Antibiotics Review _ __________________________________________________________________________
Monobactams Aztreonam
IV: 1–2 g every 8 to 12 hrs
>9 mos: 30–50 mg/ kg/dose every 6 to 8 hrs Max: 120 mg/kg/day >7 years of age (nebulizer): Same as adult dosing
IV, IM, oral inhalation
Rash, nausea, vomiting, phlebitis at infusion site
Rare cross-sensitivity with allergy to other beta-lactams.
For oral inhalation, pretreatment with a bronchodilator is recommended.
Nebulizer: 75 mg 3 times/day at least 4 hours apart for 28 days; do not repeat for 28 days after completion.
Prescribing information is given for comparison purposes only. The higher dosage ranges reflect dosages for more severe infections. Please consult the manufacturer’s package insert for the antibiotic for complete prescribing information, maximum dosages, and indications. CNS = central nervous system; LFTs = liver function tests (liver enzymes). Source: [6; 16] Table 3
SIDE EFFECTS/TOXICITY Frequent adverse reactions include elevations of liver enzymes and transient eosinophilia. Less common reactions include phlebitis at the infusion site, rash, diarrhea, and nausea [6; 76]. There have been a few reports of cross-allergy reactions in patients who are allergic to ceftazidime, but patients with penicillin and cephalosporin allergy can usually tolerate aztreo- nam [77]. Aztreonam is contraindicated in patients with prior allergic reactions to it or to any component of the formulation. DRUG INTERACTIONS No drug interactions have been reported with aztreonam [6; 78]. SPECIAL POPULATIONS Aztreonam is pregnancy category B, based on animal studies that have shown no ill effects of the drug. There are no human data available [6]. Aztreonam is secreted in breast milk in low concentrations; breastfeeding is not recommended because the effects of the drug have not been studied in young infants [78]. Aztreonam has not been studied for use in children younger than 1 month of age but appears safe in children older than 1 month of age, although it should be noted that manufacturer recommendations are for children older than 9 months of age [6; 78]. It has been shown to be very useful in children with respiratory symptoms of cystic fibrosis [79].
AMINOGLYCOSIDES The first aminoglycoside, streptomycin, was derived from Streptomyces griseus during the 1940s. Actinomycetes were studied for possible antimicrobial byproducts, and it was found that Micromonospora and Streptomyces produced useful agents. As newer, safer, and more effective aminoglycosides have been developed, the use of streptomycin is now confined primarily to certain management strategies for the treatment of tuberculosis. MECHANISM OF ACTION The basic structure of the aminoglycosides is an aminocyclitol ring. Different members of the family have different glycosidic linkages and side groups. The aminoglycosides have at least two effects on the bacterial cell that ultimately result in cell death. These agents bind nega- tive charges in the outer phospholipid membrane, displacing the cations that link the phospholipids together. This leads to disruption in the wall and leakage of cell contents. In addition, they inhibit protein synthesis by binding to the 30S subunit of the ribosome, causing miscoding and termination [80]. Although resistance to aminoglycosides is less common than with many other antibiotics, it can develop as a result of three known mechanisms. The most common pattern of resistance involves modification of the aminoglycoside molecule itself by enzymes produced by some bacteria. After the aminogly- coside is altered, it cannot bind as well to the ribosomes. The genes that encode for these enzymes are carried on plasmids, allowing rapid transfer of resistance between bacteria. Of note, amikacin has an S-4 amino 2-hydroxybutyryl (AHB) side chain that protects it against deactivation by many bacte- rial enzymes and is therefore less susceptible to this bacterial defense mechanism [81].
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