Antibiotics cross resistance

Tolypomycin Y (48) shows strong antibacterial activity against gram-positive bacteria and Neisseriagonorrheae. When adininistered by subcutaneous, intraperitoneal, and intravenous routes, tolypomycin Y is effective in mice infected with Staphylococcus aureus Streptococcuspyrogenes and Diplococcuspneumoniae. Cross-resistance is observed with rifampicia but not with other antibiotics. Resistance to tolypomycin Y develops rapidly. The bioactivity of tolypomycin R... 

Although the antibacterial spectmm is similar for many of the sulfas, chemical modifications of the parent molecule have produced compounds with a variety of absorption, metaboHsm, tissue distribution, and excretion characteristics. Administration is typically oral or by injection. When absorbed, they tend to distribute widely in the body, be metabolized by the Hver, and excreted in the urine. Toxic reactions or untoward side effects have been characterized as blood dyscrasias crystal deposition in the kidneys, especially with insufficient urinary output and allergic sensitization. Selection of organisms resistant to the sulfonamides has been observed, but has not been correlated with cross-resistance to other antibiotic families (see Antibacterial AGENTS, synthetic-sulfonamides). 

Some polymyxins are sold for second-line systemic therapy. Polymyxin B sulfate and colistimethate sodium can be used for intravenous, intramuscular, or intrathecal administration, especially for Pseudomonas aerupinosa mP QXiosis, but also for most other gram-negative organisms, such as those resistant to first-line antibiotics. Nephrotoxicity and various neurotoxicities are common in parenteral, but not in topical, use. Resistance to polymyxins develops slowly, involves mutation and, at least in some bacteria, adaptation, a poorly understood type of resistance that is rapidly lost on transfer to a medium free of polymyxin. Resistance can involve changes in the proteins, the lipopolysaccharides, and lipids of the outer membrane of the cell (52). Polymyxin and colistin show complete cross-resistance. 

Staphylococcus aureus cells can acquire large DNA fragments containing the mecA gene which encodes a complete new penicillin binding protein 2A (PBP 2A), as part of a transposon. PBP2A can substitute the natural set of penicillin-sensitive PBPs thereby mediating a complete cross resistance to all (3-lactam antibiotics. 

Since rifamycins are important drugs for the treatment of M. tuberculosis infection [36, 86, 87] the activity of rifaximin on and interference with this bacterium have been carefully studied. Indeed, a potential problem of the treatment with this antibiotic is represented by the possibility that even very low blood levels achieved by oral administration might be able to select mutants, cross-resistant to rifamycins [85], in patients treated for GI infections and harboring M. tuberculosis. 

Much information on the mechanism of action and cross-resistance of purine analogues has been obtained in bacteria, some of which are quite sensitive to certain of these compounds in vitro. There is a great deal of variation in response of the various bacteria to a particular agent and of a particular bacterium to the various cytotoxic purine analogues. Some, if not most, of these differences are probably due to differences in the anabolism of the various compounds. Despite the fact that certain purine analogues have quite a spectrum of antibacterial activity in vitro, none has been useful in the treatment of bacterial infections in vivo because their toxicity is not selective—the metabolic events whose blockade is responsible for their antibacterial activity are also blocked in mammalian cells and thus inhibition of bacterial growth can only be attained at the cost of prohibitive host toxicity. In contrast, the sulpha drugs and antibiotics such as penicillin act on metabolic events peculiar to bacteria. 

Viomycin is a complex polypeptide antibiotic that is active against MDR strains of tuberculosis. Cross-resistance between viomycin and kanamycin is less frequent than between viomycin and capreomycin. 

Macrolides inhibit growth of bacteria by inhibiting protein synthesis on ribosomes. Bacterial resistance to macrolides is often accompanied by cross-resistance to lincosamide and sireptogramin B antibiotics (MLS-resistance), which can be either inducible or constitutive. 14-Membered... 

Xu M, Zhou YN, Goldstein BP et al (2005) Cross-resistance of Escherichia coli RNA polymerases conferring rifampin resistance to different antibiotics. J Bacteriol 187 2783-2792... 

It is well documented that antimicrobial agents cause cross-resistance. Use of antibiotics causes alterations in normal microbial flora of the body. The suprain-fection is a common problem associated with antibiotic therapy and is very difficult to treat. Prolonged uses of antibiotics alter the microflora of the intestine and cause vitamin deficiency. Neomycin causes morphologic abnormalities in the intestinal mucosa. 

Resistance to erythromycin is becoming a serious clinical problem. For example, most strains of staphylococci in hospital isolates are resistant to this drug. Several mechanisms have been identified (1) the inability of the organism to take up the antibiotic (2) a decreased affinity of the 50S ribosomal subunit for the antibiotic resulting from the methylation of an adenine of the 23S bacterial ribosomal RNA and (3) presence of a plasmid-associated erythromycin esterase. Both clarithromycin and azithromycin show cross-resistance with erythromycin. 

The resistance mechanisms that cause the inactivation of penicillins, cephalosporins, aminoglycosides, macrolides and tetracyclines do not apply to fluoroquinolones, and there is therefore no cross-resistance between quinolones and other antibiotics. 

Although many workers have reported that gentamicin resistant strains of Ps. aeruginosa are sensitive to tobramycin [170,218,219], complete cross-resistance between the two antibiotics was found in 1972 [220]. 

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