Primary focus in congenital tuberculosis:

• Liver (primary complex in the liver with periportal lymphadenopathy, acquired via transumbilical route) or Lungs (acquired via aspiration of infected amniotic fluid).

Management plan as per IAP:

• Continue breastfeeding (safe if mother wears a surgical mask and practices hand hygiene; breast milk does not transmit TB).
• Administer BCG vaccine at birth.
• Perform Chest X-ray (CXR) and clinical evaluation of the neonate:
  • If asymptomatic with normal CXR: Give Isoniazid (INH) chemoprophylaxis ($10\text{ mg/kg/day}$) for 6 months (6 HR/INH prophylaxis), followed by Mantoux testing.
  • If symptomatic or abnormal CXR / suspected congenital TB: Perform gastric aspirate for CBNAAT (GeneXpert) and initiate full Anti-Tubercular Therapy (ATT): 2 months intensive phase ($2\text{ HRZ}\pm \text{E}$) + 4–7 months continuation phase ($4\text{–}7\text{ HR}$).

Smear finding & parasite form:

• Leishman-Donovan (LD) bodies — Amastigote form of Leishmania donovani (intracellular non-flagellated round-to-oval bodies with a nucleus and rod-shaped kinetoplast within reticuloendothelial macrophages).

Culture media:

• NNN medium (Novy-MacNeal-Nicolle medium) — shows flagellated promastigote forms.

Drugs used to treat resistant cases / Kala-azar:

• Liposomal Amphotericin B (Drug of choice)
• Miltefosine (Oral)
• Paromomycin (Aminosidine)
• Pentamidine isethionate
• Recombinant IFN-$\gamma$ as an adjunct
• Adjunct splenectomy in severe refractory hypersplenism

Direct evidences (demonstration of parasite):

• Microscopic visualization of LD bodies (amastigotes) in bone marrow, splenic, liver, or lymph node aspirates.
• Culture of promastigotes on Novy-MacNeal-Nicolle (NNN) medium.
• Leishmania DNA detection by Polymerase Chain Reaction (PCR).

Indirect evidences (serology / non-specific tests):

• rK39 antigen-based rapid immunochromatographic dipstick test / ELISA
• Aldehyde test of Napier (formol-gel test; positive after 3 months of illness due to hypergammaglobulinemia) and Chopra's antimony test
• Peripheral blood examination showing pancytopenia (anemia, leukopenia, thrombocytopenia) with reversal of A:G ratio.

Most probable diagnosis:

• Erythema infectiosum (Fifth disease / "Slapped cheek" syndrome)

Causative organism:

• Parvovirus B19 (Single-stranded DNA virus)

Two life-threatening situations:

• Transient Aplastic Crisis (TAC) in patients with underlying chronic hemolytic anemias (e.g., Sickle Cell Disease, Hereditary Spherocytosis, Thalassemia, Autoimmune Hemolytic Anemia).
• Non-immune Hydrops Fetalis / intrauterine fetal demise during maternal infection in pregnancy (due to severe fetal anemia and myocardial failure).
• Pure Red Cell Aplasia / chronic marrow failure in immunocompromised individuals (HIV, chemotherapy, SCID).

TB Contact & Treatment:

• Definition: Any child living in a household with an adult or family member who has active pulmonary TB or was treated with ATT in the past 2 years.
• Preventive Treatment (TPT): After ruling out active TB (normal CXR and no symptoms):
  • Isoniazid (INH) at $10\text{ mg/kg/day}$ daily for 6 months (6H), OR
  • 3 months of daily Isoniazid + Rifampicin (3HR), OR
  • 3 months of weekly Rifapentine + Isoniazid (3HP).

Treatment failure (RNTCP / NTEP definition):

• A tuberculosis patient whose biological specimen is smear- or culture-positive at the end of the intensive phase / at 12 weeks of treatment or at the end of treatment despite full adherence, or who becomes smear/culture-positive again during continuation phase.

Treatment for BCG adenitis:

• Non-suppurative BCG adenitis: Conservative management / reassurance; no active intervention or ATT is required as most resolve spontaneously within weeks to months.
• Suppurative BCG adenitis: Needle aspiration (avoids sinus formation); avoid surgical incision and drainage.

Malarial treatment failure / Drug resistance (WHO Classification):

• Early Treatment Failure (ETF):
  • Development of danger signs or severe malaria on Days 1, 2, or 3 with parasitemia;
  • Parasitemia on Day 2 higher than on Day 0, irrespective of temperature;
  • Parasitemia on Day 3 with axillary temp $\ge {37.5}^{\circ }\text{C}$;
  • Parasitemia on Day 3 $\ge 25\mathrm{\%}$ of Day 0 count.
• Late Clinical Failure (LCF):
  • Development of danger signs / severe malaria in presence of parasitemia on any day between Day 4 and Day 28 (or Day 42) in patients not meeting ETF criteria;
  • Parasitemia on any day between Day 4 and Day 28 (or Day 42) with axillary temp $\ge {37.5}^{\circ }\text{C}$ (or history of fever).
• Late Parasitological Failure (LPF):
  • Presence of parasitemia on any day between Day 7 and Day 28 (or Day 42) with axillary temp $<{37.5}^{\circ }\text{C}$ in patients not meeting ETF or LCF criteria.
• Adequate Clinical and Parasitological Response (ACPR):
  • Absence of parasitemia on Day 28 (or Day 42) without previously meeting criteria for ETF, LCF, or LPF.

Premunition:

• A state of acquired partial non-sterilizing immunity seen in individuals living in malaria-endemic areas. Low-level asymptomatic parasitemia persists, suppressing inflammatory cytokine storm and protecting against severe life-threatening disease and death upon subsequent reinfection.

Drugs used for chronic Hepatitis B:

• Nucleos(t)ide Analogues: Entecavir (ETV), Tenofovir Disoproxil Fumarate (TDF), Tenofovir Alafenamide (TAF), Lamivudine, Adefovir.
• Immunomodulators: Pegylated Interferon alfa-2a (PEG-IFN-$\alpha$) / Interferon alfa-2b.

Favorable predictors of treatment response:

• High baseline serum ALT/SGPT levels ($>2\text{–}5\times \text{ ULN}$)
• Low baseline serum HBV DNA levels ($<{10}^7\text{ IU/mL}$)
• Higher histological activity score on liver biopsy
• Older age / acquired later in childhood
• HBV Genotypes A and B (respond better to interferon than C and D)

Endpoints of therapy:

• Ideal/Definitive endpoint: Loss of HBsAg with or without development of anti-HBs seroconversion.
• Satisfactory intermediate endpoints:
  • Undetectable serum HBV DNA by sensitive PCR
  • In HBeAg-positive patients: Loss of HBeAg with seroconversion to anti-HBe
  • Normalization of serum ALT levels
  • Histological improvement (reduction of necroinflammation and fibrosis)

Management of acute HBV contact (unvaccinated/non-immune):

• Administer Hepatitis B Immune Globulin (HBIG) at $0.06\text{ mL/kg}$ IM immediately (ideally within 24 hours, maximum 7 days).
• Simultaneously initiate the complete Hepatitis B vaccine series ($10\mu \text{g}$ / pediatric dose IM) at 0, 1, and 6 months at a different anatomical site.

Hepatitis B prophylaxis in hemodialysis / immunocompromised patients:

• Administer double the standard dose ($40\mu \text{g}$ or high-dose formulation) on a 4-dose schedule at 0, 1, 2, and 6 months.
• No HBIG required unless acute parenteral exposure.
• Check annual anti-HBs titers; administer booster if anti-HBs falls $<10\text{ mIU/mL}$.

Criteria to define polio eradication:

• Zero cases of paralytic poliomyelitis caused by indigenous wild poliovirus for at least 3 consecutive years.
• Routine immunization coverage maintained at $\ge 80\mathrm{\%}$.
• High-quality, certified acute flaccid paralysis (AFP surveillance) system meeting WHO benchmarks (non-polio AFP rate $\ge 2$ per 100,000 children $<15$ years and adequate stool specimen collection $\ge 80\mathrm{\%}$).
• Poliovirus laboratory containment.

Incidence of VAPP after 1st dose:

• Approximately 1 case per 1.4 to 2.8 million first doses of OPV (highest risk with the first dose).

Effectiveness of IPV after 3 doses:

• Near 100% (99–100%) protective seroconversion against all three poliovirus serotypes (Types 1, 2, and 3).

Minimal age for IPV and rationale:

• 6 to 8 weeks of age (routinely given at 6 and 14 weeks as fractional IPV / fIPV or 6, 10, 14 weeks as full-dose IPV).
• Rationale: High levels of transplacentally acquired maternal anti-polio antibodies in the first few weeks can interfere with the infant's active immune response to injectable IPV; giving it after 6–8 weeks allows maternal antibodies to decline sufficiently.

WHO definition of a confirmed case of Japanese Encephalitis (JE):

• A suspected case of Acute Encephalitis Syndrome (AES) with laboratory confirmation by ANY of:
  • Presence of JE-specific IgM antibodies in CSF (or serum) by IgM capture ELISA;
  • A $\ge 4$-fold rise in JE-specific antibody titers in paired acute and convalescent sera;
  • Detection of JE virus genome in serum, CSF, or brain tissue by RT-PCR;
  • Isolation of JE virus from CSF, serum, or brain tissue.

Vector transmitting JE in India:

• Culex tritaeniorhynchus and Culex vishnui group mosquitoes (breed in irrigated rice paddies).

MRI findings:

• Bilateral symmetric hyperintensity on T2/FLAIR in the thalami (classic), basal ganglia, and midbrain substantia nigra ("Eye of the Tiger" / "Double Panda" sign in midbrain/pons).

Most probable diagnosis:

• Subacute Sclerosing Panencephalitis (SSPE) (slow virus encephalitis caused by mutant, defective Measles virus).

Clinical stages of Jabbour:

• Stage I (Behavioral & Cognitive): Subtle changes in personality, declining school performance, mood changes, irritability, lethargy.
• Stage II (Myoclonic stage): Stereotypic massive myoclonic jerks/spasms, drop attacks, choreoathetosis, visual deficits, dementia.
• Stage III (Extrapyramidal & Pyramidal stage): Rigidity, spasticity, decerebrate/decorticate posturing, autonomic instability, unresponsiveness.
• Stage IV (Terminal/Vegetative stage): Akinetic mutism, loss of cortical function, coma, flaccidity, autonomic failure, death.

Diagnostic modalities:

• CSF and Serum anti-measles IgG antibody titers: Markedly elevated (with oligoclonal bands and high CSF:serum ratio $>1:4$).
• Electroencephalography (EEG): Pathognomonic periodic, high-amplitude, slow-wave complexes (Radermecker complexes) occurring synchronously every 4–10 seconds against a suppressed background.
• Neuroimaging (MRI/CT): Progressive multifocal white matter T2/FLAIR hyperintensities, diffuse cortical atrophy, and ventricular dilatation.

Available treatment:

• No curative therapy; treatment is largely palliative and slows progression:
  • Oral Isoprinosine (Inosiplex) ($100\text{ mg/kg/day}$)
  • Intraventricular / Intrathecal Interferon-alpha (IFN-$\alpha$) via Ommaya reservoir
  • Antiepileptics (Valproate, Clonazepam) for myoclonus
  • Intrathecal/oral Ribavirin, IVIG, supportive nursing care.

Most probable diagnosis:

• Brain Abscess (Right cerebral hemisphere, causing left-sided focal seizures / left upper motor neuron facial palsy).

Expected etiological agents:

• Streptococcus viridans, Streptococcus milleri / anginosus group, Staphylococcus aureus, anaerobic streptococci, Bacteroides species (polymicrobial in cyanotic CHD due to right-to-left shunt bypassing pulmonary phagocytic filtration).

Diagnostic modalities:

• Contrast-Enhanced CT (CECT) Head / MRI Brain with DWI: Shows a ring-enhancing lesion with surrounding vasogenic edema and restricted central diffusion on DWI.
• Blood cultures.
• Lumbar puncture is CONTRAINDICATED due to high risk of uncal/transtentorial herniation.

Initial medical treatment:

• Empirical IV Antibiotics (for 4–6 weeks):
  • Third-generation Cephalosporin (Ceftriaxone / Cefotaxime) + Metronidazole + Vancomycin.
• Antiepileptics: IV Phenytoin or Levetiracetam for seizure control.
• Anti-edema measures: IV Mannitol / 3% Hypertonic Saline, Dexamethasone if severe mass effect with impending herniation.

Indications for surgical intervention (Burr hole aspiration / excision):

• Abscess diameter $>2.5\text{ cm}$
• Significant mass effect, midline shift, or impending herniation
• Threatened rupture into ventricles
• Gas-containing abscess or fungal etiology
• Failure to improve / expanding lesion after 2–3 weeks of targeted medical therapy
• Readily accessible superficial unilocular lesion.

Immediate Serological Testing:

• Immediately test maternal serum for Varicella-Zoster Virus (VZV) IgG antibodies.
• If results are available within 72–96 hours:
  • If VZV IgG positive: Mother is immune; reassure her, no further prophylaxis is needed.
  • If VZV IgG negative (non-immune) or results unavailable within 96 hours:
    • Administer Varicella-Zoster Immune Globulin (VZIG) at a dose of $125\text{ units per }10\text{ kg}$ IM (minimum 125 units, maximum 625 units) as soon as possible, ideally within 96 hours (acceptable up to 10 days post-exposure).

Oral Antiviral Therapy:

• If VZIG is not available or if the pregnant woman subsequently develops fever/rash: Initiate oral Acyclovir ($800\text{ mg}$ 5 times daily for 7 days) or IV Acyclovir ($10\text{–}15\text{ mg/kg}$ 8-hourly for varicella pneumonia/severe disease).
• Note: Live attenuated Varicella vaccine is strictly contraindicated during pregnancy.

Antiretroviral Therapy (ART) Regimen:

• Preferred First-line Regimen (WHO / NACO Guidelines):
  • ABC + 3TC + DTG (Abacavir + Lamivudine + Dolutegravir)
  • Alternative / Protease Inhibitor Regimen: AZT + 3TC + LPV/r (Zidovudine + Lamivudine + Lopinavir/ritonavir)
• Dosages:
  • Zidovudine (AZT): $180\text{–}240{\text{ mg/m}}^2/\text{dose}$ PO BID (or $9\text{–}12\text{ mg/kg/dose}$ BID)
  • Lamivudine (3TC): $4\text{ mg/kg/dose}$ PO BID
  • Abacavir (ABC): $8\text{ mg/kg/dose}$ PO BID
  • Dolutegravir (DTG): $15\text{–}25\text{ mg}$ PO once daily (weight-band based)
  • Lopinavir/ritonavir (LPV/r): $300/75{\text{ mg/m}}^2/\text{dose}$ PO BID
  • Also initiate Cotrimoxazole Preventive Therapy (CPT).

Laboratory tests to order:

• Prior to initiation (Baseline):
  • Complete Blood Count (Hb, TLC, DLC, Platelet count) — especially check for anemia/thrombocytopenia before ZDV
  • Baseline CD4 count / CD4 percentage and plasma HIV viral load
  • Renal function tests (BUN, Serum Creatinine, electrolytes)
  • Liver function tests (SGOT/AST, SGPT/ALT, Bilirubin)
  • Fasting lipid profile & blood glucose (for PI regimens)
  • Screening for active TB, Hepatitis B, and Hepatitis C
  • HLA-B*5701 testing (if initiating Abacavir)
• At 15–30 days post-initiation:
  • Repeat CBC (monitor for ZDV-induced bone marrow suppression/anemia)
  • Repeat LFT and RFT (monitor for drug-induced hepatotoxicity / nephrotoxicity)
  • Clinical assessment for drug adherence, adverse effects, and Immune Reconstitution Inflammatory Syndrome (IRIS).

Probable diagnosis:

• Meningococcemia (Fulminant Neisseria meningitidis sepsis / Purpura fulminans / Waterhouse-Friderichsen syndrome).

First step in management (Circulation):

• Aggressive fluid resuscitation: Establish rapid IV/IO access and infuse isotonic crystalloid boluses ($20\text{ mL/kg}$ over 10–15 minutes, repeated up to $40\text{–}60\text{ mL/kg}$) while monitoring for signs of fluid overload.

Class of antibiotics:

• Third-generation Cephalosporins: IV Ceftriaxone ($100\text{ mg/kg/day}$) or IV Cefotaxime.

Drug for dopamine-refractory shock:

• Norepinephrine (for warm shock/vasodilatory shock) or Epinephrine (for cold shock).
• IV Hydrocortisone (for suspected absolute/relative adrenal insufficiency in catecholamine-resistant septic shock / Waterhouse-Friderichsen syndrome).

Diagnosis:

• Neonatal Tetanus (Tetanus neonatorum / Clostridium tetani infection).

Treatment:

• Neutralization of toxin: Human Tetanus Immunoglobulin (HTIG) $500\text{–}3000\text{ IU}$ IM single dose (or Equine Tetanus Antitoxin $10,000\text{–}20,000\text{ IU}$).
• Eradicate vegetative bacteria: IV/oral Metronidazole ($30\text{ mg/kg/day}$ divided 6-hourly) for 10–14 days (preferred over penicillin).
• Control muscle spasms: IV Diazepam ($0.5\text{–}2.0\text{ mg/kg/dose}$), Midazolam infusion, Baclofen, and neuromuscular blockade with mechanical ventilation if refractory.
• Supportive care: Minimal handling in a dark, quiet environment, umbilical wound debridement, tube feeding / TPN, airway protection.
• Active immunization: Administer DTwP/Td vaccine at recovery (tetanus infection does NOT confer natural immunity).

Usual cause of death:

• Respiratory failure / Apnea secondary to severe laryngospasm, chest wall muscle rigidity, aspiration pneumonia, and autonomic nervous system dysfunction (cardiovascular collapse).

Clinical types of tetanus:

• 1. Generalized tetanus
• 2. Neonatal tetanus
• 3. Localized tetanus
• 4. Cephalic tetanus

Diagnosis:

• Varicella (Chickenpox) — classic "dewdrops on a rose petal" pleomorphic vesicular lesions.

Three complications:

• Secondary bacterial skin and soft tissue infection (Staphylococcus aureus, Group A Streptococcus)
• Acute cerebellar ataxia / Varicella encephalitis
• Varicella pneumonia
• Acute Disseminated Encephalomyelitis (ADEM) / Reye's syndrome
• Purpura fulminans / hemorrhagic varicella

Period of infectivity:

• From 1 to 2 days before the onset of rash until all lesions have crusted over (usually 5–7 days after the appearance of the rash).

Diagnosis:

• Scabies (Infestation characterized by intensely pruritic burrows, papules, and vesicles).

Causative organism:

• Sarcoptes scabiei var. hominis (Itch mite).

Topical treatment:

• 5% Permethrin dermal cream: Applied from neck to toe (including scalp, face, and neck in infants), left on for 8–14 hours, then washed off. Repeat after 7–14 days.
• Alternatives: 1% Gamma benzene hexachloride (Lindane - avoid in infants), 10% Crotamiton cream, 5–10% precipitated sulfur ointment in petrolatum (safe in neonates).

Oral treatment:

• Oral Ivermectin: $200\mu \text{g/kg}$ single dose with food; repeat dose after 1–2 weeks (indicated for crusted/Norwegian scabies, institutional outbreaks, or failure of topicals; approved for children $\ge 15\text{ kg}$).
• Note: All household members and close contacts must be treated simultaneously.

Post-Exposure Prophylaxis (PEP) Regimen:

• Recommended 3-drug regimen:
  • Tenofovir Disoproxil Fumarate (TDF) $300\text{ mg}$ + Lamivudine (3TC) $300\text{ mg}$ (or Emtricitabine $200\text{ mg}$) + Dolutegravir (DTG) $50\text{ mg}$ once daily.
  • Alternative: TDF + 3TC + Lopinavir/ritonavir ($400/100\text{ mg}$ BID) or Atazanavir/ritonavir.
  • Timing: Initiate as soon as possible, ideally within 2 hours (maximum within 72 hours).
  • Duration: Complete 28 days (4 weeks) of therapy.

HIV Testing Schedule:

• Baseline: At the time of exposure (to rule out pre-existing HIV infection)
• 6 weeks post-exposure
• 12 weeks (3 months) post-exposure
• 6 months post-exposure (especially if exposed to co-infected HCV patient).

Description of lesion:

• Eschar — a painless, round-to-oval ulcer with a central black necrotic crust surrounded by an erythematous indurated halo and regional lymphadenopathy (resembling a cigarette burn).

Diagnosis:

• Scrub Typhus (Tsutsugamushi disease).

Causative organism:

• Orientia tsutsugamushi (obligate intracellular bacterium).

Transmission vector:

• Bite of the larval stage (chigger) of trombiculid mites (Leptotrombidium deliense).

Three complications:

• Meningoencephalitis / acute cerebellitis
• Acute Respiratory Distress Syndrome (ARDS) / pneumonitis
• Acute Kidney Injury (AKI)
• Myocarditis / circulatory collapse / shock
• Disseminated Intravascular Coagulation (DIC)

Two available treatments:

• Doxycycline: $4.5\text{ mg/kg/day}$ PO divided BID (or $100\text{ mg}$ BID) for 7–10 days.
• Azithromycin: $10\text{ mg/kg/day}$ PO once daily for 5 days (drug of choice in young children and pregnant women).

Description of images:

• Image 1 (Throat): Exudative tonsillopharyngitis with marked tonsillar enlargement, pharyngeal erythema, palatal petechiae, and thick grayish-white pseudomembrane.
• Image 2 (Peripheral smear): Atypical reactive lymphocytes (Downey cells) — large pleomorphic lymphocytes with abundant basophilic cytoplasm scalloping around adjacent red blood cells.

Diagnosis:

• Infectious Mononucleosis ("Glandular fever" caused by Epstein-Barr Virus / EBV).

Three complications:

• Splenic rupture (spontaneous or traumatic)
• Upper airway obstruction due to massive tonsillar hypertrophy
• Autoimmune hemolytic anemia (AIHA) / severe thrombocytopenia
• Neurological complications: Guillain-Barré syndrome, meningoencephalitis, Bell's palsy
• Hepatitis / fulminant hepatic necrosis.

Contraindicated medication:

• Ampicillin / Amoxicillin (and aminopenicillins), which trigger a characteristic pruritic maculopapular rash in $>90\mathrm{\%}$ of patients.

Treatment:

• Supportive: Rest, hydration, antipyretics/analgesics.
• Strict avoidance of contact sports / strenuous exercise for at least 3–4 weeks to prevent splenic rupture.
• Systemic corticosteroids (Prednisolone): Indicated for impending airway obstruction, severe thrombocytopenia, or autoimmune hemolytic anemia.

Diagnosis:

• Meningococcal Infection / Meningococcemia (Neisseria meningitidis — Gram-negative diplococci with adjacent flat surfaces / bean-shaped).

Drug treatment and dose:

• IV Ceftriaxone: $100\text{ mg/kg/day}$ IV once daily (or in 2 divided doses, max $4\text{ g/day}$) for 7 days.
• Alternative: IV Cefotaxime ($200\text{ mg/kg/day}$ in 4 divided doses) or IV Crystalline Penicillin G ($250,000\text{–}400,000\text{ units/kg/day}$ divided 4-hourly).

Chemoprophylaxis for close contact (sister):

• Rifampicin: $10\text{ mg/kg/dose}$ (max $600\text{ mg}$) PO BID for 2 days (4 doses), OR
• Ceftriaxone: $125\text{ mg}$ IM single dose ($250\text{ mg}$ if $>12$ years), OR
• Ciprofloxacin: $500\text{ mg}$ PO single dose (in adults/older adolescents).

Protection / Prevention:

• Meningococcal Conjugate Vaccine (MenACWY / MenB): Quadrivalent conjugate vaccine containing serogroups A, C, W-135, and Y (and Serogroup B recombinant vaccine).

Identification of rash:

• Erythema Marginatum — an evanescent, non-pruritic, erythematous maculopapular rash with sharp, raised outer borders and central clearing (serpiginous / polycyclic appearance), commonly distributed on the trunk and proximal limbs, sparing the face.

Condition:

• Acute Rheumatic Fever (ARF) (one of the Major Jones criteria).

Child A (Image A):

• Diagnosis: Irritant Diaper Dermatitis (Contact / Ammoniacal diaper dermatitis).
• Characteristic features: Involves convex surfaces of the buttocks, lower abdomen, and perineum; characteristically spares the intertriginous skin folds/creases.
• Management: Frequent diaper changes, barrier creams containing Zinc Oxide / petroleum jelly, aeration.

Child B (Image B):

• Diagnosis: Candidal Diaper Dermatitis (Candida albicans infection).
• Characteristic features: Beefy-red confluent erythema with elevated margins, involvement of deep intertriginous skin folds/creases, and distinct pinpoint satellite papules and pustules.
• Management: Topical antifungal cream (Clotrimazole, Miconazole, or Nystatin) applied 2–3 times daily for 7–10 days.

Most likely diagnosis:

• Pneumocystis jirovecii Pneumonia (PJP / PCP) (opportunistic fungal infection in an immunocompromised host).

Chest X-ray findings:

• Bilateral diffuse perihilar symmetrical interstitial/alveolar ground-glass infiltrates with classic apical sparing.

Best diagnostic modality:

• Bronchoalveolar Lavage (BAL) with microscopic staining or PCR (Induced sputum is an alternative).

Stains for confirmation:

• Grocott-Gomori Methenamine Silver (GMS) stain (stains cyst walls black/brown)
• Toluidine Blue O stain
• Direct Fluorescent Monoclonal Antibody (DFA) stain
• Giemsa / Calcofluor white stain.

Diagnosis:

• Stevens-Johnson Syndrome (SJS) / Toxic Epidermal Necrolysis (TEN) overlap.

Description of lesions:

• Atypical targetoid maculopapular lesions with dusky purpuric centers, flaccid bullae, epidermal detachment, and extensive hemorrhagic crusting/erosions involving $\ge 2$ mucous membranes (vermilion border of lips, oral mucosa, conjunctivae, genital mucosa).

Causes:

• Infections (2): Mycoplasma pneumoniae, Herpes Simplex Virus (HSV), Cytomegalovirus.
• Drugs (2): Sulfonamides (Cotrimoxazole), Antiepileptics (Carbamazepine, Phenytoin, Lamotrigine, Phenobarbital), NSAIDs, Aminopenicillins.

Management plan:

• Immediate discontinuation of all potential offending/suspect drugs.
• Transfer to a burn intensive care unit or specialized pediatric ICU.
• Supportive care: Fluid and electrolyte maintenance, temperature regulation, nutritional support, meticulous non-adherent wound dressing.
• Ophthalmologic care: Lubricating eye drops, topical antibiotic/steroid drops, glass rodding / amniotic membrane transplantation to prevent symblepharon.
• Immunomodulatory therapy: IVIG ($1\text{–}2\text{ g/kg}$), pulse Methylprednisolone, or Cyclosporine.

Two complications:

• Ocular: Cicatricial symblepharon, trichiasis, corneal ulceration, blindness.
• Systemic: Sepsis, Acute Tubular Necrosis (ATN) / renal failure, respiratory tract sloughing/failure, esophageal/urethral strictures.

Diagnosis:

• Erythema Infectiosum (Fifth disease / Slapped cheek rash).

Causative organism:

• Parvovirus B19.

Hematological complication:

• Transient Aplastic Crisis (TAC) / Pure Red Cell Aplasia.

Orthopedic complication:

• Post-infectious symmetric polyarthropathy / polyarthritis (involves small joints of hands, wrists, knees, ankles).

Cause of intrauterine fetal demise:

• Non-immune Hydrops Fetalis (due to severe viral tropism for fetal erythroid progenitor cells leading to severe fetal anemia, high-output congestive heart failure, and hydrops).

Treatment for severe hematological complications:

• Intravenous Immunoglobulin (IVIG) ($400\text{ mg/kg/day}$ for 5 days or $1\text{ g/kg/day}$ for 2 days) and Packed Red Blood Cell (PRBC) transfusion.

Diagnosis:

• Erythema Nodosum (Septal panniculitis characterized by tender, non-ulcerative, erythematous subcutaneous nodules over the anterior tibial surfaces).

Common Triggers:

• Infections (2): Group A $\beta$-hemolytic Streptococcus (pharyngitis), Mycobacterium tuberculosis (Primary TB), Mycoplasma pneumoniae, Yersinia, Histoplasmosis.
• Drugs (2): Sulfonamides, Oral Contraceptives, Penicillins, Bromides/Iodides.

Non-infectious systemic disorders (2):

• Sarcoidosis (Löfgren's syndrome)
• Inflammatory Bowel Disease (Crohn's disease, Ulcerative Colitis)
• Behçet's disease
• Malignancies (Lymphomas/Leukemia).

Identification:

• Strongyloides stercoralis larva (Rhabditiform / Filariform larva with short buccal cavity and prominent genital primordium).

Route of entry:

• Transcutaneous penetration of intact skin by infective filariform larvae from contaminated soil (walking barefoot).

Two high-risk conditions:

• Immunosuppressive therapy (especially systemic corticosteroids)
• HTLV-1 infection
• Malnutrition / PEM
• Hematologic malignancies / Solid organ transplantation / HIV infection.

Hematological clue:

• Marked Peripheral Blood Eosinophilia.

Drug of choice:

• Oral Ivermectin: $200\mu \text{g/kg/day}$ for 1–2 days (repeated in 2 weeks; continued for $\ge 5\text{–}7\text{ days}$ in hyperinfection syndrome). Alternative: Albendazole.

Severe complication:

• Strongyloides Hyperinfection Syndrome / Disseminated Strongyloidiasis (with secondary Gram-negative bacterial sepsis, meningitis, and ARDS).

Most probable diagnosis:

• Kawasaki Disease (showing strawberry tongue, non-exudative bulbar conjunctival injection, and erythema of extremities).

Predictors of severity / Kobayashi & Harada Risk Criteria:

• Demographic: Male sex, age $<1\text{ year}$ or $>9\text{ years}$
• Clinical: Prolonged fever ($>10\text{ days}$), recurrence/recrudescence of fever after initial defervescence, presence of hepatomegaly or cardiomegaly
• Laboratory parameters:
  • Serum Albumin $\le 3.0\text{ g/dL}$ (hypoalbuminemia)
  • Serum Sodium $\le 133\text{ mEq/L}$ (hyponatremia)
  • Platelet count $<300,000/\mu \text{L}$ (early thrombocytopenia) or extreme thrombocytosis ($>1,000,000/\mu \text{L}$) later
  • C-Reactive Protein (CRP) $\ge 10\text{ mg/dL}$ or markedly elevated ESR
  • Peripheral blood absolute neutrophil count (ANC) $\ge 80\mathrm{\%}$ / high band count
  • Serum ALT/SGPT $\ge 80\text{ IU/L}$
  • Low hemoglobin for age.

PCR positive within 48 hours:

• Implies in utero (transplacental / antenatal) transmission; typically associated with higher viral load and more rapidly progressive disease.

PCR negative at 48 hours but positive at 7–90 days:

• Implies intrapartum (during delivery) or early postpartum (breastfeeding) transmission; associated with relatively slower disease progression.

p24 antigen testing:

• Can be detected by 4 to 6 weeks of age (not recommended before 1 month due to high false-negative rates and circulating maternal antibodies; HIV DNA PCR is the gold standard).

Labeling a newborn as HIV infected:

• Requires two positive virological tests (HIV DNA PCR, HIV RNA PCR, or viral culture) performed on separate blood samples.

HIV ELISA diagnostic age, sensitivity & specificity:

• Considered definitive after 18 months of age (when passively acquired maternal anti-HIV IgG antibodies have completely cleared).
• Sensitivity and specificity are both $>99\text{–}100\mathrm{\%}$.

Biomedical Waste Segregation:

• i. Blood agar media: Yellow bag (microbiology and biotechnological waste)
• ii. Used injection needle: White translucent puncture-proof container (Sharps)
• iii. Amikacin injection with expiry: Yellow bag / Cardboard box with blue marking (expired/discarded pharmaceutical waste)
• iv. Blood-soaked cotton swab: Yellow bag (soiled anatomical waste)
• v. IV set: Red bag (recyclable contaminated plastic tubing)
• vi. Incinerated ash: Black container / landfill (disposal in secure landfill)

Organism Identification & Treatment:

• Organism: Entamoeba histolytica (Trophozoite demonstrating single nucleus with central karyosome and ingested erythrocytes).
• Treatment:
  • Tissue amebicide: Metronidazole ($35\text{–}50\text{ mg/kg/day}$ in 3 divided doses for 7–10 days) or Tinidazole ($50\text{ mg/kg/day}$ once daily for 3 days).
  • Followed by a luminal amebicide: Diloxanide furoate ($20\text{ mg/kg/day}$ for 10 days) or Paromomycin ($30\text{ mg/kg/day}$ in 3 divided doses for 7 days) to eliminate luminal cyst carriage.

Diagnosis:

• Neonatal Varicella (Perinatal varicella infection acquired when mother develops varicella 5 days before to 2 days after delivery).

Complications across 4 organ systems:

• Hematological: Disseminated Intravascular Coagulation (DIC), purpura fulminans, severe thrombocytopenia.
• Central Nervous System (CNS): Varicella meningoencephalitis, acute cerebellar ataxia, transverse myelitis.
• Respiratory: Varicella pneumonitis / Acute Respiratory Distress Syndrome (ARDS).
• Hepatic: Acute hepatitis, fulminant hepatic failure / Reye's syndrome.
• Ophthalmic: Chorioretinitis, keratitis, optic neuritis.
• Dermatological: Secondary severe invasive bacterial infection (Staphylococcus, Group A Streptococcus) with toxic shock syndrome.

X-ray finding:

• Lateral soft tissue neck X-ray demonstrates marked widening and thickening of the retropharyngeal soft tissue prevertebral space ($>7\text{ mm}$ at C2, $>14\text{ mm}$ at C6, or width greater than the adjacent vertebral body diameter) with anterior displacement of the airway and loss of normal cervical lordosis.

Possible diagnosis:

• Retropharyngeal Abscess (RPA).

Treatment:

• Airway management: Maintain airway, keep patient in a position of comfort, avoid agitation, prepare for emergency intubation or tracheostomy if needed.
• Intravenous Antibiotics: High-dose IV broad-spectrum coverage:
  • Ampicillin-Sulbactam ($200\text{ mg/kg/day}$ 6-hourly) OR Ceftriaxone + Clindamycin / Metronidazole $\pm$ Vancomycin (for MRSA).
• Surgical drainage: Urgent transoral or external surgical incision and drainage if large abscess, airway compromise, lack of clinical improvement after 24–48 hours of IV antibiotics, or evidence of fluctuance/gas.

Otoscopic findings:

• Marked erythema (hyperemia) and vascular injection of the tympanic membrane
• Bulging / outward fullness of the tympanic membrane
• Loss of normal landmarks (loss of cone of light, obscured handle of malleus)
• Decreased or absent mobility of the tympanic membrane on pneumatic otoscopy.

Diagnosis:

• Acute Otitis Media (AOM).

Pathogenesis:

• Viral Upper Respiratory Infection (URI) $\to$ Eustachian tube inflammation, mucosal edema, and dysfunction $\to$ failure of middle ear clearance resulting in negative middle ear pressure $\to$ accumulation of middle ear effusion $\to$ secondary colonization and bacterial proliferation (Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis) $\to$ acute purulent middle ear inflammation.

Risk factors in children $\le 6$ years:

• Age-dependent anatomical factors (shorter, wider, and more horizontally oriented Eustachian tubes in infants/young children)
• Day care attendance and crowding
• Absence of exclusive breastfeeding / supine bottle propping
• Exposure to environmental tobacco smoke (second-hand smoke)
• Pacifier use
• Craniofacial anomalies (e.g., cleft palate, Down syndrome)
• Allergic rhinitis and recurrent viral URIs.

Possible diagnosis:

• Alagille Syndrome (Arteriohepatic Dysplasia / JAG1 mutation).

Differential diagnoses:

• Biliary Atresia
• Idiopathic Neonatal Hepatitis
• Congenital TORCH infections (CMV, Rubella)
• Progressive Familial Intrahepatic Cholestasis (PFIC)
• Alpha-1 Antitrypsin Deficiency
• Galactosemia / Inborn errors of bile acid metabolism.

Diagnostic tests:

• Liver Function Tests: Conjugated hyperbilirubinemia, elevated serum bile acids, marked elevation of serum GGT and alkaline phosphatase.
• Liver Biopsy: Demonstrates paucity of intrahepatic interlobular bile ducts (bile duct ductopenia).
• Echocardiography: Assess for Peripheral Pulmonary Artery Stenosis (PPS), Tetralogy of Fallot, or VSD.
• Ophthalmologic Examination (Slit-lamp): Evaluate for posterior embryotoxon (prominent Schwalbe's line).
• Spinal X-ray: Check for butterfly vertebrae (anterior sagittal clefting).
• Genetic testing: Sequence analysis for JAG1 (97% of cases) or NOTCH2 gene mutations.

Deficiencies & Prevention:

• Deficiencies: Severe deficiency of fat-soluble vitamins (Vitamins A, D, E, and K) and essential fatty acids due to chronic severe cholestasis and impaired micellar fat absorption.
• Prevention & Management:
  • High-dose daily oral supplementation of water-soluble / water-miscible forms of Vitamins A, D, E, and K.
  • High-calorie formula supplemented with Medium-Chain Triglycerides (MCT oil) (absorbed directly into portal circulation without requiring bile salts).
  • Ursodeoxycholic Acid (UDCA): $15\text{–}20\text{ mg/kg/day}$ to stimulate bile flow and treat pruritus.