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Letter
Staphylococcus aureus
and Escherichia hermanii in Diabetes Patient
Gabriel Adrian Popescu,*‡
Ioana Daha,†‡ Cristina Popescu,*‡ and Elena Mitache*
*Matei Bals Infectious Diseases Institute, Bucharest, Romania; †Colentina
Hospital, Bucharest, Romania; and ‡Carol Davila University of Medicine,
Bucharest, Romania
Suggested citation
for this article: Popescu GA, Daha I, Popescu C, Mitache E. Staphylococcus
aureus and Escherichia hermanii in diabetes patient [letter].
Emerg Infect Dis [serial on the Internet]. 2004 Jul [date cited].
Available from: http://www.cdc.gov/ncidod/EID/vol10no7/03-0567.htm
To the Editor: Polymicrobial invasive infections are infrequent,
representing <10% of the invasive infections of known etiology (1).
They are often correlated with a predisposing factor: immunodeficiency
(e.g., diabetes mellitus, malignancies, extremes of age) or use of a central
catheter. Escherichia hermanii is an extremely rare etiologic agent
for invasive infections; only four cases were published from 1980 to 2002.
We report the first case of double invasive infection by E. hermanii
and Staphylococcus aureus and emphasize the importance of screening
of all the septic foci for demonstrating a polymicrobial invasive infection.
In August 2000, a 54-year-old comatose man was admitted to our infectious
diseases department with a 10-day history of fever. He had a medical history
of vertebral arthrosis (lumbar laminectomy in 1989) and insulin-dependent
diabetes mellitus. Six weeks before, he had received for 3 days gluteal
injections with kebusone (an intramuscular nonsteriodal antiinflammatory
drug [NSAID]) for acute lower back pain. Twenty-eight days after the first
injection, a gluteal abscess developed, which was surgically drained,
without perioperative antimicrobial therapy. Three days later, he became
febrile, and pyrexia persisted despite local wound management and treatment
with oxacillin, 4 g/day for 3 days; cefuroxime, 3 g/day, and gentamicin,
160 mg/day for another 7 days.
The patient became comatose and was transferred to our department. At
that time, the physical examination showed fever (40.2°C), neck stiffness,
Brudzinski sign, thoracic dullness, and bilateral crackling rales. The
level of C-reactive protein was 123 mg/L. Renal failure was noted with
a creatinine blood level of 312 mmol/L and uncontrolled diabetes with
fasting glucose of 24.75 mmol/L. Computed tomographic (CT) scan of the
brain did not show brain abscesses or tumors. Examination of the cerebrospinal
fluid (CSF) indicated a protein level of 2.67 g/L, decreased glucose concentration
of 0.55 mmol/L, and a leukocyte count of 2.3 x 109/L with 96%
neutrophils; no microbial pathogens were demonstrable under direct examination
of CSF. Chest x-ray identified bronchopneumonia and bilateral pleural
effusion. The pleural fluid analysis revealed a purulent exudate—protein,
4.5 g/L—containing 55% neutrophils. A urine specimen and three blood samples
were obtained for cultures over the first 4 hours after admission. A bacterial
invasive infection was considered and the antibiotic therapy was started
with ceftriaxone, 2 g/day, and rifampin, 1,200 mg/day. Concomitantly,
the patient received colloids to reestablish blood volume, intravenous
dexamethasone, 6 mg four times daily, to diminish the cerebral edema;
and fast-acting insulin to control hyperglycemia.
On day 3, the urine and CSF cultures were positive for E. hermanii,
and the pleural fluid and all three blood cultures yielded methicillin-susceptible
S. aureus. The E. hermanii strain produced a yellow pigment.
The drug susceptibility was assessed by AtB Expression system (BioMerieux,
Marcy l'Etoile, France). The Staphylococcus strain was susceptible
to oxacillin, cotrimoxazole, tetracycline, and ciprofloxacin and resistant
only to penicillin. E. hermanii is naturally resistant to aminopenicillins
and carbenicillin; this strain was susceptible to third-generation cephalosporins,
carbapenems, cotrimoxazole, and quinolones and resistant to aminoglycosides.
The patient's clinical central nervous system status improved, and he
came out of the coma, but his temperature remained >37.5°C. He
started to report lumbar pain. On day 5, the antimicrobial regimen was
switched to meropenem. After 24 hours, the patient became apyretic, and
glucose and creatinine levels were normal on day 8. However, on day 10,
fever, inflammation of the right thumb, and intensified lower back pain
developed. The abdominal CT and bone scintigraphy indicated abscess of
the psoas, L4-L5 spondylitis, and thumb periostitis. Intravenous ciprofloxacin
was added, 400 mg twice daily, and apyrexia occurred on day 14. On day
21, open surgery was performed, consisting of drainage of the psoas abscess
and curettage of the L4-L5 disc. On day 30, clinical improvement and C-reactive
protein level of 4.2 mg/L, led to a change to oral antimicrobial agents:
cotrimoxazole 2 g/day and ciprofloxacin 1.5 g/day. This regimen was continued
for 2 months while the patient was seen as an outpatient. The patient
remained afebrile and inflammation-free for the entire 24-month followup
period.
Polymicrobial invasive infections represent a major therapeutic problem.
However, they are infrequent: only 3.2% of infectious endocarditis (2)
cases and 6.27% of 2,188 community-acquired bacteremia cases (3)
were polymicrobial. Polymicrobial infections and elevated bacteremia levels
are more frequently associated with diabetes; 20%–35% of the skin and
soft tissue infections in persons with diabetes are polymicrobial (4),
and 15.7%–20% of the community-acquired bacteremia cases were registered
in persons with diabetes (3,4). The probable entry site
for S. aureus was cutaneous. Intramuscular NSAIDs are known to
cause aseptic necrosis, predisposing the patient to staphylococcal abscesses.
Hyperglycemia itself is a risk factor for soft-tissue infections. The
role of perioperative antimicrobial therapy in preventing the dissemination
of infection from a surgically drained abscess is controversial (5).
E. hermanii usually produces wound or gastrointestinal tract infections;
in our patient, E. hermanii probably originated from the skin or
from the gastrointestinal tract (6–9). E. hermanii
could be involved more frequently in polymicrobial invasive infections;
of E. hermanii invasive infections noted in four published reports,
two were polymicrobial (6,7).
Initial antimicrobial drug therapy was established empirically for probable
staphylococcal meningitis. The ongoing fever and persistent metabolic
disturbances led to an escalation of therapy. Some authors recommend carbapenems
as the initial regimen against invasive methicillin-susceptible S.
aureus infections with meningeal or bone involvement (10).
The patient's lower back and the invasive staphylococcal infection urged
us to consider septic bone involvement. The imaging studies confirmed
the existence of vertebral osteomyelitis; ciprofloxacin was used based
on its excellent bone diffusion and its in vitro activity on the two isolated
strains. Surgical intervention eradicated of one of the septic foci and
decreased risk for spinal cord injury; 27 (47%) of the 58 patients with
spondylodiscitis who were treated surgically had a better outcome than
the other patients with medical care only (11). Control
of the infection allowed changing to an oral regimen after 1 month. We
selected cotrimoxazole and ciprofloxacin for their in vitro effectiveness
against the two pathogens. Although this agent is not usually used to
treat bone infection, we used cotrimoxazole on the basis of evidence provided
by several communications that indicated a superior efficiency to referential
regimens (12).
In conclusion, the identification of all organisms involved in polymicrobial
invasive infections may require cultures of specimens from all accessible
septic foci. For E. hermanii, a role of "associated"
pathogen in a polymicrobial invasive infection could be considered. Medical
therapy alone could be insufficient, and the combined therapy allowed
for a successful outcome in invasive infection with lumbar spondilodiscitis.
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