Sphingomonas paucimobilis
Authors: Michael Ryan, Ph.D., Adeel A. Butt, M.D., Catherine C. Adley, Ph.D.
GENERAL DESCRIPTION
Sphingomonas paucimobilis was initially known as CDC Group IIk, biotype 1, subsequently receiving its own taxonomic status in 1977, when it was named Pseudomonas paucimobilis (14). In 1990 the bacteria was placed into its own genus Sphingomonas and as the type strain of the genus (36). It shares biochemical properties, fatty acid content and DNA homology with species of Flavobaterium (27). The first infection under the name P. paucimobilis was reported in 1979 in a sailor who had developed a leg ulcer, and the organism was isolated in pure culture from the wound specimen (25). Subsequently, many more cases of infection with the organism were reported along with a number of persons colonized with the organism, without any identifiable disease (28). S. paucimobilis was originally regarded as the only representative of the Sphingomonas genus to be of clinical importance. However two other Sphingomonas spp. species – Sphingomonas mucosissima (2) and Sphingomonas adhesiva (28) have recently been implicated in infection.
Microbiology
S. paucimobilis is a yellow pigmented, aerobic, non-fermenting Gram-negative rod with a polar flagellum. The name "paucimobilis" derives from the fact that few bacteria are motile in broth culture. The organism can be cultured on a variety of non-selective media, including blood and chocolate agar, but not on McConkey or media selective for enterobacteria. It is both oxidase and catalase positive (27). It grows optimally at 30°C, and also grows at 37°C, but does not grow at 5°C or 42°C (21). Unlike other gram-negative rods, it lacks Lipopolysaccharide (LPS) in its outer capsule (14). Instead, it possesses at least two different kinds of sphingolipids (where its name derives from). These sphingolipids have a unique sphingoglycolipid with the long-chain base dihydrosphingosin, ubiquinone 10 (Q-10), and 2-hydroxymyristic acid (2-OH C14:0) and the absence of 3-hydroxy fatty acids (13). These are capable of inducing tumor necrosis factor (TNF), Interleukin (IL) 6, and IL-1 from mononuclear cells (14).
Epidemiology
S. paucimobilis can be widely found in the natural environment. It has been isolated from water, soil and other sources (27). It has frequently been isolated from hospital equipment (such as ventilators) and water sources (6). Many cases of infection with S. paucimobilis are due to contaminated solutions (9, 6, 18, 27). These solutions can include a wide range of substances including distilled water, haemodialysis fluid, and sterile drug solutions (10, 17, 26). These have led to both bloodstream (bacteraemia) and peritoneal infections. In many of these cases contamination of the product could happen at the manufacturing stage. There could potentially be many reasons for this, but one of the most important may be the ability of S. paucimobilis to pass through the 0.2 μm filters that are used for the terminal sterilisation of several medicinal products, e.g. sterile drug solutions (17). Investigations in our laboratory have also found that S. paucimobilis can penetrate 0.2 μm filters (1).
Other sources of infections have included mechanical ventilators such as in a Belgian neonatal intensive care unit were the source of tracheal colonization in 85 mechanically ventilated babies. The temperature probes of the ventilators were found to be the source of contamination, and proper sterilization of the probes was successful in eradicating the organism from the unit (16). In a pediatric ward, it has been isolated from the atomizer units of cool mist tents (5). In this instance, the atomizer units repeatedly grew S. paucimobilis during routine maintenance cultures despite decontamination and sterilization with sterile water. Further investigations revealed a leaking ice chamber that was thought to be responsible for the contamination. Fortunately, no human cases were reported and the cultures became sterile after the cooling ice was placed in plastic bags. In one Japanese hospital, water obtained from a reverse osmosis system, as well as from an ultra-filtration unit tested positive for S. paucimobilis, and the level of contamination was higher than that in tap water from the same hospital. Further studies showed a correlation between the chlorine level in the water and the amount of growth of this organism, suggesting that chlorination of the water may have some inhibitory effect on its growth (22). The organism has also been grown in low numbers from dialysis water, although no infection was reported around the time of isolation of the organism (5, 17). In many cases of infection the aetiology of S. paucimobilis was unknown (28).
Clinical Manifestations
Initially S. paucimobilis was thought to be a non-pathogenic environmental isolate (6) however it has since been reported to cause a variety of infections. Cases have included wound infections, meningitis (18, 20), a case of septic shock in a burns patient (3), catheter associated bacteremia (19), ventilator associated pneumonia (19), splenic abscess (32), urinary tract infection, empyema (7) and several cases of bacteremia and peritonitis (6, 8, 18, 19, 31). There have also been cases of invasive infections such as meningitis and osteomyelitis (34). Most infected persons are immunocompromised having underlying co-morbid medical illnesses, and several have an indwelling catheter that required removal in about half the cases for a cure. No deaths have yet been reported in association with S. paucimobilis. It has been isolated from many patients with no signs or symptoms attributable to infection due to this organism (9). Four patients were reported to have the organism isolated from maxillary sinus irrigation, and the saline irrigation solution was found be to be the contaminated with the organism. None of the patients had clinical disease (9). A breakdown of the instances of S. paucimobilis infection can be seen in Table 1.
Laboratory Diagnosis
The laboratory diagnosis is made by culturing the organism in appropriate media. The specimen could be blood, other bodily fluids or tissue, as appropriate, depending on the clinical presentation. The existing Biochemical Identification commercial systems that are offered on the market, e.g. the autoSCAN-W/A, the bioMérieux Vitek AutoMicrobic System or the bioMérieux API 20NE, do not always give the most dependable identification for some genera and species, especially Gram-negative non-fermenting rods including S. paucimobilis, which is hard to identify using the above standard biochemical test kits (33). No species specific PCR primers exist for S. paucimobilis however both genus specific PCR primers and a selective media for Sphingomonas species is available (37).
Pathogenesis
It does not display the virulence typically associated with other pseudomonads and this has been attributed to the lack of the typical LPS capsule (18). A recent study has identified several virulence genes in the genome of S. paucimobilis. that have similarity to those of Pseudomonas aeruginosa including Pyoverdine and Pyochelin (sidephores-iron chelating agents), alginate genes (alginate, an anionic polysaccharide, can have antiphagocytosis activity), Rhamnolipid (a biosurfactant), Phospholipase C (a toxin), several Protease genes (Alkaline protease and LasA and LasB) and several genes involved in adherence such as flagella genes and Type IV pili genes (30). The effects the protein products of these genes might have in vivo is unknown.
SSUSCEPTIBILITY IN VITRO AND IN VIVO
Single Drug
In vitro susceptibility testing has shown that most strains of S. paucimobilis are susceptible to ampicillin, carbenicillin, ceftizoxime, cefotaxime, fluoroquinolones and trimethoprim/ sulfamethoxazole. It is usually resistant to piperacillin, first generation cephalosporins, cefmetazole and cefoperazone (19, 36). Unfortunately only one large scale study with 29 S. paucimobilis isolates has been carried out (Results can be seen in Table 2). No antibiotic resistance mechanisms have yet been elucidated for S. paucimobilis.
Combinations of Antimicrobials
There is no data available on combination therapy with two or more agents. Given the low mortality from this organism, combination therapy is not warranted in most patients.
ANTIMICROBIAL THERAPY
Drug of Choice
Infections due to S. paucimobilis have not been associated with mortality. Only one death was noted in all the reported cases, and the patient died due to Candida and P. aeruginosa bacteremia. Because of the limited number of cases, assessment of attributable mortality is difficult. Similarly, randomized, controlled trials of treatment are not possible. From the case reports and small case series, it appears that the patients recover, even if the initial therapy is with antibiotics to which the organism is subsequently found to be resistant. Fluoroquinolones, third generation cephalosporins, and carbapenems seem to have excellent activity, and each may be used as initial therapy (2, 21, 17). As with all infections, patients must be carefully monitored for response, and care providers should be aware of local antibiotic susceptibility patterns. Therapy should be adjusted when the susceptibility results are available, or if the patient fails to respond to initial therapy. The organism has variable susceptibility to aminoglycosides, and was reported to be resistant to aztreonam and piperacillin in one report (15).
A study carried out on an outbreak of S. paucimobilis in a pediatric hospital the carbapenem group of antibiotics was found to be the most effective in treating a range of infections (4). The drug of choice may be a fluoroquinolone because of the susceptibility patterns and ease of administration. Levofloxacin in a dose of 500 mg per day for 2 weeks, or ciprofloxacin 500 mg twice a day for 2 weeks are good choices. Other newer fluoroquinolones may be substituted based on local availability or cost. Alternatively, a third generation cephalosporin such as cefotaxime in a dose of 1 gram every 8 hours, or a carbepenam such as imipenem in the dose of 500 mg every six hours may be used. Piperacillin-tazobactam (150 mg/kg/day) may also be effective (23).
Combination Therapy
There is no good data on combination therapy with two drugs for S. paucimobilis.
ADJUNCTIVE THERAPY
The removal of infected catheters or medical devices is indicated in many patients. The case for removal of such catheters and devices has to be individualized, based on the need and utility of the catheter or device and the risk of ongoing infection. No controlled trials have been performed to answer this question specifically. It would seem prudent to remove such devices in patients who are very sick and those who do not respond promptly to initial antimicrobial therapy.
ENDPOINTS FOR MONITORING THERAPY
Success of therapy is measured by clinical resolution of infection. Negative blood cultures in bacteremic patients document bacteriologic cure. The need for repeat cultures in patients who have responded well to therapy has not been studied for this organism.
VACCINES
There are no available vaccines for this organism.
PREVENTION OR INFECTION CONTROL MEASURES
As with all other infections, universal precautions must be followed.
CAVEATS
There are no controlled trials of therapy for S. paucimobilis. All of the recommendations contained in this chapter are based on the results of in vitro susceptibility studies, case studies, and anecdotal reports.
COMMENTS
S. paucimobilis is a frequently encountered organism in the environment. It contaminates water supplies and hospital equipment. In addition to the occasional propensity to cause human disease, it is implicated in microbial influenced corrosion of water pipes. Because of their ability to accumulate copper in their cell walls, Sphingomonas spp. can bind to copper in the copper containing water pipes, facilitating an anodic reaction and corrosion of copper (35). Heating the water to 64°C decreases these reactions and microbial growth, as does low concentrations of antibiotics like cefoxitin, in the circulating water (35).
Sphingomonas spp. show antagonism to some plant pathogens, such as the fungus Verticillium dahliae, which affects several commercial plant species. Several Sphingomonas species have been recovered from sub-surface tunnels, where they may account for up to 11% of the culturable bacteria. Many species (though not S. paucimobilis) can degrade toluene, naphthalene, benzoate and other refractory environmental contaminants, suggesting a potential role in ecological clearance of such materials, including use for oil spills (35). More research is needed to determine how much of a threat S. paucimobilis can be clinical situations.
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Tables
Table 1. Breakdown of conditions caused by Sphingomonas paucimobilis infections
| Condition | No. of instances reported in the Literature |
|---|---|
Bacteraemia/septicaemia |
25 |
Peritonitis |
6 |
Lung infections/pneumonia |
3 |
Urinary tract infection |
3 |
Pseudo-infection |
2 |
Leg ulcer |
2 |
Meningitis |
2 |
Septic Arthritis |
2 |
Osteomyelitis |
1 |
Endophthalmitis |
1 |
Bacteraemia/diarrhoeal disease |
1 |
Splenic abscess |
1 |
Empyema |
1 |
Bacteraemia/septic arthritis |
1 |
Bacteraemic biliary tract infection |
1 |
Cervical adenitis |
1 |
Wound infection |
1 |
Bromhidrosis |
1 |
Calf myositis |
1 |
Catheter-related sepsis |
1 |
Endophthalmitis |
1 |
Infection |
1 |
Pyomyoma |
1 |
Submandibular sialolithiasis |
1 |
Table 2. In vitro susceptibility of Sphingomonas paucimobilis to selected antibiotics
| Antibiotic | MIC50 mg/ml (range) | MIC90 mg/ml (range) | % of strains susceptibl | % of strains resistant | No. of strains tested |
|---|---|---|---|---|---|
Amikacin |
2 |
32 |
85.7 |
7.1 |
29 |
Amoxicillin/Clavulanate |
<2 |
>16 |
82.1 |
17.9 |
29 |
Aztreonam |
>16 |
>16 |
7.1 |
82.1 |
29 |
Ceftazidime |
4 |
>16 |
71.4 |
25 |
29 |
Cefepime |
4 |
>16 |
71.4 |
21.4 |
29 |
Ceftriaxone |
4 |
>32 |
71.4 |
17.9 |
29 |
Ciprofloxacin |
0.5 |
2 |
89.3 |
7.1 |
29 |
Gatifloxacin |
0.12 |
1 |
96.4 |
3.6 |
29 |
Gentamicin |
<2 |
>8 |
89.3 |
7.1 |
29 |
Imipenem |
<0.5 |
>8 |
85.7 |
14.3 |
29 |
Levofloxacin |
<0.5 |
1 |
94.6 |
3.6 |
29 |
Meropenem |
0.12 |
>8 |
85.7 |
10.7 |
29 |
Piperacillin |
32 |
>128 |
39.3 |
28.6 |
29 |
Piperacillin/Tazobactam |
4 |
64 |
75 |
7.1 |
29 |
Tetracycline |
<4 |
<4 |
96.4 |
3.6 |
29 |
Ticarcillin/Clavulanate |
<16 |
64 |
78.6 |
7.1 |
29 |
Tobramycin |
0.5 |
>16 |
67.9 |
25 |
29 |
Trimethoprim/Sulphamethoxazole |
<0.5 |
>2 |
89.3 |
10.7 |
29 |
Information for the table was taken from [29]
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