1045
CORRESPONDENCE Stomatococcus mucllaginosus Meningitis in a Child with Leukemia
G. SouilIet, M. Chomarat, G. Barbe, N. Balouck, C. Ploton, and N. Philippe Department ofHaematology-lmmunotogy. Department ofBone Marrow Transplantation. and Laboratory of Bacteriology, Hiipital d'enfants Debrousse, Lyon; and the Laboratory ofBacteriology, Centre Hospitalier Lyon-Sud, Pierre-Benite, France References I. Ascher DP. Zbick C White C Fischer GW. Infections due to Stomatococcus mucilaginosus: 10 cases and review. Rev Infect Dis 1991;
13:1048-52.
Correspondence: Dr. M. Chomarat, Laboratory of Bacteriology. Centre Hospitalier Lyon-Sud. 69310 Pierre-Benite, France.
2. Lemozy J. Maestre Ph. Huguet H. Chomarat M. Dabernat H. Lareng MB. Source of infection in Stomatococcus mucilaginosus septicaemia. Lancet 1990; I :416. 3. Magee JT. Burnett IA, Hindmarch JM. Spencer RC. Micrococcus and Stomatococcus spp. from human infections. J Hosp Infect 1990;
Clinical Infectious Diseases 1992;15:1045 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1506-0017$02.00
4. Weinblatt ME, Sahdev I. Berman M. Stomatococcus mucilaginosus infections in children with leukemia. Pediatr Infect Dis J 1990;9:678-9.
16:67-73.
Downloaded from cid.oxfordjournals.org at Emory University on August 16, 2015
SIR-Infections due to Stomatococcus mucilaginosus are still rarely reported [1-4]. To emphasize the role of this newly recognized opportunistic bacterium, we describe what we believe to be the second reported case of meningitis in a child with aplasia after allogeneic bone marrow transplantation (BMT). An II t-year-old boy with acute lymphoblastic leukemia received a T cell-depleted haploidentical bone marrow transplant from his father on 5 April. The preparative regimen included the use of etoposide, high-dose cytosine/arabinoside cyclophosphamide, fractionated total-body irradiation, and antithymocyte globulin (Institut Merieux, Marcy L'Etoile, France). He received granulocyte macrophage-colony stimulating factor for 3 months. He was kept in a sterile isolator. Selective gut decontamination was achieved by administration of colimycin and tobramycin. Standard oral therapy was administered with chlorhexidine and amphotericin B. Four days after BMT, while he was aplastic, he became febrile; blood cultures were performed, and therapy with intravenous antibiotics (piperacillin, amikacin, and vancomycin) was started. S. mucilaginosus was isolated from four blood cultures on 9 and 10 April. On 12 April, as fever (temperature, 40°C) persisted and the child had frontal headaches associated with faint nuchal rigidity, a lumbar puncture was performed; culture of the CSF was sterile. Gram-stained smears of CSF specimens obtained during 2227 April revealed gram-positive cocci in clusters, and S. mucilaginosus was cultured from the first three CSF specimens. Piperacillin and amikacin were hence replaced with fosfomycin, ceftriaxone, and gentamicin in the therapeutic regimen. In addition, gentamicin and vancomycin were administered intrathecally for 3 days. On I May fever and headaches were persistent (the blood and CSF were sterile); the child became sleepy and photophobic and had great nuchal rigidity and cutaneous hyperesthesia. Empiric therapy with amphotericin B was given for 3 weeks. On 4 May, as he was still neutropenic «0.1 polymorphonuclear lymphocytes/rnm"), gentamicin was replaced by thiamphenicol until 6 July to achieve better antibiotic penetration into the CSF, despite any inflammatory reaction. Two
weeks after eradication of S. mucilaginosus from the CSF, the child convulsed. Results of cranial computerized tomography were normal, but sequelae were observed: disorientation, cutaneous hyperesthesia, and unilateral blindness. After transitory improvement in his behavior, he became unconscious and then died with aplasia on 8 September. All the isolated strains were susceptible to piperacillin, ceftriaxone, cefotaxime, imipenem, gentamicin, vancomycin, fosfomycin, chloramphenicol, fusidic acid, and macrolides. They were resistant to amikacin; tobramycin; penicillins A, G, and M; trimethoprim-sulfamethoxazole; and fluoroquinolones. S. mucilaginosus, an encapsulated bacterium, is a normal inhabitant of the human oral cavity. The portal of entry for the organism is usually a venous catheter [1, 3] but sometimes an oral lesion [2]. In the present case, which involved no buccal lesions, S. mucilaginosus grew in routine gum tissue cultures on day I and was associated with the presence of Streptococcus mitis. On day 4 mouth rinses with vancomycin were instituted; subsequent gum tissue cultures yielded no S. mucilaginosus. Intravenous catheter cultures were consistently sterile. Despite appropriate therapy for septicemia, meningitis occurred 11 days after blood cultures became negative. It seems that S. mucilaginosus seeded precociously into the CSF and that the antibiotic diffusion was insufficient to prevent the occurrence of meningitis. The development of sequelae in spite of eradication of bacteria illustrates the virulence of this opportunistic pathogen in neutropenic patients and suggests the importance of prophylactic buccal decontamination.
CORRESPONDENCE Stomatococcus mucllaginosus Meningitis in a Child with Leukemia
G. SouilIet, M. Chomarat, G. Barbe, N. Balouck, C. Ploton, and N. Philippe Department ofHaematology-lmmunotogy. Department ofBone Marrow Transplantation. and Laboratory of Bacteriology, Hiipital d'enfants Debrousse, Lyon; and the Laboratory ofBacteriology, Centre Hospitalier Lyon-Sud, Pierre-Benite, France References I. Ascher DP. Zbick C White C Fischer GW. Infections due to Stomatococcus mucilaginosus: 10 cases and review. Rev Infect Dis 1991;
13:1048-52.
Correspondence: Dr. M. Chomarat, Laboratory of Bacteriology. Centre Hospitalier Lyon-Sud. 69310 Pierre-Benite, France.
2. Lemozy J. Maestre Ph. Huguet H. Chomarat M. Dabernat H. Lareng MB. Source of infection in Stomatococcus mucilaginosus septicaemia. Lancet 1990; I :416. 3. Magee JT. Burnett IA, Hindmarch JM. Spencer RC. Micrococcus and Stomatococcus spp. from human infections. J Hosp Infect 1990;
Clinical Infectious Diseases 1992;15:1045 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1506-0017$02.00
4. Weinblatt ME, Sahdev I. Berman M. Stomatococcus mucilaginosus infections in children with leukemia. Pediatr Infect Dis J 1990;9:678-9.
16:67-73.
Downloaded from cid.oxfordjournals.org at Emory University on August 16, 2015
SIR-Infections due to Stomatococcus mucilaginosus are still rarely reported [1-4]. To emphasize the role of this newly recognized opportunistic bacterium, we describe what we believe to be the second reported case of meningitis in a child with aplasia after allogeneic bone marrow transplantation (BMT). An II t-year-old boy with acute lymphoblastic leukemia received a T cell-depleted haploidentical bone marrow transplant from his father on 5 April. The preparative regimen included the use of etoposide, high-dose cytosine/arabinoside cyclophosphamide, fractionated total-body irradiation, and antithymocyte globulin (Institut Merieux, Marcy L'Etoile, France). He received granulocyte macrophage-colony stimulating factor for 3 months. He was kept in a sterile isolator. Selective gut decontamination was achieved by administration of colimycin and tobramycin. Standard oral therapy was administered with chlorhexidine and amphotericin B. Four days after BMT, while he was aplastic, he became febrile; blood cultures were performed, and therapy with intravenous antibiotics (piperacillin, amikacin, and vancomycin) was started. S. mucilaginosus was isolated from four blood cultures on 9 and 10 April. On 12 April, as fever (temperature, 40°C) persisted and the child had frontal headaches associated with faint nuchal rigidity, a lumbar puncture was performed; culture of the CSF was sterile. Gram-stained smears of CSF specimens obtained during 2227 April revealed gram-positive cocci in clusters, and S. mucilaginosus was cultured from the first three CSF specimens. Piperacillin and amikacin were hence replaced with fosfomycin, ceftriaxone, and gentamicin in the therapeutic regimen. In addition, gentamicin and vancomycin were administered intrathecally for 3 days. On I May fever and headaches were persistent (the blood and CSF were sterile); the child became sleepy and photophobic and had great nuchal rigidity and cutaneous hyperesthesia. Empiric therapy with amphotericin B was given for 3 weeks. On 4 May, as he was still neutropenic «0.1 polymorphonuclear lymphocytes/rnm"), gentamicin was replaced by thiamphenicol until 6 July to achieve better antibiotic penetration into the CSF, despite any inflammatory reaction. Two
weeks after eradication of S. mucilaginosus from the CSF, the child convulsed. Results of cranial computerized tomography were normal, but sequelae were observed: disorientation, cutaneous hyperesthesia, and unilateral blindness. After transitory improvement in his behavior, he became unconscious and then died with aplasia on 8 September. All the isolated strains were susceptible to piperacillin, ceftriaxone, cefotaxime, imipenem, gentamicin, vancomycin, fosfomycin, chloramphenicol, fusidic acid, and macrolides. They were resistant to amikacin; tobramycin; penicillins A, G, and M; trimethoprim-sulfamethoxazole; and fluoroquinolones. S. mucilaginosus, an encapsulated bacterium, is a normal inhabitant of the human oral cavity. The portal of entry for the organism is usually a venous catheter [1, 3] but sometimes an oral lesion [2]. In the present case, which involved no buccal lesions, S. mucilaginosus grew in routine gum tissue cultures on day I and was associated with the presence of Streptococcus mitis. On day 4 mouth rinses with vancomycin were instituted; subsequent gum tissue cultures yielded no S. mucilaginosus. Intravenous catheter cultures were consistently sterile. Despite appropriate therapy for septicemia, meningitis occurred 11 days after blood cultures became negative. It seems that S. mucilaginosus seeded precociously into the CSF and that the antibiotic diffusion was insufficient to prevent the occurrence of meningitis. The development of sequelae in spite of eradication of bacteria illustrates the virulence of this opportunistic pathogen in neutropenic patients and suggests the importance of prophylactic buccal decontamination.
