Comamonas testosteroni is an aerobic, motile, non-spore-forming, medium-to-long gram-negative bacillus which occurs singly or in pairs and is known to use testosterone.1 It is an environmental organism of worldwide distribution that is found in water, soil, and on plants.1 Indeed, it has also been found in the water of in-use hospital oxygen humidifier reservoirs.2 It is part of the Pseudomonas rRNA homology group III which is now classified in the Comamonadaceae family that includes the genera Comamonas, Delftia, and Acidovorax.1 Pseudomonas testosteroni and Pseudomonas acidovorans were reclassified as members of the genus Comamonas in 1987, of which Comamonas terrigena had been a sole species since 1985 when the genus was created.1,3 They were reclassified based on phenotypic characteristics, chemotaxonomic characters, and DNA homology.3 Comamonas acidovorans has since been reclassified as Delftia acidovorans.1 C. testosteroni received its name as it is reported that it decomposes testosterone, although this same property has been demonstrated by other Pseudomonas species and some fungi.3,4
The pathogenic potential of this organism has not been well recognized, and it is normally considered to be a commensal in most cases. The following is the description of a patient with septic shock secondary to C. testosteroni bacteremia who had metastatic esophageal carcinoma.
A 54-year-old previously well-functioning woman presented with a one-day history of right breast pain, chills, and fever of 40°C. She had a history of esophageal cancer with metastases to lung and bones and had been receiving chemotherapy for 6 months through an upper extremity peripherally inserted central venous catheter (PICC), which had been replaced 1 week earlier. On examination, she was found to be cachectic and lethargic, although arousable. She was hypotensive, with a blood pressure of 71/47 mm Hg, and tachycardic, with a heart rate of 118 beats per minute, and had a fever of 39°C. Her breathing was shallow, and her oxygen saturation was 92% with 2 L O2 via nasal cannula. There were decreased breath sounds at both apices. A chest radiograph revealed a right middle lobe infiltrate. The white blood cell count was 22,500 cells/mm3 and her serum lactate level was 1.7 units. She was admitted to the intensive care unit for septic shock unresponsive to fluid boluses and given cefepime, vancomycin, and azithromycin. Shortly after admission, she was intubated and given drotrecogin alfa, glucocorticosteroids, and pressor support with norepinephrine and vasopressin. On hospital day 2, 2/2 aerobic bottles inoculated with blood grew non-lactose-fermenting gram-negative rods, and the PICC was discontinued. Infectious disease was consulted, and the antibiotics were modified to cefepime and ciprofloxacin. Sputum cultures grew Pseudomonas aeruginosa, but the gram-negative bacillus that was isolated from blood cultures was subsequently identified as C. testosteroni. Cefepime was discontinued, and she was treated with ciprofloxacin for a total of 16 days, with resolution of her infection. Although she recovered from her C. testosteroni infection, she died approximately one year later secondary to esophageal cancer.
Comamonas testosteroni has traditionally been considered a nonpathogenic microorganism. To date, only 27 patients have been reported in the literature in which C. testosteroni (or P. testosteroni) was identified as a potential pathogen. Of these 27 patients, there was clinical information available for only 16 (Table 1).
The most commonly identified sites of infection were the abdominal cavity (6 cases) and, including the patient described herein, blood (6 cases). There were 2 patients in whom the organism was isolated from the cerebrospinal fluid, 1 patient with a urinary isolate, and 1 patient with nosocomial pneumonia in whom both C. testosteroni and C. acidovorans were isolated. Among the 6 patients with intraperitoneal isolates, 5 had perforated appendices. The sixth patient with an abdominal infection had alcoholic cirrhosis, ascites, and primary bacterial peritonitis. All of the individuals with abdominal infections survived.
Among the 6 patients with bacteremic infections, there were 2 infections in neonates. In 1 case, the child was stillborn, whereas the other child was premature. In both of these cases, there was maternal intravenous drug abuse, and both of the neonates died. Two patients with bacteremic infections, one of which was presumed to be endocarditis had no apparent predisposing risk factors for the development of this infection. The other 2 patients, one of whom is the subject of this case report, had metastatic cancer and indwelling central venous catheters. Thus, C. testosteroni is a potential pathogen in both immunocompromised and healthy individuals.
C. testosteroni has been isolated from environmental sources, such as soil and water, but has not been recognized to be a component of the endogenous human microflora. The isolation of this organism from 5 patients with perforated appendices is rather striking and suggests that this organism may have a unique ecological niche within the appendix.
C. testosteroni is susceptible to a wide variety of antibiotics including most cephalosporins, penicillins, aminoglycosides, fluoroquinolones, and trimethoprim/sulfamethoxazole. Beta-lactam antibiotics, along with other agents in some cases, were given to every one of the 15 patients who received therapy. Cefoxitin was the most frequently used antibiotic and was given to 5 patients. The isolate in this case was found to be sensitive to a broad range of antibiotics, including cefepime and ciprofloxacin and, as with most of the previously reported cases, her infection resolved with appropriate antibiotic therapy.
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