Impetigo neonatorum associated with late onset group B streptococcal meningitis

Ananya Guha, Michael Eisenhut^, , Paul Shears and Mark Dalzell

Royal Liverpool Childrens NHS Trust, Alder Hey, Eaton Road, Liverpool L12 2AP, UK

Accepted 13 April 2003. ; Available online 29 May 2003.

1. Introduction

Impetigo neonatorum is a form of impetigo occurring in neonates from birth to the second week of life. Skin areas predominantly affected are moist areas under the diaper, around the neck, groins and axillae.[1] Organisms isolated from the lesions included Staphylococcus (S.) aureus and Group B streptococcus (GBS).[2, 3, 4 and 5] Impetigo in neonates has not been associated with systemic manifestations. Skin lesions reported in late onset GBS meningitis are erysipelas and cellulitis. [6 and 7] We report the first case of GBS meningitis associated with impetigo neonatorum.

2. Case report

This male infant was born at term by normal vaginal delivery with a birth weight of 3.2 kg. There was no history of prolonged rupture of membranes, no maternal pyrexia or evidence of maternal GBS carriage, or impetigo in close contacts. He was breast-fed from birth and had mild physiological jaundice on the second day. Mother had cracked nipples on the fourth day but she continued with breast-feeding.

Two days prior to admission mother noted pin prick like, red spots over the lower abdomen in the area covered by the diaper. A few more similar lesions appeared the day before admission. A yellow crust on an enlarged erythematous base developed and the infant became unwell with poor feeding and an abnormal cry.

On admission, on the twelfth day of life, the infant was pyrexial (38.5 °C) and irritable. There were no symptoms or signs of cardiovascular or respiratory compromise. The anterior fontanelle was full. Three skin lesions compatible with impetigo were noted over the infraumbilical region (see Fig. 1). An infection screen was performed and intravenous cefotaxime commenced. Cerebrospinal fluid (CSF) revealed gram-positive bacteria on staining, which were identified as GBS. CSF glucose was <0.5 mmol/l, protein 3.8 g/l (normal range 0.3–1.2 g/l), and the cell count showed 723 white blood cells per microliter. Blood cultures also isolated GBS. A urine culture was sterile and a chest X-ray was normal. From skin swabs of the impetigo lesions S. aureus was isolated. Culture of maternal breast milk also revealed a growth of this organism.

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Figure 1. Impetigo neonatorum in a case of group B streptococcal meningitis.

The infant made an uneventful recovery. The skin lesions healed within five days after admission without scar or abnormal pigmentation. A 2-week course of intravenous cefotaxime was completed.

3. Discussion

Although GBS was not cultured from skin lesions we think the skin lesions and the GBS meningitis were not a mere coincidence. In nonbullous impetigo S. aureus has previously been detected together with GBS in the same lesions.[8] Mitis Salivarius agar plates conducive to growth of GBS, were not used for culture in this instance. This may have prevented detection of streptococci in the mixture with S. aureus. S. aureus is known to produce an anti-streptococcal bacteriocin inhibiting concomitant growth of GBS.[9]

Breastmilk has previously been described as an important source of infection in late onset group B streptococcal meningitis.[10] We could not exclude maternal breast milk as a source of the infection because S. aureus cultured from the milk may have obscured the presence of GBS.

This case illustrates that the skin may be an entry site for GBS causing late-onset meningitis. Early systemic antibiotic therapy covering both S. aureus and GBS in impetigo neonatorum is necessary to prevent this potentially fatal complication.

References

1. L.A. Schachner and S. Press, Vesicular, bullous, and pustular disorders. In: L.A. Schachner and R.C. Hansen, Editors, Pediatric Dermatology, Churchill Livingstone, London (1988), p. 823.

2. A. Kline and E. O'Donnell, Group B streptococcus as a cause of neonatal bullous skin lesions. Pediatr Infect Dis J 12 (1993), pp. 165–166.

3. T.K. Belgaumkar, Impetigo neonatorum congenita due to group B betahemolytic streptococcus infection. J Pediatr 86 (1975), pp. 982–983.

4. J.B. Lopez, P. Gross and T.R. Boggs, Skin lesions in association with beta-hemolytic streptococcus group B. Pediatrics 58 (1976), pp. 859–861.

5. W. Kunze, Impetigo neonatorum congenita durch B-Streptokokken. Zbl Gynaekol 102 (1980), pp. 1075–1076.

6. R.S. Ramamurthy, G. Srinivasan and N.M. Jacobs, Necrotizing fasciitis and necrotizing cellulitis due to group B Streptococcus. Am J Dis Child 131 (1977), pp. 1169–1170.

7. J.B. Howard and G.H. McCracken, The spectrum of group B streptococcal infections in infancy. Am J Dis Child 128 (1974), pp. 815–818.

8. H. Akiyama, O. Yamasaki, H. Kanzaki, J. Tada and J. Arata, Streptococci isolated from various skin lesions: the interaction with Staphylococcus aureus strains. J Dermatol Sci 19 (1999), pp. 17–22. SummaryPlus | Full Text + Links | PDF (69 K)

9. A. Iqbal, S.A. Ali, A. Abbasi, W. Volter and S.A. Rasool, Production, purification and some properties of Bac201, a bacteriocin-like inhibitory substance produced by Staphylococcus aureus AB201. J Basic Microbiol 41 (2001), pp. 25–36.

10. J. Dinger, D. Mueller, N. Pargac and R. Schwarze, Breast milk transmission of group B streptococcal infection. Pediatr Infect Dis J 21 (2002), pp. 567–568.

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Abstract

Article Outline

1. Introduction

2. Case report

3. Discussion

References