Antimicrobe.org: Achromobacter (Alcaligenes) Species
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Updated March, 2009
Sally A Roberts MBChB, FRACP, FRCPA, Selwyn D R Lang, MBChB, FRACP, FRCPA
GENERAL DESCRIPTION
Microbiology Guided Medline Search
The genus Achromobacter is regarded as a member of the Alcaligenaceae family belonging to the Proteobacteria beta group. The present members of the genus Achromobacter are Achromobacter. xylosoxidans, Achromobacter xylosoxidans subsp. xylosoxidans, Achromobacter xylosoxidans subsp. denitrificans, Achromobacter denitrificans, Achromobacter insolitus, Achromobacter ruhlandii, Achromobacter piechaudii. and Achromobacter spanius (81). Members of the genus Achromobacter are motile, non-fermentative, oxidase- and catalase-positive, gram-negative bacilli which grow overnight, under aerobic conditions on most solid media, including MacConkey. A. xylosoxidans subsp. denitrificans is also able to grow anaerobically utilizing nitrate as an electron acceptor. Colonies are typically small with a thin, irregular, spreading edge. In general Achromobacter species produce alkaline reactions with carbohydrates, A. xylosoxidans is the exception, acidifying OF glucose and OF xylose.
A. piechaudii differs from A. xylosoxidans and A. xylosoxidans subsp. denitrificans by its ability to grow in 6.5% salt. A. piechaudii and A. ruhlandii reduce nitrate to nitrite but not further, whereas A. xylosoxidans and A. xylosoxidans subsp. denitrificans reduce nitrate to free nitrogen gas. Achromobacter spp. can utilize citrate as a sole carbon source except for A. piechaudii.
The genus Alcalignes contains one member, Alcaligenes faecalis. A. faecalis is a motile, nonfermentative, oxidase- and catalase-positive gram-negative bacillus. The colonial morphology is similar to Achromobacter but A. faecalis can be distinguished by the presence of a fruity odor (hence the previous name A. odorans) and it may cause green discoloration of blood agar. It produces an alkaline reaction with carbohydrates and is able to utilize citrate as a sole source of carbon. Like A. piechaudii, A. faecalis is able to grow in 6.5% salt.
Epidemiology Guided Medline Search
Achromobacter and Alcaligenes species are ubiquitous in soil and water and can be recovered from the human respiratory tract and gastrointestinal tract in hospitalized patients (69). Environmental sources such as well water, tap water and swimming pools have been identified (30, 68). Colonization of patients is facilitated by contamination of fluids in use in hospitals, including soaps and disinfectants and devices such as nebulizers, pressure transducers, incubators and humidifiers. In these circumstances, it is sometimes difficult to distinguish between colonization and infection. Achromobacter and Alcaligenes species are occasionally recovered in pure culture from normally sterile sites and are recognized as significant pathogens, particularly in the immunocompromised and the hospital environment.
Clinical Manifestations Guided Medline Search
The literature on infections due to Achromobacter and Alcaligenes species is comprised of case reports, reviews of case reports and case series. Infections include: bacteremia (1, 10, 17, 19, 25, 37, 39, 41, 68, 73, 74, 82); meningitis (13, 16); prosthetic joint infection (72); sternal osteomyelitis (78); ophthalmic infections (31, 53, 57, 60, 70, 71); chronic otitis media (54, 80); lung infection (26, 42); spontaneous and peritoneal dialysis-associated peritonitis (8, 21, 48), liver abscess (3,75) and endocarditis (12, 49, 52). The majority of these infections occurred in adult patients who had underlying malignancy or were otherwise immunocompromised.
Legrand et al. (39) reviewed 10 cases of bacteremia due to A. xylosoxidans occurring in patients with underlying malignancies and reviewed 23 other cases of bacteremia reported in the literature. Duggan et al. (19) described 77 cases of bacteremia due to A. xylosoxidans including the 23 cases reported by the previous authors (38). The episode of bacteremia was nosocomially acquired in 54 (70%) patients and for 28 (36%) of the patients infection was associated with an outbreak, or following contact with a contaminated solution or piece of equipment within the hospital. The most common clinical syndromes associated with the episode of bacteremia were; primary bacteremia 19%, intravascular catheter associated bacteremia 19%, and pneumonia 16%. Of the more recently published case series, three with over 30 patients each (1, 25, 64) reported rates of nosocomial bacteremia ranging between 33 – 96%. In two of the series (1, 64) 17.5 and 52% of episodes were polymicrobial. Case series of pseudobacteremia have been reported (11, 46, 66); the most likely source in these events were contaminated disinfectant solutions or containers, and nonsterile blood collection tubes.
Weitkamp et al. (79) reported a patient with hyper-IgM syndrome with recurrent episodes of bacteremia due to A. xylosoxidans over a 3.5 year period; lymphoid tissue was considered the most likely source for his recurrent A. xylosoxidans bacteremia. Eight cases of bacteremia and/or respiratory disease caused by A. xylosoxidans in patient infected with the immunodeficiency virus have been reported (26, 42). There are several reports of neonatal infections, especially bacteremia and meningitis, including maternal-fetal transfer (29).
Both colonization and infection with A. xylosoxidans in children with cystic fibrosis have been described (14, 15, 20, 23, 34, 47, 55, 59). Dunne et al. (20) reported an epidemiological investigation of 16 cases of A. xylosoxidans, of which 8 occurred in patients with cystic fibrosis. Cross infection between patients with A. xylosoxidans has been reported (59). Colonization with A. xylosoxidans can be long term; Moissenet et al. reported that 8 of 120 children with cystic fibrosis were persistently colonized with A. xylosoxidans for a mean of 3.5 years despite various antibiotic treatments including intravenous ticarcillin, piperacillin, ceftazidime and imipenem, oral trimethoprim-sulphamethoxazole and ciprofloxacin and nebulized colistin (47). Peltroche-Llacsahuanga et al. (55) described two brothers with cystic fibrosis with long-standing colonization with A. xylosoxidans. Colonization of the second brother occurred three years after the first and there did not appear to be any evidence of a change in clinical status over the observation periods of six and three years, respectively. A retrospective case control study of patients did not show decline in lung function over time for patients colonized with A. xylosoxidans (15) but Rønne Hansen et al reported an increase in lung function decline in a group of patients with rapidly increasing specific A. xylosoxidans antibodies (59). There is little evidence to suggest that colonisation with panresistant Gram-negative bacilli in cystic fibrosis patients undergoing lung transplantation including A. xylosoxidans impacts on survival (28).
The great majority of clinical reports of infection caused by this genus implicate A. xylosoxidans. Other Achromobacter spp. and Alcaligenes faecalis are less frequently isolated. Morrison et al. (48) reported three cases of peritonitis due to A. xylosoxidans subsp. denitrificans and Cheron et al. (9) reported 10 patients with respiratory tract colonization due to A. xylosoxidans subsp. denitrificans, two of whom were found to have been exposed to contaminated water used in a nebulizer. A. piechaudii has been associated with chronic otorrhoea in one patient (54) and recurrent bacteremia in association with an intravascular catheter in another patient (35).
Alcaligenes faecalis is seldom isolated from clinical material; Bizet et al. (7) described six patients from whom A. faecalis was isolated from urine (3), ear discharge (1) and pus from discharging wounds (2). Bacteraemia due to A. faecalis accounted for only one of 52 (2%) episodes of bacteraemia in cancer patients caused by A. xylosoxidans and Alcaligenes sp. over a ten year period (1) Post-operative ophthalmic infections have also been reported (33, 36, 44).Ahmed MS et al. Achromobacter xylosoxidans, an Emerging Pathogen in Catheter-related Infection in Dialysis Population Causing Prosthetic Valve Endocarditis: A Case Report and Review of Literature. Clin Nephrol. 2009 Mar;71(3):350-4.
Reddy AK, Garg P, et al. Clinical, Microbiological Profile and Treatment Outcome of Ocular Infections Caused by Achromobacter xylosoxidans. Cornea. 2009 Aug 31. [Epub ahead of print]
SUSCEPTIBILITY IN VITRO AND IN VIVO Guided Medline Search In Vitro and In Vivo
Achromobaceter xylosoxidans (recently Alcaligenes xylosoxidans subsp. xylosoxidans)
Four published studies provide MIC50 and MIC90 data for a wide range of antibiotics for clinical isolates of A. xylosoxidans (Table 1) (6, 24, 32, 76). The most consistently active antibiotics among those tested were imipenem, meropenem, trimethoprim-sulphamethoxazole, piperacillin, ticarcillin/clavulanate and ceftazidime. All isolates were resistant to aminoglycosides, ampicillin, amoxicillin, mecillinam (amidinocillin) and aztreonam; most were resistant to first, second, third and fourth generation cephalosporins, other than ceftazidime, and to the quinolones. These are in keeping with the results from two small series (4, 19). The addition of clavulanate to amoxicillin and to ticarcillin reduced the mean MICs of these antibiotics such that a majority of isolates were susceptible to ticarcillin-clavulanate in vitro (Table 1).
A detailed study of the susceptibility of 56 clinical isolates and two reference strains of A. xylosoxidans (formerly known as Alcaligenes denitrificans subsp. xylosoxydans) to 12 β-lactam antibiotics, and of the effect of β-lactamase inhibitors, was conducted by Mensah et al. (45). All strains produced β-lactamase, but two phenotypic classes of activity were observed: 41 strains produced β-lactamase inhibited by cloxacillin (type S) but not by clavulanic acid, whereas the other 17 (type R) strains showed β-lactamase activity inhibited by clavulanic acid. Tables 2 and 3 show the susceptibilities of these two groups of isolates. All were susceptible to imipenem and to moxalactam. The 41 type S strains were highly susceptible to ticarcillin, piperacillin and azlocillin. Susceptibility to cephalosporins was more variable. These strains were highly resistant to cefuroxime and cefoxitin, resistant to cefotaxime and cefamandole, and susceptible to cefoperazone and ceftazidime. In the case of the type R strains, Table 3, clavulanic acid potentiated amoxicillin, ticarcillin, cefoperazone and, to a lesser extent, ceftazidime, but not cefuroxime or cefotaxime; tazobactam potentiated piperacillin. The authors note in their discussion that isolates resistant to penicillins are also resistant to sulphonamides, however, others have found no cross-resistance with trimethoprim-sulphamethoxazole (16). Saiman et al. (61) looked specifically at A. xylosoxidans isolates from patients with cystic fibrosis, Table 4.
Achromobacter xylosoxidans subsp. denitrificans
In one series (6) the antibiogram for A. xylosoxidans subsp. denitrificans isolates, Table 5, did not differ significantly from that for A. xylosoxidans, Table 1.
Achromobacter piechaudii and Alcaligenes faecalis
These organisms are less commonly encountered clinically and there is a relative paucity of in vitro susceptibility data. Tables 6 and 7 show what has been reported (6, 76). Achromobacter piechaudii isolates showed a resistance pattern similar to A. faecalis, but were more markedly resistant to cefoxitin and cefotaxime, Table 6. Alcaligenes faecalis isolates, Table 7, were less resistant to cephalosporins than A. xylosoxidans and clavulanate rendered most susceptible to amoxicillin and to ticarcillin. Piperacillin had slightly greater intrinsic activity than ticarcillin, but was not investigated in combination with tazobactam. The quinolones showed variable activity. All were resistant to aztreonam and most to the aminoglycosides.
Two strains of extended-spectrum ß-lactamase producing A. faecalis have been reported (18, 56). A strain of A. faecalis with PER-1 extended-spectrum beta-lactamase production was isolated from a patient's urine (56). The authors raised the concern that A. faecalis may be an efficient shuttle for spreading of this resistance gene among other opportunistic pathogens that are normally commensal microbiota. The second strain, also isolated from a patient’s urine, (18) contained a gene for blaTEM-21 located on the chromosome.
Jorgensen et al. reported that all 14 isolates of Achromobacter spp., other than A. xylosoxidans, in their series were susceptible to meropenem (MIC90 0.25μg/ml) and to imipenem (MIC90 1μg/ml) (32). In contrast the MIC90 of meropenem and of imipenem for 15 isolates of A. xylosoxidans were 4μg/ml and 8μg/ml respectively (32). A. xylosoxidans strains carrying metallo-ß-lactamases were first reported in Japan in the mid-1990’s (67). These strains carried metallo-ß-lactamases IMP enzymes. More recently VIM-2 enzymes have been detected in two strains isolated from clinical specimens (65, 67) in Korea and Greece; the MICs for imipenem and meropenem were between 16 – 64 mg/L.
In summary, Achromobacter spp. and A. faecalis are susceptible to the carbapenems, imipenem and meropenem but strains carrying metallo-ß-lactamases have been reported (65, 67). Most isolates are susceptible to trimethoprim-sulphamethoxazole, piperacillin (especially with tazobactam) and ticarcillin/clavulanate. Susceptibility is variable to cephalosporins, among which moxalactam and ceftazidime are the most active. Tetracyclines, chloramphenicol, macrolides and quinolones show variable activity. Achromobacter spp. and A. faecalis are generally resistant to aminoglycosides, ampicillin, penicillin and rifampicin (63).
A further feature of note is that A. xylosoxidans, and perhaps other Achromobacter spp. also, is commonly tolerant to many antibiotics including trimethoprim-sulphamethoxazole, ticarcillin, mezlocillin, piperacillin and cefoperazone (2, 51). Tolerance is of potential importance in patients with endocarditis, meningitis, neutropenic sepsis or prosthetic device infection, conditions in which bactericidal activity is deemed relevant. Most case reports of treatment of infections due to Achromobacter spp. do not describe bactericidal titres. However, a titre of 1:16 was obtained in the CSF of a patient successfully treated with a combination of ceftazidime, gentamicin and trimethoprim-sulphamethoxazole (13). There are very few reports of the effects of combinations of antibacterials against Achromobacter spp., other than β-lactam plus β-lactamase inhibitor and trimethoprim plus sulphamethoxazole. Despite resistance to amikacin, synergy has been reported with amikacin plus ceftazidime, a combination used successfully to treat intravascular catheter-related sepsis due to A. xylosoxidans in a child with AIDS (10). Since in this case synergy was detected by disc diffusion testing and bactericidal titres were not reported, it is not certain whether the combination was bactericidal. The two-disk approximation method and time-kill assays (16) have shown that the combination of a beta-lactam drug or trimethoprim-sulphamethoxazole with gentamicin can be synergistic but the combination of a beta-lactam drug and trimethoprim-sulphamethoxazole is uniformly antagonistic. In vitro testing using combinations of azithromycin-tobramycin, azithromycin-ceftazidime and azithromycin-doxycycline or azithromycin trimethoprim-sulfamethoxazole inhibited 22% of A. xylosoxidans strains from patients with cystic fibrosis. The authors rightly state that in vitro synergy studies do not predict in vivo efficacy (62).
ANTIMICROBIAL THERAPY Guided Medline Search Smart search
There are no large series and no randomized controlled trials. On the basis of in vitro data, carbapenems are likely to replace trimethoprim-sulphamethoxazole as the agents of first choice for serious infections due to Achromobacter spp. and A. faecalis. Piperacillin with or without tazobactam and ticarcillin with clavulanate are alternatives. It should be noted that a β-lactamase hyperproducing variant of A. xylosoxidans has been selected in vivo in a patient treated initially with piperacillin and pefloxacin (16). The CSF cultures were still culture-positive after one month of therapy. Although the therapy was changed to trimethoprim-sulphamethoxazole the patient, who had acute lymphoblastic leukemia, died a few days later (16). Combination therapy may be more effective than a single agent in treating patients with serious A. xylosoxidans infections, even if the isolate does not appear to be susceptible to aminoglycosides (19).
Combination therapy with ceftazidime and amikacin for 14 days has been used successfully in treating Broviac catheter related sepsis where the catheter was not removed (10). If synergy, as was shown in vitro in this case, can be shown with an aminoglycoside, then combination therapy could be considered.
(Printable Version of Antimicrobial Therapy for Achromobacter)
ENDPOINTS FOR MONITORING THERAPY Guided Medline Search
For invasive infections, repeat cultures at the original site is indicated if symptoms or fever persists on antibiotic therapy.
VACCINES Guided Medline Search
No vaccine is available for Achromobacter spp.
PREVENTION AND INFECTION CONTROL Guided Medline Search Smart search
Achromobacter spp. are often associated with an aqueous environment and rapidly colonizes these sorts of environments within the hospital setting, they are less often found on fomites or in nonaquatic surroundings. Outbreaks related to contaminated saline (9, 27, 43), chlorhexidine (77, 73, 46) deionized water (58) and quaternary ammonium solutions (22) have been reported. Alcaligenes denitrificans subsp. xylosoxydans has been isolated from unopened samples of benzalkonium chloride, the distilled water used by the company's manufacturing plant was found to be the source (51).
The majority of infections caused by Achromobacter spp. are nosocomially acquired (19). An appreciation of the hospital sources of the organism and the environments in which they are likely to colonize is important. As described above, aqueous fluids and disinfectants containing alcohol or quaternary ammonium compounds and nonbacteriostatic saline are perfect culture media for Achromobacter spp.. When investigating a suspected outbreak due to Achromobacter spp. phenotypic typing methods are of little use due to the predictable pattern of antibiotic susceptibility and the limited range of biochemical reactions. A number of different molecular genotyping methods including pulse-field gel electrophoresis, restriction fragment-length polymorphism, polymerase chain reaction and randomly amplified polymorphic DNA have been utilized (2, 4, 9, 40, 46, 73, 77,) to assist with the epidemiological investigation of suspected outbreaks. Benaoudia et al. (5) was able to show that nine isolates of A. xylosoxidans were genotypically distinct whereas phenotypically the isolates were indistinguishable and as the period of hospitalization of five of the patients overlapped they were able exclude a common source of exposure or patient-to-patient contact.
Along with good adherence to hand hygiene by healthcare workers special attention should be paid to maintaining sterility in aqueous fluids used in the irrigation of wounds and body parts. In the event of an outbreak the use of multi-use containers for aqueous fluids used for patient contact should be avoided. Sodium hypochlorite or povidine-iodine solutions are effective disinfectants against Achromobacter spp. (63).
TABLES
Table 1. Susceptibilities of Achromobacter xylosoxidans
Table 2. Susceptibilities of cloxacillin-sensitive ß-lactamase-producing Achromobacter xylosoxidans
Table 5. In vitro susceptibilities of Achromobacter xylosoxidans subsp. denitifricans
Table 6. In vitro susceptibilities of Achromobacter piechaudii
Table 7. In vitro susceptibilities of Alcaligenes faecalis
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| Table 1. Susceptibilities of Achromobacter xylosoxidansa | |||||||
| Antibiotic | n | Range | MIC50 | MIC90 | Breakpointb | % Susceptible | Reference |
| AmikacinAmikacin | 3350 | 8-12816->128 | 128>128 | 128>128 | <16≤16 | 1376 | |
| Gentamicin | 33 | 4-64 | 64 | 64 | <4 | 13 | |
| Gentamicin | 16 | 256 | 256 | 256 | <4 | 0 | 5 |
| GentamicinGentamicin | 1550 | 1-644->128 | >6464 | >64>128 | <4≤4 | 2076 | |
| Kanamycin | 16 | 64-512 | 128 | 256 | <16 | 0 | 5 |
| Netilmicin | 33 | 8-64 | 64 | 64 | <8 | 13 | |
| Netilmicin | 16 | 64-256 | 128 | 256 | <8 | 0 | 5 |
| Tobramycin | 33 | 16-64 | 32 | 64 | <4 | 0 | 13 |
| Amidinocillin | 33 | 32->256 | 256 | >256 | 13 | ||
| AmpicillinAmpicillin | 3350 | 16->1284->128 | 3232 | >128128 | <8≤8 | 0 | 1376 |
| Amoxycillin | 16 | 32-512 | 64 | 256 | <8 | 0 | 5 |
| Amoxycillin clavulanate | 16 | 16-64 | 32 | 64 | <8/4 | 0 | 5 |
| Amoxycillin clavulanate | 33 | 4->128 | 16 | 64 | <8/4 | 13 | |
| Piperacillin | 33 | 0.5->128 | 0.5 | 64 | <16 | 13 | |
| Piperacillin | 16 | 0.5-8 | 4 | 8 | <16 | 100 | 5 |
| PiperacillinPiperacillinPiperacillin tazobactam | 155050 | <2->2560.06-40.06-2 | <20.50.5 | 25621 | <16≤16≤16/2 | 207676 | |
| Temocillin | 33 | 64->256 | >256 | >256 | 13 | ||
| Ticarcillin | 15 | <2->256 | 4 | >256 | <16 | 20 | |
| Ticarcillin | 16 | 4-512 | 16 | 128 | <16 | 5 | |
| Ticarcillin clavulanate | 16 | 2-16 | 4 | 8 | <16/2 | 100 | 5 |
| Ticarcillin clavulanate | 33 | 0.25-64 | 1 | 32 | <16/2 | 13 | |
| Ticarcillin clavulanate | 15 | <2-128 | <2 | 128 | <16/2 | 20 | |
| Cefamandole | 33 | 4-128 | 16 | 32 | <8 | 13 | |
| Cefazolin | 33 | 16-128 | 128 | 128 | <8 | 0 | 13 |
| Ceforanide | 33 | 4-256 | 256 | 256 | 13 | ||
| Cefotaxime | 33 | 8-64 | 32 | 64 | <8 | 13 | |
| Cefotaxime | 16 | 64-256 | 256 | 256 | <8 | 0 | 5 |
| Cefotaxime | 15 | 16->64 | 64 | >64 | <8 | 0 | 20 |
| Cefotetan | 33 | 16-256 | 128 | 256 | <16 | 13 | |
| Cefoxitin | 16 | 256 | 256 | 256 | <8 | 0 | 5 |
| Ceftazidime | 33 | 1-64 | 4 | 16 | <8 | 13 | |
| CeftazidimeCeftazidime | 1550 | 2->641-32 | 84 | 1616 | <8≤8 | 2076 | |
| CeftriaxoneCefoperazoneCefoperazone sulbactamCefepime | 33505050 | 2-1282-81-48-128 | 322232 | 6444128 | <8≤16≤16/8<8 | 13767676 | |
| Cefuroxime | 33 | 32-128 | 64 | 64 | <8 | 0 | 13 |
| Cephalothin | 16 | 128-256 | 128 | 256 | <8 | 0 | 5 |
| Aztreonam | 16 | 32-64 | 64 | 64 | <8 | 0 | 5 |
| AztreonamAztreonam | 1550 | 32->6464-128 | 6464 | >64128 | <8≤8 | 0 | 2076 |
| Imipenem | 33 | 0.25-4 | 0.5 | 2 | <4 | 100 | 13 |
| ImipenemImipenem | 1550 | 1->160.5-4 | 22 | 84 | <4≤4 | 2076 | |
| MeropenemMeropenem | 1550 | 0.25-40.25-4 | 11 | 42 | ≤4 | 2076 | |
| Ciprofloxacin | 33 | 1-64 | 4 | 16 | <1 | 13 | |
| Ciprofloxacin | 16 | 2-8 | 4 | 8 | <1 | 0 | 5 |
| CiprofloxacinCiprofloxacin | 1550 | 1->81->128 | 322 | 6416 | <1≤1 | 2076 | |
| NorfloxacinNorfloxacin | 3350 | 8-648->128 | 3216 | 6464 | ≤4 | 1376 | |
| Ofloxacin | 33 | 1-64 | 4 | 32 | <2 | 13 | |
| Pefloxacin | 33 | 1-64 | 4 | 32 | 13 | ||
| Pipemidic acid | 16 | 512 | 512 | 512 | 5 | ||
| Nalidixic acidColistinChloramphenicolErythromycinRifampicinMinocycline | 165050505050 | 1281-648->1288->1288-642-64 | 12843264164 | 12832128>128328 | ≤2≤8≤1≤4≤4 | 57676767676 | |
| Trimethoprim-sulphamethoxazolecTrimethoprim-sulphamethoxazolec | 33 50 | 0.12-64 0.06-64 | 0.2 1 | 12 32 | <2/38 ≤2/38 | 13 76 | |
a Modified from (6, 24, 32)
b Current NCCLS interpretive standards for susceptibility (µg/ml) (50).
c Trimethoprim-sulphamethoxazole tested in a ratio of 1:19. Concentration refers to the
trimethoprim component.
| Table 2. Susceptibilities of cloxacillin-sensitive ß-lactamase-producing Achromobacter xylosoxidansa | |||||||
| Antibiotic | n | Range | MIC50 | MIC90 | Breakpointb | % Susceptible | |
| Amoxicillin | 41 | 4-64 | 8 | 64 | <8 | ||
| Amoxicillin clavulanate c | 41 | 2-32 | 4 | 8 | <8/4 | ||
| Azlocillin | 41 | <0.12-2 | 0.25 | 0.5 | |||
| Piperacillin | 41 | <0.12-1 | 0.5 | 0.5 | <16 | 100 | |
| Piperacillin tazobactamd | 41 | <0.12-1 | 0.5 | 0.5 | <16/4 | 100 | |
| Ticarcillin | 41 | 0.25-8 | 1 | 4 | <16 | 100 | |
| Ticarcillin clavulanate c | 41 | 0.25-2 | 1 | 1 | <16/2 | 100 | |
| Cefamandole | 41 | 4-64 | 16 | 32 | <8 | ||
| Cefoperazone | 41 | 0.5-4 | 2 | 4 | <16 | 100 | |
| Cefoperazone clavulanate c | 41 | <0.12-4 | 2 | 2 | <16 | 100 | |
| Cefotaxime | 41 | 16-128 | 64 | 64 | <8 | 0 | |
| Cefotaxime clavulanate c | 41 | 16-64 | 64 | 64 | <8 | 0 | |
| Cefoxitin | 41 | 64->256 | 256 | 256 | <8 | 0 | |
| Ceftazidime | 41 | 1-16 | 4 | 8 | <8 | ||
| Ceftazidime clavulanate c | 41 | 1-16 | 4 | 8 | <8 | ||
| Cefuroxime | 41 | >256 | >256 | >256 | <8 | 0 | |
| Cefuroxime clavulanate c | 41 | >256 | >256 | >256 | <8 | 0 | |
| Moxalactam | 41 | 0.25-8 | 2 | 4 | <8 | 100 | |
| Imipenem | 41 | 1-4 | 2 | 2 | <4 | 100 | |
a Modified from (45).
b Current NCCLS interpretive standards for susceptibility (µg/ml) (45).
c Clavulanate (2µg/ml).
d Tazobactam (4µg/ml).
| Table 3. Susceptibilities of cloxacillin/clavulanic acid-susceptible ß-lactamase-producing Achromobacter xylosoxidans a | |||||||
| Antibiotic | n | Range | MIC50 | MIC90 | Breakpointb | % Susceptible | |
| Amoxicillin | 17 | >256 | >256 | >256 | <8 | 0 | |
| Amoxicillin clavulanate c | 17 | <2-128 | 64 | 128 | <8/4 | ||
| Azlocillin | 17 | 4-64 | 32 | 64 | |||
| Piperacillin | 17 | 4-128 | 32 | 64 | <16 | ||
| Piperacillin tazobactamd | 17 | 0.5-16 | 1 | 4 | <16/4 | 100 | |
| Ticarcillin | 17 | 64->256 | >256 | >256 | <16 | 0 | |
| Ticarcillin clavulanate c | 17 | 0.5-64 | 16 | 64 | <16/2 | ||
| Cefamandole | 17 | 16-256 | 32 | 128 | <8 | ||
| Cefoperazone | 17 | 16-128 | 64 | 128 | <16 | ||
| Cefoperazone clavulanate c | 17 | 1-8 | 2 | 8 | <16 | 100 | |
| Cefotaxime | 17 | 64->256 | 64 | >256 | <8 | 0 | |
| Cefotaxime clavulanate c | 17 | 32->256 | 256 | >256 | <8 | 0 | |
| Cefoxitin | 17 | 128->256 | 256 | >256 | <8 | 0 | |
| Ceftazidime | 17 | 2-32 | 16 | 32 | <8 | ||
| Ceftazidine clavulanate c | 17 | 2-16 | 4 | 8 | <8 | ||
| Cefuroxime | 17 | >256 | >256 | >256 | <8 | 0 | |
| Cefuroxime clavulanate c | 17 | >256 | >256 | >256 | <8 | 0 | |
| Moxalactam | 17 | 0.5-8 | 2 | 2 | <8 | 100 | |
| Imipenem | 17 | 1-2 | 2 | 2 | <4 | 100 | |
a Adapted from (45).
b Current NCCLS interpretive standards for susceptibility (µg/ml) (50).
c Clavulanate (2µg/ml).
d Tazobactam (4µg/ml).
Table 4. In vitro susceptibilities of Achromobacter xylosoxidans isolates from patients with Cystic Fibrosis (61)
| Antibiotic | Range | MIC50 | MIC90 | Breakpointa | % Susceptible |
Ticarcillin clavulanate 4->128 128 >128 ≤16/2 40
Piperacillin 4->128 32 >128 ≤16 50
Piperacillin tazobactam 4->128 32 >128 ≤16/4 55
Ceftazidime 2->64 64 128 ≤8 45
Imipenem 1->16 4 >16 ≤4 59
Meropenem 0.5->16 8 >16 ≤4 51
Ciprofloxacin 0.5->8 >8 >8 ≤1 9
Tobramycinb 4->256 >256 >256 ≤4 3
Trimethoprim-
Sulfamethoxazole >16 >16 >16 ≤2/38 0
Chloramphenicol 8->64 32 >64 ≤8 22
Minocycline 1-32 8 16 ≤4 51
Colistinb 100->200 92
---------------------------------------------------------------------------------------------------------------------------------------------------------------
a b Current NCCLS interpretive standards for susceptibility (µg/ml) (50).
b Higher concentrations tested such as those achieved by aerosolization
| Table 5. In vitro susceptibilities of Achromobacter xylosoxidans subsp. denitifricansa | |||||||
| Antibiotic | n | Range | MIC50 | MIC90 | Breakpointb | % Susceptible | |
| Amoxycillin | 10 | 0.5-512 | 32 | 128 | <8 | ||
| Amoxycillin clavulanate c | 10 | 0.5-128 | 16 | 32 | <8/4 | ||
| Piperacillin | 10 | 0.125-1024 | 1 | 4 | <16 | ||
| Ticarcillin | 10 | 0.125-256 | 8 | 64 | <16 | ||
| Ticarcillin clavulanate c | 10 | 0.125-256 | 2 | 4 | <16/2 | ||
| Cefotaxime | 10 | 0.125-256 | 2 | 4 | <16/2 | ||
| Cefoxitin | 10 | 0.125-256 | 128 | 256 | <8 | ||
| Cephalothin | 10 | 0.125-128 | 32 | 128 | <8 | ||
| Aztreonam | 10 | 32-64 | 32 | 64 | <8 | 0 | |
| Ciprofloxacin | 10 | 0.125-8 | 2 | 8 | <1 | ||
| Pipemidic acid | 10 | 8-512 | 256 | 512 | |||
| Nalidixic acid | 10 | 2-128 | 128 | 256 | |||
| Gentamicin | 10 | 0.125-256 | 128 | 256 | <4 | ||
| Kanamycin | 10 | 0.125-512 | 128 | 256 | <16 | ||
| Netilmicin | 10 | 0.125-256 | 128 | 256 | <8 | ||
a Modified from (6).
b Current NCCLS interpretive standards for susceptibility (µg/ml) (50).
c Clavulanate (2µg/ml).
| Table 6. In vitro susceptibilities of Achromobacter piechaudiia | |||||||
| Antibiotic | n | Range | MIC50 | MIC90 | Breakpointb | % Susceptible | |
| Amoxycillin | 5 | 4-64 | 16 | 32 | <8 | ||
| Amoxycillin clavulanate c | 5 | 1-2 | 2 | 2 | <8/4 | 100 | |
| Piperacillin | 5 | 0.5-1 | 0.5 | 1 | <16 | 100 | |
| Ticarcillin | 5 | 8-32 | 8 | 16 | <16 | 100 | |
| Ticarcillin clavulanate c | 5 | 1-4 | 2 | 2 | <16/2 | 100 | |
| Cefotaxime | 5 | 64 | 64 | 64 | <8 | 0 | |
| Cefoxitin | 5 | 64 | 64 | 64 | <8 | 0 | |
| Cephalothin | 5 | 8-16 | 8 | 16 | <8 | ||
| Aztreonam | 5 | 16 | 16 | 16 | <8 | 0 | |
| Ciprofloxacin | 5 | 2-8 | 2 | 4 | <8 | 0 | |
| Pipemidic acid | 5 | 256 | 256 | 256 | |||
| Nalidixic acid | 5 | 2-32 | 4 | 8 | |||
| Gentamicin | 5 | 16-128 | 32 | 64 | <4 | 0 | |
| Kanamycin | 5 | 8-32 | 8 | 8 | <16 | ||
| Netilmicin | 5 | 2-32 | 4 | 8 | <8 | ||
a Modified from (6).
b Current NCCLS interpretive standards for susceptibility (µg/ml) (50).
c Clavulanate (2µg/ml).
| Table 7. In vitro susceptibilities of Alcaligenes faecalis | |||||||
| AntibioticAmpicillin | N18 | Range2->128 | MIC508 | MIC90>128 | Breakpointa<8 | Reference 76 | |
| Amoxycillin | 34 | 2-1024 | 16 | 64 | <8 | 6 | |
| Amoxycillin clavulanate b | 34 | 0.5-128 | 2 | 4 | <8/4 | 6 | |
| PiperacillinPiperacillinPiperacillin tazobactam | 341818 | 1-2560.5-5120.25-256 | 410.5 | 166432 | <16<16<16/2 | 67676 | |
| Ticarcillin | 34 | 1-512 | 16 | 64 | <16 | 6 | |
| Ticarcillin clavulanate b | 34 | 0.5-32 | 2 | 8 | <16/2 | 6 | |
| Cefotaxime | 34 | 0.5-128 | 2 | 8 | <8 | 6 | |
| Cefoxitin | 34 | 2-128 | 4 | 8 | <8 | 6 | |
| CephalothinCefoperazoneCefoperazone sulbactamCeftazidimeCefepime | 3418181818 | 2-1281-320.5-21-324-64 | 810.548 | 3282816 | <8<16<16/8<8<8 | 676767676 | |
| Aztreonam | 34 | 32 | 32 | 32 | <8 | 6 | |
| Ciprofloxacin | 34 | 0.5-8 | 2 | 4 | <1 | 6 | |
| Pipemidic acid | 34 | 8-512 | 256 | 256 | 6 | ||
| Nalidixic acid | 34 | 128 | 128 | 128 | 6 | ||
| Gentamicin | 34 | 32-512 | 32 | 64 | <4 | 6 | |
| Kanamycin | 34 | 4-512 | 128 | 256 | <16 | 6 | |
| Netilmicin | 34 | 1-256 | 8 | 16 | <8 | 6 | |
a Current NCCLS interpretive standards for susceptibility (µg/ml) (50).
b Clavulanate (2µg/ml).
Review ArticlesAhmed MS et al. Achromobacter xylosoxidans, an Emerging Pathogen in Catheter-related Infection in Dialysis Population Causing Prosthetic Valve Endocarditis: A Case Report and Review of Literature. Clin Nephrol. 2009 Mar;71(3):350-4.
