Part 1 obgyn notes Sri Lanka
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    Microbiology
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    HSV

    HSV

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    1. HSV – Virology & Microbiology (What is this virus?)

    1.1 Basic classification

    • Family: Herpesviridae
    • Type: Enveloped, double-stranded DNA virus
    • Subfamily: Alphaherpesviridae (rapid replication, latency in sensory ganglia)
    • Serotypes:
      • HSV-1 – classically orolabial, but increasingly genital
      • HSV-2 – classically genital (most recurrent genital herpes in adults)

    Key memory:

    Herpes = enveloped dsDNA + lifelong latent in sensory ganglia

    1.1 Basic classification — Active Recall (Fill in the Blanks)

    1. Family: _____________
    2. Type: _____________, _____________-stranded _____________ virus
    3. Subfamily: _____________ (rapid replication, latency in _____________ _____________)

    Serotypes

    1. HSV-1 – classically _____________, but increasingly _____________
    2. HSV-2 – classically _____________ (most _____________ genital herpes in _____________)

    Key Memory Line

    1. Herpes = _____________ _____________ + lifelong _____________ in _____________ _____________

    1.2 Structure

    • Core: linear dsDNA genome
    • Capsid: icosahedral
    • Tegument: protein layer around capsid (contains viral proteins that help early replication)
    • Envelope: lipid bilayer derived from host, with multiple glycoproteins (gB, gC, gD, gH, etc.) → needed for binding & entry.

    Clinical relevance:

    • Envelope → sensitive to drying, detergents, disinfectants
    • Close contact required (sexual, perinatal, mucosal).

    1.2 Structure — Active Recall (Fill in the Blanks)

    • Core: linear __________ genome
    • Capsid: __________ symmetry
    • Tegument: __________ layer around capsid containing viral __________ that help __________ replication
    • Envelope: __________ bilayer derived from __________, with multiple __________ (gB, gC, gD, gH, etc.) required for __________ and __________

    Clinical Relevance — Active Recall

    • Presence of envelope → virus is __________ to __________, __________, and __________
    • Therefore, transmission requires __________ __________
    • Common modes: __________, __________, and __________ contact

    1.3 Replication cycle (why latency/recurrent?)

    1. Attachment to host cell
      • Viral glycoproteins bind to host receptors (e.g. heparan sulfate, nectin-1).
    2. Fusion & entry
      • Envelope fuses with cell membrane → capsid + tegument enter cytoplasm.
    3. Transport to nucleus
      • Capsid goes to nuclear pore → viral DNA enters nucleus.
    4. Gene expression (immediate-early → early → late genes)
      • Immediate-early: regulatory proteins
      • Early: DNA polymerase etc.
      • Late: structural proteins (capsid, glycoproteins)
    5. DNA replication – rolling circle mechanism.
    6. Assembly in nucleus → nucleocapsids.
    7. Envelopment via host membranes → virions released by exocytosis or cell lysis.

    Active Recall — Fill in the Blanks

    1. Attachment to host cell

    • Viral _____________ bind to host receptors such as _____________ _____________ and _____________-___________.

    2. Fusion & entry

    • Viral _____________ fuses with the _____________ _____________ → _____________ + _____________ enter the _____________.

    3. Transport to nucleus

    • _____________ travels to the _____________ _____________ → viral _____________ enters the _____________.

    4. Gene expression sequence

    • Occurs in the order: __ → _____________ → _____________ genes.

    Subtypes

    • Immediate-early genes code for _____________ _____________.
    • Early genes code for _____________ _____________ (e.g., _____________ _____________).
    • Late genes code for _____________ _____________ such as _____________ and _____________.

    5. DNA replication

    • Viral DNA replicates via the _____________ _____________ mechanism.

    6. Assembly

    • Assembly occurs in the _____________ forming _____________.

    7. Envelopment & release

    • Envelopment occurs via _____________ _____________ → virions released by _____________ or _____________ _____________.

    1.4 Latency & reactivation (very examworthy)

    • After primary infection, virus travels retrograde in sensory nerves to the sensory ganglia:
      • Genital HSV → sacral dorsal root ganglia (S2–S4)
      • Oral HSV → trigeminal ganglion
    • In latency:
      • Viral DNA persists as episome in nucleus
      • Only latency-associated transcripts (LATs) expressed – no full viral replication.
    • Reactivation triggers:
      • Stress, fever, sunlight, menstruation, immunosuppression, pregnancy.
    • Reactivation → virus travels anterograde down nerve → recurrent lesions on skin/mucosa.

    Key exam line:

    HSV establishes lifelong latency in sensory ganglia with periodic reactivation causing recurrent lesions.

    1.4 Latency & Reactivation — Active Recall (Fill in the Blanks)

    After Primary Infection

    1. After primary infection, HSV travels _____________ in _____________ nerves to the _____________ _____________.
    2. Genital HSV → _____________ _____________ _____________ _____________ (–)
    3. Oral HSV → _____________ _____________

    During Latency

    1. Viral DNA persists in the nucleus as an _____________.
    2. Only _____________ (_________) are expressed.
    3. During latency, there is no full viral _____________.

    Reactivation Triggers

    1. Common reactivation triggers include:

    Reactivation & Recurrence

    1. During reactivation, virus travels _____________ down the nerve.
    2. This results in _____________ _____________ on the _____________ or _____________.

    Key Exam Line (Fill in the Blanks)

    1. HSV establishes lifelong _____________ in _____________ _____________ with periodic _____________ causing _____________ _____________.

    1.5 Transmission (focus on pregnancy)

    • Sexual contact – genital-genital, oral-genital.
    • Vertical transmission:
      • Mostly intrapartum (during delivery) from contact with infected genital secretions.
      • Rarely in utero (transplacental) or postnatally (direct contact, kissing, breast lesions).

    Transmission risk is highest when:

    • Mother has primary HSV infection near term, especially if she is shedding virus and has no antibodies yet.

    1.5 Transmission (Focus on Pregnancy) — Active Recall

    Modes of Transmission

    1. Sexual contact includes:
      • –
      • –

    Vertical Transmission

    1. Vertical transmission occurs most commonly _____________ (during _____________).
    2. The main mechanism is contact with infected _____________ _____________.
    3. Vertical transmission may rarely occur:
      • _____________ (_____________)
      • _____________ (direct _____________, _____________, _____________ _____________)

    Highest Risk Scenario

    1. Transmission risk is highest when the mother has _____________ HSV infection _____________ _____________.
    2. Risk is especially high if she is _____________ _____________ and has _____________ _____________ yet.

    1.6 Immune response (why primary infection is dangerous)

    • Innate:
      • Interferons, NK cells.
    • Adaptive:
      • Humoral: neutralizing antibodies → reduce severity of subsequent infections.
      • Cell-mediated immunity is critical (CD8+ T cells).
    • In primary infection in pregnancy, mother is seronegative, no pre-existing antibodies → higher viraemia, higher risk to fetus/neonate.

    1.6 Immune Response (Why Primary Infection Is Dangerous)

    Active Recall — Fill in the Blanks

    Innate Immunity

    1. Key innate immune components include _____________ and _____________ .

    Adaptive Immunity

    1. Humoral immunity involves _____________ _____________ which reduce the _____________ of subsequent infections.
    2. Cell-mediated immunity is _____________ and is mediated mainly by _____________+ __cells.

    Primary Infection in Pregnancy

    1. In primary HSV infection during pregnancy, the mother is _____________.
    2. There are no pre-existing _____________.
    3. This leads to higher _____________ and increased risk to the _____________

    2. Clinical patterns of HSV relevant to pregnancy

    2.1 Primary genital HSV infection

    • First episode in seronegative woman (no prior HSV-1/2 antibodies).
    • Features:
      • Painful grouped vesicles → ulcers on vulva, vagina, cervix, perineum.
      • Marked pain, dysuria, tender inguinal lymphadenopathy, fever, malaise.
      • Lesions last longer (2–3 weeks) than recurrent episodes.
    • Obstetric importance:
      • If occurs in 1st trimester → small risk miscarriage / congenital HSV (rare).
      • If occurs in 3rd trimester, especially near delivery → high risk of neonatal HSV if vaginal birth.

    2.1 Primary Genital HSV Infection — Active Recall

    Definition

    1. Primary genital HSV infection is the first episode in a _____________ woman with no prior __________- / _____________.

    Clinical Features

    1. Painful _____________ _____________ progress to _____________ on the _____________, _____________, _____________, and _____________.
    2. Associated symptoms include:
      • Marked _____________
      • Tender _____________ _____________
    3. Lesions persist for __– _____________, which is _____________ than recurrent episodes.

    Obstetric Importance

    1. Infection in the _____________ trimester carries a small risk of _____________ or _____________ HSV (_____________).
    2. Infection in the _____________ trimester, especially _____________ _____________, carries a _____________ risk of _____________ HSV if _____________ birth occurs.

    2.2 Non-primary first episode

    • Genital infection with one HSV type in a woman already immune to the other type
    • (e.g. prior HSV-1 orolabial → now genital HSV-2).

    • Less severe than true primary, some cross-protection.

    2.2 Non-Primary First Episode — Active Recall

    1. A non-primary first episode is a _____________ infection with one _____________ type in a woman already _____________ to the _____________ type.
    2. Example: prior _____________ _____________ infection → current _____________ _____________ infection.
    3. Compared to a true primary infection, this episode is _____________ _____________.
    4. This is because there is partial between HSV types.

    2.3 Recurrent genital HSV

    • Reactivation from sacral ganglia.
    • Mild prodromal tingling, burning → fewer lesions, faster healing (5–7 days).
    • Systemic symptoms usually minimal.
    • In pregnancy: much lower risk of neonatal infection compared with primary, because maternal antibodies present.

    2.3 Recurrent Genital HSV — Active Recall

    1. Recurrent genital HSV results from _____________ from the _____________ _____________.
    2. Patients often experience mild _____________ symptoms such as _____________ and _____________ before lesions appear.
    3. Recurrent episodes are characterized by _____________ lesions and _____________ healing.
    4. Lesions typically heal within __– ____ _________.
    5. _____________ symptoms are usually _____________ .

    Pregnancy Relevance

    1. In pregnancy, recurrent genital HSV carries a _____________ _____________ of _____________ infection compared with primary infection.
    2. This reduced risk is because _____________ _____________ are _____________.

    2.4 HSV in the fetus/neonate (for viva/short notes)

    • In utero (congenital) – rare:
      • Microcephaly, chorioretinitis, skin scarring, IUGR, hydrocephalus.
    • Neonatal HSV – acquired around delivery:
      • Localized skin/eye/mouth disease.
      • CNS disease – encephalitis.
      • Disseminated disease – multi-organ failure, high mortality.

    Risk of neonatal HSV:

    • Primary maternal infection near delivery: up to ~30–50%
    • Recurrent infection with lesions at delivery: ~1–3%
    • Asymptomatic shedding: smaller but real risk.

    (Exact numbers vary by source, but concept = primary near term = highest risk.)

    2.4 HSV in the Fetus / Neonate — Active Recall

    In Utero (Congenital) Infection

    1. In-utero (congenital) HSV infection is _____________.
    2. Congenital HSV may present with:

    Neonatal HSV (Around Delivery)

    1. Neonatal HSV is usually acquired _____________ _____________.
    2. The three major clinical forms are:
      • _____________ _____________ / _____________ / _____________ disease
      • _____________ disease – _____________
      • _____________ disease – failure with _____________ mortality

    Risk of Neonatal HSV

    1. Risk with _____________ maternal infection _____________ _____________ is approximately _____________–___________%.
    2. Risk with _____________ infection and _____________ at delivery is approximately _____________–___________%.
    3. _____________ viral _____________ carries a _____________ but _____________ risk.

    3. Diagnosis (mother during pregnancy)

    • Clinical: characteristic painful vesicles/ulcers.
    • Lab tests:
      • PCR from lesion swab – most sensitive & specific (type-specific, HSV-1 vs HSV-2).
      • Viral culture (less used now).
      • Type-specific HSV serology (IgG) to distinguish primary vs recurrent:
        • Primary = no prior antibodies, new seroconversion.
    • In pregnancy, diagnosis often clinical + PCR if needed.

    Diagnosis (mother during pregnancy) – Active Recall

    Clinical

    • Diagnosis is often __________ based on __________ painful __________ / __________.

    Laboratory tests

    • Most sensitive and specific test: __________ from __________ swab
      • Can differentiate __________ vs __________.
    • Older method now less used: __________ __________.
    • To distinguish primary vs recurrent infection:
      • Type-specific HSV __________ (__________)
      • Primary infection = no prior __________, with new __________.

    In pregnancy

    • Diagnosis is usually __________ + __________ (if confirmation is needed).

    4. Antiviral drugs (Mechanism + names)

    • Acyclovir (and its prodrug valacyclovir): mainstay.
    • They are guanosine analogues:
      • Activated by viral thymidine kinase → acyclovir triphosphate.
      • Inhibits viral DNA polymerase → chain termination.
    • Safe and widely used in pregnancy and breastfeeding (especially acyclovir).

    4. Antiviral drugs (Mechanism + names) – Active Recall

    Main drugs

    • First-line drug for HSV: __________
    • Prodrug with better oral bioavailability: __________

    Drug class

    • These drugs are __________ analogues.

    Activation

    • Initial phosphorylation is done by __________ __________ __________.
    • Active form is __________ __________ .

    Mechanism of action

    • Inhibits __________ __________ __________.
    • Results in __________ __________ of viral DNA.

    Use in pregnancy

    • These drugs are considered __________ and used in __________ and __________.

    5. HSV in Pregnancy – Management Strategy

    Think in 3 big questions:

    1. Is this primary or recurrent genital herpes?
    2. What gestation? Early vs near term.
    3. At delivery, are there active lesions / prodromal symptoms?

    5.1 General principles

    • Do not terminate pregnancy solely for genital herpes.
    • Aim to:
      • Treat maternal symptoms.
      • Reduce viral shedding.
      • Prevent neonatal HSV – especially at delivery.

    5. HSV in Pregnancy – Management Strategy (Active Recall)

    Three key questions

    1. Is the infection __________ or __________ genital herpes?
    2. What is the __________ age? __________ vs __________ pregnancy.
    3. At delivery, are there __________ __________ or __________ __________?

    5.1 General principles

    • Pregnancy should __________ be __________ solely due to genital herpes.
    • Management aims to:
      • __________ maternal symptoms.
      • __________ viral shedding.
      • __________ __________ HSV, especially at __________.

    5.2 Management of primary genital HSV in pregnancy

    A. During pregnancy (not at labour)

    • Confirm clinically ± PCR.
    • Oral acyclovir:
      • Typical regimen: Acyclovir 400 mg TDS (three times daily) for 5–10 days
      • (Exact dose/duration can vary by guideline; know “acyclovir for 5–10 days”).

    • Analgesia, local care (saline baths, topical anesthetic gel).
    • Counsel:
      • Avoid sexual contact (especially oral-genital) during active lesions.
      • Use condoms thereafter (reduces but does not fully prevent transmission).

    If primary infection occurs in 1st or 2nd trimester:

    • Treat with acyclovir as above.
    • Reassure: congenital infection is rare.
    • Document HSV status in notes.
    • Plan suppressive therapy from 36 weeks onwards (see below).

    If primary infection occurs in 3rd trimester, especially within 6 weeks of delivery:

    • High risk of neonatal infection if vaginal birth.
    • Start oral acyclovir immediately.
    • Plan elective caesarean section at onset of labour / rupture of membranes IF active lesions or infection within last ~6 weeks.
    • Also start suppressive therapy from 36 weeks (see below) to reduce viral shedding and necessity for emergency CS.

    5.2 Management of primary genital HSV in pregnancy – Active Recall

    A. During pregnancy (not at labour)

    • Diagnosis is __________ ± __________.
    • First-line antiviral:
      • Oral __________
      • Typical regimen: __________ mg __________ (__________ times daily) for – days
    • Supportive care:
      • __________
      • __________ care (e.g. saline baths, topical __________ gel)

    Counselling

    • Avoid __________ contact during active lesions (especially –).
    • Use __________ thereafter:
      • Reduces transmission but does __________ fully __________ it.

    If primary infection occurs in 1st or 2nd trimester

    • Treat with __________ as above.
    • Reassure: congenital infection is __________.
    • __________ HSV status clearly in antenatal notes.
    • Plan __________ therapy from __________ weeks onwards.

    If primary infection occurs in 3rd trimester (especially within __________ weeks of delivery)

    • Risk of __________ HSV infection is __________ if vaginal delivery.
    • Start oral __________ __________.
    • Plan __________ caesarean section at:
      • Onset of __________ or
      • __________ of membranes
      • IF __________ lesions are present or infection occurred within last __________ weeks.
    • Also commence __________ therapy from __________ weeks to:
      • Reduce __________ shedding
      • Reduce need for __________ CS.

    5.3 Management of recurrent genital HSV in pregnancy

    • Recurrent episodes:
      • Treat with short course oral acyclovir (e.g. 400 mg TDS for 5 days).
    • Routine antenatal care continues.

    Suppressive therapy (very exam-high-yield)

    • For women with:
      • Frequent recurrences, OR
      • Primary infection earlier in pregnancy, OR
      • Known genital HSV to reduce lesions at delivery.

    From 36 weeks until delivery:

    • Acyclovir 400 mg orally TDS
    • (or Valacyclovir 500 mg BD where available).

    Benefits:

    • Reduces clinical recurrences.
    • Reduces asymptomatic shedding.
    • Reduces need for caesarean for HSV.

    5.3 Management of recurrent genital HSV in pregnancy – Active Recall

    Recurrent episodes

    • Managed with __________ course oral __________.
    • Example regimen: __________ mg __________ for __________ days.
    • __________ antenatal care continues.

    Suppressive therapy (exam-high-yield)

    Indications (any ONE):

    • __________ recurrences
    • __________ infection earlier in pregnancy
    • Known __________ HSV to reduce lesions at delivery

    Timing

    • Start from __________ weeks until __________.

    Drug & dose

    • __________ __________ mg orally __________
    • Alternative (where available): __________ __________ mg __________

    Benefits

    • Reduces __________ recurrences
    • Reduces __________ viral __________
    • Reduces need for __________ section for HSV

    5.4 Management at time of delivery

    A. Primary genital HSV near term or at labour

    • Active primary lesions or prodromes (pain, burning) at onset of labour:
      • Recommend caesarean section to reduce neonatal HSV.
      • Ideally done within 4–6 hours of membrane rupture for maximal benefit, but still beneficial later.
      • if > 6 hrs has passed give iv Acyclovir to baby for 10 days

    B. Recurrent genital HSV at labour

    • If recurrent lesions or prodrome present at onset of labour:
      • Many guidelines recommend caesarean section, especially if first episode or frequent recurrences.
    Recurrent lesions at labour → offer caesarean section to reduce neonatal risk.
    • If no active lesions and no prodromes at delivery:
      • Vaginal delivery is safe, even if maternal history of HSV.
      • Suppressive acyclovir from 36 weeks helps.

    C. Spontaneous rupture of membranes (SROM)

    • Primary HSV with active lesions + SROM:
      • Proceed to caesarean section as soon as possible; risk increases with duration of ruptured membranes.
    • Recurrent HSV with lesions + SROM:
      • Usually still offer CS, but risk somewhat lower.

    5.4 Management at time of delivery – Active Recall

    A. Primary genital HSV near term or at labour

    • If __________ primary __________ or __________ (__________, __________) are present at __________ of __________:
      • __________ caesarean section to reduce __________ HSV.
    • Optimal timing:
      • Ideally within – hours of __________ rupture.
      • Still __________ even if done later.

    B. Recurrent genital HSV at labour

    • If __________ lesions or __________ present at __________ of __________:
      • Most guidelines recommend __________ __________, especially if:
        • __________ episode, or
        • __________ recurrences.
    • Exam-standard rule:
      • Recurrent lesions at labour → __________ __________ to reduce __________ risk.
    • If __________ active lesions AND __________ prodromes at delivery:
      • __________ delivery is __________.
      • Applies even with __________ history of HSV.
      • __________ acyclovir from __________ weeks reduces risk.

    C. Spontaneous rupture of membranes (SROM)

    • __________ HSV with __________ lesions + __________:
      • Proceed to __________ section as __________ as possible.
      • Neonatal risk __________ with __________ of ruptured membranes.
    • __________ HSV with __________ lesions + __________:
      • Usually still __________ CS.
      • Risk is __________ than with primary infection.

    5.5 Postnatal management & breastfeeding

    • Breastfeeding:
      • HSV is not transmitted via breast milk.
      • Breastfeeding is allowed if:
        • No herpetic lesions on the breast.
        • Mother practices hand hygiene.
      • If lesions on breast → avoid feeding from that side until fully healed.
    • Contact precautions:
      • No kissing baby if orolabial lesions present.
      • Handwashing after touching lesions.
      • 5.5 Postnatal management & breastfeeding – Active Recall (Blanks)

        Breastfeeding:

      • HSV is not transmitted via __________ __________.
      • Breastfeeding is __________ if:
        • No __________ __________ on the __________.
        • Mother practices __________ __________.
      • If __________ on the breast → avoid feeding from that __________ until fully __________.
      • Contact precautions:

      • No __________ baby if __________ lesions are present.
      • __________ after touching __________.

    6. Neonatal HSV – what to mention in an answer

    If baby is born to mother with active genital HSV at delivery (especially primary):

    • Assess neonate:
      • Examine for lesions.
      • Swabs (mouth, nasopharynx, conjunctiva, rectum) for HSV PCR.
      • Blood tests, ± CSF if symptomatic.
    • Empirical IV acyclovir if:
      • Maternal primary HSV near delivery or
      • Neonate symptomatic (lethargy, fever, seizures, respiratory distress, vesicles).

    Typical neonatal regimen (conceptual, do not need exact doses in OBGYN exam):

    • IV acyclovir for 14–21 days depending on disease type (local vs CNS vs disseminated).

    Neonatal HSV – Active Recall (Fill in the Blanks)

    If baby is born to mother with active __________ HSV at delivery (especially __________):

    Assess neonate:

    • Examine for __________.
    • Swabs (__________, __________, __________, __________) for HSV __________.
    • __________ tests, ± __________ if __________.

    Empirical IV __________ if:

    • Maternal __________ HSV near delivery or
    • Neonate __________ (__________, __________, __________, __________, __________).

    Typical neonatal regimen

    (conceptual – exact doses not required in OBGYN exam):

    • IV __________ for – days depending on disease type (__________ vs __________ vs __________).

    7. HSV & pregnancy counselling points (for OSCE / viva)

    • Explain:
      • HSV is common; many adults infected.
      • Once infected, virus stays in body and can recur.
      • In pregnancy:
        • High risk if first infection in late pregnancy.
        • Lower risk with recurrent HSV because woman has antibodies.
      • We use antiviral tablets (acyclovir) to:
        • Make symptoms better.
        • Reduce chances of passing virus to baby.
      • We may recommend caesarean if infection is new or there are lesions at birth.
      • Baby will be monitored, and if high risk, may need IV acyclovir.

    8. “20% that gives 80% marks” – Exam-style condensation

    If you’re short on time, this is what you MUST remember:

    1. Virus & latency
      • HSV-1, HSV-2; enveloped dsDNA; Herpesviridae.
      • Establishes lifelong latency in sensory ganglia with periodic reactivation.
    2. Transmission & pregnancy risk
      • Transmission by sexual contact and perinatally during vaginal delivery.
      • Highest risk of neonatal infection when primary maternal genital HSV occurs near term (mother seronegative, high shedding).
    3. Primary vs recurrent
      • Primary: severe, systemic symptoms, longer duration, no antibodies, high neonatal risk if close to delivery.
      • Recurrent: milder, shorter, antibodies reduce fetal/neonatal risk.
    4. Antiviral of choice
      • Acyclovir – safe in pregnancy & breastfeeding.
      • Treatment: e.g. 400 mg TDS for 5–10 days for acute episodes.
      • Suppressive therapy from 36 weeks: acyclovir 400 mg TDS until delivery to reduce recurrences and viral shedding.
    5. Mode of delivery
      • Primary HSV with active lesions or first-episode near term → caesarean section recommended to prevent neonatal HSV (especially if lesions or prodrome at labour).
      • Recurrent HSV with no lesions / prodrome at labour → vaginal delivery is acceptable (especially if on suppressive therapy).
      • Recurrent HSV with active lesions or prodrome at labour → usually offer caesarean.
    6. Neonate
      • Risk: skin/eye/mouth disease, CNS disease, or disseminated infection.
      • If high risk → investigate and give IV acyclovir early.

    Herpetic whitlow = lesions on fingers from autoinnoculations

    Eczema herpeticum = localized (on the eczema), Monomorphic lesions, pain full

    TZANCK CELLS = inclusion bodies = Cowdry

    complications

    Erythema multiforme

    steven Johnson syndrome

    Sacral radiculopathy

    Perfect — I’ll condense everything you listed into exam-safe, zero-omission master tables, arranged so you can revise fast, answer vivas, and convert to XMind easily.

    No fluff, no missing links.

    🦠 HSV — COMPLETE HIGH-YIELD TABLE SET (Zero Omission)

    TABLE 1 — HSV VIROLOGY & STRUCTURE (FOUNDATION TABLE)

    Aspect
    Details
    Virus family
    Herpesviridae
    Subfamily
    Alphaherpesvirinae
    Genome
    Double-stranded DNA (linear)
    Envelope
    Present (lipid bilayer from host)
    Capsid
    Icosahedral
    Tegument
    Protein layer between capsid & envelope
    Glycoproteins
    gB, gC, gD, gH (attachment & fusion)
    Replication speed
    Rapid
    Site of replication
    Nucleus
    DNA replication
    Rolling circle mechanism
    Latency site
    Sensory ganglia
    Environmental stability
    Fragile (envelope sensitive)

    📌 Exam hook: Enveloped dsDNA virus → nuclear replication → lifelong latency

    TABLE 2 — HSV-1 vs HSV-2 (SEROTYPE COMPARISON)

    Feature
    HSV-1
    HSV-2
    Classical site
    Orolabial
    Genital
    Current trend
    Increasing genital infections
    Still main cause of recurrent genital HSV
    Latency ganglion
    Trigeminal
    Sacral (S2–S4)
    Neonatal HSV risk
    Possible
    Higher
    Recurrence frequency
    Less frequent genital recurrence
    More frequent recurrence

    TABLE 3 — HSV REPLICATION CYCLE (STEPWISE EXAM TABLE)

    Step
    Key Events
    Attachment
    Glycoproteins bind heparan sulfate, nectin-1
    Entry
    Envelope fuses with cell membrane
    Transport
    Capsid → nuclear pore
    Gene expression
    Immediate-early → Early → Late
    Early genes
    DNA polymerase, thymidine kinase
    Late genes
    Capsid proteins, envelope glycoproteins
    DNA replication
    Rolling circle
    Assembly
    Nucleus
    Release
    Exocytosis or cell lysis

    TABLE 4 — LATENCY & REACTIVATION (VERY EXAM-WORTHY)

    Aspect
    Details
    Nerve transport to ganglion
    Retrograde axonal transport
    Genital HSV latency site
    Sacral dorsal root ganglia (S2–S4)
    Oral HSV latency site
    Trigeminal ganglion
    Latent genome form
    Episome
    Genes expressed
    Latency-associated transcripts (LATs)
    Full replication in latency
    Absent
    Reactivation transport
    Anterograde
    Reactivation triggers
    Stress, fever, sunlight, menstruation, pregnancy, immunosuppression

    📌 Key line: HSV establishes lifelong latency with periodic reactivation.

    TABLE 5 — TRANSMISSION (WITH PREGNANCY FOCUS)

    Mode
    Details
    Sexual
    Genital–genital, oral–genital
    Vertical (main)
    Intrapartum during delivery
    Mechanism
    Contact with infected genital secretions
    In utero
    Rare (transplacental)
    Postnatal
    Kissing, skin contact, breast lesions
    Highest neonatal risk
    Primary maternal infection near term
    Why high risk
    No maternal antibodies + high viral shedding

    TABLE 6 — IMMUNE RESPONSE & PREGNANCY RISK

    Component
    Role
    Innate immunity
    Interferons, NK cells
    Humoral immunity
    Neutralizing antibodies
    Cell-mediated immunity
    CD8⁺ T cells (CRITICAL)
    Primary infection in pregnancy
    Mother seronegative
    Consequence
    Higher viraemia
    Neonatal risk
    High

    TABLE 7 — CLINICAL TYPES OF GENITAL HSV (PREGNANCY-RELEVANT)

    Type
    Features
    Neonatal Risk
    Primary
    Severe, systemic, long duration
    Highest
    Non-primary first episode
    Partial immunity, milder
    Moderate
    Recurrent
    Mild, short, prodrome
    Low

    TABLE 8 — PRIMARY GENITAL HSV (DETAIL TABLE)

    Aspect
    Details
    Immune status
    Seronegative
    Lesions
    Painful vesicles → ulcers
    Sites
    Vulva, vagina, cervix, perineum
    Systemic features
    Fever, malaise, dysuria, lymphadenopathy
    Duration
    2–3 weeks
    1st trimester risk
    Rare miscarriage / congenital HSV
    Near term risk
    High neonatal HSV risk

    TABLE 9 — RECURRENT GENITAL HSV

    Feature
    Details
    Source
    Reactivation from sacral ganglia
    Prodrome
    Tingling, burning
    Lesions
    Fewer
    Healing time
    5–7 days
    Systemic symptoms
    Minimal
    Pregnancy risk
    Low (antibodies present)

    TABLE 10 — FETAL & NEONATAL HSV

    Type
    Key Features
    Congenital (in utero)
    Rare
    Congenital features
    Microcephaly, hydrocephalus, chorioretinitis, skin scarring, IUGR
    Neonatal (around delivery)
    Most common
    Neonatal forms
    SEM / CNS / Disseminated
    Disseminated disease
    Multi-organ failure, high mortality

    TABLE 11 — NEONATAL HSV RISK (NUMBERS TABLE)

    Scenario
    Risk
    Primary maternal HSV near delivery
    30–50%
    Recurrent HSV with lesions
    1–3%
    Asymptomatic shedding
    Low but real

    📌 Exam logic: Primary near term = worst.

    TABLE 12 — DIAGNOSIS IN PREGNANCY

    Method
    Role
    Clinical
    Painful vesicles / ulcers
    PCR from lesion
    Gold standard
    Viral culture
    Older method
    HSV IgG serology
    Primary vs recurrent
    Pregnancy approach
    Clinical ± PCR

    TABLE 13 — ANTIVIRAL DRUGS (MECHANISM TABLE)

    Aspect
    Details
    Drug of choice
    Acyclovir
    Prodrug
    Valacyclovir
    Drug class
    Guanosine analogue
    Activation
    Viral thymidine kinase
    Active form
    Acyclovir triphosphate
    Action
    Inhibits viral DNA polymerase
    Effect
    Chain termination
    Pregnancy safety
    Safe
    Breastfeeding
    Safe

    TABLE 14 — MANAGEMENT IN PREGNANCY (BIG PICTURE)

    Question
    Why
    Primary or recurrent?
    Determines neonatal risk
    Gestation age
    Near term = high risk
    Lesions at delivery?
    Determines mode of delivery

    TABLE 15 — PRIMARY HSV MANAGEMENT IN PREGNANCY

    Scenario
    Management
    Any trimester
    Oral acyclovir 400 mg TDS 5–10 days
    1st / 2nd trimester
    Treat + reassure
    3rd trimester / <6 weeks to delivery
    High risk
    Near term
    Elective CS if lesions or recent infection
    ≥36 weeks
    Start suppressive therapy

    TABLE 16 — SUPPRESSIVE THERAPY (VERY HIGH-YIELD)

    Aspect
    Details
    Start
    36 weeks
    Drug
    Acyclovir
    Dose
    400 mg TDS
    Alternative
    Valacyclovir 500 mg BD
    Benefits
    ↓ recurrences, ↓ shedding, ↓ CS

    TABLE 17 — DELIVERY DECISIONS

    Situation
    Mode of Delivery
    Primary HSV + lesions/prodrome
    Caesarean
    Recurrent HSV + lesions
    Usually CS
    No lesions or prodrome
    Vaginal delivery OK
    SROM + primary HSV
    Urgent CS
    SROM + recurrent HSV
    CS usually offered

    TABLE 18 — POSTNATAL & BREASTFEEDING

    Aspect
    Guidance
    Breast milk
    Virus not transmitted
    Breastfeeding
    Allowed if no breast lesions
    Breast lesions
    Avoid that side
    Kissing
    Avoid if orolabial lesions
    Hygiene
    Strict handwashing

    TABLE 19 — NEONATAL MANAGEMENT

    Step
    Action
    Assessment
    Look for lesions
    Swabs
    Mouth, NP, eye, rectum
    Tests
    Blood ± CSF
    Empirical treatment
    IV acyclovir
    Duration
    14–21 days

    TABLE 20 — SPECIAL HSV ENTITIES & COMPLICATIONS

    Condition
    Key Features
    Herpetic whitlow
    Finger lesions, autoinoculation
    Eczema herpeticum
    Painful monomorphic lesions on eczema
    Tzanck cells
    Multinucleated giant cells
    Cowdry type A inclusions
    Intranuclear inclusions
    Erythema multiforme
    Immune-mediated
    Stevens–Johnson syndrome
    Severe mucocutaneous reaction
    Sacral radiculopathy
    Urinary retention, neural pain

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