Bactroban is used to treat certain skin infections such as impetigo and furuncle. It works by stopping the growth of bacteria.
Other names for this medication:
Also known as: Mupirocin.
Bactroban is an antibiotic ointment that is effective in treating impetigo, and other skin infections that bacteria causes. It is important to note that this ointment will not work on fungal infections or infections caused by viruses.
Bactroban consists of 2 medications: sulfamethoxazole and trimethoprim. The first inhibits synthesis of dihydrofolic acid (the substance important for human and bacterial metabolism) while the last blocks next stage of its biochemical cycle: formation of tetrahydrofolic acid which occurs only in microorganisms.
This medication is effective against streptococci, staphylococci, pneumococci, bacillus dysentery, typhoid fever, E. coli, Proteus, and ineffective against Mycobacterium tuberculosis, spirochetes, Pseudomonas aeruginosa. Bactrim is applied in treatment of pneumonia and other diseases of respiratory, gastrointestinal systems, urogenital systems caused by bacterial infections which develop after surgery and others.
Bactroban is an antibacterial. It works by stopping the production of essential proteins needed by the bacteria to survive.
Bactroban is also known as Mupirocin, Centany.
Generic name of Bactroban is Mupirocin.
Follow the directions for using this medicine provided by your doctor. Use Bactroban exactly as directed.
Bactroban should be applied directly to the skin.
This ointment is normally applied to the skin 3 times per day, normally for 1 to 2 weeks.
Before you apply the ointment, ensure that the affected area is clean and dry.
Apply a thin film of the ointment to the affected area. After applying the ointment, you may use a gauze to cover the affected area.
Wash your hands immediately after using Bactroban.
If you overdose Bactroban and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of overdose: dizziness, drowsiness, nausea, vomiting, loss of appetite, stomach pain, headache, yellowing of your skin or eyes, blood in your urine, fainting.
Store at a room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away the after the expiration date. Keep out of the reach of children.
The most common side effects associated with Bactroban are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Bactroban if you are allergic to Bactroban components.
It is not known whether Bactroban will harm an unborn baby. Do not use this medicine without your doctor's advice if you are pregnant or breast-feeding.
Do not take Bactroban if you suffer from asthma or have severe kidney or liver disorders.
Do not take Bactroban if you have anemia caused by folic acid deficiency.
Bactroban should be used with extreme caution in children younger than 5 years old; safety and effectiveness in these children have not been confirmed.
Do not drink alcohol or use medicines that may cause drowsiness (e.g., sleep aids, muscle relaxers) while you are using Bactroban; it may add to their effects. Ask your pharmacist if you have questions about which medicines may cause drowsiness.
Do not use Bactroban on large areas of broken or damaged skin, especially if you suffer from reduced kidney function.
Avoid exposure to sunlight or getting tanned.
Do not stop taking Bactroban suddenly.
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The objective of the study was to investigate the trend of mupirocin resistance among methicillin-resistant Staphylococcus aureus (MRSA) in Trinidad. No premarketing susceptibility surveillance was ever done following the introduction of mupirocin in 1986. A total of 188 MRSA strains recovered over a 2-year period from various body sites were tested for mupirocin resistance via the disc diffusion method. The major sources of MRSA were surgical site infections (74.0%) and bloodstream infections (8.0%). High-level and low-level mupirocin resistance were detected in 26.1 and 44.1% of MRSA stains, respectively. Resistances to other non-beta-lactam antibiotics were also high. Ninety-eight percent of all MRSA were resistant to erythromycin. This was followed by resistance rates of 96.8, 95.2, 94.1, 93.6, and 93.1%, for gentamicin, ciprofloxacin, amikacin and tobramycin, co-trimoxazole, and tetracycline, respectively. No MRSA strains were found to be resistant to vancomycin, linezolid, and quinupristin-dalfopristin. The study showed that mupirocin resistance among Trinidadian MRSA strains was relatively high compared to that seen in other countries. Because of the increasing prevalence of MRSA at the San Fernando General Hospital (SFGH) and the apparently increasing resistance to mupirocin, frequent monitoring of MRSA susceptibility patterns and infection control initiatives may be helpful in reducing the incidence of MRSA with a concomitant decrease in mupirocin resistance. This report is the first after 20 years of continuous use of the drug at the SFGH.
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The emergence of antimicrobial resistance severely threatens our ability to treat bacterial infections. While acquired resistance has received considerable attention, relatively little is known of intrinsic resistance that allows bacteria to naturally withstand antimicrobials. Gene products that confer intrinsic resistance to antimicrobial agents may be explored for alternative antimicrobial therapies, by potentiating the efficacy of existing antimicrobials. In this study, we identified the intrinsic resistome to a broad spectrum of antimicrobials in the human pathogen, Staphylococcus aureus. We screened the Nebraska Transposon Mutant Library of 1920 single-gene inactivations in S. aureus strain JE2, for increased susceptibility to the anti-staphylococcal antimicrobials (ciprofloxacin, oxacillin, linezolid, fosfomycin, daptomycin, mupirocin, vancomycin, and gentamicin). Sixty-eight mutants were confirmed by E-test to display at least twofold increased susceptibility to one or more antimicrobial agents. The majority of the identified genes have not previously been associated with antimicrobial susceptibility in S. aureus. For example, inactivation of genes encoding for subunits of the ATP synthase, atpA, atpB, atpG and atpH, reduced the minimum inhibitory concentration (MIC) of gentamicin 16-fold. To elucidate the potential of the screen, we examined treatment efficacy in the Galleria mellonella infection model. Gentamicin efficacy was significantly improved, when treating larvae infected with the atpA mutant compared to wild type cells with gentamicin at a clinically relevant concentration. Our results demonstrate that many gene products contribute to the intrinsic antimicrobial resistance of S. aureus. Knowledge of these intrinsic resistance determinants provides alternative targets for compounds that may potentiate the efficacy of existing antimicrobial agents against this important pathogen.
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Prophylactic intranasal MPN is safe, inexpensive, and very effective in reducing the overall sternal wound infections by 66.6%.
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Pragmatic cluster-randomized trial.
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All decolonisation strategies improved health outcomes and reduced costs. Although universal decolonisation (regardless of MRSA status) was the most cost effective in the short term, strategies using screening to target MRSA carriers may be preferred owing to the reduced risk of selecting for resistance. Among such targeted strategies, universal admission and weekly screening with polymerase chain reaction coupled with decolonisation using nasal mupirocin was the most cost effective. This finding was robust to the size of intensive care units, prevalence of MRSA on admission, proportion of patients classified as high risk, and precise value of willingness to pay for health benefits. All strategies using isolation but not decolonisation improved health outcomes but costs were increased. When the prevalence of MRSA on admission to the intensive care unit was 5% and the willingness to pay per QALY gained was between £20,000 (€23,000; $32,000) and £30,000, the best such strategy was to isolate only those patients at high risk of carrying MRSA (either pre-emptively or after identification by admission and weekly screening for MRSA using chromogenic agar). Universal admission and weekly screening using polymerase chain reaction based detection of MRSA coupled with isolation was unlikely to be cost effective unless prevalence was high (10% of patients colonised with MRSA on admission).
The rate of the MRSA strains, particularly at burn centers, is increasing worldwide. Detection of mupirocin resistance MRSA strains in the burn centers particularly from personnel will help to control these strains. For this purpose, a total of 116 Staphylococcus aureus isolates from the patients (burns) and personnel (nostrils) in Ahvaz Taleghani hospital (Iran) were investigated. The methicillin and mupirocin resistant isolates were detected by multiplex amplification of the mecA and ileS-2 genes. The mecA was found among 80% of isolates. The rates of mupirocin resistant strains among personnel and patients were 70% and 6%, respectively. The carriage rates of the S. aureus, MRSA and MRSA with high-level mupirocin resistance in the personnel were 40%, 34% and 28%, respectively. In conclusions, the high prevalence of MRSA strains in the patients showed the potential outbreak of the MRSA in the burn center and highlighted the need of antibiotic susceptibility monitoring of MRSA. Moreover being personnel as a main reservoir in terms of MRSA strains with high-level mupirocin resistance emphasizes the screening of the personnel in terms of the MRSA in the healthcare system especially in the burn center.
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