Ticarcillin, which has the chemical formula alpha-carboxyl 3-thienyl methyl penicillin, is very similar to carbenicillin but is more active against Pseudomonas aeruginosa [1]. It is unstable in acidic environment, therefore the drug is administered parenterally.Nowadays, it is now exclusively used as a fixed combination with clavulanic acid.

Therapeutic use

Ticarcillin is normally used as a fixed combination with clavulanic acid. Alone it was a useful and preferable alternative to carbenicillin for the treatment of pseudomonas infections. It has been used with success in P. aeruginosa septicemia [2], including in patients with neutropenia and underlying neoplastic disease 3-4], in P. aeruginosa pneumonia [5], and in pulmonary infections in patients with cystic
fibrosis [6]. P. aeruginosa urinary tract infections may also respond to ticarcillin therapy [2]. Results with ticarcillin have been similar to those previously achieved with larger doses of carbenicillin. As ticarcillin is administered in a lower dosage, it probably causes less bleeding, sodium overload, and hypokalemia than carbenicillin. For these reasons, ticarcillin largely replaced carbenicillin [7], and now piperacillin has largely replaced ticarcillin.

There may be in vitro synergism between ticarcillin and aminoglycosides, such as gentamicin, tobramycin, and amikacin [4]. Such synergistic combinations have been extensively used, but the results have been usually about the same as those obtained by ticarcillin alone [2,6]. Some authors consider that when serious Pseudomonas infections are treated, ticarcillin should always be combined with a second drug, such as gentamicin, to prevent emergence of ticarcillin-resistant P. aeruginosa strains during treatment [8]. This is controversial, except for Pseudomonas meningitis [9] and Pseudomonas endocarditis, in which case it is generally agreed that treatment should be by a combination of ticarcillin with an aminoglycoside, such as gentamicin, tobramycin, or amikacin. For P. aeruginosa endocarditis, a regimen of ticarcillin 18 g/day combined with tobramycin 8 mg/kg body weight per day has been recommended [10]. Right-sided Pseudomonas endocarditis in i.v. drug users may often be cured by such chemotherapy alone, but leftsided endocarditis usually needs 6 weeks’ chemotherapy and an early valve replacement [11]. In one retrospective analysis of 410 episodes of Pseudomonas bacteremia, cure rates of patients who received an anti-pseudomonal b-lactam antibiotic, such as carbenicillin or ticarcillin, with (72%) or without an aminoglycoside (71%), were higher than in patients who received an aminoglycoside alone (29%) [12]. 

Ticarcillin–gentamicin or ticarcillin–tobramycin combinations have been used with success as initial empiric chemotherapy for patients with granulocytopenia and neoplastic disease with a suspected severe infection [13-16]. In one trial ticarcillin plus either gentamicin, amikacin or netilmicin were all equally effective for this purpose [17]. Ticarcillin plus an aminoglycoside such as gentamicin, tobramycin, or amikacin is suitable for initial therapy of patients with febrile neutropenia, although now there are many other preferred empiric regimens including piperacillin, imipenem, meropenem, or ceftazidime which may be substituted for ticarcillin [18-26].

Ticarcillin usually inactivates gentamicin and tobramycin at a slower rate in vivo than carbenicillin [27-28]. Nevertheless, inactivation of gentamicin and tobramycin by ticarcillin may be significant in all patients, and especially in those with renal failure [29-30]. Serum level monitoring and dosage adjustment of the aminoglycoside are necessary in both patients with normal and impaired renal function when gentamicin or tobramycin is used with ticarcillin.

Ticarcillin alone has been used for Proteus infections [3] and occasionally for the treatment of E. coli, Enterobacter spp., and S. marcescens infections [2,14]. Bacteremia due to Achromobacter xylosoxidans rarely occurs in cancer patients. Ticarcillin may be suitable therapy, either alone or in combination with other drugs [31-32]. Ticarcillin has also been used for treatment of Gram-negative anaerobic infections [33]. Ticarcillin, chloramphenicol, and clindamycin, each in combination with gentamicin, were equally effective in therapy for intra-abdominal or female genital tract sepsis in one study [34].

Dosage and Administration

 Both carbenicillin and ticarcillin are best given in six to eight divided doses. For instance, if a total daily dose of 30 g carbenicillin or 18 g of ticarcillin is to be administered, doses of 5 or 3 g, respectively, can be given every 4 hours; each dose can be dissolved in 50–100 ml of i.v. fluid in a pediatric buretrol for infusion over 30–60 minutes [35]. Alternatively, the drugs may be already dispensed in a secondary i.v. bottle. These doses can be infused at a faster rate but, similar to penicillin G, the infusion rate does not appear to influence their clinical efficiency. Probenecid in doses of 1–2 g orally per day may be administered to delay the excretion of either carbenicillin or ticarcillin.

The adult dose of ticarcillin for severe infections due to P. aeruginosa is 18–24 g/day.


The dose of ticarcillin for severe infections due to P. aeruginosa in children is 300–400 mg/kg/day. In the first week of life, a ticarcillin dose of 75 mg/kg should be given every 12 hours to infants weighing less than 2000 g (total daily dose 150 mg/kg) and 75 mg/kg is administered every 8 hours to those weighing more than 2000 g (total daily dose 225 mg/kg). For babies who still weigh less than 2000 g after 1 week of age, the dosage should be increased to 75 mg/kg 8-hourly (total daily dose 225 mg/kg), and for those who weigh more than 2000 g after 1 week of age, the dosage should be increased to 100 mg/kg 8-hourly (total daily dose 300 mg/kg). The drug can be administered either i.m. or i.v., usually by intermittent 30-minute infusions. With these dosage schedules, serum levels 30 minutes after the completion of the infusion are approximately 150 mg/ml, and trough levels just before the next dose are 25–50 mg/ml [36-37].

Impaired renal function

The half-lives of both carbenicillin and ticarcillin, normally about 1 hour, are prolonged to 13–14 hours in patients with severe renal failure, so that dosage reduction is necessary. All patients with any degree of renal failure should be given an initial loading dose of 5 g carbenicillin or 3 g ticarcillin i.v. Thereafter, patients with a creatinine clearance >60 ml/min may be treated with usual doses of both drugs. If the creatinine clearance is 30–60 ml/min, 3 g carbenicillin or 2 g ticarcillin should be given 4-hourly, and if it is 10–30 ml/min, the dose is 3 g carbenicillin or 2 g ticarcillin every 8 hours. Dosages for patients with severe renal failure (creatinine clearance o10 ml/min), are carbenicillin 2 g every 8–12 hours and ticarcillin 2 g every 12 hours [2,38].


As with other penicillins, neurotoxic reactions may arise when very high doses of ticarcillin are administered, especially in patients with impaired renal function.

Hypersensitivity reactions

Carbenicillin and ticarcillin may provoke any of the reactions which occur with penicillin G in penicillin-sensitive subjects. Anaphylaxis due to carbenicillin has been reported [39]. These drugs are contraindicated in patients with a history of penicillin hypersensitivity. Eosinophilia has been fairly frequently noted during ticarcillin therapy [2,40], and occasionally this has been associated with a urticarial rash [23]. Carbenicillin can also cause drug fever [40].


High doses of i.v. carbenicillin and ticarcillin, similar to ‘‘massive’’ doses of penicillin G, may cause neurotoxicity. This is more likely to occur in patients with renal failure. In one case report two patients with severe renal failure developed convulsions whilst receiving a daily i.v. carbenicillin dose of only 4 g [41]. One patient with end-stage renal failure receiving maintenance hemodialysis who was treated with ticarcillin 8 g i.v. daily developed severe neurotoxicity after 23 days of therapy. However, 12 hours after discontinuation of ticarcillin, the serum level was 850 mg/ml and the CSF level was 120 mg/ml [42]. It is possible that relatively low serum and CSF carbenicillin or ticarcillin levels may provoke convulsions in some uremic patients. Patients with underlying central nervous system disease may also be more prone to convulsions with high serum levels of any of the penicillins.

Bleeding disorders

These have been noted in association with carbenicillin and ticarcillin given i.v. Because of carbenicillin effect on platelet function, a study on 17 volunteers who received i.v. ticarcillin for periods of 3–10 days, in doses of 100, 200, or 300 mg/kg/day (7–21 g/day) was performed [43]. Blood coagulation was unaffected, but platelet function was impaired in all subjects. Lower doses produced only mild defects in platelet function, but with a dose of 300 mg/kg/day hemostasis was more seriously impaired and the defects were similar in degree to those produced by the same dose of carbenicillin. It is possible that bleeding disorders may be less common with ticarcillin because clinically it is used in lower doses than carbenicillin. Two patients in whom prolongation of the bleeding time appeared to be caused by ticarcillin were reported; one had received a high dose of 400 mg/kg/day but the other only 275 mg/kg/day [44]. Another patient who had renal failure and inadvertently received a full dosage of ticarcillin developed a bleeding disorder characterized by petechiae, ecchymoses and epistaxis; the serum ticarcillin level 9 hours after the last dose was 1050 mg/ml [14]. In another study, 156 adult patients were treated with either ticarcillin, piperacillin, mezlocillin, or cefotaxime. Increases in bleeding times occurred in 73% of patients receiving ticarcillin, 43% of those treated with piperacillin, 25% of patients receiving mezlocillin, and 17% of those receiving cefotaxime. Significant bleeding occurred in 34% of patients treated with ticarcillin, 17% of those receiving piperacillin, 2% with mezlocillin, and 5% with cefotaxime [45]. Platelet dysfunction may be caused by virtually all penicillins, but it is more severe with carbenicillin and ticarcillin. The penicillins disturb platelet membrane function by interfering with adenosine diphosphate (ADP) receptors and leaving them unavailable for agonists to induce aggregation [45-46]. It appears that carbenicillin and ticarcillin usually affect only the platelet component of hemostasis, and other causes for bleeding, although reported (see above), are rare [47].


Severe neutropenia in one adult patient occurred in association with i.v. ticarcillin therapy; it resolved when the drug was stopped and recurred on re-exposure to ticarcillin [48]. Ticarcillin associated neutropenia was also reported in a child with cystic fibrosis [49]. In this case the authors favored an immunologic basis because the time for onset of neutropenia was rapid (4 days) and there were other features suggestive of an allergic reaction such as fever, diarrhea, serum glutamic oxaloacetic transaminase (SGOT) elevation, and eosinophilia.


There has generally been a lower frequency of hepatic injury with ticarcillin compared with carbenicillin [50]. In three patients increases in serum glutamic pyruvic transaminase (SGPT) developed during treatment with carbenicillin; these decreased after carbenicillin was stopped and they rose minimally or not at all during subsequent therapy with ticarcillin [51].

Electrolyte and acid–base disturbances

Electrolyte disturbances similar to those caused by i.v. carbenicillin may occur with ticarcillin therapy. Hypokalemia has been observed in several patients treated by high doses i.v. [6,14].


Protein binding 45%
Half-life 1.1 hrs
Cmax (mg/ml)  
tmax (hrs)  
Distribution volume Vd  


Carbenicillin and ticarcillin are not absorbed from the gastrointestinal tract and must be administered either i.m. or i.v. The dosage used  can be varied widely depending on the nature of the infection and the susceptibility of the pathogen. Carindacillin and carfecillin are well absorbed from the gastrointestinal tract but they are not suitable for the treatment of systemic infections because therapeutic serum levels are not attained. They are useful for oral treatment of certain urinary tract infections because adequate urine concentrations of carbenicillin are achieved.


Serum levels after both i.m. and i.v. administration of ticarcillin are similar to those of carbenicillin, and its serum half-life (70 minutes) is
only slightly longer than that of carbenicillin (60 minutes) [35-52]. After administration of 1 g of ticarcillin i.m. to adults, a mean peak serum level of 35 mg/ml is reached in 1 hour; thereafter, it falls, and at 6 hours it is only about 6 mg/ml [53]. Following a rapid 5-minute i.v. infusion of 3 g ticarcillin, the mean serum level 15 minutes later is 257 mg/ml; this falls to 218 mg/ml at 30 minutes, 119 mg/ml at 1 hour, 70 mg/ml at 2 hours, and after 4 hours it is 30 mg/ml (Figure 1 [35]. If a 3 g i.v. ticarcillin dose is infused slowly over 90–120 min, every 4 hours, the mean peak serum level at the end of the infusion is 239 mg/ml and the mean trough level at the end of the 4-hour interval is 94 mg/ml [2]. When ticarcillin is administered i.v. at either of these rates in a dose of 3 g every 4 hours, serum levels are adequate for the treatment of systemic P. aeruginosa infections [35].

Figure 1. Pharmacokinetic profile of ticarcillin following a 5 minutes i.v. infusion of a 3 grams dose.

As with other penicillins, probenecid increases both serum levels and the half-life of ticarcillin. Carbenicillin and ticarcillin are probably distributed in body fluids and tissues similarly to penicillin G. Both drugs diffuse well into human interstitial fluid [54]. Insignificant amounts of carbenicillin and ticarcillin appear in the cerebrospinal fluid (CSF) of patients with uninflamed meninges, but higher and sometimes therapeutically effective CSF levels against P. aeruginosa occur in patients with meningitis treated by large doses i.v. [2].

These drugs penetrate into bronchial secretions, but concentrations reached are usually lower than those needed for inhibition of P. aeruginosa. In cystic fibrosis patients, sputum levels of ticarcillin ranged from 2.8 to 12 mg/ml when the drug was given i.v. in the usual dosage [2].

Ticarcillin penetrates into peritoneal and pleural fluids, where the average concentrations are, respectively, 34% and 22% of concomitant serum levels [2]. After a single i.v. dose of 5 g of ticarcillin, mean concentrations in serum, muscle, and fat were 185, 18, and 32 mg/ml, respectively, 1.0–1.5 h after the injection [55]. Significant ticarcillin concentrations are not attained in normal bone after usual i.v. doses [56].


Carbenicillin and ticarcillin are excreted in urine by glomerular filtration and tubular secretion. Probenecid reduces their rate of excretion by partially blocking renal tubular secretion. High urinary concentrations of active carbenicillin or ticarcillin are obtained after the administration of the usual i.m. or i.v. doses; urinary levels of 65–2475 mg/ml are reached during the first 3 hours after a single 3-g i.v. dose of ticarcillin [35,57]. When ticarcillin is given in appropriate doses to patients with renal failure, urinary concentrations are high irrespective of the degree of renal impairment. Even in patients with a creatinine clearance of 10 ml/min, urinary ticarcillin concentrations are in the range 250–3900 mg/ml [58].

Approximately 80% of an i.v.-administered dose of ticarcillin can be recovered from the urine as the active drug during the first 6 hours after administration. This is less than the comparable figure for carbenicillin (95%) because more ticarcillin is inactivated before renal
excretion. Approximately 10% of the administered dose of ticarcillin is excreted in the urine as penicilloic acid [35].

Some ticarcillin is metabolized in the liver to produce antibacterially inactive penicilloic acid. In severely uremic or anuric patients the serum half-lives of carbenicillin and ticarcillin are 13–14 hours, compared with about 3 hours for penicillin G and 8 hours for ampicillin.



Mechanism of Action

Ticarcillin's antibiotic properties arise from its ability to prevent cross-linking of peptidoglycan during cell wall synthesis when the bacteria tries to divide, causing death. Their increased activity against organisms such as P. aeruginosa and M. morganii is mainly due to their superior ability to penetrate the outer cell membrane of these Gram-negative bacilli.

Antibacterial activity

The in vitro activity of carbenicillin and ticarcillin in comparison with ampicillin against common pathogens is shown in Table 1. The key clinical target of activity for these drugs is P. aeruginosa, although they have activity against a variety of other Gram-negative and positive pathogens.

Table 1. Comparative in vitro susceptibilities of carbenicillin, ticarcillin, and ampicillin [1,57,59-64].


MIC (mg/ml)

Organism Carbenicillin Ticarcillin Ampicillin
S.aureus (non penicillinase producers) 1.25 1.25 0.06
Steptococcus pyogenes 0.15 0.5 0.008
Streptococcus pneumoniae 0.15 1.25 0.008
Enterococcus faecalis 25.0 125.0 1.0-5.0
Listeria monocytogenes 10.0 0.08–0.32
Clostridium tetani 0.25 0.5
Clostridium perfringens 0.25 0.5
Escherichia coli 12.5 5.0 5.0
Enterobacter spp. 50.0 5.0 100.0
Klebsiella pneumoniae >250.0 500.0 1.56
Serratia marcescens 12.5 12.5 200.0
Proteus mirabilis 3.12 1.25 1.25
Proteus vulgaris 25.0 2.5 100.0
Providencia rettgeri 0.78 2.5 25.0
Morganella morganii 6.25 2.5 200.0
Neisseria gonorrhoeae 0.3 0.02 0.02–0.6
Neisseria meningitidis 0.1 0.25
Haemophilus influenzae 0.5 0.25 0.05
Haemophilus influenzae (ampicillin-resistant) 4.0–32.0 4.0–32.0 3.0–500
Pseudomonas aeruginosa 50.0 25.0 500.0
Prevotella melaninogenica 0.1–4.0 0.1–4.0 0.1–4.0
Bacteroides fragilis 4.0–128.0  4.0–128.0 4.0–256

Gram-negative aerobic bacteria

Pseudomonas aeruginosa
Ticarcillin is consistently at least twice, and sometimes four times, as active as carbenicillin against P. aeruginosa [1,65] (see Table 1). Strains of all bacteria, including P. aeruginosa, which have become resistant to carbenicillin are also ticarcillin resistant [66-67]. In most hospitals the majority of P. aeruginosa strains used to be ticarcillin sensitive [68]. However, resistance is now much more common and In 2007, in a French multicenter study performed in 2004, 62% of 450 P. aeruginosa strains were resistant to ticarcillin and 61% to ticarcillin–
clavulanic acid [69]. Similar to carbenicillin, ticarcillin combined with an aminoglycoside, such as gentamicin, tobramycin, or amikacin, exhibits in vitro synergism against some strains of P. aeruginosa.

Other Gram-negative aerobic bacteria
These exhibit similar susceptibility to carbenicillin and ticarcillin [1]. Compared with ampicillin, carbenicillin and ticarcillin have a relatively high activity against Proteus vulgaris, Providencia rettgeri,and Morganella morganii (see Table 1). Their activity against other Gram-negative bacteria is similar to that of ampicillin; they are effective to a degree against Escherichia coli, P.mirabilis, salmonellae, shigellae, and also Haemophilus influenzae, Neisseria meningitidis, and N. gonorrhoeae. Ampicillin is preferred for treatment of infections due to these bacteria because it is the more active drug. Carbenicillin and ticarcillin have some activity against ampicillin-resistant H. influenzae strains, but this activity is less (MIC 4–32 mg/ml) than their activity against ampicillin-sensitive strains (MIC 0.25–1.0 mg/ml) [63-70]. Klebsiella spp. are almost invariably resistant to carbenicillin and ticarcillin, but some strains of Enterobacter spp. are relatively sensitive [1,71]. Some Serratia marcescens strains are susceptible to these drugs in relatively low concentrations (25 mg/ml); others are either highly resistant (MIC >8000 mg/ml) or moderately resistant (MIC <2000 mg/ml) [1,72]. In a study in French outpatients [73], resistance to ticarcillin in Enterobacteriaceae varied between 100% in strains of Klebsiella spp. and Y. enterocolitica and 22% in Proteus spp.; 42% of 1902 isolates of E. coli were resistant to ticarcillin.

Gram-negative anaerobic bacteria

Most strains of Prevotella (previously Bacteroides) melaninogenica and Fusobacterium spp. are sensitive to carbenicillin and ticarcillin, with MICs in the range of 0.1–8.0 mg/ml. Bacteroides fragilis is more resistant, but 80% of strains can be inhibited by 64 mg/ml and 95% by 128 mg/ml carbenicillin, both of which are clinically attainable concentrations [64,74]. Ticarcillin may be slightly more active than carbenicillin against B. fragilis and other Bacteroides spp. [75-77].

Gram-positive bacteria

Carbenicillin and ticarcillin are active against S. aureus (non penicillinase producers), Streptococcus pyogenes, and S. pneumoniae. Enterococcus faecalis and Listeria monocytogenes are not so sensitive and usually need quite high carbenicillin and ticarcillin concentrations for inhibition (see Table 1) [1,62]. b-lactamase-producing staphylococci are resistant to these drugs. Anaerobic Gram-positive bacteria, such as Peptococcus and Peptostreptococcus spp., anaerobic streptococci, Clostridium, Lactobacillus, Actinomyces, and Propionibacterium spp., are all usually susceptible to low carbenicillin and ticarcillin concentrations [64,76,78]. Clostridium difficile is also ticarcillin sensitive [79].

Other pharmacological effects


Medicinal Chemistry

CAS number: 34787-01-4 EINECS: 252-213-5

Molecular Formula:  C15H16N2O6S2

Average mass: 384.427307 Da

Monoisotopic mass:  384.044983 Da

Systematic name: 6-{[Carboxy(3-thienyl)acetyl]amino}-3,3-dimethyl-7-oxo-4-thia-1-azabicyclo[3.2.0]heptane-2-carboxylic acid

SMILES: CC1([C@@H](N2[C@H](S1)[C@@H](C2=O)NC(=O)[C@@H](c3ccsc3)C(=O)O)C(=O)O)C

Std. InChI: 1S/C15H16N2O6S2/c1-15(2)9(14(22)23)17-11(19)8(12(17)25-15)16-10(18)7(13(20)21)6-3-4-24-5-6/h3-5,7-9,12H,1-2H3,(H,16,18)(H,20,21)(H,22,23)/t7-,8-,9+,12-/m1/s1

ACD/LogP: 1.239 # of Rule of 5 Violations: 0
ACD/LogD (pH 5.5): -3.47 ACD/LogD (pH 7.4): -3.51
ACD/BCF (pH 5.5): 1.00 ACD/BCF (pH 7.4): 1.00
ACD/KOC (pH 5.5): 1.00 ACD/KOC (pH 7.4): 1.00
#H bond acceptors: 8 #H bond donors: 3
#Freely Rotating Bonds: 5 Polar Surface Area: 177.55 Å2
Index of Refraction: 1.694 Molar Refractivity: 90.746 cm3
Molar Volume: 236.449 cm3 Polarizability: 35.975 10-24cm3
Surface Tension: 86.0250015258789 dyne/cm Density: 1.626 g/cm3
Flash Point: 418.431 °C Enthalpy of Vaporization: 117.35 kJ/mol
Boiling Point: 768.264 °C at 760 mmHg Vapour Pressure: 0 mmHg at 25°C

Major Impurities:


Melting point:

Optical rotation:


logP: 1.01




1. Sutherland R., Burnett J., Rolinson G.N. "X-carboxy-3thienylmethyl penicillin (BRL 2288), a new semisynthetic penicillin: in vitro evaluation". Antimicrob. Agents Chemother. 1970: 390, (1971).

2. Parry M.F., Neu H.C. "Ticarcillin for treatment of serious infections with Gram-negative bacteria". J. Infect. Dis. 134: 476, (1976).

3. Rodriguez V., Bodey G.P., Horikoshi N. et al. "Ticarcillin therapy of infections". Antimicrob. Agents Chemother. 4: 427, (1973).

4. Korvick J.A., Yu V.L. "Antimicrobial agent therapy for Pseudomonas aeruginosa". Antimicrob. Agents Chemother. 35: 2167, (1991).

5. Ervin F.R., Bullock Jr. W.E. "Clinical and pharmacological studies of ticarcillin in Gram-negative infections". Antimicrob. Agents Chemother. 9: 94, (1976).

6. Parry M.F., Neu H.C., Merlino M. et al. "Treatment of pulmonary infections in patients with cystic fibrosis: a comparative study of ticarcillin and gentamicin". J. Pediatr. 90: 144, (1977).

7. Bodey G.P., Bolivar R., Fainstein V., Jadeja L. "Infections caused by Pseudomonas aeruginosa". Rev. Infect. Dis. 5: 279, (1983).

8. Peterson C.D., Kaatz B.L., Angaran D.M. "Drug evaluation data, ticarcillin and carbenicillin. A comparison". Drug Intellig. Clin. Pharm. 11: 482, (1977).

9. Rahal J.J., Simberkoff M.S. "Host defense and antimicrobial therapy in adult Gram-negative bacillary meningitis". Ann. Intern. Med. 96: 468, (1982).

10. Reyes M.P., Lerner A.M. "Current problems in the treatment of infective endocarditis due to Pseudomonas aeruginosa". Rev. Infect. Dis. 5: 314, (1983).

11. Komshian S.V., Tablan O.C., Palutke W., Reyes M.P. "Characteristics of leftsided endocarditis due to Pseudomonas aeruginosa in the Detroit medical center". Rev. Infect. Dis. 12: 693, (1990).

12. Bodey G.P., Jadeja L., Elting L. "Pseudomonas bacteremia. Retrospective analysis of 410 episodes". Arch. Intern. Med. 145: 1621, (1985).

13. Klastersky J., Hensgens C., Debusscher L. "Empiric therapy for cancer patients: comparative study of ticarcillin-tobramycin, ticarcillin-cephalothin, and cephalothin-tobramycin". Antimicrob. Agents Chemother. 7: 640, (1975).

14. Schimpff S.C., Landesman S., Hahn D.M. et al. "Ticarcillin in combination with cephalothin or gentamicin as empiric antibiotic therapy in granulocytopenic cancer patients". Antimicrob. Agents Chemother. 10: 837, (1976).

15. Murillo J., Standiford H.C., Schimpff S.C., Tatem B.A. "Comparison of serum bactericidal activity among three antimicrobial combinations". Antimicrob. Agents Chemother. 13: 992, (1978).

16. Klastersky J. "Empiric treatment of infections in neutropenic patients with cancer". Rev. Infect. Dis. 5 (Suppl 1): 21, (1983).

17. Love L.J., Schimpff S.C., Hahn D.M. et al. "Randomized trial of empiric antibiotic therapy with ticarcillin in combination with gentamicin, amikacin or netilmicin in febrile patients with granulocytopenia and cancer". Am. J. Med. 66: 603, (1979).

18. Klastersky J. "Concept of empiric therapy with antibiotic combinations". Am. J. Med. 80:2, (1986).

19. Schimpff S.C. "Empiric antibiotic therapy for granulocytopenic cancer patients". Am. J. Med. 80: 13, (1986).

20. Rolston K.V.I., Jones P.G., Fainstein V. et al. "Ceftizoxime plus ticarcillin: double beta-lactam therapy for infections in cancer patients". J. Antimicrob. Chemother. 19: 367, (1987).

21. Rubin R.H. "Empiric antibacterial therapy in granulocytopenia induced by cancer chemotherapy". Ann. Intern. Med. 108: 134, (1988).

22. Sage R., Hann I., Prentice H.G. et al. "A randomized trial of empirical antibiotic therapy with one of four beta-lactam antibiotics in combination with netilmicin in febrile neutopenic patients". J. Antimicrob. Chemother. 22: 237, (1988).

23. Hughes W.T., Armstrong D., Bodey G.P. et al. "Guidelines for the use of antimicrobial agents in neutropenic patients with unexplained fever". J. Infect. Dis. 161: 381, (1990).

24. Pizzo P.A. "Management of fever in patients with cancer and treatment induced neutropenia". N. Engl. J. Med. 328: 1323, (1993).

25. Aquino V.M., Pappo A., Buchanan G.R. et al. "The changing epidemiology of bacteremia in neutropenic children with cancer". Pediatr. Infect. Dis. J. 14: 140, (1995).

26. Martino R., Subirà M., Manteiga R. et al. "Viridans streptococcal bacteremia and viridans streptococcal shock syndrome in neutropenic patients: comparison between children and adults receiving chemotherapy or undergoing bone marrow transplantation". Clin. Infect. Dis. 20: 476, (1995).

27. Ervin F.R., Bullock Jr. W.E., Nuttall C.E. "Inactivation of gentamicin by penicillins in patients with renal failure". Antimicrob. Agents Chemother. 9: 1004, (1976).

28. Pickering L.K., Gearhart P. "Effect of time and concentration upon interaction between gentamicin, tobramycin, netilmicin, or amikacin and carbenicillin or ticarcillin". Antimicrob. Agents Chemother. 15: 592, (1979).

29. Murillo J., Standiford H.C., Schimpff S.C., Tatem B. "Gentamicin and ticarcillin serum levels". JAMA 241: 2401, (1979).

30. Chow M.S.S., Quintiliani R., Nightingale C.H. "In vivo inactivation of tobramycin by ticarcillin. A case report". JAMA 247: 658, (1982).

31. Mandell W.F., Garvey G.J., Neu H.C. "Achromobacter xylosoxidans bacteremia". Rev. Infect. Dis. 9: 1001, (1987).

32. Legrand C., Anaissie E. "Bacteremia due to Achromobacter xylosoxidans in patients with cancer". Clin. Infect. Dis. 14: 479, (1992).

33. Nichols R.L. "Empiric antibiotic therapy for intraabdominal infections". Rev. Infect. Dis. 5 (Suppl 1): 90, (1983).

34. Harding G.K.M., Buckwold F.J., Ronald A.R. et al. "Prospective randomized comparative study of clindamycin, chloramphenicol, and ticarcillin, each in combination with gentamicin in therapy for intraabdominal and female genital tract sepsis". J. Infect. Dis. 142: 384, (1980).

35. Neu H.C., Garvey G.J. "Comparative in vitro activity and clinical pharmacology of ticarcillin and carbenicillin". Antimicrob. Agents Chemother. 8: 457, (1975).

36. Nelson J.D., Kusmiesz H., Shelton S., Woodman E. "Clinical pharmacology and efficacy of ticarcillin in infants and children". Pediatrics 61: 858, (1978).

37. Nelson J.D. "Neonatal ticarcillin dosage". Pediatrics 64: 549, (1979).

38. Eastwood J.B., Curtis J.R. "Carbenicillin administration in patients with severe renal failure". BMJ 1: 486, (1968).

39. Silverblatt F., Turck M. "Laboratory and clinical evaluation of carbenicillin (carboxybenzyl penicillin)". Antimicrob. Agents Chemother. 1968: 279, (1969).

40. Lang R., Lishner M., Ravid M. "Adverse reactions to prolonged treatmenwith high doses of carbenicillin and ureidopenicillins". Rev. Infect. Dis. 13: 68, (1991).

41. Hoffman T.A., Bullock W.E. "Carbenicillin therapy of Pseudomonas and other Gram-negative bacillary infections". Ann. Intern. Med. 73: 165, (1970).

42. Kallay M.C., Tabechian H., Riley G.R., Chessin L.N. "Neurotoxicity due to ticarcillin in patient with renal failure". Lancet 1: 608, (1979).

43. Brown III C.H., Natelson E.A., Bradshaw M.W. et al. "Study of the effects of ticarcillin on blood coagulation and platelet function". Antimicrob. Agents Chemother. 7: 652, (1975).

44. Ervin F.R., Bullock Jr W.E. "Clinical and pharmacological studies of ticarcillin in Gram-negative infections". Antimicrob. Agents Chemother. 9: 94, (1976).

45. Fass R.J., Copelan E.A., Brandt J.T. et al. "Platelet-mediated bleeding caused by broad-spectrum penicillins". J. Infect. Dis. 155: 1242, (1987).

46. Ferres H., Nunn B. "Penicillin metabolites and platelet function". Lancet 2: 226, (1983).

47. Leading Article . "Antimicrobials and haemostasis". Lancet 1: 510, (1983).

48. Gastineau D., Spector R., Philips D. "Severe neutropenia associated with ticarcillin therapy". Ann. Intern. Med. 94: 711, (1981).

49. Ohning B.L., Reed M.D., Doershuk C.F., Bulmer J.L. "Ticarcillin-associated granulocytopenia". Am. J. Dis. Child. 136: 645, (1982).

50. Neu H.C. "Carbenicillin and ticarcillin". Med. Clin. N. Amer. 66: 61, (1982).

51. Graft D.F., Chesney P.J. "Use of ticarcillin following carbenicillin-associated hepatotoxicity". J. Pediatr. 100: 497, (1982).

52. Meyers B.R., Hirschman S.Z., Strougo L., Srulevitch E. "Comparative study of piperacillin, ticarcillin and carbenicillin pharmacokinetics". Antimicrob. Agents Chemother. 17: 608, (1980).

53. Rodriguez V., Inagaki J., Bodey G.P. "Clinical pharmacology of ticarcillin (x-carboxyl-3-thienylmethyl penicillin, BRL 2288)". Antimicrob. Agents Chemother. 4: 31, (1973).

54. Tan J.S., Salström S.J. "Levels of carbenicillin, ticarcillin, cephalothin, cefazolin, cefamandole, gentamicin, tobramycin and amikacin in human serum and interstitial fluid". Antimicrob. Agents Chemother. 11: 698, (1977).

55. Daschner F.D., Thoma G., Langmaack H., Dalhoff A. "Ticarcillin concentrations in serum, muscle and fat after a single intravenous injection". Antimicrob. Agents Chemother. 17: 738, (1980).

56. Summersgill J.T., Schupp L.G., Raff M.J. "Comparative penetration of metronidazole, clindamycin, choramphenicol, cefoxitin, ticarcillin and moxalactam into bone". Antimicrob. Agents Chemother. 21: 601, (1982).

57. Knudsen E.T., Rolinson G.N., Sutherland R. "Carbenicillin: a new semisynthetic penicillin active against Pseudomonas pyocyanea". BMJ 3: 75, (1967).

58. Parry M.F., Neu H.C. "Pharmacokinetics of ticarcillin in patients with abnormal renal function". J. Infect. Dis. 133: 46, (1976).

59. Butler K., English A.R., Ray V.A., Timreck A.E. "Carbenicillin: chemistry and mode of action". J. Infect. Dis. 122 (Suppl): 1, (1970).

60. Smith C.B., Wilfert J.N., Dans P.E. et al. "In vitro activity of carbenicillin and results of treatment of infections due to Pseudomonas with carbenicillin singly and in combination with gentamicin". J. Infect. Dis. 122 (Suppl): 14, (1970).

61. Adler J.L., Burke J.P., Wilcox C., Finland M. "Susceptibility of Proteus species and Pseudomonas aeruginosa to penicillins and cephalosporins". Antimicrob. Agents Chemother. 1970: 63, (1971).

62. McCracken Jr G.H., Nelson J.D., Thomas M.L. "Discrepancy between carbenicillin and ampicillin activities against enterococci and Listeria". Antimicrob. Agents Chemother. 3: 343, (1973).

63. Kammer R.B., Preston D.A., Turner J.R., Hawley L.C. "Rapid detection of ampicillin-resistant Haemophilus influenzae and their susceptibility to sixteen antibiotics". Antimicrob. Agents Chemother. 8: 91, (1975).

64. Sutter V.L., Finegold S.M. "Susceptibility of anaerobic bacteria to 23 antimicrobial agents". Antimicrob. Agents Chemother. 10: 736, (1976).

65. Prior R.B., Fass R.J. "Comparison of ticarcillin and carbenicillin activity against random and select populations of Pseudomonas aeruginosa". Antimicrob. Agents Chemother. 13: 84, (1978).

66. Kalkani E., Marketos N. "Comparative in vitro evaluation of the effects of ticarcillin and carbenicillin upon Pseudomonas aeruginosa". Antimicrob. Agents Chemother. 9: 89, (1976).

67. McGowan Jr J.E., Terry P.M. "Susceptibility of Gram-negative aerobic bacilli resistant to carbenicillin in a general hospital to piperacillin and ticarcillin". Antimicrob. Agents Chemother. 15: 137, (1979).

68. Smith J.A., Henry D.A. "Comparison of bactericidal activity of selected beta-lactam antimicrobials against Pseudomonas aeruginosa". J. Antimicrob. Chemother. 22: 849, (1988).

69. Cavallo J.D., Hocquet D., Pleisat P. et al. "Susceptibility of Pseudomonmas aeruginosa to antimicrobials: a 2004 French multicentre hospital study". J. Antimicrob. Chemother. 59: 1021, (2007).

70. Thornsberry C., Baker C.N., Kirven L.A., Swenson J.M. "Susceptibility of ampicillin-resistant Haemophilus influenzae to seven penicillins". Antimicrob. Agents Chemother. 9: 70, (1976).

71. Standiford H.C., Kind A.L., Kirby W.M.M. "Laboratory and clinical studies of carbenicillin against Gram-negative bacilli". Antimicrob. Agents Chemother.  1968: 286, (1969).

72. Hewitt W.L., Winters R.E. "The current status of parenteral carbenicillin". J. Infect. Dis. 127 (Suppl): 120, (1973).

73. Quentin C., Arpin C., Dubois V. et al. "Antibiotic resistance rates and phenotypes among isolates of Enterobacteriaceae in French extra-hospital practice". Eur. J. Clin. Microbiol. Infect. Dis. 23: 185, (2004).

74. Sutter V.L., Finegold S.M. "Susceptibility of anaerobic bacteria to carbenicillin, cefoxitin, and related drugs". J. Infect. Dis. 131: 417, (1975).

75. Roy I., Bach V., Thadepalli H. "In vitro activity of ticarcillin against anaerobic bacteria compared with that of carbenicillin and penicillin". Antimicrob. Agents Chemother. 11: 258, (1977).

76. Monif G.R.G., Clark P.R., Shuster J.J., Baer H. "Susceptibility of the anaerobic bacteria, Group D streptococci, Enterobacteriaceae, and Pseudomonas to semisynthetic penicillins: carbenicillin, piperacillin, and ticarcillin". Antimicrob. Agents Chemother. 14: 643, (1978).

77. Behra-Miellett J., Calvet L., Mory F. et al. "Antibiotic resistance among anaerobic Gram-negatiobve bacilli: lessons from a French multicentric survey". Anaerobe 9: 105, (2003).

78. Denys G.A., Jerris R.C., Swenson J.M., Thornsberry C. "Susceptibility of Propionibacterium acnes clinical isolates to 22 antimicrobial agents". Antimicrob. Agents Chemother. 23: 335, (1983).

79. Chow A.W., Cheng N., Bartlett K.H. "In vitro susceptibility of Clostridium difficile to new beta-lactam and quinolone antibiotics". Antimicrob. Agents Chemother. 28: 842, (1985).





     Hit Counter


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