Pediatrics
Final Professional MBBS — Pediatrics. Complete question bank: Long Questions (10 marks) and Short Notes (5 marks) across all 15 systems, with clinical pearls, drug doses, staging tables, mnemonics and key-point recaps.
DEFINITION
Tuberculosis (TB) is a chronic granulomatous infectious disease caused by Mycobacterium tuberculosis. Children usually develop primary, paucibacillary disease acquired from an infectious adult (the index case) with sputum-positive pulmonary TB.
PATHOGENESIS
- Inhaled bacilli form a subpleural Ghon focus; with the draining lymphangitis and regional (hilar) lymph node this is the primary (Ghon) complex.
- Most primary infections are contained (latent TB); progression gives primary disease, and reactivation later gives post-primary TB.
- Haematogenous spread → miliary TB and TB meningitis (especially in young/immunocompromised children).
TYPES
- Pulmonary TB — commonest (hilar lymphadenopathy, consolidation, effusion).
- Extrapulmonary — lymph node (commonest EP), TB meningitis, miliary, abdominal, spinal (Pott's), pleural, osteoarticular.
CLINICAL FEATURES
- Persistent fever and/or cough > 2 weeks, weight loss / failure to thrive / no weight gain, and fatigue.
- A history of contact with an adult TB case is a very important clue.
- Site-specific — matted cervical lymphadenopathy, meningitis, gibbus (spinal), abdominal distension/ascites.
DIAGNOSTIC APPROACH
- History of contact + suggestive symptoms.
- Tuberculin skin test (Mantoux) — ≥ 10 mm positive (≥ 5 mm if HIV/severely malnourished).
- Chest X-ray — hilar/mediastinal lymphadenopathy, consolidation, miliary mottling.
- Microbiology — sputum or gastric aspirate for AFB; CBNAAT/GeneXpert (rapid; also detects rifampicin resistance); culture (gold standard).
- IGRA where available; site-specific samples (CSF, lymph-node FNAC, pleural fluid).
MANAGEMENT — ATT (daily regimen, weight-band dosing)
- Intensive phase — 2 months of HRZE (isoniazid, rifampicin, pyrazinamide, ethambutol).
- Continuation phase — 4 months of HRE (total 6 months for drug-sensitive TB).
- TB meningitis / miliary / osteoarticular — prolonged therapy (about 12 months) and corticosteroids for TBM.
- Directly observed treatment, nutritional support, and monitoring for adherence, response and drug toxicity.
LATENT TB vs ACTIVE TB DISEASE
Feature Latent TB infection Active TB disease Symptoms None Present (fever, cough, weight loss) Mantoux Positive Positive Chest X-ray Normal Abnormal Infectious No Possible Treatment INH preventive therapy Full ATT MONITORING ON TREATMENT
- Clinical response — resolution of fever, weight gain, improved appetite (usually within weeks).
- Watch for drug toxicity — hepatotoxicity (H, R, Z), optic neuritis (ethambutol), and ensure adherence.
- Follow-up radiology/microbiology as indicated; document treatment outcome.
TB & HIV
HIV co-infection increases the risk of active TB, extrapulmonary and disseminated disease, and atypical presentations; all children with TB should be offered HIV testing, and ART is combined with ATT (with attention to drug interactions).
BCG VACCINE
- Live attenuated vaccine given at birth; protects mainly against severe childhood forms (miliary TB and TB meningitis).
- Does not reliably prevent primary pulmonary infection; a normal scar indicates prior vaccination.
💊KEY DRUG DOSES (viva)- Isoniazid (H) 10 mg/kg (7–15); Rifampicin (R) 15 mg/kg (10–20).
- Pyrazinamide (Z) 35 mg/kg (30–40); Ethambutol (E) 20 mg/kg (15–25).
- Prednisolone 2 mg/kg/day (TBM/pericardial) × 4 weeks, then taper.
- INH chemoprophylaxis 10 mg/kg/day × 6 months (contacts < 5 yr; HIV+).
PREVENTION
- BCG vaccination at birth (protects against severe forms — miliary TB and TBM).
- Contact screening and chemoprophylaxis (INH) for under-5 and HIV-positive contacts.
- Prompt treatment of infectious adults; infection control; addressing malnutrition.
⚠️DANGER / REMEMBER: Multidrug-resistant TB (MDR-TB) — resistance to at least isoniazid and rifampicin — is suspected in treatment failure/contact of an MDR case, and needs specialised second-line regimens (guided by drug-susceptibility testing).📝CLINICAL / APPLIED POINTS- Always ask for and evaluate the adult source (index) case — child TB means recent transmission.
- A positive Mantoux indicates infection, not necessarily active disease; interpret with clinical/radiological features.
- Use CBNAAT/GeneXpert early — it is rapid and flags rifampicin resistance.
- BCG protects against the dangerous forms (miliary TB, TBM), not against primary infection.
- Under-5 and HIV-positive contacts need INH preventive therapy after excluding active disease.
🔑KEY POINTS TO REMEMBER- Primary paucibacillary disease from an adult index case; Ghon (primary) complex.
- Fever/cough > 2 weeks + weight loss + contact history; pulmonary commonest; TBM/miliary dangerous.
- Mantoux ≥ 10 mm, CXR, gastric aspirate/CBNAAT (Xpert = rifampicin resistance), culture.
- ATT: 2 months HRZE + 4 months HRE (12 months + steroids for TBM).
- Prevent with BCG, contact screening and INH prophylaxis (< 5 yr, HIV).
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics; NTEP (RNTCP) paediatric TB guidelines.DEFINITION
Enteric fever is a systemic infection caused by Salmonella enterica serotype Typhi (and Paratyphi A/B). It is transmitted by the faeco-oral route through contaminated food and water, and is common where sanitation is poor.
PATHOGENESIS
Ingestion of the organism → Invasion via Peyer's patches of the ileum → Spread to mesenteric lymph nodes → bacteraemia → Seeding of the reticulo-endothelial system (liver, spleen, marrow) → Secondary bacteraemia → clinical illness
CLINICAL FEATURES (by week)
- Week 1 — stepladder (rising) fever, headache, malaise, relative bradycardia (Faget sign), coated tongue, constipation or diarrhoea.
- Week 2 — sustained high fever, rose spots (blanching pink macules on the trunk), hepatosplenomegaly, abdominal distension, toxaemia.
- Week 3 — complications (intestinal perforation/haemorrhage from Peyer's-patch ulceration), 'typhoid state' (apathy, delirium).
INVESTIGATIONS
- Blood culture — the gold standard (highest yield in the first week).
- Widal test — rising O and H agglutinin titres (positive from week 2; has limitations/false results).
- Bone-marrow culture — the most sensitive (unaffected by prior antibiotics); stool/urine culture positive later.
- Typhidot (IgM); CBC — leucopenia with aneosinophilia.
MANAGEMENT
- Antibiotics — ceftriaxone is the usual drug of choice for hospitalised/severe cases; cefixime or azithromycin for uncomplicated outpatient treatment (fluoroquinolone resistance is now common).
- Supportive care — hydration, antipyretics, and adequate nutrition (soft diet).
- Dexamethasone for severe disease with shock, delirium or encephalopathy.
- Monitor for and manage complications (surgery for perforation).
DIFFERENTIAL DIAGNOSIS OF PROLONGED FEVER
- Malaria, tuberculosis, urinary tract infection, and other bacteraemias.
- Viral infections (dengue), abscess, and (less commonly) malignancy/connective-tissue disease.
THE CHRONIC CARRIER STATE
A small proportion continue to excrete the organism for > 1 year (usually from chronic gallbladder carriage, sometimes with gallstones). Carriers are an important source of transmission and may need prolonged antibiotics or cholecystectomy.
PARATYPHOID FEVER
Salmonella Paratyphi A/B causes a clinically similar but generally milder illness ('paratyphoid'); together with typhoid it constitutes 'enteric fever'.
EPIDEMIOLOGY
- Endemic where sanitation and safe water are lacking; humans are the only reservoir.
- Spread by the faeco-oral route via contaminated food/water and by carriers handling food.
CLINICAL COURSE & MONITORING
- Defervescence usually occurs within 3–5 days of effective antibiotics; slow response suggests resistance or complication.
- Monitor for the third-week complications (perforation, haemorrhage) and for relapse after apparent recovery.
PATHOLOGY (why the third week is dangerous)
The organism proliferates in the Peyer's patches of the terminal ileum, which undergo hyperplasia, necrosis and ulceration; these ulcers can perforate or bleed in the third week — the classic surgical emergencies of typhoid.
KEY EXAM POINT
A toxic, febrile child with relative bradycardia and hepatosplenomegaly, then a sudden temperature drop with abdominal rigidity, suggests perforation — a surgical emergency needing resuscitation and operation.
ANTIMICROBIAL RESISTANCE
- Multidrug-resistant (MDR) typhoid (to older first-line drugs) and widespread fluoroquinolone resistance now guide empirical therapy toward ceftriaxone/azithromycin.
- Culture with sensitivity testing directs definitive treatment; de-escalate once results are available.
DIETARY & SUPPORTIVE CARE
- Maintain hydration and a soft, easily digestible, high-calorie diet during the febrile illness.
- Antipyretics for comfort; monitor closely for abdominal signs heralding perforation/bleeding.
💊KEY DRUG DOSES (viva)- Ceftriaxone 75 mg/kg/day IV (once daily) × 10–14 days.
- Cefixime 15–20 mg/kg/day oral × 10–14 days.
- Azithromycin 10–20 mg/kg/day × 7 days.
- Dexamethasone 3 mg/kg then 1 mg/kg 6-hourly (severe/encephalopathy).
COMPLICATIONS
- Intestinal perforation and haemorrhage (3rd week — the most feared).
- Myocarditis, hepatitis, encephalopathy, nephritis.
- Relapse and a chronic carrier state (persistent gallbladder carriage).
PREVENTION
- Typhoid conjugate vaccine (TCV).
- Safe drinking water, sanitation, hand hygiene and food safety; identification and treatment of carriers.
📝CLINICAL / APPLIED POINTS- Suspect enteric fever in any child with prolonged fever and a toxic look in an endemic setting.
- Send a blood culture before antibiotics — it is the gold standard, best in week 1.
- A single Widal is unreliable; a rising titre or a positive culture is more meaningful.
- Watch the third week for perforation/haemorrhage — a sudden fall in temperature with abdominal signs is a red flag.
- Treat carriers and vaccinate (TCV) to interrupt transmission.
🔑KEY POINTS TO REMEMBER- Systemic Salmonella Typhi infection; faeco-oral; invades Peyer's patches → bacteraemia.
- Stepladder fever, relative bradycardia, rose spots, hepatosplenomegaly; perforation in week 3.
- Blood culture (gold standard, week 1); marrow culture most sensitive; Widal from week 2.
- Ceftriaxone (severe) / cefixime or azithromycin (uncomplicated); steroids for severe.
- Complications: perforation/haemorrhage, relapse, carrier state; prevent with TCV + sanitation.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Malaria is a protozoal infection caused by Plasmodium species (P. falciparum, P. vivax, ovale, malariae, knowlesi), transmitted by the bite of the female Anopheles mosquito. P. falciparum causes the most severe disease.
LIFE CYCLE (in brief)
Mosquito injects sporozoites → Liver (exo-erythrocytic) stage — vivax/ovale form dormant hypnozoites → Release into blood → RBC (erythrocytic) cycle → RBC rupture → fever paroxysm + release of merozoites → Gametocytes taken up by mosquito
Hypnozoites of vivax/ovale cause later relapses — hence the need for anti-relapse therapy.
CLINICAL FEATURES
- Uncomplicated malaria — classical paroxysm of cold stage → hot stage → sweating stage, with periodicity (tertian/quartan), plus anaemia and splenomegaly.
- Severe (mostly falciparum) malaria — cerebral malaria (coma, seizures), severe anaemia, hypoglycaemia, acute kidney injury (blackwater fever), respiratory distress/ARDS, shock, metabolic acidosis and DIC.
INVESTIGATIONS
- Peripheral blood smear (thick and thin) — the gold standard; identifies species and parasite density.
- Rapid diagnostic test (RDT) — detects parasite antigen (HRP-2, pLDH).
- Supportive tests — blood glucose, haemoglobin, renal function (to detect severe disease).
MANAGEMENT
- Uncomplicated P. falciparum — Artemisinin-based Combination Therapy (ACT) (in India, artesunate + sulfadoxine-pyrimethamine) plus a single dose of primaquine (gametocidal).
- P. vivax — chloroquine (3 days) plus primaquine × 14 days for radical cure of hypnozoites (check G6PD status first).
- Severe malaria — IV artesunate is the drug of choice; manage complications (hypoglycaemia, seizures, anaemia, fluids).
PLASMODIUM SPECIES (comparison)
Species Note P. falciparum Most severe; no relapse; cerebral/severe malaria P. vivax Commonest in India; relapses (hypnozoites); benign tertian P. ovale Relapses (hypnozoites) P. malariae Quartan; may cause nephrotic syndrome CEREBRAL MALARIA
- A severe falciparum complication — impaired consciousness/coma and seizures with sequestration in cerebral microvasculature.
- Manage the airway, treat seizures and hypoglycaemia, give IV artesunate, and provide intensive supportive care; it carries significant mortality and a risk of neurological sequelae.
MONITORING
- Serial parasitaemia, blood glucose, haemoglobin and urine output.
- Reassess for evolving danger signs — malaria can deteriorate quickly.
EPIDEMIOLOGY
- A major cause of febrile illness in endemic areas; P. vivax predominates in much of India, P. falciparum causes most severe disease/deaths.
- Transmission by the female Anopheles mosquito, mainly at dusk/dawn.
CONGENITAL & TRANSFUSION MALARIA
Malaria can rarely be transmitted transplacentally (congenital malaria — fever, anaemia, splenomegaly in a neonate) or through blood transfusion; consider it in at-risk neonates.
KEY EXAM POINT
In severe malaria, treat empirically and urgently with IV artesunate and actively look for and correct hypoglycaemia (common, and worsened by quinine), seizures, severe anaemia and acidosis — these determine survival.
PROGNOSIS
Uncomplicated malaria treated promptly recovers fully; severe falciparum malaria is a medical emergency with appreciable mortality, so early recognition, IV artesunate and management of complications are essential.
💊KEY DRUG DOSES (viva)- IV artesunate 2.4 mg/kg at 0, 12 and 24 h, then daily (severe malaria).
- Chloroquine 25 mg/kg total over 3 days (10, 10, 5) — vivax.
- Primaquine 0.25–0.5 mg/kg/day × 14 days (vivax radical cure; single 0.75 mg/kg dose as falciparum gametocidal) — after G6PD screening.
- Manage hypoglycaemia with IV 10% dextrose 2–5 mL/kg.
COMPLICATIONS (severe falciparum)
- Cerebral malaria, severe anaemia, hypoglycaemia, renal failure, ARDS, shock, acidosis, DIC.
- High mortality if untreated — severe malaria is a medical emergency.
PREVENTION
- Vector control — insecticide-treated bed nets (LLINs), indoor residual spraying, source reduction.
- Chemoprophylaxis for travellers; early diagnosis and prompt treatment; malaria vaccines (RTS,S/R21) in endemic Africa.
📝CLINICAL / APPLIED POINTS- Any child with fever from an endemic area needs a smear/RDT for malaria — don't miss it.
- Check G6PD before primaquine (it can cause haemolysis in deficient children).
- Falciparum can rapidly become severe — assess for danger signs (coma, seizures, hypoglycaemia, severe anaemia).
- IV artesunate is the drug of choice for severe malaria (has replaced quinine).
- Always treat hypoglycaemia and other complications alongside antimalarials.
🔑KEY POINTS TO REMEMBER- Plasmodium via female Anopheles; falciparum most severe; vivax/ovale relapse (hypnozoites).
- Paroxysmal fever (cold–hot–sweating), anaemia, splenomegaly; severe = cerebral/anaemia/hypoglycaemia.
- Thick & thin smear (gold standard) + RDT.
- ACT + primaquine (falciparum); chloroquine + 14-day primaquine (vivax); IV artesunate (severe).
- Check G6PD before primaquine; prevent with bed nets and vector control.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics; National Vector Borne Disease Control Programme.DEFINITION
Dengue is an acute arboviral infection caused by the dengue virus (a flavivirus, 4 serotypes DEN 1–4), transmitted by the Aedes aegypti mosquito. A second infection with a different serotype increases the risk of severe disease (antibody-dependent enhancement).
PHASES OF ILLNESS
Febrile phase (2–7 days) → Critical phase (around defervescence, days 3–7) — plasma leakage → Recovery phase — reabsorption of fluid
WHO CLASSIFICATION (2009)
Category Features Dengue without warning signs Fever + 2 of: nausea/vomiting, rash, aches, leucopenia, positive tourniquet test Dengue WITH warning signs Abdominal pain, persistent vomiting, mucosal bleeding, lethargy, liver > 2 cm, rising haematocrit with rapid fall in platelets, clinical fluid accumulation Severe dengue Severe plasma leakage (shock/DSS, fluid accumulation with respiratory distress), severe bleeding, or organ impairment CLINICAL FEATURES
- High fever with severe headache, retro-orbital pain, myalgia and arthralgia ('breakbone fever'), and rash.
- Positive tourniquet test, thrombocytopenia and leucopenia.
- Plasma leakage (pleural effusion, ascites, rising haematocrit) in the critical phase → hypovolaemic shock (dengue shock syndrome).
INVESTIGATIONS
- NS1 antigen (positive early, days 1–5); IgM/IgG serology (after day 5).
- CBC — thrombocytopenia, leucopenia, and a rising haematocrit (a key marker of plasma leakage).
- Serial monitoring of haematocrit, platelets and warning signs.
MANAGEMENT
- No specific antiviral — treatment is supportive, centred on careful fluid management.
- Isotonic crystalloid for those with warning signs/leakage, titrated to the haematocrit and vital signs (avoid both under- and over-hydration).
- Paracetamol for fever; avoid aspirin and NSAIDs (bleeding risk).
- Platelet transfusion only for significant bleeding — not for a low count alone.
- Manage dengue shock syndrome with prompt fluid resuscitation.
OLDER (DHF/DSS) GRADING
Grade Features DF Fever + non-specific symptoms DHF I Above + thrombocytopenia/haemoconcentration + positive tourniquet test DHF II Grade I + spontaneous bleeding DHF III (DSS) Circulatory failure (narrow pulse pressure, hypotension) DHF IV (DSS) Profound shock (undetectable BP/pulse) PATHOPHYSIOLOGY OF SEVERE DENGUE
Immune activation increases vascular permeability, causing plasma leakage (into pleural/peritoneal spaces), haemoconcentration and hypovolaemic shock; thrombocytopenia and coagulopathy contribute to bleeding — hence the emphasis on monitoring haematocrit and careful fluid therapy.
CRITERIA FOR DISCHARGE
- Afebrile > 24–48 h without antipyretics, improving clinically and appetite returning.
- Rising platelet trend, stable haematocrit, and no respiratory distress from effusions/ascites.
TOURNIQUET TEST
A blood-pressure cuff is inflated midway between systolic and diastolic for ~5 minutes; > 10–20 petechiae per square inch is positive, indicating capillary fragility — a simple bedside clue in dengue.
WARNING SIGNS TO WATCH
- Severe abdominal pain, persistent vomiting, mucosal bleeding, lethargy/restlessness.
- Tender enlarging liver, and a rising haematocrit with a rapid drop in platelets — trigger closer monitoring/admission.
PROGNOSIS
With timely recognition of the critical phase and careful fluid management, most children recover fully; deaths occur mainly from unrecognised plasma leakage/shock or severe bleeding — both largely preventable with monitoring.
💊KEY DRUG DOSES (viva)- Paracetamol 10–15 mg/kg/dose (max 4 doses/day) — NEVER aspirin/NSAIDs.
- Isotonic crystalloid (0.9% saline / Ringer lactate) 5–10 mL/kg/hour for leakage, titrated to haematocrit.
- DSS: 10–20 mL/kg bolus, then reassess; colloid if refractory.
PREVENTION
- Vector control — eliminate Aedes breeding sites (stored water), larvicides, personal protection.
- Community awareness; dengue vaccine only in seropositive individuals (per current guidance).
📝CLINICAL / APPLIED POINTS- The danger period is the CRITICAL phase, around defervescence — not the peak of fever.
- A rising haematocrit with a falling platelet count signals plasma leakage — watch it serially.
- Never give aspirin/NSAIDs in dengue; use paracetamol.
- Give fluids judiciously — over-hydration causes as much harm as shock.
- Transfuse platelets only for bleeding, not for a number.
🔑KEY POINTS TO REMEMBER- Flavivirus (DEN 1–4) via Aedes aegypti; second heterologous infection → severe (ADE).
- WHO 2009: without warning signs / with warning signs / severe dengue.
- Breakbone fever, retro-orbital pain, thrombocytopenia; plasma leakage in the critical phase.
- NS1 (early), IgM (later); monitor haematocrit + platelets + warning signs.
- Supportive — careful isotonic fluids, paracetamol (no NSAIDs), platelets only for bleeding.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics; WHO/National dengue guidelines.DEFINITION
Measles is a highly contagious viral illness caused by the measles virus (a paramyxovirus, RNA), spread by respiratory droplets. It remains an important cause of childhood morbidity and mortality (largely preventable by vaccination).
CLINICAL FEATURES
- Prodrome — high fever with the '3 Cs': cough, coryza and conjunctivitis.
- Koplik spots — small white spots on the buccal mucosa — are pathognomonic and appear before the rash.
- Exanthem — an erythematous maculopapular rash with cephalocaudal spread (from behind the ears/hairline → face → trunk → limbs), which later fades with brownish staining and fine desquamation.
COMPLICATIONS (measles is dangerous through its complications)
- Otitis media (commonest) and pneumonia (commonest cause of death).
- Diarrhoea (with dehydration and worsening malnutrition), laryngotracheitis (croup).
- Neurological — febrile seizures, acute post-measles encephalitis, and the late, fatal subacute sclerosing panencephalitis (SSPE) years later.
- Vitamin A depletion → keratomalacia and blindness; reactivation of tuberculosis; severe malnutrition.
INVESTIGATIONS
- Usually a clinical diagnosis (prodrome, Koplik spots, typical rash).
- Measles-specific IgM serology confirms when needed (surveillance).
MANAGEMENT
- Supportive care — fluids, antipyretics, nutrition, and eye/mouth care.
- Vitamin A for all children with measles (reduces mortality and eye complications).
- Prompt treatment of complications — antibiotics for secondary bacterial pneumonia/otitis media.
EPIDEMIOLOGY & INFECTIVITY
- One of the most contagious human infections; spread by respiratory droplets and aerosols.
- Infectious from ~4 days before to 4 days after rash onset; incubation ~10–14 days.
STAGES OF ILLNESS
Incubation (~10–14 days) → Prodrome — fever + 3 Cs + Koplik spots (2–4 days) → Exanthem — cephalocaudal maculopapular rash → Recovery — staining and desquamation
DIFFERENTIAL DIAGNOSIS OF A MACULOPAPULAR RASH
- Rubella (milder, posterior-auricular nodes), roseola, scarlet fever, drug rash.
- Koplik spots and the prodrome of 3 Cs help identify measles.
MODIFIED & ATYPICAL MEASLES
- Modified measles — milder illness in those with partial immunity (e.g. after immunoglobulin, young infants with maternal antibody).
- Immunocompromised children may have severe or atypical disease (e.g. giant-cell pneumonia) without the classical rash.
ROLE OF NUTRITION
Measles and malnutrition form a vicious cycle — measles precipitates or worsens malnutrition and vitamin A deficiency, and malnourished children have far more severe measles; nutritional support and vitamin A are therefore integral to care.
KEY EXAM POINT
Every child with measles should receive vitamin A (two doses, age-based) regardless of nutrition; it reduces mortality and prevents blinding keratomalacia. Two doses of a measles-containing vaccine remain the key to elimination.
💊KEY DRUG DOSES (viva)- Vitamin A (2 consecutive days): < 6 mo 50,000 IU; 6–12 mo 100,000 IU; > 12 mo 200,000 IU (repeat a 3rd dose at 2–4 weeks if eye signs of deficiency).
- Antibiotics (e.g. amoxicillin) only for secondary bacterial complications.
PREVENTION
- Measles-containing vaccine (MR/MMR) — two doses (9–12 months and 16–24 months in the Indian schedule).
- Post-exposure prophylaxis — vaccine within 72 hours, or immunoglobulin for high-risk/immunocompromised contacts.
- Vaccination is the cornerstone of measles elimination.
📝CLINICAL / APPLIED POINTS- Koplik spots are pathognomonic and precede the rash — a valuable early clue.
- Most measles deaths are from complications (pneumonia, diarrhoea) — anticipate and treat them.
- Give vitamin A to every child with measles regardless of nutritional status.
- SSPE is a devastating late complication — another reason to vaccinate.
- Measles worsens malnutrition and can precipitate xerophthalmia — attend to nutrition and eyes.
🔑KEY POINTS TO REMEMBER- Highly contagious paramyxovirus; droplet spread; vaccine-preventable.
- Prodrome = 3 Cs (cough, coryza, conjunctivitis) + Koplik spots (pathognomonic); cephalocaudal maculopapular rash.
- Complications: otitis media (commonest), pneumonia (commonest killer), diarrhoea, encephalitis, SSPE, keratomalacia.
- Supportive care + vitamin A for all; treat secondary infections.
- Prevent with two doses of MR/MMR; PEP with vaccine within 72 h.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics; WHO/UIP immunisation schedule.DEFINITION & TRANSMISSION
Paediatric HIV is infection with the human immunodeficiency virus, causing progressive immunodeficiency. In children the commonest route is vertical (mother-to-child) transmission — intrauterine, intrapartum, or through breastfeeding; also via infected blood/products.
CLINICAL FEATURES
- Failure to thrive, recurrent/severe or unusual infections, chronic diarrhoea, persistent oral thrush.
- Generalised lymphadenopathy, hepatosplenomegaly, parotid enlargement, developmental delay.
- Opportunistic infections (e.g. Pneumocystis pneumonia, TB); WHO clinical staging I–IV.
DIAGNOSIS
- Under 18 months — a virological (HIV DNA/RNA PCR) test is required, because maternal antibody persists and antibody tests can be falsely positive.
- Over 18 months — HIV antibody testing (as in adults).
MANAGEMENT & PREVENTION
- Antiretroviral therapy (ART) for all diagnosed children (combination regimen), with adherence support.
- Co-trimoxazole prophylaxis against opportunistic infection; routine and additional immunisation; nutrition; treat infections/TB.
- Prevention of mother-to-child transmission (PMTCT) — maternal ART, safe delivery, infant ARV prophylaxis and safe infant-feeding counselling.
WHO CLINICAL STAGING (overview)
- Stage 1 — asymptomatic/persistent generalised lymphadenopathy.
- Stage 2 — recurrent respiratory infections, skin conditions.
- Stage 3 — moderate (chronic diarrhoea, oral thrush, TB).
- Stage 4 — severe (AIDS-defining: PCP, severe wasting, malignancy).
KEY EXAM POINT
In an infant with unexplained failure to thrive, recurrent infections and oral thrush, test the mother's HIV status and perform a virological (DNA PCR) test on the infant — antibody tests are unreliable under 18 months.
💊KEY DRUG DOSES (viva)- Co-trimoxazole prophylaxis — daily, dosed by weight/age (HIV-exposed and infected infants).
- Infant ARV prophylaxis (e.g. nevirapine/zidovudine) per national PMTCT protocol.
🔑KEY POINTS TO REMEMBER- Mainly vertical (mother-to-child) transmission, including via breastfeeding.
- FTT, recurrent infections, thrush, lymphadenopathy/hepatosplenomegaly; WHO stage I–IV.
- < 18 months: virological (DNA/RNA PCR); > 18 months: antibody test.
- ART for all + co-trimoxazole prophylaxis + immunisation; prevent by PMTCT.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics; NACO/WHO paediatric HIV guidelines.DEFINITION
Tetanus is a disease caused by the neurotoxin tetanospasmin of Clostridium tetani, which enters through a contaminated wound (or the umbilical stump in neonates) and blocks inhibitory neurotransmission, causing sustained muscle rigidity and spasms.
NEONATAL TETANUS
- Follows unclean cord-cutting/dressing practices in an unimmunised mother.
- Presents at day 3–14 with inability to suck, excessive crying, stiffness and spasms.
CLINICAL FEATURES
- Trismus (lockjaw), risus sardonicus (fixed grimace), neck/back stiffness and opisthotonus.
- Generalised spasms triggered by stimuli (light, sound, touch); autonomic instability.
- Consciousness is preserved (an important feature).
MANAGEMENT
- Neutralise unbound toxin — human tetanus immunoglobulin (TIG) (or antitetanus serum).
- Antibiotics — metronidazole (drug of choice; penicillin is an alternative).
- Control spasms — diazepam (± magnesium sulfate); nurse in a quiet, dark environment.
- Wound care/debridement; airway protection and ventilation for severe spasms; supportive care.
PATHOPHYSIOLOGY
Tetanospasmin travels retrogradely up motor nerves to the spinal cord and blocks release of the inhibitory neurotransmitters GABA/glycine, so unopposed motor activity causes sustained rigidity and reflex spasms.
PROGNOSIS
- Neonatal and severe generalised tetanus carry high mortality, especially with autonomic instability.
- Outcome depends on early antitoxin, spasm control and good supportive/intensive care.
💊KEY DRUG DOSES (viva)- Human tetanus immunoglobulin 500 IU IM (or 3000–6000 IU); infiltrate around the wound.
- Metronidazole 30 mg/kg/day (or IV penicillin) × 7–10 days.
- Diazepam to control spasms (titrated); magnesium sulfate infusion in severe cases.
PREVENTION
- Immunisation — DPT in infancy, boosters (Td), and maternal tetanus toxoid in pregnancy.
- Clean delivery and cord care; appropriate wound prophylaxis (TIG + toxoid).
🔑KEY POINTS TO REMEMBER- Tetanospasmin of C. tetani via wound/umbilical stump; preserved consciousness.
- Neonatal: day 3–14, poor sucking + spasms (unclean cord, unimmunised mother).
- Trismus, risus sardonicus, opisthotonus, stimulus-triggered spasms.
- TIG + metronidazole + diazepam + wound care/ventilation; prevent with immunisation & clean delivery.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Chickenpox is a highly contagious primary infection with the varicella-zoster virus (VZV), spread by respiratory droplets and direct contact. The virus becomes latent in dorsal-root ganglia and can later reactivate as herpes zoster (shingles).
CLINICAL FEATURES
- Mild fever and malaise, followed by an intensely itchy vesicular rash.
- Rash is centripetal (trunk more than limbs), begins as macules → papules → vesicles ('dew drop on a rose petal') → crusts.
- Pleomorphism — lesions in different stages simultaneously (a key distinguishing feature).
COMPLICATIONS
- Secondary bacterial infection of skin lesions (commonest).
- Pneumonia (especially adolescents/adults), cerebellar ataxia and encephalitis.
- Congenital varicella syndrome (early-pregnancy maternal infection) and severe neonatal varicella.
MANAGEMENT & PREVENTION
- Supportive — antipyretics (not aspirin — Reye syndrome risk), antihistamines and skin care.
- Aciclovir for high-risk groups — immunocompromised, neonates, adolescents/adults, and severe disease.
- Post-exposure — VZIG for susceptible high-risk contacts; varicella vaccine for prevention.
INCUBATION & INFECTIVITY
- Incubation ~14–16 days; infectious from ~1–2 days before the rash until all lesions crust.
- Susceptible contacts (household) are at high risk — hence isolation.
KEY EXAM POINT
The combination of a centripetal, intensely itchy rash with lesions at different stages at the same time distinguishes chickenpox from smallpox (historically) and from other vesicular rashes.
HERPES ZOSTER (reactivation)
After primary chickenpox, VZV stays latent in the dorsal-root ganglia and can reactivate years later as herpes zoster (shingles) — a painful dermatomal vesicular rash — particularly with waning immunity or immunosuppression.
💊KEY DRUG DOSES (viva)- Aciclovir 20 mg/kg/dose (max 800 mg) 4–5 times/day oral (high-risk); IV 10 mg/kg 8-hourly for severe/immunocompromised.
- VZIG for susceptible high-risk exposed individuals.
🔑KEY POINTS TO REMEMBER- Primary VZV infection; latency in dorsal-root ganglia → later zoster.
- Itchy centripetal vesicular rash; 'dew drop on rose petal'; lesions in different stages (pleomorphism).
- Complications: secondary bacterial infection, pneumonia, cerebellar ataxia; congenital varicella.
- Supportive (no aspirin); aciclovir for high-risk; prevent with vaccine/VZIG.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Mumps is an acute viral infection caused by the mumps virus (a paramyxovirus), spread by respiratory droplets, characteristically causing parotid gland inflammation (parotitis).
CLINICAL FEATURES
- Fever, malaise and headache, followed by painful swelling of the parotid gland(s) (uni- then often bilateral).
- Ear pain, pain on chewing, and obliteration of the angle of the jaw; the opening of Stensen's duct may be red.
- Usually self-limiting over about a week.
COMPLICATIONS
- Orchitis (in post-pubertal males — pain/swelling, small risk to fertility), oophoritis.
- Meningoencephalitis, pancreatitis, and sensorineural hearing loss.
MANAGEMENT & PREVENTION
- Supportive — analgesia, antipyretics, adequate fluids and soft diet.
- Prevention — the MMR vaccine (two doses).
DIAGNOSIS & EPIDEMIOLOGY
- Largely clinical (parotitis + contact history); serology (IgM) or PCR if confirmation is needed.
- Spread by droplets; infectious from before to after the swelling; incubation ~16–18 days.
DIFFERENTIAL DIAGNOSIS OF PAROTID SWELLING
- Suppurative (bacterial) parotitis, recurrent parotitis, lymphadenitis, and a parotid duct stone.
- Bilateral, non-suppurative swelling with systemic viral features favours mumps.
COMPLICATIONS — NOTE ON ORCHITIS
Mumps orchitis occurs mainly in post-pubertal males, is usually unilateral, and, although it can rarely impair fertility, does so uncommonly; supportive care (analgesia, scrotal support) is used.
KEY EXAM POINT
Bilateral, tender parotid swelling with systemic viral symptoms in an unimmunised child is mumps until proven otherwise; MMR vaccination has made it uncommon where uptake is high.
PREVENTION NOTE
Mumps is prevented by the MMR vaccine (given with measles and rubella); high two-dose coverage has made mumps and its complications (orchitis, meningoencephalitis, deafness) uncommon.
🔑KEY POINTS TO REMEMBER- Paramyxovirus; droplet spread; causes parotitis.
- Fever + painful parotid swelling (Stensen's duct); self-limiting.
- Complications: orchitis, meningoencephalitis, pancreatitis, deafness.
- Supportive care; prevent with MMR vaccine.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Rubella (German measles) is a mild viral illness caused by the rubella virus (a togavirus). Its major importance is that infection in early pregnancy causes the severe congenital rubella syndrome (CRS) in the fetus.
POSTNATAL RUBELLA (in the child)
- Low-grade fever with a fine maculopapular rash (face → trunk, fades quickly).
- Tender posterior-auricular and sub-occipital lymphadenopathy (characteristic); Forchheimer spots on the palate.
- Usually mild and self-limiting.
CONGENITAL RUBELLA SYNDROME (CRS)
- Results from maternal infection in the first trimester.
- Classic triad — cataract, congenital heart disease (especially PDA) and sensorineural deafness.
- Also microcephaly, growth restriction, hepatosplenomegaly and a 'blueberry muffin' rash.
PREVENTION
- Rubella-containing vaccine (MR/MMR); ensuring immunity in women of child-bearing age is key to preventing CRS.
- Avoid the vaccine in pregnancy (live vaccine).
DIAGNOSIS
- Postnatal rubella — clinical + rubella IgM if needed.
- CRS — maternal history, characteristic features, rubella IgM in the infant and virus detection.
KEY EXAM POINT
The importance of rubella lies almost entirely in pregnancy — a mild childhood illness, but a first-trimester maternal infection can devastate the fetus (CRS), which is why immunising girls/women is a public-health priority.
EXTENDED FEATURES OF CRS
- Ophthalmic — cataract, glaucoma, 'salt-and-pepper' retinopathy.
- Cardiac — PDA and pulmonary artery stenosis; CNS — microcephaly, intellectual disability.
- Others — hepatosplenomegaly, thrombocytopenia, 'blueberry muffin' rash, growth restriction.
WHY VACCINATION MATTERS
Because there is no treatment for CRS, prevention through population immunity (MR/MMR) — especially in girls before child-bearing age — is the only effective strategy.
🔑KEY POINTS TO REMEMBER- Togavirus; mild in children (rash + posterior-auricular/sub-occipital lymphadenopathy).
- Major risk = congenital rubella syndrome after first-trimester maternal infection.
- CRS triad: cataract + congenital heart disease (PDA) + sensorineural deafness.
- Prevent with MR/MMR vaccine (immunise women of child-bearing age).
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Diphtheria is an acute infection caused by toxigenic Corynebacterium diphtheriae, whose exotoxin causes local pseudomembrane formation and distant toxic effects (heart, nerves). It spreads by respiratory droplets.
CLINICAL FEATURES
- Sore throat and low-grade fever with a greyish, adherent pseudomembrane over the tonsils/pharynx that bleeds on attempted removal.
- 'Bull neck' — marked cervical lymphadenopathy with soft-tissue oedema.
- Extension into the larynx → airway obstruction (a medical emergency).
COMPLICATIONS
- Toxic myocarditis (a leading cause of death).
- Neuropathy — palatal palsy (nasal speech, regurgitation) and later peripheral neuritis.
- Airway obstruction.
MANAGEMENT & PREVENTION
- Diphtheria antitoxin — give early (neutralises unbound toxin; do not wait for culture).
- Antibiotics — penicillin or erythromycin (eradicate the organism, stop toxin production).
- Airway management, cardiac monitoring, isolation and bed rest; treat contacts.
- Prevention — DPT vaccination (and boosters).
CLINICAL TYPES
- Pharyngo-tonsillar (commonest) — pseudomembrane + bull neck.
- Laryngeal — hoarseness, stridor, airway obstruction.
- Nasal — serosanguineous discharge; cutaneous diphtheria (skin).
KEY EXAM POINT
Do not wait for laboratory confirmation — give diphtheria antitoxin early on clinical suspicion, because it only neutralises unbound toxin; delay allows irreversible binding to heart and nerves.
EPIDEMIOLOGY & CONTROL
- Re-emerges where immunisation coverage falls; humans are the reservoir.
- Manage close contacts (chemoprophylaxis, immunisation status check) and isolate cases; notify.
KEY EXAM POINT
The triad to remember is pseudomembrane + bull neck + toxin complications (myocarditis, neuropathy); early antitoxin saves lives, and DPT immunisation prevents the disease.
💊KEY DRUG DOSES (viva)- Diphtheria antitoxin 20,000–100,000 units (by site/severity), given early after a test dose.
- Erythromycin 40–50 mg/kg/day, or penicillin, × 14 days.
🔑KEY POINTS TO REMEMBER- Toxigenic C. diphtheriae; exotoxin-mediated; droplet spread.
- Greyish adherent pseudomembrane (bleeds on removal) + 'bull neck'; airway obstruction.
- Complications: myocarditis, palatal/peripheral neuropathy, airway obstruction.
- Early diphtheria antitoxin + antibiotics + airway care; prevent with DPT.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Kala-azar (visceral leishmaniasis) is a chronic protozoal infection caused by Leishmania donovani, transmitted by the bite of the female sandfly (Phlebotomus). It is endemic in parts of eastern India (Bihar).
CLINICAL FEATURES
- Prolonged (> 2 weeks) fever, often with a double rise, and progressive weakness.
- Massive splenomegaly and hepatomegaly; pancytopenia (anaemia, leucopenia, thrombocytopenia).
- Weight loss and darkening of the skin ('kala-azar' = black fever).
INVESTIGATIONS
- Splenic or bone-marrow aspirate — demonstrates LD bodies (amastigotes) (most specific).
- rK39 rapid antibody test (widely used); aldehyde (formol-gel) test.
- Pancytopenia and hypergammaglobulinaemia on supportive tests.
MANAGEMENT & PREVENTION
- Liposomal amphotericin B — the drug of choice.
- Miltefosine (oral) and paromomycin are alternatives.
- Post-kala-azar dermal leishmaniasis (PKDL) may follow treatment and acts as a reservoir.
- Prevention — vector (sandfly) control and early diagnosis/treatment of cases.
POST-KALA-AZAR DERMAL LEISHMANIASIS (PKDL)
PKDL is a skin condition (hypopigmented macules, papules, nodules) appearing months to years after apparently successful treatment; it is important because these patients act as a reservoir for continued transmission, hindering elimination.
KEY EXAM POINT
Consider kala-azar in any child from an endemic area with prolonged fever, massive splenomegaly and pancytopenia; the rK39 test is a useful bedside screen, and marrow/splenic aspirate showing LD bodies confirms it.
SUPPORTIVE CARE & COMPLICATIONS
- Manage anaemia, malnutrition and intercurrent/secondary infections (which commonly complicate advanced disease).
- Untreated kala-azar has high mortality; relapse and PKDL require follow-up.
💊KEY DRUG DOSES (viva)- Liposomal amphotericin B — single dose 10 mg/kg (or short course) — first-line.
- Miltefosine 2.5 mg/kg/day × 28 days (oral alternative).
🔑KEY POINTS TO REMEMBER- Leishmania donovani via sandfly (Phlebotomus); endemic in Bihar/eastern India.
- Prolonged fever + massive splenomegaly + pancytopenia + skin darkening.
- Marrow/splenic aspirate (LD bodies) + rK39 test.
- Liposomal amphotericin B (first-line); miltefosine oral; watch for PKDL.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics; National Kala-azar Elimination Programme.