Book contents
- Frontmatter
- Contents
- Contributors
- Foreword
- Preface
- Section 1 General principles
- Section 2 Fetal disease
- Chapter 6 Red cell alloimmunization
- Chapter 7 Fetal and neonatal alloimmune thrombocytopenia
- Chapter 8.1 Fetal dysrhythmias
- Chapter 8.2 Fetal dysrhythmias
- Chapter 9.1 Structural heart disease
- Chapter 9.2 Structural heart disease
- Chapter 9.3 Structural heart disease
- Chapter 10.1 Manipulation of amniotic fluid volume
- Chapter 10.2 Manipulation of amniotic fluid volume
- Chapter 11.1 Twin-to-twin transfusion syndrome
- Chapter 11.2 Twin-to-twin transfusion syndrome
- Chapter 11.3 Twin-to-twin transfusion syndrome
- Chapter 11.4 Twin-to-twin transfusion syndrome
- Chapter 11.5 Twin-to-twin transfusion syndrome
- Chapter 12.1 Twin reversed arterial perfusion (TRAP) sequence
- Chapter 12.2 Twin reversed arterial perfusion (TRAP) sequence
- Chapter 13.1 Fetal infections
- Chapter 13.2 Fetal infections
- Chapter 14.1 Fetal urinary tract obstruction
- Chapter 14.2 Fetal urinary tract obstruction
- Chapter 14.3 Fetal urinary tract obstruction
- Chapter 14.4 Fetal urinary tract obstruction
- 15.1 Fetal lung growth, development, and lung fluid
- Chapter 15.2 Fetal lung growth, development, and lung fluid
- Chapter 16.1 Neural tube defects
- Chapter 16.2 Neural tube defects
- Chapter 17.1 Fetal tumors
- Chapter 17.2 Fetal tumors
- Chapter 18.1 Intrauterine growth restriction
- Chapter 18.2 Intrauterine growth restriction
- Chapter 19.1 Congenital diaphragmatic hernia
- Chapter 19.2 Congenital diaphragmatic hernia
- Chapter 20.1 Fetal stem cell transplantation
- Chapter 20.2 Fetal stem cell transplantation
- Chapter 20.3 Fetal stem cell transplantation
- Chapter 21 Gene therapy
- Chapter 22 The future
- Glossary
- Index
- References
Chapter 13.2 - Fetal infections
Clinical management
from Section 2 - Fetal disease
Published online by Cambridge University Press: 05 February 2013
- Frontmatter
- Contents
- Contributors
- Foreword
- Preface
- Section 1 General principles
- Section 2 Fetal disease
- Chapter 6 Red cell alloimmunization
- Chapter 7 Fetal and neonatal alloimmune thrombocytopenia
- Chapter 8.1 Fetal dysrhythmias
- Chapter 8.2 Fetal dysrhythmias
- Chapter 9.1 Structural heart disease
- Chapter 9.2 Structural heart disease
- Chapter 9.3 Structural heart disease
- Chapter 10.1 Manipulation of amniotic fluid volume
- Chapter 10.2 Manipulation of amniotic fluid volume
- Chapter 11.1 Twin-to-twin transfusion syndrome
- Chapter 11.2 Twin-to-twin transfusion syndrome
- Chapter 11.3 Twin-to-twin transfusion syndrome
- Chapter 11.4 Twin-to-twin transfusion syndrome
- Chapter 11.5 Twin-to-twin transfusion syndrome
- Chapter 12.1 Twin reversed arterial perfusion (TRAP) sequence
- Chapter 12.2 Twin reversed arterial perfusion (TRAP) sequence
- Chapter 13.1 Fetal infections
- Chapter 13.2 Fetal infections
- Chapter 14.1 Fetal urinary tract obstruction
- Chapter 14.2 Fetal urinary tract obstruction
- Chapter 14.3 Fetal urinary tract obstruction
- Chapter 14.4 Fetal urinary tract obstruction
- 15.1 Fetal lung growth, development, and lung fluid
- Chapter 15.2 Fetal lung growth, development, and lung fluid
- Chapter 16.1 Neural tube defects
- Chapter 16.2 Neural tube defects
- Chapter 17.1 Fetal tumors
- Chapter 17.2 Fetal tumors
- Chapter 18.1 Intrauterine growth restriction
- Chapter 18.2 Intrauterine growth restriction
- Chapter 19.1 Congenital diaphragmatic hernia
- Chapter 19.2 Congenital diaphragmatic hernia
- Chapter 20.1 Fetal stem cell transplantation
- Chapter 20.2 Fetal stem cell transplantation
- Chapter 20.3 Fetal stem cell transplantation
- Chapter 21 Gene therapy
- Chapter 22 The future
- Glossary
- Index
- References
Summary
Introduction
This chapter focuses upon pathogenic organisms that may be responsible for fetal infection during pregnancy and may have significant effects on outcome. Many infections have associated serious consequences including fetal/perinatal mortality and significant morbidity. Each of the pathogenic organisms will be discussed in turn and specific risks and morbidity outlined.
Introduction
Parvovirus B19 was discovered by chance in 1975 during a systematic search of hepatitis B surface antigen (HBsAg) in sera from blood donors. The name of B19 refers to the number of blood bag in which the virus was discovered. It was not until 1984 that its responsibility in the occurrence of fetal hydrops was proven.
Parvovirus B19 belongs to the Parvoviridae family. This is a naked virus whose genome is linear single-stranded DNA-like. Parvovirus nucleotide variability is low (<1%). After penetration through the respiratory tract, the virus replicates in the nasopharynx, viremia occurs and then a non-specific febrile syndrome appears eight days after primary infection. IgM are present and an antigen–antibody complex is formed causing the rash that appears approximately three weeks after infection in infected children. Therefore, the patient is no longer contagious because the virus is not present in the nasopharynx.
Keywords
- Type
- Chapter
- Information
- Fetal TherapyScientific Basis and Critical Appraisal of Clinical Benefits, pp. 208 - 237Publisher: Cambridge University PressPrint publication year: 2012