attachment
attachment

Answer the question for psm first 2 question r 10 marks other r 5 marks

Reading File
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Reading File
Reading File
Reading File
Reading File
Reading File
Reading File
Finding Sources
Reading File
Reading File
Here are complete, exam-ready answers for all questions based on Park's Textbook of Preventive and Social Medicine:

PSM Exam Answers


LONG ESSAYS (10 Marks Each)


Q1. Describe the epidemiological determinants of Malaria. Discuss the approaches and strategies for Malaria in India with emphasis on Falciparum Malaria.

Epidemiological Determinants of Malaria

Agent Factors:
  • Causative agent: Plasmodium species - P. falciparum, P. vivax, P. malariae, P. ovale
  • P. falciparum is the most dangerous, causing cerebral malaria and severe malaria
  • P. vivax is the most widespread in India but usually less lethal
  • The parasite must complete its sexual cycle in the mosquito (extrinsic incubation period: 10-14 days for P. falciparum)
  • Drug resistance is a major challenge, especially chloroquine-resistant P. falciparum
Host Factors:
  1. Age - All ages are susceptible; children under 5 and pregnant women are most vulnerable
  2. Sex - Males are more exposed due to outdoor activity; females more susceptible during pregnancy
  3. Immunity - People in endemic areas develop partial immunity with repeated infections
  4. Genetic factors - Sickle cell trait, G6PD deficiency, and Duffy blood group negativity offer some protection
  5. Nutritional status - Malnutrition increases susceptibility
  6. Occupation - Labourers, farmers, forest workers, tribal populations are at high risk
Environmental Factors:
  1. Climate - Temperature 20-30°C and humidity >60% favour mosquito breeding; rainfall creates breeding sites
  2. Altitude - Malaria does not usually occur above 2000 metres
  3. Season - Transmission peaks after monsoon (July-November in India)
  4. Geography - Forested, hilly, tribal areas in North-East India, Odisha, Jharkhand, Chhattisgarh are high-burden
  5. Breeding sites - Stagnant water, irrigation channels, ponds, rice fields
  6. Urbanization - Urban malaria due to construction sites and water storage
Vector Factors:
  • Vector: Anopheles mosquitoes - A. culicifacies (rural), A. stephensi (urban), A. fluviatilis, A. minimus
  • A. culicifacies is the principal vector in India, responsible for ~65% of malaria cases
  • Mosquitoes bite at night (dusk to dawn); are endophilic and zoophilic/anthropophilic depending on species

National Strategies for Malaria Control in India

National Framework for Malaria Elimination (NFME) 2016-2030: The goal is to eliminate malaria from India by 2030, through a phased approach.
Phase I (2016-2020): Eliminate malaria from 26 states/UTs where API (Annual Parasite Incidence) <1 Phase II (2020-2022): Reduce incidence in remaining states Phase III (2022-2027): Nationwide elimination Phase IV (2027-2030): Prevent re-introduction
Key Strategies:
1. Early Diagnosis and Prompt Treatment (EDPT):
  • Use of Rapid Diagnostic Tests (RDTs) at village level by ASHAs
  • Microscopy at PHC/CHC level for confirmation
  • For P. falciparum: Artemisinin-based Combination Therapy (ACT) - Artesunate + Sulfadoxine-Pyrimethamine (AS+SP) given under direct observation
  • For P. vivax: Chloroquine + Primaquine (for radical cure, to eliminate hypnozoites)
  • Severe P. falciparum: Injectable Artesunate or Artemether
2. Special Emphasis on Falciparum Malaria:
  • P. falciparum causes complications: cerebral malaria, severe anaemia, acute respiratory distress, renal failure, blackwater fever
  • High-risk states (Odisha, Jharkhand, Chhattisgarh, MP, North-East) receive priority
  • Village Health Workers (ASHA/MPW) given RDTs and ACT for early treatment
  • ABER (Annual Blood Examination Rate) target: minimum 10% of population tested
3. Vector Control:
  • Indoor Residual Spraying (IRS): DDT, Malathion, Deltamethrin sprayed on interior walls twice a year in high-risk areas
  • Insecticide Treated Bed Nets (ITNs)/Long Lasting Insecticide-Treated Nets (LLINs): Distributed free in tribal and forested areas
  • Larval control: Biological (Gambusia fish, Bacillus thuringiensis israelensis), chemical (larvicides) and environmental management (anti-larval measures, source reduction)
4. Integrated Vector Management (IVM):
  • Combines chemical, biological and environmental methods
  • Community participation emphasized
5. Surveillance:
  • API (Annual Parasite Incidence) = Number of positive cases per 1000 population per year; high-risk = API >2
  • SPR (Slide Positivity Rate) = % of slides positive
  • ABER (Annual Blood Examination Rate) = % of population whose blood is examined
  • SFR (Slide Falciparum Rate) = % of slides showing P. falciparum
  • Sentinel surveillance sites established
6. Epidemic Preparedness and Response
7. Behaviour Change Communication (BCC) and IEC:
  • Public education on mosquito prevention, sleeping under nets, seeking early care
8. International Initiatives:
  • India is signatory to WHO Global Technical Strategy for Malaria 2016-2030
  • "High Burden to High Impact" (HBHI) approach adopted

Q2. Explain the concept of the Natural History of Disease. Discuss the various levels of prevention and modes of the interventions corresponding to the natural history with an example.

Natural History of Disease

Disease results from a complex interaction between agent, host, and environment. The natural history of disease refers to the progression of a disease process in an individual over time in the absence of treatment or prevention. It was described by Leavell and Clark (1965).
The natural history consists of two phases:

1. Prepathogenesis Phase

  • Period before the disease begins in man
  • The disease agent has NOT yet entered the human host
  • Causative factors (Agent, Host, Environment - the Epidemiological Triad) exist but have not yet interacted to cause disease
  • This is "man in the midst of disease" or "man exposed to risk of disease"
  • Example (TB): Mycobacterium tuberculosis exists in the environment; susceptible host (malnourished, immunocompromised) lives in overcrowded housing - these factors are present but disease has not begun yet

2. Pathogenesis Phase

  • Begins with entry of the disease agent into the susceptible host
  • The disease progresses through:
    • Early pathogenesis - subclinical/inapparent infection, tissue changes begin, no symptoms yet
    • Advanced disease/discernible early disease - signs and symptoms begin to appear
    • Late pathogenesis - disease advanced, complications develop
  • Final outcome: Recovery, Disability, or Death
The natural history illustrates two important concepts:
  • Spectrum of disease - from subclinical to severe
  • Iceberg phenomenon - only the tip (clinical cases) is visible; many subclinical cases remain submerged

Levels of Prevention (Leavell and Clark)

Prevention has four levels corresponding to stages in natural history:

1. Primordial Prevention

  • Prevents the emergence of risk factors in populations where they have not appeared
  • Directed at the entire population - healthy individuals
  • Operates in the prepathogenesis phase, BEFORE risk factors develop
  • Example: Discouraging children from adopting unhealthy lifestyles (smoking, unhealthy diet) to prevent later hypertension and obesity
  • Main intervention: Individual and mass education

2. Primary Prevention

  • Defined as "action taken prior to the onset of disease which removes the possibility that a disease will ever occur"
  • Operates in the prepathogenesis phase when agent and host have not yet interacted
  • Two modes:
    • Health promotion (non-specific): nutrition, personal hygiene, antenatal care, health education
    • Specific protection: immunization, chemoprophylaxis, use of specific nutrients, protection from carcinogens
  • Example (TB): BCG vaccination, improving nutritional status, proper ventilation

3. Secondary Prevention

  • Defined as "action which halts the progress of a disease at its incipient stage and prevents complications"
  • Operates in the early pathogenesis phase
  • Two modes:
    • Early diagnosis and treatment - mass screening, surveillance, case-finding
    • Disability limitation - adequate treatment to prevent complications
  • Example (TB): Sputum examination of symptomatic contacts, early treatment with anti-TB drugs to prevent spread and complications

4. Tertiary Prevention

  • Defined as "all measures available to reduce or limit impairments and disabilities, minimize suffering caused by existing departures from good health and to promote the patient's adjustment to irremediable conditions"
  • Operates in the late pathogenesis phase
  • Modes:
    • Disability limitation - prevent further deterioration
    • Rehabilitation - physical, mental, social, and vocational rehabilitation
  • Example (TB): Pulmonary rehabilitation for patients with residual lung damage; vocational rehabilitation for those with prolonged disability

Modes of Intervention

LevelPhaseMode
PrimordialPre-pathogenesisHealth promotion (population level)
PrimaryPre-pathogenesisHealth promotion + Specific protection
SecondaryEarly pathogenesisEarly diagnosis + Prompt treatment
TertiaryLate pathogenesisDisability limitation + Rehabilitation
Example with Coronary Heart Disease (CHD):
  • Primordial: Discourage adoption of sedentary lifestyle, high-fat diet in children
  • Primary: Dietary modification, exercise, smoking cessation, treatment of hypertension (specific protection)
  • Secondary: ECG screening, cholesterol testing, treatment of angina before infarction
  • Tertiary: Cardiac rehabilitation, prevention of recurrent infarction, vocational guidance
(Based on Park's Textbook of Preventive and Social Medicine)

SHORT ESSAYS (5 Marks Each)


Q3. Illustrate the diagnostic algorithm for drug-sensitive pulmonary tuberculosis under the National Tuberculosis Elimination Programme (NTEP)

Diagnostic Algorithm for Drug-Sensitive Pulmonary TB (NTEP)

Case Definition:
  • Presumptive TB case: Any person with cough for >=2 weeks, fever >=2 weeks, significant weight loss, or night sweats; or a person with any symptoms who has been in contact with a confirmed TB patient
Step-by-step Algorithm:
Step 1 - Identify Presumptive TB Case All patients presenting with above symptoms at any health facility are identified as presumptive TB cases and referred for diagnostic workup.
Step 2 - CBNAAT/TrueNat Testing (Preferred First Test)
  • Cartridge-Based Nucleic Acid Amplification Test (CBNAAT/GeneXpert) or TrueNat MTB assay is the preferred first-line test
  • Simultaneously detects M. tuberculosis AND tests for Rifampicin resistance
  • Result in ~2 hours
  • Recommended for: all presumptive TB cases, HIV-positive individuals, previously treated cases, children, extra-pulmonary TB
Step 3 - Sputum Smear Microscopy (where CBNAAT unavailable)
  • Collect 2 sputum samples (spot-morning or spot-spot)
  • Examine for Acid-Fast Bacilli (AFB) using ZN staining
  • Smear positive = pulmonary TB confirmed
Step 4 - Chest X-Ray
  • Done for all presumptive TB cases
  • If X-ray suggestive but smear negative, proceed to CBNAAT
  • Helps identify cavitary disease, infiltrates
Step 5 - Diagnosis and Classification
  • Bacteriologically confirmed TB: Positive by smear, culture, or molecular test (CBNAAT)
  • Clinically diagnosed TB: Clinical and X-ray evidence but bacteriologically negative; treated as TB if clinician decides
Step 6 - Treatment Initiation for Drug-Sensitive TB
  • New patients: 2HRZE/4HR (2 months Isoniazid + Rifampicin + Pyrazinamide + Ethambutol, then 4 months Isoniazid + Rifampicin)
  • Treatment given as Daily Fixed-Dose Combination (FDC) tablets under DOTS (Direct Observation of Treatment, Short-course)
  • All patients registered on Ni-kshay portal (web-based TB notification system)
  • Ni-kshay Poshan Yojana - Rs. 500/month nutritional support during treatment
Note: If CBNAAT detects Rifampicin resistance, the patient is referred for drug-resistant TB (DR-TB) evaluation and treatment.

Q4. Discuss the role of family in health and disease.

Role of Family in Health and Disease

The family is considered the basic unit of society and plays a central role in determining the health status of its members. Family medicine recognizes the family as the "focal point of health care."
1. Biological Role:
  • Family is the unit of reproduction; hereditary diseases and genetic traits are transmitted through family
  • Consanguineous marriages increase risk of genetic disorders
  • Family determines nutritional status through food availability and eating patterns
2. Family as a Source of Infection:
  • Infectious diseases (TB, hepatitis, meningitis, chickenpox) spread rapidly within family due to close contact
  • Index case in the family often leads to secondary cases
  • Family members share the same water, food, air - making common-source outbreaks possible
  • Concept of "family contact" is used in disease control (e.g., TB contact tracing)
3. Role in Aetiology and Causation:
  • Unhealthy family lifestyles contribute to non-communicable diseases - obesity, hypertension, diabetes, cardiovascular disease
  • Family dietary habits influence nutritional status
  • Family stress and dysfunctional relationships contribute to mental illness
  • Family smoking habits influence children's risk of respiratory disease
4. Influence on Health Behaviour:
  • Family shapes health beliefs, practices and healthcare-seeking behaviour
  • Attitude to immunization, contraception, antenatal care, and treatment compliance is influenced by family
  • Health literacy within family determines early recognition of illness
5. Family as a Unit of Health Care:
  • First level of care is provided within the family
  • Family members are the first to identify illness, provide home care, and decide on treatment-seeking
  • Elderly care, maternal care, child nutrition - all are family responsibilities
6. Role in Prevention and Rehabilitation:
  • Family provides social support during illness and recovery
  • Compliance with treatment (e.g., anti-TB drugs, diabetic medications) depends on family support
  • Family care is critical in rehabilitation of disabled members
  • Emotional support from family reduces morbidity in chronic illnesses (cancer, mental illness)
7. Family Cycle and Health:
  • Different stages of the family life cycle carry different health risks (e.g., pregnancy, infancy, adolescence, old age)
  • Health services can be tailored to family needs at each stage
Role of PHC in family health: The Primary Health Centre (PHC) is the first contact point between the community and the health system; health workers (ASHA, ANM) visit families and deliver preventive and promotive services.

Q5. Define incubation period. Explain its epidemiological importance.

Definition

Incubation period is defined as "the time interval between invasion by an infectious agent and the appearance of the first sign or symptom of the disease in question" (WHO definition).
  • For non-infectious diseases, the equivalent term is latent period - defined as "the period from disease initiation to disease detection"
  • The median incubation period is the time required for 50% of cases to occur following exposure
During the incubation period, the infectious agent multiplies in the host until it builds up sufficient density to disturb the health equilibrium and cause overt disease.
Factors determining incubation period:
  1. Generation time of the pathogen
  2. Infective dose
  3. Portal of entry
  4. Individual susceptibility of host
Examples:
DiseaseIncubation Period
Food poisoning (Staph)1-6 hours
Cholera1-3 days
Influenza1-3 days
Typhoid10-14 days
Measles10-14 days
Chickenpox14-21 days
Hepatitis A15-45 days
Hepatitis B45-180 days
Rabies2 weeks - 6 months
Leprosy2-5 years

Epidemiological Importance

  1. Tracing the source of infection:
    • Short incubation period (hours to days) - easy to trace source (e.g., food poisoning, cholera). "Follow the trail" is simple
    • Long incubation period - many contacts and events have occurred; source tracing is difficult, cause-effect relationship is diluted
  2. Surveillance and quarantine:
    • Duration of quarantine is based on the maximum incubation period of the disease
    • e.g., quarantine for COVID-19 was 14 days based on its incubation period
  3. Determination of time of exposure:
    • Working backward from onset of disease, the incubation period helps identify when exposure occurred
    • Useful in investigating common-source epidemics (food poisoning outbreaks)
  4. Evaluation of epidemic curve:
    • In a point-source epidemic, all cases occur within one incubation period
    • The epidemic curve shape and the incubation period help determine whether it is a point-source or propagated epidemic
  5. Period of communicability:
    • As a rule, infectious diseases are NOT communicable during incubation period
    • Exceptions: measles, chickenpox, whooping cough, and hepatitis A are communicable in the LATER part of incubation period
    • This knowledge guides isolation/quarantine decisions
  6. Estimation of immune status:
    • If disease occurs earlier than the minimum incubation period, it suggests pre-existing immunity or non-specific infection
  7. Medicolegal importance:
    • Used to determine time of exposure in cases of occupational disease or food poisoning litigation
(Park's Textbook of PSM)

Q6. Discuss the steps in conducting a case-control study.

Case-Control Study

A case-control study is an observational, retrospective, analytical epidemiological study that compares persons who have a disease (cases) with persons who do not have the disease (controls) to identify factors that may have contributed to the disease.

Steps in Conducting a Case-Control Study:

Step 1 - Formulate the Research Question and Hypothesis
  • Define the disease and the exposure(s) of interest
  • State the null hypothesis and alternative hypothesis
  • Example: "Is cigarette smoking associated with lung cancer?"
Step 2 - Define and Select Cases
  • A case = a person with the disease/outcome under study
  • Source of cases: hospitals (hospital-based), community (population-based), disease registries
  • Apply inclusion and exclusion criteria clearly
  • Ensure cases are truly affected by the disease (use diagnostic criteria)
  • Use incident (new) cases if possible to avoid survival bias
Step 3 - Define and Select Controls
  • A control = a person without the disease but from the same population as cases
  • Source: hospital controls, community controls, neighbourhood controls, relatives
  • Controls must be from the same "reference population" that gave rise to the cases
  • Matching (individual or frequency matching) can be done to control confounding - match for age, sex, socioeconomic status
  • Usually 1:1 to 1:4 case-to-control ratio
Step 4 - Measure Exposure
  • Collect data on past exposure from both cases and controls
  • Methods: structured interviews, questionnaires, medical records, biological samples
  • Both groups are questioned in the same manner to avoid interviewer bias
  • Investigators are ideally blinded to case/control status
Step 5 - Assess Potential Sources of Bias
  • Selection bias - cases and controls not representative
  • Recall bias - cases may remember exposures differently than controls (major limitation)
  • Information bias - systematic error in data collection
  • Confounding - controlled by matching, restriction, or statistical methods
Step 6 - Calculate Sample Size
  • Based on expected exposure prevalence in controls, odds ratio to detect, alpha error (type I, usually 5%), and beta error (type II, usually 20%)
Step 7 - Data Collection and Analysis
  • Construct a 2x2 contingency table:
Disease (Cases)No Disease (Controls)
Exposedab
Not exposedcd
  • Calculate Odds Ratio (OR) = (a x d) / (b x c)
    • OR >1 = positive association (risk factor)
    • OR <1 = protective factor
    • OR = 1 = no association
Step 8 - Statistical Testing
  • Chi-square test to assess statistical significance
  • Calculate 95% confidence interval for OR
  • If CI does not include 1.0, result is statistically significant
Step 9 - Interpretation and Conclusion
  • Assess whether association is causal using Bradford Hill criteria (strength, consistency, specificity, temporality, biologic plausibility, etc.)
  • Report findings
Advantages of case-control: Rapid, inexpensive, good for rare diseases and diseases with long latent periods, multiple exposures can be studied simultaneously.
Disadvantage: Cannot calculate incidence; recall bias; cannot establish temporal relationship directly.

Q7. Enumerate the steps involved in the investigation of an epidemic.

Investigation of an Epidemic

Definition: An epidemic exists when the number of observed cases exceeds the expected frequency for that population based on past experience.
The objectives of epidemic investigation are:
  • Define the magnitude in terms of time, place, and person
  • Determine conditions and factors responsible
  • Identify cause, source, and mode of transmission
  • Make recommendations to prevent recurrence

Steps in Epidemic Investigation:

Step 1 - Verification of Diagnosis
  • Confirm that the reported cases actually have the suspected disease
  • Clinical examination of a sample of cases
  • Laboratory investigations (where applicable) to confirm - but do NOT delay investigation waiting for lab results
  • Rule out misdiagnosis or misclassification
Step 2 - Confirmation of Existence of Epidemic
  • Compare current disease frequency with the same period in previous years
  • Epidemic exists if observed cases exceed expected by more than 2 standard errors above the endemic level
  • Common-source epidemics (cholera, food poisoning) are usually obvious without comparison
Step 3 - Define the Population at Risk
  • Identify the population exposed to the suspected source
  • Determine attack rates
Step 4 - Rapid Search for All Cases
  • Active case finding (house-to-house, health records, lab reports)
  • Prepare a line listing of cases: name, age, sex, address, date of onset, symptoms, exposures
  • Define a case definition (clinical, laboratory, epidemiological criteria)
Step 5 - Descriptive Epidemiology (Person, Place, Time)
  • Time: Draw the epidemic curve (histogram of cases by time of onset)
    • Helps distinguish common-source vs. propagated epidemic
  • Place: Spot map of cases - identify geographic clustering
  • Person: Attack rates by age, sex, occupation, food consumed, etc.
Step 6 - Formulate a Hypothesis
  • Based on descriptive data, formulate a hypothesis about the source, mode of transmission, and causative agent
  • Example: "The epidemic is due to contaminated water from the common well"
Step 7 - Test the Hypothesis (Analytical Study)
  • Conduct a case-control study or cohort study to test the hypothesis
  • Calculate attack rates in exposed vs. unexposed groups
  • Calculate Odds Ratio or Relative Risk
Step 8 - Environmental Investigation
  • Collect environmental samples (water, food, air)
  • Inspect sanitation, food handling, water supply
  • Lab testing of samples for the causative agent
Step 9 - Institute Control Measures
  • Do NOT wait for all steps to be complete before implementing control
  • Control measures directed at:
    1. Reservoir/source (eliminate contaminated food/water)
    2. Route of transmission (disinfection, isolation)
    3. Susceptible host (vaccination, prophylaxis)
Step 10 - Prepare and Submit Report
  • Prepare a complete epidemiological report including findings, conclusions, and recommendations
  • Report to appropriate public health authorities
  • Implement measures to prevent future recurrence

Q8. Define re-emerging infections with examples. Explain the factors responsible for re-emergence of infectious disease.

Definition

Re-emerging infections are infections that were once of public health importance but had declined significantly, and have since reappeared (re-emerged) as a significant threat to public health. They may be newly resistant to antibiotics/antivirals or appear in new geographic areas or new populations.
Examples of Re-emerging Infections:
  1. Tuberculosis - re-emerged globally due to HIV co-infection and drug resistance (MDR-TB, XDR-TB)
  2. Cholera - periodic re-emergence, e.g., Latin America 1991 pandemic (new O139 strain)
  3. Dengue - dramatic global re-emergence since 1970s; now endemic in 100+ countries
  4. Malaria - resurgence in areas previously under control due to drug resistance (chloroquine-resistant P. falciparum) and insecticide-resistant mosquitoes
  5. Diphtheria - re-emerged in former Soviet Union states in 1990s after vaccination programme collapse
  6. Yellow fever - re-emerging in Africa and South America
  7. West Nile fever - spread to North America
  8. Chikungunya - re-emerged in Indian Ocean islands and India in 2005-06
  9. Measles - re-emerging in countries with declining vaccination coverage
  10. Rabies - persists in new geographic areas

Factors Responsible for Re-emergence:

1. Microbial/Biological Factors:
  • Development of antimicrobial resistance (MDR-TB, drug-resistant malaria, MRSA)
  • Genetic mutations and evolution of new strains with increased virulence
  • Emergence of new variants/serotypes evading existing immunity
2. Host/Human Factors:
  • Decline in vaccination coverage - loss of herd immunity allows resurgence of vaccine-preventable diseases
  • Immunosuppression - HIV/AIDS pandemic led to re-emergence of TB, PCP, CMV, etc.
  • Increased susceptible populations - elderly, organ transplant recipients, cancer patients on chemotherapy
  • Human behaviour - unsafe sexual practices, intravenous drug use
3. Environmental Factors:
  • Climate change - global warming extends geographic range of vector mosquitoes (Aedes aegypti, Anopheles)
  • Deforestation and ecological changes bring humans into contact with new animal reservoirs
  • Natural disasters (floods, earthquakes) disrupt sanitation, causing waterborne disease resurgence
4. Social and Economic Factors:
  • Poverty and malnutrition increase susceptibility and impair immunity
  • Urbanization and overcrowding facilitate spread
  • Conflict and civil unrest - displace populations, disrupt health services and vaccination programmes
  • Collapse of public health infrastructure (e.g., Soviet Union breakup -> diphtheria re-emergence)
5. International Travel and Trade:
  • Mass international travel spreads infections across continents rapidly
  • International trade in animals and animal products can introduce infections to new regions (e.g., foot-and-mouth disease, avian influenza)
6. Iatrogenic Factors:
  • Inappropriate antibiotic use drives antimicrobial resistance
  • Nosocomial infections
  • Blood transfusion and organ transplantation can spread emerging infections
7. Technological and Industrial Factors:
  • Changes in food production and processing (large-scale food industry increases risk of food-borne outbreaks)
  • Water supply changes

Q9. Discuss common-source epidemics with examples.

Common-Source Epidemics

A common-source epidemic occurs when a group of persons are all exposed to a common infectious agent, toxin, or chemical from a single source. The exposure may be simultaneous or continuous/intermittent.

Types:

A. Common-Source, Single Exposure (Point-Source) Epidemic

  • All persons are exposed to the agent briefly and simultaneously at one point in time
  • All cases develop within one incubation period of the disease
  • Epidemic curve: rises and falls rapidly, sharp single peak, NO secondary waves
  • The curve is explosive with clustering of cases in a narrow time interval
  • Median incubation period helps identify the probable causative agent
Features:
  1. Epidemic curve rises and falls rapidly
  2. No secondary waves
  3. All cases develop within one incubation period
  4. Sharp, high single peak
Classic Examples:
  • Food poisoning (e.g., staphylococcal food poisoning at a wedding banquet - all guests who ate the contaminated food develop illness within 1-6 hours)
  • Salmonella outbreak from contaminated eggs at a common meal
  • Cholera from a contaminated common water source (John Snow's Broad Street pump, London 1854)
  • Hepatitis A from a contaminated water supply
  • Bhopal gas tragedy (1984) - exposure to methyl isocyanate gas from Union Carbide plant (non-infectious common-source)
  • Minamata disease - mercury poisoning from fish in Minamata Bay, Japan (environmental common-source)

B. Common-Source, Continuous/Multiple Exposure Epidemic

  • Exposure to the agent is prolonged or intermittent over a period of time
  • Cases continue to occur over a period longer than one incubation period
  • Epidemic curve is more spread out and plateau-shaped
  • Ends when source is identified and removed
Examples:
  • Typhoid outbreak from a contaminated piped water supply over weeks
  • Legionnaires' disease from contaminated air-conditioning cooling towers over several weeks

Distinguishing Features from Propagated Epidemics:

FeatureCommon-sourcePropagated
SourceSingle common sourcePerson to person / vector
Curve shapeSharp rise, rapid fall (point-source)Multiple waves
DurationShort (1 incubation period)Prolonged
ExamplesFood poisoning, choleraMeasles, influenza, plague

Q10. Discuss the measures to evaluate a screening test.

Screening Test Evaluation

A screening test is applied to apparently healthy (asymptomatic) persons to detect those likely to have the disease, who are then referred for definitive diagnosis.
The performance of a screening test is evaluated using the following measures, derived from a 2x2 contingency table:
Screening TestDisease PresentDisease AbsentTotal
Positivea (True Positive)b (False Positive)a+b
Negativec (False Negative)d (True Negative)c+d
Totala+cb+dN

1. Sensitivity

  • Definition: Ability of the test to correctly identify ALL those who HAVE the disease (True Positives)
  • "How good is the test at detecting disease when it IS present?"
  • Formula: Sensitivity = a / (a+c) x 100
  • High sensitivity = few false negatives; good for "ruling OUT" disease (SnNout)
  • Example: If sensitivity = 90%, then 90% of diseased people test positive, 10% give false negatives

2. Specificity

  • Definition: Ability of the test to correctly identify those who do NOT have the disease (True Negatives)
  • "How good is the test at correctly calling healthy people negative?"
  • Formula: Specificity = d / (b+d) x 100
  • High specificity = few false positives; good for "ruling IN" disease (SpPin)
  • Example: If specificity = 90%, then 90% of non-diseased people test negative, 10% give false positives

3. Predictive Value of a Positive Test (PPV / Positive Predictive Value)

  • Definition: The probability that a person with a POSITIVE test result actually HAS the disease
  • Formula: PPV = a / (a+b) x 100
  • Affected by prevalence of disease in the population - higher prevalence = higher PPV
  • Clinically important: tells the clinician how likely a positive result is a true positive

4. Predictive Value of a Negative Test (NPV / Negative Predictive Value)

  • Definition: The probability that a person with a NEGATIVE test result truly does NOT have the disease
  • Formula: NPV = d / (c+d) x 100
  • High NPV means you can confidently rule out disease in those who test negative

5. False-Negative Rate

  • Formula: c / (a+c) x 100
  • = 1 - Sensitivity
  • Proportion of diseased people missed by the test

6. False-Positive Rate

  • Formula: b / (b+d) x 100
  • = 1 - Specificity
  • Proportion of non-diseased people incorrectly labelled as having disease

7. Yield

  • Number of previously unrecognised cases identified by the screening test
  • Depends on sensitivity of the test, prevalence of disease, and proportion of population screened

8. Likelihood Ratio

  • Likelihood Ratio Positive (LR+) = Sensitivity / (1 - Specificity)
  • Combines sensitivity and specificity into one measure; LR+ >10 strongly supports diagnosis

Trade-off Between Sensitivity and Specificity:

  • As the cut-off for a positive test is lowered: sensitivity increases, specificity decreases
  • As cut-off is raised: sensitivity decreases, specificity increases
  • ROC curve (Receiver Operating Characteristic curve) is used to select the optimal cut-off point

Factors Affecting Predictive Value:

  • Prevalence (pre-test probability): Increasing prevalence increases PPV; decreasing prevalence increases NPV
  • This is why mass screening of low-prevalence populations gives many false positives

All answers based on Park's Textbook of Preventive and Social Medicine (23rd Ed.)
attachment
attachment

Answer the question for 3marks psm

Finding Sources
Finding Sources
Finding Sources
Reading File
Reading File
Reading File
Reading File
Finding Sources
Reading File
Reading File
Reading File
Reading File
Reading File
Finding Sources
Reading File
Reading File
Reading File
Reading File
Reading File
I now have all the content. Here are concise, exam-ready 3-mark answers for all questions:

PSM Short Answer Questions (3 Marks Each)


Q11. Enumerate the characteristics of an ideal indicator (health indicator)

An ideal health indicator should have the following characteristics (Park's PSM):
  1. Valid - should actually measure what it is supposed to measure
  2. Reliable and Objective - answers should be the same if measured by different people in similar circumstances
  3. Sensitive - should be sensitive to changes in the situation concerned
  4. Specific - should reflect changes ONLY in the situation concerned (not affected by other factors)
  5. Feasible - should have the ability to obtain the data needed
  6. Relevant - should contribute to the understanding of the phenomenon of interest
In reality, few indicators comply with ALL criteria. Health measurement is therefore conceived in terms of a profile employing many indicators, not a single one.

Q12. Disability Adjusted Life Years (DALY)

Definition: DALY is a measure of overall disease burden, expressed as the number of years lost due to ill-health, disability or early death. Originally developed by Harvard University for the World Bank in 1990; adopted by WHO in 2000.
Formula: DALY = YLL + YLD
  • YLL (Years of Life Lost) - calculated from the number of deaths at each age multiplied by the expected remaining years of life according to a global standard life expectancy
  • YLD (Years Lost to Disability) - number of incident cases multiplied by average duration of disease and a severity weighting factor (0 = perfect health, 1 = dead)
Key points:
  • One DALY = one year of healthy life lost
  • Japanese life expectancy is used as the standard for measuring premature death
  • A higher DALY score = greater burden of disease
  • Combines both fatal and non-fatal disabling conditions in a single measure
  • Example: 1990 WHO report showed 5 of 10 leading causes of disability were psychiatric conditions - something mortality statistics alone would miss

Q13. Explain statistical averages with examples

Statistical averages are values that describe the central tendency of a distribution. There are three main types:
1. Mean (Arithmetic Mean)
  • Sum of all values divided by the number of observations
  • Formula: x̄ = Σx / n
  • Example: DBP of 10 individuals = 83, 75, 81, 79, 71, 95, 75, 77, 84, 90. Total = 810. Mean = 810/10 = 81.0 mmHg
  • Advantage: Easy to calculate; most useful average
  • Disadvantage: Influenced by extreme values (outliers)
2. Median
  • The middle value when data is arranged in ascending/descending order
  • Not affected by extreme values
  • Example: DBP of 9 individuals arranged in order: 71, 75, 75, 77, 79, 81, 83, 84, 95 → Median = 79 mmHg
  • Used when data is skewed
3. Mode
  • The most frequently occurring value in a distribution
  • Example: In the above series, 75 appears twice - it is the mode
  • Used for categorical data or when the most common value is required

Q14. Discuss the strategies for Polio Eradication in India

India was certified polio-free on 27th March 2014.
Key strategies used:
1. Pulse Polio Immunization (PPI):
  • National Immunization Days (NIDs) - all children under 5 years given OPV on two fixed days, irrespective of previous immunization status
  • Sub-national immunization days (SNIDs) in high-risk areas
  • "Two drops of oral polio vaccine = Polio protection"
2. Sustain Routine Immunization:
  • High levels of routine OPV coverage maintained through Universal Immunization Programme (UIP)
3. Acute Flaccid Paralysis (AFP) Surveillance:
  • All AFP cases in children under 15 years mandatory reported immediately
  • Stool samples collected for virus isolation within 14 days of onset
  • 60-day follow-up for residual paralysis
  • AFP rate target: ≥2/100,000 children under 15 years
4. Mopping Up:
  • Door-to-door immunization in high-risk pockets where wild poliovirus still circulating
  • Last stage of polio eradication strategy
5. Introduction of IPV:
  • Inactivated Polio Vaccine (IPV) introduced along with bivalent OPV (bOPV) to boost immunity against all 3 serotypes, especially type 2 (switched from tOPV to bOPV in April 2016)
6. Outbreak Response:
  • Even a single confirmed case treated as an outbreak; preventive measures initiated within 48 hours of notification

Q15. Rotavirus Diseases

Rotavirus is the most common cause of severe acute gastroenteritis (diarrhoea) in infants and young children worldwide.
Disease caused:
  • Watery diarrhoea (usually 3-8 loose stools/day), vomiting, fever
  • Leading cause of diarrhoeal death in under-5 children globally
  • Affects children between 6 months to 2 years predominantly
  • Spread by fecal-oral route; highly contagious
  • Does NOT have an animal reservoir in the usual sense - primarily human-to-human
Vaccines (Rotavirus vaccine):
  • Two licensed oral, live attenuated vaccines:
    1. Rotarix™ (monovalent, human): 2 doses at ~2 and 4 months of age; complete by 24 weeks
    2. RotaTeq™ (pentavalent, bovine-human reassortant): 3 doses at 2, 4, and 6 months; complete by 32 weeks
  • Important: First dose should NOT be given after 12 weeks - risk of intussusception increases
  • Both vaccines show good safety and efficacy in clinical trials
  • Introduced in India's UIP (Universal Immunization Programme) in phases

Q16. Describe the biological effects of radiation exposure

The biological effects of ionizing radiation are classified as:
A. Somatic Effects (affect the irradiated individual):
DoseEffect
< 5 radNo observable effect
5-50 radSlight blood changes on medical evaluation
50-150 radBlood changes + nausea, fatigue, vomiting
150-1100 radSevere blood changes; bone marrow destroyed; ~50% die at 300-500 rad within 60 days; called Acute Radiation Syndrome
1100-2000 rad100% death within 1-2 weeks; GI system destroyed
>2000 radCertain death; CNS involvement; brain and muscles fail
B. Genetic Effects (affect offspring):
  • Injury to chromosomes - chromosome mutations and point mutations
  • Effects manifest in future generations
  • Include developmental abnormalities, heritable mutations
Summary of categories:
  • Somatic: Radiation sickness, Acute Radiation Syndrome, increased cancer risk (leukaemia, solid tumours), cataracts
  • Genetic: Chromosome mutations (deletions, translocations), point mutations (gene level)
High doses kill cells causing organ damage; low doses over long periods cause chronic effects including malignancy.

Q17. Discuss the strategies for prevention and control of air pollution

(WHO recommended strategies - Park's PSM)
1. Containment:
  • Prevent toxic substances from escaping into ambient air
  • Engineering methods: enclosure, ventilation, air cleaning
  • Use of "arresters" (filters, scrubbers) for removal of air contaminants
2. Replacement:
  • Replace a polluting technology with one that does not cause pollution
  • Increased use of electricity, solar power, natural gas, central heating instead of coal
  • Use of de-leaded petrol (India also using unleaded petrol)
3. Dilution:
  • Valid as long as within the self-cleaning capacity of the environment
  • Some air pollutants are removed by vegetation - establishment of green belts between industrial and residential areas
  • Limitation: atmosphere can be overburdened beyond self-cleaning capacity
4. Legislation:
  • Clean Air Acts in many countries
  • India: "The Air (Prevention and Control of Pollution) Act, 1981"
  • Covers: height of chimneys, smokeless zones, standards for ambient air quality
5. International Action:
  • WHO international network of laboratories for monitoring and study of air pollution
  • Two international centres at London and Washington; others at Moscow, Nagpur, Tokyo
6. Air Disinfection (for indoor/hospital air):
  • Mechanical ventilation
  • Ultraviolet radiation (in OTs and infectious disease wards)
  • Chemical mists (triethylene glycol vapours)
  • Dust control

Q18. Enumerate the diseases transmitted by ticks

Ticks (Order Acarina) are ectoparasites that suck blood and transmit the following diseases:
Diseases transmitted by Hard Ticks (Ixodidae):
  1. Tick Typhus (Rocky Mountain Spotted Fever, Indian Tick Typhus) - Rickettsia spp.; vector: Haemaphysalis, Dermacentor
  2. Viral Encephalitis (Russian Spring-Summer Encephalitis, Kyasanur Forest Disease)
  3. Haemorrhagic Fever (Crimean-Congo Haemorrhagic Fever)
  4. Tularaemia - Francisella tularensis; vector: Dermacentor andersoni
  5. Tick Paralysis - due to toxin injected by feeding tick
  6. Human Babesiosis - Babesia spp. (malaria-like illness)
  7. Lyme Disease - Borrelia burgdorferi; vector: Ixodes ticks
Diseases transmitted by Soft Ticks (Argasidae):
  1. Relapsing Fever - Borrelia spp.; vector: Ornithodoros moubata
In India specifically:
  • Indian Tick Typhus (Tick-borne rickettsiosis) - caused by Rickettsia conorii
  • Kyasanur Forest Disease (KFD) - vector: Haemaphysalis spinigera

Q19. UNICEF

Full name: United Nations International Children's Emergency Fund (retained initials though name changed to "UN Children's Fund" in 1953)
Establishment: 1946 by UN General Assembly, originally to rehabilitate children in war-ravaged countries
Headquarters: United Nations, New York Regional office for South Asia: Kathmandu, Nepal (covers India, Pakistan, Sri Lanka, Bangladesh, Nepal, Afghanistan, Bhutan, Maldives) Governance: 36-nation Executive Board
Functions/Activities:
  1. Child Health: Supports vaccine production; assisted India's BCG programme from inception; environmental sanitation (safe water); primary health care for mothers and children
  2. Child Nutrition: Funds protein-rich food supplements; "applied nutrition" programmes with FAO
  3. Immunization: Emphasis on routine immunization, EPI, Vitamin A supplementation
  4. Safe Water and Sanitation: Rural water supply provision
  5. MCH: Maternal and child health services; family planning
Works in collaboration with: WHO, UNDP, FAO, UNESCO
Current focus (UNICEF approach):
  • "Whole child" concept - addressing both immediate health/nutrition AND long-term development
  • Known as "country health programming"
  • Integrated approach: community participation + primary health care

Q20. Koplik's Spots

Definition: Koplik's spots are small, bluish-white spots on a red base (like table salt crystals) that appear on the buccal mucosa opposite the first and second lower molars in measles.
Features:
  • Appear 1-2 days before the rash (in the prodromal phase, around day 12-13 after exposure)
  • Smaller than the head of a pin
  • Located on buccal mucosa (inner cheek), opposite lower molar teeth
  • Pathognomonic of measles - their presence clinches the diagnosis of measles
Clinical significance:
  1. Diagnostic value: Only clinical sign specific to measles; confirms diagnosis BEFORE the rash appears
  2. Appear during the prodromal stage (fever, coryza, cough, red eyes)
  3. Disappear soon after the rash appears
  4. Diagnosis of measles can be made at the Koplik's spot stage - allows early isolation and contact tracing
When to look for them: Any child presenting with fever + coryza + cough + red eyes (the 3 Cs + fever) in the prodromal phase.

All answers based on Park's Textbook of Preventive and Social Medicine (23rd Edition)
This is a shared conversation. Sign in to Orris to start your own chat.