203.1 🎓 醫學生版

203.1.0.1 📌 一頁重點

• Virus: ssDNA parvovirus, smallest DNA virus (~ 5 kb genome)
• Receptor: erythrocyte P antigen (globoside) → tropism for erythroid precursors → erythroid hypoplasia
• Transmission: respiratory droplet (children primarily), blood/transplant, vertical
• Clinical Forms:
  1. Erythema infectiosum (5th disease, slapped cheek) — children, fever + rash
  2. Arthropathy — adults (especially women), symmetric small joint
  3. Transient aplastic crisis in chronic hemolytic anemia (sickle cell, hereditary spherocytosis, thalassemia) — sudden severe anemia, life-threatening
  4. Hydrops fetalis in pregnancy (1st-2nd trimester) — fetal anemia + heart failure
  5. Chronic anemia / pure red cell aplasia in immunocompromise (HIV, transplant)
  6. Acute symmetric polyarthritis (mimics RA)
• Universal infection (~ 70% adults seropositive)
• Diagnosis:
  • IgM (acute, weeks 1-2)
  • IgG (past + immunity)
  • PCR (viremia, chronic, fetal)
• Treatment:
  • 5th disease: supportive
  • Aplastic crisis: transfusion + supportive (sickle cell)
  • Hydrops fetalis: intrauterine transfusion (MCA Doppler-guided)
  • Chronic anemia (HIV / immunocompromise): IVIG
  • Arthropathy: NSAID, usually self-limited
• Pregnancy: serial fetal ultrasound + MCA Doppler for anemia detection; transfusion if fetal anemia confirmed

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203.1.0.2 1️⃣ Virology

• Erythroparvovirus genus, Parvoviridae family
• ssDNA, ~ 5 kb (smallest DNA virus)
• Non-enveloped (resistant to disinfectants; alcohol gel less effective)
• P antigen (globoside) receptor — present on erythroid progenitors, fetal liver, placenta
• Productive replication only in actively replicating cells
• Erythroid progenitors (CFU-E, BFU-E) → high replication → erythroid hypoplasia (transient)
• Immune complex deposition → arthritis + rash (mediated by antibodies, not direct viral effect)

203.1.0.2.1 Other Parvoviruses

• Bocavirus (HBoV) — respiratory + GI infections in children
• Parvovirus 4 (PARV4) — rare opportunistic
• Adeno-associated viruses (AAV) — used as gene therapy vectors (not pathogenic)

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203.1.0.3 2️⃣ Erythema Infectiosum (5th Disease)

203.1.0.3.1 Children Classical

• “Slapped cheek” rash — bright red facial rash
• Followed by reticular / lacy rash on trunk + extremities (days)
• Low-grade fever, mild
• Self-limited 1-2 wk
• “Fifth disease” in classification of classic childhood rashes:
  • 1st: measles
  • 2nd: scarlet fever
  • 3rd: rubella
  • 4th: filatow-Dukes (historical, possibly mistaken)
  • 5th: erythema infectiosum (parvovirus B19)
  • 6th: roseola (HHV-6)

203.1.0.3.2 Transmission Window

• Contagious before rash appears (during viremic phase)
• Not contagious once rash appears
• Implication: schools / daycare exposure usually after contagious period

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203.1.0.4 3️⃣ Arthropathy

203.1.0.4.1 Adults > Children

• Symmetric small joint (hands, wrists, knees, ankles)
• Like rheumatoid arthritis pattern
• Women > men
• Acute onset
• Usually self-limited (2-4 wk) but can persist months
• Mimics RA in differential
• RF can be transiently +
• Anti-CCP usually -

203.1.0.4.2 Treatment

• NSAID
• Self-limited

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203.1.0.5 4️⃣ Transient Aplastic Crisis

203.1.0.5.1 Setting

• Underlying chronic hemolytic anemia (sickle cell, hereditary spherocytosis, thalassemia, G6PD deficiency, PNH)
• Erythroid hypoplasia + ↑ hemolysis = catastrophic Hb drop

203.1.0.5.2 Clinical

• Sudden severe anemia (Hb 2-4 g/dL drop)
• Fatigue, pallor, dyspnea
• Worsening of underlying hemolytic disease symptoms
• Can be life-threatening

203.1.0.5.3 Diagnosis

• B19 IgM + or PCR +
• Reticulocyte count low (vs normally elevated in hemolytic anemia → marrow shutdown)

203.1.0.5.4 Treatment

• Transfusion (immediate)
• Supportive
• Self-limited (marrow recovers in days)

203.1.0.5.5 Sickle Cell + Parvovirus B19

• Common cause of aplastic crisis in sickle cell
• All sickle cell patients in aplastic crisis → suspect B19
• IgG seroconversion → immunity (won’t recur)

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203.1.0.6 5️⃣ Hydrops Fetalis

203.1.0.6.1 Mechanism

• Maternal B19 infection during pregnancy → vertical transmission → fetal erythroid suppression + cardiac involvement → severe anemia + heart failure + ascites + pleural effusion + skin edema = hydrops

203.1.0.6.2 Risk

• 1-2nd trimester highest (fetal erythropoiesis maximum)
• Vertical transmission ~ 30%
• Severe hydrops ~ 1-9% of infected pregnancies
• 3rd trimester: lower risk

203.1.0.6.3 Detection

• Maternal serology (IgM + at delivery if recent infection)
• Serial fetal ultrasound (anemia signs)
• MCA Doppler peak systolic velocity (PSV) > 1.5 MoM = fetal anemia

203.1.0.6.4 Treatment

• Intrauterine transfusion (cordocentesis with packed RBC) if severe fetal anemia
• Serial monitoring after
• Maternal IVIG — limited evidence

203.1.0.6.5 Prevention

• Healthcare workers / teachers exposed during pregnancy — counseling + serology
• Avoid contact with viremic children when possible (challenge — most adults working with kids)
• No vaccine available

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203.1.0.7 6️⃣ Chronic Anemia / Pure Red Cell Aplasia

203.1.0.7.1 Setting

• HIV (advanced)
• HSCT, solid organ transplant
• Hematologic malignancy
• Steroid / immunosuppressant
• Failure to clear B19 viremia → persistent erythroid suppression

203.1.0.7.2 Clinical

• Persistent normocytic / macrocytic anemia
• Reticulocyte low
• Bone marrow: erythroid hypoplasia + giant pronormoblasts (“lantern cells”) — pathognomonic
• Sustained B19 viremia

203.1.0.7.3 Treatment

• IVIG (2 g/kg total in divided doses) — provides antibodies to clear virus
• ART improvement in HIV
• Reduction of immunosuppression in transplant
• Repeat IVIG courses if relapse

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203.1.0.8 7️⃣ Diagnosis

203.1.0.8.1 Serology

• IgM: acute infection (positive weeks 1-2 after exposure)
• IgG: past infection / immunity
• Paired sera if needed

203.1.0.8.2 PCR

• Quantitative B19 DNA
• Useful in immunocompromise (where serology unreliable), chronic viremia, fetal blood
• Tissue samples in infants / stillbirth investigation

203.1.0.8.3 Reticulocyte Count

• Low in viremic phase
• Differentiates from other causes of anemia

203.1.0.8.4 Bone Marrow

• Erythroid hypoplasia + giant pronormoblasts (pathognomonic)
• Not routinely needed for diagnosis

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203.1.0.9 8️⃣ Treatment Summary

Form	Treatment
5th disease (children)	Supportive
Arthropathy	NSAID; self-limited
Aplastic crisis	Transfusion + supportive
Hydrops fetalis	Intrauterine transfusion (MCA Doppler-guided)
Chronic anemia (HIV/transplant)	IVIG + reduce immunosuppression / ART

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