Antimicrobial selection and dosage in the treatment of equine bacterial infections

Baggot, J. D.; Prescott, John F.

doi:10.1111/j.2042-3306.1987.tb02596.x

Cited by 24 publications

(12 citation statements)

References 10 publications

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“…1992;Wichtel et a/. 1992) and sensitivity trends for Gram-negative equine pathogens in our hospital (Baggot and Prescott 1987; Prescott and Baggot 1988), our targeted peak and trough serum concentration for amikacin were 215 pg/ml (but <30 pg/ml) and 5 3 pg/ml (but > I pg/ml), respectively. These provided peak values which were 4-5 times the mean inhibitory concentration (MIC) for common equine pathogens and trough values below 5 pg/ml which is regarded to be the upper limit to avoid nephrotoxicity.…”

Section: Measurement Of Amikacin Serum Concentrationsmentioning

confidence: 62%

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Clinical pharmacokinetics of amikacin in hypoxic premature foals

Green

Conlon

1993

Equine Veterinary Journal

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Summary The pharmacokinetics of amikacin, administered iv at 7 mg/kg, every 8 h, were evaluated over the first 48 h of hospitalisation in 7 critically ill hypoxic premature foals and compared with those in 8 full‐term nonhypoxic critically ill neonatal foals. The pharmacokinetic data were used to calculate dosage schedules that would maintain the plasma amikacin concentrations in individual foals within a target range of ≥15 μg/ml but <30 μg/ml for peak values and ≤3 μg/ml for trough values. The results indicated a statistically significant increase in the amikacin serum half‐life (5.39 ± 3.46 h) and smaller elimination rate constant (0.17 ± 0.09 h−1) in premature foals. The pharmacokinetic derangements required increasing the dose to 8.5–10.5 mg/kg bwt in 6 of 7 premature foals and an increase in the dosage interval to 12–24 h in all 7 foals. Overall, the total dosage of amikacin was decreased in the hypoxic, premature foals so that target peaks and troughs could be maintained. Our findings suggest that prematurity and hypoxia are variables related to a prolonged serum half‐life of amikacin in hypoxic, premature foals. Although there was no evidence of amikacin‐induced nephrotoxicity in any of these foals, daily monitoring and tailoring of the dose schedule to the individual foal are strongly advised.

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Section: Measurement Of Amikacin Serum Concentrationsmentioning

confidence: 62%

“…1984;Shulman and Yogev 1985;Chadwick et a/. 1986;Baggot and Prescott 1987). The emergence of gentamycin-resistant organisms (Tally et a/.…”

Section: Introductionmentioning

confidence: 99%

Clinical pharmacokinetics of amikacin in hypoxic premature foals

Green

Conlon

1993

Equine Veterinary Journal

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“…1976; National Council on Clinical Laboratory Standards 1989), previous studies on the pharmacology of amikacin in horses (Orsini et al 1985;Brown et al 1986;Adland-Davenport er al. 1990) and sensitivity trends for Gram-negative equine pathogens in our hospital (Baggot and Prescott 1987;Prescott and Baggot 1988), our targeted peak and trough serum concentrations for amikacin were I5 pg/ml and 3 @ml, respectively.…”

Section: Measurement Of Amikacin Serum Concentrationsmentioning

confidence: 82%

“…The aminoglycoside antibiotics are active against most strains of Enterohacteriaceae, Pseudornonas aeruginosa, Klehsiella spp. and Staphylococcus spp., which are common pathogens in infants and the equine neonate (Koterba et al 1984;Baggot and Prescott 1987;Shulman and Yogev 1985;Howard and McCracken 1975;Chadwick et al1986;Sardemann et al 1976). The emergence of gentamycin-resistant organisms in our hospital, and in others (Koterba et al 1984;Tally et al 1975), has necessitated the use of amikacin, a semi-synthetic aminoglycoside, for the empirical treatment of critically ill, high risk-foals.…”

Section: Introductionmentioning

confidence: 99%

Effects of hypoxia and azotaemia on the pharmacokinetics of amikacin in neonatal foals

Green

Conlon

Mama

et al. 1992

Equine Veterinary Journal

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Summary The effects of hypoxia and azotaemia on the pharmacokinetics of amikacin were evaluated in 20 full‐term neonatal critically ill foals which required 24‐h supportive care, antibiotics and dextrose‐supplemented polyionic fluids given intravenously, nasal insufflation with oxygen and nutritional supplementation. There was no association between sepsis score or survival and pharmacokinetic parameters. Concurrent hypoxia and azotaemia were associated with significantly decreased clearance and increased peak and trough serum concentrations of amikacin; however, peaks or troughs did not exceed toxic values. Derangements in serum peak, trough and clearance values, which were present on admission, persisted over the 6‐day duration of this study. Daily monitoring of serum amikacin concentration revealed a tendency to underdose (particularly in foals receiving aggressive fluid therapy), which necessitated increasing the dose/kg body weight (9–12 mg/kg) and increasing the dose interval (10–12 h) in 40% (8/20) of the cases, so that blood concentrations of amikacin could be maintained within the target range of 3–15 μg/ml. Amikacin‐induced nephrotoxicity was not indicated by conventional laboratory testing, nor was it strongly suspected after examination of post mortem lesions.

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“…use. Baggot and Prescott (1987) and Horspool et al. (1992) showed that intravenously administered ampicillin sodium has an elimination half‐life t 1/2 (d) of less than 1 h in the horse.…”

Section: Introductionmentioning

confidence: 99%

Intramuscular dosing strategy for ampicillin sodium in horses, based on its distribution into tissue chambers before and after induction of inflammation

Hoven¹,

Hierweck²,

Dobretsberger

et al. 2003

Vet Pharm & Therapeutics

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The Pharmacokinetics (PK) and distribution into tissue chamber fluid (TCF) of intramuscularly (i.m.) administered ampicillin sodium were examined in horses in order to design adequate dosing strategies. Concentration-time curves of ampicillin in plasma and TCF were determined in six horses following administration of 15 mg/kg ampicillin sodium, before and after the induction of local inflammation with 0.5% carrageenan. The calculated parameters were used to simulate various dosage-dosing interval combinations. Ampicillin was absorbed very rapidly following i.m. administration. Plasma concentrations were maximual between 18 and 21 min after administration. None of the plasma PK parameters were affected significantly by local (TC) inflammation. Penetration of ampicillin into and elimination from the TCF were affected significantly by inflammation and the half-life of elimination from the tissue fluid t1/2(d) was significantly shorter in inflammation. In the simulated dosage-dosing interval scenarios, only a dosage of 15 mg ampicillin/kg four times daily would successfully treat all ampicillin-susceptible bacterial isolates in well vascularized tissues. However a dosage as low as 10 mg/kg twice daily, would, in theory, treat all ampicillin-susceptible isolates in the inflamed poorly vascularized tissues. Decreasing the dosage results in loss of efficacy that cannot be completely compensated for by increasing the frequency of dosing.

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Antimicrobial selection and dosage in the treatment of equine bacterial infections

Cited by 24 publications

References 10 publications

Clinical pharmacokinetics of amikacin in hypoxic premature foals

Clinical pharmacokinetics of amikacin in hypoxic premature foals

Effects of hypoxia and azotaemia on the pharmacokinetics of amikacin in neonatal foals

Intramuscular dosing strategy for ampicillin sodium in horses, based on its distribution into tissue chambers before and after induction of inflammation

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