167
DIAGN MICROBIOLINFECTDIS 1991;14:167-169
CASE REPORT
Infection of an Arteriovenous Fistula with Rothia dentocariosa Rafael A. Nivar-Aristy, Leonard P. Krajewski, and John A. Washington
Rothia dentocariosa is an unusual cause of infection in humans, despite the fact that the organism is frequently isolated from the oral cavity. The authors describe a case of R. dento-
cariosa infection following revision of an arteriovenous fistula in a 46-year-old diabetic man with renal failure.
Rothia was first identified as a genus in 1967 by Georg and Brown (1967). The organism is a coccal to rod-shaped, Gram-positive bacterium that morphologically resembles Actinomyces, Arachnia, Corynebacterium, and Nocardia (Barksdale, 1979), and is a component of the normal oral flora that may also be recovered from dental caries and plaque (Barksdale, 1979; Dzierzanowska et al., 1979). Since its original description, documented cases of infections with Rothia dentocariosa have included periodontal inflammatory disease (Dzierzanowska et al., 1979), infection of a pilonidal cyst (Lutwick and Rockhill, 1978), a periappendiceal abscess (Scharfen, 1975), and at least four cases of infective endocarditis (Broeren and Peel, 1984; Isaacson and Grenko, 1988; Pape et al., 1979; Schafer et al., 1979), including one with a brain abscess (Isaacson and Grenko, 1988). Although only the sources of the isolates were listed, Brown et al. (1969) at the Centers for Disease Control described the laboratory identification of 50 isolates of R. dentocariosa that were predominantly from the oral cavity and upper respiratory tract, but that also included one isolate each from a postoperative wound, leg-stump drainage, leg ulcer, tissue (not specified), cerebrospinal fluid, urine, and blood.
CASE REPORT
From the Departments of Microbiologyand Vascular Surgery, ClevelandClinicFoundation, Cleveland, Ohio, USA. Address reprint requests to Dr. J. A. Washington, Department of Microbiology,ClevelandClinicFoundation, One ClinicCenter, 9500 Euclid Avenue, Cleveland, OH 44195-5140, USA. Received 10 June 1990; revised and accepted 16 July 1990. © 1991 Elsevier Science PublishingCo., Inc. 655 Avenue of the Americas, New York, NY 10010 0732-8893/91/$3.50
The patient was a 46-year-old diabetic man who underwent gastric stapling and small intestinal resection for morbid obesity in 1985. Postoperatively, the patient had numerous complications, including a retroperitoneal abscess, Gram-negative septicemia, pancreatitis, and pulmonary emboli, necessitating inferior vena cava ligation. The patient also developed renal insufficiency that required hemodialysis for the first time in March 1989. Since that time, he had undergone several attempts at construction of vascular access. The patient was transferred to the Cleveland Clinic Foundation because of a poorly functioning right brachial axillary polytretoflorethylene (PTFE) fistula. As a result of this inadequate vascular access, he was not able to be hemodialized effectively. On admission, the patient was noted to have lymphedema over both arms, chest, and lower extremities. There was a right pleural effusion. Neither the popliteal nor pedal pulses were palpable. There were open ulcerations on both feet. A white blood cell scan was positive for osteomyelitis of the left foot. A blood culture following admission grew Escherichia coli. A fistulogram demonstrated that the right brachial artery to axillary-vein fistula was functioning poorly. There was also a previously placed left axillary artery to right internal jugular-vein PTFE fistula, which extended across the anterior chest. There was moderate, soft tissue induration surrounding this vascular graft. Eleven days following admission, the left axillary-jugular fistula was revised by inter-
168
posing another segment of PTFE from the distal left brachial artery to the previous graft at the infraclavicular area. This revision extended the length of the graft available for needle puncture and thus adequate vascular access. Postoperatively, the left antecubital and infraclavicular incisions drained a clear serous discharge and the left arm remained lymphedematous. On the tenth postoperative day, a thick slightly yellow exudate was expressed from the left infraclavicular and left-midarm incisions. This material was submitted for culture. Of interest was the fact that the patient stated that the same kind of drainage had occurred from prior upper-extremity incisions for attempts at vascular access placement. The patient was treated with vancomycin and gentamicin during the course of his hospitalization. The drainage from the left-arm incisions gradually subsided and the incisions healed quickly. The leftarm PTFE graft has been used for vascular access for the past 5 months without evidence of local or systemic infection. The patient did require left belowknee amputation for osteomyelitis, which was unresponsive to antibiotic therapy. BACTERIOLOGY On receipt in the laboratory, the specimen, which was described as an abscess site from the left-arm arteriovenous fistula, was cultured for aerobic and anaerobic bacteria. Growth was noted after 6 days of incubation in thioglycollate medium. A Gramstained smear revealed a branching Gram-positive rod that grew on subculture on blood agar plates that were incubated both anaerobically and in an atmosphere of increased carbon dioxide. An acidfast stain of the organism was negative. On subculture the colonies were creamy white, dry, and crumbly. The organism was catalase-, nitrate-, Voges-Poskauer-, and esculin-positive, and fermented glucose, trehalose, sucrose, and maltose. Negative reactions included oxidase, urease, and indole. The organism did not grow in 6% sodium chloride medium. Minimal inhibitory concentrations, obtained with a microbroth dilution method incubated for 24 hr at 35°C in ambient air, were penicillin, ~0.5 ~g/ml; amoxicillin, ~1 ~g/ml; oxacillin, ~0.5 ~g/ml; cefazolin, ~4 ~g/ml; erythromycin, ~0.5 ~g/ml; vancomycin, ~2 ~,g/ml; tetracycline, >8 ~g/rnl; gentamicin, ~1 ~g/ml; and trimethoprim/sulfamethoxazole, >8/160 ~,g/ml. DISCUSSION
Despite its presence normally in the oral cavity, R. dentocariosa appears rarely to cause infection outside
R.A. Nivar-Aristy et al.
the oral cavity. In addition to a patient with a periappendecial abscess and one with infected pilonidal cyst (Lutwick and Rockhill, 1978; Scharfen, 1975), there have been four cases of endocarditis, including one complicated by a brain abscess (Broeren and Peel, 1984; Isaacson and Grenko, 1988; Pape et al., 1979; Schafer et al., 1979). Isolates from blood cultures from the cases with endocarditis grew in a variety of blood culture media, including Columbia broth, biphasic brain-heart infusion medium, and fluid thioglycollate medium. Where noted, detection of growth in these media required as long as 8 days of incubation. Rothia dentocariosa from an abscess associated with an infected pilonidal cyst occurred on ordinary blood agar, although the incubation time required for its detection was not noted (Lutwick and Rockhill, 1978). Growth from pus from a periappendiceal abscess required - 1 4 days of incubation under anaerobic conditions; however, it is not clear from this report what primary isolation medium was used (Scharfen, 1975). In our laboratory the primary agar-based media used for bacterial culture are discarded after 48 hr of incubation; however, fluid thioglycollate medium is incubated aerobically for a total of 5 days and another fluid thioglycollate medium is incubated anaerobically for 7 days. Our isolate was only detected in fluid thioglycollate medium that had been incubated anaerobically for 6 days. In any event, it does appear that the organism is slow growing and generally will only be recognized after prolonged incubation. Information about the antimicrobial susceptibility of R. dentocariosa is sketchy and has been determined in a few cases by a variety of methods. Diskdiffusion susceptibility testing by Pape et al. (1979) and by Schafer et al. (1979) demonstrated that the organism was susceptible to penicillins, cephalospofins, erythromycin, vancomycin, aminoglycosides, tetracycline, chloramphenicol, and trimethoprim/ sulfamethoxazole. Minimal inhibitory concentrations determined by Schafer et al. (1979) confirmed the disk-diffusion test results. Penicillin, cefazolin, gentamicin, and rifampin have demonstrated good bactericidal activity. Dzierzanowska et al. (1979) used agar dilution to determine the susceptibility of 90 strains of R. dentocariosa isolated from dental plaques, caries, and periodontal tissue and found that most strains were susceptible to penicillins, cephalospofins, erythromycin, and tetracyclines. Susceptibility to clindamycin was variable. Although R. dentocariosa was the only microorganism isolated from this patient's incisionial w o u n d drainage, we can only speculate about the pathogenic role of the microorganism in this case as R. dentocariosa was not isolated repeatedly or from multiple sites.
Case Report
169
REFERENCES Barksdale L (1979) Identifying Rothia dentocariosa. Ann Intern Med 91:786. Broeren SA, Peel MM (1984) Endocarditis caused by Rothia dentocariosa. J Clin Pathol 37:1298. Brown JM, Georg LK, Waters LC (1969) Laboratory identification of Rothia dentocariosa and its occurrence in human clinical materials. Appl Microbiol 17:150. Dzierzanowska D, Miksza-Zytkiewicz R, Czerniawska M, Linda H, Borowski J (1979) Sensitivity of Rothia dentocariosa. J Antimicrob Chemother 4:469. Georg LK, Brown JM (1967) Rothia gen. nov., an aerobic genus of the family Actinomycetacaeae. Intern J Syst Bacteriol 17:79.
Isaacson H, Grenko R (1988) Rothia dentocariosa endocarditis complicated by brain abscess. Am J Med 84:352. Lutwick L, RockhiU R (1978) Abscess associated with Rothia dentocariosa. J Clin Microbiol 8:612. Pape J, Singer C, Kiehn T, Lee BJ, Armstrong D (1979) Infective endocarditis caused by Rothia dentocariosa. Ann Intern Med 91:746. Schafer FJ, Wing EJ, Norden CW (1979) Infectious endocarditis caused by Rothia dentocariosa. Ann Intern Med 91:747. Scharfen J (1975) Untraditional glucose fermenting actinomycetes as human pathogens. II. Rothia dentocariosa as a cause of abdominal actinomycosis and a pathogen for mice. Zbl Bakteriol Mikrobiol Hyg [A] 233:80.
DIAGN MICROBIOLINFECTDIS 1991;14:167-169
CASE REPORT
Infection of an Arteriovenous Fistula with Rothia dentocariosa Rafael A. Nivar-Aristy, Leonard P. Krajewski, and John A. Washington
Rothia dentocariosa is an unusual cause of infection in humans, despite the fact that the organism is frequently isolated from the oral cavity. The authors describe a case of R. dento-
cariosa infection following revision of an arteriovenous fistula in a 46-year-old diabetic man with renal failure.
Rothia was first identified as a genus in 1967 by Georg and Brown (1967). The organism is a coccal to rod-shaped, Gram-positive bacterium that morphologically resembles Actinomyces, Arachnia, Corynebacterium, and Nocardia (Barksdale, 1979), and is a component of the normal oral flora that may also be recovered from dental caries and plaque (Barksdale, 1979; Dzierzanowska et al., 1979). Since its original description, documented cases of infections with Rothia dentocariosa have included periodontal inflammatory disease (Dzierzanowska et al., 1979), infection of a pilonidal cyst (Lutwick and Rockhill, 1978), a periappendiceal abscess (Scharfen, 1975), and at least four cases of infective endocarditis (Broeren and Peel, 1984; Isaacson and Grenko, 1988; Pape et al., 1979; Schafer et al., 1979), including one with a brain abscess (Isaacson and Grenko, 1988). Although only the sources of the isolates were listed, Brown et al. (1969) at the Centers for Disease Control described the laboratory identification of 50 isolates of R. dentocariosa that were predominantly from the oral cavity and upper respiratory tract, but that also included one isolate each from a postoperative wound, leg-stump drainage, leg ulcer, tissue (not specified), cerebrospinal fluid, urine, and blood.
CASE REPORT
From the Departments of Microbiologyand Vascular Surgery, ClevelandClinicFoundation, Cleveland, Ohio, USA. Address reprint requests to Dr. J. A. Washington, Department of Microbiology,ClevelandClinicFoundation, One ClinicCenter, 9500 Euclid Avenue, Cleveland, OH 44195-5140, USA. Received 10 June 1990; revised and accepted 16 July 1990. © 1991 Elsevier Science PublishingCo., Inc. 655 Avenue of the Americas, New York, NY 10010 0732-8893/91/$3.50
The patient was a 46-year-old diabetic man who underwent gastric stapling and small intestinal resection for morbid obesity in 1985. Postoperatively, the patient had numerous complications, including a retroperitoneal abscess, Gram-negative septicemia, pancreatitis, and pulmonary emboli, necessitating inferior vena cava ligation. The patient also developed renal insufficiency that required hemodialysis for the first time in March 1989. Since that time, he had undergone several attempts at construction of vascular access. The patient was transferred to the Cleveland Clinic Foundation because of a poorly functioning right brachial axillary polytretoflorethylene (PTFE) fistula. As a result of this inadequate vascular access, he was not able to be hemodialized effectively. On admission, the patient was noted to have lymphedema over both arms, chest, and lower extremities. There was a right pleural effusion. Neither the popliteal nor pedal pulses were palpable. There were open ulcerations on both feet. A white blood cell scan was positive for osteomyelitis of the left foot. A blood culture following admission grew Escherichia coli. A fistulogram demonstrated that the right brachial artery to axillary-vein fistula was functioning poorly. There was also a previously placed left axillary artery to right internal jugular-vein PTFE fistula, which extended across the anterior chest. There was moderate, soft tissue induration surrounding this vascular graft. Eleven days following admission, the left axillary-jugular fistula was revised by inter-
168
posing another segment of PTFE from the distal left brachial artery to the previous graft at the infraclavicular area. This revision extended the length of the graft available for needle puncture and thus adequate vascular access. Postoperatively, the left antecubital and infraclavicular incisions drained a clear serous discharge and the left arm remained lymphedematous. On the tenth postoperative day, a thick slightly yellow exudate was expressed from the left infraclavicular and left-midarm incisions. This material was submitted for culture. Of interest was the fact that the patient stated that the same kind of drainage had occurred from prior upper-extremity incisions for attempts at vascular access placement. The patient was treated with vancomycin and gentamicin during the course of his hospitalization. The drainage from the left-arm incisions gradually subsided and the incisions healed quickly. The leftarm PTFE graft has been used for vascular access for the past 5 months without evidence of local or systemic infection. The patient did require left belowknee amputation for osteomyelitis, which was unresponsive to antibiotic therapy. BACTERIOLOGY On receipt in the laboratory, the specimen, which was described as an abscess site from the left-arm arteriovenous fistula, was cultured for aerobic and anaerobic bacteria. Growth was noted after 6 days of incubation in thioglycollate medium. A Gramstained smear revealed a branching Gram-positive rod that grew on subculture on blood agar plates that were incubated both anaerobically and in an atmosphere of increased carbon dioxide. An acidfast stain of the organism was negative. On subculture the colonies were creamy white, dry, and crumbly. The organism was catalase-, nitrate-, Voges-Poskauer-, and esculin-positive, and fermented glucose, trehalose, sucrose, and maltose. Negative reactions included oxidase, urease, and indole. The organism did not grow in 6% sodium chloride medium. Minimal inhibitory concentrations, obtained with a microbroth dilution method incubated for 24 hr at 35°C in ambient air, were penicillin, ~0.5 ~g/ml; amoxicillin, ~1 ~g/ml; oxacillin, ~0.5 ~g/ml; cefazolin, ~4 ~g/ml; erythromycin, ~0.5 ~g/ml; vancomycin, ~2 ~,g/ml; tetracycline, >8 ~g/rnl; gentamicin, ~1 ~g/ml; and trimethoprim/sulfamethoxazole, >8/160 ~,g/ml. DISCUSSION
Despite its presence normally in the oral cavity, R. dentocariosa appears rarely to cause infection outside
R.A. Nivar-Aristy et al.
the oral cavity. In addition to a patient with a periappendecial abscess and one with infected pilonidal cyst (Lutwick and Rockhill, 1978; Scharfen, 1975), there have been four cases of endocarditis, including one complicated by a brain abscess (Broeren and Peel, 1984; Isaacson and Grenko, 1988; Pape et al., 1979; Schafer et al., 1979). Isolates from blood cultures from the cases with endocarditis grew in a variety of blood culture media, including Columbia broth, biphasic brain-heart infusion medium, and fluid thioglycollate medium. Where noted, detection of growth in these media required as long as 8 days of incubation. Rothia dentocariosa from an abscess associated with an infected pilonidal cyst occurred on ordinary blood agar, although the incubation time required for its detection was not noted (Lutwick and Rockhill, 1978). Growth from pus from a periappendiceal abscess required - 1 4 days of incubation under anaerobic conditions; however, it is not clear from this report what primary isolation medium was used (Scharfen, 1975). In our laboratory the primary agar-based media used for bacterial culture are discarded after 48 hr of incubation; however, fluid thioglycollate medium is incubated aerobically for a total of 5 days and another fluid thioglycollate medium is incubated anaerobically for 7 days. Our isolate was only detected in fluid thioglycollate medium that had been incubated anaerobically for 6 days. In any event, it does appear that the organism is slow growing and generally will only be recognized after prolonged incubation. Information about the antimicrobial susceptibility of R. dentocariosa is sketchy and has been determined in a few cases by a variety of methods. Diskdiffusion susceptibility testing by Pape et al. (1979) and by Schafer et al. (1979) demonstrated that the organism was susceptible to penicillins, cephalospofins, erythromycin, vancomycin, aminoglycosides, tetracycline, chloramphenicol, and trimethoprim/ sulfamethoxazole. Minimal inhibitory concentrations determined by Schafer et al. (1979) confirmed the disk-diffusion test results. Penicillin, cefazolin, gentamicin, and rifampin have demonstrated good bactericidal activity. Dzierzanowska et al. (1979) used agar dilution to determine the susceptibility of 90 strains of R. dentocariosa isolated from dental plaques, caries, and periodontal tissue and found that most strains were susceptible to penicillins, cephalospofins, erythromycin, and tetracyclines. Susceptibility to clindamycin was variable. Although R. dentocariosa was the only microorganism isolated from this patient's incisionial w o u n d drainage, we can only speculate about the pathogenic role of the microorganism in this case as R. dentocariosa was not isolated repeatedly or from multiple sites.
Case Report
169
REFERENCES Barksdale L (1979) Identifying Rothia dentocariosa. Ann Intern Med 91:786. Broeren SA, Peel MM (1984) Endocarditis caused by Rothia dentocariosa. J Clin Pathol 37:1298. Brown JM, Georg LK, Waters LC (1969) Laboratory identification of Rothia dentocariosa and its occurrence in human clinical materials. Appl Microbiol 17:150. Dzierzanowska D, Miksza-Zytkiewicz R, Czerniawska M, Linda H, Borowski J (1979) Sensitivity of Rothia dentocariosa. J Antimicrob Chemother 4:469. Georg LK, Brown JM (1967) Rothia gen. nov., an aerobic genus of the family Actinomycetacaeae. Intern J Syst Bacteriol 17:79.
Isaacson H, Grenko R (1988) Rothia dentocariosa endocarditis complicated by brain abscess. Am J Med 84:352. Lutwick L, RockhiU R (1978) Abscess associated with Rothia dentocariosa. J Clin Microbiol 8:612. Pape J, Singer C, Kiehn T, Lee BJ, Armstrong D (1979) Infective endocarditis caused by Rothia dentocariosa. Ann Intern Med 91:746. Schafer FJ, Wing EJ, Norden CW (1979) Infectious endocarditis caused by Rothia dentocariosa. Ann Intern Med 91:747. Scharfen J (1975) Untraditional glucose fermenting actinomycetes as human pathogens. II. Rothia dentocariosa as a cause of abdominal actinomycosis and a pathogen for mice. Zbl Bakteriol Mikrobiol Hyg [A] 233:80.
