- Email: [email protected]
Urinary tract infection associated with Comamonas acidovorans
CORRESPONDENCE
Urinary tract infection associated with Cornamonas acidovorans
of infections caused by C. acidovorans have been sporadically reported, including endocarditis [ 3 ] ,ocular infections [4,5], acute suppurative otitis [6] and bacteremia [7-91. This microorganism has also been recovered from inhalation equipment and from clinical specimens, but it was considered to be a contaminant in these cases [lo]. The susceptibility pattern of our isolate shows a similar resistance phenotype to those strains reported previously. Although C. acidovorans is probably of low pathogenicity, its presence in any type of specimen would certainly warrant susceptibility testing. Because of the ubiquitous character of this microorganism, establishing its pathogenicity may be difficult. O u r patient presented with a clear case of UTI due to a Gram-negative rod. C. acidouorans was the only organism isolated from the urine of this patient and, since the symptoms resolved after the organism was eliminated by antibiotic treatment, we believe that this organism was the etiologic agent of the infection. Further studies should clarifj the precise contribution of C. acidovorans to the pathogenicity of infection, especially in irnmunocompromised patients.
Clin Microbiol Inject 1999; 5: 443-444 Cornamonas acidovorans (formerly Pseudomonas acidovorans) is a ubiquitous Gram-negative rod commonly found in soil and water. Although generally considered to be non-pathogenic, C. acidovorans has been associated with serious infections. In a comprehensive search of the scientific literature from the last 10 years (MEDLINE) we found no published case reports of urinary tract infections (UTIs) due to C. acidouorans. This paper appears to be the first report of the isolation of this microorganism from a U T I and its identification as a pathogen. A 61-year-old male with hemiplegia was hospitalized to allow the study of a vertiginous syndrome. Six days later, the patient developed oliguria and a vesical catheter was put in place to control diuresis. The patient’s clinical condition worsened, and he developed urethral discomfort and pyuria. The urine obtained at this time was strongly foul-smelling; the p H was 8 and the microscopic analysis showed pyuria (>50 leukocytes per high-power field), microhematuria and bacteriuria. The nitrite test was positive. Gram staining showed Gram-negative rods. Urine culture was done in CLED agar and yielded pure growth of Gram-negative, oxidase-positive rods (> 100 000 CFU/mL urine). The biochemical characteristics of the isolate were studied with the API 20 N E system (bioMerieux, Marcy l’Etoile, France). The strain was identified as C. acidouorans by the API 20 NE identification system; its analytical profile was 1004466. Antimicrobial susceptibility measured by the disk agar diffusion method showed that our strain was susceptible to ticarcillin, cefotaxime, aztreonam, imipenem, norfloxacin, ciprofloxacin and co-trimoxazole and resistant to ampicillim, tobramicin, amikacin and fosfomicin. The patient was treated with a 2-week course of norfloxacin (400 mg orally twice daily). A prompt therapeutic response was acoinpanied by resolution of the dysuria and frequency. Further urine analysis showed four to seven leukocytes per highpower field, and cultures were negative. The genus Cornamonas was created in 1985 by De Vos et a1 [l] and initially included only one species, C. terr
Maria del Mar Ojeda- thyas ‘, Andy& Strhrez-Alonso I , Maria de 10s Angela Pbrez-Ceruantes 2r Esther SuCirez-Gil and Carmelo A40nz6n-MorenoL * Servicio de Microbiologia, Hospital Insular de Gran Canaria, ’UD Microbiologia, Centro de Ciencias de la Salud, ULPGC, PO Box 550, 35080 Las Palmas de Gran Canaria, Canary Islands, Spain
’
*Tel: +928 45 34 05 Fax: +928 45 14 13 E-mail: [email protected]
References 1. De Vos P, Kersters K, Falsen E, et al. Comamonas Davis and Park 1962 gen. nov. nom. rev. emend., and Comarnonas terrtqena Hugh 1962 sp. nov., nom. rev. Int J Syst Bacteriol 1985; 35: 443-53. 2. Tamaoka J, Ha DM, Komagata K. Reclassification of Pseudomonar acidovorans den Dooren de Jong 1926 and Pseudomonas terfosteroni Marcus and Talalay 1956 as Cornamonas an’dotwans comb. nov. and Cornamonas tcstosteroni comb. nov., with an amended description of the genus Cornamonas. Int J Syst Bacteriol 1987; 37: 52-9. 3. Horowitz H, Gilroy S, Feinstein S, Gilardi G. Endocarditis
443
444
C l i n i c a l M i c r o b i o l o g y and I n f e c t i o n , Volume 5 N u m b e r 7, J u l y 1999
associated with Comamonas acidovorans. J Clin Microbiol 1990; 28: 1 4 S 5 . 4. Brinser JH, Torczynski E. Unusual Pseudomonas corneal ulcers. Am J Ophthalmol 1977; 84: 462. 5. Stonecipher KG, Jensen HG, Kastl PR, Faulkner A, Rowsey J. Ocular infections associated with Cornamonas acidovorans. Am J Ophthalmol 1991; 112: 46-9. 6. Reina J, Llompart I, Alomar P. Acute suppurative otitis caused by Cornamonas an'dovorans. Clin Microbiol Newslett 1991; 13: 38-9. 7. Castagnola E, Tasso L, Conte M, et al. Central venous catheterrelated infection due to Cornamonas acidovorans in a child with non-Hodgkm's lymphoma. Clin Infect Dis 1994; 29: 55940. 8. Ender PT, Dooley DP, Moore RH. Vascular catheter-related Cornamonas acidovorans bacteremia managed with preservation of the catheter. Pediatr Infect Dis J 1996; 15: 918-20. 9. Castagnola E, Conte M, Venzano P, et al. Broviac catheterrelated bacteraemias due to unusual pathogens in children with cancer: case report with literature review. J Infect 1997; 34(3): 215-1 8. 10. Weinstein RA, Stamm E, Kramer L, Corey L. Pressure monitoring devices: an overlooked source of nosocomial infection. JAMA 1976; 236: 936-8.
High-level cephalosporinase-producingEnterobacter cloacae meningitis in a newborn
Clin Microbiol Inzct 1999; 5: 444-446 Enterobacter cloacae is an uncommon cause of meningitis. The organism is known to mutate to produce large amounts of cephalosporinase able to hydrolyze thirdgeneration cephalosporins [l], which are often thought to be responsible for the selection of such resistant mutants. A newborn female, born at full term by vaginal delivery, was admitted to the neonatal intensive care unit with a lumbar meningomyelocele. Apgar scores were 10 and 10 at 1 and 5 min, respectively. Physical examination revealed an active neonate with only bladder dysfunction. No signs of neonatal infection were noted, and the serum C-reactive protein (CRP) level was less than 10 mg/L. Surgical closure of the meningomyelocele was performed 2 days later (day 3). Preoperative smears of the meningomyelocele were obtained for bacteriologic culture, and scanty Staphylococcus haemolyticus, Escherichia
coli and Enterobacter cloacae were isolated. Postoperatively, the patient became subfebrile. The peripheral white blood cell count was 10760/mm3, including 63% polymorphonuclear leukocytes and 21% lymphocytes, and serum C R P increased to 37 mg/L on day 4 and then to 99 mg/L on day 5. The antibiotic susceptibilities of the Enterobacter cloacae is shown in Table 1. Therapy was initiated on day 5 with cefotaxime and vancomycin given intravenously (50 mg/kg 6-hourly and 10 mg/kg 12-hourly, respectively). Eight days after surgery, the patient had a rectal temperature between 38 and 39OC, and developed vomiting, a stiff neck and convulsions. She developed severe apnea and brachycardia which required mechanical ventilation. Serum C R P levels remained increased at 196 mg/L on day 11, when we replaced vancomycin with fosfomycin (100 mg/kg 12-hourly). O n day 12, cerebrospinal fluid cultures yielded Enterobacter cloacae. Cerebrospinal fluid (CSF) contained 1094 nucleated cells/mm3 (86%neutrophils, 14% monocytes). This isolate was susceptible in vitro to carbapenems, cefepime, ciprofloxacin, fosfomycin and aminoglycosides but was shown to produce high-level, derepressed cephalosporinase. In order to verify that the two Enterobacter cloacae isolates were clondy related, pulsedfield gel electrophoresis was performed on intact DNA preparations, as previously described for S. aureus [2], except that lysostaphin was not added (Figure 1). The results indicated that the two isolates were related. The second strain was therefore considered to be a resistant mutant of the previous strain. This prompted us to replace cefotaxime with imipenem (50 mg/kg three times daily). However, the infant developed ventricular dilatation, and on day 15 a ventricular external shunt was put in place. At this time, the CSF white cell count was 230/mm3, with 98% polymorphonuclear leukocytes, the protein content was 439 mg/mL and no glucose was found in the CSE Enterobacter cloacae was isolated from further CSF cultures. On day 17, because of poor CSF concentrations of imipenem (day 17, 1 mg/L; day 18, 0.1 mg/L) and according to previously published data [3], cefepime (37.5 mg/kg every 6 h) was substituted and on day 19 amikacin (7.5 mg/kg every 12 h) was added. The in vitro bactericidal activity of this combination was
Table 1 Antibiotic susceptibhty of the two strains isolated from cerebrospinal fluid before and after treatment with cefotaxime Methods
Antibiotics
Enterobacter cloacae 1
Enterobacter cloacae 2
MIC/MBC by macro broth dilutions (mg/L)
Amikacin Cefotaxime Cefepime Imipenem
4/16 1/4 4/16 2/32
4/16 32/256 4/16 4/32
Urinary tract infection associated with Cornamonas acidovorans
of infections caused by C. acidovorans have been sporadically reported, including endocarditis [ 3 ] ,ocular infections [4,5], acute suppurative otitis [6] and bacteremia [7-91. This microorganism has also been recovered from inhalation equipment and from clinical specimens, but it was considered to be a contaminant in these cases [lo]. The susceptibility pattern of our isolate shows a similar resistance phenotype to those strains reported previously. Although C. acidovorans is probably of low pathogenicity, its presence in any type of specimen would certainly warrant susceptibility testing. Because of the ubiquitous character of this microorganism, establishing its pathogenicity may be difficult. O u r patient presented with a clear case of UTI due to a Gram-negative rod. C. acidouorans was the only organism isolated from the urine of this patient and, since the symptoms resolved after the organism was eliminated by antibiotic treatment, we believe that this organism was the etiologic agent of the infection. Further studies should clarifj the precise contribution of C. acidovorans to the pathogenicity of infection, especially in irnmunocompromised patients.
Clin Microbiol Inject 1999; 5: 443-444 Cornamonas acidovorans (formerly Pseudomonas acidovorans) is a ubiquitous Gram-negative rod commonly found in soil and water. Although generally considered to be non-pathogenic, C. acidovorans has been associated with serious infections. In a comprehensive search of the scientific literature from the last 10 years (MEDLINE) we found no published case reports of urinary tract infections (UTIs) due to C. acidouorans. This paper appears to be the first report of the isolation of this microorganism from a U T I and its identification as a pathogen. A 61-year-old male with hemiplegia was hospitalized to allow the study of a vertiginous syndrome. Six days later, the patient developed oliguria and a vesical catheter was put in place to control diuresis. The patient’s clinical condition worsened, and he developed urethral discomfort and pyuria. The urine obtained at this time was strongly foul-smelling; the p H was 8 and the microscopic analysis showed pyuria (>50 leukocytes per high-power field), microhematuria and bacteriuria. The nitrite test was positive. Gram staining showed Gram-negative rods. Urine culture was done in CLED agar and yielded pure growth of Gram-negative, oxidase-positive rods (> 100 000 CFU/mL urine). The biochemical characteristics of the isolate were studied with the API 20 N E system (bioMerieux, Marcy l’Etoile, France). The strain was identified as C. acidouorans by the API 20 NE identification system; its analytical profile was 1004466. Antimicrobial susceptibility measured by the disk agar diffusion method showed that our strain was susceptible to ticarcillin, cefotaxime, aztreonam, imipenem, norfloxacin, ciprofloxacin and co-trimoxazole and resistant to ampicillim, tobramicin, amikacin and fosfomicin. The patient was treated with a 2-week course of norfloxacin (400 mg orally twice daily). A prompt therapeutic response was acoinpanied by resolution of the dysuria and frequency. Further urine analysis showed four to seven leukocytes per highpower field, and cultures were negative. The genus Cornamonas was created in 1985 by De Vos et a1 [l] and initially included only one species, C. terr
Maria del Mar Ojeda- thyas ‘, Andy& Strhrez-Alonso I , Maria de 10s Angela Pbrez-Ceruantes 2r Esther SuCirez-Gil and Carmelo A40nz6n-MorenoL * Servicio de Microbiologia, Hospital Insular de Gran Canaria, ’UD Microbiologia, Centro de Ciencias de la Salud, ULPGC, PO Box 550, 35080 Las Palmas de Gran Canaria, Canary Islands, Spain
’
*Tel: +928 45 34 05 Fax: +928 45 14 13 E-mail: [email protected]
References 1. De Vos P, Kersters K, Falsen E, et al. Comamonas Davis and Park 1962 gen. nov. nom. rev. emend., and Comarnonas terrtqena Hugh 1962 sp. nov., nom. rev. Int J Syst Bacteriol 1985; 35: 443-53. 2. Tamaoka J, Ha DM, Komagata K. Reclassification of Pseudomonar acidovorans den Dooren de Jong 1926 and Pseudomonas terfosteroni Marcus and Talalay 1956 as Cornamonas an’dotwans comb. nov. and Cornamonas tcstosteroni comb. nov., with an amended description of the genus Cornamonas. Int J Syst Bacteriol 1987; 37: 52-9. 3. Horowitz H, Gilroy S, Feinstein S, Gilardi G. Endocarditis
443
444
C l i n i c a l M i c r o b i o l o g y and I n f e c t i o n , Volume 5 N u m b e r 7, J u l y 1999
associated with Comamonas acidovorans. J Clin Microbiol 1990; 28: 1 4 S 5 . 4. Brinser JH, Torczynski E. Unusual Pseudomonas corneal ulcers. Am J Ophthalmol 1977; 84: 462. 5. Stonecipher KG, Jensen HG, Kastl PR, Faulkner A, Rowsey J. Ocular infections associated with Cornamonas acidovorans. Am J Ophthalmol 1991; 112: 46-9. 6. Reina J, Llompart I, Alomar P. Acute suppurative otitis caused by Cornamonas an'dovorans. Clin Microbiol Newslett 1991; 13: 38-9. 7. Castagnola E, Tasso L, Conte M, et al. Central venous catheterrelated infection due to Cornamonas acidovorans in a child with non-Hodgkm's lymphoma. Clin Infect Dis 1994; 29: 55940. 8. Ender PT, Dooley DP, Moore RH. Vascular catheter-related Cornamonas acidovorans bacteremia managed with preservation of the catheter. Pediatr Infect Dis J 1996; 15: 918-20. 9. Castagnola E, Conte M, Venzano P, et al. Broviac catheterrelated bacteraemias due to unusual pathogens in children with cancer: case report with literature review. J Infect 1997; 34(3): 215-1 8. 10. Weinstein RA, Stamm E, Kramer L, Corey L. Pressure monitoring devices: an overlooked source of nosocomial infection. JAMA 1976; 236: 936-8.
High-level cephalosporinase-producingEnterobacter cloacae meningitis in a newborn
Clin Microbiol Inzct 1999; 5: 444-446 Enterobacter cloacae is an uncommon cause of meningitis. The organism is known to mutate to produce large amounts of cephalosporinase able to hydrolyze thirdgeneration cephalosporins [l], which are often thought to be responsible for the selection of such resistant mutants. A newborn female, born at full term by vaginal delivery, was admitted to the neonatal intensive care unit with a lumbar meningomyelocele. Apgar scores were 10 and 10 at 1 and 5 min, respectively. Physical examination revealed an active neonate with only bladder dysfunction. No signs of neonatal infection were noted, and the serum C-reactive protein (CRP) level was less than 10 mg/L. Surgical closure of the meningomyelocele was performed 2 days later (day 3). Preoperative smears of the meningomyelocele were obtained for bacteriologic culture, and scanty Staphylococcus haemolyticus, Escherichia
coli and Enterobacter cloacae were isolated. Postoperatively, the patient became subfebrile. The peripheral white blood cell count was 10760/mm3, including 63% polymorphonuclear leukocytes and 21% lymphocytes, and serum C R P increased to 37 mg/L on day 4 and then to 99 mg/L on day 5. The antibiotic susceptibilities of the Enterobacter cloacae is shown in Table 1. Therapy was initiated on day 5 with cefotaxime and vancomycin given intravenously (50 mg/kg 6-hourly and 10 mg/kg 12-hourly, respectively). Eight days after surgery, the patient had a rectal temperature between 38 and 39OC, and developed vomiting, a stiff neck and convulsions. She developed severe apnea and brachycardia which required mechanical ventilation. Serum C R P levels remained increased at 196 mg/L on day 11, when we replaced vancomycin with fosfomycin (100 mg/kg 12-hourly). O n day 12, cerebrospinal fluid cultures yielded Enterobacter cloacae. Cerebrospinal fluid (CSF) contained 1094 nucleated cells/mm3 (86%neutrophils, 14% monocytes). This isolate was susceptible in vitro to carbapenems, cefepime, ciprofloxacin, fosfomycin and aminoglycosides but was shown to produce high-level, derepressed cephalosporinase. In order to verify that the two Enterobacter cloacae isolates were clondy related, pulsedfield gel electrophoresis was performed on intact DNA preparations, as previously described for S. aureus [2], except that lysostaphin was not added (Figure 1). The results indicated that the two isolates were related. The second strain was therefore considered to be a resistant mutant of the previous strain. This prompted us to replace cefotaxime with imipenem (50 mg/kg three times daily). However, the infant developed ventricular dilatation, and on day 15 a ventricular external shunt was put in place. At this time, the CSF white cell count was 230/mm3, with 98% polymorphonuclear leukocytes, the protein content was 439 mg/mL and no glucose was found in the CSE Enterobacter cloacae was isolated from further CSF cultures. On day 17, because of poor CSF concentrations of imipenem (day 17, 1 mg/L; day 18, 0.1 mg/L) and according to previously published data [3], cefepime (37.5 mg/kg every 6 h) was substituted and on day 19 amikacin (7.5 mg/kg every 12 h) was added. The in vitro bactericidal activity of this combination was
Table 1 Antibiotic susceptibhty of the two strains isolated from cerebrospinal fluid before and after treatment with cefotaxime Methods
Antibiotics
Enterobacter cloacae 1
Enterobacter cloacae 2
MIC/MBC by macro broth dilutions (mg/L)
Amikacin Cefotaxime Cefepime Imipenem
4/16 1/4 4/16 2/32
4/16 32/256 4/16 4/32