Diagnostic Microbiology and Infectious Disease 79 (2014) 108–110
Contents lists available at ScienceDirect
Diagnostic Microbiology and Infectious Disease journal homepage: www.elsevier.com/locate/diagmicrobio
Case Reports
Muscular abscess caused by Cupriavidus gilardii in a renal transplant recipient☆ Daniel Tena a,⁎, Cristina Losa a, María José Medina b, Juan Antonio Sáez-Nieto b a b
Sección de Microbiología, Hospital Universitario de Guadalajara, Guadalajara, Spain Servicio de Bacteriología, Centro Nacional de Microbiología, Majadahonda, Madrid, Spain
a r t i c l e
i n f o
Article history: Received 12 August 2013 Received in revised form 13 January 2014 Accepted 21 January 2014 Available online 30 January 2014 Keywords: Cupriavidus species Cupriavidus gilardii Muscular abscess Renal transplant Immunocompromised patient
a b s t r a c t Cupriavidus gilardii is a rare cause of human infection. We report a muscular abscess on the right thigh caused by this organism in a renal transplant recipient, who had suffered a septic shock associated with an extensive cellulitis caused by Streptococcus pyogenes. The patient was successfully treated with surgical drainage and intravenous ciprofloxacin for 13 days. This is the first time that C. gilardii is isolated from a human abscess. C. gilardii should be considered as a cause of human infection, especially in immunocompromised patients. Infection caused by this organism may be underdiagnosed because the identification is very difficult. © 2014 Elsevier Inc. All rights reserved.
1. Introduction
2. Case report
Cupriavidus spp. are ubiquitous environmental organisms that are mostly found in soil, water, and plants. This organism is not commonly isolated from clinical specimens. Actually, there are 13 species described, but species known to cause human disease include Cupriavidus pauculus (formerly CDC group IV c-2), Cupriavidus gilardii, and Cupriavidus metallidurans (Langevin et al., 2011; Vay et al., 2007; Wauters et al., 2001). C. pauculus is the species most frequently isolated. C. pauculus is a rare but recognized cause of bacteremia, especially in patients with hematologic malignances and AIDS (Anderson et al., 1997; Arance et al., 1997; Musso et al., 1994). In addition, there have been reported nosocomial outbreaks caused by C. pauculus associated with contamination of equipments or tap water (Balada-Llasat et al., 2010; Stovall et al., 2010). However, C. gilardii rarely causes human infections. To our knowledge, only 2 clinical infections have been previously reported (Karafin et al., 2010; Wauters et al., 2001). In the present report, we describe a muscular abscess on the right thigh caused by C. gilardii in an immunocompromised patient, who had suffered a septic shock associated with an extensive cellulitis caused by Streptococcus pyogenes. This is the first time that C. gilardii is isolated from a human abscess.
A 36-year-old man with a history of renal transplant in treatment with prednisone, tacrolimus, and mycophenolic acid was admitted to our hospital, with a 24-h history of intense pain on the right thigh and difficulty for walking. There was no history of trauma. On admission, the patient appeared with bad general aspect but conscious. Vital signs were the following: blood pressure, 110/80 mm Hg; respiratory rate, 40 breaths/min; heart rate, 50 beats/min; oxygen saturation of 100% on ambient air and temperature of 39 °C. Examination of the right thigh revealed marked edema with intense pain to palpation. The skin appeared painful, cold, erythematous, and smelly. Pulses were detected, and a small wound was observed on the right arm without apparent exudate. Blood parameters revealed the following values: white blood cells 18.370/mm 3 (neutrophils 97.1%, lymphocytes 1.3%, monocytes 1.5%), creatinine 5.7 mg/dL, and creatine kinase 548 IU/L. The rest of blood parameters were within normal limits. The ultrasound scan of the right thigh revealed diffuse edema of the subcutaneous cellular tissue without signs of abscess. The patient was transferred to the intensive care unit due to a multi-organ failure. Blood samples were obtained for culture and aggressive management with intravenous fluids and vasoactive drugs, and empiric antibiotic treatment with meropenem (1 g/12 h i.v.), linezolid (600 mg/12 h i.v.), and voriconazole (3 mg/kg of body weight/12 h i.v.) was initiated. A day after, examination with abdominopelvic computed tomography (CT) revealed an increased subcutaneous cellular tissue on the right hemipelvis and a located abscess on the right flank. The abscess was evacuated by percutaneous drainage, and purulent fluid was obtained for culture. In addition, a surgical debridement was performed without opening of the fascia. Gram stain of the aspirate revealed abundant leukocytes and gram-positive cocci grouped in pairs. S. pyogenes was
☆ Conflict of interest: The authors declare no conflicts of interests. ⁎ Corresponding author. Tel.: +34-949-209236; fax: +34-949-209213. E-mail address: [email protected] (D. Tena). 0732-8893/$ – see front matter © 2014 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.diagmicrobio.2014.01.023
D. Tena et al. / Diagnostic Microbiology and Infectious Disease 79 (2014) 108–110
isolated from the blood and the abscess aspirate using conventional methods. The strain was susceptible to penicillin and clindamycin. Treatment with voriconazole was discontinued, and clindamycin was added (600 mg/8 h i.v.). Additional debridements of necrotic material were necessary in the following days and the patient progressively improved. Twenty days after admission, a new CT was performed, and 2 subfascial abscesses were observed on the right thigh. A surgery intervention was performed by opening the fascia, and the abscesses were drained. Two samples were obtained for culture. The Gram stain of both samples revealed gram-negative rods. After 24 h of incubation, the strain grew on Columbia agar and McConkey agar. The isolate was nonfermenting and oxidase positive. The Vitek system (bioMerieux, Marcy L´Etoile, France) and the API 20 NE system (bioMèrieux) failed to identify the organism. The isolate was sent to the National Center of Microbiology (Majadahonda, Madrid, Spain) for identification. The 16S rDNA sequence analysis of a fragment of 1333 bp obtained by a PCR method previously described (Drancourt et al., 2000) showed a homology of 99.3% with C. gilardii from the GenBank (accession number EF114428 and others). Antimicrobial susceptibility testing was performed using the disk diffusion method on Muller-Hinton agar plates incubated for 24 h. The breakpoints used were those defined by the CLSI for other non-Enterobacteriaceae (CLSI, 2013). The strain was susceptible to cefuroxime, cefotaxime, ciprofloxacin, amikacin, trimethoprim/sulfamethoxazole, and tigecycline and resistant to penicillin, amoxicillin/clavulanic acid, imipenem, meropenem, gentamicin, and tobramycin. After knowing the result of the antibiogram, treatment with linezolid was discontinued, and ciprofloxacin was added (200 mg/12 h i.v.). Surgical cures were performed daily, and the patient's condition gradually improved. Twenty-five days after admission, the patient was transferred to the surgery ward, and antibiotic treatment with meropenem, clindamycin and ciprofloxacin was continued for 10 more days. A rehabilitation program was initiated due to difficulty for moving the right hip. The patient was discharged from the hospital 35 days after admission and continues in an intensive rehabilitation program.
3. Discussion C. gilardii is an aerobic, Gram-negative, glucose-nonfermenting bacillus that was first identified by Coenye et al. (1999). This organism has been isolated from a number of ecological niches, including plants and soils contaminated with heavy metals (Coenye et al., 2002). The taxonomic history for this species is complex. The organism has been known by various names, including Ralstonia gilardii, Wautersia gilardii, and C. gilardii (Vandamme and Coenye, 2004; Wauters et al., 2001). C. gilardii rarely causes human infection. Only 2 clinical infections have been previously reported, including a catheter sepsis in a child with acute lymphoblastic leukemia, and a fatal sepsis in a child with aplastic anemia (Karafin et al., 2010; Wauters et al., 2001). C. gilardii has been identified in respiratory secretions of cystic fibrosis patients, but the clinical role is unclear (Coenye et al., 2002). Furthermore, C. gilardii has been isolated from cerebrospinal fluid, a furuncle, and a bone marrow, but no information on clinical relevance is available (Coenye et al., 1999). In our case, C. gilardii was clinically significant because the organism was isolated from 2 subfascial abscesses in pure culture, and samples were obtained after surgery. In addition, the strain was resistant to meropenem, and the patient was previously treated with this antibiotic for 6 days. This finding suggests that the infection could be mixed from the beginning and that C. gilardii was selected after the treatment with meropenem. It's possible that C. gilardii was not initially isolated due to a low bacterial inoculum or due to a high growth of S. pyogenes. However, we cannot rule out the possibility of a superinfection caused by C. gilardii. It's also possible that the organism could be introduced during the postdrainage management of the presenting S. pyogenes soft tissue
109
abscess. The source of the infection is difficult to determine. The origin could be environmental because Cupriavidus spp. has been usually isolated from environmental niches (Coenye et al., 2002; Langevin et al., 2011); however, the portal of entry in this case is not known. Unfortunately, environmental cultures were not performed. Our patient illustrates that infections caused by environmental organisms can occasionally occur in immunocompromised hosts. The pathogenic mechanisms of Cupriavidus spp. in human infections are unknown. The rare occurrence of this organism among clinical isolates and the high frequency in immunocompromised patients reflect its low pathogenicity. Identification of Cupriavidus spp. based on conventional methods is very difficult and should be confirmed with molecular assays. Consequently, the frequency of this infection can be masked because this organism could be underdiagnosed. The 16S rDNA gene sequencing appears to be useful for the identification of Cupriavidus spp. (Langevin et al., 2011; Wauters et al., 2001). In the last past years, the taxonomy laboratory of reference in Spain has identified another 21 strains of the genus Cupriavidus using this method, including: C. pauculus (13 strains), C. metallidurans (6), Cupriavidus basilensis (1) and Cupriavidus respiraculi (1) (data not published). There is no information about the clinical significance of these isolates. Cupriavidus spp. is usually resistant to many antibiotics, including ampicillin, amoxicillin/clavulanic acid, gentamicin, and tobramycin (Ramos et al., 1993; Vay et al., 2007; Wauters et al., 2001). All isolates previously reported have been found to be active in vitro to ciprofloxacin (Azcona-Gutiérrez et al., 2008; Ramos et al., 1993; Vay et al., 2007; Wauters et al., 2001). Resistance to cotrimoxazole, piperacillin/tazobactam, and cefotaxime is very infrequent, and the activity of amikacin has been reported as variable (Arduino et al., 1993; Karafin et al., 2010; Vay et al., 2007). Like our isolate, C. gilardii can be resistant to imipenem, resulting in difficulty with treatment (Karafin et al., 2010). The optimal therapeutic regimen for treating infections caused by Cupriavidus spp. remains unclear because of the limited data. Patients with bacteremia have been successfully treated with third-generation cephalosporins (associated or not with amikacin), imipenem, and ciprofloxacin (Arance et al., 1997; Moissenet et al., 1996; Ramos et al., 1993; Vay et al., 2007). Other infections, such as peritonitis in patients on continuous ambulatory peritoneal dialysis, have been cured after treating with ciprofloxacin or cotrimoxazole, but removal of the intraperitoneal catheter is usually required (Ramos et al., 1993; Zapardiel et al., 1991). Our patient was successfully treated with ciprofloxacin when the antibiogram was available, but surgical drainage is the most important procedure for treating clinical abscesses. Although the clinical evolution of infections due to Cupriavidus spp. is usually good, cases with fatal outcome have been described, especially in patients with hematologic malignances (Karafin et al., 2010; Salar et al., 1998). In conclusion, C. gilardii should be considered as a cause of human infection, especially in immunocompromised patients. Infection caused by this organism may be underdiagnosed because the identification is very difficult. More cases will be required in the future to identify sources of infection and therapeutic options. References Anderson RR, Warnick P, Schreckenberger PC. Recurrent CDC IV c-2 bacteremia in a human with AIDS. J Clin Microbiol 1997;35:780–2. Arance A, Montes A, Cisnal M, Mesía R, Falo C, García del Muro J, et al. CDC group IV c-2 infection in a stem cell transplant recipient. Bone Marrow Transplant 1997;20: 1005–6. Arduino S, Villar H, Veron MT, Koziner B, Dictar M. CDC Group IV c-2 as a cause of catheter-related sepsis in an immunocompromised patient. Clin Infect Dis 1993;17: 512–3. Azcona-Gutiérrez JM, Buendía-Moreno B, Sáez-Nieto JA, López-Brea-Calvo M. Aislamiento de Cupriavidus pauculus en la unidad de cuidados intensivos. Enferm Infecc Microbiol Clin 2008;26:397–8. (in Spanish). Balada-Llasat JM, Elkins C, Swyers L, Bannerman T, Pancholi P. Pseudo-outbreak of Cupriavidus pauculus infection in an outpatient clinic related to rinsing culturette swabs in tap water. J Clin Microbiol 2010;48:2645–7.
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Clinical and Laboratory Standards Institute (CLSI). Performance standards for antimicrobial susceptibility testing, 23th informational supplement. M100-S23, vol. 33, no. 1. Wayne, PA: CLSI; 2013. Coenye T, Falsen E, Vancanneyt M, Hoste N, Govan JRW, Kersters K, et al. Classification of some Alcaligenes faecalis-like isolates from the environment and human clinical samples as Ralstonia gilardii sp. Nov. Int J Syst Bacteriol 1999;49:405–13. Coenye T, Vandamme P, LiPuma JJ. Infection by Ralstonia species in cystic fibrosis patients: identifications of R. pickettii and R. mannitolytica by polymerase chain reaction. Emerg Infect Dis 2002;8:692–6. Drancourt M, Bollet C, Carliotz A, Martelin R, Gayralt JP, Raoult D. 16s ribosomal DNA sequence analysis of a large collection of environmental and clinical identified bacterial isolates. J Clin Microbiol 2000;38:2623–30. Karafin M, Romagnoli M, Fink DL, Howard T, Rau R, Milstone AM, et al. Fatal infection caused by Cupriavidus gilardii in a child with aplastic anemia. J Clin Microbiol 2010;48:1005–7. Langevin S, Vincelette J, Bekal S, Gaudreau C. First case of invasive human infection caused by Cupriavidus metallidurans. J Clin Microbiol 2011;49:744–5. Moissenet D, Tabone MD, Girardet JP, Leverger G, Garbarg-Chenon A, Vu-Thien H. Nosocomial CDC Group IV c-2 bacteremia: epidemiological investigation by randomly amplified polymorphic DNA analysis. J Clin Microbiol 1996;34: 1264–6.
Musso D, Drancourt M, Bardot J, Legre R. Human infection due to the CDC group IV c-2 bacterium: case report and review. Clin Infect Dis 1994;18:482–4. Ramos JM, Soriano F, Bernacer M, Esteban J, Zapardiel J. Infection caused by the nonfermentative gram-negative bacillus CDC Group IV c-2: case report and literature review. Eur J Clin Microbiol Infect Dis 1993;12:456–8. Salar A, Carratalá J, Zurita A, González-Barca E, Grañena A. Bacteremia caused by CDC Group IV c-2 in a patient with acute leukemia. Haematology 1998;83:670–2. Stovall SH, Wisdom C, McKamie W, Ware W, Dedman H, Fiser RT. Nosocomial transmission of Cupriavidus pauculus during extracorporeal membrane oxygenation. ASAIO J 2010;56:486–7. Vandamme P, Coenye T. Taxonomy of the genus Cupriavidus: a tale of lost and found. Int J Syst Evol Microbiol 2004;54:2285–9. Vay C, García S, Alperovich G, Almuzara M, Lasala MB, Famiglietti A. Bacteremia due to Cupriavidus pauculus (formerly CDC group IV c-2) in a hemodialysis patient. Clin Microbiol Newsl 2007;29:30–2. Wauters G, Claeys G, Verschraegen G, De Baere T, Vandecruys E, van Simaey L, et al. Case of catheter sepsis with Ralstonia gilardii in a child with acute lymphoblastic leukemia. J Clin Microbiol 2001;39:4583–4. Zapardiel J, Blum G, Caramelo C, Fernández-Roblas R, Rodríguez-Tudela JL, Soriano F. Peritonitis with CDC Group IV c-2 bacteria in a patient on continuous ambulatory peritoneal dialysis. Eur J Clin Microbiol Infect Dis 1991;10:509–11.
Contents lists available at ScienceDirect
Diagnostic Microbiology and Infectious Disease journal homepage: www.elsevier.com/locate/diagmicrobio
Case Reports
Muscular abscess caused by Cupriavidus gilardii in a renal transplant recipient☆ Daniel Tena a,⁎, Cristina Losa a, María José Medina b, Juan Antonio Sáez-Nieto b a b
Sección de Microbiología, Hospital Universitario de Guadalajara, Guadalajara, Spain Servicio de Bacteriología, Centro Nacional de Microbiología, Majadahonda, Madrid, Spain
a r t i c l e
i n f o
Article history: Received 12 August 2013 Received in revised form 13 January 2014 Accepted 21 January 2014 Available online 30 January 2014 Keywords: Cupriavidus species Cupriavidus gilardii Muscular abscess Renal transplant Immunocompromised patient
a b s t r a c t Cupriavidus gilardii is a rare cause of human infection. We report a muscular abscess on the right thigh caused by this organism in a renal transplant recipient, who had suffered a septic shock associated with an extensive cellulitis caused by Streptococcus pyogenes. The patient was successfully treated with surgical drainage and intravenous ciprofloxacin for 13 days. This is the first time that C. gilardii is isolated from a human abscess. C. gilardii should be considered as a cause of human infection, especially in immunocompromised patients. Infection caused by this organism may be underdiagnosed because the identification is very difficult. © 2014 Elsevier Inc. All rights reserved.
1. Introduction
2. Case report
Cupriavidus spp. are ubiquitous environmental organisms that are mostly found in soil, water, and plants. This organism is not commonly isolated from clinical specimens. Actually, there are 13 species described, but species known to cause human disease include Cupriavidus pauculus (formerly CDC group IV c-2), Cupriavidus gilardii, and Cupriavidus metallidurans (Langevin et al., 2011; Vay et al., 2007; Wauters et al., 2001). C. pauculus is the species most frequently isolated. C. pauculus is a rare but recognized cause of bacteremia, especially in patients with hematologic malignances and AIDS (Anderson et al., 1997; Arance et al., 1997; Musso et al., 1994). In addition, there have been reported nosocomial outbreaks caused by C. pauculus associated with contamination of equipments or tap water (Balada-Llasat et al., 2010; Stovall et al., 2010). However, C. gilardii rarely causes human infections. To our knowledge, only 2 clinical infections have been previously reported (Karafin et al., 2010; Wauters et al., 2001). In the present report, we describe a muscular abscess on the right thigh caused by C. gilardii in an immunocompromised patient, who had suffered a septic shock associated with an extensive cellulitis caused by Streptococcus pyogenes. This is the first time that C. gilardii is isolated from a human abscess.
A 36-year-old man with a history of renal transplant in treatment with prednisone, tacrolimus, and mycophenolic acid was admitted to our hospital, with a 24-h history of intense pain on the right thigh and difficulty for walking. There was no history of trauma. On admission, the patient appeared with bad general aspect but conscious. Vital signs were the following: blood pressure, 110/80 mm Hg; respiratory rate, 40 breaths/min; heart rate, 50 beats/min; oxygen saturation of 100% on ambient air and temperature of 39 °C. Examination of the right thigh revealed marked edema with intense pain to palpation. The skin appeared painful, cold, erythematous, and smelly. Pulses were detected, and a small wound was observed on the right arm without apparent exudate. Blood parameters revealed the following values: white blood cells 18.370/mm 3 (neutrophils 97.1%, lymphocytes 1.3%, monocytes 1.5%), creatinine 5.7 mg/dL, and creatine kinase 548 IU/L. The rest of blood parameters were within normal limits. The ultrasound scan of the right thigh revealed diffuse edema of the subcutaneous cellular tissue without signs of abscess. The patient was transferred to the intensive care unit due to a multi-organ failure. Blood samples were obtained for culture and aggressive management with intravenous fluids and vasoactive drugs, and empiric antibiotic treatment with meropenem (1 g/12 h i.v.), linezolid (600 mg/12 h i.v.), and voriconazole (3 mg/kg of body weight/12 h i.v.) was initiated. A day after, examination with abdominopelvic computed tomography (CT) revealed an increased subcutaneous cellular tissue on the right hemipelvis and a located abscess on the right flank. The abscess was evacuated by percutaneous drainage, and purulent fluid was obtained for culture. In addition, a surgical debridement was performed without opening of the fascia. Gram stain of the aspirate revealed abundant leukocytes and gram-positive cocci grouped in pairs. S. pyogenes was
☆ Conflict of interest: The authors declare no conflicts of interests. ⁎ Corresponding author. Tel.: +34-949-209236; fax: +34-949-209213. E-mail address: [email protected] (D. Tena). 0732-8893/$ – see front matter © 2014 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.diagmicrobio.2014.01.023
D. Tena et al. / Diagnostic Microbiology and Infectious Disease 79 (2014) 108–110
isolated from the blood and the abscess aspirate using conventional methods. The strain was susceptible to penicillin and clindamycin. Treatment with voriconazole was discontinued, and clindamycin was added (600 mg/8 h i.v.). Additional debridements of necrotic material were necessary in the following days and the patient progressively improved. Twenty days after admission, a new CT was performed, and 2 subfascial abscesses were observed on the right thigh. A surgery intervention was performed by opening the fascia, and the abscesses were drained. Two samples were obtained for culture. The Gram stain of both samples revealed gram-negative rods. After 24 h of incubation, the strain grew on Columbia agar and McConkey agar. The isolate was nonfermenting and oxidase positive. The Vitek system (bioMerieux, Marcy L´Etoile, France) and the API 20 NE system (bioMèrieux) failed to identify the organism. The isolate was sent to the National Center of Microbiology (Majadahonda, Madrid, Spain) for identification. The 16S rDNA sequence analysis of a fragment of 1333 bp obtained by a PCR method previously described (Drancourt et al., 2000) showed a homology of 99.3% with C. gilardii from the GenBank (accession number EF114428 and others). Antimicrobial susceptibility testing was performed using the disk diffusion method on Muller-Hinton agar plates incubated for 24 h. The breakpoints used were those defined by the CLSI for other non-Enterobacteriaceae (CLSI, 2013). The strain was susceptible to cefuroxime, cefotaxime, ciprofloxacin, amikacin, trimethoprim/sulfamethoxazole, and tigecycline and resistant to penicillin, amoxicillin/clavulanic acid, imipenem, meropenem, gentamicin, and tobramycin. After knowing the result of the antibiogram, treatment with linezolid was discontinued, and ciprofloxacin was added (200 mg/12 h i.v.). Surgical cures were performed daily, and the patient's condition gradually improved. Twenty-five days after admission, the patient was transferred to the surgery ward, and antibiotic treatment with meropenem, clindamycin and ciprofloxacin was continued for 10 more days. A rehabilitation program was initiated due to difficulty for moving the right hip. The patient was discharged from the hospital 35 days after admission and continues in an intensive rehabilitation program.
3. Discussion C. gilardii is an aerobic, Gram-negative, glucose-nonfermenting bacillus that was first identified by Coenye et al. (1999). This organism has been isolated from a number of ecological niches, including plants and soils contaminated with heavy metals (Coenye et al., 2002). The taxonomic history for this species is complex. The organism has been known by various names, including Ralstonia gilardii, Wautersia gilardii, and C. gilardii (Vandamme and Coenye, 2004; Wauters et al., 2001). C. gilardii rarely causes human infection. Only 2 clinical infections have been previously reported, including a catheter sepsis in a child with acute lymphoblastic leukemia, and a fatal sepsis in a child with aplastic anemia (Karafin et al., 2010; Wauters et al., 2001). C. gilardii has been identified in respiratory secretions of cystic fibrosis patients, but the clinical role is unclear (Coenye et al., 2002). Furthermore, C. gilardii has been isolated from cerebrospinal fluid, a furuncle, and a bone marrow, but no information on clinical relevance is available (Coenye et al., 1999). In our case, C. gilardii was clinically significant because the organism was isolated from 2 subfascial abscesses in pure culture, and samples were obtained after surgery. In addition, the strain was resistant to meropenem, and the patient was previously treated with this antibiotic for 6 days. This finding suggests that the infection could be mixed from the beginning and that C. gilardii was selected after the treatment with meropenem. It's possible that C. gilardii was not initially isolated due to a low bacterial inoculum or due to a high growth of S. pyogenes. However, we cannot rule out the possibility of a superinfection caused by C. gilardii. It's also possible that the organism could be introduced during the postdrainage management of the presenting S. pyogenes soft tissue
109
abscess. The source of the infection is difficult to determine. The origin could be environmental because Cupriavidus spp. has been usually isolated from environmental niches (Coenye et al., 2002; Langevin et al., 2011); however, the portal of entry in this case is not known. Unfortunately, environmental cultures were not performed. Our patient illustrates that infections caused by environmental organisms can occasionally occur in immunocompromised hosts. The pathogenic mechanisms of Cupriavidus spp. in human infections are unknown. The rare occurrence of this organism among clinical isolates and the high frequency in immunocompromised patients reflect its low pathogenicity. Identification of Cupriavidus spp. based on conventional methods is very difficult and should be confirmed with molecular assays. Consequently, the frequency of this infection can be masked because this organism could be underdiagnosed. The 16S rDNA gene sequencing appears to be useful for the identification of Cupriavidus spp. (Langevin et al., 2011; Wauters et al., 2001). In the last past years, the taxonomy laboratory of reference in Spain has identified another 21 strains of the genus Cupriavidus using this method, including: C. pauculus (13 strains), C. metallidurans (6), Cupriavidus basilensis (1) and Cupriavidus respiraculi (1) (data not published). There is no information about the clinical significance of these isolates. Cupriavidus spp. is usually resistant to many antibiotics, including ampicillin, amoxicillin/clavulanic acid, gentamicin, and tobramycin (Ramos et al., 1993; Vay et al., 2007; Wauters et al., 2001). All isolates previously reported have been found to be active in vitro to ciprofloxacin (Azcona-Gutiérrez et al., 2008; Ramos et al., 1993; Vay et al., 2007; Wauters et al., 2001). Resistance to cotrimoxazole, piperacillin/tazobactam, and cefotaxime is very infrequent, and the activity of amikacin has been reported as variable (Arduino et al., 1993; Karafin et al., 2010; Vay et al., 2007). Like our isolate, C. gilardii can be resistant to imipenem, resulting in difficulty with treatment (Karafin et al., 2010). The optimal therapeutic regimen for treating infections caused by Cupriavidus spp. remains unclear because of the limited data. Patients with bacteremia have been successfully treated with third-generation cephalosporins (associated or not with amikacin), imipenem, and ciprofloxacin (Arance et al., 1997; Moissenet et al., 1996; Ramos et al., 1993; Vay et al., 2007). Other infections, such as peritonitis in patients on continuous ambulatory peritoneal dialysis, have been cured after treating with ciprofloxacin or cotrimoxazole, but removal of the intraperitoneal catheter is usually required (Ramos et al., 1993; Zapardiel et al., 1991). Our patient was successfully treated with ciprofloxacin when the antibiogram was available, but surgical drainage is the most important procedure for treating clinical abscesses. Although the clinical evolution of infections due to Cupriavidus spp. is usually good, cases with fatal outcome have been described, especially in patients with hematologic malignances (Karafin et al., 2010; Salar et al., 1998). In conclusion, C. gilardii should be considered as a cause of human infection, especially in immunocompromised patients. Infection caused by this organism may be underdiagnosed because the identification is very difficult. More cases will be required in the future to identify sources of infection and therapeutic options. References Anderson RR, Warnick P, Schreckenberger PC. Recurrent CDC IV c-2 bacteremia in a human with AIDS. J Clin Microbiol 1997;35:780–2. Arance A, Montes A, Cisnal M, Mesía R, Falo C, García del Muro J, et al. CDC group IV c-2 infection in a stem cell transplant recipient. Bone Marrow Transplant 1997;20: 1005–6. Arduino S, Villar H, Veron MT, Koziner B, Dictar M. CDC Group IV c-2 as a cause of catheter-related sepsis in an immunocompromised patient. Clin Infect Dis 1993;17: 512–3. Azcona-Gutiérrez JM, Buendía-Moreno B, Sáez-Nieto JA, López-Brea-Calvo M. Aislamiento de Cupriavidus pauculus en la unidad de cuidados intensivos. Enferm Infecc Microbiol Clin 2008;26:397–8. (in Spanish). Balada-Llasat JM, Elkins C, Swyers L, Bannerman T, Pancholi P. Pseudo-outbreak of Cupriavidus pauculus infection in an outpatient clinic related to rinsing culturette swabs in tap water. J Clin Microbiol 2010;48:2645–7.
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