Introduction

Parvovirus B19 is a single-stranded DNA virus of the family Parvoviridae and genus Erythrovirus; it is responsible for erythema infectiosum. It is also known as fifth disease because it was the fifth of six classic exanthematous diseases of childhood.¹

Epidemiology

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  Parvovirus B19 infection is extremely common. Seropositivity rates are 5–10 per cent among children aged two to five years, increasing to 50 per cent by age 15 years and 60 per cent by age 30 years. A small percentage of adults every year acquire the infection, resulting in a cumulative incidence of approximately 90 per cent in adults older than 60 years.

  
  
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  The annual conversion rate among pregnant women is 15 per cent.²

  
  
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  Nursery school teachers have a three-fold higher risk of acute infection than other pregnant women, and other school teachers have a 1.6-fold increased risk. The population-attributable risk of infection in susceptible pregnant women is about 55 per cent from their own children and 6 per cent for occupational exposure.

People at Increased Risk

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   1. Mothers of preschool children

   
   
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   2. School age children

   
   
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   3. Workers at daycare centres

   
   
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   4. School teachers

Assessment of immunity at the beginning of the pregnancy can be considered in these populations.

Signs and Symptoms

Infection is often asymptomatic, and up to 50 per cent of non-pregnant women, and up to 70 per cent of infected pregnant women are asymptomatic.³

Pathogenesis

Mode of transmission is through respiratory secretions and hand-to-mouth contact.⁵

Other modes of transmission are blood product infusion and transplacental transfer which occurs in up to 33 per cent of cases. Infected patients are contagious for 5–10 days after exposure, only during the week before the onset of the rash. Approximately 50 per cent of women are at risk if exposed to an infected household member.

Outbreaks usually occur yearly, with larger epidemics every four to five years, and may last up to six months.

Without known exposure, about 1–3 per cent of susceptible pregnant women will develop serologic evidence of infection in pregnancy, rising to over 10 per cent in epidemic periods.⁶

Diagnosis of Maternal Infection

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   1. Parvovirus serology (enzyme-linked immunoassay (ELISA), radioimmunoassay, or immunofluorescence)

   
   
   
   
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     For detection of anti-parvovirus B19 immunoglobulin M (IgM) and immunoglobulin G (IgG) antibodies)

   
   
   
   
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   2. Polymerase chain reaction (PCR) testing for parvovirus B19

   
   
   
   
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     To detect viral DNA present in the blood or other tissues/fluids

     
     
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     The differentiation between acute and chronic infection requires standard DNA hybridisation or quantitative (real-time) PCR in combination with serologic assays for B19-specific IgG, IgM, or both⁷

     
     
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     Monitoring the quantitative PCR viral load in neonates with congenital parvovirus infection helps direct follow-up and the need for transfusions⁷

     
     
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     PCR may be performed on fetal serum or amniotic fluid to detect virus⁷

   
   

Management of Maternal Infection

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   1. Maternal parvovirus B19 infection is managed with symptomatic therapy.

   
   
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   2. There is no specific antiviral treatment.

   
   
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   3. High-dose intravenous immunoglobulin is occasionally used for treating persistent aplastic anaemia associated with parvovirus B 19 infection.

   
   
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   4. Maternal complications are uncommon. Parvovirus infection is usually a self-limited viral infection.

Pregnancy and Parvovirus

Over 50 per cent of pregnant women in the USA are immune to parvovirus.

Pregnancy does not appear to affect the course of the infection, but infection may expose the fetus to the risks of miscarrying, hydrops fetalis and fetal loss.

The transmission rate of maternal parvovirus infection to the fetus is 17–33 per cent.

Fetal Implications

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   1. Spontaneous abortion

Spontaneous abortion or fetal death occurs in less than 10 per cent of infected pregnancies. Most usually occur between 10 and 20 weeks’ gestation, and the spontaneous abortions 4–6 weeks after infection.

The spontaneous loss rate of fetuses affected with parvovirus B19 before 20 weeks’ gestation is 13.0 per cent, and after 20 weeks’ gestation is 0.5 per cent.⁸

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   2. Congenital anomalies

Currently, there does not appear to be any evidence that parvovirus infection increases the risk of congenital anomalies in humans, though there have been case reports of central nervous system, craniofacial, musculoskeletal and eye anomalies.⁹

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   3. Fetal loss

If infection is acquired before 19–20 weeksʼ gestation (14.8 per cent), the fetal loss rate is higher than if the infection is acquired after 20 weeks (2.3 per cent).¹⁰

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   4. Hydrops fetalis

Ultrasound picture of hydrops fetalis includes: ^{11, 12}

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  Ascites

  
  
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  Skin oedema

  
  
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  Pleural and pericardial effusions

  
  
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  Placental oedema

  
  
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  Possible mechanisms for hydrops include fetal anaemia due to transplacental infection, combined with the shorter half-life of fetal red blood cells (especially during the hepatic stage of hematopoiesis)

  
  
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  Other possible causes include fetal viral myocarditis leading to cardiac failure, and impaired hepatic function caused by direct damage to hepatocytes and indirect damage due to haemosiderin deposits

  
  
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  Parvovirus infection accounts for 8–10 per cent of non-immune hydrops, although some studies found molecular evidence in 18–27 per cent of cases of non-immune hydrops