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Fulminant neonatal sepsis due to Streptococcus milleri
88
Letters to the editor References
I. Christie AB. Infectious diseases; epidemiology and clinic practice. 3rd edition. Edinburgh: Churchill Livingstone, I98o. 2. Ruthow IM. Rupture of the spleen in infectious mononucleosis. Arch Surg I978; II3: 718-720. 3. SmithJN. Complicationsof infectiousmononucleosis.Ann Intern Med 1956; 44: 86x-864. 4. Sakulsky SB, Wallace RB, SilversteinMN, Docherty MB. Ruptured spleen in infectious mononucleosis. Arch Surg I967; 94: 349-350.
F u l m i n a n t n e o n a t a l sepsis due to
Streptococcus m i l l e r i
Sir, We report a case of fulminating sepsis due to Streptococcus milleri, a condition, as far as we know, not previously reported in the newborn. T h e patient was a 3.28 kilogram boy of approximately 37 weeks gestation~ born by spontaneous vertex delivery to a gravid a 3, apparently healthy mother. Ante-natal care revealed no weight gain after 35 weeks gestation and one day prior to delivery the mother stopped feeling any foetal movement. There was no vaginal discharge nor prolonged rupture of membranes. At birth the baby was asphyxiated and there was marked meconium-stained liquor, which was immediately aspirated. Clinical examination showed the baby had hepatosplenomegaly, but there were no petechiae, and the rest of the examination was normal. He had spontaneous but weak respiration, remained cyanosed and was initially nursed with 4o per cent oxygen in an incubator. At six hours he still remained ill and cyanosed with no evidence of cardiac abnormality. A full sepsis screening was performed and treatment with benzyl penicillin and gentamicin was commenced plus oxygen given by continuous positive airway pressure using a facemask. A peripheral W.B.C. at this time was I 1.6 x io9/1 with 50"9 per cent neutrophils showing toxic left shift. After 16 hours the baby developed repeated convulsions which could not be controlled, and 24 hours after birth he suffered a cardiac arrest and died. Prior to death a blood culture, swabs from ears, eyes, nose, throat, axilla and umbilicus were taken and all yielded a heavy pure growth of beta-haemolytic streptococci, which was later identified as Streptococcus milleri, fully sensitive to penicillin. Post-mortem samples of lung, spleen and cerebrospinal fluid also yielded the same organism in pure culture. At post-mortem the relevant findings were that both lungs appeared purple, congested and unexpanded. All other organs, including the brain, appeared normal. Histologically, in the lung most of the alveoli contained aspirated, meconium-stained material and the lung had a consolidated appearance with early focal bronchopneumonia; the brain showed a widespread meningitis with large numbers of polymorphs in the pia arachnoid and occasional small foci of necrosis but no identifiable organisms. Similar foci of necrosis and acute inflammation were present in the adrenal glands and in several mesenteric and cervical lymph nodes. T h e r e are striking similarities between the infection in this baby and that in cases of septicaemia in the newborn caused by beta-haemolytic streptococci group B. Given that Streptococcus milleri is a normal member of the vaginal
Letters to the editor
89
flora and it has some capacity for causing harm, as cases of endocarditis, intracranial, abdominal and liver abscesses demonstrate, 1 it is therefore not so surprising to find it causing death in a neonate. However, to our knowledge this organism has not been previously described as such a cause of fulminating neonatal sepsis. It seems to be yet another organism to be aware of when dealing with severe infection in the newborn. (We thank Dr G. Coleman of the Streptococcal Reference Centre for identifying this organism.)
Barnsley District General Hospital, Gawber Road, Barnsley, South Yorkshire
R. C° Spencer ~" C. S. Nanayakarra A. J. Coup
* Present address : Dept of Bacteriology, Royal Hallamshire Hospital, Sheffield SIo 2JF.
Reference
r. Murray HW, Gross KC, Masier H, Robert RB. Seriousinfectionscausedby Streptococcus milleri. Am J Med I978; 64: 75% P e n i c i l l i n r e s i s t a n c e in v i r i d a n s s t r e p t o c o c c i
Sir, It is unusual to find penicillin-resistant viridans streptococci from clinical material, except from patients treated with penicillin. 1, 2 I report two resistant strains that were isolated from two completely unrelated patients who were not receiving antibiotics. Strain one
This was isolated from blood cultures of a febrile leukaemic patient. Before the culture and sensitivity results were known, the patient received high doses of flucloxacillin, benzyl penicillin and gentamicin for three days without clinical improvement. By disc diffusion test the strain was found to be resistant to penicillin, amplicillin, tetracycline, cotrimoxazole and gentamicin and sensitive to cefuroxime. At this stage all his antibiotics were stopped and cefuroxime was prescribed at a dose of 75o mg thrice daily intravenously. T h e patient was better after 48 hours and the temperature settled to normal. T h e r e were no more signs or symptoms of infection and repeat blood cultures were negative. T h e m i n i m u m inhibitory concentration (MIC) of penicillin against the organism done on antibiotic incorporated solid medium was found to be 5 mg/1 on repeated occasions. It was not a fl-lactamase (chromogenic cephalosporin test) producer. T h e strain was later identified as Streptococcus milleri (one member of the 'viridans' group) by the Streptococcal Reference Unit, Central Public Health Laboratory London. Detailed study of patient's case notes and enquiry from the general practitioner did not show evidence of use of antibiotics within the previous three months.
Letters to the editor References
I. Christie AB. Infectious diseases; epidemiology and clinic practice. 3rd edition. Edinburgh: Churchill Livingstone, I98o. 2. Ruthow IM. Rupture of the spleen in infectious mononucleosis. Arch Surg I978; II3: 718-720. 3. SmithJN. Complicationsof infectiousmononucleosis.Ann Intern Med 1956; 44: 86x-864. 4. Sakulsky SB, Wallace RB, SilversteinMN, Docherty MB. Ruptured spleen in infectious mononucleosis. Arch Surg I967; 94: 349-350.
F u l m i n a n t n e o n a t a l sepsis due to
Streptococcus m i l l e r i
Sir, We report a case of fulminating sepsis due to Streptococcus milleri, a condition, as far as we know, not previously reported in the newborn. T h e patient was a 3.28 kilogram boy of approximately 37 weeks gestation~ born by spontaneous vertex delivery to a gravid a 3, apparently healthy mother. Ante-natal care revealed no weight gain after 35 weeks gestation and one day prior to delivery the mother stopped feeling any foetal movement. There was no vaginal discharge nor prolonged rupture of membranes. At birth the baby was asphyxiated and there was marked meconium-stained liquor, which was immediately aspirated. Clinical examination showed the baby had hepatosplenomegaly, but there were no petechiae, and the rest of the examination was normal. He had spontaneous but weak respiration, remained cyanosed and was initially nursed with 4o per cent oxygen in an incubator. At six hours he still remained ill and cyanosed with no evidence of cardiac abnormality. A full sepsis screening was performed and treatment with benzyl penicillin and gentamicin was commenced plus oxygen given by continuous positive airway pressure using a facemask. A peripheral W.B.C. at this time was I 1.6 x io9/1 with 50"9 per cent neutrophils showing toxic left shift. After 16 hours the baby developed repeated convulsions which could not be controlled, and 24 hours after birth he suffered a cardiac arrest and died. Prior to death a blood culture, swabs from ears, eyes, nose, throat, axilla and umbilicus were taken and all yielded a heavy pure growth of beta-haemolytic streptococci, which was later identified as Streptococcus milleri, fully sensitive to penicillin. Post-mortem samples of lung, spleen and cerebrospinal fluid also yielded the same organism in pure culture. At post-mortem the relevant findings were that both lungs appeared purple, congested and unexpanded. All other organs, including the brain, appeared normal. Histologically, in the lung most of the alveoli contained aspirated, meconium-stained material and the lung had a consolidated appearance with early focal bronchopneumonia; the brain showed a widespread meningitis with large numbers of polymorphs in the pia arachnoid and occasional small foci of necrosis but no identifiable organisms. Similar foci of necrosis and acute inflammation were present in the adrenal glands and in several mesenteric and cervical lymph nodes. T h e r e are striking similarities between the infection in this baby and that in cases of septicaemia in the newborn caused by beta-haemolytic streptococci group B. Given that Streptococcus milleri is a normal member of the vaginal
Letters to the editor
89
flora and it has some capacity for causing harm, as cases of endocarditis, intracranial, abdominal and liver abscesses demonstrate, 1 it is therefore not so surprising to find it causing death in a neonate. However, to our knowledge this organism has not been previously described as such a cause of fulminating neonatal sepsis. It seems to be yet another organism to be aware of when dealing with severe infection in the newborn. (We thank Dr G. Coleman of the Streptococcal Reference Centre for identifying this organism.)
Barnsley District General Hospital, Gawber Road, Barnsley, South Yorkshire
R. C° Spencer ~" C. S. Nanayakarra A. J. Coup
* Present address : Dept of Bacteriology, Royal Hallamshire Hospital, Sheffield SIo 2JF.
Reference
r. Murray HW, Gross KC, Masier H, Robert RB. Seriousinfectionscausedby Streptococcus milleri. Am J Med I978; 64: 75% P e n i c i l l i n r e s i s t a n c e in v i r i d a n s s t r e p t o c o c c i
Sir, It is unusual to find penicillin-resistant viridans streptococci from clinical material, except from patients treated with penicillin. 1, 2 I report two resistant strains that were isolated from two completely unrelated patients who were not receiving antibiotics. Strain one
This was isolated from blood cultures of a febrile leukaemic patient. Before the culture and sensitivity results were known, the patient received high doses of flucloxacillin, benzyl penicillin and gentamicin for three days without clinical improvement. By disc diffusion test the strain was found to be resistant to penicillin, amplicillin, tetracycline, cotrimoxazole and gentamicin and sensitive to cefuroxime. At this stage all his antibiotics were stopped and cefuroxime was prescribed at a dose of 75o mg thrice daily intravenously. T h e patient was better after 48 hours and the temperature settled to normal. T h e r e were no more signs or symptoms of infection and repeat blood cultures were negative. T h e m i n i m u m inhibitory concentration (MIC) of penicillin against the organism done on antibiotic incorporated solid medium was found to be 5 mg/1 on repeated occasions. It was not a fl-lactamase (chromogenic cephalosporin test) producer. T h e strain was later identified as Streptococcus milleri (one member of the 'viridans' group) by the Streptococcal Reference Unit, Central Public Health Laboratory London. Detailed study of patient's case notes and enquiry from the general practitioner did not show evidence of use of antibiotics within the previous three months.