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Cross-resistance can take place between compounds that are chemically similar, like antibiotics within similar and different classes. [9] That said, structural similarity is a weak predictor of antibiotic resistance, and does not predict antibiotic resistance at all when aminoglycosides are disregarded in the comparison. [10]
Nevertheless, the risk of cross-reactivity is sufficient to warrant the contraindication of all β-lactam antibiotics in patients with a history of severe allergic reactions (urticaria, anaphylaxis, interstitial nephritis) to any β-lactam antibiotic. Rarely, allergic reactions have been triggered by exposure from kissing and sexual contact ...
Lincosamides are often used clinically as an alternative antibiotic for patients who are allergic to penicillin. Of the lincosamides, clindamycin is most commonly used within the clinic due to its higher bioavailability, higher oral absorption and efficacy within the target organism spectrum. [ 23 ]
Monobactam antibiotics exhibit no IgE cross-reactivity reactions with penicillin but have shown some cross reactivity with cephalosporins, most notably ceftazidime, which contains an identical side chain as aztreonam. [8] Monobactams can trigger seizures in patients with history of seizures, although the risk is lower than with penicillins.
Cross-reactivity, in a general sense, is the reactivity of an observed agent which initiates reactions outside the main reaction expected. This has implications for any kind of test or assay , including diagnostic tests in medicine, and can be a cause of false positives .
Clindamycin is a lincosamide antibiotic medication used for the treatment of a number of bacterial infections, including osteomyelitis (bone) or joint infections, pelvic inflammatory disease, strep throat, pneumonia, acute otitis media (middle ear infections), and endocarditis. [5]
All types of microbes can develop drug resistance. Thus, there are antibiotic, antifungal, antiviral and antiparasitic resistance. [4] [8] Antibiotic resistance is a subset of antimicrobial resistance. This more specific resistance is linked to bacteria and thus broken down into two further subsets, microbiological and clinical.
Penicillin is a cyclic analogue of the D-Ala-D-Ala terminated carbonyl donors, therefore in the presence of this antibiotic, the reaction stops at the level of the serine ester-linked penicilloyl enzyme. [11] Thus β-lactam antibiotics force these enzymes to behave like penicillin binding proteins. [12]