Letters to the Editor Staphylococcus schleiferi Meningitis in a Child To the Editors:
S
taphylococcus schleiferi subsp. schleiferi was described in 1988 by Freney et al.1 It is a member of the human preaxillary skin flora,2 but it is not known whether carriage is persistent or transient. It has been implicated as the causative agent of several human infections. We here report the first case of meningitis in a child with this infection. A 6-year-old female child had a history of fever, headache and vomiting. She had 1 episode of generalized tonic clonic seizure on the day of presentation, and developed left focal seizures followed by left hemiparesis within 20 minutes of admission. She had no prior history of seizures. The child was developmentally normal and academically brilliant. The heart rate was 100/min; capillary refill time, 2 seconds; respiratory rate, 24/min and blood pressure, 120/84 mm Hg. The Glasgow coma scale score at admission was 10/15, both pupils were of equal size and well reacting to light and fundus examination was normal. Facial nerve palsy, increased motor tone, brisk deep tendon reflexes, was evident on the left side. Bilateral plantar reflexes were extensor. The child had nuchal rigidity, and Kernig and Brudzinski signs were present. She had intermittent decorticate posturing. The liver was enlarged with a span of 12 cm. She was clinically diagnosed as meningitis/ meningoencephalitis with raised intracranial pressure. The white blood cell count was 13900/dL with 79% neutrophils. Cerebrospinal fluid (CSF) had 2200 cells/dL with 90% neutrophils and 10% lymphocytes, protein 107 mg/dL and glucose 45 mg/dL (blood glucose 122 mg/dL). Gram staining of CSF did not reveal any organism but CSF and blood cultures grew abundant coagulase-negative staphylococcal species. The isolate was identified by Microscan Autoscan 4 (Siemens, West Sacramento, CA) as S. schleiferi. The identification was confirmed by phenotypic tests for sugar fermentation and showed the following: mannitol negative, maltose negative, lactose negative, mannose positive and trehalose negative. By Microscan Autoscan 4 system, the organism was susceptible to ciprofloxacin, clindamycin, erythromycin, gentamicin, The author has no funding or conflicts of interest to disclose. Copyright © 2015 by Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0891-3668/15/3403-0329 DOI: 10.1097/INF.0000000000000561
moxifloxacin, oxacillin, rifampin, tetracycline, trimethoprim–sulfamethoxazole and vancomycin. The patient was treated with intravenous cloxacillin. Hypertonic saline (3%) was used in infusion at 0.2–1 ml/kg/h as osmotherapy. She responded well to this therapy and was discharged with residual left hemiparesis. At 3 months follow-up examination, she was walking without assistance with mild residual weakness of the left upper and lower limbs. She has started attending school. Most S. schleiferi infections have been reported in dogs.1 Infections in human have been wound infection, prosthetic infections and bacteremia.2–6 S. schleiferi is often mistaken for S. aureus because both express clumping factor and heat stable DNase. The subspecies schleiferi does not produce a staphylocoagulase, but can produce a pseudocoagulase and therefore is sometimes described as coagulase positive. Protease inhibitors and anticoagulants can frequently inhibit clotting activity and therefore it is usually reported as coagulase negative.7 A review of 28 reported cases4 in 2001 reported that all isolates were coagulase negative: 50% of cultures were from wound infections, 19.4% were found in blood cultures, 13.8% from catheter tips, 8.3% from ear exudates and 5.5% from CSF. Other sites included pleural fluid, corneal exudate, biliary drainage and urine. Most patients were older men (mean age of 64 years) and the most common underlying comorbidity was immunosuppression and malignancy. The series included 2 patients with meningism secondary to neoplasms (meningioma, multiple cholesteatoma), and both of them had ventriculo-peritoneal shunts. S. schleiferi was recovered from CSF and the parietal reservoir in one of them. This is the first reported case of meningitis by this organism in humans in the absence of an indwelling intracranial device. We suspect that this patient became infected with S. schleiferi through contact with her dog. This dog had numerous skin pustules and ear infection and culture from his ears and hairs grew S. schleiferi.
Atul Jindal, MBBS, MD, DM
Department of Pediatrics All India Institute of Medical Sciences Raipur, Chhattisgarh, India
Deepak Shivpuri, MBBS, MD
Department of Pediatrics Centre for Advanced Pediatrics Fortis Escorts Hospital
Smita Sood, MBBS, MD
Department of Microbiology Fortis Escorts Hospital Jaipur, Rajasthan, India
The Pediatric Infectious Disease Journal • Volume 34, Number 3, March 2015
REFERENCES 1. Freney J, Brun Y, Bes M, et al. Staphylococcus lugdunensis sp. nov. and Staphylococcus schleiferi sp. nov., two species from human clinical specimens. Int J Syst Bacteriol. 1988;38:168– 172. 2. Célard M, Vandenesch F, Darbas H, et al. Pacemaker infection caused by Staphylococcus schleiferi, a member of the human preaxillary flora: four case reports. Clin Infect Dis. 1997;24:1014–1015. 3. Da Costa A, Lelièvre H, Kirkorian G, et al. Role of the preaxillary flora in pacemaker infections: a prospective study. Circulation. 1998;97:1791– 1795. 4. Hernández JL, Calvo J, Sota R, et al. Clinical and microbiological characteristics of 28 patients with Staphylococcus schleiferi infection. Eur J Clin Microbiol Infect Dis. 2001;20:153–158. 5. Kumar D, Cawley JJ, Irizarry-Alvarado JM, et al. Case of Staphylococcus schleiferi subspecies coagulans endocarditis and metastatic infection in an immune compromised host. Transpl Infect Dis. 2007;9:336–338. 6. Latorre M, Rojo PM, Unzaga MJ, et al. Staphylococcus schleiferi: a new opportunistic pathogen. Clin Infect Dis. 1993;16:589–590. 7. Vandenesch F, Lebeau C, Bes M, et al. Clotting activity in Staphylococcus schleiferi subspecies from human patients. J Clin Microbiol. 1994;32:388–392.
Neonatal Pityriasis Versicolor To The Editors:
A
premature (32 + 3 weeks gestational age) black skinned neonate with low birthweight (852 g) was placed in an incubator at the intensive care unit. The infant was receiving total parenteral nutrition (TPN) and broad spectrum antibiotics. He was examined for noncongenital depigmented areas at the age of 3 weeks. Physical examination revealed numerous hypopigmented macules and patches on the upper part of the trunk, face and neck (see Fig., Supplemental Digital Content 1, http:// links.lww.com/INF/C25) where no lesions had been previously present. A fine scale was demonstrable when the surface of a lesion was scraped. Clinical examination of the parents did not reveal any skin eruption. The potassium hydroxide preparation demonstrated spherical yeast forms and hyphae. These characteristic findings supported the
The authors declare no conflicts of interest. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (www.pidj.com). Copyright © 2015 by Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0891-3668/15/3403-0329 DOI: 10.1097/INF.0000000000000568
www.pidj.com | 329
S
taphylococcus schleiferi subsp. schleiferi was described in 1988 by Freney et al.1 It is a member of the human preaxillary skin flora,2 but it is not known whether carriage is persistent or transient. It has been implicated as the causative agent of several human infections. We here report the first case of meningitis in a child with this infection. A 6-year-old female child had a history of fever, headache and vomiting. She had 1 episode of generalized tonic clonic seizure on the day of presentation, and developed left focal seizures followed by left hemiparesis within 20 minutes of admission. She had no prior history of seizures. The child was developmentally normal and academically brilliant. The heart rate was 100/min; capillary refill time, 2 seconds; respiratory rate, 24/min and blood pressure, 120/84 mm Hg. The Glasgow coma scale score at admission was 10/15, both pupils were of equal size and well reacting to light and fundus examination was normal. Facial nerve palsy, increased motor tone, brisk deep tendon reflexes, was evident on the left side. Bilateral plantar reflexes were extensor. The child had nuchal rigidity, and Kernig and Brudzinski signs were present. She had intermittent decorticate posturing. The liver was enlarged with a span of 12 cm. She was clinically diagnosed as meningitis/ meningoencephalitis with raised intracranial pressure. The white blood cell count was 13900/dL with 79% neutrophils. Cerebrospinal fluid (CSF) had 2200 cells/dL with 90% neutrophils and 10% lymphocytes, protein 107 mg/dL and glucose 45 mg/dL (blood glucose 122 mg/dL). Gram staining of CSF did not reveal any organism but CSF and blood cultures grew abundant coagulase-negative staphylococcal species. The isolate was identified by Microscan Autoscan 4 (Siemens, West Sacramento, CA) as S. schleiferi. The identification was confirmed by phenotypic tests for sugar fermentation and showed the following: mannitol negative, maltose negative, lactose negative, mannose positive and trehalose negative. By Microscan Autoscan 4 system, the organism was susceptible to ciprofloxacin, clindamycin, erythromycin, gentamicin, The author has no funding or conflicts of interest to disclose. Copyright © 2015 by Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0891-3668/15/3403-0329 DOI: 10.1097/INF.0000000000000561
moxifloxacin, oxacillin, rifampin, tetracycline, trimethoprim–sulfamethoxazole and vancomycin. The patient was treated with intravenous cloxacillin. Hypertonic saline (3%) was used in infusion at 0.2–1 ml/kg/h as osmotherapy. She responded well to this therapy and was discharged with residual left hemiparesis. At 3 months follow-up examination, she was walking without assistance with mild residual weakness of the left upper and lower limbs. She has started attending school. Most S. schleiferi infections have been reported in dogs.1 Infections in human have been wound infection, prosthetic infections and bacteremia.2–6 S. schleiferi is often mistaken for S. aureus because both express clumping factor and heat stable DNase. The subspecies schleiferi does not produce a staphylocoagulase, but can produce a pseudocoagulase and therefore is sometimes described as coagulase positive. Protease inhibitors and anticoagulants can frequently inhibit clotting activity and therefore it is usually reported as coagulase negative.7 A review of 28 reported cases4 in 2001 reported that all isolates were coagulase negative: 50% of cultures were from wound infections, 19.4% were found in blood cultures, 13.8% from catheter tips, 8.3% from ear exudates and 5.5% from CSF. Other sites included pleural fluid, corneal exudate, biliary drainage and urine. Most patients were older men (mean age of 64 years) and the most common underlying comorbidity was immunosuppression and malignancy. The series included 2 patients with meningism secondary to neoplasms (meningioma, multiple cholesteatoma), and both of them had ventriculo-peritoneal shunts. S. schleiferi was recovered from CSF and the parietal reservoir in one of them. This is the first reported case of meningitis by this organism in humans in the absence of an indwelling intracranial device. We suspect that this patient became infected with S. schleiferi through contact with her dog. This dog had numerous skin pustules and ear infection and culture from his ears and hairs grew S. schleiferi.
Atul Jindal, MBBS, MD, DM
Department of Pediatrics All India Institute of Medical Sciences Raipur, Chhattisgarh, India
Deepak Shivpuri, MBBS, MD
Department of Pediatrics Centre for Advanced Pediatrics Fortis Escorts Hospital
Smita Sood, MBBS, MD
Department of Microbiology Fortis Escorts Hospital Jaipur, Rajasthan, India
The Pediatric Infectious Disease Journal • Volume 34, Number 3, March 2015
REFERENCES 1. Freney J, Brun Y, Bes M, et al. Staphylococcus lugdunensis sp. nov. and Staphylococcus schleiferi sp. nov., two species from human clinical specimens. Int J Syst Bacteriol. 1988;38:168– 172. 2. Célard M, Vandenesch F, Darbas H, et al. Pacemaker infection caused by Staphylococcus schleiferi, a member of the human preaxillary flora: four case reports. Clin Infect Dis. 1997;24:1014–1015. 3. Da Costa A, Lelièvre H, Kirkorian G, et al. Role of the preaxillary flora in pacemaker infections: a prospective study. Circulation. 1998;97:1791– 1795. 4. Hernández JL, Calvo J, Sota R, et al. Clinical and microbiological characteristics of 28 patients with Staphylococcus schleiferi infection. Eur J Clin Microbiol Infect Dis. 2001;20:153–158. 5. Kumar D, Cawley JJ, Irizarry-Alvarado JM, et al. Case of Staphylococcus schleiferi subspecies coagulans endocarditis and metastatic infection in an immune compromised host. Transpl Infect Dis. 2007;9:336–338. 6. Latorre M, Rojo PM, Unzaga MJ, et al. Staphylococcus schleiferi: a new opportunistic pathogen. Clin Infect Dis. 1993;16:589–590. 7. Vandenesch F, Lebeau C, Bes M, et al. Clotting activity in Staphylococcus schleiferi subspecies from human patients. J Clin Microbiol. 1994;32:388–392.
Neonatal Pityriasis Versicolor To The Editors:
A
premature (32 + 3 weeks gestational age) black skinned neonate with low birthweight (852 g) was placed in an incubator at the intensive care unit. The infant was receiving total parenteral nutrition (TPN) and broad spectrum antibiotics. He was examined for noncongenital depigmented areas at the age of 3 weeks. Physical examination revealed numerous hypopigmented macules and patches on the upper part of the trunk, face and neck (see Fig., Supplemental Digital Content 1, http:// links.lww.com/INF/C25) where no lesions had been previously present. A fine scale was demonstrable when the surface of a lesion was scraped. Clinical examination of the parents did not reveal any skin eruption. The potassium hydroxide preparation demonstrated spherical yeast forms and hyphae. These characteristic findings supported the
The authors declare no conflicts of interest. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (www.pidj.com). Copyright © 2015 by Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0891-3668/15/3403-0329 DOI: 10.1097/INF.0000000000000568
www.pidj.com | 329
