Hepatitis - PSM (Community Medicine) for RGUHS Exams

Comparative Table of Hepatitis Viruses

HEPATITIS A (Infectious Hepatitis)

Epidemiological Determinants (Park's)

• Causative agent: HAV - an enterovirus (type 72) of Picornaviridae family
• Multiplies only in hepatocytes
• Only one serotype known; no chronic carrier state
• Resistance: Survives >10 weeks in well water; withstands 60°C for 1 hour; resistant to chlorine at usual doses; inactivated by boiling for 5 min, UV rays, autoclaving, or formalin
• Faecal shedding is highest during the later part of incubation period and early acute phase

• All ages susceptible; children usually have subclinical (anicteric) infection
• Period of infectivity: 2 weeks before to 1 week after onset of jaundice
• Infective material: mainly faeces; blood during brief viraemia phase

• Poor sanitation and hygiene
• Overcrowding
• Contaminated food/water (fecal-oral)

Endemicity Patterns

• High endemicity (poor sanitation): Most infected in childhood - subclinical; adults are immune; outbreaks rare
• Intermediate endemicity (developing countries): Paradoxically higher disease burden - children escape early infection, then get infected as adolescents/adults - large outbreaks possible
• Low endemicity (developed countries): Disease in high-risk groups (IV drug users, homosexual men, travellers)

Prevention and Control

• Early reporting and isolation (enteric precautions for 1 week after onset of jaundice)
• Sanitary disposal of faeces
• Investigation and notification

• Safe water supply - 1 mg/L free residual chlorine inactivates virus in 30 min at pH ≤8.5
• Boil water during epidemics
• Proper sewage disposal
• Food hygiene and hand washing

• Inactivated (formaldehyde) vaccines - most commonly used worldwide; licensed for ≥12 months age; 2 doses in deltoid; interval 6-12 months (can extend to 18-36 months); protective efficacy ~94% after 2 doses; can be given simultaneously with other vaccines
• Live attenuated vaccine - manufactured in China; single subcutaneous dose
• Both provide long-lasting, possibly lifelong protection
• Combination vaccines (Hep A+B or Hep A+typhoid) available for travellers

• 0.02 ml/kg: protection for ~1-2 months
• 0.06 ml/kg: protection for ~3-5 months
• 80-90% effective when given before or within 14 days of exposure
• Now declining in use due to short duration and cost

HEPATITIS B (Serum Hepatitis)

Key Facts

• Caused by HBV - a Hepadnavirus (partially double-stranded DNA)
• Can be acute or chronic; may range from asymptomatic to fulminant
• Acute HBV: case fatality rate 0.5 to 1%
• HBV + delta virus (HDV) = severe virulent hepatitis
• HBsAg prevalence defines endemicity: ≥8% = highly endemic, <2% = low endemic

Global Burden (Park's)

• 257 million persons living with chronic HBV infection (2015)
• 887,220 deaths in 2015 (HCC 337,454; cirrhosis 462,690; acute hepatitis 87,076)
• Most burden from perinatal/early childhood infection (more likely to become chronic)
• Africa (6.1%) and Western Pacific (6.2%) have highest prevalence
• India: HBsAg prevalence ~3.7% (intermediate endemicity)

Transmission Routes

• Parenteral (blood transfusion, needles, injections)
• Sexual contact
• Perinatal (mother-to-child) - major route in high endemic areas
• Household contact (sharing razors, toothbrushes)

Markers and Their Significance

Prevention and Control

• Recombinant DNA vaccine (yeast-derived HBsAg)
• Schedule under UIP in India: Birth dose + 6, 10, 14 weeks (as pentavalent)
• Birth dose within 24 hours of birth is critical to prevent perinatal transmission
• 3-dose schedule gives >95% protection (anti-HBs ≥10 mIU/mL = seroprotection)
• High-risk groups: healthcare workers, IV drug users, dialysis patients, sexual contacts

• Used for post-exposure prophylaxis (needlestick, newborn of HBsAg+ mother)
• Given within 12 hours of birth for perinatal exposure (along with vaccine)
• Also used for percutaneous/mucosal exposure in unvaccinated persons

HEPATITIS C

• ssRNA virus, Flaviviridae family
• Mainly parenteral transmission (IV drug use, transfusions, needlestick)
• Most common cause of post-transfusion hepatitis

• 80% cases progress to chronic hepatitis (highest chronicity among all hepatitis viruses)

• Major risk of cirrhosis and hepatocellular carcinoma
• No vaccine available
• Diagnosis: ELISA for anti-HCV antibodies; PCR for HCV RNA
• Treatment: Direct-acting antivirals (DAAs) - sofosbuvir-based regimens

HEPATITIS D (Delta Hepatitis)

• Defective ssRNA virus; requires HBV (HBsAg) as helper for replication
• 2 patterns:
  • Co-infection (simultaneous HBV+HDV): Usually self-limiting; 10% chronicity
  • Superinfection (HDV on chronic HBV): 90-100% chronicity; severe disease
• Prevention: HBV vaccination automatically prevents HDV

HEPATITIS E

• ssRNA virus, Hepeviridae
• Fecal-oral route (like Hep A) - waterborne epidemics
• Incubation period: 4-5 weeks (longer than Hep A)
• Special feature: Very high mortality in pregnant women (20%) - most important exam point
• No chronic state (except in immunocompromised)
• Diagnosis: Serum IgM/IgG antibodies
• No vaccine approved in India (HEV vaccine approved in China)
• Common in India, Southeast Asia, Africa - endemic areas similar to Hep A

RGUHS Previous Year Questions on Hepatitis (PSM Paper)

1. Prevention and control of Hepatitis A
2. Epidemiology of Viral Hepatitis
3. Serological markers of Hepatitis B
4. Rationality of giving Hepatitis B vaccine to infants (S'10)
5. Hepatitis E in pregnancy
6. Universal Precautions (linked to Hep B, Hep C)

• Describe the epidemiology and prevention of Viral Hepatitis / Hepatitis B

• Window period in Hepatitis B
• HBsAg carriers
• HBIG
• HAV vaccine
• Differences between Hepatitis A and E

High-Yield Points for RGUHS Exam

1. HAV and HEV - fecal-oral; HAV never chronic; HEV fatal in pregnancy (20%)
2. HBV - most important from vaccination standpoint; perinatal infection - 90% chronicity
3. HCV - most common cause of post-transfusion hepatitis; >80% chronicity; no vaccine
4. HDV - requires HBV; prevented by HBV vaccine
5. HBsAg = first marker; anti-HBs = immunity; HBeAg = high infectivity
6. HAV vaccine: 2 doses, 6-12 months apart, 94% efficacy
7. HBV vaccine: birth dose within 24 hours is key for perinatal prevention
8. HBIG for newborns of HBsAg+ mothers: within 12 hours of birth
9. IgG dose for HAV passive prophylaxis: effective up to 14 days post-exposure
10. HAV infectivity: highest 2 weeks before jaundice onset; drops after jaundice appears

LYMPHATIC FILARIASIS

PSM / Community Medicine - RGUHS 10 Mark Answer

DEFINITION

CAUSATIVE ORGANISMS

PROBLEM STATEMENT

• Affects 49 countries; tropics and subtropics of Africa, Asia, Western Pacific, Americas
• 893 million people at risk; 120 million infected; 40 million with overt disease
• 15 million with lymphoedema; 25 million men with urogenital swelling (hydrocele)
• 90% of cases caused by W. bancrofti

• Endemic in 256 districts, 16 states and 5 UTs
• 630 million people exposed to risk
• Heavily infected areas: Uttar Pradesh, Bihar, Jharkhand, Andhra Pradesh, Odisha, Tamil Nadu, Kerala, West Bengal, Gujarat
• National Filaria Control Programme (NFCP) operating since 1955

EPIDEMIOLOGICAL DETERMINANTS

A. Agent Factors

• Adult worms live in lymphatic vessels; microfilariae (Mf) circulate in peripheral blood
• W. bancrofti Mf: sheathed, no nuclei in tail tip; nocturnal periodicity (appear in peripheral blood between 10 PM - 2 AM)
• B. malayi Mf: sheathed, two distinct nuclei in tail tip; nocturnal subperiodicity (always present but peak at night)
• Only infective (L3) larvae transmitted by mosquito bites

B. Host Factors

• (a) Age: All ages susceptible; microfilaria (Mf) rate rises with age and plateaus in middle age; filarial disease appears in >10 years age group
• (b) Sex: Mf rate higher in males in most endemic areas
• (c) Migration: Movement of people extends filariasis into new non-endemic areas
• (d) Immunity: Resistance develops only after many years of repeated exposure; immunological basis unclear
• (e) Social factors: Linked to urbanization, industrialization, poverty, illiteracy, poor sanitation

C. Environmental Factors

• (a) Climate: Temperature 22-38°C favours Culex quinquefasciatus breeding; relative humidity 70% optimal for longevity
• (b) Drainage: Bad drainage promotes vector breeding in polluted water
• (c) Town planning: Inadequate sewage disposal increases breeding of C. quinquefasciatus in cesspools, soakage pits, open drains, septic tanks, burrow pits

VECTORS

• Bancroftian filariasis in India: Culex quinquefasciatus (formerly C. fatigans) - urban vector; breeds in polluted/stagnant water
• Brugian filariasis in India: Mansonia (Mansonoides) annulifera and M. uniformis - breed in water containing aquatic plants (Pistia stratiotes); cannot breed without these plants

• W. bancrofti: Culex, Anopheles, Aedes
• Brugia spp: Mansonia, Anopheles, Coquillettidia

MODE OF TRANSMISSION

• Bite of infected vector mosquito
• Infective L3 larvae deposited near puncture site
• Larvae penetrate skin and reach lymphatic system
• Transmission depends on infective biting rate (man-mosquito contact)

INCUBATION PERIOD

• Prepatent period (inoculation → appearance of Mf in blood): information lacking
• Clinical incubation period (inoculation → clinical manifestations): 8 to 16 months (may be longer)

CLINICAL MANIFESTATIONS

1. Lymphatic Filariasis (4 stages)

• Hydrocele (most common in Bancroftian)
• Elephantiasis (legs, scrotum, arms, penis, vulva, breasts - in decreasing frequency)
• Chyluria (milky urine due to lymph in urine)
• Brugian filariasis: genitalia rarely involved (key difference from Bancroftian)

2. Occult Filariasis (Tropical Pulmonary Eosinophilia - TPE)

• Due to immune hyperresponsiveness to Mf
• Features: paroxysmal nocturnal cough and wheeze, fever, weight loss
• Very high eosinophilia (>3000/mm³), raised IgE
• Bilateral diffuse infiltrates on CXR
• Treatment: DEC (diethylcarbamazine)

DIAGNOSIS

1. Night blood examination (10 PM - 2 AM) - demonstration of Mf in thick blood smear (gold standard)
2. Knott's concentration technique - for low Mf density
3. Membrane filtration technique - more sensitive
4. Immunochromatographic card test (ICT) - detects circulating filarial antigen of W. bancrofti; can be done at any time of day
5. ELISA - for antibody detection
6. USG - "filarial dance sign" (movement of adult worms in dilated lymphatics)
7. Lymphoscintigraphy - for lymphatic damage assessment

PREVENTION AND CONTROL

A. Vector Control (Anti-larval Operations)

• Source reduction: Elimination of breeding places - filling up of cesspools, soakage pits, burrow pits; proper drainage
• Anti-larval measures:
  • Polystyrene beads (floating layer over drains) - physical suffocation of larvae
  • Bacterial larvicides: Bacillus sphaericus (highly effective against Culex), B. thuringiensis israelensis (Bti)
  • Temephos (Abate) - chemical larvicide
• Anti-adult measures: Pyrethrum spray, DDT residual spraying, insecticide-treated bed nets
• Destruction of Pistia plants - eliminates Mansonia breeding for Brugian filariasis

B. Mass Drug Administration (MDA) - KEY STRATEGY

• Drug regimen:
  • DEC (Diethylcarbamazine citrate) 6 mg/kg as single annual dose
  • DEC + Albendazole 400 mg - combined since 2007 in India (more effective)
  • Where onchocerciasis is co-endemic: Ivermectin + Albendazole (DEC avoided)
• Target: Reduce Mf prevalence to <1% to interrupt transmission
• Duration: Minimum 5 rounds of MDA with coverage ≥65% of total population
• Exclusions: Pregnant women, children <2 years, seriously ill persons
• India: MDA starts in November annually; all 250 LF endemic districts covered

C. Morbidity Management

• Home-based limb care/foot hygiene to prevent acute attacks of lymphangitis
• Hydrocele operations at CHCs/district hospitals/medical colleges
• Physiotherapy and limb elevation for lymphoedema

D. Surveillance and Case Detection

• Night blood surveys (Mf rate, microfilaria carrier detection)
• Treatment of Mf carriers
• Transmission Assessment Surveys (TAS) - to assess if MDA can be stopped

NATIONAL FILARIA CONTROL PROGRAMME (NFCP)

• Established: 1955
• In 1978: Merged with Urban Malaria Scheme
• Training centres: Calicut (Kerala), Rajahmundry (A.P.), Varanasi (U.P.) (under NICD, Delhi)
• Implementation: 206 filaria control units, 199 filaria clinics, 27 survey units (urban towns)
• Rural areas: Services through primary health care system

Elimination Goal

• National Health Policy 2002: ELF (Elimination of Lymphatic Filariasis) target by 2015 (later extended)
• Elimination defined as: Mf carriers <1% AND children born after ELF initiation free from circulating antigenaemia
• Strategy:
  1. Annual MDA with DEC + Albendazole for 5+ years
  2. Home-based morbidity management + hydrocele operations
• By 2017: 94 districts (221 million population) completed 1st TAS and stopped MDA

HIGH-YIELD EXAM POINTS (RGUHS)