Rothia dentocariosa
Authors: Sara Droz and Reinhard Zbinden
Author, First Edition, R. Zbinden, M.D., MSc
Microbiology
The Genus Rothia has encountered many taxonomic changes in the last 15 years. Rothia dentocariosa, the type species of the genus, is an aerobic coccoid to rod-shaped, non-sporogenic, non-motile, catalase-positive Gram-positive bacterium; younger colonies are round, convex, smooth or creamy and, therefore, may resemble those of corynebacteria and staphylococci; mature colonies may be raised and highly convoluted (19). According to the amended description, some strains form charcoal-black colonies and are catalase negative (13). The very similar genomo-var II of R. dentocariosa was included in the newly described Rothia aeria (33); this species might encounter further taxonomic changes in the near future since many isolates of Rothia spp. most closely related to R. aeria from blood cultures are very similar to R. dentocariosa, but easily differentiated by 16S rRNA gene sequencing (20). Stomatococcus mucilaginosus was reclassified as Rothia mucilaginosa (11). Only these three species are further discussed in this chapter. Rothia nasimurium has been isolated from the nose of a mouse (11), Rothia amarae isolated from sludge of a water sewer (17), Rothia terrae isolated from soil in Taiwan (10) and Rothia endophytica isolated from healthy roots of Dysophylla stellata (Lour.) (72); these four species are not associated with human infections.
Epidemiology
R. dentocariosa was originally isolated from dental plaques and caries. It is found in the oral cavity and pharynx of man where it forms part of the normal microflora (19). An investigation of throat swabs showed that R. dentocariosa is present in over 30% of healthy individuals (21). Therefore, it can also be isolated from respiratory tract specimens as part of the normal oral flora (68, 29). However, clinical relevant isolates of R. dentocariosa have been found in patients with periodontal lesions which might be the source for transient bacteremia resulting in systemic diseases, similar to other oral bacteria (3). The habitat of R. mucilaginosa and the Rothia strains closely related to R. aeria are similar to that of R. dentocariosa (11, 33).
Clinical Manifestations
Periodontal disease is the most common infection where R. dentocariosa is involved together with other established oral bacteria . It can also be isolated together with anaerobic and facultatively anaerobic microflora from pericoronal pockets of mandibular third molars showing symptoms of acute, severe pericoronitis (45).
Over the past 40 years, several infectious disease entities caused by R. dentocariosa have been reported of which infective endocarditis is the predominant and most severe clinical manifestation (3, 4, 5). Three valve involvement and prosthetic valve endocarditis have been documented (3, 52). Sequelae and complications of endocarditis include abdominal aneurysm (70), perivalvular abscess (3, 22, 61), cerebral abscess (3, 25), intracerebral hemorrhages (3, 51, 54), and vertebral osteomyelitis (34).
Other complications include: bacteremia (55, 60, 71, 73), endophthalmitis (36), corneal ulcer (41), infection of an arteriovenous fistula (43), septic arthritis (18) and peritonitis associated with continuous ambulatory peritoneal dialysis (2, 15, 28), periappendiceal abscess (57), and pilonidal abscess (35). There is some evidence that R. dentocariosa must be considered a cause of opportunistic pulmonary infection. The first case of R. dentocariosa pneumonia was described in an 84-year-old woman with acute myelocytic leukemia; the diagnosis was based on a positive culture of a transthoracic needle aspirate (58). Two further cases of pneumonia were described in patients with lung cancer; the diagnosis was based on isolation of pure cultures of R. dentocariosa from pleural fluid and bronchoalvelar lavage (65).
R. aeria has been mainly associated with endocarditis (29) which were complicated by embolization (42) and cerebral hemorrhage (62). Other described infections are septic arthritis (66), bronchitis (38), neck abscess (16), neonatal sepsis (39), intrauterine infection with fetal death (27) and prosthetic -associated knee infections, mainly in immunocompromised patients (29).
R. mucilaginosa has caused septicaemia and meningitis, especially in children with hematological malignancies (8, 32, 49), pneumonia (9), septic arthritis (66), peritonitis associated with peritoneal dialysis (23, 24), peritonitis mostly in neutropenic patients (8), infectious granulomatous dermatitis (40), soft tissue infections (64) and prosthetic valve endocarditis (7).
Laboratory Diagnosis
Colonies of R. dentocariosa are nonhemolytic on human or sheep blood agar and with raised and highly convoluted morphology after some days (19). R. dentocariosa ferments glucose, maltose, fructose, and sucrose, but not lactose (13), xylose or mannitol; other positive reactions are reduction of nitrate, esculin hydrolysis, and catalase; oxidase and urease reactions are negative (68, 69). Some strains might be negative for catalase and nitrate, and positive for urease (43, 69). Lactic acid is the major end product from glucose, together with acetic acid and a small amount of succinic acid (68). Rothia is in the database of the API Coryne V2.0 (bioMérieux sa, France); positive enzyme reactions in this test strip are the pyrazinamidase and α-glucosidase (66), negative enzyme reactions comprise the alkaline phosphatase (13) and β-glucuronidase (68). The conventional methods cannot differentiate R. aeria from R. dentocariosa but the MALDI-TOF method can do so (16, 49). The reactions of R. mucilaginosa are similar but catalase is usually negative; the mucoid and adherent colonies to agar surfaces differentiate them from R. dentocariosa (11) Since R. mucilaginosa forms predominately Gram-positive cocci, it is in the databases of the commercial kits of Gram-positive cocci.
SUSCEPTIBILITY IN VITRO AND IN VIVO
R. dentocariosa seems universally susceptible to penicillin. An earlier investigation of 90 strains of R. dentocariosa isolated from dental plaques, carious lesions, and periodontal tissue showed high sensitivity against penicillins, cephalosporins, erythromycin and tetracycline. However, lincomycin and to a lesser extent clindamycin showed poor activity (14). An investigation of ten strains mostly isolated from blood showed susceptibility to penicillin G, penicillin V, ampicillin, piperacillin, cefuroxime, cefotaxime, imipenem, gentamicin, tetracycline, erythromycin, clindamycin, chloramphenicol, rifampicin, vancomycin, and ciprofloxacin (31). However, resistance to aminoglycosides (3, 30, 36, 52) and ciprofloxacin (36, 52) have been reported. Table 1) shows all published minimal inhibitory concentrations of R. dentocariosa and R. aeria isolated from the cases of endocarditis and bacteremia.
R. mucilaginosa is generally susceptible to penicillin, ampicillin, cefotaxime, imipenem, rifampicin and vancomycin are partially resistant to penicillin. It is frequently resistant to clindamycin, aminoglycosides, trimethoprim-sulfamethoxazole and ciprofloxacin (7). The in vitro susceptibility of 63 strains of R. mucilaginosa to antimicrobial agents showed for penicillin a MIC (mg/L) range of ≤0.03-1, a MIC 50% of ≤0.03 and a MIC 90 % of 0.125; the corresponding values for gentamicin were ≤0.03-16, 2 and 4, for erythromycin ≤0.03->16, 1 and 1, for clindamycin ≤0.03->16, 0.5 and 2, for fosfomycin ≤0.03->16, 1 and >16, for fusidic acid ≤0.03-0.5, 0.5 and 0.5, for vancomycin ≤0.03->1, 0.5 and 1, respectively; all strains had an MIC ≤0.03 against rifampicin (67).
ANTIMICROBIAL THERAPY
Drug of Choice
Penicillins and cephalosporins have an excellent activity against R. dentocariosa, R. aeria and R. mucilaginosa and are the drugs of choice (3, 7, 67). However, animal studies (19) and in vitro bactericidal studies are limited (6) and clinical studies are not available. Combination therapy is advisable for severe infections. A synergistic antimicrobial effect between aminoglycosides and penicillin or vancomycin might be expected but probably depends on the particular isolate of Rothia sp. A few multiple resistant strains as well as strains resistant to penicillins and cephalosporins due to production of β-lactamase have been described (14, 67). Therefore, susceptibility testing is necessary for all relevant isolates of Rothia sp. in associated with prosthetic device infections; an antibiotic combination with rifampicin might be successful (3, 7).
Special Situations
Endocarditis
Penicillin or cephalosporins for 6 weeks, with or without an aminoglycoside for the initial 1 to 2 weeks, is the treatment of choice (51). However, decreased susceptibility to aminoglycosides has been reported in which case combinination of a β-lactam with rifampicin is recommended (3). In addition to penicillin, vancomycin has been regarded as a first-line drug in the treatment of endocarditis due to R. dentocariosa. However, its in vitro susceptibility to vancomycin was less favorable as assessed by minimal inhibitory concentrations (3). Furthermore, clinical failure of vancomycin has been reported (61). Surgery is recommended in cases of associated paravalvular abscess (22). The clinical outcome after appropriate antibiotic treatment for at least 6 weeks was favorable despite presence of prosthetic valves or occurrence of extra-cardiac complications including brain abscess and mycotic and aortic aneurysms (3). Three deaths have been reported in patients with R. dentocariosa endocarditis; one of these patients died after emergency aortic valve reconstruction and replacement due to progressive cardiac failure (3), and two patients had paravalvular abscesses (22, 61). Fatal outcome of endocarditis has also been described for R. aeria with hemorrhagic complications (43, 62) and for R. mucilaginosa in intravenous drug users with a prior valve replacement (7). A summary of is listed in Table 2.
Other Infections:
Patients with R. dentocariosa pneumonia were cured with ceftriaxone (2 g per day) or amoxicillin/clavulanate (2 g per day) for 2 weeks (65) or with clindamycin for several weeks (58). An abdominal infection with R. dentocariosa was successfully treated with 2,400,000 U penicillin for 9 days after surgical intervention (57). A patient with peritonitis receiving continuous ambulatory peritoneal dialysis (CAPD) became afebrile with oral amoxicillin/clavulanate (500/125 mg, three times daily) and intravenous amikacin (125 mg per day) (2). Intraperitoneal cefazolin (250 mg per bag four times daily) plus netilmicin (50 mg once per day into the night bag) therapy cured another CAPD patient with peritonitis within 5 days (15). Alternative therapy of relapsing peritonitis using intraperitoneal ciprofloxacin and amikacin was successful (28).
Prosthetic joint infections with Rothia spp. usually requires removal of the prosthesis plus antibacterial agent therapy (37).
R. mucilaginosa is increasingly recognized as a cause of prosthetic device infections (7).
Underlying Diseases
Extensive periodontal disease or multiple carious teeth have been reported in most cases of endocarditis (22).
Peridontal disease is a predisposing risk factor for infections with R. dentocariosa. Most patients with R. dentocariosa endocarditis were over 40 years old and only one patient with endocarditis was described in a female patient (3, 25). Most patients had underlying valvular heart disease or prosthetic valves (3). Recent dental manipulation (6, 56) or intravenous drug abuse were also reported (61). Endocarditis prophylaxis might be useful for dental procedures associated with gingival bleeding (5).
R. aeria is an opportunistic pathogen of immunocompromised (29). History of dental caries or tooth extraction might be a risk factor (42).
The major clinical manifestation of R. mucilaginosa infection is bacteremia, mainly in patients with neutropenia associated chemotherapy (39).
Alternative Therapy
In patients allergic to penicillin, a combination of rifampicin and a second antimicrobial agent with activity against R. dentocariosa, e.g., ciprofloxacin, is suggested for treatment of endocarditis (3). Other infections can be treated with macrolides, tetracycline or clindamycin. However, susceptibility testing is warranted for each clinical isolate of Rothia sp.
ADJUNCTIVE THERAPY
Dental procedures and extractions to remove pockets of infection may be necessary. Cure of endocarditis may require valvular replacement.
ENDPOINTS FOR MONITORING THERAPY
For patients with endocarditis, blood cultures are indicated if objective signs of infection persist while receiving appropriate antibiotic therapy. For periodontal infection, the endpoints should be based on clinical response since these infections are polymicrobial and Rothia species are normal flora.
VACCINES
No vaccines are available for this uncommon pathogen which is part of the normal flora of the oropharynx.
PREVENTION
The American Heart Association's recommendations for antibiotic prophylaxis for dental procedures should theoretically minimize the risk of endocarditis associated with dental procedures.
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Tables
Table 1. In vitro Susceptibilities (MICs) of Rothia dentocariosa and Rothia aeria Ioslated from Cases of Endocarditis and Bacteremia
| Antimicrobial Agent | n | Range | MIC50 (mg/mL) | MIC90 (mg/mL) | Reference |
|---|---|---|---|---|---|
Penicillin |
22 |
0.001-0.75 |
0.016 |
0.12 |
1,3,4,6,12,23,28,32,45,47, 57-59,62,65,70,73 |
Cefazolin |
4 |
0.016-2 |
0.25 |
0.25 |
28, 57, 59, 73 |
Ceftriaxone |
10 |
0.016-1 |
0.02 |
4 |
1,3,12,28,58,62,65 |
Gentamicin |
15 |
0.25-8 |
2 |
3 |
1,3,4,6,12,23,32,45,58,59,73 |
Vancomycin |
15 |
0.25-4 |
1.5 |
3,12,23,32,45,57,62,65 |
|
Rifampicin |
5 |
0.004-0.5 |
0.016 |
1,3,6,12 |
|
Clindamycin |
9 |
0.048-2 |
0.5 |
3,4,57,58,65,73 |
|
Ciprofloxacin |
9 |
0.06-1 |
0.75 |
1,3,12,45,57,58 |
|
Erythromycin |
6 |
0.016-0.12 |
0.02 |
3,32,57,59,73 |
|
Tetracycline |
4 |
0.16-1 |
0.5 |
3,57,59 |
Table 2. for Treatment of R. dentocariosa, R. aeria and R. mucilaginosa Endocarditis
| Patient Age/Sex | Antibiotic Treatment | Duration | Special Condition | Reference |
|---|---|---|---|---|
R. dentocariosa |
||||
50/M |
Ceftriaxone, rifampicin |
6 weeks |
Intracerebral hemorrhage |
3 |
67/M |
Ceftriaxone, teicoplanin, netilmicin followed by rifampicin, ciprofloxacin |
4 weeks/6 weeks |
Bioprosthesis |
3 |
61/F |
Penicillin |
6 weeks |
Mitral valve replacement |
4 |
17/F |
Penicillin, amikacin* |
4 weeks/1week* |
Aortic valve replacement |
4 |
6/F |
Ceftriaxone |
6 weeks |
Surgery, 2 months later |
5 |
53/M |
Gentamicin, rifampicin, penicillin |
8 weeks, 6 weeks* |
Rheumatic mitral valve disease |
6 |
27/F |
Penicillin, gentamicin followed by penicillin |
1 week/6 weeks |
Brain abscess |
28 |
37M |
Penicillin, netilimicin |
6 weeks, 3 weeks* |
Triple-valve surgery |
33 |
62/M |
Penicillin, gentamicin followed by ceftriaxone |
4 weeks, 2weeks*/2weeks |
Vertebral osteomyelitis |
36 |
58/M |
Penicillin, gentamicin |
7 weeks, 4 weeks* |
Valve replacement |
47 |
49/M |
Vancomycin, gentamicin followed by penicillin |
3 weeks, 10 days*/6 weeks |
Multiple intracranial hemorrhages |
54 |
71/M |
Penicillin, gentamicin followed by ceftriaxone followed by penicillin |
1 week/1 week/4 weeks |
Prosthetic aortic valve |
55 |
55/M |
Penicillin G, gentamicin |
6 weeks, 2 weeks* |
Multiple cerebellar hemorrhages |
57 |
57/M |
Penicillin, streptomycin |
6 weeks, 2 weeks* |
Mitral valve prolapse |
59 |
37/M |
Vancomycin, penicillin G followed by ceftriaxone |
1 week/6 weeks |
Mitral valve prolapse |
59 |
17/M |
Ceftriaxone followed by penicillin, gentamicin |
1 week/ 6 weeks, 2 weeks* |
Abdominal aneurysm |
70 |
R. aeria |
||||
48/M |
Benzylpenicillin, gentamicin followed by benzylpenicillin, ceftriaxone followed by rifampicin, ciprofloxacin |
2 weeks/ 8 weeks/ 12 weeks |
Brain septic embolization; spleen and left kidney infacrtion; right renal artery and hepatic artery aneurysms |
12 |
53/M |
Ceftriaxone |
4 weeks |
Aortic valve replacement, permanent pacemaker implantation |
32 |
25/M |
Ampicillin |
5 weeks |
Bicuspid aortic valve |
45 |
63/M |
Penicillin G |
8 weeks |
Brain septic embolization |
45 |
61/M |
Benzylpenicilllin, rifampicin, gentamicin |
4 weeks, 1 week* |
Brain septic embolization |
66 |
R. mucilaginosa |
||||
35/M |
Vancomycin, gentamicin |
8 weeks, 4 weeks* |
Aortic valve replacement, intravenous drug abuse (IVD) |
7 |
36/M |
Vancomycin |
6 weeks |
Prosthetic valve, IVD |
7 |
44/M |
Penicillin G |
6 weeks |
Mitral valve prolapse, cerebral mycotic aneurysm |
49 |
46/M |
Penicillin G |
6 weeks |
Mitral valve prolapse |
51 |
34/F |
Penicillin G |
6 weeks |
Mitral valve prolapse, IVD |
53 |
63/M |
Penicillin G |
5 weeks |
Rheumatic carditis |
56 |
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