Cardiobacterium hominis
Authors:Selwyn D R Lang, MBChB, FRACP, FRCPA, Victor L. Yu, M.D.
Authors (First Edition 1998, Second Edition 2002): Selwyn D R Lang, MBChB, FRACP, FRCPA, Arthur J Morris, BSc (Hons), MD, Dip ABMM, FRCPA
Cardiobacterium hominis is a slow-growing, fastidious, capnophilic, Gram-negative bacillus represented by the "C" in HACEK, an acronym for Haemophilusspecies, Actinobacillus actinomycetemcomitans, C. hominis, Eikenella corrodens and Kingella species (20). All these organisms have the propensity to cause endocarditis, but in the case of C. hominis this disease is, with rare exceptions, its only pathological manifestation (56).
C. hominis was first isolated from four patients with subacute bacterial endocarditis in 1962 and was described as a Pasteurella-like organism, designated "CDC group 11-D". The patients were middle-aged, from various parts of the United States and presented over a 10 month period (65). The name C. hominis was conferred in 1964 (58) and there is only the single species in the genus.
A recent review of endocarditis due to rare and fastidious bacteria (6) notes that C. hominis endocarditis has been recorded in 76 patients. For comparison, numbers due to other HACEK organisms are: Haemophilus species [178], Actinobacillus actinomycetemcomitans [93], Eikenella corrodens [19] and Kingella species [33] (6). To these should be added a single case due to Suttonella indologenes (formerly Kingella indologenes) (22). However, the term HACEK has not been replaced by HACEKS because of this report.
Microbiology
Although growth of C. hominis in modern commercial media is usually detectable after 3 to 5 days, incubation for 2 to 3 weeks is recommended before reporting a culture as negative (68,70). Routine Gram-staining and subculturing is essential since there is likely to be no visible change, such as turbidity or haemolysis, in the blood culture medium. On initial isolation the 1-3 μm long bacilli may be Gram-variable. They are frequently bulbous at one or both ends and arranged in short chains or rosettes. When grown in media containing yeast extract, these characteristic features may be lost and the cells appear as regular, regularly staining, Gram-negative bacilli (70). C. hominis grows on blood or chocolate agar at 35°C when there is adequate humidity and an atmosphere enriched by CO2. It will seldom grow on MacConkey agar or other enteric media. Small glistening opaque colonies usually become apparent after 2 or 3 days, but occasionally take up to 2 weeks. These colonies produce slight β-haemolysis and develop a rough appearance with serpentine growth at the edge (70). With further incubation C. hominis colonies may pit the agar. C. hominis is oxidase-positive, catalase-negative, nitrate-negative, urease-negative and indole-positive. These reactions may be weak on initial isolation but become more obvious with subculture (56). The positive indole reaction is useful in distinguishing C. hominis from other "HACEK" organisms, though it should be noted thatSuttonella indologenes, its closest relative based on 16S ribosomal RNA sequence analysis, is also indole-positive. C. hominis has white or yellowish, opaque colonies whereas those of S. indologenes are gray and translucent. C. hominis also differs from S. indologenes in giving a negative alkaline phosphatase reaction.
Epidemiology
Cardiobacterium hominis is a member of the normal upper respiratory flora in humans and may be found rarely on other mucosal surfaces. Slotnik, using a labeled, hyperimmune, rabbit antiserum and selective culture, was able to detect C. hominis in the upper respiratory flora of 68% of normal subjects. There was no predilection for any particular age or sex (59). C. hominis was also recovered from 2 of 159 cervical and vaginal smears (60). Organisms binding the specific antibody were seen in 70% of stool samples but could not be cultured (59). C. hominis has not been isolated from animals, soil, water or hospital equipment.
Human infection is endogenously acquired. Almost all cases reported have been endocarditis, or possible endocarditis (1-3,5-9,11-15, 17-21,23-27, 29-43,46-52,54,56,57,61,62,65-67,69-73). Although C. hominis was responsible for only 2 of 1,989 cases of endocarditis accumulated from 13 published series before 1983, it accounted for 14 of 111 cases in case reports of endocarditis due to "unusual organisms" (2). At least 75% of patients have had underlying anatomical cardiac defects such as rheumatic heart disease or congenital abnormalities (6, 70). Prosthetic heart valves were infected in 13%, all as late complications of the cardiac surgery (6, 70). In 44% of cases of endocarditis due to C. hominis there had been a prior dental procedure or evidence of gingival infection (6). One case followed gastrointestinal endoscopy (51). Most cases have been in middle-aged adults and, in contrast to endocarditis due to other HACEK organisms, the aortic valve is most frequently involved (6). Cases in children are rare but three cases have been reported in children (63)
Clinical Manifestations
Endocarditis due to C. hominis tends to be exceptionally low grade and insidious. In one case, systemic symptoms preceded the eventual diagnosis for 12 months (37) and of 34 cases identified up to 1983, the average duration of symptoms preceding diagnosis was 169 days (70). Despite, or perhaps in keeping with its chronicity, C. hominis tends to form large friable vegetations associated with frequent embolic complications (31, 43, 54, 70). The clinical presentation has included low-grade fever [86%], splenomegaly [59%], emboli [44%] and congestive heart failure [44%] (6). Several cases have presented with, or have developed, neurological symptoms and signs (18,19,29,34,47,69). One of these presented with meningitis (19). Intracranial mycotic aneurysm (34) and ruptured mycotic aneurysm of the superior mesenteric artery (57) illustrate the propensity forC. hominisendocarditis to embolize. Francioli et al noted that emboli were reported in 13 of 31 [42%] cases (19). Vasculitic manifestations such as glomerulonephritis (32), arthralgia and skin rashes, including a bullous eruption (12), may complicate C. hominis endocarditis and false positive tests for syphilis have been reported (70).
The outcome, with appropriate treatment, is generally good: overall 87% have survived with 30% undergoing valve replacement (6). In a review of 22 cases of infective endocarditis due to C. hominis, Robison et al reported a bacteriological cure in all but one case, and in an Enterococcus species, not C. hominis, was recovered from vegetations on the valve at postmortem (54).
Currie et al have reviewed 10 cases of C. hominis infection involving prosthetic valves to which they add the first reported involvement of an aortic homograft valve (13). In six cases the aortic valve alone was involved, in three the mitral valve alone and in two, both aortic and mitral valves. All were cured, five undergoing valve replacements primarily for haemodynamic reasons (13).
Rare cases of C. hominis focal infection, without endocarditis, include a pacemaker lead infection with vertebral osteomyelitis (45) and an abdominal abscess (53). In addition, there are occasional reported cases of sepsis and bacteraemia without evidence of endocarditis (16, 55).
Laboratory Diagnosis
In the clinical laboratory, C. hominis is recovered almost exclusively from blood cultures from patients with endocarditis. Automated blood culture systems generally produce small incremental changes in growth indices after 3-5 days, however, incubation in a liquid medium for at least 14 days is recommended before cultures are presumed to be negative (37). In one recent report, the organism was recovered only after terminal subculture following 10 days incubation of a BACTEC 6A blood culture bottle (35). C. hominis has also been cultured from vegetations on a native heart valve following failure of antibiotic treatment (36) and from an infected prosthetic valve in a patient whose blood cultures had remained negative (64). Characteristics that help distinguish C. hominis from other bacteria of the HACEK group are described in the section on microbiology (above).
In one reported case, in which cultures of blood and valve tissue remained negative, the diagnosis of C. hominis endocarditis was established by examining arterio-embolic tissue removed by percutaneous, transluminal, embolectomy, using polymerase chain reaction amplification of the 16 rRNA gene followed by single chain sequencing (43). Further support for the diagnosis of C. hominis infection in this patient was provided by his developing a high titer of antibody to C. hominis. The assay used was one described in measuring the antibody response to C. hominis during treatment (72). Healthy upper respiratory carriers of C. hominis do not develop an antibody response (70). In another case of endocarditis, MALDI-TOF mass spectrometry plus nucleotide sequencing was used to identify this bacterium (10).
Pathogenesis
C. hominis is of low virulence (56). Using the original clinical isolate, Tucker et al were unable to produce disease in animals. Between 107 and 108 viable organisms were injected intravenously, intraperitoneally or subcutaneously into mice, guinea pigs, rabbits, hamsters and pigeons, but produced no evidence of infection (65). It has been suggested that this is in keeping with the tendency of C. hominis to affect previously damaged or prosthetic valves and to run a relatively chronic course (56).
SUSCEPTIBILITY IN VITRO AND IN VIVO
Susceptibility testing of C. hominis can be difficult owing to the fastidious nature and slow growth rate of the organism. It is important, however, to perform susceptibility testing because the result is never entirely predictable.
Table 1 summarizes representative susceptibilities of several strains to a range of antibiotics (21). Notably, all 22 isolates tested against penicillin were susceptible; however, one isolate developed resistance to ampicillin during treatment (52). More recently, Kugler et al tested 29 antimicrobials against HACEK organisms, including five isolates of C. hominis, using the E-test method. None were β-lactamase producers. MIC50 values were ≤ 0.016 µg/ml in the case of penicillin, ampicillin, ampicillin/sulbactam, ticarcillin, piperacillin/tazobactam, cefixime, ceftibuten, cefpodoxime, cefdinir, cefuroxime, cefoxitin, imipenem and meropenem and ≤ 0.2 µg/ml in the case of cefprozil, cefotaxime, ceftriaxone, ceftazidime, cefepime, cefpirome, ciprofloxacin, clinafloxacin, grepafloxacin, levofloxacin, sparfloxacin, trovafloxacin and rifampicin. Carbapenems were the most active of all the agents tested. Oxacillin was the least active β-lactam (range MIC 0.5-4 µg/ml), and ofloxacin the least active fluoroquinolone (range MIC 0.032-8 µg/ml). The MIC range of trimethoprim/sulphamethoxazole was 0.5-1.5 µg/ml (28).
There are very few published data on the bactericidal activity of antibiotics for C. hominis. Chloramphenicol has been noted to achieve bactericidal titers in serum of 1:32 in a patient with C. hominis infection successfully treated with this drug (52). Vogt et al. reported MIC/MBC (µg/ml) for a single isolate: penicillin 0.06/0.06, mezlocillin 0.5/0.5, tobramycin 1/2, imipenem 0.06/0.25, and ciprofloxacin 0.06/0.06 (66). Their patient developed renal toxicity while receiving treatment with mezlocillin and gentamicin, relapsed on mezlocillin alone, and was cured with ciprofloxacin. Both peak and trough sera were rapidly bactericidal while the patient received ciprofloxacin.
Although ampicillin-resistance was reported to have emerged during treatment of a case of C. hominis endocarditis in 1977 (52), there have been only two case reports of C. hominis endocarditis due to β-lactamase producing strains (34,35). In each case β-lactamase production was confirmed using a chromogenic cephalosporin test and susceptibility to amoxicillin was restored in the presence of clavulanic acid. Since different susceptibility testing methods were used, direct comparison of the susceptibilities of the two isolates is difficult. The French isolate (33) was tested using a disc diffusion method and was noted to be susceptible to tetracycline, rifampicin, vancomycin, and imipenem but resistant to cefotaxime, erythromycin, cotrimoxazole and gentamicin. The Taiwan isolate (35) was tested using a broth dilution method and the breakpoints for Streptococcus pneumoniae (44). Minimum inhibitory concentrations (μg/ml) of penicillin and ampicillin were >256 and that of amoxicillin/clavulanate 0.5; cephalothin 4.0; cefotaxime and ceftriaxone 1.0; tetracycline 4.0; gentamicin 0.5; ciprofloxacin 0.5; trimethoprim/sulphamethoxazole 0.25 and vancomycin 8.0.
ANTIMICROBIAL THERAPY
General
For many years, penicillin or ampicillin, alone, or in combination with an aminoglycoside, were regarded as the standard treatment for endocarditis due to HACEK organisms (20). Serum bactericidal titers for C. hominis in patients given penicillin alone have ranged from 1:256 to 1:2560 and the average duration of treatment for cured patients was 37 days with a range of 12-49 days (71). Twenty-seven [87%] of 31 patients with C. hominis endocarditis, including all 4 patients with prosthetic heart valve involvement, were cured (71). However, with the emergence of β-lactamase producing strains within the HACEK group of organisms an ad hoc writing group for the American Heart Association (68) now recommends cefotaxime or ceftriaxone as the drugs of choice for treatment of HACEK endocarditis, an approach endorsed by others (4). The recommended dose of ceftriaxone is 2g once daily intravenously or intramuscularly. The recommended duration of treatment is 3-4 weeks for native valve disease and 6 weeks when a prosthetic valve is involved (68). A successful outcome has been reported in 11 patients with C. hominis infection of prosthetic valves (13). Treatment regimens ranged from ampicillin or ceftriaxone alone for 4 weeks, to penicillin or ampicillin, plus gentamicin for almost 6 weeks, and in the only reported case of aortic homograft valve infection, ceftriaxone and gentamicin for 18 days followed by oral amoxicillin.
Although third generation cephalosporins have been recommended because of the occurrence of β-lactamase-producing HACEK organisms (68), this might be questioned for C. hominis infection since ceftriaxone was seemingly ineffective in both cases due to β-lactamase-producing strains. The one patient, whose organism was resistant to cefotaxime in vitro, remained febrile after receiving ceftriaxone for 6 days, and was eventually cured using a combination of vancomycin and rifampicin followed by amoxicillin/clavulanate and rifampicin (33). The other patient received ampicillin and gentamicin for two weeks, then ceftriaxone (MIC 1.0 μg/ml) 2 g 12 hourly for a further three weeks. At this time she developed a skin rash and was changed to intravenous ciprofloxacin 400 mg 12 hourly, before undergoing aortic valve replacement for progressive heart failure (35). Although neither patient was proven to have bacteriological failure following the recommended course of ceftriaxone, they illustrate the importance of determining susceptibilities in each case and the occasional need for alternative treatment options. Based on limited data, it would seem reasonable to treat infection due to β-lactamase producing strains of C. hominis with a carbapenem, a β-lactam/β-lactamase-inhibitor combination or a fluoroquinolone. It should, however, be noted that the fluoroquinolones have variable activity e.g. ofloxacin MIC as high as 8.0 μg/ml (28).
Alternative Therapy
The American Heart Association's preferred alternative to a third generation cephalosporin is combination treatment with ampicillin and gentamicin, providing the isolate does not produce β-lactamase (68). The recommended dose of ampicillin is 12g/day intravenously, either continuously or in 6 equally divided doses and that of gentamicin is 1mg/kg intramuscularly or intravenously 8-hourly. Monotherapy with ampicillin is no longer recommended. These recommendations are necessarily made on the basis of scanty published data.
There are few precedents for managing infection due to isolates resistant to penicillins or cephalosporins, or for treating patients unable to tolerate these antibiotics. Gentamicin alone for 6 weeks has been reported to be successful (5). However, the suggested treatments for those with β-lactam allergies are aztreonam or fluoroquinolones or trimethoprim-sulphamethoxazole, provided susceptibility is confirmed (68). While combination treatment with a β-lactam plus an aminoglycoside is commonly used, there is no evidence that it is superior to monotherapy for C. hominis endocarditis.
(Printable Version of Antimicrobial Therapy for Cardiobacterium hominis)
ADJUNCTIVE THERAPY
Adjunctive therapy is primarily valve replacement when required. Steroid treatment has been used for glomerulonephritis complicating C. hominis endocarditis (32).
As in the prevention of any endocarditis due to normal oral flora, prevention entails good dental hygiene. Regimens recommended to prevent viridans streptococcal endocarditis are generally likely to be effective. However, exceptions are inevitable: one case report documents C. hominis endocarditis due to a strain resistant to erythromycin (MIC 12.5 μg/ml) and vancomycin (MIC 25μg/ml) in a penicillin allergic patient who had received prophylactic erythromycin for a dental extraction (50).
ENDPOINTS FOR MONITORING THERAPY
The endpoints are similar for other causes of endocarditis. Blood cultures should be repeated if fever persists during antibiotic therapy or recurs following conclusion of long-term therapy.
VACCINES
There are no vaccines available for C. hominis.
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Tables
Table 1. In Vitro Susceptibilities Cardiobacterium hominisa
| Antimicrobial agent | n | Representative MIC (µg/ml)b | Breakpointc | n (%) susceptible |
|---|---|---|---|---|
| Penicillin | 22 | 0.05 | 22 (100%) | |
| Ampicillin | 16 | <0.4 | < 1 | 15 (94%) |
| Oxacillin | 3 | NAd | 2 (67%) | |
| Carbenicillin | 5 | <1.6 | 5 (100%) | |
| Cephalothin | 11 | <0.4 | 11 (100%) | |
| Chloramphenicol | 17 | 1.25 | 17 (100%) | |
| Colistin | 2 | NA | 2 (100%) | |
| Trimethoprim-sulphamethoxazole | 3 | NA | <0.5/9.5 | 3 (100%) |
| Sulfonamide | 1 | NA | 0 (0%) | |
| Tetracycline | 19 | 0.25 | <2 | 19 (100%) |
| Erythromycin | 14 | NA | 11 (79%) | |
| Gentamicin | 9 | <0.8 | 8 (89%) | |
| Kanamycin | 6 | <0.8 | 1 (17%) | |
| Streptomycin | 14 | 1.6 | 14 (100%) | |
| Tobramycin | 2 | NA | 2 (100%) | |
| Rifampin | 1 | NA | < 1 | 1 (100%) |
| Vancomycin | 3 | 25 | 1 (33%) | |
| Clindamycin | 2 | 5 | 0 (0%) |
aModified from Wormser GP, Bottone EJ. Cardiobacterium hominis: review of microbiological and clinical features. Rev Infect Dis 1983; 5:680-691.(70)
bMIC50, MIC90 and MIC Range not reported.
cNational Committee for Clinical Laboratory Standards. 2001. Performance Standards for Antimicrobial Susceptibility Testing; Eleventh Informational Supplement. NCCLS document M100-S11; MIC Interpretive Standards (µg/ml) for Haemophilus spp. National Committee for Laboratory Standards, Wayne, Pa.
dNA = Data not available
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