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PSM - Epidemiology of Communicable Diseases (10-Marker Notes)

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1. TUBERCULOSIS

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2. POLIOMYELITIS

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3. MUMPS

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4. DIARRHOEAL DISEASES

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5. CHOLERA

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6. MALARIA

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7. RABIES

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8. JAPANESE ENCEPHALITIS (JE)

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9. HIV/AIDS

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Quick Revision Table

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All points drawn from Park's Textbook of Preventive and Social Medicine (PSM) - the standard reference for these 10-marker exam questions. Each disease section covers agent, source, transmission, incubation, infective period, risk factors, key epidemiological indicators, and control measures - the standard format expected in a 10-marker answer.

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PSM - EPIDEMIOLOGY OF COMMUNICABLE DISEASES

Full 10-Marker Answers | Park's Textbook of PSM

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1. TUBERCULOSIS

Definition

Agent Factors

• Causative agent: Mycobacterium tuberculosis (human type); M. bovis (bovine type - rare)
• Acid-fast bacillus (AFB), aerobic, non-spore-forming, non-motile
• Can survive in dried sputum for 6-8 months but killed by sunlight and UV light
• Infectivity: One sputum-positive case can infect 10-15 persons per year
• 1/3rd of the global population is infected asymptomatically; only 5-10% develop clinical disease in their lifetime

Source of Infection

• Open case of pulmonary TB (sputum-positive patient) = most important source
• Infected cattle (bovine TB) via unpasteurized milk

Mode of Transmission

• Droplet infection (main route) - inhalation of infected droplet nuclei (1-10 microns) that remain suspended in air
• Droplet contact - large droplets settling on mucous membranes
• Alimentary tract - ingestion of infected milk (bovine TB)
• Direct inoculation - skin (rare, lab workers - "anatomist's wart")
• Transplacental - very rare, congenital TB

Incubation Period

• 4-6 weeks from infection to primary lesion (tuberculin positivity develops)
• Disease may not manifest for months or years (latent TB)

Period of Communicability

• As long as viable tubercle bacilli are present in sputum
• Sputum-positive > sputum-negative (more infectious)

Host Factors

• Age: All ages; risk highest in infants, elderly, adolescents
• Sex: Males > Females (2:1) due to occupational exposure, smoking, alcohol
• Nutrition: Malnutrition greatly increases susceptibility
• Immunity: Reduced in HIV, DM, silicosis, steroid use, malignancy
• Genetic factors: Some genetic predisposition exists

Environmental Factors

• Poverty, overcrowding, poor ventilation = major risk factors
• Social determinants: poor housing, sanitation, lack of education
• Season: Peak in winter/spring (overcrowding indoors)

Epidemiological Indicators

• Annual Risk of Infection (ARI): Most sensitive indicator; % of population getting newly infected per year; ARI of 1% = ~50 new smear-positive cases per 1,00,000 population
• Tuberculin positivity rate: Measures infection prevalence in community
• MDR-TB (resistant to at least Rifampicin + Isoniazid) and XDR-TB are emerging threats

Pathophysiology

• Inhaled bacilli reach alveoli → phagocytosed by macrophages → Ghon's focus (primary lesion, usually in mid-lung zone)
• Bacilli spread to regional lymph nodes → Ghon's complex (primary focus + lymph node)
• Cell-mediated immunity (CMI) develops in 4-6 weeks → tuberculin sensitivity
• If CMI fails → progressive primary TB or post-primary reactivation

Clinical Features

• Pulmonary TB: Cough (>2 weeks), hemoptysis, fever, night sweats, weight loss, anorexia
• Extrapulmonary: Lymphadenopathy (most common extrapulmonary), pleural effusion, TB meningitis, TB spine (Pott's disease), miliary TB

Diagnosis

• Sputum smear microscopy (Ziehl-Neelsen stain): AFB
• Sputum culture (gold standard): Lowenstein-Jensen (LJ) medium
• Cartridge-Based NAAT (CBNAAT/GeneXpert): rapid molecular test
• Tuberculin skin test (Mantoux): 5 TU PPD, read at 48-72 hours; induration ≥10 mm = positive

Control Measures - RNTCP / NTEP

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2. POLIOMYELITIS

Definition

Agent Factors

• Agent: Poliovirus - Enterovirus, family Picornaviridae, RNA virus
• Three serotypes: Type 1 (Brunhilde) - most common cause of paralysis; Type 2 (Lansing); Type 3 (Leon)
• Stable in water/sewage for months; killed by heat, UV, chlorination
• WPV Type 2 eradicated in 1999; WPV Type 3 last detected 2012; only Type 1 remains in circulation

Source of Infection

• Cases (both clinical and inapparent)
• Inapparent infections are the main source - ratio of inapparent to paralytic = 100:1 or more
• No animal reservoir - strictly human disease

Mode of Transmission

• Feco-oral route (main) - ingestion of contaminated food/water
• Droplet infection (minor, early stage of illness)
• Crowding, poor sanitation, and contaminated water facilitate spread

Incubation Period

• Minor illness: 3-5 days
• Major illness (paralytic): 7-14 days (range 3-35 days)

Period of Communicability

• Virus present in throat: 1 week before and 1 week after onset
• Virus present in feces: 3-6 weeks (can be longer in immunodeficient)
• Patient is most infectious in first few days before and after onset

Host Factors

• Age: Mainly affects children < 5 years (hence "infantile paralysis"); adults also susceptible if unimmunized
• Sex: Males more susceptible to paralytic disease
• Immunity: Type-specific and lifelong after infection; maternal antibodies protect infants for 6 months
• Provocation polio: IM injections, tonsillectomy, dental extractions during incubation period increase risk of paralysis at that site
• Pregnancy increases risk of paralysis

Pathophysiology (4 Stages)

1. Inapparent infection (90-95%): Virus multiplies in GI tract; immune response clears it
2. Abortive polio (4-8%): Minor illness - fever, sore throat, nausea; no CNS involvement
3. Non-paralytic polio (1-2%): Aseptic meningitis; no paralysis; full recovery
4. Paralytic polio (<1%): Virus enters CNS via bloodstream → destroys anterior horn cells → Lower Motor Neuron (LMN) type flaccid paralysis

Types of Paralytic Polio

• Spinal: Most common - asymmetric flaccid paralysis of limbs
• Bulbar: Cranial nerve involvement - most dangerous; respiratory paralysis
• Bulbospinal: Combined form
• Polioencephalitis: Rare, in infants

Clinical Features

• Biphasic fever (dromedary pattern)
• Flaccid, asymmetric paralysis (LMN type)
• No sensory loss (distinguishes from GBS)
• Paralysis maximum at 48 hours; some recovery possible

Diagnosis

• AFP (Acute Flaccid Paralysis) surveillance: Any child < 15 years with AFP = suspected polio
• Two stool specimens 24-48 hours apart within 14 days of onset
• Virus isolation from stool = gold standard

Vaccines

Control - India's Polio Eradication

• Pulse Polio Immunization (PPI): National Immunization Days (NIDs) - OPV to all children < 5 yrs
• Sub-National Immunization Days (SNIDs): High-risk areas
• AFP Surveillance: All AFP cases in < 15 yrs must be investigated
• Mop-up operations: Targeted campaigns around confirmed cases
• India polio-free since 27th March 2014 (WHO certified)
• bOPV (bivalent Types 1+3) replaced tOPV in 2016; fIPV introduced in UIP

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3. MUMPS

Definition

Agent Factors

• Agent: Myxovirus parotiditis - RNA virus, family Paramyxoviridae, genus Rubulavirus
• Only ONE serotype (unlike influenza); no significant antigenic variation
• Source of infection: Both clinical and subclinical cases; subclinical = 30-40% of all infections
• Virus isolated from saliva (Stenson's duct), blood, urine, breast milk, CSF
• Secondary attack rate: ~86% among susceptibles

Mode of Transmission

• Droplet infection (main route)
• Direct contact with infected saliva

Incubation Period

• 2-4 weeks; usually 14-18 days (range 12-25 days)

Period of Communicability

• 4-6 days before onset of symptoms to 1 week or more after onset
• Maximum infectivity: Just before and at the onset of parotitis
• Once parotid swelling subsides, the case is no longer infectious
• Key exam point: Infectious 48 hours BEFORE symptoms appear (similar to Park's "period of maximum infectivity is just before onset")

Host Factors

• Age: Most common in children 5-9 years; average age higher than measles/chickenpox
• Disease more severe in adults than children
• One attack (clinical or subclinical) = lifelong immunity
• Infants < 6 months protected by maternal antibodies

Environmental Factors

• Endemic globally; peak incidence in winter and spring
• Epidemics every 2-5 years in unimmunized populations
• Overcrowding promotes spread

Clinical Features

• Prodrome: Fever, malaise, headache, anorexia (1-2 days)
• Parotitis: Unilateral or bilateral swelling and tenderness of parotid glands; bilateral in ~70-80%
• Redness of Stenson's duct opening - pathognomonic sign
• Pain on chewing/swallowing

Complications

Diagnosis

• Clinical (parotid swelling)
• Serology: Rise in antibody titre (S and V antigens)
• Virus isolation from saliva/CSF
• Increased serum amylase

Control

• Isolation: For 9 days from onset of parotid swelling
• MMR vaccine: Live attenuated; given at 9-12 months + booster at 15-18 months
• No specific treatment; symptomatic management
• Mumps surveillance: Reporting all cases

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4. DIARRHOEAL DISEASES

Definition

Classification (WHO)

Causative Agents

• Viruses: Rotavirus (most common in children < 2 years globally), Norovirus, Adenovirus
• Bacteria: ETEC (traveller's diarrhoea), Shigella, Salmonella, V. cholerae, Campylobacter, C. difficile
• Parasites: Giardia lamblia, Entamoeba histolytica, Cryptosporidium

Source of Infection

• Feces of infected persons or animals
• Contaminated food and water

Mode of Transmission - "4 F's + 1"

Incubation Period

• Bacterial toxins: 6-48 hours
• ETEC: 10-12 hours
• Viral (Rotavirus): 24-48 hours
• Parasitic (Giardia): 1-3 weeks

Host Factors - Risk Factors

• Age < 2 years (immature immunity)
• Malnutrition (vicious cycle: diarrhoea → malnutrition → more diarrhoea)
• Bottle feeding (lack of protective antibodies in breast milk)
• Lack of access to safe water and sanitation
• Immunodeficiency (HIV, malnutrition)

Pathophysiology

• Secretory diarrhoea (e.g., cholera, ETEC): Toxin activates adenylate cyclase → increased cAMP → hypersecretion of Cl⁻ and Na⁺ into intestinal lumen → watery diarrhoea
• Invasive diarrhoea (e.g., Shigella): Organism invades intestinal mucosa → inflammation → bloody diarrhoea/dysentery
• Osmotic diarrhoea (e.g., Rotavirus): Villous damage → reduced absorption → osmotic gradient → watery stool

ORS (Oral Rehydration Solution)

Zinc Supplementation

• 20 mg/day for children > 6 months for 14 days
• 10 mg/day for infants < 6 months for 14 days
• Reduces severity, duration, and future episodes

Control Measures

• Safe water supply and sanitation (WASH program)
• Handwashing with soap (most cost-effective single intervention)
• Exclusive breastfeeding for 6 months
• Rotavirus vaccine (in NIS since 2016 in India)
• ORS + Zinc treatment (IMNCI guidelines)
• Improved food hygiene
• Oral Zinc + ORS = "Two-pillar" approach (UNICEF/WHO)

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5. CHOLERA

Definition

Agent Factors

• Agent: Vibrio cholerae - Gram-negative comma-shaped bacillus ("Koch's comma bacillus")
• Serogroups causing epidemics: O1 and O139
• Biotypes of O1: Classical (El Tor now predominant worldwide)
• El Tor advantages over Classical: Longer survival, more carriers produced, hardier in environment, causes milder disease
• Seventh pandemic (1961-present): Due to El Tor biotype; O139 (Bengal strain) identified in 1992 in Bangladesh
• Grows best in alkaline media (pH 8.2); does not survive below pH 6
• Killed by heat (55°C for 15 min), chlorination, drying

Source of Infection

• Cases (clinical and subclinical)
• Carriers: 75% of infections are inapparent; El Tor produces more carriers than Classical type
• Contaminated water (main source) and food

Mode of Transmission

• Waterborne (most important) - contaminated drinking water
• Foodborne - contaminated fish, vegetables, rice
• Feco-oral route
• Person-to-person (less common)

Carriers in Cholera

• Contact carrier: Infected during epidemic
• Convalescent carrier: After recovery; carries for a few weeks
• Healthy (Chronic) carrier: Rare; most significant epidemiologically; can carry for months to years (especially El Tor)

Incubation Period

• Few hours to 5 days; usually 1-2 days (range 6 hours to 5 days)

Period of Communicability

• During diarrhoeal phase (profuse shedding)
• Carriers: weeks to months

Pathophysiology

• V. cholerae → colonizes small intestine → produces cholera toxin (CT)
• CT = A subunit (active) + B subunit (binding)
• B subunit binds GM1 ganglioside on enterocytes
• A subunit → permanently activates adenylate cyclase → cAMP ↑↑↑
• cAMP → hypersecretion of Cl⁻ and water into lumen, inhibits Na⁺ absorption
• Result: "Rice-water stools" - profuse, odourless, watery diarrhoea (up to 20 litres/day)

Clinical Features

• Sudden onset, effortless profuse watery diarrhoea
• "Rice-water stools" - watery, fishy/inoffensive odour, flecks of mucus
• Painless vomiting (no nausea initially)
• Severe dehydration → "washer-woman's hands," sunken eyes, skin tenting
• Muscle cramps, oliguria/anuria
• Case fatality untreated: 50-60%; with treatment: < 1%

Diagnosis

• Dark-field microscopy: "Shooting stars" motility
• Culture: TCBS (Thiosulfate Citrate Bile Salts Sucrose) agar - yellow colonies (El Tor)
• String test: Vibrios agglutinate in string-like fashion
• Serotyping with O1 and O139 antisera

Treatment

• ORS (mainstay) for mild-moderate dehydration
• IV Ringer's Lactate for severe dehydration (not normal saline)
• Tetracycline (drug of choice for adults, single dose 2g OR 4x500mg x 3 days)
• Doxycycline alternative; Azithromycin for children and pregnant women
• Zinc supplementation for children

Control

• Safe water supply - most effective long-term measure
• Proper sewage disposal and sanitation
• Notification within 24 hours
• Oral cholera vaccine (OCV): Shanchol, OrchoL - 2 doses, 14 days apart; 65-85% efficacy for 2-3 years
• Food and water precautions during outbreaks
• Dead bodies: Epidemics have NEVER arisen from dead bodies

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6. MALARIA

Definition

Agent Factors

Vector

• Female Anopheles mosquito (only female feeds on blood for egg development)
• Dusk-to-dawn biter (peak biting: 9pm - 5am)
• Breeds in clean, still water (not stagnant/organic waste water)
• Anopheles culicifacies = main vector in rural India
• Anopheles stephensi = main vector in urban India

Source of Infection

• Infected humans (gametocyte carriers)
• Simian malaria (P. knowlesi in Southeast Asia)

Mode of Transmission

• Bite of infected female Anopheles (main)
• Blood transfusion (transfusion malaria - no pre-erythrocytic stage, shorter IP)
• Congenital/Transplacental (rare)
• Syringe-transmitted (IV drug users)

Life Cycle (Key Points)

• In mosquito (Definitive host): Sexual cycle (sporogony); infective stage = sporozoites
• In man (Intermediate host): Asexual cycle (schizogony)
  • Pre-erythrocytic (Exo-erythrocytic) phase: Sporozoites → liver → merozoites (14 days for P. vivax)
  • Erythrocytic phase: Merozoites → RBC → ring form → trophozoite → schizont → merozoites (rupture of RBC = fever)
  • Hypnozoites: Dormant liver forms in P. vivax and P. ovale → cause RELAPSES
  • P. falciparum = NO hypnozoites, but RBC sequestration in capillaries → complications

Clinical Features (Classic Triad)

1. Cold stage: Rigor (15-60 min); patient feels very cold
2. Hot stage: High fever 39-41°C (2-6 hours)
3. Sweating stage: Profuse sweating, temperature falls, patient feels better

Complications (P. falciparum - Severe Malaria)

• Cerebral malaria: Altered consciousness, coma, seizures (most dangerous)
• Blackwater fever: Massive hemolysis → hemoglobinuria → "black urine"; renal failure
• Algid malaria: Circulatory collapse
• Malarial hypoglycemia (falciparum + quinine treatment)
• Acute renal failure, pulmonary edema, severe anemia, DIC
• Hyperreactive Malarial Splenomegaly (HMS) / Tropical Splenomegaly Syndrome

Epidemiological Indicators

Treatment

• P. vivax: Chloroquine (25 mg/kg over 3 days) + Primaquine (0.25 mg/kg x 14 days for radical cure - kills hypnozoites; contraindicated in G6PD deficiency, pregnancy)
• P. falciparum: ACT - Artesunate + Sulphadoxine-Pyrimethamine (AS+SP) or Artemether-Lumefantrine
• Severe malaria: IV Artesunate (drug of choice) or IV Quinine

Control

• Vector control: Indoor Residual Spraying (IRS) with DDT/synthetic pyrethroids
• Insecticide-Treated Nets (ITNs)/LLINs - Proven most effective
• Environmental management: Source reduction, biological control (Gambusia fish - larvivorous)
• Personal protection: Repellents, protective clothing, mosquito nets
• National Programme: NVBDCP (National Vector Borne Disease Control Programme)
• Malaria vaccine: RTS,S/AS01 (Mosquirix) - first WHO-approved malaria vaccine (Oct 2021); limited efficacy (~36%)

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7. RABIES

Definition

Agent Factors

• Agent: Rabies virus - Lyssavirus type 1, family Rhabdoviridae
• Morphology: Bullet-shaped, enveloped, RNA virus; 75 x 180 nm
• Negri bodies: Eosinophilic, intracytoplasmic inclusion bodies in neurons (especially Purkinje cells of cerebellum and hippocampal neurons) - pathognomonic of rabies
• "Street virus": Wild-type; variable incubation; Negri bodies present
• "Fixed virus": Lab-adapted; short, fixed incubation; no Negri bodies; used for vaccine

Source of Infection

• Saliva of infected animals (most important)
• Dogs = 97% of human rabies in India
• Other sources: Cats, foxes, jackals, wolves, bats (Americas - vampire and insectivorous bats)
• No human-to-human transmission (except organ transplant - very rare)

Reservoir

• Domestic: Dogs (developing world)
• Wildlife: Foxes (Europe), Raccoons/skunks (North America), Bats (Americas)
• Man = dead-end host

Mode of Transmission

• Bite of rabid animal - main route; virus in saliva enters through wound
• Lick on abraded skin or mucous membrane - no bite needed
• Aerosol inhalation - in bat caves (rare)
• Corneal/organ transplant - very rare

Incubation Period

• Range: 10 days to 1 year (exceptionally longer)
• Usual: 2-8 weeks (20-90 days)
• Factors affecting IP:
  • Site of bite: Shorter for head/neck/face (virus closer to brain), longer for lower limbs
  • Severity of bite: Deep bites = shorter IP
  • Amount of virus inoculated

Period of Communicability

• Dogs become infectious 3-10 days BEFORE symptoms appear (and remain so)
• This is why dogs must be observed for 10 days after biting a person

Pathophysiology

• Virus inoculated → replicates locally in muscle → binds nicotinic acetylcholine receptors at neuromuscular junction → enters peripheral nerves → travels centripetally via fast axonal transport (8 mm/hour) → reaches CNS (brainstem and limbic system) → encephalitis → travels centrifugally to salivary glands, cornea, skin

Clinical Features

• Fever, headache, malaise
• Pain/tingling/paresthesia at bite site (pathognomonic warning sign)

• Furious rabies (80%): Hydrophobia (fear of water - laryngeal/pharyngeal spasm on seeing water), aerophobia, photophobia, hyperexcitability, autonomic instability
• Dumb (paralytic) rabies (20%): Ascending flaccid paralysis; resembles GBS; NO hydrophobia; less dramatic

Diagnosis

• Ante-mortem: DFA (Direct Fluorescent Antibody) test on skin biopsy (nape of neck), corneal impressions, saliva; RT-PCR
• Post-mortem: Negri bodies on brain (hippocampus, cerebellum) by Sellers staining

WHO Bite Categories and Management

Post-Exposure Prophylaxis (PEP)

1. Wound washing: Immediate and thorough washing with soap and water for 15 minutes; apply iodine/70% alcohol
2. Anti-Rabies Vaccine (ARV): HDCV or PCECV; IM (Deltoid): Days 0, 3, 7, 14 (Essen regimen) OR Intradermal (ID): 2-site ID on Days 0, 3, 7, 28 (Updated Thai regimen)
3. Rabies Immunoglobulin (RIG): Only for Category III; Human RIG (HRIG) 20 IU/kg OR Equine RIG (ERIG) 40 IU/kg; infiltrate maximum into/around wound

Control

• Dog vaccination: Mass annual vaccination of dogs (>70% coverage breaks transmission cycle)
• Stray dog control: Registration, neutering, elimination of stray dogs
• Pre-exposure prophylaxis (PrEP): For high-risk groups (vets, lab workers); Days 0, 7, 28
• Once clinical symptoms appear: No treatment is effective (rare "Milwaukee protocol" with limited success)

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8. JAPANESE ENCEPHALITIS (JE)

Definition

Agent Factors

• Agent: JE virus - Flavivirus (RNA virus), related to West Nile, Dengue, Yellow fever viruses
• Single serotype; multiple genotypes (I-V) with different geographical distributions
• Initial viral replication occurs in local/regional lymph nodes; CNS invasion via blood
• Leading cause of viral encephalitis in Asia - occurring in 24 Asian and Western Pacific countries

Reservoir and Amplifying Host

Vector

• Primary vector: Culex tritaeniorhynchus (main), Culex vishnui, Culex pseudovishnui
• Night-biting mosquito
• Breeds in paddy (rice) fields, flooded irrigation channels - explains rural/agricultural distribution
• Also breeds in ground pools, slow-flowing water with aquatic vegetation

Mode of Transmission

• Bite of infected Culex mosquito
• NOT person-to-person transmission

Incubation Period

• 5-15 days (range 5-15 days)

Inapparent: Clinical ratio

• 300:1 to 500:1 - vast majority of infections are inapparent/subclinical
• Only 1 in 300-500 infected persons develops clinical encephalitis

Epidemiology in India

• First recognized in India in 1955 in Tamil Nadu
• Endemic in 21 states
• States with annual outbreaks: UP, Bihar, Assam, Karnataka, West Bengal, Tamil Nadu, Haryana (contribute ~55% of cases and deaths)
• ~375 million population at risk
• Reported under umbrella of AES (Acute Encephalitis Syndrome)
• Seasonal: Rainy season / monsoon and post-monsoon period (June-October)
• Transmission mainly in rural agricultural areas with flooded irrigation

Clinical Features

• Sudden onset with high fever
• Altered sensorium → stupor → coma
• Convulsions (especially in children)
• Headache, nuchal rigidity, signs of meningeal irritation
• Parkinsonism-like features (tremors, rigidity) - characteristic of JE
• Case fatality: 20-30%
• Neurological sequelae in 30-50% of survivors (epilepsy, cognitive impairment, behavioral changes, motor deficits)

Diagnosis

• IgM ELISA in CSF (gold standard) - JE-specific IgM appears 3-8 days after onset; CSF IgM is diagnostic
• Serum IgM ELISA: Suggestive but cross-reactive with other Flaviviruses (Dengue, WNV)
• CT/MRI: Bilateral thalamic lesions (characteristic of JE)
• CSF: Lymphocytic pleocytosis, elevated protein, normal/low glucose

Treatment

• No specific antiviral treatment - mainly supportive
• Manage raised ICP, seizures, respiratory failure
• ICU care for severe cases

Vaccines (JE Vaccines)

• SA 14-14-2 vaccine added to NIS in India in 2013 for children 1-15 years in endemic districts

Control

• Vaccination (most important long-term measure)
• Vector control: Larviciding of rice fields, biological control
• Pig sties away from human habitation (prevent amplification)
• Personal protection: Mosquito nets, repellents, protective clothing at night
• Surveillance of AES cases
• Health education about the disease

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9. HIV / AIDS

Definition

Agent Factors

• Agent: HIV - Retrovirus (family Retroviridae, subfamily Lentivirus)
• HIV-1: Global distribution; more virulent; responsible for majority of infections worldwide
• HIV-2: Mainly West Africa; less virulent; slower progression to AIDS; lower transmissibility
• Structure: Enveloped RNA virus; contains reverse transcriptase enzyme (RNA → DNA)
• Key surface proteins: gp120 (binds CD4 receptor), gp41 (membrane fusion); p24 antigen (capsid protein - marker of viral replication)

Source of Infection

• Blood (and blood products)
• Semen and pre-seminal fluid
• Vaginal/rectal secretions
• Breast milk
• NOT transmitted by: Saliva, tears, sweat, urine, feces (in absence of blood), casual contact, mosquitoes

Mode of Transmission

• Sexual transmission (most common globally): Unprotected heterosexual (main in developing countries) and homosexual (main in developed countries); receptive anal intercourse = highest risk
• Parenteral transmission: Blood transfusion (high risk), IV drug use (needle sharing), needlestick injuries (0.3% risk per exposure)
• Mother-to-Child Transmission (MTCT/Vertical): During pregnancy (25%), delivery (65%), breastfeeding (10-15%); overall risk without intervention = 25-40%

Incubation Period

• Window period: 6-12 weeks from infection to seroconversion (test becomes positive); patient is infectious but test-negative during this period
• Clinical latency: Average 10 years from HIV infection to AIDS (range 2-15 years)
• Acute HIV syndrome: 2-4 weeks after infection; flu-like illness (fever, lymphadenopathy, rash, myalgia)

Period of Communicability

• Lifelong once infected
• Highest viral load = highest infectivity: (1) Acute HIV (first 2-3 months) and (2) Late-stage AIDS
• Effective ART reduces viral load to undetectable levels = U=U (Undetectable = Untransmittable)

Pathophysiology

• HIV gp120 binds CD4 receptor + co-receptor (CCR5 or CXCR4) on T-helper lymphocytes
• Virus enters cell → reverse transcriptase converts RNA to DNA → integrase integrates viral DNA into host genome (provirus)
• Viral replication → CD4+ T-cell destruction
• Normal CD4 count: 500-1500 cells/µL
• AIDS: CD4 < 200 cells/µL (or < 15% of total lymphocytes)
• Progressive immunosuppression → susceptibility to opportunistic infections (OIs)

WHO Clinical Staging (Summary)

Opportunistic Infections (Important for Exams)

• TB - most common OI in India (and globally)
• Pneumocystis jirovecii Pneumonia (PCP) - most common OI in developed countries
• Cryptococcal meningitis - fungal; India India most common fungal OI
• CMV retinitis - presents with floaters, visual loss; CD4 < 50
• MAC (Mycobacterium avium complex) - disseminated; CD4 < 50
• Toxoplasmosis - cerebral; ring-enhancing lesions on CT
• Kaposi's sarcoma - HHV-8; violaceous skin lesions; AIDS-defining

Global and Indian Burden

• Global: ~38 million people living with HIV (PLHIV); 1.5 million new infections per year; Sub-Saharan Africa most affected
• India: ~2.3 million PLHIV; Adult HIV prevalence ~0.2%; High-burden states: Maharashtra, Andhra Pradesh/Telangana, Karnataka, Manipur, Mizoram
• NACO (National AIDS Control Organisation): Apex body for HIV/AIDS in India; runs NACP (National AIDS Control Programme)

Diagnosis

• ELISA (Enzyme-Linked Immunosorbent Assay): Screening test; detects HIV antibodies; positive result requires confirmation
• Western Blot: Confirmatory test (gold standard)
• Rapid tests: Point-of-care; India uses 3-test strategy
• PCR (Viral Load): Monitors treatment response; early diagnosis in infants (< 18 months)
• CD4 count: Monitors immune status and guides treatment
• p24 antigen: Detectable before antibodies (during window period); used in 4th generation combo tests

Treatment - ART (Antiretroviral Therapy)

• WHO: ART for ALL PLHIV regardless of CD4 count (Test and Treat policy)
• Standard first-line regimen: TDF + 3TC + DTG (Tenofovir + Lamivudine + Dolutegravir)
• ART reduces viral load, restores CD4, prevents OIs, reduces transmission
• ART does NOT cure HIV - must be taken lifelong
• IRIS (Immune Reconstitution Inflammatory Syndrome): Paradoxical worsening after starting ART due to recovering immune system

Control Measures - India (NACP)

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QUICK MASTER TABLE

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