicin or colistin may be used. For<unk>  wound infections, acetic acid with concentrations from 0.5% to 5% can be an effective bacteriostatic agent in eliminating the bacteria from the wound. Usually a sterile gauze soaked with acetic acid is placed on the wound after irrigation with normal saline. Dressing would be done once per day.<unk>  is usually eliminated in 90% of the cases after 10 to 14 days of treatment. Antibiotic resistance One of the most worrisome characteristics of<unk>  is its low antibiotic susceptibility, which is attributable to a concerted action of multidrug efflux pumps with chromosomally encoded antibiotic resistance genes (e.g., mexAB, mexXY, etc.) and the low permeability of the bacterial cellular envelopes. In addition to this intrinsic resistance,<unk>  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<unk>  isolates requires several different genetic events, including acquisition of different mutations and/or horizontal transfer of antibiotic resistance genes. Hypermutation favours the selection of mutation-driven antibiotic resistance in<unk>  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 phenotypic resistance associated to biofilm formation or to the emergence of small-colony variants may be important in the response of<unk>  populations to antibiotics treatment. Mechanisms underlying antibiotic resistance have been found to include production of antibiotic-degrading or antibiotic-inactivating enzymes, outer membrane proteins to evict the antibiotics and mutations to change antibiotic targets. Presence of antibiotic-degrading enzymes such as extended-spectrum β-lactamases like PER-1, PER-2, VEB-1, AmpC cephalosporinases, carbapenemases like serine oxacillinases, metallo-b-lactamases, OXA-type carbapenemases, aminoglycoside-modifying enzymes, among others have been reported.<unk>  can also modify the targets of antibiotic action, for example methylation of 16S rRNA to prevent aminoglycoside binding and modification of DNA, or topoisomerase to protect it from the action of quinolones.<unk>  has also been reported to possess multidrug efflux pumps systems that confer resistance against a number of antibiotic classes and the MexAB-OprM (Resistance-nodulation-division (RND) family) is considered as the most important. An important factor found to be associated with antibiotic resistance is the decrease in the virulence capabilities of the resistant strain. Such findings have been reported in the case of rifampicin-resistant and colistin-resistant strains, in which decrease in infective ability, quorum sensing and motility have been documented. Mutations in DNA gyrase are commonly associated with antibiotic resistance in<unk> . These mutations, when combined with others, confer high resistance without hindering survival. Additionally, genes involved in cyclic-di-GMP signaling may contribute to resistance. When grown in vitro conditions designed to mimic a cystic fibrosis<unk> tient's lungs, these genes mutate repeatedly. Two small RNAs : Sr0161 and ErsA were shown to interact with mRNA encoding the major porin OprD responsible for the uptake of carbapenem antibiotics into the periplasm. The sRNAs bind to the 5'UTR of oprD causing increase in bacterial resistance to meropenem. Another sRNA: Sr006 was suggested to positively regulate (post-transcriptionally) the expression of<unk> gL, an enzyme responsible for deacylation of lipid A. This reduces the pro-inflammatory property of lipid A. Furthermore, similarly to study in Salmonella Sr006 regulation of<unk> gL expression was suggested to aid in polymyxin B resistance. Prevention Probiotic prophylaxis may prevent colonization and delay onset of<unk>  infection in an ICU setting. Immunoprophylaxis against<unk>  is being investigated. The risk of contracting<unk>  can be reduced by avoiding pools, hot tubs, and other bodies of standing water; regularly disinfecting and/or replacing equipment that regularly encounters moisture (such as contact lens equipment and solutions); and washing one's hands often (which is protective against many other<unk> thogens as well). However, even the best hygiene practices cannot totally protect an individual against<unk> , given how common<unk>  is in the environment. Experimental therapies Phage therapy against<unk>  has been investigated as a possible effective treatment, which can be combined with antibiotics, has no contraindications and minimal adverse effects. Phages are produced as sterile liquid, suitable for intake, applications etc. Phage therapy against ear infections caused by<unk>  was reported in the journal Clinical Otolaryngology in August 2009.
Pseudomonas aeruginosa
Acinetobacter baumannii
Staphylococcus aureus
Streptococcus bovis
Enterobacter cloacae
Bacillus cereus
Bacillus anthracis
Pasteurella