Part 1 obgyn notes Sri Lanka
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    PARVO B19

    PARVO B19

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    1. MICROBIOLOGY OF PARVOVIRUS B19 (FULL DETAILS)

    Structure

    • Smallest DNA virus infecting humans
    • Family: Parvoviridae
    • Genus: Erythroparvovirus
    • Non-enveloped
    • Icosahedral capsid
    • Replicates in nucleus of rapidly dividing cells

    KEY POINT

    🩸 Tropism for erythroid precursors → infects pronormoblasts in bone marrow via P antigen receptor.(in fetal myocardiocytes,hepatocytes)

    Replication & Pathogenesis

    • Infects erythroid progenitors → temporarily stops red cell production.
    • In immunocompetent hosts → transient aplastic crisis if underlying hemolysis (e.g., sickle cell).
    • In pregnancy → fetal anemia → high-output heart failure → hydrops fetalis.

    Transmission

    • Respiratory droplets (most common)
    • Vertical transmission: transplacental
    • Blood products
    • Incubation: 4–14 days

    Clinical Features in Adults

    • 50% asymptomatic (important for pregnancy diagnosis!)
    • Flu-like illness
    • Arthralgia: common in women

      • – Small joints of hands, wrists, knees

    • Mild rash (less common than in kids- Slapped cheek)

    Immunity

    • One serotype → lifelong immunity.
    • IgM appears first, persists 2–3 months
    • IgG lifelong → immunity

    2. EFFECTS IN PREGNANCY

    Vertical Transmission Rate

    • 30% of maternal infections → fetal transmission

    Fetal Risks

    1. Severe fetal anemia

    • Virus destroys fetal erythroblasts

    2. Hydrops fetalis

    • Due to high-output cardiac failure from anemia
    • Peak risk: 9–20 weeks, highest before 20 weeks

    3. Fetal loss

    • Overall <10%
    • Risk highest if infection before 20 weeks

    4. No structural anomalies

    • NOT teratogenic
    • Effects are due to anemia, not malformations

    3. MATERNAL INVESTIGATIONS

    When to test the mother?

    • Exposure
    • Symptoms
    • Hydrops on scan

    Maternal Tests

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    ✔ Parvovirus B19 IgM

    • Positive → recent infection (last 2–3 months)

    ✔ Parvovirus B19 IgG

    • Positive → immunity
    • IgG+ / IgM– → immune → NO RISK

    ✔ PCR (Maternal blood)

    • Detects active viremia
    • Useful when serology is unclear

    4. FETAL INVESTIGATIONS

    Ultrasound

    • Hydrops fetalis
    • Ascites
    • Pericardial effusion
    • Pleural effusion
    • Placental thickening
    • Polyhydramnios

    Fetal MCA Doppler

    • Peak systolic velocity (PSV)
    • >1.5 MoM → significant fetal anemia → needs transfusion

    5. MANAGEMENT OF MATERNAL PARVOVIRUS B19 INFECTION

    STEP 1 — Determine Maternal Immune Status

    1. IgG– / IgM–

    → Susceptible

    → Repeat serology in 2–3 weeks

    2. IgM+ (with or without IgG)

    → Recent infection

    3. IgG+ / IgM–

    → Immunity

    → NO fetal monitoring required

    STEP 2 — After Confirmed Maternal Infection

    Monitor fetus for 12 weeks

    • Weekly US
    • Weekly MCA Doppler

    If MCA-PSV >1.5 MoM → severe fetal anemia

    → Intrauterine transfusion (IUT)

    • Via intraperitoneal or intravascular transfusion
    • Dramatically reduces fetal mortality

    STEP 3 — Hydrops Fetalis Treatment

    ✔ IUT is the main treatment

    • Corrects anemia
    • Hydrops usually resolves after transfusion

    ✔ Repeat transfusions may be needed every 1–2 weeks

    ✔ Deliver if viable after multiple transfusions depending on GA

    STEP 4 — Maternal Treatment

    • No antiviral available
    • No vaccine
    • Supportive care only

    6. PROGNOSIS

    • Most pregnancies do well
    • Hydrops + anemia treated with IUT → survival up to 80–90%
    • No long-term congenital infection issues

    7. DIFFERENTIALS FOR HYDROPS

    • Rh isoimmunization
    • Alpha-thalassemia major
    • CMV
    • Parvo B19 (most common viral cause)
    • Twin–twin transfusion

    EXAM TIP (Always asked):

    MCA Doppler > 1.5 MoM = fetal anemia

    → Do intrauterine transfusion.

    PARVOVIRUS B19 IN PREGNANCY — COMPLETE MASTER TABLE (ZERO-OMISSION)

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    DOMAIN
    SUBSECTION
    DETAILS (NO OMISSIONS)
    MICROBIOLOGY
    Virus type
    Smallest DNA virus infecting humans
    Family
    Parvoviridae
    Genus
    Erythroparvovirus
    Envelope
    Non-enveloped
    Capsid
    Icosahedral
    Replication site
    Nucleus
    Target cells
    Rapidly dividing cells
    Cell tropism (KEY)
    Erythroid precursors (pronormoblasts)
    Receptor
    P antigen (globoside)
    PATHOGENESIS
    Core mechanism
    Infection of erythroid progenitors → temporary arrest of erythropoiesis
    Normal host
    Usually asymptomatic or mild illness
    Hemolytic disorders
    Transient aplastic crisis (e.g. sickle cell disease)
    Pregnancy
    Fetal anemia → high-output cardiac failure → hydrops fetalis
    TRANSMISSION
    Route 1
    Respiratory droplets (most common)
    Route 2
    Vertical (transplacental)
    Route 3
    Blood products
    Incubation period
    4–14 days
    ADULT CLINICAL FEATURES
    Asymptomatic
    ~50% (critical in pregnancy)
    Systemic
    Flu-like illness
    Joints
    Arthralgia (common in women)
    Joints involved
    Small joints of hands, wrists, knees
    Rash
    Mild rash, less common than in children
    IMMUNITY
    Serotype
    Single serotype
    Duration
    Lifelong immunity
    IgM
    Appears first, persists 2–3 months
    IgG
    Lifelong, protective
    PREGNANCY — TRANSMISSION
    Vertical transmission rate
    ~30%
    PREGNANCY — FETAL RISKS
    Severe anemia
    Viral destruction of fetal erythroblasts
    Hydrops fetalis
    Due to high-output cardiac failure
    Peak risk period
    9–20 weeks, highest <20 weeks
    Fetal loss
    <10% overall, highest if infection <20 weeks
    Teratogenicity
    NOT teratogenic
    Nature of damage
    Functional (anemia-related), no structural anomalies
    MATERNAL INVESTIGATION — INDICATIONS
    When to test
    Exposure, maternal symptoms, hydrops on ultrasound
    MATERNAL TESTS
    IgM
    Positive = recent infection (last 2–3 months)
    IgG
    Positive = immunity
    IgG+/IgM–
    Immune → NO fetal risk
    PCR (maternal blood)
    Detects active viremia, useful if serology unclear
    FETAL INVESTIGATIONS
    Ultrasound signs
    Hydrops, ascites, pericardial effusion, pleural effusion
    Placenta
    Placental thickening
    Liquor
    Polyhydramnios
    MCA Doppler
    Peak systolic velocity (PSV)
    Critical cutoff
    >1.5 MoM = significant fetal anemia
    MANAGEMENT — STEP 1
    IgG– / IgM–
    Susceptible → repeat serology in 2–3 weeks
    IgM+ ± IgG
    Recent infection
    IgG+ / IgM–
    Immune → NO fetal monitoring needed
    MANAGEMENT — STEP 2
    Fetal surveillance
    12 weeks monitoring after infection
    Frequency
    Weekly ultrasound + weekly MCA Doppler
    Severe anemia
    MCA-PSV >1.5 MoM
    Action
    Intrauterine transfusion (IUT)
    Route
    Intravascular or intraperitoneal
    Effect
    Markedly reduces fetal mortality
    MANAGEMENT — STEP 3
    Hydrops treatment
    IUT = mainstay
    Outcome
    Correction of anemia → hydrops resolution
    Repeat IUT
    Every 1–2 weeks if needed
    Delivery
    If viable, depending on gestational age
    MANAGEMENT — STEP 4
    Maternal therapy
    No antiviral, no vaccine
    Care
    Supportive only
    PROGNOSIS
    Overall outcome
    Most pregnancies do well
    With IUT
    Survival 80–90%
    Long-term effects
    No chronic congenital infection issues
    DIFFERENTIALS OF HYDROPS
    Immune
    Rh isoimmunization
    Hematologic
    Alpha-thalassemia major
    Infectious
    CMV
    Viral (most common)
    Parvovirus B19
    Placental
    Twin–twin transfusion
    EXAM LOCK
    One-liner
    MCA-PSV >1.5 MoM = fetal anemia → IUT
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