Z Geburtshilfe Neonatol 2015; 219(01): 52-56
DOI: 10.1055/s-0034-1395537
Case Report
© Georg Thieme Verlag KG Stuttgart · New York

An 8-Month History of Meningitis in an Extremely Low Birth Weight Infant? – Long-lasting Infection with Ureaplasma parvum

Neonatale Meningitis – 8 Monate unentdeckt?
K. Glaser
1   University Children’s Hospital Würzburg, University of Würzburg, Germany
,
M. Wohlleben
1   University Children’s Hospital Würzburg, University of Würzburg, Germany
,
C. P. Speer
1   University Children’s Hospital Würzburg, University of Würzburg, Germany
› Author Affiliations
Further Information

Publication History

Publication Date:
19 December 2014 (online)

Abstract

Introduction: Ureaplasma spp. have been implicated in the pathogenesis of both preterm labor and neonatal morbidity including pneumonia and sepsis and the development of chronic lung disease of prematurity. Data on Ureaplasma meningitis are limited and partly controversially discussed.

Patient: We report the unique case of a 9-month-old infant with progressive internal hydrocephalus of unknown origin and developmental delay due to a history of>200 days of inflammation of the central nervous system. The female extremely low birth weight infant had been referred to our hospital for ventriculoperitoneal shunt implantation. She had been born at 26+3 weeks of gestation with a birth weight of 940 g. With the exception of a moderate respiratory distress syndrome, postnatal period had been reported uneventful. However, internal hydrocephalus had become manifest at 4 weeks of postnatal age. Intraventricular hemorrhage had not been documented by cranial ultrasound and magnetic resonance imaging. Cerebrospinal fluid (CSF) analysis had repetitively revealed pronounced inflammation reflected by pleocytosis (50–86 leukocytes/μL, 60% lymphocytes), CSF protein levels of 578–1 026 mg/dL and undetectable CSF glucose. Although suggesting bacterial meningitis, microbial diagnostics had not been indicative, and empirical antibiotics had not affected the CSF findings. On admission to our hospital, CSF analysis still documented significant inflammation (125 leukocytes/μL, CSF protein 565 mg/dL, CSF glucose<2 mg/dL).

Results: Due to a prenatal history of cerclage, we initiated microbial diagnostics on Ureaplasma spp. and Mycoplasma hominis. U. parvum was detected in CSF by culture and PCR, no other pathogens were isolated. On intravenous treatment with chloramphenicol, CSF profile continuously normalized, and cultures and PCR became negative. Treatment was continued for 3 weeks, and the infant was discharged after uncomplicated ventriculoperitoneal shunt placement. During a 12-month observation period she has shown encouraging recovery.

Conclusion: In preterm infants, in particular, internal hydrocephalus of unknown origin and sustained CSF inflammation are highly suggestive of Ureaplasma meningitis. Our case highlights that infection may escape detection if not explicitly considered, since microbial diagnosis requires complex media and PCR.

Zusammenfassung

Hintergrund: Ein Zusammenhang zwischen perinataler Ureaplasmen-Infektion und vorzeitiger Wehentätigkeit sowie neonataler Pneumonie und Sepsis wird vermutet, eine Assoziation mit der Entwicklung einer bronchopulmonalen Dysplasie diskutiert. Zur Ureaplasmen-Meningitis, deren klinische Relevanz unsicher ist, gibt es nur wenige Daten.

Patient: Wir berichten den besonderen Fall eines 9 Monate alten Säuglings mit progredientem Hydrozephalus internus unklarer Genese und Entwicklungsverzögerung verursacht durch eine mehr als 200 Tage andauernde Inflammation des zentralen Nervensystems. Das weibliche Frühgeborene der 26+3. Schwangerschaftswoche, Geburtsgewicht 940 g, war zur Anlage eines ventrikulo-peritonealen Shunts in unsere Klinik überwiesen worden. Mit Ausnahme eines moderaten Atemnotsyndroms Dokumentation eines unauffälligen postnatalen Verlaufs, dennoch Manifestation eines Hydrozephalus internus 4 Wochen postnatal. Eine intraventrikuläre Hämorrhagie war weder neurosonografisch noch kernspintomografisch dargestellt worden, in repetitiven Liquor-Untersuchungen jedoch Nachweis einer Inflammation (50–86 Zellen/μL, 60% Lymphozyten, Eiweiß 578–1 026 mg/dL, Glukose nicht messbar). Trotz vermuteter bakterieller Meningitis kein Erregernachweis, kein Effekt empirischer Antibiotika-Regime. Bei Aufnahme in unsere Klinik bestanden unverändert eine Pleozytose (125 Zellen/μL), eine Proteinerhöhung im Liquor (565 mg/dL) und eine signifikant verminderte Glukosekonzentration (<2 mg/dL).

Verlauf: Aufgrund einer Cerclage in der Pränatal-Anamnese initiierten wir die mikrobiologische Diagnostik auf Ureaplasmen und Mycoplasma hominis. Es gelang der Nachweis von U. parvum in Liquorkultur und PCR, kein Nachweis sonstiger Erreger. Unter i. v.-antibiotischer Therapie mit Chloramphenicol normalisierten sich die Liquorbefunde kontinuierlich, Liquorkultur und PCR blieben ohne Erregernachweis. Die Therapie wurde über 3 Wochen fortgeführt, der Säugling nach unkomplizierter VP-Shunt-Anlage nach Hause entlassen. In den nachfolgenden 12 Monaten zeigte sich eine erfreuliche Aufholentwicklung.

Fazit: Insbesondere bei Frühgeborenen sollten ein Hydrozephalus internus unklarer Genese sowie eine chronische Inflammation des ZNS an eine Ureaplasmen-Meningitis denken lassen. Unser Fallbericht verdeutlicht, dass die Infektion der Diagnostik entgeht, falls keine Ureaplasmen-spezifische Diagnostik initiiert wird.

 
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