Amikacin indications

Gram-negative cocci Non-tuberculous mycobacteria Nocardia Ceftriaxone 50 mg/mL or Ceftazidime 50 mg/mL or Fluoroquinolones 3 mg/mL Amikacin 20-40 mg/mL or Oral clarithromycin 500 mg every 12 hours Amikacin 20-40 mg/mL or Trimethoprim 16 mg/mL and sulfamethoxazole 80 mg/mL wearers as indicated... 

Amikacin is indicated for the treatment of genital tract infections in the mare by intra-uterine infusion. 

E. The patient has exudative pharyngitis, presumably secondary to group A streptococcus. Antibiotic treatment is indicated to reduce the duration and severity of symptoms and to prevent acute rheumatic fever. The antibiotic of first choice is penicillin V. Other reasonable alternatives are benzathine penicillin G, erythromycin, cephalosporin, clindamycin, azithromycin, and clarithromycin. Amikacin, lome-fioxacin, metronidazole, and netilmicin are not active against group A streptococcus. 

Structures of several important aminoglycoside antibiotics. Ring II is 2-deoxystreptamine. The resemblance between kanamycin and amikacin and between gentamicin, netilmicin, and tobramycin can be seen. The circled numerals on the kanamycin molecule indicate points of attack of plasmid-mediated bacterial transferase enzymes that can inactivate this drug. , , and , acetyltransferase , phosphotransferase , adenylyltransferase. Amikacin is resistant to modification at , , , and . 

Penicillin plus streptomycin is effective for enterococcal endocarditis and 2-week therapy of viridans streptococcal endocarditis. Gentamicin has largely replaced streptomycin for these indications. Streptomycin remains a useful agent for treating enterococcal infections, however, because approximately 15% of enterococcal isolates that are resistant to gentamicin (and therefore to netilmicin, tobramycin, and amikacin) will be susceptible to streptomycin. 

Figure 5 Pharmacological effects of liposome and liposome-free incubations for amikacin (A [132]) and for triamcinolone acetonide phosphate (B, unpublished observation) in cell culture. A represents situation A in figure 3. B, represents situation B in Figure 3. Note the right shift for the liposomal preparation, indicating a less favorable uptake of liposomal encapsulated drug. Such formulations are only working as slow-release depot formulations of the drug.

Schreier et al. [85] examined the effects of liposome encapsulation on the pharmacokinetics in sheep of amikacin, a water-soluble aminoglycoside. The dmg was formulated in 200 nm liposomes and administered by means of intratracheal instillation. The liposome formulations were soy PC/phosphatidyl glycerol (PG) (7 3 molar ratio) and soy PC/PG/CH (4 3 3). They found that both liposome formulations reduced plasma Cmax and prolonged the plasma half-life of the amikacin compared with the dmg administered as a solution, once again indicating that liposomes were controlling dmg delivery in the lungs. The inclusion of cholesterol in liposomes more than tripled the plasma half-life for the dmg compared with the liposomes without cholesterol. Cholesterol reduces the fluidity and permeability of liposomes in their liquid crystalline phase. 

Results from animal studies indicate that while furosemide enhanced cephaloridine nephrotoxicity no increased renal toxicity was observed by combining of piperacillin with furosemide [142]. Latamoxef and flo-moxef may decrease nephrotoxicity of vancomycin by inhibiting its uptake into the kidney [146,147]. The results of a retrospective study including renal transplant patients indicate that aztreonam can be safely administered with cyclosporine [148]. Combination therapy with ampicillin/aztreonam in neonates showed a lower renal toxicity than in the group with concurrent administration of oxacillin/ amikacin [149]. 

Amikacin sulfate is approved for i.m. or s.c. injection in horses (50 or 250 mg/ml solution) and for intrauterine infusion (250 mg/ml solution). Other routes of administration that are not within the label indications (i.v. and intraarticular) are used frequently. 

Preliminary studies indicate that amikacin may be less... 

Indications Neuromuscular blockade, endotracheal intubation Category Non-depolarizing neuromuscular blocker Half-life initial 2 minutes terminal 20 minutes Clinically important, potentially hazardous interactions with amikacin, aminoglycosides, anesthetics, antibiotics, gentamicin, halothane, kanamycin, neomycin, piperacillin, streptomycin, tobramycin... 

Renal excretion mechanisms appear to mature within the first 2 weeks after birth in foals, calves, lambs, kids and piglets, while their maturation in puppies may take 4-6 weeks. In a study of the pharmacokinetics of amikacin in critically ill full-term foals ranging in age from 2 to 12 days, the systemic clearance of the aminoglycoside was lower (indicating impaired renal function) and the half-life was considerably prolonged in uraemic compared with non-uraemic foals (Adland-Davenport et al., 1990). 

In the second study [16], 62 subjects were treated with intravenous ceftazidime and amikacin. The treatment group also received aerosolized amikacin 100 mg twice daily. Treatments were given for an average of 15 days, and subjects were reevaluated four to six weeks after hospital discharge. During treatment, transient improvements in several outcome measures were noted (e.g., x-ray score, inflammation indices, and percentage underweight) however, there were no differences in any measure at the final evaluation point. As in the earlier study, eradication of bacteria from sputum was also transient. 

A newly Isolated, plasmid-determined acetyl transferase [AAC(3)-III] inactivates most aminoglycosides, including gentamicin and apramycln, but not butirosin, amikacin or fortlmlcin. Earlier data had indicated no cross-resistance of apramycln with other aminoglycosides. " A broad-... 

Unfortunately, MAC is resistant to the standard drugs used for tuberculosis, such as isoniazid and pyrazinamide. Multiple agents such as rifampin, rifabutin (ansamycin), clofazimine, imipenem, amikacin, ethambutol, ciprofloxacin, clarithromycin, and azithromycin have varying degrees of in vitro anti-MAC activity. Controversy formerly existed as to whether treatment for MAC is beneficial, but data indicate that an aggressive therapeutic approach decreases symptoms... 

A few other fluorinated kanamycins, including 5-deoxy-5-epi-fluoroamikacin, 5-deoxy-5-ep(-fluoroarbekacin, and their related analogs, have been prepared to study the fluorination-toxicity relationship. In contrast to the low toxicities of the 5-fluoro derivatives [121], these epi-fluoro compounds showed acute toxicity values identical to those of arbekacin and amikacin [122]. This indicates the importance of stereo-electronic effects of the fluoro group at position 5 of the 2-deoxystreptomine moiety in toxicity of aminoglycoside antibiotics. 

Kanamycin is all but obsolete, and there are few indications for its use. It has been employed to heat tuberculosis in combination with other effective drugs. It has no therapeutic advantage over streptomycin or amikacin and probably is more toxic either should be used instead, depending on susceptibility of the isolate. 

Amikacin is indicated for treatment of tuberculosis suspected to be caused by streptomycin-resistant or multidrag-resistant mycobacterial strains. To avoid emergence of resistance, amikacin should always be used in combination drug regimens. 

Both animal and human studies indicate that nephrotoxicity may be increased by the concurrent use of ciclosporin and gentamicin. This has also been shown for tobramycin. Cases of renal impairment have been reported for amikacin and gentamicin. 

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