- Email: [email protected]
Rothia dentocariosa Endocarditis
J. Infect. Dis. 18 1:344-348. 20. Mounts, A.W. et al. 1999. Casscontrol study of risk factors for avian influenza A (H5Nl) disease, Hong Kong, 1997. J. Infect. Dis. 180:505-508.
21. Peiris, M. et al. 1999. Human infection with influenza H9N2. Lancet 354:9 16917. 22. Guo, Y.J. et al. 1999. Discovery of humans infected by avian influenza A (H9N2) virus. Chinese J. Exp. Clin.
Virol. 15:105-108. 23. Lin, Y.P. et al. 2000. Avian-to-human transmission of H9N2 subtype influenza A viruses: Relationship between H9N2 and H5Nl human isolates. Proc. Natl. Acad. Sci. U.S.A. 97:9654-9658.
Case Report
Rothia dentocariosa Endocarditis Julie Larkin, M.D.
Jose Montero, M.D. Marcel0 Targino, M.S. Alex Powers, M.S. CathyAccurso,B.A.,M.P.H. Monica Campbell, B.S. Division of Infectious Disease Department of Internal Medicine University of South Florida Tampa, FL 33602-1289 Rothia dentocariosa is a pleomorphic gram-positive bacillus, which is part of the normal flora in the human oral cavity but is rarely reported to cause human disease. This organism was first isolated in 1949 by Onisi from carious dentine and named Actinomyces dentocariosus (1). The bacterium was later renamed Nocardia dentocariosus due to its preference for aerobic conditions of growth (2). In 1967, Georg and Brown placed the organism under the Actinomycetaceae family within a new genus Rothia (3). In this report, we describe a case of R. dentocariosa endocarditis diagnosed after vascular embolic complications were noted. Furthermore, we review the literature and present previously known cases of R. dentocariosa endocarditis.
Case Report A 6 l-year-old white female was admitted to the hospital on 715197with acute bilateral lower extremity pain. An aortogram demonstrated an occluded left common iliac artery (consistent with an acute thrombus) as well as occlusion of the right superficial femoral artery at its origin. There were also several occluded vessels emerging from the right profumla femoral artery, again suggesting embolic disease. The patient underwent an emergent right femoral and left iliac embolectomy. Her previous cardiac history was notable for Clinical Microbiology
Newsletter 23:2,2001
chronic atrial fibrillation and longstanding mitral stenosis. She had no documented history of rheumatic heart disease. Seventeen days after initial admission, the patient developed a fever of 102OFand was readmitted. She denied fever or chills prior to admission but noted that she had “chest congestion.” Physical examination revealed an absence of native dentition with full upper and lower dentures present, and an irregular heart rhythm with a grade II/VI diastolic murmur. There was no evidence of hepatomegaly, splinter hemorrhages, or change in mental status. Her recent surgical wounds had minor incisional ecchymoses and hematomas but were otherwise healing appropriately. Laboratory data revealed a leukocyte count of 9.0 x 109/1,a hemoglobin value of 10.2 g/dl, and urinalysis was remarkable only for three to five erythrocytes. Blood cultures were performed and revealed growth of gram-positive bacilli within 72 h of incubation. Intravenous vancomycin therapy was started, but was changed to intravenous penicillin when Actinomyces-like organisms were found growing on culture. Transthoracic and transesophageal echocardiogram demonstrated severe mitral stenosis with thick mitral valve leaflets consistent with rheumatic heart disease. No vegetations were found but a thrombus was seen in the atria1 appendage. Blood cultures grew R. dentocariosa and the patient was treated with a six-week course of intravenous penicillin for a presumed endovascular infection with R. dentocariosa. Following her antibiotic therapy, she underwent elective mitral valve replacement.
Blood Culture Methods and Microbiology A specimen for blood culture drawn 0 2001 Elsevier Science Inc.
from a peripheral site was placed on the BacT/Alert automated blood culture instrument (Organon Technika, Durham, NC). The anaerobic culture bottle flagged positive after 2.5 days of incubation. The Gram stain results showed diphtheroid-like, gram-positive rods. The organism was subcultured to blood and chocolate agars for isolation. It was also subcultured on two CDC anaerobic plates placed at different atmospheres (aerobic and anaerobic) for oxygen requirement evaluation. Results of the subculture revealed a non-pigmented, catalase-positive, non-motile, nonhemolytic, non-spore forming, pleomorphic, aerobic bacillus. Further testing indicated that the organism was nonacid fast, nitrate positive, esculin positive, urea negative, and gram positive. Because R. dentocariosa is a rare isolate, definitive identification is a challenge. When the Gram stain showed gram-positive rods, the initial impression was a Propionibacterium acnes-like or coryneform-like organism. Because the organism grew aerobically and anaerobically on blood agar, a Propionibacterium spp. was ruled out. The catalasepositive and acid fast-negative test results placed the organism into the aerobic, non-spore-forming, gram-positive bacillus category similar to Corynebacterium spp. An ANI (Vitek, Hazelwood, MO) test identified, with 98% certainty, the isolate as Actinomyces odontolyticus. The Rapid ANA II system identified the organism as Actinomyces israelii (95 percent certainty). However, after the organism was found to be aerobic and catalase positive, neither identification could be accepted. These identification systems are restricted to anaerobic isolate identification thus demonstrating the need to determine whether a gram0196-4399/00 (see frontmatter)
13
positive rod will grow in air. A Rapid Coryne (bioMerieux S.A.) test strip was unable to identify the organism. Conventional tube biochemicals were performed as per Table 1. At this point, review of the cumulative information available in conjunction with standard microbiological reference textbooks identified the organism as R. dentocariosa (4). The National Committee for Clinical Laboratory Standards (NCCLS) does not have standards for R. dentocariosa susceptibility testing. No susceptibility testing was performed on our isolate. Discussion Clinical infection due to R. dentocariosa has been reported rarely. Although this organism is considered to be of low virulence, there have been reports of clinical infections including periappendiceal abscess (5), pilonidal abscess (6) pneumonitis in an immunocompromised host (7), septicemia in a patient with chronic lymphocytic leukemia (B), and infection of an arteriovenous fistula (9). The most frequent clinical manifestation of serious infection by R. dentocariosa has been infective endocarditis, previously reported in 13 patients (1 O-22). Table 2 summarizes all reported cases of R. dentocariosa endocarditis, the antibiotics used to treat them, and the result of treatment.
Table 1. Summary of isolate properties Result Test
Our isolate
Type strain
Aerobic
+
+
Catalase
+
V
CDC aerobic
4+ growth
+
CDC anaerobic
4+ growth
+
+
Esculin
+
Hemolytic on blood agar
NR
Kinyoun stain Motility Nitrate
+
t
Nutrient agar
1+
t
ONPG
+
NR
Pigment
NR +
+
AlWAcid
NR
weak+
NR
Pleomorphic Spore forming TSI Urease VP
Key: +, positive; -, negative; NR, not reported; V, variable
Although four previous cases required surgery, medical management generally resulted in cure. Three deaths have been reported (15,19,30), two as a result of complicated valvular surgeries. All previously reported cases of endocarditis caused by R. dentocariosa
had antecedent signs and symptoms consistent with endocarditis. Our case is atypical in that our patient demonstrated fever only after admission to the hospital and treatment for her vascular embolic disease. As well, most cases have been associated with periodontal
Table 2. Previous cases and outcomes PT. age/sex
Case (Ref.)
Outcome
Antibiotic treatment
Cure
1(10)
58/M
Penicillin + gentamicin
2(ll)
57/M
Penicillin + streptomycin
Cure
3(12)
53iM
Penicillin + gentamicin + rifampin
Cure
4(13)
27/F
Penicillin + gentamicin
Cure
504)
41/M
Penicillin, then vancomycin + gentamicin Retreated with penicillin + vancomycin
Cure
6(16)
4olM
Vancomycin + gentamicin
Cure
7(l7)
71/M
Penicillin + gentamicin; failed ceftriaxone
Cure
8(15)
35/M
Vancomycin + gentamicin
9(18)
17/M
Amoxicillin/clavulanate
lO(19)
7oiM
Penicillin + netilmicin + vancomycin
ll(19)
67N
Rifampin + ciprofloxacin
Cure
12(19)
SO/M
Rifampin + ceftriaxone
Cure
13(20)
37/M
Amoxicillin
Perivalvular abscess; death
+ gentamicin
+ metronidazole
Penicillin + vancomycin
+ gentamicin
Cure Cerebral abscesses;
Cure Para-aortic root abscess; death
14(21)
54A4
15(22)
6/F
Ceftriaxone
Cure
16 (present case)
61/F
Penicillin
Cure
14
0196-4399/00
(see frontmatter)
8 2001 Elaevier Science Inc.
death
Clinical Microbiology Newsletter 23:2,2001
disease or dental manipulation. Our patient was edentulous and had no history of recent dental manipulation. Another recent case report is similar in that a child with congenital heart disease also had no predisposing oral factor other than spontaneous loss of a deciduous tooth (22). Although cultures were not obtained from the acute thrombi removed from our patient during surgery, it is assumed that these originated from a cardiac source as a result of her chronic atria1 fibrillation. Her remaining atria1 thrombi on echocardiogram prompted prolonged treatment with intravenous penicillin and oral coumadin. Although R. dentocariosa is susceptible to many antimicrobial agents in vitro, it is uniformly susceptible to penicillin, which should be regarded as the antibiotic of choice for treatment. References 1. Onisi, M. 1949. Study on the actino-
myces isolated from the deeper layers of carious dentine. J. Dent. 6:278-3 18. 2. Roth, G.D. 1957. Proteolytic organisms of the carious lesion. Oral Surg. 10:1105-1117. 3. Georg, L.K. and J.M. Brown. 1967. Rothia, gen. nov., an aerobic genus of the family Actinomycetaceae. Int. J. Syst. Bacterial. 17:79-88. 4. Clarridge, J.E. and C.A. Spiegal. 1995. Corynebacterium and miscellaneous
Clinkal Microbiology Newsletter 23:2,2001
irregular gram-positive rods, Etysipelothin and Gardnerella, p. 357-378. In P. Murray et al. (ed.), Manual of clinical microbiology, ASM Press, Washington, DC. 5. Scharfen, J. 1975. Untraditional glucose fermenting Actinomycetes as human pathogens. Part II: Rothia dentocariosa as a cause of abdominal actinomycosis and a pathogen for mice. Zentralbl. Bakteriol. (Orig. A) 233:80-92. 6. Lutwick, L.I. and R.C. Rockhill. 1978. Abscess associated with Rothia dentocuriosa. J. Clin. Microbial. 8:612-613. 7. Schiff, M.J. and M.H. Kaplan. 1987. Rothia dentocariosa pneumonia in an immunocompromised patient. Lung 165:279-282. 8. Pers, C. et al. 1987. Rothia dentocariosa septicaemia in a patient with chronic lymphocytic leukemia and toxic granulocytopenia. Dan. Med. Bull. 34:322-323. 9. Nivar-Aristy, R.A., L.P. Krajewski, and J.A. Washington. 1991. Infection of an arteriovenous fistula with Rothiu dentocuriosa. Diag. Microbial. Infect. Dis. 14:167-169. 10. Pape, J. et al. 1979. Infective endocarditis caused by Rothia dentocariosa. Ann. Intern. Med. 91:746-747. 11. Schafer, F.J., E.J. Wing, and C.W. Norden. 1979. Infectious endocarditis caused by Rothia dentocariosa. Ann. Intern. Med. 91:747-748. 12, Broeren, S.A. and M.M. Peel. 1984.
8 2001 Elsevier Science Inc.
Endocarditis caused by Rothia dentocariosa. J. Clin. Pathol. 37:1298-1300. 13. Issacson, J.H. and R.T. Grenko. 1988. Rothia dentocariosa endocarditis complicated by brain abscess. Am. J. Med. 841352-354. 14. Shands, J.J. 1988. Rothia dentocuriosa endocarditis. Am. J. Med. 85:280-281. 15. Sudduth, E.J., J.D. Rozich, and W.E. Farrar. 1993. Rothia dentocariosa endocarditis complicated by perivalvular abscess. Clin. Infect. Dis. 17:722-725. 16. Anderson, M.D. et al. 1993. Prosthetic valve endocarditis due to Rothiu dentocariosa. Clin. Infect. Dis. 17:945-956. 17. Ruben, S.J. 1993. Rothia dentocariosa endocarditis. West. J. Med. 159690-691. 18. Weersink, A.J.L. et al. 1994. Rothia dentocariosa endocarditis complicated by an abdominal aneurysm. Clin. Infect. Dis. 18:489-490. 19. Binder, D. et al. 1997. Native and prosthetic endocarditis caused by Rothia dentocariosa: diagnostic and therapeutic considerations. Infection 25122-26. 20. Kong, R. et al. 1988. Case of triple endocarditis caused by Rothia dentocariosa and results of a survey in France. J. Clin. Microbial. 36:309-3 10. 21. Ferraz, V. et al. 1998. Rothia dentocariosa endocarditis and aortic root abscess. J. Infect. 37:292-295. 22. Braden, D.S., S. Feldman, and A.L. Palmer. 1999. Rothia endocarditis in a child. South. Med. J. 92:815-816.
01964399100 (see fmlltmatter)
15
21. Peiris, M. et al. 1999. Human infection with influenza H9N2. Lancet 354:9 16917. 22. Guo, Y.J. et al. 1999. Discovery of humans infected by avian influenza A (H9N2) virus. Chinese J. Exp. Clin.
Virol. 15:105-108. 23. Lin, Y.P. et al. 2000. Avian-to-human transmission of H9N2 subtype influenza A viruses: Relationship between H9N2 and H5Nl human isolates. Proc. Natl. Acad. Sci. U.S.A. 97:9654-9658.
Case Report
Rothia dentocariosa Endocarditis Julie Larkin, M.D.
Jose Montero, M.D. Marcel0 Targino, M.S. Alex Powers, M.S. CathyAccurso,B.A.,M.P.H. Monica Campbell, B.S. Division of Infectious Disease Department of Internal Medicine University of South Florida Tampa, FL 33602-1289 Rothia dentocariosa is a pleomorphic gram-positive bacillus, which is part of the normal flora in the human oral cavity but is rarely reported to cause human disease. This organism was first isolated in 1949 by Onisi from carious dentine and named Actinomyces dentocariosus (1). The bacterium was later renamed Nocardia dentocariosus due to its preference for aerobic conditions of growth (2). In 1967, Georg and Brown placed the organism under the Actinomycetaceae family within a new genus Rothia (3). In this report, we describe a case of R. dentocariosa endocarditis diagnosed after vascular embolic complications were noted. Furthermore, we review the literature and present previously known cases of R. dentocariosa endocarditis.
Case Report A 6 l-year-old white female was admitted to the hospital on 715197with acute bilateral lower extremity pain. An aortogram demonstrated an occluded left common iliac artery (consistent with an acute thrombus) as well as occlusion of the right superficial femoral artery at its origin. There were also several occluded vessels emerging from the right profumla femoral artery, again suggesting embolic disease. The patient underwent an emergent right femoral and left iliac embolectomy. Her previous cardiac history was notable for Clinical Microbiology
Newsletter 23:2,2001
chronic atrial fibrillation and longstanding mitral stenosis. She had no documented history of rheumatic heart disease. Seventeen days after initial admission, the patient developed a fever of 102OFand was readmitted. She denied fever or chills prior to admission but noted that she had “chest congestion.” Physical examination revealed an absence of native dentition with full upper and lower dentures present, and an irregular heart rhythm with a grade II/VI diastolic murmur. There was no evidence of hepatomegaly, splinter hemorrhages, or change in mental status. Her recent surgical wounds had minor incisional ecchymoses and hematomas but were otherwise healing appropriately. Laboratory data revealed a leukocyte count of 9.0 x 109/1,a hemoglobin value of 10.2 g/dl, and urinalysis was remarkable only for three to five erythrocytes. Blood cultures were performed and revealed growth of gram-positive bacilli within 72 h of incubation. Intravenous vancomycin therapy was started, but was changed to intravenous penicillin when Actinomyces-like organisms were found growing on culture. Transthoracic and transesophageal echocardiogram demonstrated severe mitral stenosis with thick mitral valve leaflets consistent with rheumatic heart disease. No vegetations were found but a thrombus was seen in the atria1 appendage. Blood cultures grew R. dentocariosa and the patient was treated with a six-week course of intravenous penicillin for a presumed endovascular infection with R. dentocariosa. Following her antibiotic therapy, she underwent elective mitral valve replacement.
Blood Culture Methods and Microbiology A specimen for blood culture drawn 0 2001 Elsevier Science Inc.
from a peripheral site was placed on the BacT/Alert automated blood culture instrument (Organon Technika, Durham, NC). The anaerobic culture bottle flagged positive after 2.5 days of incubation. The Gram stain results showed diphtheroid-like, gram-positive rods. The organism was subcultured to blood and chocolate agars for isolation. It was also subcultured on two CDC anaerobic plates placed at different atmospheres (aerobic and anaerobic) for oxygen requirement evaluation. Results of the subculture revealed a non-pigmented, catalase-positive, non-motile, nonhemolytic, non-spore forming, pleomorphic, aerobic bacillus. Further testing indicated that the organism was nonacid fast, nitrate positive, esculin positive, urea negative, and gram positive. Because R. dentocariosa is a rare isolate, definitive identification is a challenge. When the Gram stain showed gram-positive rods, the initial impression was a Propionibacterium acnes-like or coryneform-like organism. Because the organism grew aerobically and anaerobically on blood agar, a Propionibacterium spp. was ruled out. The catalasepositive and acid fast-negative test results placed the organism into the aerobic, non-spore-forming, gram-positive bacillus category similar to Corynebacterium spp. An ANI (Vitek, Hazelwood, MO) test identified, with 98% certainty, the isolate as Actinomyces odontolyticus. The Rapid ANA II system identified the organism as Actinomyces israelii (95 percent certainty). However, after the organism was found to be aerobic and catalase positive, neither identification could be accepted. These identification systems are restricted to anaerobic isolate identification thus demonstrating the need to determine whether a gram0196-4399/00 (see frontmatter)
13
positive rod will grow in air. A Rapid Coryne (bioMerieux S.A.) test strip was unable to identify the organism. Conventional tube biochemicals were performed as per Table 1. At this point, review of the cumulative information available in conjunction with standard microbiological reference textbooks identified the organism as R. dentocariosa (4). The National Committee for Clinical Laboratory Standards (NCCLS) does not have standards for R. dentocariosa susceptibility testing. No susceptibility testing was performed on our isolate. Discussion Clinical infection due to R. dentocariosa has been reported rarely. Although this organism is considered to be of low virulence, there have been reports of clinical infections including periappendiceal abscess (5), pilonidal abscess (6) pneumonitis in an immunocompromised host (7), septicemia in a patient with chronic lymphocytic leukemia (B), and infection of an arteriovenous fistula (9). The most frequent clinical manifestation of serious infection by R. dentocariosa has been infective endocarditis, previously reported in 13 patients (1 O-22). Table 2 summarizes all reported cases of R. dentocariosa endocarditis, the antibiotics used to treat them, and the result of treatment.
Table 1. Summary of isolate properties Result Test
Our isolate
Type strain
Aerobic
+
+
Catalase
+
V
CDC aerobic
4+ growth
+
CDC anaerobic
4+ growth
+
+
Esculin
+
Hemolytic on blood agar
NR
Kinyoun stain Motility Nitrate
+
t
Nutrient agar
1+
t
ONPG
+
NR
Pigment
NR +
+
AlWAcid
NR
weak+
NR
Pleomorphic Spore forming TSI Urease VP
Key: +, positive; -, negative; NR, not reported; V, variable
Although four previous cases required surgery, medical management generally resulted in cure. Three deaths have been reported (15,19,30), two as a result of complicated valvular surgeries. All previously reported cases of endocarditis caused by R. dentocariosa
had antecedent signs and symptoms consistent with endocarditis. Our case is atypical in that our patient demonstrated fever only after admission to the hospital and treatment for her vascular embolic disease. As well, most cases have been associated with periodontal
Table 2. Previous cases and outcomes PT. age/sex
Case (Ref.)
Outcome
Antibiotic treatment
Cure
1(10)
58/M
Penicillin + gentamicin
2(ll)
57/M
Penicillin + streptomycin
Cure
3(12)
53iM
Penicillin + gentamicin + rifampin
Cure
4(13)
27/F
Penicillin + gentamicin
Cure
504)
41/M
Penicillin, then vancomycin + gentamicin Retreated with penicillin + vancomycin
Cure
6(16)
4olM
Vancomycin + gentamicin
Cure
7(l7)
71/M
Penicillin + gentamicin; failed ceftriaxone
Cure
8(15)
35/M
Vancomycin + gentamicin
9(18)
17/M
Amoxicillin/clavulanate
lO(19)
7oiM
Penicillin + netilmicin + vancomycin
ll(19)
67N
Rifampin + ciprofloxacin
Cure
12(19)
SO/M
Rifampin + ceftriaxone
Cure
13(20)
37/M
Amoxicillin
Perivalvular abscess; death
+ gentamicin
+ metronidazole
Penicillin + vancomycin
+ gentamicin
Cure Cerebral abscesses;
Cure Para-aortic root abscess; death
14(21)
54A4
15(22)
6/F
Ceftriaxone
Cure
16 (present case)
61/F
Penicillin
Cure
14
0196-4399/00
(see frontmatter)
8 2001 Elaevier Science Inc.
death
Clinical Microbiology Newsletter 23:2,2001
disease or dental manipulation. Our patient was edentulous and had no history of recent dental manipulation. Another recent case report is similar in that a child with congenital heart disease also had no predisposing oral factor other than spontaneous loss of a deciduous tooth (22). Although cultures were not obtained from the acute thrombi removed from our patient during surgery, it is assumed that these originated from a cardiac source as a result of her chronic atria1 fibrillation. Her remaining atria1 thrombi on echocardiogram prompted prolonged treatment with intravenous penicillin and oral coumadin. Although R. dentocariosa is susceptible to many antimicrobial agents in vitro, it is uniformly susceptible to penicillin, which should be regarded as the antibiotic of choice for treatment. References 1. Onisi, M. 1949. Study on the actino-
myces isolated from the deeper layers of carious dentine. J. Dent. 6:278-3 18. 2. Roth, G.D. 1957. Proteolytic organisms of the carious lesion. Oral Surg. 10:1105-1117. 3. Georg, L.K. and J.M. Brown. 1967. Rothia, gen. nov., an aerobic genus of the family Actinomycetaceae. Int. J. Syst. Bacterial. 17:79-88. 4. Clarridge, J.E. and C.A. Spiegal. 1995. Corynebacterium and miscellaneous
Clinkal Microbiology Newsletter 23:2,2001
irregular gram-positive rods, Etysipelothin and Gardnerella, p. 357-378. In P. Murray et al. (ed.), Manual of clinical microbiology, ASM Press, Washington, DC. 5. Scharfen, J. 1975. Untraditional glucose fermenting Actinomycetes as human pathogens. Part II: Rothia dentocariosa as a cause of abdominal actinomycosis and a pathogen for mice. Zentralbl. Bakteriol. (Orig. A) 233:80-92. 6. Lutwick, L.I. and R.C. Rockhill. 1978. Abscess associated with Rothia dentocuriosa. J. Clin. Microbial. 8:612-613. 7. Schiff, M.J. and M.H. Kaplan. 1987. Rothia dentocariosa pneumonia in an immunocompromised patient. Lung 165:279-282. 8. Pers, C. et al. 1987. Rothia dentocariosa septicaemia in a patient with chronic lymphocytic leukemia and toxic granulocytopenia. Dan. Med. Bull. 34:322-323. 9. Nivar-Aristy, R.A., L.P. Krajewski, and J.A. Washington. 1991. Infection of an arteriovenous fistula with Rothiu dentocuriosa. Diag. Microbial. Infect. Dis. 14:167-169. 10. Pape, J. et al. 1979. Infective endocarditis caused by Rothia dentocariosa. Ann. Intern. Med. 91:746-747. 11. Schafer, F.J., E.J. Wing, and C.W. Norden. 1979. Infectious endocarditis caused by Rothia dentocariosa. Ann. Intern. Med. 91:747-748. 12, Broeren, S.A. and M.M. Peel. 1984.
8 2001 Elsevier Science Inc.
Endocarditis caused by Rothia dentocariosa. J. Clin. Pathol. 37:1298-1300. 13. Issacson, J.H. and R.T. Grenko. 1988. Rothia dentocariosa endocarditis complicated by brain abscess. Am. J. Med. 841352-354. 14. Shands, J.J. 1988. Rothia dentocuriosa endocarditis. Am. J. Med. 85:280-281. 15. Sudduth, E.J., J.D. Rozich, and W.E. Farrar. 1993. Rothia dentocariosa endocarditis complicated by perivalvular abscess. Clin. Infect. Dis. 17:722-725. 16. Anderson, M.D. et al. 1993. Prosthetic valve endocarditis due to Rothiu dentocariosa. Clin. Infect. Dis. 17:945-956. 17. Ruben, S.J. 1993. Rothia dentocariosa endocarditis. West. J. Med. 159690-691. 18. Weersink, A.J.L. et al. 1994. Rothia dentocariosa endocarditis complicated by an abdominal aneurysm. Clin. Infect. Dis. 18:489-490. 19. Binder, D. et al. 1997. Native and prosthetic endocarditis caused by Rothia dentocariosa: diagnostic and therapeutic considerations. Infection 25122-26. 20. Kong, R. et al. 1988. Case of triple endocarditis caused by Rothia dentocariosa and results of a survey in France. J. Clin. Microbial. 36:309-3 10. 21. Ferraz, V. et al. 1998. Rothia dentocariosa endocarditis and aortic root abscess. J. Infect. 37:292-295. 22. Braden, D.S., S. Feldman, and A.L. Palmer. 1999. Rothia endocarditis in a child. South. Med. J. 92:815-816.
01964399100 (see fmlltmatter)
15