Nafcillin, 6-(2-ethoxy-1-naphthamido) penicillanic acid, is a semisynthetic, narrow-spectrum[1] b-lactam antibiotic [2] derived from the penicillin nucleus, 6-aminopenicillanic acid. As a b-lactamase-resistant penicillin, it is used to treat infections caused by Gram-positive bacteria, in particular, species of staphylococci that are resistant to other penicillins. Developed in 1961, it has since been widely used in the United States and a small number of other countries for the parenteral treatment of serious b-lactamase-producing staphylococcal infections.

Nafcillin is considered therapeutically equivalent to oxacillin, although its safety profile is somewhat different.

Therapeutic use

Nafcillin is indicated in the treatment of staphylococcal infections, except those caused by MRSA. U.S. clinical practice guidelines recommend either nafcillin or oxacillin as the first-line treatment of choice for staphylococcal endocarditis in patients without artificial heart valves [3].

S. aureus infections

Parenteral nafcillin has been used successfully for the treatment of severe S. aureus infections, such as septicemia, endocarditis, osteomyelitis, septic arthritis, pneumonia, meningitis, skin and skin structure infections, and pyomyositis [4-12]. In the USA, nafcillin is
widely regarded as the preferred drug for treatment of S. aureus endocarditis [13-14].

Although the synergistic combination of nafcillin plus gentamicin has usually demonstrated superior therapeutic effect, compared with nafcillin alone, in experimental animals [15], it remains somewhat uncertain whether this synergistic nafcillin–gentamicin combination is clinically superior to nafcillin alone for the treatment of human endocarditis caused by tolerant or nontolerant S. aureus strains. It may be reasonable to initiate combination therapy in patients with S. aureus endocarditis, but the aminoglycoside should be stopped after clearance of bacteremia (3–5 days) and that nafcillin alone be continued for a total of 6 weeks [16].

The high prevalence of S. aureus as a cause of acute and chronic osteomyelitis means that nafcillin is widely used for initial treatment of this condition [17-18]. A rifampicin–nafcillin combination has been used to treat chronic staphylococcal osteomyelitis, with a trend towards better outcomes; however, the advantages of this combination are not definitive [19].

In Australia and in Europe, one of the parenteral isoxazolyl penicillins, such as cloxacillin or flucloxacillin, is commonly used, while in the USA, oxacillin is an effective alternative. The response obtained in severe staphylococcal infections is about the same with all of these drugs, provided they are given parenterally in appropriate doses.

Because of its better penetration into the CSF, some authors regard nafcillin as the drug of choice for staphylococcal meningitis [20-21]. If nafcillin is used for this purpose, the parenteral dose should be at least 2 g 4 hourly for adults [22-23]. For the treatment of staphylococcal meningitis, a nafcillin–rifampicin combination may prove to be more effective [24].

Infections due to coagulase-negative staphylococci

Nafcillin can be used to treat severe hospital-acquired infections caused by these organisms, such as prosthetic valve endocarditis, provided the strain is methicillin sensitive. The addition of either gentamicin or rifampicin, or both, to the nafcillin regimen may improve the results of treatment [25]. If the strain is methicillin resistant, which is frequent if the infection is hospital acquired, vancomycin should be used and the addition of either rifampicin or gentamicin, or both, may be of beneficial [26-27]. Chemoprophylaxis with nafcillin plus rifampicin has been used for patients undergoing cardiac valve surgery. However, in one study, more than half of the patients receiving such chemoprophylaxis became colonized by S. epidermidis strains resistant to methicillin, gentamicin, and rifampicin [28].

Dosage and Administration

Nafcillin comes as a 1- and 2-g parenteral formulation for intravenous and intramuscular use.


Owing to low and unpredictable absorption, nafcillin is not recommended for oral administration. Nafcillin can be given either i.m. or i.v. Intramuscular administration results in a peak concentration of 5–8  mg/ml after 500-mg to 1-g doses. The usual adult i.v. dosage is 1 g 4-hourly, but this can be doubled for the treatment of severe infections, in particular endocarditis. Doses of up to 18 g i.v. daily have been given to adults with no ill effects. The drug should be given i.v. using techniques as described for penicillin G. Nafcillin has been given prophylactically directly into surgical wounds at the time of closure [29] and can be used to treat continuous ambulatory peritoneal dialysis-associated peritonitis by instillation in the dialysate at a concentration of 125 mg/l [30]. Nafcillin is quite stable in peritoneal dialysate solutions [31].

Newborn infants and children

The usual parenteral pediatric dose is 25 mg/kg 4-hourly; higher doses of 50 mg/kg 4-hourly can be given safely. In newborns, the recommended dosage for severe infection is 100 mg/kg/day, given in two divided doses for infants less than 7 days of age, and in three divided doses for those older than 7 days [32]. In those with birth weights less than 2000 g, a dose of 20 mg/kg body weight, administered 8-hourly, is probably sufficient [32].

Impaired renal function

Nafcillin is eliminated from the body rapidly and primarily by nonrenal mechanisms [33], so that dosage reduction is not needed in patients with renal impairment. The plasma nafcillin elimination half-life is unaltered in anuric patients during hemodialysis and in the interval between dialyses, so that patients can be treated by a nafcillin dosage used for patients with normal renal function [34].

Impaired hepatic function

As nafcillin is normally cleared through the liver, impaired hepatic function alters kinetics. Cirrhosis and extrahepatic biliary obstruction alter clearance to some extent, although there is at least partial compensation through increased renal clearance 35]. Thus, serum levels may need to be monitored in patients with severe hepatic impairment, and dosage adjustments need to be made accordingly. There are no formal recommendations for dosage reduction, with each patient’s individual situation requiring consideration.


Serious toxicity is unlikely following large doses of nafcillin. Acute ingestion of large doses of nafcillin may cause nausea, vomiting, diarrhea and abdominal pain. Acute oliguric renal failure and hematuria may occur following large doses.

Organism Test Type Route Reported Dose (Normalized Dose) Effect Source
child TDLo unreported 1050mg/kg/1W- (1050mg/kg) KIDNEY, URETER, AND BLADDER: INTERSTITIAL NEPHRITIS JAMA, Journal of the American Medical Association. Vol. 225, Pg. 178, 1973

Adverse reactions

Overall adverse reaction rates to nafcillin when used as definitive treatment are approximately 20–30% [36-37]. Different rates, either higher or lower, have been recorded when used for prolonged periods, such as for outpatient treatment [38-39]. Serious reaction rates are <5%.

Hypersensitivity reactions

Nafcillin, like other penicillins, may cause the same hypersensitivity reactions that occur with penicillin G. Most common is skin rash [38]. The drug is contraindicated in any patient with a history of penicillin sensitivity. Rash is less likely with nafcillin than with oxacillin [37]. 


A patient who developed renal damage due to methicillin, resolved when lincomycin was substituted [40]. Later, when therapy was changed to nafcillin, the hypersensitivity nephritis recurred. Nephropathy has been reported on many occasions with methicillin, but less commonly with other penicillinase-resistant penicillins. If nephropathy develops after the use of one penicillin analog, it is likely to recur if any other penicillin is subsequently used.


Nafcillin administered in large doses i.v. (200 mg/kg/day) can cause hypokalemia and associated alkalosis [41]. Nafcillin acts as a non-reabsorbable anion and increases passive renal distal tubular potassium excretion. This is similar to what occurs with other penicillins used in large doses, such as penicillin G. Hypokalemia may resolve when the nafcillin dose is reduced [42].

False-positive tests

Nafcillin in the urine can cause a false-positive urine reaction for protein when the sulfasalicylic test is used, but not with the dipstick test. Unrecognized, this may lead to unnecessary cessation of the drug and even renal biopsy [43]. Penicillin G and oxacillin can also cause false-positive urine protein determinations, but to a lesser degree.

Hematologic side-effects

Neutropenia with concomitant fever occurred in one patient receiving a daily dose of 12 g i.v. nafcillin. This complication resolved when the drug was stopped [44]. In another patient, i.v. nafcillin therapy (12 g daily) was associated with the development of agranulocytosis, which only improved after the drug was discontinued [45]. Four of 29 patients with serious staphylococcal infections treated with nafcillin had fever rash and neutropenia [46]. Neutropenia appears to be a common complication of prolonged outpatient intravenous therapy [37]. Two patients treated with high daily doses of nafcillin i.v. (12–14 g) developed abnormal bleeding times and one had a bleeding episode. This was due to platelet dysfunction, similar to that described with penicillin G [47].

Skin and tissue necrosis

This can occur after accidental subcutaneous extravasation of i.v. nafcillin, and may necessitate multiple tissue debridements and skin grafting. In animals, tissue necrosis occurs after subcutaneous inoculation of nafcillin, but not with oxacillin, methicillin, and cephalothin [48]. In humans, nafcillin-induced tissue injury can be prevented by prompt administration of hyaluronidase into the site of extravasation [49].


Hepatotoxicity has been described with all the antistaphylococcal penicillins. Rates of toxicity, at least in the setting of outpatient intravenous therapy, are significantly lower for nafcillin than oxacillin [37].



Protein binding 89.9 ±1.5%
Metabolism <30% hepatic
Half-life 33 to 61 minutes
Cmax (mg/ml)  
tmax (hrs)  
Distribution volume Vd  
Excretion bile, kidney


Nafcillin is comparatively poorly and inconsistently absorbed from the gastrointestinal tract compared with the isoxazolyl penicillins [50]. Doses of 500 mg and 1 g orally yield peak concentrations of 3.2 ± 1.9 mg/ml and 7.7 ± 2.7 mg/ml, respectively; thus, serum levels following oral nafcillin are low and irregular. Administration with food halves absorption [50-52]. Therefore, oral administration of nafcillin is not recommended. The elimination half-life of nafcillin in normal adults ranges from 0.7 to 1.4 hours [33, 53-54]; in children, it is 0.76 ± 0.03 hours and is little influenced by age [55]. Nafcillin has a high degree of protein binding to serum albumin, depending on the type of assay, binding ranges from 79% to 90% with an average of around 88% [56].


Following i.v. infusion of a 0.5 g dose of nafcillin over 15 minutes to adults, the serum level is 11 mg/ml at the end of the infusion and 0.5 mg/ml at 6 hours [57]. After an i.m. injection of 1 g nafcillin, a peak serum level of about 8 mg/ml is reached 1 hour later; it falls to about 0.5 mg/ml at 6 hours [52]. Concomitant oral administration of probenecid increases and prolongs nafcillin levels, similar to other penicillins [58]. Probenecid reduces urinary recovery by 50%, decreases both renal and nonrenal clearance, and doubles the AUC [59].

In children with active infection administered 37.5 mg/kg of nafcillin 6-hourly, infused over 15 minutes, concentrations at 30 minutes (near peak) were around 50 mg/ml [55], whereas in children having cerebrospinal fluid (CSF) shunt replacement, peaks after 50 mg/kg were 22–107 mg/ml. The kinetics of nafcillin in children are summarized in Table 1.

Table 1. Nafcillin kinetics in children.

Subjects (n) Dose (mg/kg) Cmax (mg/l) t1/2 (h) Clearance Vd (l/kg)
Children with general infections (24) [55] 37.5 48.1 ± 3.5 0.76 ± 0.03 595 ± 5 (ml/min/1.73m2) 0.89 ± 0.08
Children having CSF shunt replacement (10) [60] 50 22-107 0.5 ± 0.1 0.90 ± 0.55 (l/kg/h) 0.70 ± 0.52
Premature neonates <21days old (10) [60] 33-50 - 3.4 ± 0.9 1.07 ± 0.19 (ml/min/kg) 0.33 ± 0.08
Premature neonates >21days old (10) [61] 33.3 - 1.8 ± 0.6 1.98 ± 0.68 (ml/min/kg) 0.30 ± 0.03

Tissue penetration of nafcillin is probably similar to the isoxazolyl penicillins. It penetrates into the CSF of rabbits with experimental staphylococcal meningitis to about the same extent as oxacillin, producing CSF concentrations which are 1.4–2% of simultaneous serum levels [62]. Higher nafcillin CSF concentrations have been detected in patients with and without meningitis. An adult patient with staphylococcal meningitis was treated with a nafcillin dose of 200 mg/kg/day; a high CSF concentration of 9.5 mg/ml was reached 45 minutes after a 3 g i.v. dose, administered over 5 minutes [63]. Penetration of i.v. administered nafcillin into the ventricular fluid of hydrocephalic children has been studied; in seven with bacterial ventriculitis, concentrations of nafcillin in ventricular fluid were 0.8–20.4% of the peak serum level, whereas in seven others without bacterial ventriculitis, these levels were <0.02–4% of peak serum concentrations [64]. After a dose of 50 mg/kg of nafcillin, CSF concentrations ranged from 0.02 to 0.30 (mean 0.16 ± 0.11) mg/l.


About 30% of an i.m. administered dose of nafcillin can be recovered from the urine where concentrations reach as high as 1000 mg/ml. A considerably smaller amount of active nafcillin (about 19% of the administered dose) is recovered from the urine after i.m. administration if it is given with probenecid [58-59]. A small amount of active drug, probably only about 8% of an i.m. dose, is eliminated via the bile [65]. The remainder of administered nafcillin appears to be inactivated in the liver [65].


There is evidence that it induces cytochrome P-450 enzymes [66].

The other aspect of this medication is that this medication contains lots of salts as media. So it could cause some edema or fluid accumulation. It would be prudent to avoid this medication if there were a concern for a congestive heart failure or kidney disease.

Mechanism of Action

Penicillinase-resistant penicillins exert a bactericidal action against penicillin-susceptible microorganisms during the state of active multiplication. All penicillins inhibit the biosynthesis of the bacterial cell wall. It acts like other penicillins in the penicillin-binding proteins, principally PBPs 1a, 1b, and 2.

Antibacterial activity

The in vitro susceptibility of key pathogens to nafcillin are summarized in Tables 2 and 3.

Table 2. In vitro activity of nafcillin.

Species Nr. strains tested MIC50 (mg/ml) MIC90 (mg/ml) Range (mg/ml) Emerging
Staphylococcus aureus, methicillin susceptible 20 0.5 0.5 0.25–1.0  
  29 0.25 0.5 0.25–1.0  
  25 0.5 0.5 0.25–2  
  114 0.5 0.5 0.25–1  
Staphylococcus aureus, methicillin resistant 16 64 256 8–>256  
  24 64 >64 32–>64  
  29 >16 >16 16–>16  
Staphylococcus aureus, penicillin susceptible 40 0.25 0.5 0.25–0.5  
Coagulase-negative Staphylococcus spp., methicillin susceptible 29 0.25 4 0.016–8  
Coagulase-negative Staphylococcus spp., methicillin resistant 23 32  >64 1–>6  
Staphylococcus epidermidis 100 0.5 16 <0.125–>16 Yes
  3 0.16  0.16–0.312 Yes
Staphylococcus saprophyticus 49  1 0.25–2 Yes
Staphylococcus haemolyticus 75 >16 >16  <0.125–>16 Yes
Staphylococcus hominis 36   <0.125 1 <0.125–>16 Yes
Streptococcus pyogenes 9 0.004–0.016  
  0.08 <0.08–0.312  
Streptococcus agalactiae 10 0.25  0.25 0.25  
Streptococcus pneumoniae 10 0.125  8 0.06–16 Yes
        0.03–0.06  Yes
Viridans group Streptoccoccus spp. 10  4   64 0.06–64 Yes
Rhodococcus spp. 14 >256  >256 8–>256  
Leuconostoc spp. 12 8 16 0.5–32  
Pediococcus spp. 17 32 32 16–128  
Corynebacterium spp. 13 64 >256 1–>256  
Lactobacillus spp. 11 4 16 4–16  
Enterococcus faecalis 15 8 8 8  
Bacillus anthracis 13 0.5  0.5 0.5  
Neisseria gonorrhoeae 25 0.5–16  
Neisseria meningitidis 2  –  0.5  
Moraxella catarrhalis 0.06–0.5  
Haemophilus influenzae 12 4–32  

Table 3. Minimum inhibitory concentration (MIC) distributions for nafcillin among key species.

Species MIC (mg/ml)
0.125 0.25 0.5 1 2 4 8
Clostridium difficile   1       10 4
Staphylococcus aureus   2 15 18      
Staphylococcus aureus (penicillin-susceptible) 1 21 18        
Staphylococcus aureus (methicillin-susceptible) 3 41 68 3      
Staphylococcus epidermidis   23 81 34 24 5  

Nafcillin has a very similar antibacterial spectrum to the isoxazolyl penicillins (Isoxazolyl Penicillins: Oxacillin, Cloxacillin, Dicloxacillin and Flucloxacillin). It is about as active as oxacillin against both penicillin G-susceptible and penicillin G-resistant Staphylococcus aureus strains [51]. Stability of nafcillin in the presence of staphylococcal b-lactamase (penicillinase) is similar to that of methicillin and greater than that of the isoxazolyl penicillins. Nafcillin shows superior activity to glycopeptides in an animal model of subcutaneous abscesses induced by methicillin-susceptible S. aureus [67]. Methicillin-resistant S. aureus strains are resistant to all penicillinase-resistant penicillins, including nafcillin [68-69]. Both penicillin G-susceptible and b-lactamase-producing strains of coagulase-negative staphylococci are nafcillin susceptible. In many settings, over 50% of coagulase-negative staphylococci are methicillin-resistant, and these are resistant to nafcillin [70]. Penicillin tolerant S. aureus and coagulase-negative staphylococci are usually also tolerant to nafcillin.

As with isoxazolyl penicillins, this may vary in vivo in different parts of the body. Thus, in the presence of polyvinylchloride catheters, the minimum bactericidal concentrations (MBCs) of nafcillin for coagulase-negative staphylococci are considerably higher than in the absence of such catheters [71]. Nafcillin and gentamicin (and other aminoglycosides) are synergistic in vitro against most S. aureus strains [72-73].
Nafcillin has greater activity than methicillin and the isoxazolyl penicillins against pneumococci and b-hemolytic streptococci. Enterococcus
and almost all Gram-negative bacteria are intrinsically resistant. A nafcillin/ampicillin combination is synergistic in vitro against ampicillin-resistant Haemophilus influenzae strains; these strains are inhibited when both drugs are used in a concentration of 0.78 mg/ml. The combination is effective for the treatment of experimental H. influenzae sepsis in animals, and it was used to treat successfully a child with osteomyelitis due to an ampicillin-resistant H. influenzae strain [74-75]. Minimum inhibitory concentrations (MICs) of nafcillin against some selected bacteria are shown in Tables 2 and 3.

Other pharmacological effects

 Nafcillin is a semisynthetic antibiotic substance derived from 6-amino-penicillanic acid. The drugs in this class are highly resistant to inactivation by staphylococcal penicillinase and are active against penicillinase-producing and non penicillinase-producing strains of Staphylococcus aureus. The penicillinase- resistant penicillins are active in vitro against a variety of other bacteria.

Like other penicillins, the antistaphylococcal penicillins show only slight concentration-dependent killing, with maximum effects reached at concentrations 3- to 4-fold higher than the MIC [76]. The in vitro postantibiotic effect of antistaphylococcal penicillins against S. aureus is moderate at most, of the order of 1.5-2 hours depending on concentration and time of exposure [77]. In vivo, the postantibiotic effect is somewhat longer, for example 3 hours for nafcillin against S. aureus  [77].

Medicinal Chemistry

CAS number: 147-52-4  EINECS: 205-690-9

Molecular Formula:  C21H22N2O5S

Average mass: 436.457

Monoisotopic mass: 436.106887157

Systematic name: (2S,5R,6R)-6-(2-ethoxynaphthalene-1-amido)-3,3-dimethyl-7-oxo-4-thia-1-azabicyclo[3.2.0]heptane-2-carboxylic acid

SMILES: [H][C@]12SC(C)(C)[C@@H](N1C(=O)[C@H]2NC(=O)C1=C(OCC)C=CC2=CC=CC=C12)C(O)=O

Std. InChI: 1S/C21H22N2O5S/c1-4-28-13-10-9-11-7-5-6-8-12(11)14(13)17(24)22-15-18(25)23-16(20(26)27)21(2,3)29-19(15)23/h5-10,15-16,19H,4H2,1-3H3,(H,22,24)(H,26,27)/t15-,16+,19-/m1/s1

CD/LogP: 3.52±0.24 # of Rule of 5 Violations: 0
ACD/LogD (pH 5.5): 0.47 ACD/LogD (pH 7.4): -0.21
ACD/BCF (pH 5.5): 1.00 ACD/BCF (pH 7.4): 1.00
ACD/KOC (pH 5.5): 1.75 ACD/KOC (pH 7.4): 1.00
#H bond acceptors: 7 #H bond donors: 2
#Freely Rotating Bonds: 5 Polar Surface Area: 121.24 Å2
Index of Refraction: 1.686 Molar Refractivity: 110.3±0.4 cm3
Molar Volume: 289.9±5.0 cm3 Polarizability: 43.7±0.5 10-24cm3
Surface Tension: 70.0±5.0 dyne/cm Density: 1.4±0.1 g/cm3
Flash Point: 385.7±32.9 °C Enthalpy of Vaporization: 109.6±3.0 kJ/mol
Boiling Point: 714.1±60.0 °C at 760 mmHg Vapour Pressure: 0.0±2.4 mmHg at 25°C

Major Impurities:


Melting point:

Optical rotation:

Solubility: soluble in water

logP: 3.3




1. Palmer D.L., Pett S.B., Akl B.F. "Bacterial wound colonization after broad-spectrum versus narrow-spectrum antibiotics". Ann. Thorac. Surg. 59 (3): 626–31, (1995).

2. Tan AK, Fink AL (January 1992). "Identification of the site of covalent attachment of nafcillin, a reversible suicide inhibitor of beta-lactamase". Biochem. J. 281 (1): 191–6, (1992).

3. Bonow R.O., Carabello B.A., Kanu C., et al. "ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): developed in collaboration with the Society of Cardiovascular Anesthesiologists: endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons". Circulation 114 (5): e84–231, (2006).

4. Eickhoff T.C., Kislak J.W., Finland M. "Clinical evaluation of nafcillin in patients with severe staphylococcal disease". N. Engl. J. Med. 272: 699, (1965).

5. Goldenberg D.L., Cohen A.S. "Acute infectious arthritis. A review of patients with nongonococcal joint infections (with emphasis on therapy and prognosis)". Am. J. Med. 60: 369, (1976).

6. Parker R.H., Fossieck Jr B.E. "Intravenous followed by oral antimicrobial therapy for staphylococcal endocarditis". Ann. Intern. Med. 93: 832, (1980).

7. Carney D.N., Fossieck Jr B.E., Parker R.H., Minna J.D. "Bacteremia due to Staphylococcus aureus in patients with cancer: report on 45 cases in adults and review of the literature". Rev. Infect. Dis. 4:1, (1982).

8. Watanakunakorn C. "Bacteremic Staphylococcus aureus pneumonia". Scand. J. Infect. Dis. 19: 623, (1987).

9. Kim J.H., van der Horst C., Mulrow C.D., Corey G.R. "Staphylococcus aureus meningitis: review of 28 cases". Rev. Infect. Dis. 11: 698, (1989).

10. Daly J.S., Worthington M.G., Andrews R.J. et al. "Randomized, double-blind trial of cefonicid and nafcillin in the treatment of skin and skin structure infections". Antimicrob. Agents Chemother. 34: 654, (1990).

11. Walling D.M., Kaelin Jr W.G. "Pyomyositis in patients with diabetes mellitus". Rev. Infect. Dis. 13: 797, (1991).

12. Givner L.B., Kaplan S.L. "Meningitis due to Staphylococcus aureus in children". Clin. Infect. Dis. 16: 766, (1993).

13. Masur H., Murray H.W., Roberts R.B. "Nafcillin therapy for Staphylococcus aureus endocarditis". Antimicrob. Agents Chemother. 14: 457, (1978).

14. Sande M.A., Scheld W.M. "Combination antibiotic therapy of bacterial endocarditis". Ann. Intern. Med. 92: 390, (1980).

15. Fantin B., Carbon C. "In vivo antibiotic synergism: contribution of animal models". Antimicrob. Agents Chemother. 36: 907, (1992).

16. Korzeniowski O., Sande M.A. "The National Collaborative Endocarditis Study Group. Combination antimicrobial therapy for Staphylococcus aureus endocarditis in patients addicted to parenteral drugs and in nonaddicts". Ann. Intern. Med. 97: 496, (1982).

17. Kaplan S.L., Mason Jr E.O., Feigin R.D. "Clindamycin versus nafcillin or methicillin in the treatment of Staphylococcus aureus osteomyelitis in children". South Med. J. 75: 138, (1982).

18. Gentry L.O., Rodriguez G.G. "Oral ciprofloxacin compared to parenteral antibiotics in the treatment of osteomyelitis". Antimicrob. Agents Chemother. 34: 40, (1990).

19. Norden C.W., Bryant R., Plamer D. et al. "Chronic osteomyelitis caused by Staphylococcus aureus: controlled clinical trial of nafcillin therapy and naficillin-rifampin therapy". South Med. J. 79: 947, (1986).

20. Ruiz D.E., Warner J.F. "Nafcillin treatment of Staphylococcus aureus meningitis". Antimicrob. Agents Chemother. 9: 554, (1976).

21. Fossieck Jr B.E., Kane J.G., Diaz C.R., Parker R.H. "Nafcillin entry into human cerebrospinal fluid". Antimicrob. Agents Chemother. 11: 965, (1977).

22. Kane J.G., Parker R.H., Jordan G.W., Hoeprich P.D. "Nafcillin concentration in cerebrospinal fluid during treatment of staphylococcal infections". Ann. Intern. Med. 87: 309, (1977).

23. Quintiliani R., Cooper B.W. "Current concepts in the treatment of staphylococcal meningitis". J. Antimicrob. Chemother. 21 (Suppl. C): 107, (1988).

24. Gordon J.J., Harter D.H., Phair J.P. "Meningitis due to Staphylococcus aureus. Am. J. Med. 78: 965, (1985).

25. Sande M.A., Scheld W.M. "Combination antibiotic therapy of bacterial endocarditis". Ann. Intern. Med. 92: 390, (1980).

26. Karchmer A.W., Archer G.L., Dismukes W.E. "Staphylococcus epidermidis causing prosthetic valve endocarditis: microbiologic and clinical observations as guides to therapy". Ann. Intern. Med. 98: 447, (1983).

27. Caputo G.M., Archer G.L., Calderwood S.B. et al. "Native valve endocarditis due to coagulase-negative staphylococci. Clinical and microbiological features". Am. J. Med. 83: 619, (1987).

28. Archer G.L., Armstrong B.C. "Alteration of staphylococcal flora in cardiac surgery patients receiving antibiotic prophylaxis". J. Infect. Dis. 147: 642, (1983).

29. Griego R.D., Zitelli J.A. "Intra-incisional prophylactic antibiotics for dermatological surgery". Arch. Dermatol. 134: 688, (1998).

30. Piraino B., Bailie G.R., Bernadini J. et al. "Peritoneal dialysis-related infections recommendations: 2005 update". Periton. Dial. Int. 25: 107, (2005).

31. Sewell D.L., Golper T.A. "Stability of antimicrobial agents in peritoneal dialysate". Antimicrob. Agents Chemother. 21: 528, (1982).

32. Banner Jr W., Gooch W.M., Burckart G., Korones S.B. "Pharmacokinetics of nafcillin in infants with low birth weights". Antimicrob. Agents Chemother. 17: 691, (1980).

33. Kind A.C., Tupasi T.E., Standiford H.C., Kirby W.M.M. "Mechanisms responsible for plasma levels of nafcillin lower than those of oxacillin". Arch. Intern. Med. 125: 685, (1970).

34. Diaz C.R., Kane J.G., Parker R.H., Pelsor F.R. "Pharmacokinetics of nafcillin in patients with renal failure". Antimicrob. Agents Chemother. 12: 98, (1977).

35. Marshall 2nd J.P., Salt W.B., Elam R.O. et al. "Disposition of nafcillin in patients with cirrhosis and extrahepatic biliary obstruction". Gastroenterology 73: 1388, (1977).

36. Kancir L.M., Tuazon C.U., Cardella T.A., Sheagren J.N. "Adverse reactions to methicillin and nafcillin during treatment of serious Staphylococcus aureus infections". Arch. Intern. Med. 138: 909, (1978).

37. Maraqa N.F., Gomez M.M., Rathmore M.H., Alvarez A.M. "Higher occurrence of hepatotoxicity and rash in patients treated with oxacillin, compared to those treated with nafcillin and other commonly used antimicrobials". Clin. Infect. Dis. 34: 50, (2002).

38. Dahlgren A.F. "Adverse drug reactions in home care patients receiving nafcillin or oxacillin". Am. J. Health Syst. Pharm. 54: 1176, (1997).

39. Wynn M., Dalovisio J.R., Tice A.D., Jian X. "Evaluation of the efficacy and safety of outpatient parenteral antimicrobial therapy for infections with methicillin-sensitive Staphylococcus aureus". South Med. J. 98: 590, (2005).

40. Parry M.F., Ball W.D., Conte Jr J.E., Cohen S.N. "Nafcillin nephritis". JAMA 225: 178, (1973).

41. Mohr J.A., Clark R.M., Waack T.C., Whang R. "Naficillin-associated hypokalemia". JAMA 242: 544, (1979).

42. Andreoli S.P., Kleiman M.B., Glick M.R., Bergstein J.M. "Nafcillin, pseudoproteinuria and hypokalemic alkalosis". J. Pediatr. 97: 841, (1980).

43. Line D.E., Adler S., Fraley D.S., Burns F.J. "Massive pseudoproteinuria caused by nafcillin". JAMA 235: 1259, (1976).

44. Sandberg M., Tuazon C.U., Sheagren J.M. "Neutropenia probably resulting from nafcillin". JAMA 232: 1152, (1975).

45. Markowitz S.M., Rothkopf M., Holden F.D. et al. "Nafcillin-induced agranulocytosis". JAMA 232: 1150, (1975).

46. Kancir L.M., Tuazon C.U., Cardella T.A., Sheagren J.N. "Adverse reactions to methicillin and nafcillin during treatment of serious Staphylococcus aureus infections". Arch. Intern. Med. 138: 909, (1978).

47. Alexander D.P., Russo M.E., Fohrman D.E., Rothstein G. "Nafcillin induced platelet dysfunction and bleeding". Antimicrob. Agents Chemother. 23: 59, (1983).

48. Tilden S.J., Craft J.C., Cano R., Daum R.S."Cutaneous necrosis associated with intravenous nafcillin therapy". Am. J. Dis. Child. 134: 1046, (1980).

49. Zenk K.E., Dungy C.I., Greene G.R. "Nafcillin extravasation injury". Am. J. Dis. Child. 135: 1113, (1981).

50. Watanakunakorn C. "Absorption of orally administered nafcillin in normal healthy volunteers". Antimicrob. Agents Chemother. 11: 1007, (1977).

51. Klein J.O., Finland M., Wilcox C. "Nafcillin. Antibacterial action in vitro and absorption and excretion in normal young men". Am. J. Med. Sci. 246: 10, (1963).

52. Whitehouse A.C., Morgan J.G., Schumacher J., Hamburger M. "Blood levels and anti-staphylococcal titers produced in human subjects by a penicillinase resistant penicillin, nafcillin, compared with similar penicillins". Antimicrob. Agents Chemother. 1962: 384, (1963).

53. Rudnick M., Morrison G., Walker B., Singer I. "Renal failure, hemodialysis, and nafcillin kinetics". Clin. Pharmacol. Ther. 20: 413, (1976).

54. Waller E.S., Sharanevych M.A., Yakatan G.J. "The effect of probenecid on nafcillin disposition". J. Clin. Pharmacol. 22: 482, (1982).

55. Feldman W.E., Nelson J.D., Stanberry L.R. "Clinical and pharmacokinetic evaluation of nafcillin in infants and children". J. Pediatr. 93: 1029, (1978).

56. Craig W.A., Suh B. "Protein binding and the antimicrobial effects: methods for determination of protein binding". In Antibiotics in Laboratory Medicine (Lorian V, ed.), 3rd edn, p. 367. Baltimore MD: Williams & Wilkins, (1991).

57. Neu H.C. "Antistaphylococcal penicillins". Med. Clin. N. Am. 66: 51, (1982).

58. Klein J.O., Finland M., Wilcox C. "Nafcillin. Antibacterial action in vitro and absorption and excretion in normal young men". Am. J. Med. Sci. 246: 10, (1963).

59. Waller E.S., Sharanevych M.A., Yakatan G.J. "The effect of probenecid on nafcillin disposition". J. Clin. Pharmacol. 22: 482, (1982).

60. Nahata M.C., Fan-Havard P., Kosnik E.J. et al. "Pharmacokinetics and cerebrospinal fluid concentration of nafcillin in pediatric patients undergoing cerebrospinal fluid shunt replacement". Chemotherapy 36: 98, (1990).

61. Banner Jr W., Gooch W.M., Burckart G., Korones S.B. "Pharmacokinetics of nafcillin in infants with low birth weights". Antimicrob. Agents Chemother. 17: 691, (1980).

62. Strausbaugh L.J., Murray T.W., Sande M.A. "Comparative penetration of six antibiotics into the cerebrospinal fluid of rabbits with experimental staphylococcal meningitis". J. Antimicrob. Chemother. 6: 363, (1980).

63. Ruiz D.E., Warner J.F. "Nafcillin treatment of Staphylococcus aureus meningitis". Antimicrob. Agents Chemother. 9: 554, (1976).

64. Yogev R., Schultz W.E., Rosenman S.B. "Penetrance of nafcillin into human ventricular fluid: correlation with ventricular pleocytosis and glucose levels". Antimicrob. Agents Chemother. 19: 545, (1981).

65. Kind A.C., Tupasi T.E., Standiford H.C., Kirby W.M.M. "Mechanisms responsible for plasma levels of nafcillin lower than those of oxacillin". Arch. Intern Med. 125: 685, (1970).

66. Lang C.C., Jamal S.K., Mohamed Z., Mustafa M.R., Mustafa A.M., Lee T.C. "Evidence of an interaction between nifedipine and nafcillin in humans". Br. J. Clin. Pharmacol. 55 (6): 588–90, (2003).

67. Wood C.A., Wisniewski R.M. "Beta-lactams versus glycopeptides in treatment of subcutaneous abscesses infected with Staphylococcus aureus". Antimicrob. Agents Chemother. 38: 1023, (1994).

68. Barber M., Waterworth P.M. "Penicillinase-resistant penicillins and cephalosporins". Br. Med. J. 2: 344, (1964).

69. Richmond A.S., Simberkoff M.S., Schaefler S., Rahal Jr J.J. "Resistance of Staphylococcus aureus to semisynthetic penicillin and cephalothin". J. Infect. Dis. 135: 108, (1977).

70. Karchmer A.W., Archer G.L., Dismukes W.E. "Staphylococcus epidermidis causing prosthetic valve endocarditis: microbiologic and clinical observations as guides to therapy". Ann. Intern. Med. 98: 447, (1983).

71. Sheth N.K., Franson T.R., Sohnle P.G. "Influence of bacterial adherence to intravascular catheters on in-vitro antibiotic susceptibility". Lancet 2: 1266, (1985).

72. Watanakunakorn C., Glotzbecker C. "Enhancement of antistaphylococcal activity of nafcillin and oxacillin by sisomicin and netilmicin". Antimicrob. Agents Chemother. 12: 346, (1977).

73. Eliopoulos G.M., Moellering Jr R.C. "Antibiotic synergism and antimicrobial combinations in clinical infections". Rev. Infect. Dis. 4: 282, (1982).

74. Yogev R., Kabat W.J. "Synergistic action of nafcillin and ampicillin against ampicillin-resistant Haemophilus influenzae. Type B bacteremia and meningitis in infant rats". Antimicrob. Agents Chemother. 18: 122, (1980).

75. Yogev R., Burkholder E., Davis A.T. "Synergistic action of ampicillin and nafcillin against ampicillin-resistant Haemophilus influenzae". Antimicrob. Agents Chemother. 17: 461, (1980).

76. Craig W.A., Ebert S.C. "Killing and regrowth of bacteria in vivo: a review". Scand. J. Infect. Dis. 64: 63, (1991).

77. Craig W.A., Gudmundsson S. "Postantibiotic effect". In Antibiotics in Laboratory Medicine (Lorian V, ed.), 4th edn, p. 296. Baltimore MD:Williams & Wilkins, (1996).



     Hit Counter


Send mail to stefano.biondi@innovativesolution.it with questions or comments about this web site.
Copyright © 2010 Innovative Solution di Biondi Stefano