CASE REPORT
Emerging Escherichia Pathogen Quanhathai Kaewpoowat,a Nitipong Permpalung,a Deborah E. Sentochnikb,c Department of Internal Medicine, Bassett Medical Center, Cooperstown, New York, USAa; Division of Infectious Diseases, Bassett Medical Center, Cooperstown, New York, USAb; College of Physicians and Surgeons, Columbia University, New York, New York, USAc
Escherichia hermannii was first identified as a new species in 1982. It has rarely been reported as a human pathogen. We report the first case of E. hermannii as the sole pathogen in a catheter-related bloodstream infection.
CASE REPORT
A
63-year-old Caucasian man presented with 1 week of fever and lethargy. His medical history included dialysis-dependent end-stage kidney disease secondary to diabetic nephropathy. Hemodialysis had been instituted 1 year previously via left arm arteriovenous fistula (AVF). Two months later, the fistula thrombosed. A silicone double-lumen catheter was then placed in the right subclavian vein. It was used as temporary dialysis access for 7 months. Three weeks prior to admission, a left forearm AVF placed 5 months before became his new dialysis access. The double-lumen catheter was maintained as a backup port. One week before admission, the patient felt weak and had a low-grade fever. At hemodialysis 2 days prior to admission, he was noted to be febrile (38.5°C). Hospitalization was advised but refused. A set of blood cultures was drawn from his AVF, and another set was drawn from the central venous catheter. One gram of vancomycin was then administered intravenously before the patient left the dialysis unit. Within 24 h, both sets of blood cultures grew Gram-negative bacilli. The patient was immediately contacted and admitted to the hospital. Physical findings on admission were remarkable for a fever of 39.3°C, a heart rate 97/min, a respiratory rate 22/min, a blood pressure of 143/54 mmHg, and somnolence. A physical examination did not reveal signs of localized infection. Laboratory testing showed a white blood cell count of 3,700/ml with 79.6% neutrophils and 10.9%. lymphocytes. Chest X-ray and urinalysis findings were unremarkable. Two sets of repeat blood cultures were drawn peripherally. Broad-spectrum antibiotic therapy with vancomycin, levofloxacin, and metronidazole was then immediately initiated for severe sepsis. A computed tomography scan of the abdomen and pelvis with contrast did not reveal any site of infection. On hospital day 3, the central venous catheter was removed. The culture plate from the catheter tip grew Gram-negative rods with yellow colony pigmentation. The organism was identical to the one that was isolated from the previous blood cultures (drawn from his AVF, the central venous catheter, and two sets from peripheral veins). It was identified by MicroScan (Siemens) rapid Gram-negative panel. The culture was finally identified as Escherichia hermannii (99.99% probability) on the basis of yellow colony pigmentation and positive chemical reactions to glucuronic acid, arabinose, inositol, ornithine, glucose, alpha-Lglutamic acid, L-pyroglutamic acid, and tryptophan. The organism was sensitive to amikacin, aztreonam, cefoxitin, ceftazidime, ceftriaxone, ciprofloxacin, gentamicin, trimethoprim-sulfamethoxazole (TMP-SMX), tetracycline, and tobramycin (Table 1 con-
August 2013 Volume 51 Number 8
TABLE 1 Antibiotic susceptibility of the E. hermannii isolate described in this report Antibiotic
Sensitivitya
MIC (g/ml)
Amikacin Ampicillin-sulbactam Aztreonam Cefoxitin Ceftazidime Ceftriaxone Ciprofloxacin Gentamicin TMP-SMX Tetracycline Tobramycin
S S S S S S S S S S S
ⱕ16 ⱕ8/4 ⱕ8 ⱕ8 ⱕ2 ⱕ4 ⱕ1 ⱕ1 ⱕ0.5/9.5 ⱕ4 ⱕ4
a
S, susceptible.
tains further details). Vancomycin was discontinued on day 3. Intravenous levofloxacin and metronidazole were continued as treatment for a possible enteric source of infection. The patient’s symptoms improved. He was discharged on hospital day 6 and completed a 2-week antibiotic course with oral levofloxacin and oral metronidazole. The patient has been followed up for 17 months and has been doing well.
E. hermannii was first proposed as a new species by Brenner et al. in 1982 (1). Previously, it was known as an E. coli-like biogroup. By the DNA hybridization technique, E. hermannii showed only 35 to 45% relatedness to E. coli. It has been isolated primarily from wounds (50%), sputum (25%), and stool samples (20%) (1). A mouse model study failed to cause a fatal infection (2). In vitro studies have found that E. hermannii is inherently resistant to penicillin, ampicillin, and carbenicillin but sensitive to other betalactam antibiotics (cephalosporins, carbapenems, and monobactam) (2, 3). During the past 30 years, there have been sporadic reports
Received 11 April 2013 Returned for modification 14 May 2013 Accepted 31 May 2013 Published ahead of print 5 June 2013 Address correspondence to Quanhathai Kaewpoowat,
[email protected]. Copyright © 2013, American Society for Microbiology. All Rights Reserved. doi:10.1128/JCM.00983-13
Journal of Clinical Microbiology
p. 2785–2786
jcm.asm.org
2785
Case Report
TABLE 2 Clinical features of previously reported cases of E. hermannii as a potential pathogen Concurrently isolated organism(s)
Reference
Age
Sexa
Comorbidity
Country
Site(s) of isolation
4
27 days
F
Premature birth
USA
6
69 yr
F
Korea
7
80 yr
F
Leiomyosarcoma receiving chemotherapy C. albicans fungemia
Belgium
CSF, peritoneal fluid, blood Tip of Hickman catheter, blood Blood
8
5 days
NR
USA
CSF, cephalohematoma
9
54 yr
M
Prenatal history of prolonged rupture of membrane, hyperbilirubinemia Diabetes, vertebral arthrosis
Romania
Urine, CSF
MSSA (in 3 blood cultures, pleural fluid)
5
38 yr
M
None
Greece
Eye discharge
None
a
Serratia liquefaciens (blood) Leclercia adecarboxylata Enterococcus faecalis, Leclercia adecarboxylata None
Antibiotics used Oxacillin, moxalactam Not reported Not reported
Ceftriaxone, cefotaxime⫹ ampicillin⫹ gentamicin⫹ acyclovir Ceftriaxone ⫹ rifampin, meropenem ⫹ ciprofloxacin, TMPSMX ⫹ ciprofloxacin Oral cefuroxime ⫹ ciprofloxacin eye drops
F, female; M, male; NR, not reported.
worldwide describing E. hermannii as a human pathogen (Table 2). E. hermannii has been isolated from various sites, including wounds (2, 3), peritoneal fluid (4), eye discharge (5), blood (4, 6, 7), cerebrospinal fluid (CSF) (4, 8, 9), a neonatal cephalohematoma (8), and urine (9). Although E. hermannii was considered as a possible cause of illness, most of the cases reported coinfection with other known human-pathogenic bacteria, e.g., methicillinsusceptible Staphylococcus aureus (MSSA) and Leclercia adecarboxylata. Only two of them described E. hermannii as the sole isolate (5, 8). There is insufficient clinical data for antibiotic recommendations. The treatment used in previously reported cases has included expanded- and broad-spectrum cephalosporins, sometimes in combination therapy with a fluoroquinolone (levofloxacin or ciprofloxacin). Our patient’s is the first reported case in which levofloxacin was used successfully as the sole agent to treat an E. hermannii infection. ACKNOWLEDGMENTS Thanks to Edward Bischof for reviewing the manuscript and to the Bassett microbiology laboratory for providing microbiology data. We have no commercial or other association that might pose a conflict of interest. None of the information in this report has ever been presented at any meeting or conference. This study received no financial support.
2786
jcm.asm.org
REFERENCES 1. Brenner DJ, Davis BR, Steigerwalt AG, Riddle CF, McWhorter AC, Allen SD, Farmer JJ, III, Saitoh Y, Fanning GR. 1982. Atypical biogroups of Escherichia coli found in clinical specimens and description of Escherichia hermannii sp. nov. J. Clin. Microbiol. 15:703–713. 2. Pien FD, Shrum S, Swenson JM, Hill BC, Thornsberry C, Farmer JJ, III. 1985. Colonization of human wounds by Escherichia vulneris and Escherichia hermannii. J. Clin. Microbiol. 22:283–285. 3. Stock I, Wiedemann B. 1999. Natural antibiotic susceptibility of Escherichia coli, Shigella, E. vulneris and E. hermannii strains. Diagn. Microbiol. Infect. Dis. 33:187–199. 4. Ginsberg HG, Daum RS. 1987. Escherichia hermannii sepsis with duodenal perforation in a neonate. Pediatr. Infect. Dis. J. 6:300 –302. 5. Poulou A, Dimitroulia E, Markou F, Tsakris A. 2008. Escherichia hermannii as the sole isolate from a patient with purulent conjunctivitis. J. Clin. Microbiol. 46:3848 –3849. 6. Lee NY, Ki CS, Kang WK, Peck KR, Kim S, Song JH. 1999. Hickman catheter-associated bacteremia by Leclercia adecarboxylata and Escherichia hermannii: a case report. Korean J. Infect. Dis. 31:167–170. 7. de Baere T, Wauters G, Huylenbroeck A, Claeys G, Peleman R, Verschraegen G, Allemeersch D, Vaneechoutte M. 2001. Isolations of Leclercia adecarboxylata from a patient with chronically inflamed gallbladder and from a patient with sepsis without focus. J. Clin. Microbiol. 39:1674 –1675. 8. Dahl KM, Barry J, DeBiasi RL. 2002. Escherichia hermannii infection of a cephalohematoma: case report, review of the literature, and description of a novel invasive pathogen. Clin. Infect. Dis. 35:e96 – e98. 9. Popescu GA, Daha I, Popescu C, Mitache E. 2004. Staphylococcus aureus and Escherichia hermannii in diabetes patient. Emerg. Infect. Dis. 10:1335– 1337.
Journal of Clinical Microbiology
