Common viral exanthems — formative SAQs

SAQ 1 (10 marks)

A 26-year-old woman who is 22 weeks pregnant presents to her general practitioner. Two days ago her 6-year-old son was diagnosed with erythema infectiosum (fifth disease) after developing slapped cheeks and a lacelike rash. She has no history of parvovirus B19 infection and is unsure whether she has had it before. She is currently well with no rash or fever. [1]

Question: Outline the assessment and management of this pregnant woman, including the risk to the fetus, the investigations, the surveillance pathway and the role of treatment. (10 marks) [3]

Model answer

Risk to the fetus (2 marks). Parvovirus B19 crosses the placenta and is tropic for fetal erythroid precursors via the P blood group antigen. In a non-immune pregnant woman who acquires primary infection, the fetus is at risk of severe anaemia, high-output cardiac failure and hydrops fetalis, and of non-hydropic late intrauterine fetal death. The risk is concentrated in the second trimester because fetal erythropoiesis is massive and the red-cell lifespan is short. Critically, these are risks of anaemia and hydrops, not of a congenital malformation syndrome — so termination is not indicated, and a hydropic fetus can be rescued by intrauterine transfusion if recognised in time. [3] [1]

Investigations (3 marks). The first step is to determine the mother's immune status, because an immune woman needs no further action. Send parvovirus B19 IgG and IgM. IgG positive with IgM negative means past infection and immunity — reassure her, the fetus is protected. IgG negative means she is susceptible and at risk of primary infection, and a rising IgM or seroconversion over the next two to four weeks confirms infection. PCR has a role where the picture is atypical or the woman is immunocompromised and may not seroconvert. The single most important point is that she should not be reassured without serology. [1] [3]

Surveillance pathway (3 marks). If she is non-immune and seroconverts, refer her to fetal medicine for serial fetal ultrasound for ten to twelve weeks after the infection. Ultrasound looks for the earliest signs of hydrops — ascites, pleural or pericardial effusions, skin oedema, polyhydramnios, and raised middle cerebral artery peak systolic velocity as a marker of fetal anaemia. The surveillance window reflects the time over which fetal anaemia can develop after maternal infection. Liaise early with obstetrics and fetal medicine so that a plan is in place should hydrops emerge. [3]

Treatment (2 marks). If ultrasound surveillance detects hydrops, the intervention is intrauterine transfusion to correct the fetal anaemia, which can rescue a fetus that would otherwise die. There is no vaccine and no role for antiviral prophylaxis or immunoglobulin in the immunocompetent pregnant woman. Counselling is central: explain the risk honestly, the surveillance plan, and the fact that timely transfusion gives an excellent outcome — the aim is to detect and treat, not to abort. [3] [1]

SAQ 2 (10 marks)

A 5-year-old boy with sickle cell disease (HbSS) is brought to the emergency department with two days of fever, increasing pallor, fatigue and breathlessness. He has no rash. His baseline haemoglobin is 78 g/L; today it is 41 g/L with a reticulocyte count near zero. A classmate had a febrile rash illness last week. [1]

Question: Describe the diagnosis, the pathophysiology, the immediate management and the disposition of this child. (10 marks) [2]

Model answer

Diagnosis and pathophysiology (3 marks). The diagnosis is parvovirus B19 transient aplastic crisis. The precipitous haemoglobin fall with profound reticulocytopenia in a child with chronic haemolytic anaemia is the fingerprint: the marrow has stopped producing red cells. Parvovirus B19 uses the P antigen (globoside) on erythroid precursors as its receptor and halts red-cell production. In a child with normal haemopoiesis this brief arrest is invisible, but in sickle cell disease the red-cell lifespan is short (fifteen to twenty days) and the marrow runs at high output just to maintain baseline, so even a brief arrest causes a dangerous drop. Note that the aplastic crisis often occurs without the classic fifth-disease rash. [1] [2]

Immediate management (4 marks). This is a haematological emergency. Take blood urgently for a full blood count, reticulocytes, group and cross-match, and send parvovirus B19 serology and PCR. Transfuse packed red cells for the severe symptomatic anaemia, titrated to relieve symptoms and restore a safe haemoglobin, monitoring carefully for the complications of transfusion in sickle cell disease. Monitor for high-output cardiac failure and give oxygen and fluid balance support as needed. Involve haemato-oncology early. The crisis is transient — the marrow recovers as the virus clears — so the goal is to tide the child over the nadir. Do not attribute the presentation to a vaso-occlusive pain crisis, because reticulocytopenia points to aplasia, not sequestration or haemolysis. [1]

Disposition and follow-up (3 marks). Admit for transfusion, monitoring and haematology care. The child should be nursed with attention to standard sickle cell precautions — oxygenation, hydration, infection surveillance — and transfused until the haemoglobin is safe and the reticulocyte count begins to recover. After recovery, counsel the family that parvovirus B19 is a recognised precipitant of aplastic crisis in sickle cell disease and that any future febrile illness with pallor needs urgent assessment. The broader lesson is that any child with chronic haemolytic anaemia and a sudden haemoglobin drop has parvovirus B19 until proven otherwise, and the reticulocyte count is the key discriminator. [1] [2]