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Journal of Clinical Microbiology, May 2000, p. 2015-2017, Vol. 38, No. 5
0095-1137/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Infective Endocarditis Complicated with Progressive Heart Failure
due to 
-Lactamase-Producing Cardiobacterium
hominis
Po-Liang
Lu,1
Po-Ren
Hsueh,1,2
Chien-Ching
Hung,1
Lee-Jene
Teng,3
Tsrang-Neng
Jang,4 and
Kwen-Tay
Luh1,2,*
Departments of Internal
Medicine1 and Laboratory
Medicine,2 National Taiwan University Hospital,
School of Medical Technology, National Taiwan University
College of Medicine,3 and Department of
Medicine, Shin Kong Wu Ho-Su Memorial
Hospital,4 Taipei, Taiwan
Received 30 December 1999/Returned for modification 15 February
2000/Accepted 28 February 2000
 |
ABSTRACT |
We describe a 66-year-old woman with infective endocarditis due to
Cardiobacterium hominis whose condition, complicated by severe aortic regurgitation and congestive heart failure, necessitated aortic valve replacement despite treatment with ceftriaxone followed by
ciprofloxacin. The blood isolate of C. hominis produced
-lactamase and exhibited high-level resistance to penicillin (MIC,
256 µg/ml) and reduced susceptibility to vancomycin (MIC, 8 µg/ml).
| |
CASE REPORT |
A 66-year-old woman who had been
well except for having diabetes mellitus was admitted to a district
hospital in the city of Taipei, Taiwan, on 4 April 1998 because of
chest discomfort and fatigability that worsened during the course of a
day. She was not febrile on admission. Dental caries were noted. Grade II systolic and diastolic murmurs were heard at the cardiac apex and at
the left lower and right upper sternal borders. Otherwise, the physical
examination was unremarkable. The white blood cell count was 8,500 cells/mm3, with 75% neutrophils, 20% lymphocytes, and 5%
monocytes. The hemoglobin level was 9.9 g/dl, and the platelet count
was 199,000/mm3. The remaining laboratory results were
within normal limits.
Transthoracic and transesophageal echocardiography revealed vegetation
at the aortic valve in addition to severe aortic regurgitation and
dilation of the left ventricle and atrium. Infective endocarditis was
suspected, and treatment with ampicillin (2 g every [q] 4 h) and
gentamicin (60 mg q 12 h), administered intravenously, was begun
after blood specimens were obtained for culture. Blood cultures showed
no growth after incubation for a week. The patient's symptoms were
aggravated, and exertional dyspnea developed after treatment for 14 days; she was then referred to National Taiwan University Hospital. On
admission, her temperature was 37.5°C. A repeat echocardiography
revealed findings similar to those obtained previously, but without
perivalvular abscess.
Ampicillin and gentamicin were replaced by ceftriaxone (2 g q 12 h) on 20 April 1998. Because skin rashes developed 3 weeks later,
ceftriaxone was replaced by intravenous ciprofloxacin (400 mg q 12 h), which was continued for 1 week. On 13 May 1998, the patient
developed worsening dyspnea on mild exertion and orthopnea. She
underwent aortic valve replacement because of progressive heart failure
on 21 May 1998. Perforation of the noncoronary cusp of the aortic valve
was found. Cultures of blood and the aortic valves were negative. The
postoperative course was uneventful and she remained well during the 8 months of follow-up care.
Microbiology.
Ten milliliters of blood was obtained from the
patient upon her admission to the first hospital. A 5-ml volume of the
original blood sample was added to each of two blood cultures (BACTEC
6A aerobic and BACTEC 7A anaerobic bottles; Becton Dickinson, Sparks, Md.) by using the BACTEC 860 System (Becton Dickinson). After a 10-day
incubation (prolonged incubation because of clinical suspicion of
infective endocarditis caused by organisms of the group
[Haemophilus species, Actinobacillus
actinomycetemcomitans, Cardiobacterium hominis,
Capnocytophaga spp., Eikenella corrodens, and
Kingella species]), HACEK a terminal subculture of the
BACTEC 6A aerobic bottle grew a gram-negative bacillus and the
microorganism was reported as Pasteurella multocida. The
isolate was sent to National Taiwan University Hospital for further
identification. A tiny, glistening, opaque colony was observed on
trypticase soy agar supplemented with 5% sheep blood (BBL Microbiology
Systems, Cockeysville, Md.) after culture at 37°C in an atmosphere of
5% carbon dioxide for more than 2 days. No hemolysis was observed on
blood agar. Rods with one or both ends swollen were seen observed after
Gram staining of the colony. The isolate was oxidase-positive, catalase-negative, nitrate-negative, indole-positive, urease-negative, and nonmotile. The organisms fermented glucose, sucrose, and lactose. The biochemical profiles of the isolate were in accord with the identification of C. hominis (2). Cellular fatty
acid chromatograms of the isolate, obtained as previously described
(3), corresponded to the pattern of C. hominis
which contained a high percentage (
3%) of 18:1 
7c/9t/12t
fatty acid methyl ester (FAME), 16:0 FAME, 14:0 FAME, 12:0 FAME, and
16:1 7c/15-2-OH FAME (Fig. 1) (17).
View larger version (10K):
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|
FIG. 1.
Gas chromatography of FAMES of C. hominis.
The designations refer to the number of carbon atoms (number before the
colon) and the number of double bonds (number after the colon). 3-OH,
hydroxyl group at carbon 3 (Microbial Identification System; Microbial
ID Inc., Newark, Del.).
|
|
The MICs of 11 antimicrobial agents were determined by using the broth
dilution method with cation-adjusted Mueller-Hinton broth with 5%
lysed horse blood as described by the National Committee for Clinical
Laboratory Standards for susceptibility testing for Streptococcus
pneumoniae (11), and the results were read after 24 h of incubation at 37°C in an ambient air. S. pneumoniae ATCC 49619 was used as control strain. The MICs of the
11 antimicrobial agents for the control strain were within the ranges
provided by the National Committee for Clinical Laboratory Standards
(11). The MICs for the C. hominis isolate were as
follows: penicillin, >256 µg/ml; ampicillin, >256 µg/ml;
amoxicillin-clavulanic acid, 0.5 µg/ml; cephalothin, 4.0 µg/ml;
cefotaxime, 1.0 µg/ml; ceftriaxone, 1.0 µg/ml; tetracycline, 4 µg/ml; gentamicin, 0.5 µg/ml; ciprofloxacin, 0.5 µg/ml;
trimethoprim-sulfamethoxazole, 0.25 µg/ml; and vancomycin, 8 µg/ml.
The isolate produced -lactamase by means of the nitrocefin-based test (Cefinase disk; BBL Microbiology Systems).
Discussion.
C. hominis is a member of the HACEK group,
exhibiting the common characteristics of a slow growth rate and a
requirement of CO2 for optimal growth and causing similar
clinical syndromes (9, 10). Nearly one-third of the isolates
of Haemophilus aphrophilus and 40% of A. actinomycetemcomitans were reported to be resistant to penicillin
in 1961 (6). Compared with the other members of HACEK group,
C. hominis is rarely reported to be resistant to penicillin,
and penicillin or ampicillin has been considered the drug of choice for
treating infective endocarditis caused by this organism (1, 4, 9,
10, 13, 17, 18). Although a strain of penicillin-resistant
C. hominis was reported as early as in 1977 (J. J. Rahal, Jr., and M. S. Simberkoff, Program Abstr. 17th Intersci.
Conf. Antimicrob. Agents Chemother., abstr. 5, 1977), infection with a
-lactamase-producing strain was not reported until 1994 (8) and there was no further report of such a -lactamase
producer. Herein, we have reported another case of infective
endocarditis complicated with severe congestive heart failure due to
-lactamase-producing C. hominis.
It is not unusual for C. hominis to be misidentified
(7). The first case of endocarditis due to C. hominis in the Kingdom of Saudi Arabia was diagnosed as
Brucella endocarditis (5). The isolate we
reported was the first isolate of C. hominis in Taiwan and
was initially misidentified as P. multocida. Interestingly, C. hominis was described as a Pasteurella-like
organism when it was first isolated in 1962. The resemblance between
C. hominis and several other organisms may explain why this
bacterium, one of the upper respiratory tract flora (4), had
never been described until 1962 (14).
For correct identification of C. hominis in clinical
laboratory, it should be distinguished from other members of the HACEK group and from Pasteurella, Brucella,
Streptobacillus moniliformis, and Bordetella
parapertussis. The main characteristics of C. hominis distinguishing it from other closely related organisms are absence of
catalase activity, positive oxidase reaction, production of indole, and
absence of nitrate production (14). For example, Pasteurella is distinguished from C. hominis by
catalase positivity. The laboratory diagnosis of the HACEK group of
organisms requires a high index of suspicion. Organisms of this group
should be suspected in all cases of endocarditis in which a
gram-negative coccobacillary organism is isolated, an organism which
has failed to grow on MacConkey agar or any medium selective for
Enterobacteriaceae, shows characteristic rosette formation
upon Gram staining, and has a stellate colonial appearance.
The American Heart Association suggested that
trimethoprim-sulfamethoxazole, a fluoroquinolone, and aztreonam
could be considered as alternative regimens in patients unable to
tolerate -lactam therapy (17). Our patient developed an
allergic reaction to ceftriaxone, and ciprofloxacin was used to
complete the 4-week antimicrobial course. Bacteriologic cure was
documented with negative culture results from the excised aortic
valve and from a blood specimen after therapy.
Serious complications, such as embolic events and congestive heart
failure, among patients with C. hominis endocarditis during the course of therapy are not uncommon (44% for each complication), although bacteriologic cure may be achieved (10, 18). Severe cardiac failure demanding surgical intervention developed in our case
in spite of successful ceftriaxone and then ciprofloxacin therapy to
eradicate the pathogen.
Our case is the second reported case of endocarditis due to
-lactamase-producing C. hominis. The first reported
-lactamase-producing C. hominis isolated in France had an
antibiogram different from ours (8). That isolate was
susceptible to vancomycin and that patient was successfully treated,
with no sequels, with vancomycin and rifampin for 4 weeks, followed by
amoxicillin-clavulanate for 2 weeks. The MICs of gentamicin and
trimethoprim-sulfamethoxazole for our isolate were 0.5 and 0.25 µg/ml, respectively, whereas the previously reported isolate was
resistant to the two antimicrobial agents.
In vitro susceptibility testing may be difficult to perform and
interpret because of the fastidious nature and slow growth of C. hominis (7). There are no breakpoints for this
organism, nor have the correct medium or atmosphere and time of
incubation been established (11). Penicillin or ampicillin
has been the antibiotic of choice for C. hominis until now
(1, 4, 10, 13, 17, 18). In contrast to other members of the
HACEK group with a high frequency of penicillin resistance, C. hominis has rarely been reported to be penicillin-resistant
(5, 8, 9; J. J. Rahal, Jr., and M. S. Simberkoff, 17th ICAAC). Because of difficulties inherent in performing
antimicrobial susceptibility testing, in 1995 the American Heart
Association recommended that HACEK microorganisms should be considered
ampicillin-resistant and the third-generation cephalosporins should be
considered the antibiotics of choice (15). The facts that
the MICs of cefotaxime and ceftriaxone for this isolate were both
elevated (1.0 µg/ml) and that the previous -lactamase-producing
C. hominis was resistant to cefotaxime suggested that we
should be alert to the occurrence of -lactamase-producing C. hominis, noting its susceptibility to penicillin and the
third-generation cephalosporins.
Susceptibility of C. hominis to vancomycin is variable
(10). Our isolate showed reduced susceptibility to
vancomycin (MIC, 8 µg/ml). It should be noted that vancomycin and
erythromycin are recommended for prophylaxis of infective endocarditis
in patients allergic to penicillins. Failure of prophylaxis with
erythromycin for dental extractions may occur in the face of C. hominis resistant to erythromycin and vancomycin (12).
A therapy regimen including vancomycin as did the previous successful
treatment for -lactamase-producing C. hominis was not
suitable for our patient.
In summary, our case report has provided evidence that C. hominis, like the other HACEK microorganisms, can produce
-lactamase, and our results support the recommendation of American
Heart Association that the third-generation cephalosporins should be
considered the antibiotic of choice for the treatment of HACEK endocarditis.
| |
FOOTNOTES |
*
Corresponding author. Mailing address: Department of
Laboratory Medicine, National Taiwan University Hospital, No. 7 Chung-Shan South Rd., Taipei, Taiwan. Phone: 886-2-23562149. Fax:
886-2-23224263. E-mail: luhkt{at}ha.mc.ntu.edu.tw.
| |
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Journal of Clinical Microbiology, May 2000, p. 2015-2017, Vol. 38, No. 5
0095-1137/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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