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
The Pediatric Infectious Disease Journal • Volume 34, Number 3, March 2015
Letters
clinical diagnosis of pityriasis versicolor (PV). No specific cultures or polymerase chain reaction techniques were performed. He was treated with intravenous fluconazole for 2 weeks with total resolution of the lesions on follow-up after 3 months with no postinflammatory hypopigmentation. Colonization by Malassezia in neonates begins in the first days of life, and increases during the first weeks.1 The mother seems to be the reservoir for the child’s colonization.2 Malassezia furfur, M. sympodalis and M. globosa are the most common colonizing species. Molecular analysis has proven that M. globosa produces PV. PV is characterized by multiple oval to round hypo- or hyperpigmented patches or thin plaques that are covered with fine scales. The lesions are often confluent and preferentially distributed in the seborrheic areas of the skin surface. In children, it often involves the face, in contrast to the rarity of facial involvement in adults. Typical PV has rarely been reported in neonates. Pityriasis alba, tuberous sclerosis and postinflammatory hypopigmentation are the main differential diagnoses. Factors associated with risk of neonatal infection by Malassezia include genetic inheritance, gestational age, birth weight, length of stay in an intensive care unit, use of TPN, use of antibiotics, use of corticosteroids, elevated temperature and humidity of the incubator and the presence of central venous catheters.3 Potentially severe fungemia has been reported in association with M. sympodalis, M. furfur and M. pachydermatis in infants receiving TPN via an indwelling central venous catheter,4 but in none of these cases were skin lesions suggestive of PV were described. Studies investigating the colonization of central venous lines specifically by Malassezia spp. have demonstrated colonization rates of 2.4–32% in critically ill neonates.5 It is suggested that the organism is introduced into the nursery on the hands of health care workers. The clinical signs and symptoms of Malassezia fungemia and sepsis are fever and respiratory distress that can result in pneumonia or bronchopneumonia with an interstitial pattern on chest radiology. PV is usually treated with topical antimycotic drugs. Systemic treatment with different oral antifungals, such as ketoconazole, itraconazole and fluconazole may be an option in extensive lesions and in those patients at risk of invasive disease, as in our case.
Ana Bauzá, MD
Department of Dermatology Hospital Universitari Son Espases Palma de Mallorca, Spain REFERENCES 1. Bernier V, Weill FX, Hirigoyen V, et al. Skin colonization by Malassezia Species in Neonates. Arch Dermatol. 2002;138:215–218. 2. Nagata R, Nagano H, Ogishima D, et al. Transmission of the major skin microbiota, Malassezia, from mother to neonate. Pediatr Int. 2012;54:350–355. 3. Ahtonen P, Lehtonen OP, Kero P, et al. Malassezia furfur colonization of neonates in an intensive care unit. Mycoses. 1990;33:543–547. 4. Gaitanis G, Magiatis P, Hantschke M, et al. The Malassezia genus in skin and systemic diseases. Clin Microbiol Rev. 2012;25:106–141. 5. Aschner JL, Punsalang A Jr, Maniscalco WM, et al. Percutaneous central venous catheter colonization with Malassezia furfur: incidence and clinical significance. Pediatrics. 1987;80: 535–539.
Corneal Melting Caused by Neisseria gonorrhoeae in an Adolescent To the Editors: e treated a 17-year-old Hispanic male who had a 7-day history of left eye pain with movement, edema, decreased vision and copious purulent drainage caused by Neisseria gonorrhoeae. He had been evaluated 3 times at other hospitals where he was treated with gentamicin eye drops for 4 days and then artificial tears for 2 days with worsening symptoms. The patient was otherwise healthy. Evaluation of his social history revealed multiple sexual partners over the course of a 1-month period occasionally without protection and did not have any knowledge of possible gonococcal infection in sexual partners. The patient had a fever of 101.2°F and was in mild distress. The left eye was remarkable for external erythema, conjunctival erythema, tenderness to touch and milky discharge from his eye. Genitourinary examination did not reveal any rashes, lesions or discharge. An ophthalmologic examination on hospital day 2 revealed a corneal lesion with a tetrahedral area of 2.5 × 1×1 mm with 10% of thickness remaining. The rest of the physical examination was normal. A computed tomography scan performed on admission revealed left preseptal
W
Elisabet Jubert, MD Ana Martín-Santiago, MD
The authors have no funding or conflicts of interest to disclose.
Marta Bernardino, MD
Copyright © 2015 by Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0891-3668/15/3403-0330 DOI: 10.1097/INF.0000000000000583
Department of Dermatology Department of Pediatrics
330 | www.pidj.com
cellulitis with no drainable postseptal fluid collection evident. Culture of left eye purulent drainage was positive for N. gonorrhoeae and negative for Chlamydia trachomatis. Urine DNA amplification was weakly positive for N. gonorrhoeae and negative for C. trachomatis. The boy was treated with oral doxycycline, copious irrigation with artificial tears and moxifloxacin ophthalmic drops. For corneal melting, he was treated with prednisolone drops and oral vitamin C. Patient was discharged home after 5 hospital days with moxifloxacin ophthalmic drops, oral doxycycline and oral vitamin C with instructions to wear an eye shield while sleeping. At a 1-month follow-up, there was a 1.7 × 1.3 × 1.5 mm area of epithelialization over the corneal defect. Gonococcal conjunctivitis is very rare outside of the neonatal period. There has been 1 other published case of periorbital cellulitis caused by N. gonorrhoeae in a child, 1 reported case of gonococcal orbital cellulitis in an adolescent, and 2 reported cases of gonococcal preseptal cellulitis in adults.1–4 Unlike other bacterial infections, N. gonorrhoeae is able to penetrate intact corneal epithelium causing corneal melt, which occurred in our patient. This destruction of the epithelium and stroma can quickly lead to vision loss or corneal perforation that might require corneal grafting.6,7
Mary Kate Claiborne, MD Joshua Atkinson, MS IV Austin Hoy, MS IV Katrina McBeth, MD
The University of Texas Medical School at Houston Houston, Texas REFERENCES
1. Upile NS, Munir N, Leong SC, et al. Who should manage acute periorbital cellulitis in children? Int J Pediatr Otorhinolaryngol. 2012;76: 1073–1077. 2. Frazier JJ, Miller J, Pickering LK. Orbital cellulitis due to Neisseria gonorrhoeae in an enucleated socket. Arch Ophthalmol. 1979;97:2345. 3. Green JA, Lim J, Barkham T. Neisseria gonorrhoeae: a rare cause of preseptal cellulitis? Int J STD AIDS. 2006;17:137–138. 4. Henderson TR, Booth AP, Morrell AJ. Neisseria gonorrhoeae: a previously unreported cause of pre-septal cellulitis. Eye (Lond). 1997;11 (Pt 1):130–132. 5. Hauser A, Fogarasi S. Periorbital and orbital cellulitis. Pediatr Rev. 2010;31:242–249. 6. Tipple C, Smith A, Bakowska E, et al. Corneal perforation requiring corneal grafting: a rare complication of gonococcal eye infection. Sex Transm Infect. 2010;86:447–448. 7. Day AC, Ramkissoon YD, George S, et al. Don’t forget gonococcus! Eye (Lond). 2006;20: 1400–1402.
© 2015 Wolters Kluwer Health
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
The Pediatric Infectious Disease Journal • Volume 34, Number 3, March 2015
Letters
clinical diagnosis of pityriasis versicolor (PV). No specific cultures or polymerase chain reaction techniques were performed. He was treated with intravenous fluconazole for 2 weeks with total resolution of the lesions on follow-up after 3 months with no postinflammatory hypopigmentation. Colonization by Malassezia in neonates begins in the first days of life, and increases during the first weeks.1 The mother seems to be the reservoir for the child’s colonization.2 Malassezia furfur, M. sympodalis and M. globosa are the most common colonizing species. Molecular analysis has proven that M. globosa produces PV. PV is characterized by multiple oval to round hypo- or hyperpigmented patches or thin plaques that are covered with fine scales. The lesions are often confluent and preferentially distributed in the seborrheic areas of the skin surface. In children, it often involves the face, in contrast to the rarity of facial involvement in adults. Typical PV has rarely been reported in neonates. Pityriasis alba, tuberous sclerosis and postinflammatory hypopigmentation are the main differential diagnoses. Factors associated with risk of neonatal infection by Malassezia include genetic inheritance, gestational age, birth weight, length of stay in an intensive care unit, use of TPN, use of antibiotics, use of corticosteroids, elevated temperature and humidity of the incubator and the presence of central venous catheters.3 Potentially severe fungemia has been reported in association with M. sympodalis, M. furfur and M. pachydermatis in infants receiving TPN via an indwelling central venous catheter,4 but in none of these cases were skin lesions suggestive of PV were described. Studies investigating the colonization of central venous lines specifically by Malassezia spp. have demonstrated colonization rates of 2.4–32% in critically ill neonates.5 It is suggested that the organism is introduced into the nursery on the hands of health care workers. The clinical signs and symptoms of Malassezia fungemia and sepsis are fever and respiratory distress that can result in pneumonia or bronchopneumonia with an interstitial pattern on chest radiology. PV is usually treated with topical antimycotic drugs. Systemic treatment with different oral antifungals, such as ketoconazole, itraconazole and fluconazole may be an option in extensive lesions and in those patients at risk of invasive disease, as in our case.
Ana Bauzá, MD
Department of Dermatology Hospital Universitari Son Espases Palma de Mallorca, Spain REFERENCES 1. Bernier V, Weill FX, Hirigoyen V, et al. Skin colonization by Malassezia Species in Neonates. Arch Dermatol. 2002;138:215–218. 2. Nagata R, Nagano H, Ogishima D, et al. Transmission of the major skin microbiota, Malassezia, from mother to neonate. Pediatr Int. 2012;54:350–355. 3. Ahtonen P, Lehtonen OP, Kero P, et al. Malassezia furfur colonization of neonates in an intensive care unit. Mycoses. 1990;33:543–547. 4. Gaitanis G, Magiatis P, Hantschke M, et al. The Malassezia genus in skin and systemic diseases. Clin Microbiol Rev. 2012;25:106–141. 5. Aschner JL, Punsalang A Jr, Maniscalco WM, et al. Percutaneous central venous catheter colonization with Malassezia furfur: incidence and clinical significance. Pediatrics. 1987;80: 535–539.
Corneal Melting Caused by Neisseria gonorrhoeae in an Adolescent To the Editors: e treated a 17-year-old Hispanic male who had a 7-day history of left eye pain with movement, edema, decreased vision and copious purulent drainage caused by Neisseria gonorrhoeae. He had been evaluated 3 times at other hospitals where he was treated with gentamicin eye drops for 4 days and then artificial tears for 2 days with worsening symptoms. The patient was otherwise healthy. Evaluation of his social history revealed multiple sexual partners over the course of a 1-month period occasionally without protection and did not have any knowledge of possible gonococcal infection in sexual partners. The patient had a fever of 101.2°F and was in mild distress. The left eye was remarkable for external erythema, conjunctival erythema, tenderness to touch and milky discharge from his eye. Genitourinary examination did not reveal any rashes, lesions or discharge. An ophthalmologic examination on hospital day 2 revealed a corneal lesion with a tetrahedral area of 2.5 × 1×1 mm with 10% of thickness remaining. The rest of the physical examination was normal. A computed tomography scan performed on admission revealed left preseptal
W
Elisabet Jubert, MD Ana Martín-Santiago, MD
The authors have no funding or conflicts of interest to disclose.
Marta Bernardino, MD
Copyright © 2015 by Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0891-3668/15/3403-0330 DOI: 10.1097/INF.0000000000000583
Department of Dermatology Department of Pediatrics
330 | www.pidj.com
cellulitis with no drainable postseptal fluid collection evident. Culture of left eye purulent drainage was positive for N. gonorrhoeae and negative for Chlamydia trachomatis. Urine DNA amplification was weakly positive for N. gonorrhoeae and negative for C. trachomatis. The boy was treated with oral doxycycline, copious irrigation with artificial tears and moxifloxacin ophthalmic drops. For corneal melting, he was treated with prednisolone drops and oral vitamin C. Patient was discharged home after 5 hospital days with moxifloxacin ophthalmic drops, oral doxycycline and oral vitamin C with instructions to wear an eye shield while sleeping. At a 1-month follow-up, there was a 1.7 × 1.3 × 1.5 mm area of epithelialization over the corneal defect. Gonococcal conjunctivitis is very rare outside of the neonatal period. There has been 1 other published case of periorbital cellulitis caused by N. gonorrhoeae in a child, 1 reported case of gonococcal orbital cellulitis in an adolescent, and 2 reported cases of gonococcal preseptal cellulitis in adults.1–4 Unlike other bacterial infections, N. gonorrhoeae is able to penetrate intact corneal epithelium causing corneal melt, which occurred in our patient. This destruction of the epithelium and stroma can quickly lead to vision loss or corneal perforation that might require corneal grafting.6,7
Mary Kate Claiborne, MD Joshua Atkinson, MS IV Austin Hoy, MS IV Katrina McBeth, MD
The University of Texas Medical School at Houston Houston, Texas REFERENCES
1. Upile NS, Munir N, Leong SC, et al. Who should manage acute periorbital cellulitis in children? Int J Pediatr Otorhinolaryngol. 2012;76: 1073–1077. 2. Frazier JJ, Miller J, Pickering LK. Orbital cellulitis due to Neisseria gonorrhoeae in an enucleated socket. Arch Ophthalmol. 1979;97:2345. 3. Green JA, Lim J, Barkham T. Neisseria gonorrhoeae: a rare cause of preseptal cellulitis? Int J STD AIDS. 2006;17:137–138. 4. Henderson TR, Booth AP, Morrell AJ. Neisseria gonorrhoeae: a previously unreported cause of pre-septal cellulitis. Eye (Lond). 1997;11 (Pt 1):130–132. 5. Hauser A, Fogarasi S. Periorbital and orbital cellulitis. Pediatr Rev. 2010;31:242–249. 6. Tipple C, Smith A, Bakowska E, et al. Corneal perforation requiring corneal grafting: a rare complication of gonococcal eye infection. Sex Transm Infect. 2010;86:447–448. 7. Day AC, Ramkissoon YD, George S, et al. Don’t forget gonococcus! Eye (Lond). 2006;20: 1400–1402.
© 2015 Wolters Kluwer Health
