- Email: [email protected]
Isolation of Leclercia adecarboxylata from blood and burn wound after a hydrofluoric acid chemical injury
burns 35 (2009) 443–445
available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/burns
Case report
Isolation of Leclercia adecarboxylata from blood and burn wound after a hydrofluoric acid chemical injury M. Dalamaga a,b,*, M. Pantelaki c, K. Karmaniolas a, K. Daskalopoulou c, I. Migdalis a a
Department of Internal Medicine, NIMTS General Hospital, Athens, Greece Department of Clinical Biochemistry, Attikon University General Hospital, Athens University Medical School, Athens, Greece c Department of Clinical Microbiology, Elpis General Hospital, Athens, Greece b
article info Article history: Accepted 21 January 2008
1.
Introduction
Chemical injuries following exposure to hydrofluoric acid (HF) occur with ever-increasing frequency due to the wide use of this highly corrosive inorganic acid in research and industry [1,2]. The majority of exposures involve small surface areas and are from dilute HF [3]. Topical exposures to concentrated HF have a fatal outcome even if very small areas of body surface are involved due to systemic manifestations of hypocalcemia and hypomagnesemia [4] if severe. Leclercia adecarboxylata constitutes a rare opportunistic human pathogen [5]. L. adecarboxylata strains are rarely isolated from clinical specimens of hospitalized patients [5– 7]. Most strains have been isolated from peritoneal fluid [8–10], synovial fluid [11] as well as from sputum and wound exudates as part of a mixed microbial growth [12,13]. Few cases of bacteremia in patients with compromised immunity and chronic inflammation diseases are cited in the literature [5– 7,14,15]. The treatment of these infections represent a challenge since strains of L. adecarboxylata are becoming resistant against a variety of antimicrobial agents [6]. To the best of our knowledge, this paper reports a very rare infection caused by L. adecarboxylata that included bacteremia and wound infection in a patient suffering from HF-related chemical burn injury—an interesting complication.
2.
Case report
A 53-year-old white man, without relevant medical antecedents, while working in a chemical industry suffered a chemical injury involving 4% of his body surface area from exposure to 60% HF. The injury involved the left arm and knee area. He immediately showered in the workplace. A colleague applied a 5% calcium gluconate gel over the affected parts of his body and took him to the emergency department of our hospital where he arrived 1 h later. Physical examination revealed a blood pressure of 100/ 60 mmHg, a pulse of 100 beats per minute and a body temperature of 37 8C. There were no signs of respiratory distress. Examination also revealed the presence of erythema affecting his left arm as well as a second-degree burn of 2 cm2 on the left knee which was infiltrated with 10 mL of 10% of calcium gluconate. Wound cultures were performed. Cardiac monitoring was immediately established. The electrocardiogram showed ventricular tachycardia with prolongation of the QT interval. Serum concentrations of calcium and magnesium were monitored. Initial hemogram, basic biochemistry, coagulation tests and acid–base equilibrium were normal. Serum total calcium was 5.9 mg/dL, (reference range: 8.2–10.4 mg/dL), ionic calcium level 0.8 mmol/L (reference range: 1.15–1.32 mmol/L for pH 7.4) and magnesium
* Corresponding author at: 19, 28th October street, Agia Paraskevi, TK 153 41 Athens, Greece. Tel.: +30 6977440344; fax: +30 2106082467. E-mail address: [email protected] (M. Dalamaga). 0305-4179/$36.00 # 2008 Elsevier Ltd and ISBI. All rights reserved. doi:10.1016/j.burns.2008.01.002
444
burns 35 (2009) 443–445
0.68 mmol/L (reference range: 0.65–1.05 mmol/L). Hypocalcemia was corrected by intravenous administration of 18 mequiv. calcium gluconate. Three hours later, serum calcium levels had normalized (10.2 mg/dL) and cardiac rhythm returned to sinus. Fifteen hours after his arrival at the hospital, he presented with fever, chills and malaise. Physical examination revealed a blood pressure of 150/75 mmHg, a pulse of 98 beats per minute and a body temperature of 39.2 8C. The lungs were clear and the heart sounds were normal without any murmur. Laboratory findings included a hematocrit of 44%, a white blood cell count of 15,400/mm3 (granulocytes 83%) with left shift and toxic granulation, a platelet count of 475,000/mm3, an erythrocyte sedimentation rate of 65 mm per hour and a CRP level of 18.9 mg/L. Basic biochemistry tests as well as urine test and sediment analysis were all normal. Chest X-ray did not reveal any abnormalities. Three consecutive sets of blood cultures, each set consisting of an aerobic bottle and an anaerobic bottle (BACTEC bottles; Johnston laboratories, Inc., Towson, MD) were obtained. Blood cultures (4 out of 6) as well as left knee area wound cultures revealed the growth of L. adecarboxylata (TSI and MacConkey agar). Gram’s stain of left knee wound and microscopic examination disclosed a moderate number of Gram-negative rods as well as many polymorphonuclear cells. The Gram-negative rod had a biochemical profile number of 1044053 – corresponding to L. adecarboxylata – when tested by the API 20E System (Biome´rieux, Marcy l’Etoile, France). Furthermore, identification of Gram-negative microorganisms and susceptibility testing were performed by two automated systems (Phoenix Trade Mark; Becton Dickinson, USA and Microscan; Dade Behring Inc., West Sacramento, CA) using a combined Gram-negative identification panel and an automated microbroth dilution method [16]. Criteria for identification acceptance were 90% and >85% agreement in accordance with manufacturer recommendations. Criteria for resistance were in accordance with Clinical and Laboratory Standards Institute Guideline [17]. The isolate presented the susceptibility pattern shown in Table 1. As soon as L. adecarboxylata infection was confirmed and according to the results of the antibiotic susceptibility testing, cefriaxone (1 g every 8 h i.v.) and amikacin (500 mg every 12 h i.v.) were administered parenterally for 12 days with clinical success. Apyrexia was achieved 5 days later. New wound and blood cultures were performed; these were sterile. The general condition of the patient was improved and he was discharged from the hospital 19 days after admission with a residual erythema on his left knee and on the anterior aspect of right arm but without any electrolyte abnormalities. Follow-up showed a complete recovery.
3.
Discussion
HF is a weak acid when compared to other hydrogen halides but it is very corrosive in particular at higher concentrations [1,2]. Due to its corrosiveness, HF penetrates skin and mucous membranes provoking deep tissue layer destruction [1]. In biologic tissues, HF splits into hydrogen cation and the fluoride moiety [4]. The most significant factor influencing deep tissue
Table 1 – Minimal inhibitory concentrations of antibiotics to Leclercia adecarboxylata Antimicrobial agent Amikacin Gentamicin Tobramycin Meropenem Imipenem Aztreonam Ampicillin Amoxicillin/clavulanate Piperacillin/tazobactam Cefazolin Cefuroxime sodium Cefoxitin Ceftazidime Cefriaxone Cefepime Aztreonam Ampicillin Piperacillin Trimethoprim/sulfamethoxazole Nitrofurantoin Ciprofloxacin Norfloxacin Fosfomycin w/G6PD
Minimal inhibitory concentration (mg/mL) 8 (S)a 8 (R) 8 (R) 1 (S) 1 (S) 2 (S) >16 (R) >16/8 (R) 4/4 (S) 16 (R) 4 (S) 4 (S) 1 (S) 2 (S) 2 (S) 2 (S) >16 (R) >64 (R) >2/38 (R) 16 (S) 0.125 (S) 2 (S) 16 (S)
a In parentheses is indicated the susceptibility status (S = susceptible, I = intermediate susceptible; R = resistant).
destruction and acute systemic toxicity of HF is the total amount of fluoride ion absorbed [3,4]. The dissociated fluoride anion can bind divalent cations such as calcium and magnesium and form insoluble salts causing hypocalcemia and hypomagnesemia, respectively [4], as it can be seen in our case. Hypocalcemia may be developed in chemical injuries of greater than 1% body surface area resulted from exposure 50% or greater HF concentration [1]. Electrocardiographic monitoring as well as determination of serum calcium and magnesium should be established as soon as possible. In addition to the aforementioned, infectious complications are probable after HF burn injuries even not reported in the literature. L. adecarboxylata was first described by Leclerc in 1962 as Escherichia adecarboxylata and was formerly known as Enteric group 41 [5,18]. L. adecarboxylata is a motile, aerobic, oxidase negative, catalase positive Gram-negative rod belonging to the Enterobacteriaceae family [18]. This microorganism has been rarely isolated from environmental and clinical specimens [5]. In clinical specimens, L. adecarboxylata has most often been isolated as part of mixed flora from sputum and traumaassociated lower extremity wound infections [12,13,18,19]. It has been isolated in blood cultures from patients with compromised immune defense by an underlying medical condition [6,7,10,15] and sepsis [7] as well as from the blood donation of an apparently healthy individual representing more likely contamination by epidermal flora or transient asymptomatic bacteremia [14]. Finally, L. adecarboxylata has been isolated from feces in patients with diarrhea [20], from gallbladder tissue in a patient with chronic cholecystitis [7], from peritoneal fluid in a child receiving chronic peritoneal dialysis [9] and from synovial fluid in a patient with septic
burns 35 (2009) 443–445
arthritis [11]. To the best of our knowledge, this is the first reported case of L. adecarboxylata simultaneous isolation from blood and wound cultures in an otherwise healthy patient suffering from HF burn injury—an interesting complication. It is important to highlight that (1) L. adecarboxylata isolated from wound culture was not a part of mixed flora and (2) the acid environment due to HF-related chemical injury allowed paradoxically the growth of L. adecarboxylata. This case report suggests that the spectrum of infections due to L. adecarboxylata may continue to expand. Possible means of bacterial transmission in patients suffering from burns are cross-infection and contact of the burned areas (main entrance for bacteria) with contaminated aqueous environment and inanimate objects. We cannot rule out that this bacterium was acquired from the patient’s own skin flora. In our case, all L. adecarboxylata isolates exhibited the same susceptibility profile and were identical. In all reported cases with L. adecarboxylata, all strains were found to be susceptible to most antibiotics except one strain which produced an SHV-12 ExtendedSpectrum Beta-Lactamase [6]. In conclusion, this is the first report of L. adecarboxylata infection and subsequent bacteremia in any burned patient or other skin injury. Given the expansive spectrum of infections following burn injuries and the microorganism potential resistance to antimicrobial therapy, isolation of the bacterium from blood as well as burn wound cultures should prompt the commencement of adequate antibiotic treatment.
[6]
[7]
[8]
[9]
[10]
[11]
[12]
[13]
[14]
[15]
Conflict of interest [16]
None.
references [17] [1] Greco RJ, Hartford CE, Haith LR, Patton ML. Hydrofluoric acid-induced hypocalcemia. J Trauma 1988;28:1593–6. [2] Shewmake SW, Anderson BG. Hydrofluoric acid burns: a report of a case and review of the literature. Arch Dermatol 1979;115:593–6. [3] Sheridan RL, Ryan CM, Quinby Jr WC, Blair J, Tompkins RG, Burke JF. Emergency management of major hydrofluoric acid exposures. Burns 1995;21:62–4. [4] Muriale L, Lee L, Genovese J, Trend S. Fatality due to acute fluoride poisoning following dermal contact with hydrofluoric acid in a palynology laboratory. Ann Occup Hyg 1996;40:705–10. [5] Abbott SL. Klebsiella, Enterobacter, Citrobacter, Serratia, Plesiomonas, and other Enterobacteriaceae. In: Murray PR, Baron EJ, Jorgensen JH, Pfaller MA, Yolken RH, editors.
[18]
[19]
[20]
445
Manual of clinical microbiology. 8th ed., Washington, DC: American Society for Microbiology Press; 2003. p. 684–700. Mazzariol A, Zuliani J, Fontana R, Cornaglia G. Isolation from blood culture of a Leclercia adecarboxylata strain producing an SHV-12 extended-spectrum beta-lactamase. J Clin Microbiol 2003;41:1738–9. De Baere T, Wauters G, Huylenbroeck A, Claeys G, Peleman R, Verschraegen G, et al. Isolation of Leclercia adecarboxylata from a patient with a chronically inflamed gallbladder and from a patient with sepsis without focus. J Clin Microbiol 2001;39:1674–5. Rodriguez JA, Sanchez FJ, Gutierrez N, Garcia JE, GarciaRodriguez JA. Bacterial peritonitis due to Leclercia adecarboxylata in a patient undergoing peritoneal dialysis. Enferm Infecc Microbiol Clin 2001;19:237–8. Fattal O, Deville JG. Leclercia adecarboxylata peritonitis in a child receiving chronic peritoneal dialysis. Pediatr Nephrol 2000;15:186–7. Daza RM, Iborra J, Alonso N, Vera I, Portero F, Mendaza P. Isolation of Leclercia adecarboxylata in a cirrhotic patient. Enferm Infecc Microbiol Clin 1993;11:53–4. Perez-Moreno MO, Anguera J, Carulla M, Perez-Moreno M. Septic arthritis due to Leclercia adecarboxylata of probable iatrogenic origin. Enferm Infecc Microbiol Clin 2003;21:167–8. Temesgen Z, Toal DR, Cockerill FR. Leclercia adecarboxylata infection: case report and review. Clin Infect Dis 1997;25:79–81. Beltran A, Molinero AV, Capilla S, Polo AM. Isolation of Leclercia adecarboxylata from wound exudates of a diabetic patient. Med Clin (Barc) 2004;122:159. Davenport P, Land KJ. Isolation of Leclercia adecarboxylata from the blood culture of an asymptomatic platelet donor. Transfusion 2007;47:1816–9. Longhurst CA, West DC. Isolation of Leclercia adecarboxylata from an infant with acute lymphoblastic leukemia. Clin Infect Dis 2001;32:1659. O’Hara CM, Weinstein MP, Miller JM. Manual and automated systems for detection and identification of microorganisms. In: Murray PR, Baron EJ, Jorgensen JH, Pfaller MA, Yolken RH, editors. Manual of clinical microbiology. 8th ed., Washington, DC: American Society for Microbiology Press; 2003. p. 197–9. Wikler MA, Cockerill FR, Craig WA, Dudley MN, Eliopoulos GM, Hecht DW, et al. Enterobacteriaceae. Performance standards for antimicrobial susceptibility testing; fifteenth informational supplement, vol. 25, no. 1. Wayne, PA, USA: Clinical and Laboratory Standards Institute Trade Mark; 2005. pp. 34–38. Tamura K, Sakazaki R, Kosako Y, Yoshizaki E. Leclercia adecarboxylata gen.nov., comb. nov., formerly known as Escherichia adecarboxylata. Curr Microbiol 1986;13:179–84. Martinez MM, Sanchez G, Gomez J, Mendaza P, Daza RM. Isolation of Leclercia adecarboxylata in ulcer exudate. Enferm Infecc Microbiol Clin 1998;16:345. Cai M, Dong X, Wei J, Yang F, Xu D, Zhang H, et al. Isolation and identification of Leclercia adecarboxylata in clinical isolates in China. Wei Sheng Wu Hsueh Pao (Acta Microbiologica Sinica) 1992;32:119–23.
available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/burns
Case report
Isolation of Leclercia adecarboxylata from blood and burn wound after a hydrofluoric acid chemical injury M. Dalamaga a,b,*, M. Pantelaki c, K. Karmaniolas a, K. Daskalopoulou c, I. Migdalis a a
Department of Internal Medicine, NIMTS General Hospital, Athens, Greece Department of Clinical Biochemistry, Attikon University General Hospital, Athens University Medical School, Athens, Greece c Department of Clinical Microbiology, Elpis General Hospital, Athens, Greece b
article info Article history: Accepted 21 January 2008
1.
Introduction
Chemical injuries following exposure to hydrofluoric acid (HF) occur with ever-increasing frequency due to the wide use of this highly corrosive inorganic acid in research and industry [1,2]. The majority of exposures involve small surface areas and are from dilute HF [3]. Topical exposures to concentrated HF have a fatal outcome even if very small areas of body surface are involved due to systemic manifestations of hypocalcemia and hypomagnesemia [4] if severe. Leclercia adecarboxylata constitutes a rare opportunistic human pathogen [5]. L. adecarboxylata strains are rarely isolated from clinical specimens of hospitalized patients [5– 7]. Most strains have been isolated from peritoneal fluid [8–10], synovial fluid [11] as well as from sputum and wound exudates as part of a mixed microbial growth [12,13]. Few cases of bacteremia in patients with compromised immunity and chronic inflammation diseases are cited in the literature [5– 7,14,15]. The treatment of these infections represent a challenge since strains of L. adecarboxylata are becoming resistant against a variety of antimicrobial agents [6]. To the best of our knowledge, this paper reports a very rare infection caused by L. adecarboxylata that included bacteremia and wound infection in a patient suffering from HF-related chemical burn injury—an interesting complication.
2.
Case report
A 53-year-old white man, without relevant medical antecedents, while working in a chemical industry suffered a chemical injury involving 4% of his body surface area from exposure to 60% HF. The injury involved the left arm and knee area. He immediately showered in the workplace. A colleague applied a 5% calcium gluconate gel over the affected parts of his body and took him to the emergency department of our hospital where he arrived 1 h later. Physical examination revealed a blood pressure of 100/ 60 mmHg, a pulse of 100 beats per minute and a body temperature of 37 8C. There were no signs of respiratory distress. Examination also revealed the presence of erythema affecting his left arm as well as a second-degree burn of 2 cm2 on the left knee which was infiltrated with 10 mL of 10% of calcium gluconate. Wound cultures were performed. Cardiac monitoring was immediately established. The electrocardiogram showed ventricular tachycardia with prolongation of the QT interval. Serum concentrations of calcium and magnesium were monitored. Initial hemogram, basic biochemistry, coagulation tests and acid–base equilibrium were normal. Serum total calcium was 5.9 mg/dL, (reference range: 8.2–10.4 mg/dL), ionic calcium level 0.8 mmol/L (reference range: 1.15–1.32 mmol/L for pH 7.4) and magnesium
* Corresponding author at: 19, 28th October street, Agia Paraskevi, TK 153 41 Athens, Greece. Tel.: +30 6977440344; fax: +30 2106082467. E-mail address: [email protected] (M. Dalamaga). 0305-4179/$36.00 # 2008 Elsevier Ltd and ISBI. All rights reserved. doi:10.1016/j.burns.2008.01.002
444
burns 35 (2009) 443–445
0.68 mmol/L (reference range: 0.65–1.05 mmol/L). Hypocalcemia was corrected by intravenous administration of 18 mequiv. calcium gluconate. Three hours later, serum calcium levels had normalized (10.2 mg/dL) and cardiac rhythm returned to sinus. Fifteen hours after his arrival at the hospital, he presented with fever, chills and malaise. Physical examination revealed a blood pressure of 150/75 mmHg, a pulse of 98 beats per minute and a body temperature of 39.2 8C. The lungs were clear and the heart sounds were normal without any murmur. Laboratory findings included a hematocrit of 44%, a white blood cell count of 15,400/mm3 (granulocytes 83%) with left shift and toxic granulation, a platelet count of 475,000/mm3, an erythrocyte sedimentation rate of 65 mm per hour and a CRP level of 18.9 mg/L. Basic biochemistry tests as well as urine test and sediment analysis were all normal. Chest X-ray did not reveal any abnormalities. Three consecutive sets of blood cultures, each set consisting of an aerobic bottle and an anaerobic bottle (BACTEC bottles; Johnston laboratories, Inc., Towson, MD) were obtained. Blood cultures (4 out of 6) as well as left knee area wound cultures revealed the growth of L. adecarboxylata (TSI and MacConkey agar). Gram’s stain of left knee wound and microscopic examination disclosed a moderate number of Gram-negative rods as well as many polymorphonuclear cells. The Gram-negative rod had a biochemical profile number of 1044053 – corresponding to L. adecarboxylata – when tested by the API 20E System (Biome´rieux, Marcy l’Etoile, France). Furthermore, identification of Gram-negative microorganisms and susceptibility testing were performed by two automated systems (Phoenix Trade Mark; Becton Dickinson, USA and Microscan; Dade Behring Inc., West Sacramento, CA) using a combined Gram-negative identification panel and an automated microbroth dilution method [16]. Criteria for identification acceptance were 90% and >85% agreement in accordance with manufacturer recommendations. Criteria for resistance were in accordance with Clinical and Laboratory Standards Institute Guideline [17]. The isolate presented the susceptibility pattern shown in Table 1. As soon as L. adecarboxylata infection was confirmed and according to the results of the antibiotic susceptibility testing, cefriaxone (1 g every 8 h i.v.) and amikacin (500 mg every 12 h i.v.) were administered parenterally for 12 days with clinical success. Apyrexia was achieved 5 days later. New wound and blood cultures were performed; these were sterile. The general condition of the patient was improved and he was discharged from the hospital 19 days after admission with a residual erythema on his left knee and on the anterior aspect of right arm but without any electrolyte abnormalities. Follow-up showed a complete recovery.
3.
Discussion
HF is a weak acid when compared to other hydrogen halides but it is very corrosive in particular at higher concentrations [1,2]. Due to its corrosiveness, HF penetrates skin and mucous membranes provoking deep tissue layer destruction [1]. In biologic tissues, HF splits into hydrogen cation and the fluoride moiety [4]. The most significant factor influencing deep tissue
Table 1 – Minimal inhibitory concentrations of antibiotics to Leclercia adecarboxylata Antimicrobial agent Amikacin Gentamicin Tobramycin Meropenem Imipenem Aztreonam Ampicillin Amoxicillin/clavulanate Piperacillin/tazobactam Cefazolin Cefuroxime sodium Cefoxitin Ceftazidime Cefriaxone Cefepime Aztreonam Ampicillin Piperacillin Trimethoprim/sulfamethoxazole Nitrofurantoin Ciprofloxacin Norfloxacin Fosfomycin w/G6PD
Minimal inhibitory concentration (mg/mL) 8 (S)a 8 (R) 8 (R) 1 (S) 1 (S) 2 (S) >16 (R) >16/8 (R) 4/4 (S) 16 (R) 4 (S) 4 (S) 1 (S) 2 (S) 2 (S) 2 (S) >16 (R) >64 (R) >2/38 (R) 16 (S) 0.125 (S) 2 (S) 16 (S)
a In parentheses is indicated the susceptibility status (S = susceptible, I = intermediate susceptible; R = resistant).
destruction and acute systemic toxicity of HF is the total amount of fluoride ion absorbed [3,4]. The dissociated fluoride anion can bind divalent cations such as calcium and magnesium and form insoluble salts causing hypocalcemia and hypomagnesemia, respectively [4], as it can be seen in our case. Hypocalcemia may be developed in chemical injuries of greater than 1% body surface area resulted from exposure 50% or greater HF concentration [1]. Electrocardiographic monitoring as well as determination of serum calcium and magnesium should be established as soon as possible. In addition to the aforementioned, infectious complications are probable after HF burn injuries even not reported in the literature. L. adecarboxylata was first described by Leclerc in 1962 as Escherichia adecarboxylata and was formerly known as Enteric group 41 [5,18]. L. adecarboxylata is a motile, aerobic, oxidase negative, catalase positive Gram-negative rod belonging to the Enterobacteriaceae family [18]. This microorganism has been rarely isolated from environmental and clinical specimens [5]. In clinical specimens, L. adecarboxylata has most often been isolated as part of mixed flora from sputum and traumaassociated lower extremity wound infections [12,13,18,19]. It has been isolated in blood cultures from patients with compromised immune defense by an underlying medical condition [6,7,10,15] and sepsis [7] as well as from the blood donation of an apparently healthy individual representing more likely contamination by epidermal flora or transient asymptomatic bacteremia [14]. Finally, L. adecarboxylata has been isolated from feces in patients with diarrhea [20], from gallbladder tissue in a patient with chronic cholecystitis [7], from peritoneal fluid in a child receiving chronic peritoneal dialysis [9] and from synovial fluid in a patient with septic
burns 35 (2009) 443–445
arthritis [11]. To the best of our knowledge, this is the first reported case of L. adecarboxylata simultaneous isolation from blood and wound cultures in an otherwise healthy patient suffering from HF burn injury—an interesting complication. It is important to highlight that (1) L. adecarboxylata isolated from wound culture was not a part of mixed flora and (2) the acid environment due to HF-related chemical injury allowed paradoxically the growth of L. adecarboxylata. This case report suggests that the spectrum of infections due to L. adecarboxylata may continue to expand. Possible means of bacterial transmission in patients suffering from burns are cross-infection and contact of the burned areas (main entrance for bacteria) with contaminated aqueous environment and inanimate objects. We cannot rule out that this bacterium was acquired from the patient’s own skin flora. In our case, all L. adecarboxylata isolates exhibited the same susceptibility profile and were identical. In all reported cases with L. adecarboxylata, all strains were found to be susceptible to most antibiotics except one strain which produced an SHV-12 ExtendedSpectrum Beta-Lactamase [6]. In conclusion, this is the first report of L. adecarboxylata infection and subsequent bacteremia in any burned patient or other skin injury. Given the expansive spectrum of infections following burn injuries and the microorganism potential resistance to antimicrobial therapy, isolation of the bacterium from blood as well as burn wound cultures should prompt the commencement of adequate antibiotic treatment.
[6]
[7]
[8]
[9]
[10]
[11]
[12]
[13]
[14]
[15]
Conflict of interest [16]
None.
references [17] [1] Greco RJ, Hartford CE, Haith LR, Patton ML. Hydrofluoric acid-induced hypocalcemia. J Trauma 1988;28:1593–6. [2] Shewmake SW, Anderson BG. Hydrofluoric acid burns: a report of a case and review of the literature. Arch Dermatol 1979;115:593–6. [3] Sheridan RL, Ryan CM, Quinby Jr WC, Blair J, Tompkins RG, Burke JF. Emergency management of major hydrofluoric acid exposures. Burns 1995;21:62–4. [4] Muriale L, Lee L, Genovese J, Trend S. Fatality due to acute fluoride poisoning following dermal contact with hydrofluoric acid in a palynology laboratory. Ann Occup Hyg 1996;40:705–10. [5] Abbott SL. Klebsiella, Enterobacter, Citrobacter, Serratia, Plesiomonas, and other Enterobacteriaceae. In: Murray PR, Baron EJ, Jorgensen JH, Pfaller MA, Yolken RH, editors.
[18]
[19]
[20]
445
Manual of clinical microbiology. 8th ed., Washington, DC: American Society for Microbiology Press; 2003. p. 684–700. Mazzariol A, Zuliani J, Fontana R, Cornaglia G. Isolation from blood culture of a Leclercia adecarboxylata strain producing an SHV-12 extended-spectrum beta-lactamase. J Clin Microbiol 2003;41:1738–9. De Baere T, Wauters G, Huylenbroeck A, Claeys G, Peleman R, Verschraegen G, et al. Isolation of Leclercia adecarboxylata from a patient with a chronically inflamed gallbladder and from a patient with sepsis without focus. J Clin Microbiol 2001;39:1674–5. Rodriguez JA, Sanchez FJ, Gutierrez N, Garcia JE, GarciaRodriguez JA. Bacterial peritonitis due to Leclercia adecarboxylata in a patient undergoing peritoneal dialysis. Enferm Infecc Microbiol Clin 2001;19:237–8. Fattal O, Deville JG. Leclercia adecarboxylata peritonitis in a child receiving chronic peritoneal dialysis. Pediatr Nephrol 2000;15:186–7. Daza RM, Iborra J, Alonso N, Vera I, Portero F, Mendaza P. Isolation of Leclercia adecarboxylata in a cirrhotic patient. Enferm Infecc Microbiol Clin 1993;11:53–4. Perez-Moreno MO, Anguera J, Carulla M, Perez-Moreno M. Septic arthritis due to Leclercia adecarboxylata of probable iatrogenic origin. Enferm Infecc Microbiol Clin 2003;21:167–8. Temesgen Z, Toal DR, Cockerill FR. Leclercia adecarboxylata infection: case report and review. Clin Infect Dis 1997;25:79–81. Beltran A, Molinero AV, Capilla S, Polo AM. Isolation of Leclercia adecarboxylata from wound exudates of a diabetic patient. Med Clin (Barc) 2004;122:159. Davenport P, Land KJ. Isolation of Leclercia adecarboxylata from the blood culture of an asymptomatic platelet donor. Transfusion 2007;47:1816–9. Longhurst CA, West DC. Isolation of Leclercia adecarboxylata from an infant with acute lymphoblastic leukemia. Clin Infect Dis 2001;32:1659. O’Hara CM, Weinstein MP, Miller JM. Manual and automated systems for detection and identification of microorganisms. In: Murray PR, Baron EJ, Jorgensen JH, Pfaller MA, Yolken RH, editors. Manual of clinical microbiology. 8th ed., Washington, DC: American Society for Microbiology Press; 2003. p. 197–9. Wikler MA, Cockerill FR, Craig WA, Dudley MN, Eliopoulos GM, Hecht DW, et al. Enterobacteriaceae. Performance standards for antimicrobial susceptibility testing; fifteenth informational supplement, vol. 25, no. 1. Wayne, PA, USA: Clinical and Laboratory Standards Institute Trade Mark; 2005. pp. 34–38. Tamura K, Sakazaki R, Kosako Y, Yoshizaki E. Leclercia adecarboxylata gen.nov., comb. nov., formerly known as Escherichia adecarboxylata. Curr Microbiol 1986;13:179–84. Martinez MM, Sanchez G, Gomez J, Mendaza P, Daza RM. Isolation of Leclercia adecarboxylata in ulcer exudate. Enferm Infecc Microbiol Clin 1998;16:345. Cai M, Dong X, Wei J, Yang F, Xu D, Zhang H, et al. Isolation and identification of Leclercia adecarboxylata in clinical isolates in China. Wei Sheng Wu Hsueh Pao (Acta Microbiologica Sinica) 1992;32:119–23.