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9.1 DISEASE: CLASSIFICATION, DESCRIPTION, MEASUREMENT, DIAGNOSIS, and PROGNOSIS
9.1.1 Classification of Disease
9.1.2 Disease Description
9.1.3 Disease Measurement
9.1.4 Disease Diagnosis
9.1.5 Disease Prognosis
9.2 DISEASE DETERMINANTS
9.2.1 Concepts of Disease Causation
9.3.2 Concept of Exposure
9.2.3. Disease Determinants
9.2.4 Variation of Disease Risk with Age
9.3 DISEASE CONTROL, ERADICATION, AND PREVENTION
9.3.1 Control
9.3.2 Eradication
9.3.3 Prevention
9.3.4 Preventive Medicine: Legal Basis
9.3.5 Preventive Medicine: Moderation, Balance and Equilibrium
9.4 DISEASE SURVEILLANCE
9.4.1 Definition
9.4.2 History of Surveillance
9.4.3 Objectives, Methods, and Scope
9.4.4 Surveillance System
9.4.5 Data Collection, Analysis, and Interpretation
9.5 DISEASE SURVEILLANCE
9.5.1 Definition, Objectives, Organization, And Benefits
9.5.2 Characteristics of Disease and Screening Tests
9.5.3 Epidemiologic Evaluation of Screening Programs
9.5.4 Cost Benefit Analysis of Screening Programs
9.5.5 Ethical Issues
UNIT 9.1
DISEASE CLASSIFICATION, DESCRIPTION, MEASUREMENT, DIAGNOSIS, and PROGNOSIS
Learning Objectives:
· Disease description: symptoms, signs
· Disease classification criteria
· Time characteristics of disease: trends, duration, natural history
· Place characteristics of disease: urban/rural, boundaries (political & natural), institutions
· Person characteristics of disease: age, gender, race/ethnicity, SES, marital status
· Epidemicity: epidemic, endemic, pandemic, epidemic curve, slow and acute epidemics, visibility of the epidemic
· Measures of disease occurrence and excess disease risk
Key Words and Terms:
· Disease classification
- Disorder classification
- Epidemic disease
- Ethnicity
- Etiology of disease
- Heredity
- Infection
- Morbidity
- Mortality
- Nomeclature of disease
- Nosology
- Risk ratio
- Risk difference
- Incidence rate ratio
- Incidence rate difference
- Odds ratio
- Cumulative incidence
- Morbidity
- Mortality
UNIT OUTLINE
9.1.1 CLASSIFICATION OF DISEASE
A. History of disease classification
B. Purpose of disease classification
C. Classification criteria
D. Commonly used classifications
International classification of disease
9.1.2 DISEASE DESCRIPTION
A. Purpose of disease description
B. Time characterization of disease:
C. Place characterization of disease:
D. Person characterization of disease:
E. Clustering and epidemics
9.1.3 DISEASE MEASUREMENT
A. States and Events
B. Incidence
C. Prevalence
D. Measures of Excess Disease Occurrence
E. Measures of Disease Impact & Measures of Survival
9.1.4 DISEASE DIAGNOSIS
A. Disease Identification
B. Symptoms and Signs
C. Diagnostic Tests
9.1.5 DISEASE PROGNOSIS
A. Objective Assessment of Prognosis
B. Study Design for Prognostic Factors
C. Parameters Used in Study of Prognosis
9.1.1 CLASSIFICATION OF DISEASE
A. HISTORY OF DISEASE CLASSIFICATION
In 1853 William Farr (1807-1883) introduced standard nomenclature for causes of death. In 1893 J Bertillon (1851-1922) introduced a new classification of causes of disease. In 1946 WHO introduced an International Classification of Diseases, Trauma, and Cause of Death. In 1975 the 9th revision of ICD was published. The 10th version was published in 1992.
B. PURPOSE OF DISEASE CLASSIFICATION
Disease classification serves the following five functions: explanation & description, prediction of disease course, prognosis, planning treatment, and disease prevention.
C. CLASSIFICATION CRITERIA
4 types of classification criteria can be identified: manifestational, causal, abstract, operational or pragmatic. Manifestational criteria, symptoms and signs, are used in the absence of knowledge of cause. Causal criteria are based on certain knowledge of cause examples: birth trauma, silicosis, syphilis, lead poisoning, AIDS. Abstract criteria are not natural and are a product of human intellectual effort often with little practical use. Operational/pragmatic criteria, like the International Classification of Diseases, are practically-oriented but may not have good theoretical foundation.
D. COMMONLY USED CLASSIFICATIONS
In practice the following 5 methods are used in classification or cross-classification of diseases: etiologic agent or force, disease process, organ system affected, method of transmission, and portal of entry. Etiologic agent/force of morbidity can be microbiological agents, genetic anomalies, metabolic disorders, environmental factors (water and air pollution), human behavior, stress (anxiety and depression), or traumatic injury. In practice most diseases are multi-causal. Disease process may be neoplastic, metabolic, infectious, or inflammatory. The organ system involved may be cardio-vascular, respiratory, nervous, genital, and urinary. The method of transmission may be water-borne, food-borne, air-borne, vector-borne, and STD. Portals of entry are the respiratory, GIT, and parenteral routes.
Medical test books use their own classification of diseases designed to suit their pedagogical approach and the sequence of presenting information.
E. INTERNATIONAL CLASSIFICATION OF DISEASE
The International Classification of Diseases (ICD) was evolved by the World Health Organization to be used uniformly by all countries in reporting disease statistics. It makes possible an international comparison of disease occurrence. The 10th version, called the International Statistical Classification of Diseases and Related Health Conditions (ICD-10), has 31 chapters listed as follows. Chapter I (A0-B99): Certain Infections and Parasitic Diseases. Chapter II (C00-C97): Neoplasms. Chapter III (D50-D89): Diseases of the Blood Forming organs and Certain Disorders involving the Immune Mechanism. Chapter IV (E00-E90): Endocrine, nutritional, and metabolic diseases. Chapter V (F00-F99): Mental and Behavioral Disorders. Chapter VI (G00-G99): Diseases of the Nervous System. Chapter VII (.H00-H69): Diseases of the Eye and Adnexa. Chapter VIII (H60-H95): Diseases of the Ear and Mastoid process. Chapter IX (I00-I99): Diseases of the Circulatory System. Chapter X (J00-J99): Diseases of the Respiratory System. Chapter XI (K00-K98): Diseases of the Digestive System. Chapter XII (L00-L99): Diseases of the Skin and sub-cutaneous tissue. Chapter XIII (M00-M99): Diseases of the Musculoskeletal System and Connective Tissue. Chapter XIV (N00-N99): Diseases of the Genitourinary System. Chapter XV (O00-O99): Pregnancy, Childbirth, and the Puerperium. Chapter XVI (P00-P96): Certain Conditions Originating in the perinatal period. Chapter XVII (Q00-Q99): Congenital Malformations, Deformations, and Chromosomal Abnormalities. Chapter XVIII (R00-R99): Symptoms, Signs, and Abnormal Clinical and Laboratory Findings Not Elsewhere Classified. XIX (S00-T98): Injury, Poisoning, and Certain Other Consequences of External Causes. XX (V01-Y99): External Causes of Morbidity and Mortality. Chapter XXI (Z00-Z99): Factors Influencing Health Status and Contact with Health Services. (page 46 John M Last: Public Health and Human Ecology. 2nd edition. Prentice Hall International, Inc ? year).
9.1.2 DISEASE DESCRIPTION
A. PURPOSE OF DISEASE DESCRIPTION
Disease description serves to answer the following questions: what, why, when, how, where, and who of a disease.
B. TIME CHARACTERIZATION OF DISEASE:
TWO TYPES OF TIME DESCRIPTION
Time can be described as calendar time or cohort time. Calendar time is time indicated or measured by days, weeks, months, seasons, and years. Calendar time is measured on the interval scale. The interval scale has an arbitrary zero and admits both positive and negative values. Cohort time is measured as time elapsed since a significant event. Examples of such events are: time since birth, age; time on the study; time since admission to hospital; and time since start of treatment. Cohort time is measured on the ratio scale. Zero on this scale has a biological significance; negative values have no meaning.
TIME TRENDS
Five different types of time trends can be described: biorhythm, periodicity, steps, linear, and curvilinear trends. Biorhythm is the daily alternation of biological phenomena referred to also as diurnal or nocturnal variation. Examples of the diurnal and nocturnal variations are the cycles of sleep and wakefulness, secretion of ACTH, and secretion of melatonin. Periodicity can be cyclic (monthly, annual, seasonal) or accidental. A distinction is made between secular trends that occur over several years in a predictable fashion and recent trends that may not be repeated in a predicable manner. The Fourier series of polynomial analysis can be used for analysis of cyclic events. Steps are short-term trends. Linear trends show a clear and definable relation between time and other variables. The linear trend may increase or decrease. Regression equations describe linear trends well. Curvilinear trends require more sophisticated descriptions using polynomial functions.
DURATION
Based on their duration, diseases can be described as acute, sub-acute, chronic, and acute exacerbations of chronic conditions. The decision of what time period is acute or chronic is arbitrary and varies from disease to disease. Acute and chronic disease: There is inaccurate perception that acute diseases are infectious and chronic diseases are non-infectious. In acute diseases, symptoms and signs are disposed of within 3 months and those who survive have complete recovery. In chronic diseases symptoms and signs continue for longer than 3 months and sometimes for life. Recovery is slow and is not complete. Acute disease can be communicable such as the common cold, pneumonia, mumps, measles, pertussis, typhoid, and cholera. They may be non communicable such as appendicitis, poisoning and traumatic injury. Chronic diseases may be communicable such as AIDS, Lyme disease, tuberculosis, syphilis, and rheumatic fever. Chronic diseases may be non communicable such as diabetes mellitus, coronary artery disease, ostoarthritis, and alcoholic liver cirrhosis.
NATURAL HISTORY
The following table summarizes the natural history of disease.
Stage | Preceding event | Contemporary events | Prevention |
Susceptibility | - | - | Primary |
Sub-clinical Disease | Exposure | Pathological changes in incubation | Secondary |
Clinical Disease | Symptom Onset | Diagnosis | Secondary |
Recovery, disability, or death | - | Treatment | Tertiary |
Source: Epidemiology Made Simple Table 2.1 page 21.
Disease can be described on a time line that traces its course of development. The time course of disease evolution is referred to as natural history. Natural history describes disease progression from the operation of the causative agent through clinical manifestations to termination. Termination may be by death, cure, or chronic complications. Disease progression is through the following stages. The pre-pathogenesis stage is the stage of operation of the risk factors. The pre-clinical stage, disease is already initiated but here are no symptoms or signs. In the clinical stage symptoms and signs appear. In the chronic stage there are complications and permanent deformities. Three time periods or intervals can be described in the natural history of disease: induction period, incubation period, latent period. The induction period is the time from causal action of the component cause to disease initiation. A co-factor may trigger the eventual disease onset. There is a different induction period with respect to each component cause. The latent period is the time between disease initiation and disease detection. The concept of latent period complicates the analysis of time-related data because it is not possible to pin -point the start of the disease process. The induction period can not be reduced. The latent period can be reduced by methods of early detection of disease.
EVENTS
Diseases can be described in relation to significant events. Significant life events include birth, death, marriage, divorce, school entry, menarche, and menopause. Point events like an earthquake or a social revolution occur for a very brief time and stop. A point event may, however, have an extended after-math like the atomic bombs whose effects were felt long after the point event itself. Some events have prolonged exposure with a start and an end. The start or end may be well defined or may be poorly defined. A good example of this type of event is air pollution.
C. PLACE CHARACTERIZATION OF DISEASE:
DISEASE AND PLACE OF RESIDENCE
Since the beginning of history, humans have known that some diseases are associated with certain places of residence. Disease can therefore be described by place of residence. The commonly used classifications are described below.
URBANIZATION
The following classifications are usually used: rural, urban, sub-urban, and slums/shacks (septic fringe). There are differences in socio-economic status, air pollution levels, nature of soil pollution, and availability of health facilities. These differences determine patterns of disease transmission.
BOUNDARIES
There are two types of boundaries: political and natural. Political boundaries separate administrative areas like the country, the district, and the city. Natural boundaries are valleys, mountains, rivers, lakes, oceans and other physical barriers to human movement. The significance of boundaries is that they restrict movement of people and therefore affect the patterns of disease transmission. Boundaries may limit the movement of disease causative agents when policies or the eco-system on one side of the boundary enhance or hinder a certain mode of disease transmission.
INSTITUTIONS
The following institutions are often used in disease description: hospital, home, school, factory, farm, and outer space. The institutional environment or the institutional activities define the type of disease found among the inmates of the institution.
MAPPING DISEASE
Geographical display and analysis can be used to relate disease phenomena to place. The following methods are used: (a) chloropeth mapping: incidence and prevalence are computed for various places and are shown on the map using different coloration (b) isopleth mapping uses contours of equal disease parameters and need not follow geo-political boundaries and can be based on sample data (c) map-on-map technique is when the map of disease distribution is superimposed on a map of risk factor distribution (d) computer displays of increasing sophistication are being developed and used.
PROXIMITY ANALYSIS
This is the of distance relations between cases of disease and the hazard. Two methods are used: the maximum ratio between the observed and the expected and the Kolmogrorov-Smirnoff statistic that tests the maximum distance between two curves.
INTERNATIONAL COMPARISONS
Different countries publish health statistics that show a wide variation in disease patterns. However gross differences especially at the country level can be misleading.
D. PERSON CHARACTERIZATION OF DISEASE:
INDIVIDUAL VARIATION
Individual variation in exposure and susceptibility varies by heredity, age, sex, SES, marital status, and ethnicity/race. Heredity operates through genetic endowment from parents ort the interaction of genetic and environmental factors in causing disease. Susceptibility to disease is high at both ends of the age spectrum due to immune incompetence. The newborn and infants have an undeveloped immune system. The immune system of the elderly in the geriatric age has undergone degenerative changes. Adolescents experience a high rate of some diseases because of their high-risk life-style and the rapid growth of the pubertal spurt. Females have disease experience different from males because of a less hazardous life style, different hormonal and reproductive functions. Females transmit X-linked hereditary diseases but do not suffer from them. Sometimes the male-female difference in disease susceptibility may be due to having different organs. Disease of the ovary and the uterus are found only in females. Disease of the prostate and testis are found only in males. SES affects disease susceptibility by determining the place of residence and hence the exposure to environmental causes of disease. Life-style, under-nutrition, and over-nutrition, type of work and hence the type of occupational exposure, and place of residence are determined by SES. Marital status is very important in that it determines psychological stability, an important ingredient in disease-related life-style. Marriage may also encourage a monogamous sexual life that prevents sexually-transmitted disease.
AGE
There are distinct disease patterns for different age groups. Diseases of childhood such as causes of IMR are different from diseases of old-age such as Alzheimer's disease. Some diseases have bimodal peaks at young and later age eg Hodgkin's Disease and testicular tumors. There is a cohort effect in disease occurrence that may translate into secular trends.
SEX
The death rate is higher for males at all ages: in utero, neonatal, and later life. The reasons for higher male mortality in later life are: smoking, accidents, firearms, and AIDS. If measured by utilization of health services, morbidity is higher for females for all diseases. The gender ratio at birth must be taken into consideration when interpreting gender-specific mortality or morbidity rates. The gender ratio at birth varies by race, birth order, and over time.
SES
Socio-economic status may be associated with high disease risk or low disease risk depending on the type of disease.
ETHNIC GROUP/RACE
The differences in disease experience among the different ethnic groups reflect socio-economic, life-style, and cultural variations. The variation of disease risk by ethnicity has no genetic basis in most cases.
MARITAL STATUS
The happily-married and their children are generally healthier than the unmarried. The married have more psychological stability. They also have more economic security. Interpretation of the effect of marital status is rather complicated because it is possible that those people who are psychologically stable and have economic security get married. Marriage therefore is a consequence and not a cause.
E. CLUSTERING and EPIDEMICS
INTERACTIONS AMONG PERSON, PLACE AND TIME CHARACTERISTICS
Sophisticated descriptions are called for when describing phenomena involving 2 or 3 dimensions at the same time. There are three usual interactions: (a) place-time (b) time-person (c) person-place. These interactions can be modeled mathematically for easier description and understanding. Sophisticated statistical methods are also available for their analysis. We will illustrate the complex interactions by study of disease clusters and epidemics.
CLUSTERING
Definition: Clustering is excessive concentration of events at a point in time or a place. Disease clustering can be described in relation to time, place, both time and place, family, and household. Clustering in place and time usually indicates an infective cause. Clustering in a family may be due to contagious infection or genetic predisposition.
Testing for clustering in time: Clustering in time is a non-linear, non-cyclical, or non-random phenomenon. The Poisson distribution is used to analyze time clustering. Clustering in time can be tested for by dividing the time of observation into short intervals and counting the number of cases of disease per time interval. The distribution should follow a Poisson distribution under the null hypothesis of no clustering. Significance deviation from the null can be tested using a chi-square test.
Testing for clustering in place: Clustering in place can be tested for by counting numbers of cases occurring per administrative unit. The number of cases per unit should follow a Poisson distribution under the null hypothesis of no clustering. Significance deviation from the null can be tested using a chi-square test.
Testing for clustering in both time and place: Description of the phenomenon of a moving cluster is quite complex because the clustering occurs in both the time and place dimensions. Testing for clustering in both time and place is more complicated. Place-time clusters can be analyzed using 2 methods: (a) the Knox method based on contingency tables (b) the Mantel-Haenszel method relating time and space intervals. Criteria of closeness are determined based on both time and place. A 4-fold table is constructed showing time (adjacent/not adjacent) and place (adjacent/not adjacent). The Poisson distribution should follow the null hypothesis of no clustering. Significant deviation from the null can be tested for using a chisquare test.
Cluster investigations are made difficult by several factors: rarity of events, vague case definitions, lack of a population base for rate computations, weak associations, multiple risk factors, long induction periods, and multiple comparisons. Cluster investigation starts by careful data collection about disease occurrence. This is followed by careful epidemiological investigation which includes defining the geographical area to be covered, the case definition, confirmation of case diagnosis by using pathological and clinical data, computing disease rates and ratios, and a study design to investigate etiology.
Comparison of outbreak and cluster investigation: Outbreaks involve infectious diseases with definable transmissible agents. Clusters are non-communicable conditions with several risk factors some of which are not well established. Outbreak investigations are short measured in days and weeks whereas cluster investigations are longer measured in weeks or months. Exposure levels and effect estimates are high in outbreaks and low in disease clusters. Exposure period in outbreaks is acute being measured in hours of days whereas disease clusters are associated with chronic exposures measured in years or decades. Laboratory confirmation of disease and exposure is easy in outbreaks but difficult in disease clusters. The cause-effect relation is easy to establish in disease outbreaks and difficult in disease clusters. Disease outbreaks are usually investigated using retrospective cohort studies whereas disease clusters are investigated using case control studies.
DISEASE OUTBREAK
A disease outbreak is usually excessive diseased occurrence of a lesser degree than an epidemic. Investigation of an outbreak starts with determining that there is an excessive occurrence based on comparison of current disease rates with surveillance data. Disease diagnosis is then confirmed using laboratory techniques. A case definition is then developed so that a definitive count of cases can be made based on the definition. Disease occurrence is then described by its place, time, and person characteristics. The susceptible population at risk of the disease is then determined. Explanatory hypotheses on causality are developed and are tested in a systematic way. A comprehensive report is prepared. Control and preventive measures are instituted. Control may involve the pathogen, the chain of transmission or the host response. Control aimed at the pathogen involves removing the source of contamination, removing persons from exposure, inactivating the pathogen, treating isolating the infected persons. Transmission is interrupted by sanitation, sterilization, disinfection, vector control, and hygiene. Host response is modified by immunization or using prophylactic therapy.
EPIDEMICS
Definition: En epidemic represents a time-person-place interaction. An epidemic is defined as excessive frequency. Most epidemics in history occurred as acute dramatic events which made many forget the existence of slow but serious epidemics. Three terms should not be confused: endemic, epidemic, and pandemic. An endemic disease is one with high prevalence in an area. An epidemic is excessive incidence over a given usually brief period of time. The following epidemics were recorded in the US: polio epidemic in in 1916, St Louis encephalitis in 1975 that affected 1815 persons, Legionnaire’s disease in 1976 that affected 235 persons, the Guillain Barre syndrome epidemic following swine virus immunization in 1976, Toxic exposure from the Love Canal in 1979, the toxic shock syndrome in 1980 that affected 877 persons, plague in 1983 that affected 40 persons, Lyme disease in 1982-1983 that affected 872 persons, the encephalomyalgia syndrome in 1990, and the ongoing AIDS epidemic starting in 1981. A pandemic is an epidemic occurring simultaneously in widely separated geographical regions. An example of a pandemic was the influenza of 1918-1919 which started in France and spread to Spain , England and the rest the rest of Europe, China , and West Africa . The current AIDS epidemic is becoming an pandemic.
Types of epidemics: An epidemic may be point source if the origin is one person or one place. It is common source if more than one origin is involved. Transmission may be person to person or the outbreak may be propagated. Epidemic progression can be described as propagated when new infections are occurring or limited when infection is limited to the initial cases.
Visibility of an epidemic: Visibility of the epidemic in increased under the following five scenarios: the cases are few but the disease is rare, a large number of cases, a distinctive illness, a swift shift from the non-epidemic to the epidemic status, and disease of very short duration. Cholera, smallpox, and plague are examples of visible epidemics. An invisible epidemic may be missed in the following five situations: a slow epidemic, disease manifesting in an unfamiliar form, lack of systematic search for the disease (eg the thalidomide disaster), and inattentiveness (e.g. the London
Identification of an epidemic: The occurrence of an epidemic can be ascertained in 3 ways: studying changes in trend over time, comparing incidence in epidemic and non-epidemic places, and comparing disease incidence among population sub-groups of the same country. Investigating an epidemic must follow certain procedures. The diagnosis must be established. A case definition must be agreed on. Based on the diagnosis and case definition a determination is made whether an epidemic exists. The epidemic is then characterized by place, time, and person. A spot map showing cases can be drawn. Incidence rates can be computed by location. Clusters can be identified but care must be taken to distinguish real from chance clusters. Hypotheses are developed about the source and route of infection. The hypotheses are tested by laboratory studies and case control studies. The pattern of spread may be common source, propagated or a mixed pattern. A point source exposure may be one-time or sporadic. A common source exposure may be continuous. Control measures are then instituted and may include sanitation, prophylaxis, diagnosis and treatment, and vector control. Surveillance is continued in the post epidemic period.
EPIZOOTIC
An epizootic is an epidemic disease in animal populations. Epizootics can become epidemics in human populations for example the St Louis encephalitis started as an epizootic condition that became an epidemic. An enzootic is an endemic disease among animals.
EPIZOODEMIC
This is an epidemic involving both human and animal populations.
9.1.3 DISEASE MEASUREMENT
A. STATES and EVENTS
State is static measured as prevalence (point or period prevalence). Event involves a time dimension. An event is a change of state. Events are measured as incidence. The term incidence is used to refer to incidence rate and cumulative incidence.
B. INCIDENCE
INCIDENCE TIME, INCIDENCE NUMBER, and ABSOLUTE RATE
Incidence is a dynamic concept that measures risk, the force of morbidity or hazard. It is a measure that deals with random events and change in status. Incidence time is the time at which new disease occurs in a population for example age at death, time on treatment. Incidence time is always measured from a zero time. Incidence number is the number of new cases detected in the time interval. The term absolute rate is also used to refer to the number of new cases in a given time interval.
INCIDENCE RATE
The incidence rate (IR) is a basic measure of disease occurrence. Incidence rate (IR) = incident number/ total person-time. Person time is defined as the sum of the product of number of persons observed by the length of time that they are observed. IR can be computed based on the first ever episode. It can alternatively be computed as episode incidence which involves the first and subsequent events. The incident number considers only the first occurrence of disease. Person-time measures the time at risk. The time dimension can be chronological or can be the duration of time on study. Use of the concept of the steady state enables us to define IR using the mid-year population as follows: IR= # newly reported cases of a disease in a year / mid-year population. The incidence rate has a lower bound of zero but has no interpretable upper bound. The upper bound depends on the unit of measurement used for example an incidence rate of 100 per person-year is the same as 10,000 per person-century. The plot of the logarithm of the incidence rate against time indicates disease trend well. The definition of the incidence rate for an open population is different from that of a closed population. The incidence rate for an open population is referred to as incidence density, person-time rate, person-time incidence rate, force of morbidity, hazard rate, disease intensity, instantaneous risk, instantaneous probability, force of mortality, and force of morbidity. The situation of an open population is depicted in the figure below:
The computation of the 95% confidence intervals for the incidence rate varies according to the number of cases, n. If n<75, the Poisson distribution is used. If n < 75 <100, either the poisson of the normal distribution is used. For n>100 the normal distribution is used. There are alternatives to the incidence rate as defined above. For example we can describe the accident rate without reference to time as the number of accidents per person-mile. The reciprocal of an incidence rate is the waiting time until occurrence of the event of interest. The average waiting time until death, for example, is the waiting time until death.
CUMULATIVE INCIDENCE
Cumulative incidence, also called incidence proportion or attach rate, is defined over a given interval of time as the number of incident cases divided by the total number of the cohort observed at the start of the observation interval. Stated otherwise it is the proportion of those who become cases among those who entered the given time interval. It can also be defined as the number of new cases as a proportion of the susceptible population at the start of the observation. Cumulative incidence = summation over time of IR. CI is a probability and a measure of risk and can be considered as the average risk over the time interval.
COMPARISON OF INCIDENCE RATE AND CUMULATIVE INCIDENCE
Both the cumulative incidence (CI) and prevalence rates (P) are based on the incidence rate (IR) but are not reliable unless follow-up is for a very short period of time. When CI is low <0.1, CI is approximately equal to IR. IR is superior to CI in that competing causes of death operate on both the numerator and denominator of IR but only on the numerator of CI. IR is suitable for study of dynamic populations. IR has the advantage that person-time can be adjusted for the effects of censoring. CI can also be used for censored data if lifetable and actuarial methods are resorted to. CI is suited to study of acute diseases with restricted risk periods. It is also suitable for study of fixed cohorts.
SURROGATE MEASURES OF INCIDENCE
Mortality rates are readily available and are used as surrogates for incidence rates. Mortality is related to the important demographic parameter of life expectancy
C. PREVALENCE
Prevalence is a static concept that is a measure of state. It is a still-picture of the disease situation at a given point in time. Whereas incidence relates to events, prevalence relates to disease states at a point in time. The prevalence number is the number of cases of disease existing at the particular point in time. The prevalence proportion = # cases of illness at a particular time / # of individuals in the population at the same time. Prevalence proportion is also called prevalence rate or point prevalence. Prevalence is not a rate but a proportion; however the term prevalence rate has become so popular in medical literature that it will take long for this error to be corrected. Prevalence is measured in cross-sectional studies. Only one observation at one point in time is needed in the determination of prevalence.
Three types of prevalence are described in epidemiological literature: point, period, and lifetime prevalence. Point prevalence is a theoretical concept that assumes ability to count cases of illness at an infinitesimal short period of time. Period prevalence refers to counting the number of illnesses over a practically reasonable length of time. This must not be so long that there is a change in the status quo by death of cases or incidence of new ones. Period prevalence is more stable and therefore more useful than point prevalence. Life-time prevalence is a special type of period prevalence referring to the whole of a person's prior life. Cumulative prevalence includes all disease conditions (cured, or resolved, continuing, and dead) in a given period of time.
There is a relation among incidence, prevalence and duration. Prevalence proportion = incidence rate x average duration of disease. A different reformulation of this formula by Richard Monson is PR = (IR - CR - MR)D. where PR=prevalence rate, CR= cure rate ie cases cured per unit time, MR= mortality rate i.e. cases dying per unit time, and D=duration in time.
Prevalence is useful for administrative purposes. It is rarely used for etiological studies except for conditions in which incidence is difficult to measure such as congenital malformations, non lethal degenerative diseases, and sero-conversion. Prevalence is not good for etiological studies for the following reasons: (a) It can not distinguish the contribution of incidence from that of disease duration (b) The time sequence is not obvious; disease and exposure are studied at the same time. PR may only give a clue about IR if IR is not available. In the extreme cases of rapidly fatal diseases, Prevalence may indicate true incidence. Average disease duration = 1R/termination rate per P-Y. Prevalence ratio (p/1-p) = IR x average duration. If p is small, p = IR x Average duration
Change in prevalence is due to: (a) Change in incidence (b) Change in duration: due to dearth or recovery (c) Both change in IR and duration.
It is sometimes useful to compute 95% confidence intervals for a proportion. The exact binomial is used of the number of cases is less than 75. The normal approximation is used for numbers above 75.
D. MEASURES OF EXCESS DISEASE OCURRENCE
Measures of excess disease occurrence, also called measures of effect, are based on measures of association. Excess disease risk is measured as an absolute effect (Rate Difference or Risk Difference) or a relative effect (Relative Risk, Rate Ratio, Risk Ratio, Prevalence Ratio, Cumulative Incidence Ratio, Incidence density Ratio, Odds Ratio, and Standard Mortality Ratio). There is no consistent relation between RD and RR. RD may be large for a small RR and vice versa. In the same way one measure may show heterogeneity of stratum-specific measures whereas the other does not. The rate ratio, the risk ratio and the odds ratio may be approximately equal under certain conditions. The rate ratio and odds ratio are commonly used in epidemiology. The odds ratio is a good estimate of the rate ratio under three conditions: the cases of the disease are representative of all diseased people in the population, the controls or comparison group are representative of all healthy people in the population, and the disease is rare. In general risk ratio > rate ratio > odds ratio. Various parameters discussed below are defined from the 2 x 2 contingency table
Disease + | Disease - | Person-time | ||
Exposure + | a | b | a + b | PT+ |
Exposure - | c | d | c + d | PT- |
a + c | b + d | N | PT |
Two odds ratios can be defined, the disease odds ratio and the exposure odds ratio. The disease odds ratio is defined as a/b ¸ c/d. The exposure odds ratio is defined as b/d ¸ a/c. It can be shown mathematically that the disease odds ratio = exposure odds ratio = ad/bc. The standard deviation used for computation of 95% confidence intervals for the odds ratio is given by OR exp [+/1 1.96 (1/a + 1/b + 1/c + 1/d)]1/2.
Relative Risk can be defined as a rate ratio based on incidence rates or as a risk ratio based on cumulative incidence or prevalence. The rate ratio is defined as {a / PT+} / {c/PT-}. The risk ratio is defined as {a/N} / {b/N}. A relative risk of >4 indicates strong association. A relative risk of 2-4 indicates moderate association. A relative risk of 1-2 indicates weak association. The prevalence ratio is defined as {a/(a + b)} / {a/(c +d)}. The exposure ratio is defined as {a/(a + c)} / {c/(c + d)}. For cumulative incidences < 0.05 the odds ratio is equal to the cumulative incidence ratio. As the time interval over which CI is measured decreases, the cumulative incidence ratio approximates the incidence density ratio.
Cordis gives the formula for computing the 95% confidence interval for the risk ratio as 95% CI = RR exp [+/1 1.96 {var(lnRR)}1/2 where var(lnRR) = [{(1 - a) / (a + c)} / {a} + {(1-b) / (b + d)} / {b}]1/2
The following interpretations of the odds ratio and risk ratio were given by Greenberg RS 1986: Prospective Studies in: Encyclopedia of Statistical Sciences Vol 7 p 315-319 eds S. Kutz and NL Johnson. John Wiley and Sons, New York
i. – 0.3 strong benefit
0.4 – 0.5 moderate benefit
0.6 – 0.8 weak benefit
0.9 – 1.1 no effect
1.2 –1.6 weak hazard
1.7 –2.5 moderate hazard
>=2.6 strong hazard
The approximate equality of the OR and RR can be proved algebraically. RR = Pr(D+|E+) / Pr (D+|E-). By substituting Pr(D+|E+) = {Pr(D+) Pr(E+|D+)} / {Pr(D+) Pr(E+|D+) + Pr(D-) Pr(E+|D-)} and Pr(D+|E-) = {Pr(D+) Pr(E-|D+)} / {Pr(D) Pr(E-|D+) + Pr(D-) Pr(E-|D-)} and crossing out like terms, RR= {Pr(E+|D+) / Pr(E-|D+)} / {Pr(E+|D-} / Pr(E-|D-)} = OR.
Two rate differences can be defined, the prevalence difference and the exposure difference. The prevalence difference is defined as {a/(a + b – c)} / {a/(c + d)}. The exposure difference is defined as {a/(a + c – b)} / {b/(b + d)}.
Four measures of excess risk are used. The excess risk among the exposed is defined as {a/(a + b – c) } / {c/(c+d)}. The population excess risk is defined as {(a + c) / (n – c)} / {c + d). The attributable fraction among the exposed is defined as [{a/(a + b)} – {c/(c + d)}] / [a/(a + b)] = {(prevalence ratio – 1) / (prevalence ratio)} x 100. The attributable fraction for the population is defined as [{(a + c) / n} / n} – {c/(c +d)}] / [(a + c) / n]. This is equivalent to {(prevalence ratio –1) x (exposure rate in population)} / {prevalence ratio – 1}.
The proportion of disease due to a particular exposure is measured by various parameters of attributable rate (AR). The attributable rate takes into consideration the population at risk. It is determined as the proportion of cases in the total population that is attributable to the risk factor. AR is a measure of the impact of eliminating a particular risk factor on disease risk. There are several formulations of AR: (a) Attributable Risk (AR) = IR(exposed) - IR (unexposed) = Pe (RR-1) / 1+ Pe (RR-1) where Pe = proportion of the population that is exposed. AR <1 indicates that the risk factor under consideration is protective. (b) AR% = AR/IR (exposed). (c) Etiologic fraction/attributable fraction (d) Population Attributable Risk (PAR).
Proportional mortality studies are used to compare the proportion of deaths among the exposed to the proportion of deaths death among the non-exposed. The proportional mortality ratio has some weaknesses. It can not distinguish between causative and preventive exposures. It can also not determine to what extent the purported exposure contributed to death. The vagueness in PMR can be resolved by treating such studies as case control studies.
E. MEASURES OF DISEASE IMPACT & MEASURES OF SURVIVAL
MEASURES OF DISEASE IMPACT
A common measure of disease impact is the years of potential life lost (YPLL).
MEASURES OF SURVIVAL
If R = incidence proportion, then the survival proportion, S = 1-R. The incidence odds is R/S = R / 1-R. If R is small, S approximates 1.0 and S/R approximates R therefore the incidence odds will approximate the incidence proportion. The case fatality rate is a type of incidence poroportion. The Kaplan-Meier formula helps compute the survival proportion over several consecutive time intervals thus S = Pk=I (Nk - Ak) / Nk where Nk = number at risk and Ak = number of cases. Cumulative survival could also be expressed using an exponential formula thus S = exp (- S Ik Dtk) where Ik = incidence in sub-interval and Dtk = length of the sub-interval. The product limit and exponential formulas do not operate well in the presence of competing risks.
9.1.4 DISEASE DIAGNOSIS
A. DISEASE IDENTIFICATION
METHODS OF DISEASE IDENTIFICATION
The following methods of disease identification will be discussed subsequently: Report of symptoms by the patient, Discovery of signs by physical examination (clinical, laboratory, radiological), Observation (direct & indirect, passive & induced), Use of an indirect marker of abnormality, and Response to a therapeutic agent e.g. the nitroglycerine test.
CASE DEFINITION
Case definition uses clinical criteria, underlying pathology, epidemiologic, and logical criteria. Certainty in case definition is at various levels: confirmed case, probable case, and possible case. Cases are a continuum and are not a dichotomy between case and non-case. Using cut-off points in case definition would be misleading.
The definition of the abnormal is based on four considerations: statistical, clinical, prognostic, and operational.
The epidemiological case definition is narrower and more rigid than the clinical case definition because of the need to standardize case definitions.
B. SYMPTOMS AND SIGNS
SYMPTOMS OF DISEASE
Symptoms are based on subjective observation hence observer error is more likely. They are reported by the patient or by close relatives, companions, or other attendants. Symptoms reflect pathology in addition to fears, attitudes, values, and beliefs of the reporter. Symptoms may be specific or non-specific.
SIGNS OF DISEASE
Signs are based on objective measurement hence measurement errors are possible. Pathognomonic signs are virtual proof of disease: e.g. Koplik spots in measles. Non-specific signs such as fever, vomiting, and weight-loss are common in several disease conditions. Qualitative signs such as the strength of the pulse are less reliable than quantitative signs such as blood pressure or pulse rate
DISEASE SYNDROMES
Syndrome (Greek for syn=together, dromos=course): is a complex of symptoms and signs. Pathognomonic syndromes are unique for certain diagnostic entities. They are often named after famous physicians. Use of the concept of syndrome is useful in diagnosis and therapy by making the identification and characterization of a group of related signs and symptoms easier.
C. DIAGNOSTIC TESTS
DEFINITION
Tests are an extension of clinical examination for signs. They are not 100% accurate or reliable. Tests are not necessarily more accurate or more objective than physical signs. Test results can not stand alone; they are interpreted in light of other relevant clinical data. The criteria of diagnostic tests must be standardized to enable comparability. The following types of diagnostic tests are used: assays of body fluids (blood, urine, and cerebrospinal fluid), radiological (x-ray, CAT scan, sonar), tissue biopsy, and function tests (e.g. LFT, RFT).
MEASURES OF TEST VALIDITY
Validity is when a test measures what it is supposed to measure. Sensitivity, specificity, and predictive value are measures of validity (accuracy). Sensitivity is a measure of the strength of association. Specificity measures the uniqueness of association. Figure 2.1 shows the relation between signs and diagnosis. We can determine the following parameters from the figure: True positives (TP) = a; True negatives (TN)=d; False negative(FN)=b; False positives (FP)=c; Sensitivity=a/a+b; Specificity=d/c+d. There is a trade-off between specificity and sensitivity. High sensitivity is associated with low specificity & vice versa. High specificity is associated with low sensitivity & vice versa. These relationships can be seen on a receiver operating curve (figure 2.2) that shows variation of sensitivity with specificity. True/correct diagnosis is based on high specificity (with low or high sensitivity). Pathognomonic signs have high specificity usually 85-95%.
PREDICTIVE VALUE OF DIAGNOSTIC TESTS
Interest focuses on how well a particular test predicts the true diagnosis. This includes the positive predictive value (detection of disease) and the negative predictive value (correct indication of absence of disease). The relationships between test results and the true diagnosis can be seen in figure 2.3. The following 2 parameters can be computed: PV+ve and PV-ve. Predictive value of positive test (PV+ve)= a/a+b. Predictive value of negative test (PV-ve)=d/c+d. PV+ve indicates the proportion of those with disease among those who are test-positive and can be alternatively expressed as PV+ = TP / {TP + FP}. PV-ve is the proportion with no disease among those who are test-negative. High prevalence of disease increases PV+ve. Stated in other words this means that common diseases are more likely to be picked up by the diagnostic test.
RELATION OF PREDICTIVE VALUE TO SENSITIVITY and SPECIFICITY
Baye's theorem can be used to relate predictive value of a positive test, PV+ve, to sensitivity. It can also relate the predictive value of a negative test, PV- , to specificity. The basic relation can be shown by the following formula: Pr(D+|T+) = Pr(T+|D+) Pr(D+) / Pr(T+) where Pr(D+) is prior probability & Pr(D+|T+) is posterior probability. Positive predictive value can be related to sensitivity and specificity by the following word formulas: PV+ = [{prevalence)(Sensitivity)}] / [(prevalence)(sensitivity) + 1-specificity)(1-prevalence). PV-=[{1-Prevalence) (Specificity)] / [{1-Prevalence) (specificity) + (1-sensitivity) (Prevalence)]. Other relations can be defined from the above relations: (a) Pr (T+|D+) / Pr (T+|D-) = Sensitivity / 1- specificity. (b) Odds of disease after test = odds of disease before test x likelihood ratio. (c) Pr (D+|T+) = sensitivity x prevalence / probability of a positive test
MEASURES OF REPRODUCIBILITY
Reproducibility consists of repeatability, consistency, reliability, and stability. Repeatability is a measure of the ability of a test to give the same answer when the subject is re-examined. Reliability is assessed differently for continuous and discrete data. The measures of repeatability used for continuous data are the standard deviation of replicate measurements and the coefficient of determination which is the standard deviation divided by the mean. For discrete data two measures are used: overall agreement and the kappa coefficient of inter-rater reliability.
The overall agreement is computed as the total of the diagonal cells in a contingency table of the scores of one rater against those of another one divided by the total number of tests as shown below:
Rater 1
Rater 2 | + | - | |
+ | a | B | P1 |
- | c | D | Q1 |
P2 | Q2 | 1.0 |
The kappa statistic measures the observer test bias and is defined as k = {2(ad – bc)} / {p1q2 + p2q1} where a, b, c, and d are actual counts and p and q are proportions. A kappa statistic >0.75 indicates excellent agreement. A kappa statistic of 0.4 to <0.75 indicates fair to good agreement. A kappa statistic <0.4 indicates poor agreement.
LIKELIHOOD RATIO
LR+ = [ (a/b) ] / [ (a + c+ / (b + d)]
LR - = [(c/d) ] / [(a + c) / (b + d) ]
Figure #2.1: Showing sensitivity and specificity
Sign + | Sign - | |
Diagnosis+ | a | b |
Diagnosis- | c | d |
Figure 2.2: Receiver operating curve
Figure 2.3 Showing predictive value of a test
Diagnosis+ | Diagnosis- | |
Test+ | A | B |
Test- | C | D |
9.1.5 DISEASE PROGNOSIS
A. OBJECTIVE ASSESSMENT OF PROGNOSIS
Clinical experience is not sufficient to identify prognostic factors because cases that come to the physician are highly selected. One physician may not follow through on all cases seen to see the final outcome. Therefore individual clinicians do not develop accurate clinical judgments about prognosis. Therefore objective methods are needed.
B. STUDY DESIGN FOR PROGNOSTIC FACTORS
Follow-up studies are used to study prognostic factors. The matching of discharge information with death certificates can also be used to study prognostic factors.
C. PARAMETERS USED IN STUDY OF PROGNOSIS
The following are used specifically: case fatality rates, survival (5-year survival rates, the survival curve, median survival time, relative survival, and comparison of actual with expected survival), and lifetable analysis.
UNIT 9.2
DISEASE DETERMINANTS
Learning Objectives
- Concepts and criteria of disease causation
- Disease Determinants
Key words and Terms
- Causal triangle
- Risk, factor
- Risk, indicator
- Causality, criteria
- Exposure
UNIT OUTLINE
9.2.1 CONCEPTS OF DISEASE CAUSATION
A. Causal Triangle
B. Risk
C. Cause
D. Disease Cause Associations
E. Criteria of Causality
9.3.2 CONCEPT OF EXPOSURE
A. Definition
B. Classification of Exposures
C. Measurement of Exposures
9.2.3. DISEASE DETERMINANTS
A. Definition of Determinants
B. Biological Determinants
C. Behavioral Determinants
D. Environmental Determinants
E. Social Determinants
9.2.4 VARIATION OF DISEASE RISK WITH AGE
A. Infancy and Childhood (0-12 Years)
B. Adolescence (13-18 Years)
C. Young Adults (19-39 Years)
D. Middle Age (40-64 Years)
E. Old Age (<64 Years)
CAUSATION
A. CAUSAL TRIANGLE
Cause is epidemiologically defined with preventive possibilities in mind. There is little benefit in studying and describing causes that can not be prevented or changed. The concept of the causal triangle (environment, host, and disease) has been used for many years to simplify epidemiological reasoning. The environment includes factors that actually cause or facilitate disease occurrence. The human host could be protected from contact with the cause of disease or could be made able to resist the disease. The disease condition is the result of the inter-play between the environment and the host. There is 2-way interactions among the three factors: agent & disease, agent & host, and host & disease.The interruption of disease causation usually involves one of the three factors.
B. RISK
DISEASE RISK
Disease risk is a probability. Risk has 2 dimensions: individual & statistical. For a single individual the risk can be 0 (no disease) or 1 (disease). Statistical probability or risk is an empirical frequentist probability based on the experiences of many people and lies between 0 and 1.
RISK FACTORS
Risk factors are established causes. A risk factor is a factor that is known empirically to be involved in disease causation. A risk factor is a characteristic that if present and acts will increase the probability of disease. It is neither the necessary nor the sufficient cause of the disease. A risk factor is often vague being a broad definition of the probable cause. Risk factors can be divided into 2: modifiable and non-modifiable risk factors. Modifiable risk factors are those over which the individual’s behavior or scientific manipulation can not change such as age, sex, and genetics. The individual has control over modifiable risk factors like smoking or alcohol.
RISK INDICATORS
Risk indicators are likely to be causes but are not yet confirmed. A risk indicator may itself not be involved in disease causation but may be a pointer to the risk.
C. CAUSE
DATA ON CAUSES
Data on causes can be obtained from animal or human experiments/observations. In animal populations each agent is assessed in a controlled experimental study. In human populations, 3 types of studies can be undertaken: clinical observations, observational epidemiology, and experimental studies
CAUSATIVE AND PREVENTIVE CAUSES
The causes may be defined as causative or preventive. A causative 'cause' directly leads to disease in a pro-active way. A 'preventive' cause leads to disease by its absence.
NECESSARY AND SUFFICIENT CAUSES
Epidemiology is the study of the occurrence relation. This is the relation between the determinant (risk factor) and outcome (disease). Several co-factors modulate this relationship. The view of causality as pure determinism is not practical. Modified determinism fits better with observed data. A risk factor's action in disease causation is affected by many other factors that operate with it. A risk factor or cause is described as sufficient when its mere presence will trigger the disease concerned. In practice a sufficient cause refers to a constellation of 2 or more risk factors since most diseases are multi-causal. One disease normally has more than 1 sufficient cause. There are some risk factors that are always present in all sufficient causes of the disease. These are referred to as necessary causes. No disease will result in the absence of the necessary cause. Cigarette smoking is not a necessary cause of lung cancer because some non-smokers get cancer. The tubercle bacillus is not a sufficient cause of TB because not every infected person gets the disease. Causes may be weak or strong depending on their contribution to the risk. Causes may interact either cooperatively in disease causation (synergy) or act against one another (antagonism). We now know that the causal chain or causal pathway is multi-stage. Initiation of the pathogenic process is by the main risk factor. The final stages of the disease onset may be to action of a promotor. Co-factors acting as promotors play a role in completing the process to the stage of clinical disease. Some co-factors may be antagonistic preventing eventual occurrence of disease. It is not necessary to know all the steps/components of the causal pathway before undertaking preventive action. It is enough to intervene against only one necessary cause/factor along the pathogenic pathway to stop the disease process.
D. DISEASE CAUSE ASSOCIATIONS
STATISTICAL and CAUSAL ASSOCIATIONS
Association between a disease and a putative risk factor can be described as statistically associated or not statistically associated. When there is no statistical association we say that disease is independent of the risk factor. Statistical association or dependence of disease on the risk factor can be causal or non-causal. In a causal association the risk factor is involved in disease causation either directly or indirectly by operating through another related intermediary or intervening factor. A non-causal relation in only apparent but is not biologically real for example presence of xanthomata is associated with coronary heart disease but one is not a biological cause of the other. The joint occurrence is because both are associated with high cholesterol. High cholesterol is associated with xanthomata and is also associated with coronary heart disease. Both associations are independent one of the other.
MODELS OF DISEASE-AGENT ASSOCIATION
There are several possible models of disease causation. (a) One disease may have 2 or more co-factors (b) One disease may have 2 quite different independent causes (c) One cause leads to 2 different diseases.
E. CRITERIA OF CAUSALITY
STEPS IN DETERMINING CAUSALITY
The first step is to test for statistical association between the risk factor/predictive factor and the disease. If there is statistical association the criteria of causality explained below are applied. This is followed by investigation of the temporal relation between the risk factor and disease using an appropriate epidemiological study. Finally all alternative causal explanations are eliminated to leave the one most probable causal link.
CRITERIA OF CAUSALITY
The first attempts to describe criteria of causality were made by Robert Koch. He listed the following 3 criteria for bacterial disease: the organism must constantly be present in cases of the disease, isolation of the organism in culture media, and reproduction of the disease in a susceptible animal. Those criteria have been modified a lot with more knowledge. Hill proposed the following criteria: strength of association, consistency, specificity, temporality, biological gradient, plausibility, coherence, experimental evidence, and analogy (Hill AB: The environment and disease: association or causation: Proceedings of the Royal Society of Medicine 58:295-300, 1965). We now know that criteria of causality are either essential criteria or back-up criteria. The essential causal criteria are four: specificity, strength, time sequence, and biological plausibility. Both the cause and the disease have to be defined as specifically as possible and the exposure must shown to have a specific effect. The strength of association is assessed by studying how disease risk (measured as odds ratio or risk ratio) increases/decreases with increase/decrease of the putative risk factor. Care must be taken in interpreting weak associations that may be due to confounding. It is only very strong associations that can overcome the effect of unknown confounding factors. The time sequence must be correct ie the cause must operate before occurrence of the disease. Biological plausibility or coherence requires that the causal relationship be understandable at the cellular level. The term coherence refers to conformity with what is known about the natural history and biology of the disease. The back-up causal criteria are five: dose-effect relationship, repetition, consistency, evidence from intervention, and experimental evidence. Under the dose-effect criterion (also called biological gradient), the more of the putative cause, the higher the risk of the disease. A unidirectional (monotonal) dose-response curve is evidence of a causal association. Under the repetition criterion, association between the 'cause' and the disease is found in different groups or populations and at different times. The cause-disease relationship must be consistent with existing knowledge. Intervention based on putative cause should lead to decreased disease occurrence. Additional support for the cause-disease relationship can be obtained from animal or in-vitro experiments. Some times a cause-disease relationship is accepted by default when there is no other explanation. The case for the putative cause may be strengthened by finding no other explanation for the disease.
9.2.2 CONCEPT OF EXPOSURE
A. DEFINITION
An exposure is defined as a substance, phenomenon, or event that has a physiological effect, can cause or protect from disease. Exposures include confounders, effect modifiers. The following are considered common exposures: (a) demographic such as age, race/ethnicity, religion, socio-economic status (b) occupational history (c) medical/surgical history (d) reproductive/sexual history (e) life style such as alcohol, smoking (f) diet (g) physical activity (h) radiation exposure (i) pollution of air, water, and soil.
B. CLASSIFICATION OF EXPOSURES
Exposures may be personal attributes or environmental agents. They may be identified based on subjective or objective data. Some exposures are current whereas others are past exposures. Exposures can be categorized as dichotomous (exposed vs unexposed). Exposures may be ranked according to importance in disease causation. Continuous exposures may be categorized into strata for example smoking duration can be categorized as =< 1 year, 1-2 years, and 2-3 years. Sometimes an exposure is categorized according to statistical criteria for example the body mass index (BMI) is categorized as high or low depending on criteria of statistical variation. In some cases exposures are left in the continuous scale such as age or cholesterol level.
C. MEASUREMENT OF EXPOSURES
Exposures may be measured quantitatively or qualitatively. Measurement of an exposure means assigning a numerical value to its magnitude. The exposure can be measured on the nominal, ordinal, or interval scales. The following are instruments used to measure exposures: questionnaires, personal interviews, biochemical analyses of biological material, physical and chemical analysis of the environment. Measurement of an exposure involves three dimensions: nature of the exposure, the dose, and time. Errors could occur in the measurement of exposures. Differential errors result in a biased odds ratio; the bias remains even of the sample size is increased. Non-differential errors make the odds ratio tend to the null value (attenuation of effect). Non differential error lowers study power and requires a larger sample size to detect a given difference. Measurement errors can be reduced by multiple assessments of the exposure such as repeat assessments of cholesterol. The effect measure can be adjusted to account for the effect of the error. The best approach is to use high quality control measures at the stage of data collection to minimize errors.
9.2.3. DISEASE DETERMINANTS
A. DEFINITION OF DETERMINANTS
Proper description of disease requires background knowledge of their determinants. The following seven determinants will be discussed: (a) demography (b) nutrition (c) infection (d) genetic anomaly (e) physical environment (f) social and economic environment: SES, occupation, and race (g) Medical care. A distinction must be made between determinants of disease and causes of disease. The latter term is more specific than the former. Determinants are general background factors that contribute to disease. Causes are the immediate antecedents of disease. Study of disease determinants is made complicated by the wide gaps in epidemiological and clinical knowledge about many diseases. It is also further complicated by the fact that the determinants are closely inter-related and it is difficult to disentangle their individual effects.
A. BIOLOGICAL DETERMINANTS
DEMOGRAPHY
The character and structure of a population affect disease patterns. There is a close relation between morbidity and mortality on one hand and population age and sex structure on the other hand. There are differentials in fertility, morbidity, and mortality in different population sub-groups. Age determines susceptibility to disease. The old have disease patterns different from the young. The elderly are usually poor due to limited income. There are gender differences in disease susceptibility and response to disease. The gender differences may operate through biological or socio-economic mediators. It has been observed that males have excess mortality in industrialized but not agrarian societies. This difference is due to occupational diseases that are higher in males. Males also tend to have more unhealthy behaviors and lifestyles like smoking, alcohol abuse, and propensity for accidents. Females are less likely to be involved in accidents or to commit suicide. Biologically males seem to have a less reactive immune system and experience higher mortality than females even in intra-uterine life. Socio-economically women are generally poorer due to low earning capacity and systematic discrimination. Marital status is also important in health. Married persons have lower mortality and a longer expectancy of life. Marriage provides a stable social and psychological environment that is conducive to health. An economic factor is also involved. A married couple can pool resources and afford a standard of living higher than that of the single person.
GENETICS
The genotype is the basic underlying genetic structure at the molecular level. Phenotype is the externally-visible expression or manifestation of the genotype. The difference between the two is due to environmental factors that limit or regulate the full expression of the genetic make-up. Pre-disposition to many diseases is inherited. Some diseases are known to be genetically-caused while the genetic basis of others is being unravelled. There are 3 types of genes: dominant, recessive, and sex-linked. Genes that control any particular genotypic expression occur in pairs, each being contributed by each parent. If both members of the pair are dominant, we have the situation of co-dominance. If a dominant gene is paired with a recessive gene, the effect of the former will be expressed while the latter is suppressed. If both pairs are recessive, the recessive genotype will manifest. The genetic anomaly may lead to an anatomical anomaly or may lead to a chemical product like enzymes or cause structural anomalies in molecules like hemoglobin and immunoglobulin molecules. The common abnormal hemoglobins are: HbS, HbC, and beta-thalassemia. The inheritable genetic disorders of HBS and GPD deficiency are an illustration of Allah's plan that what may be considered bad in one sense could be good in another sense. HbS protects against malaria because the red blood cell with HBS is not easy to infect by malarial mosquitoes. Thus children with sickle cell disease or sickle cell trait are protected against malaria that is a killer in the tropics. Glucose phosphate dehydrogenase deficiency is another inherited anomaly common in malarious areas and is protective against malaria because Plasmodium falciparum grows less in RBC with the deficiency. Thus children in the tropics with the 2 genetic anomalies survive malaria that is the leading killer of tropical childhood. HLA genes affect many aspects of cell function and immune response. Among diseases associated with HLA genes are: ankylosing spondylitis, psoriasis, diabetes mellitus, and osteoarthritis. HLA-related diseases display genetic-environmental interactions. It is difficult to analyze human disease in terms of simple genetic models because of the environmental involvement and because of polygenic influences.
B. BEHAVIORAL DETERMINANTS
LIFE STYLE:
Life-style, defined as habitual patterns of behavior, is closely related to disease. Lifestyle consists of habits and customs learned in the socialization process, diet, exercise, leisure activities (games, hobbies), health-related substance use (tea, coffee, tobacco, prescribed drugs, self medication, illicit substance use), safety practices (seat-belt use, safety equipment at home and at work), and health-seeking behaviors (immunizations, disease screening). (Page 255 John M Last Public Health and Human Ecology 2nd edition Prentice Hall International, Inc. ? year)
Culture and way of life also affect health as has been observed in changing morbidity and mortality on migration. Life-style is affected by family history, culture, socio-economic status, and religion. Behavioral determinants of health are modulated by personality, health beliefs, risk taking behavior, and stressful life events. The personality may be extrovert or introvert. It may be anxious or neurotic. Some personalities are stable while others are labile. Epidemiologists have identified the relationships between type A and B personalities and specific diseases. Life-style or behavior may act at the stage of disease initiation or the stage of disease promotion. It may also be a factor in the cure of disease. Behavioral factors can act synergistically for example obesity and high dietary cholesterol in the causation of CHD and cigarette smoking and high dietary cholesterol in the causation of CHD. Life-style can be changed by education, economic forces, and legal forces. Religion is a cultural integrating force that affects health by controlling behaviors that lead to violence, suicide, homicide, stress, physical and emotional abuse of children, spouses and the elderly. The health behaviors/habits associated with disease risk are addictions, nutrition, physical exercise, violence, and stress. Addiction to alcohol, cigarette smoking, and substance abuse (psychotropics) causes both acute and chronic diseases. Mal-nutrition due to over-eating, high dietary fat intake in the form of saturated fatty acids & cholesterol are associated with coronary heart disease (CHD). High carbohydrate and food fads are also associated with other disease conditions. Inadequate physical activity is associated with CHD. Irresponsible use of motor vehicles and violence lead to traumatic injuries. Stress is an underlying factor in physical and psychiatric disease. Physical inactivity is associated with CHD. The determinants of health-related behavior: (i) Socio-cultural: ethnicity, SES (ii) Personal: age, sex, education, previous disease experience, beliefs, knowledge (iii) Financial barriers: time availability (iv) Type of disease: chronic non-communicable diseases are usually due to human behavior. It is difficult to change human behavior from unhealthy to healthy habits. The reasons for difficulty to change human behavior are: psychological dependence, physiological dependence, and habituation. Since human behavior is a determinant of disease, its modification is important in disease prevention. Health education is one of the approaches to changing human behavior. It is defined as the combination of learning opportunities designed to facilitate voluntary adaptation of behavior to improve health. The strategies of health education: are (i) comprehension (ii) acceptance (iii) retention (iv) behavioral change
NUTRITION:
Nutritional requirements vary by age and gender. Malnutrition whether qualitative or quantitative has disease implications. Both over and under-nutrition have deleterious effects on tissue physiology. The nutritional deficiency may be general or specific. General deficiency involves several nutrients and is due to general low intake. Specific deficiency involves one or two nutrients and arises in specific situations. Under-nutrition can manifest in a gross form as starvation, marasmus, or kwashiorkor. Under-nutrition in children leads to stunting. There is synergism between under-nutrition and infection in childhood. Under-nutrition in adults leads to lower resting basal metabolic rate (BMR) and loss of weight. Over-nutrition leads to obesity and related neoplastic and cardio-vascular diseases. Relative starvation during World War II led to a fall in coronary heart disease. The increasing reliance on fast foods in the stressed industrial society of today leads to excess fat intake. Obesity is defined as 120% of ideal body weight or higher. Obesity is directly associated with coronary heart disease. It also has an indirect association through causing a rise in blood pressure. Nutrients have direct effects on body physiology. Fiber can be soluble or insoluble. Soluble fiber slows the absorption of lipids and glucose. Insoluble fiber increased stool bulk and hastens intestinal emptying. Vitamin D3 regulates DNA transcription. Anti-oxidants maintain DNA integrity. Aflatoxin damages DNA. Persons with familial cancer have a higher susceptibility to nutrient effects that lead to cancer. Epidemiological studies require reliable assessment of nutritional intake. The most commonly used method is the 24-hour recall. Actual recording of intake would be the most accurate but is cumbersome for the research subject. Presence of the observer may lead to bias.
D. ENVIRONMENTAL DETERMINANTS
INFECTION
Infection by a micro-organism is said to be established when the micro-organism replicates in the host. Infection may weaken the body's immune system thus facilitating establishment of other diseases. Micro organisms cause deleterious effects in three ways: invasion and destruction of tissues, producing toxic products, and competing with the host for food. The microbial agents involved in human disease are: viruses, rickettsia, bacteria, fungi, protozoa, and metazoa.
PHYSICAL AGENTS
The following aspects of the physical environment affect disease: climate & vegetation, housing, environmental hygiene & sanitation, and socio-economic activities. Heat and cold have direct effects on the body. Sunlight is necessary for vitamin D synthesis by the skin. Sunlight also plays a major role in the control and regulation of the biological diurnal rhythm.
Climate and vegetation affect food production and thus have an impact on the nutritional status. Some climates favor the growth and survival of disease vectors. Housing has a major impact on disease. We spend 2 /3 of the 24-hour day indoors. Environmental hygiene and sanitation greatly affect the patterns of disease transmission. Pollution of the indoor and outdoor have an acute and long-term impacts on health. Radiation, noise, and vibration are physical agents that affect health. Socio-economic activities that affect the environment such as mining, manufacturing industry, energy production, construction, automobile emissions, agriculture, forestry, fisheries, and tourism. These activites cause pollution of the air, the soil, and the water.
E. SOCIAL DETERMINANTS
SOCIO-ECONOMIC STATUS
The concept of social class is real but is difficult to define exactly. There are no perfect criteria but usually the following are used: occupation, income, education, home ownership, social prestige, race, and marital status. These factors are very inter-related and do in an imperfect way divide people into socio-economic classes which as we have seen affect health outcome. Several methods are used in social classification: occupational scales, income-based scales, socio-economic scales, and status or prestige scales. Occupational scales are crude and may not reflect actual income. They are not relevant to the non-working populations of students and housewives. The UK Registrar-General Occupational Classification is used to divide the British society into 5 social classes. Class I are leading professions and businesses such as medicine, law, stockbroking, and banking. Class II are ‘minor’ professions and businesses and include school teachers, pharmacists, and shopkeepers. Class III are skilled non manual workers such as clerks and bank tellers or skilled manual laborers such as factory foremen or crane operators. Class IV are semi-skilled workers such as truck drivers and salespersons. Class V are unskilled workers such as porters, waiters, and delivery persons.(Page 235 John M Last Public Health and Human Ecology 2nd edition Prentice Hall International, Inc. ? year). Income-based scales would be objective but are based on inaccurate data since persons are reluctant to reveal their true income to strangers. Socio-economic scales ( eg Hollingshead and Blishen scales) have been developed by combining several social indicators such as education, occupation, income, and housing. They however involve a lot of data collection from individuals.
Educational inequalities affect health-related behavior and also occupational opportunity. Education, an indicator of SES, is related to mortality and longevity. It also determines the occupational category. The SES determines the type of housing, diet, and medical care. It is also related to life-style regarding use of tobacco and alcohol. Sociologists have argued for decades about the existence of a poverty culture, poverty trap, poverty cycle which mean that inequalities are transmitted to the next generation.
The economic conditions of a society are perhaps the most powerful determinant of general health. It is the general economy that also decides the distribution of people in various SES classes. A good economic base leads to good social conditions that could mitigate the negative and harmful aspects of the physical environment. Social improvement in many countries is responsible for the demographic explosion that is seen at the moment. The fall of the death rate and increase of longevity are attributed to better nutrition, better education, political and social security. Economic improvement has paradoxical effects. On one hand it leads to fall of mortality and morbidity due to the above-mentioned factors. On the other hand it leads to increased morbidity and mortality due to a new dangerous life-style that results into accidents, suicide, and homicide.
SES differentials have been described for total mortality, infant mortality rates, and life expectancy. Cause specific differentials in morbidity and mortality have also been described. Health services utilization also varies by SES. Lower mortality is seen among those who own their homes compared to those who rent. The interaction between health and poverty is complex. Poverty leads to poor health because of inability to get healthy living conditions (housing, food, and environment). Poor health in turn leads to more poverty because of inability to work and generate income. There is a vicious cycle that is difficult to break.
CULTURE
Culture has a clear effect on health because it affects behavior and also affects the micro-environment. Culture is defined by traditions, customs, religion, and values.
SOCIAL NETWORKS
Social networks can play a supportive role that prevents the occurrence of some diseases. Their most important role is to provide psycho-social support in times of social stress. They may also provide physical support and be as source of health information. The social networks may be within the nuclear family or the extended family. The nuclear family evolves through the stages of formation, child rearing, empty nest, and bereavement when one of the spouses passes away. Divorce is a health hazard for the spouses and the children. The extended family is fast disappearing in industrialized societies and its supportive role is being lost. Other social networks may be related to the neighborhood, work, or clubs.
OCCUPATION:
Occupation is a determinant of disease occurrence but is itself influenced by education, opportunities, and local economic conditions. There are differences in life expectancy for different occupations. The economically disadvantaged, like manual workers, have higher mortality. The impact of occupation on health is seen even after retirement. Periods of unemployment are associated with stress which leads to physical and psychological illness. Sex and race are for example occupational barriers for women and disadvantaged minorities. The disadvantage continues into the next generation. Parental occupation affects the health of the offspring either directly due to occupational exposure or indirectly due to income and social class. There is occupational inequality in the work-place in terms of salaries, benefits, and security. The lowest paid is usually a health hazard due to exposure, low income, and stress.
RACE:
The impact of race on disease is more socio-economic than genetic. In the US
MEDICAL CARE:
Curative medical services might have had little impact on falling mortality rates. Major changes in mortality have been due to other factors such as sanitation, nutrition, and immunization. Formal evaluation of the impact of medical services is made difficult by lack of objective outcome measures. Data normally used in the assessment is mortality data, morbidity data, results of community surveys, and disease registers. Mortality data is difficult to interpret because of confounding. Morbidity data is usually unreliable or incomplete. Health survey data of disease incidence, morbidity, and disability is difficult to interpret. The following are 4 examples of documentation of the health impact of health intervention: immunization, antenatal care, management of heart attacks, and control of hypertension. Immunization led to control of childhood infectious disease. Ante-natal care led to improvement of obstetric outcome. Management of heart attacks led to fall of IHD mortality. Control of hypertension led to decrease of mortality due to CHD.
8.2.4 VARIATION OF DISEASE RISK WITH AGE
A. INFANCY and CHILDHOOD (0-12 YEARS)
The leading causes of death in the first 2 years of life are perinatal conditions, congenital anomalies, injuries, and infections (influenza and pneumonia) and the leading causes of morbidity are ocular mal-alignment, dental caries, and child abuse or neglect. The leading causes of death in early childhood (2-6 years) are injuries and congenital anomalies whereas the leading causes of morbidity are vision disorders, dental caries, tooth misalignment, abuse and neglect. The leading causes of mortality in late childhood (7-12 years) are injuries, congenital anomalies, and leukemia whereas the leading causes of morbidity are vision and hearing disorders, dental caries, dental misalignment, abuse and neglect.
B. ADOLESCENCE (13-18 YEARS)
The main causes of death among adolescents are injuries (mostly motor-vehicle related), and suicide. The leading causes of morbidity are depression, tooth decay, tooth misalignment, abuse and neglect.
C. YOUNG ADULTS (19-39 YEARS)
The leading causes of mortality in young adults are injuries, homicide, and suicide. The leading causes of morbidity are depression, tooth decay, tooth misalignment, malignant skin lesions.
D. MIDDLE AGE (40-64 YEARS)
The leading causes of mortality among the middle age are heart disease, lung cancer, cerebrovascular disease, breast cancer, colorectal cancer, and obstructive lung disease. The leading causes of morbidity are depression, tooth decay, gingivitis, peripheral artery disease.
E. OLD AGE (<64 YEARS)
The leading causes of mortality among the elderly are heart disease, cerebrovascular disease, obstructive lung disease, infections (pneumonia and influenza), lung cancer, and colorectal cancer. Leading causes of morbidity are depression, cognitive impairment, peripheral artery disease, dental caries, loose teeth, gingivitis, falls and fractures.
UNIT 9.3
DISEASE CONTROL, ERADICATION, and PREVENTION
Learning Objectives
· Disease control
· Disease eradication
· Disease prevention
·
Key Words and Terms
· Disease control
· Disease eradicaton
· Disease prevention
· Contact tracing
· Disease notification
· Mosquito control
· Patient isolation
· Pest control
· Rodent control
· Smoking cessation
· Universal precautions
· Vaccination
· Vector control
9.3.1 CONCEPTS OF CONTROL, ERADICATION, and PREVENTION
A. CONTROL
DEFINITION
Control is a general term for containment of disease and includes both prevention and control measures. It is used in another sense to mean limiting the transmission of a communicable disease in the population.
CONTROL OF COMMUNICABLE DISEASES
Control can be by enhancing host immune resistance by active immunization, passive immunization, or improvement of nutrition. Control can also be by interrupting disease transmission by detecting and treating infectious cases, isolating or quarantining cases, chemoprophylaxis, vector control, environmental measures, using aseptic techniques, water sanitation, sewage disposal, and food hygiene. Control can be achieved by personal measures such as personal hygiene, barrier protection such as using mosquito nets, and avoiding situations that favor transmission. Control can be achieved by inactivating the infectious agent using physical means (heat, cold, radiation) or chemical means (chlorination and disinfection) (page 119 John M Last: Public Health and Human Ecology. 2nd edition. Prentice Hall International, Inc ? year)
CONTROL OF NON-COMMUNICABLE DISEASES
Control of non-communicable diseases is mainly preventive and involves simultaneous interventions against several risk factors and lifestyle changes.
B. ERADICATION
Eradication is complete uprooting of a disease and its total elimination. This has been achieved only for smallpox. Complete eradication of a disease can occur naturally when environmental changes or changes in the host and agent make disease transmission difficult or virtually impossible for example plague as an epidemic has been eradicated in developed countries because of high levels of environmental sanitation. However when environmental, host, or agent circumstances change, previously eradicated diseases can return. Active planned disease eradication requires such drastic measures in the environment and the host that it may lead to new problems and new diseases by disturbing the eco-system. In view of these considerations disease control and prevention are preferred over disease eradication.
C. PREVENTION
DEFINITION
Prevention is planning and carrying out actions that prevent or pre-empt disease or any other undesirable outcome. Intervention is taking action during an outcome. Three types of disease prevention can be described: primary, secondary, and tertiary.
PRIMARY PREVENTION
Primary prevention is prevention of occurrence of disease or injury in the pre-pathogenic or pre-disease stage. It consists of health promotion & specific protection. Specific protection consists of immunization, antimicrobials, prevention of deficiency (iodine, iron, and vitamin), prevention of injuries, prevention of toxic exposure, and prevention of iatrogenic conditions (nosocomial infections, medication errors, surgical errors). General protection consists of character building, personality development, personal hygiene, health education, use of seat belts, dietary control, environmental control, safe housing, nutrition, and genetic counseling. Primary prevention is not always successful.
SECONDARY PREVENTION
Secondary prevention is halting the development or progress of disease or disorder by early detection and treatment. It acts at the stage of latent disease or the early pathogenic stage. It consists of early diagnosis, treatment, and prevention of disability. Early intervention limits the severity of disease and disability. Secondary prevention employs screening for early detection of disease, individual case finding, early diagnosis, and minimisation of disability. Screening can be personal or medical. Examples of screening are PKU screening in the new-born, and growth monitoring in childhood.
TERTIARY PREVENTION
Tertiary prevention deals with symptomatic disease and acts quite late in the pathogenic process. It is impeding the progress of established disease or disability by appropriate treatment or management. It is mainly disability limitation and rehabilitation. Disability limitation may be total (temporary and permanent) or partial (temporary and permanent). Rehabilitation, essentially retraining and reeducating, consists of physical therapy, assistance with activities of daily living, speech therapy, occupational therapy, and counseling. Physiotherapy is tertiary prevention in cases of cerebral palsy because it prevents further deterioration. Antibiotic prophylaxis for recurrent UTI is a tertiary prevention for UTI.
CURATIVE VS PREVENTIVE MEDICINE:
Curative medicine is mainly for the individual. Preventive medicine is for the community. The two are not opponents; they are symbiotic. There is a need for cooperation between practitioners of both types of medicine. Preventive medicine has priority and is more effective. Preventive medicine had a bigger impact on disease over the past 100 years than curative medicine. Sometimes you should start with curative and consolidate with preventive medicine.
DISEASE-ORIENTED PREVENTION STRATEGIES
General considerations:
· quarantine and isolation
· Surveillance, public health laboratory
Communicable disease
· Air-borne diseases: measles, diphtheria, rubella, meningitis. Primary prevention is by immunization
· Fecal contamination: diarrhea, hepatitis, cholera, enteric fevers, food poisoning
· Vector-borne: malaria, filariasis, japanese encephalitis, dengue
· Sexually-transmitted diseases: neisseria, syphilis, herpes, HIV
· Myco-bacterial diseases: tuberculosis, leprosy
· Helminthic: ascariasis, entrobiasis, hookworm, tenia,
Non-communicable disease
· Cancer control
· Tobacco & smoking
· Diabetes mellitus
· Cardio-vascular disease
ENVIRONMENTAL-ORIENTED PREVENTION STRATEGIES
- Environmental quality control
- Food quality control
- International public health
HOST-ORIENTED PREVENTION STRATEGIES
- Immunization
- Nutrition
- Medical Care
8.3.2 PREVENTIVE MEDICINE: LEGAL BASIS
A. CONCEPT OF PREVENTION (wiqayat)
Preventive medicine, tibb wiqa’i, is a series of pro-active measures that subsumed under the Islamic concept of prevention, wiqayat. The Qur’an has used the concept of wiqaya as taking preventive and anticipatory action against punishment (2:201, 3:16), greed (59:9, 64:16), bad acts (40:9, 40:45), injury/harm, (16:81), jealousy, oppressive rulers (3:28), annoyance (16:81), and heat (16:81). Prevention is therefore one of the fixed laws in the universe. Its application to medicine is therefore a special case of a general phenomenon.
The concept of prevention does not involve claiming to know the future or the unseen or even trying to reverse pre-destination, qadar. The human using limited empirical knowledge attempts to extrapolate, anticipate, and predict disease risk from the known distribution of risk factors. Preventive action is modification, alleviation, or reversal of the effects of risk factors. Prevention, besides avoiding any act that can hurt good health or destroy life, halaak (4:176, 67:28), also embraces activities that promote good health like physical exercise; rest; recreation; good diet; meditation, dhikr llah; and positive social relations. These activities and states of being are part of preventive medicine because they put the body in the best possible status to be able to fight and overcome any disease that occurs. All preventive measures that are taken against disease can be subsumed and explained by 2 major concepts in Islamic Law: the Purposes of the Law and Principles of the Law. There are 5 purposes of the Law, maqasid al shariat, and 5 Principles of the Law, qawaid al shariat.
B. PURPOSES OF THE LAW (maqasid al shariat)
The law was revealed to fulfil specific underlying purposes that will ensure success in this world and fulfil the interests and benefits, masaalih, of the people. The 5 Purposes of the Law, maqasid al sharia, arranged here in order of importance are: preservation of morals and religion, hifdh al diin , protection and maintenance of human life, hifdh al nafs, protection of the human intellect, hifdh al aql, protection of the progeny, hifdh al nasl, and protection of property rights, hifdh al maal. Protection of morality includes taking measures to ensure freedom, basic human rights, rule of the law, equity, and justice. Violation of these moral principles is the social root cause of much human disease. Protection of life includes health promotion, disease prevention, and treatment. Protection of the mind is avoiding what impairs human intellect like alcohol. Protection of progeny covers reproductive, fetal and child rights. Protection of property rights assures resources for health promotion and disease prevention. The 5 Purposes of the Law are permanent and are unchangeable, kulliyat abadiyat. Most of preventive medicine falls under the second Purpose of the Law. Application of this principles to public health is neither simple nor straight-forward. What we generally consider as risk factors of disease have benefitial effects as well. Cholesterol is required in metabolism but it involved in atheroma formation. Preventive measures could carry a quantum of risk such that preventing one disease creates another one. Imaam al Shatibi, the leading Muslim thinker on the Purposes of the Law, provided guidance on the resolution of such issues. He argued that there is no absolute benefit, maslahat, or harm, mafsadat. The purpose of the law is therefore to choose the best equilibrium between the harm and the benefit. It is not always true that benefits are permitted, halal, and harms are prohibited, haram; each case is considered according to its circumstances. We can safely conclude that in the field of preventive medicine, the best that humans can do is carry out empirical studies and arrive at objective conclusions but must always have the humility to admit that they could be wrong
C. PRINCIPLES OF THE LAW (qawaid al shariat)
Five principles are recognized by most scholars: intention, qasd, certainty, yaqueen, injury, dharar, difficulty, mashaqqat and custom or precedent, aadat .Each of the 5 Principles is a group of legal rulings or axioms that share a common derivation.
The Principle of Motive states that each action is judged by the intention behind it, al umuur bi maqasidiha. Means are judged with the same criteria as the intentions, al wasail laha hukm al maqasid, If the intention, qasd is wrong the means, wasiilah, is wrong. What matters are intentions, maqasid, and underlying meanings, ma’aani, and not literal terms, alfaadh, or structures, mabaani. The principle of motive applies to disease prevention messages. The recipients of the message must understand the purposes behind the behavioral change that is requested. We can speculate that failures of health education program are due to health educators providing information and instructions on behavioral change without taking time to make sure that the recipients understand the underlying motives.
The Principle of Certainty, yaqeen, states that a certainty can not be voided, changed or modified by an uncertainty, al yaqeen la yazuulu bi al shakk. The principle of certainty finds application in preventive prescriptions that seek to change people's behavior based on new evidence that is not at the level of certainty. Existing assertions should continue in force until there is compelling evidence to change them, al asl baqau ma kaana ala ma kaana. Frequent changes in preventive prescriptions could lead disinterest among the general public about disease prevention. This could have been avoided if changes were based only on evidence of highest certainty.
The Principle of Injury, dharar, states that an individual should not harm others or be harmed by others, la dharara wa la dhirar. This principle is the basis for pro-active action to prevent or treat disease rather than being fatalistic. Injury should be mitigated as much as is possible, al dharar yudfau bi qadr al imkaan and should be relieved, al dharar yuzaal, if possible. An injury should not be relieved by a similar injury, al dharar la yuzaal bi mithlihi.
The Principle of Hardship, mashaqqa states that necessity legalizes the prohibited, al dharuraat tubiihu al mahdhuuraat. Necessity is defined as what is required to preserve the 5 Purposes of the Law. If any of these 5 is at risk, permission is given to commit an otherwise legally prohibited or commonly unacceptable things like violation of individual rights. Coercive public health measures are permitted under this rubric. Prevention of a harm has priority over pursuit of a benefit of equal worth, dariu an mafasid awla min jalbi al masaalih. If the benefit has far more importance and worth than the harm, then the pursuit of the benefit has priotity. The lesser of two harms is selected, ikhtiyaar ahwan al sharrain. A lesser harm is committed in order to prevent a bigger harm, al dharar al ashadd yuzaalu bi al dharar al akhaff. Public interest has priority over individual interest, al maslahat al aamat muqaddamat ala al maslahat al khaassat.
The Principle of custom, aadat should be studied and used more by practitioners of preventive medicine. What is considered customary is what is uniform, wide-spread, and predominant, innama tutabaru al aaadat idha atradat aw ghalabat, and not rare, al ibrat li al ghaalib al shaiu la al naadir... Customs are not static, they eventually change with time and place, la yunkiru taghayyur al ahkaam bi taghayyuri al azmaan wa al ahwaal wa al aadaat wa a’raaf. Most customs are not harmful if they were they would not have survived. The aim should be the identification of those aspects that are injurious to good health rather than condemning all the customs of the people. We should be very circumspect before declaring common customs as dangerous to health. In the same way if we want our preventive messages to have an impact, we should try to include them in what is considered customary.
8.3.3. PREVENTIVE MEDICINE: MODERATION, BALANCE, and EQUILIBRIUM
A. CONCEPTUAL BASIS
The Islamic perspective of disease prevention and control was treated in general in a recent paper by the author (1). This paper will discuss three specific Islamic concepts, derived from the Qur'an, as they relate to preventive medicine. The concept of wasatiyyat, is very important in all biological, physical, social, and even spiritual phenomena in the universe The Qur;an describes wasatiyyat as a defining characteristic of the ummat (2. 2:143) and righteous individuals (3. 68:28). It is the average or center that is a good representative of the whole (4. 5:89). The Qur'anic concept of mizaan refers to establishing balance between two opposing or contradictory tendencies. Mizaan is mentioned as a general concept of balance (5. 42:17, 55:7, 57:25) and with specific application to measurements in trade (6. 6:152, 7:85, 11:84-85, 17:35, 26:182, 55:8-9, 83:1-3). The concept of 'adl is described in biology (7. 82:7), speech (8. 6:152), government (9. -45), and the judicial process (10. 5:106, 65:2, 5:8). The concept of 'adl or i'itidal is the practical active establishment of a just equilibrium. The equilibrium may be in the center or at some other optimal point. It is not easy for humans to locate the just equilibrium without the guidance of revelation, wahy.
The Qur'anic concepts mentioned above find their biological equivalent in the concept of homeostasis which refers to the ‘various physiological arrangements which serve to restore the normal state once it has been disturbed' (11. Definition due to W.B. Cannon). Homeostasis establishes and maintains biological equilibrium between internal and external environments, change and constancy, action and reaction. Homeostasis emanates from the concept of tauhid. Tauhid implies that the whole cosmos and what it contains have one deliberate creator. Thus all the contents must relate to one another in some harmonious way since they belong to one and the same scheme of creation. It is unthinkable that the one creator could create systems that are contradictory to one another. The harmony must however be looked at in a dynamic way. Because there are constant changes, there must arise from time to time contradictions in the state of flux. Homeostasis is the mechanisms that restore the status quo following temporary disturbances that are inevitable in a dynamic system. Human disease represents breakdown of homeostasis. Most disease processes are however patho-physiological disturbance that follow and attempt to reverse biological, physical, or chemical insult or injury to the body in order to return the body to the state of equilibrium. Preventive medicine involves actions and behaviors that have as the ultimate aim the support and maintenance of the homeostatic state biologically, socially, and even spiritually.
The practical life and teachings of the prophet emphasize the concept of central tendency and avoiding either extreme. Extremes of any action even if permitted, halal, are usually destructive and are not desired; the best is the equilibrium of the middle path, khair al umuur awsatuha (12. MB # 2014 p 987). There must be a balance between rest and activity, release (istifragh) and retention (ihtibaas), sadness and happiness. Applications of the concept of moderation, balance, and equilibrium is found in almost all aspects of life: human behavior, medical treatment, and use of environmental resources. The human habitat or the larger ecosystem that humans share with other living things must be maintained at a certain optimum equilibrium otherwise there will be adverse effects on life.
Disease situations are very complicated and could even involve a manifest contradiction among various preventive interventions. Imaam al Shatibi, the leading Muslim thinker on the Purposes of the Law, provided guidance on the resolution of such issues. He argued that there is no absolute benefit, maslahat, or harm, mafsadat (13). The purpose of the law is therefore to choose the best equilibrium between the harm and the benefit. Selection of the right equilibrium as well as the resolution of contradictions is further guided by the Purposes of the Law, maqasid al shariat (13), and Principles of the Law, qawaid al sharia (14).
Scientific knowledge on which preventive prescriptions are based is not perfect. This could raise serious practical problems in situations of uncertainty. We will divide these problems in two distinct groups: problems dealing with finding the moderate position and problems involving choice between two contradictory positions each with its own risks and benefits. The right solution is not always easy to find and no general rules can be given. Each situation should be considered on its own merits.
B. ESTABLISHING and MAINTAINING THE OPTIMUM
Table #1 shows examples of problems in preventive medicine involving establishing the moderate position between two extremes of the spectrum. We can be guided in the choice of the correct preventive approach by using the theory of Purposes of the Law. The law was revealed to fulfill specific underlying purposes that will ensure success in this world and fulfill the interests and benefits, masaalih, of the people. The 5 Purposes of the Law, maqasid al sharia, arranged here in order of importance are: preservation of morals and religion, hifdh al diin , protection and maintenance of human life, hifdh al nafs, protection of the human intellect, hifdh al aql, protection of the progeny, hifdh al nasl, and protection of property rights, hifdh al maal. The order of priority in selecting preventive interventions should follow the order above. Protection of religion has priority over protection of life. Protection of life has priority over protection of wealth which necessitates expending all available resources to prevent and cure disease. Protection of life has priority over protection of progeny thus in case of cancer, reproductive organs will be removed surgically to prevent disease spread. Protection of human intellect has priority over protection of progeny; persons with labile potentially psychotic personalities could be advised to avoid child-bearing whose additional stress will lead them to frank psychiatric disease. Protection of human intellect has priority over protection of wealth thus alcohol and psycho-active drugs are prohibited even if they may have economical advantages.
C. RESOLVING CONTRADICTIONS
Table #2 shows examples of choice between two positions that appear contradictory. Finding the right decision must be based on the guiding principles of the law and empirical evidence. Five principles are recognized by most scholars: intention, qasd, certainty, yaqeen, injury, dharar, difficulty, mashaqqat and custom or precedent, aadat .Each of the 5 Principles is a group of legal rulings or axioms that share a common derivation. We will refer to only two of the five principles in this paper: dharar and masghaqqat. The Principle of Injury, dharar, states that an individual should not harm others or be harmed by others, la dharara wa la dhirar. This leads to prohibition of both active smoking, harm to self, and passive smoking, harm to others. Injury should be mitigated as much as is possible, al dharar yudfau bi qadr al imkaan or should be relieved, al dharar yuzaal, if possible. This sub-principle is the basis for pro-active action to maintain homeostasis, prevent, or treat disease rather than being fatalistic. An injury should not be relieved by a similar injury, al dharar la yuzaal bi mithlihi, as happens in situations of vicious circles. The Principle of hardship, mashaqqa states that necessity legalizes the prohibited, al dharuraat tubiihu al mahdhuuraat. Necessity is defined as what is required to preserve the 5 Purposes of the Law. If any of these 5 is at risk, permission is given to commit an otherwise legally prohibited or commonly unacceptable things like violation of individual rights. Coercive public health measures are permitted under this rubric. Prevention of a harm has priority over pursuit of a benefit of equal worth, dariu an mafasid awla min jalbi al masaalih. A harmful new treatment modality is prohibited even if it has some efficacy against disease. If the benefit has far more importance and worth than the harm, then the pursuit of the benefit has priority for example when the benefits of the new treatment outweigh its harmful effects by a very large margin. When confronted with a choice between 2 harmful choices, the lesser of two harms is selected, ikhtiyaar ahwan al sharrain and a lesser harm is committed in order to prevent a bigger harm, al dharar al ashadd yuzaalu bi al dharar al akhaff. Amputation of a cancerous limb is a lesser evil that the spread of fatal malignancy. Public interest has priority over individual interest, al maslahat al aamat muqaddamat ala al maslahat al khaassat. The individual's freedom of choice is abridged by laws against smoking in public places because public interest is paramount.
D. PRACTICAL APPLICATION: DIET AND DISEASE
Generally malnutrition is an underlying factor in all diseases due to its effect on the immune system. Specific diseases are known to be related to malnutrition: hypertension, coronary heart disease (CHD), diabetes mellitus, and various types of cancer. Hypertension is associated with high sodium intake. CHD is associated with intake of saturated fat. Stomach cancer is associated with dietary intake of nitrosamines. Colon
Epidemiological evidence indicates that for most nutritional diseases, it is excessive intake that constitutes a risk. Moderate intake of nutrients is not harmful and is even needed for homeostasis. Preventive medicine could lead to elimination of much human disease by encouraging change of dietary habits. The teachings of the prophet on nutritional intake reflect the concepts of moderation, balance, and equilibrium that were defined above. The prophet taught the rule of the thirds as a guide for food intake: one third for solid food, one third for water, and one third for air (Musnad al Imaam Ahmad). He also taught that Muslims are a community who do not eat until they are hungry and when they eat they do not fill their belly. Ibn al Qayim defined three levels of food as necessary, hajat, sufficient, kifayat, and excess, fadhlat. The necessary amount of food is that necessary for maintenance of life and health. The sufficient is more than the necessary and satisfies the psychological desire for food. The excess is what is beyond the body's needs and is definitely harmful to health. Excessive intake will lead to disease by overwhelming and impairing homeostatic mechanisms.
Humans appetite for food, a survival instinct, is so strong that the important obligation of salat is delayed when food is presented (16. Muslim # 1134, 1137, 17. MB # 403 p 227). Besides the instinctive urge to eat, underlying visions of life and its purpose, culturally-dependent food preferences, patterns of social eating, food availability, and food advertising. There is a difference in attitude to feeding between the believer and non-believer (18. Shahih al Bukhari Kitaab 70 Baab 12; 19. Sahih Muslim Kitaab 36; 20. Sunan al Tirmidhi Kitaab 23 Baab 20, 21. Sunan Ibn Majah Kitaab 29 Baab 3; 22. Sunan al Darimi Kitaab 8 Baab 13; 23. Muwatta Malik Kitaab 49 Baab 9 and 10). The believer eats to get energy for ibadat. The non-believer may eat for enjoyment or to get energy for evil. There is blessing in the food of the believer; he gets satisfied easily. The non-believer has to eat more food to get the same satisfaction. The Prophet Muhammad (PBUH) in a very revealing hadith mentioned that a believer eats in one bowel whereas a non-believer eats in 7 bowels.
Fasting of Ramadhan is one the major acts of obligatory physical ibadat. Muslims are encouraged to undertake supererogatory fasting. Fasting cleanses the body, al siyam zakat al jism (24. Sunan Ibn Majah Kitaab 7 Baab 44). It is a lesson in self-control. Its biological implication is teaching self-control and self-discipline in a practical way. Fasting besides its function as a type of ibadat, is training in the control of human appetite.
UNIT 9.4
DISEASE SURVEILLANCE
Learning Objectives
- Definition and Types of surveillance
- Methods of surveillance
- Evaluation of surveillance
Key Words and Terms
- Surveillance, disease surveillance
- Surveillance, Morbidity surveillance
- Disease control.
- Surveillance, active surveillance
- Surveillance, passive surveillance
- Surveillance, sentinel surveillance
- Surveillance, laboratory-based surveillance
- Disease notification
- Disease registries
- Vital records
- Surveys for surveillance
- Uses of surveillance data
- Surveillance system
- Evaluation of surveillance
UNIT OUTLINE
9.4.1 DEFINITION
A. Who Definition
B. Disease Control and Policy
C. Active and Passive Surveillance
9.4.2 HISTORY OF SURVEILLANCE
A. Ancient Period
B. Britain:
C. US:
D. Others
9.4.3 OBJECTIVES, METHODS, and SCOPE
A. Purpose/Objectives
B. Methods/Sources of Surveillance
C. Scope of Surveillance
D. Uses of Public Health Surveillance
9.4.4 SURVEILLANCE SYSTEM
A. Essentials of a Surveillance System
B. Characteristics of a Good Surveillance System
C. Evaluation of a Surveillance System
D. Ethical and Legal Issues
9.4.5 DATA COLLECTION, ANALYSIS, and INTERPRETATION
A. Preliminary Steps
B. Data Collection
C. Data Analysis
D. Data Interpretation
E. Data Dissemination
9.4.1 DEFINITION
A. W.H.O DEFINITION
In 1968 The World Health Organization defined surveillance as systematic collection and use of epidemiological information for planning, implementing, and assessing disease control.
B. DISEASE CONTROL AND POLICY
Surveillance is a continuous process of collection, analysis, interpretation, and dissemination of information that helps disease control and contributes to policy formulation.
C. ACTIVE AND PASSIVE SURVEILLANCE
Surveillance can be active or passive. In active surveillance mechanisms are set up to actively look for and identify disease conditions. Passive surveillance does not set up any special monitoring mechanisms but relies on the existing systems to report disease occurrence.
9.4.2 HISTORY OF SURVEILLANCE
A. ANCIENT PERIOD
Hippocrates mentioned observing, collecting, and analyzing facts to decide on a course of action.
B. BRITAIN
John Graunt carried out the first recorded surveillance activity in Europe by his analysis of the bills of mortality in London England and Wales UK UK
C. US:
Lemuel Shattuck (1839-1879) wrote a report in 1850 for the Massachusetts Sanitary Commission in which he related death, infant mortality, and maternal mortality to livinhg conditions. He recommended the decennial census, standardization of disease nomenclature, and collection of health data by age, gender, occupation, socio-economic level as well as locality. In its modern form, surveillance started as collection of morbidity data. In 1741 tavern owners in Rhode Island Rhode Island US Massachusetts Italy US US US US US
D. OTHERS
Since then surveillance has developed to become a common tool in public health. It was part of the malaria and small pox eradication programs. It is carried out at the moment for HIV/AIDS. Disease registers also developed as part of the surveillance system. The first cancer registry was established in Denmark
8.4.3 OBJECTIVES, METHODS, and SCOPE
A. PURPOSE/OBJECTIVES
Surveillance systems fulfill the following purposes: (a) identification of changes in disease incidence (b) epidemiological description of disease: incidence, causes, and associated factors (c) evaluation of disease control and prevention programs (c) assessment of the burden of disease to help health care delivery (d) planning of public health programs by future projection of disease burden (e) using surveillance data for formulating public health policy (f) prediction of the occurrence of epidemics (g) provide information for researchers. The concept of surveillance has shifted from surveillance of persons to surveillance of conditions.
B. METHODS/SOURCES OF SURVEILLANCE
Surveillance can be classified as active, passive, or sentinel. Surveillance can be based on disease notification systems, laboratory-based surveillance, disease registries, surveys, data bases (vital records, immunization registries, hospital data, insurance data, worker compensation), sentinel events, and record linkage. Vital statistics provide information in disease trends. The data is essentially complete in developed countries but may not be accurate for causes. Population based immunization data is useful in evaluating control measures. Reports from public health laboratories enable monitoring changes in infectious agents but may be incomplete in coverage. Disease notification data and hospital discharge data enables assessment of the disease burden and health practices but may be incomplete. Cancer registries usually have complete information but have no national coverage. Special surveys can be set up for purposes of surveillance.
C. SCOPE OF SURVEILLANCE
Surveillance monitors events of public health importance. It covers infectious disease, occupational health, environmental health, injuries, maternal and child health, and non-communicable disease. In addition to health events, surveillance includes information on risk factors, use of preventive and curative services.
D. USES OF PUBLIC HEALTH SURVEILLANCE
Uses of surveillance information can be divided into three types: immediate, medium term, and long term. The immediate uses are detection of epidemics, emerging diseases, changes in health practices, changes in demographic characteristics, and antibiotic resistance. Medium term uses are annual dissemination of information on the magnitude of health problems, assessing control activities, setting research priorities, testing hypotheses, facilitating planning, monitoring risk factors, and monitoring changes in health practices. Long term uses include providing databases for describing the natural history of disease, facilitating epidemiologic and laboratory research, validation of preliminary research, and setting research priorities (Epidemiology and Health Services: Haroutine K Armenian and Sam Shapiro. OUP New York and Oxford
8.4.4 SURVEILLANCE SYSTEM
A. ESSENTIALS OF A SURVEILLANCE SYSTEM
The essentials of a surveillance system are: data collection, data analysis, data interpretation, and feed-back or data dissemination. Before start of surveillance, the case definition and the target population must be defined. Appropriate personnel must be selected and trained. The logistics of data collection, analysis, and dissemination must be set up. Approvals from the relevant authorities must be obtained.
B. CHARACTERISTICS OF A GOOD SURVEILLANCE SYSTEM
A good surveillance system must be ongoing, practicable, uniform, frequent and rapid, sensitive, timely, representative, high predictive value, accurate, complete, simple, flexible, and acceptable.
C. EVALUATION OF A SURVEILLANCE SYSTEM
The surveillance system is evaluated using the following criteria: (a) attainment of objectives of surveillances: decrease of incidence and prevalence, decrease of indices of disease severity such as mortality and case fatality (b ) operational characteristics (sensitivity, timelinessness, representativeness, and predictive value), acceptability, flexibility, simplicity, and cost.
D. ETHICAL and LEGAL ISSUES
The following ethical principles may be violated: autonomy, beneficence, non malefacence, justice, veracity, privacy, confidentiality, and fidelity. The following could give rise to legal challenges: mandatory reporting of disease, privacy, right of the citizen to access surveillance information, and product liability.
8.4.5 DATA COLLECTION, ANALYSIS, and INTERPRETATION
A. PRELIMINARY STEPS
The following preliminary steps are followed in setting up a surveillance system: (a) definition of the objectives (b) definition of the target population (c) identification of the health problem or public health program to be surveilled. The definition of the problem including the case definition must be clear and concise. (d) Definition of data collection procedures including types of reports to be used, forms to be used in data collection, timing and frequency of data collection, aggregation of data, and methods of data transmission (e) Definition of data management procedures: record updates, record confidentiality (f) Dissemination and use of the information.
B. DATA COLLECTION
The sources of surveillance data are: (a) mandatory morbidity and mortality notification systems (b) Health information systems: vital records (births and deaths), coroner reports, medical care records (integrated health information system & hospital discharge summary), insurance records, worker compensation records, and records of work-absence due to illness, school records (c) disease registries e.g. cancer registry (hospital-based, population-based, and exposure registers) (d) public health laboratory reports, (e) reports of disease outbreaks, epidemics, and individual case studies (f) vaccine utilization data, (g) records of hazard exposure surveillance (h) special surveys such as health interview surveys and other types of surveys (i) Sentinel surveillance that focuses on key health indicators for early warning. Sentinel events such as infant mortality and sentinel sites such as hospitals and clinics (j) Studies of animal reservoirs and vector distribution (k) study of biological markers (l) study of drug resistance (m) demographic and environmental data (n) media reports.
Computerized surveillance systems: The availability of high capacity data storage and net-working have made computerization of surveillance easier. Video and voice input allow more efficient interviewing. User friendly software.
C. DATA ANALYSIS
Data analysis procedures: Data analysis is usually descriptive and usually consists of comparing with the baseline. Data analysis should start with exploratory data displays (data plots, stem and leaf, and scatter plots), graphical displays (tables, graphs, bar diagrams), descriptive analysis and data summary (median, mean, standard deviation). More sophisticated methods such as regression and time series analysis can then be applied. Trend analysis is very crucial. A decision must be made whether the trends seen are real. If real are they seasonal or cyclic. The following measures of morbidity are used: incidence rate, attack rate, secondary attack rate, point prevalence, and period prevalence. The measures of mortality used are: crude death rate, cause-specific death rate, proportional mortality ratio, case fatality ratio, neonatal mortality ratio, infant mortality rate, and maternal mortality rate. The natality neasures used are: crude birth rate, crude fertility rate, crude rate of natural population increase, low-birth weight rate. Both direct and indirect standardization may be used. The bias due to under-reporting in most surveillance systems restricts use of more sophisticated statistical techniques. Special analytical techniques could be used to identify clusters that may be epidemics or outbreaks. Time series methods are used to analyze for secular trends, cyclic patterns, and seasonal behavior. The autoregressive integrated moving average (ARIMA).
D. DATA INTERPRETATION
Interpretation of surveillance data: Surveillance data is interpreted with the following in mind: identification of epidemics, identification of new syndromes, monitoring trends, evaluation of public policy, and projecting future needs. Observation of departures from usual disease distribution does not necessarily mean that there is a problem. Completeness of coverage of the surveillance system is an issue that may arise. Capture-recapture methods may be used to ascertain whether the surveillance system has adequate coverage. Surveillance data has limitations such as under reporting, unrepresentative case series, and inconsistent case definitions.
E. DATA DISSEMINATION
Methods of data dissemination: publications, mass media, etc. The message to be communicated must be packaged correctly and appropriately. The characteristics of the target audience must be known. Suitable channels of communication must be used. The effect of the communication must be evaluated. Data dissemination need not wait until the surveillance system is fully operational; provisional surveillance data is still useful in public health.
UNIT 9.5
DISEASE SCREENING
Learning Objectives
- Screening: definition, types, benefits
- Methods of screening
- Evaluation of screening
Key Words and Terms
- Screening, breast cancer screening
- Screening, cervical cancer screening
- Genetic screening
- Lead time bias
- Length bias
- Selection bias
- Mammography
- Mass screening
- Multi-phasic screening
- Neonatal screening
- Pap smear
- Pre-natal screening
- Vision screening
UNIT OUTLINE
9.5.1 DEFINITION, OBJECTIVES, ORGANIZATION, and BENEFITS
A. Definition of Screening
B. Objectives of the Screening Program
C. Screening Procedures
D. Benefits & Disadvantages of Screening Programs
E. Examples of Screening Programs
9.5.2 CHARACTERISTICS OF DISEASE & SCREENING TESTS
A. Suitable Disease
B. Worth-While Screening Test/Procedure
C. Process Parameters of Screening Procedures
D. Outcome Parameters of A Screening Program
E. Biases in the Interpretation of Screening Results
9.5.3 EPIDEMIOLOGIC EVALUATION OF SCREENING PROGRAMS
A. Factors of Screening Program Effectiveness
B. Process Evaluation
C. Outcome Evaluation
D. Evaluation of Specific Screening Programs
E. Improving Screening Programs
9.5.4 COST BENEFIT ANALYSIS OF SCREENING PROGRAMS
A. Financial Costs
B. Human Costs
C. Benefits
D. Hazards of Screening:
E. Recommended Screening Schedules
9.5.5 ETHICAL ISSUES
A. Benefit Vs Harm
B. Efficacy
C. Adverse Social Consequences
D. False Positive and False Negative Results
E. Others
9.5.1 DEFINITION, OBJECTIVES, ORGANIZATION, and BENEFITS
A. DEFINITION OF SCREENING
Screening is a type of secondary prevention involving identification of apparently healthy persons are at risk for further diagnostic or therapeutic interventions. It must be emphasized that screening by itself is not diagnostic. The World Health Organisation defines screening as presumptive identification of unrecognized disease or defect by the application of tests, examinations or other procedures which can be applied easily (WHO 1968). Screening can be looked at in two ways. Screening for pre-clinical disease is part of routine practice of preventive medicine for example BP measurement and x-rays. It can be extended to become mass screening of the whole population. Mass screening is population screening. Screening can be mass screening involving the whole population. It may be regular routine screening or episodic and adhoc. It may be selective or comprehensive. Screening is usually associated with chronic disease. It can also be used in infectious disease. Comprehensive cancer screening program. The players in screening programs are: public health departments, managed care organizations, community based coalitions for specific diseases, and workplace coalitions.
B. OBJECTIVES OF THE SCREENING PROGRAM
A screening program aims at achieving 3 major objectives: decrease of morbidity, decrease of mortality, and improving the quality of life. The effectiveness of the screening program is assessed on how well the above objectives are achieved. The objectives are achieved through early detection and treatment of disease. Downstaging is detection of disease at an earlier stage when it is curable. Downstaging of cervical cancer can be done by nurses and non-medical health workers who can use a simple speculum for visual inspection. Oral inspection is used to downstage oral cancer. BSE is downstaging breast cancer.
C. SCREENING PROCEDURES
Screening test/procedures can be simple or complex. Screening is occurring all the time in the clinical setting though the caregivers and the patients may not be consciously aware of it. Simple clinical questions are to identify those at risk eg maternal age for Down’s syndrome. Special tests are used for example clinical examination (breast exam), laboratory (serum AFP), and radiological (mammogram).
The target population must be identified. The population may be defined as a community or an institution (school, factory, and neighborhood). Mass screening covers the whole target population. Selective screening covers only defined segments of the target population. Risk stratification may be employed in selecting individuals to screen. The publicity for the program must ensure high coverage and uptake retention. Adequate resources must be deployed to ensure success of the program. Quality control procedures must be instituted from the beginning. An efficient referral system must be set up. All personnel must be trained. The program must be evaluated.
D. BENEFITS and DISADVANTAGES OF THE SCREENING PROGRAMS
A screening program may have public, private, and individual benefits. These benefits sometimes interact or even are contrary to one another. TB screening has a public benefit in that cases of infectious disease are identified and are treated so that they pose no further danger to the public. Screening may have a private benefit. HIV screening by insurance companies has no public benefit because the companies do not disclose the results to the public or the person screened. However the information is useful in their decisions to insure persons and what premiums to charge. Screening may have a direct benefit to the individual. It improves prognosis and enables earlier treatment with less radical therapy. Screening for childhood diseases and their subsequent treatment is beneficial to the child. Screening is reassurance for those with negative results
DISADVANTAGES OF SCREENING
There are several disadvantages associated with screening. Screen –detected cases whose disease can not be cures suffer from a longer period of morbidity. Borderline lesions may be overtreated when if left alone they would not progress to serious disease. False negatives is false reassurance that will discourage them from seeking care when early symptoms appear. False positives live with anxiety longer than necessary. False positives undergo unnecessary medical intervention. Screening tests have their own risks and costs.
E. EXAMPLES OF SCREENING PROGRAMS
CARDIOVASCULAR SCREENING: Screening for high blood pressure
CANCER SCREENING: Breast cancer screening is by mammography screening every 1-2 years is recommended in women above 50 years. There is no proof that BSE and mammography are useful in women below 50 years of age. Mammography for women below 50 years is done only if there is a family history of breast cancer. Screening mammography has a false negative rate of 10-20%. Cervical cancer screening is by use of the PAP smear test is very popular and is recommended for women above 20 years every 3 years. A positive PAP smear test may regress during follow up. Other screening tests are colposcopy, cervicography, Schiller’s test using Lugol’s iodine, the acetic acid test, and the HPV DNA test. Ovarian cancer screening by pelvic examination is of limited value. CA-125 is a cheap but non-specific test. Other tests are trans-vaginal ultrasonography, CAT, MRI, and use of monoclonal antibodies. Endometrial cancer screening is by cytology of endometrial samples. Neuroblastoma screening uses vinyl mandelic acid and homovanillic acid. Colon
GENETIC SCREENING: Genetic screening is screening for chromosomal abnormalities, single gene disorders, and multifactorial disorders. Targets of screening are neonates, older children, and pregnant women.
OTHER TYPES OF SCREENING: Screening can be carried out for congenital dislocation of the hips in the neonates and for shoulder joint dislocations.
8.5.2 CHARACTERISTICS OF DISEASE & SCREENING TESTS
A. SUITABLE DISEASE
A disease suitable for screening must have certain characteristics. It must be definable clearly. Its natural history must be known with a relatively long detectable pre-clinical phase. It must be sufficiently common (known prevalence). It must be serious with a heavy burden of suffering. It must have effective treatment if detected early. Pre-symptomatic treatment must be able to make a difference. Treatment facilities must be available.
B. WORTH-WHILE SCREENING TEST/PROCEDURE
The screening test must be simple, cheap and cost-effective, acceptable, safe, and perform optimally (high sensitivity, high specificity, low false positive, suitable cut-off level, and reliability): False negative tests are falsely reassuring and may be a reason for delay of treatment. False positive tests lead to anxiety and unnecessary diagnostic and therapeutic procedures. The test must be ethical (the test and the subsequent diagnostic and intervention procedures must be ethical).
C. PROCESS PARAMETERS OF SCREENING PROCEDURES
The following parameters are process measures that measure how effective the program is: accuracy, validity, reliability, and predictive value. They can be defined by reference to the figure below They are process measures that measure how effective the program is.
Figure #: Showing screening parameters
Test result + | Test result - | |
Disease + | A | B |
Disease - | C | D |
The accuracy of the screening test can be established by comparing findings of the test and clinical or diagnostic confirmatory tests. True positive(TP)=a . True negative(TN)=d. False negative(FN)=b. False positive(FP)=c. The validity of the screening test is assessed by its sensitivity and specificity. Sensitivity, measured as a/a+b, is the ability to pick up preclinical disease. Specificity, measured as d/c+d, is ability to classify non-diseased people correctly. A trade-off must be made between the two parameters because they are inversely related as shown in the receiver operation curve (ROC) below. Reliability is the ability of the test to give the same result, positive or negative, on repeated applications. The predictive value of a positive test (PV+), measured as a/(a+c), is the proportion of people with a positive test who actually have the disease. A high value of PV+ indicates good cost-benefit and a low value of PV+ indicates low cost benefit. The predictive value of a negative test (PV-), measured as d/(b+d), is the proportion of people with a negative test who do not have the disease. Values of PV- closer to 1.0 indicates that the test is reasuring. Both PV+ and PV- are determined by test characteristics and disease characteristics. The higher the sensitivity the higher the value of PV+. The higher the prevalence, the higher the value of PV+. It is therefore better to screen high risk populations. Prevalence has no effect on PV-. Screening results can also be stated in terms of likelihoods. The likelihood ratio of a positive screening test is computed as LR(+) = {Pr(T+|D+)} / {Pr(T+|D-)} = sensitivity / 1 – specificity. The likelihood ratio of a negative screening test is computed as LR(-) = {Pr(T-|D+)} / {Pr(T-|D-)} = 1 – sensitivity / specificity.
D. OUTCOME PARAMETERS OF A SCREENING PROGRAM
The outcome of a screening program is assessed based health outcomes (reduction of morbidity, reduction of mortality, and improvement in the quality of life) or economic outcomes. Correct interpretation of the outcome measures requires understanding of the natural history of the disease especially its time line (as shown in figure #). The natural history of the disease is intimately related to screening parameters. The time-line below shows various events in disease evolution. Disease onset is at T1. At T2 disease is detectable by screening. The screening test is done at T3. Clinical disease onset is at T4. It is possible to compute and interpret various time interval measurements. The delay time is T3-T2. The lead time is T4-T3. Total pre-clinical disease is T4-T1. The total pre-clinical detectable disease phase is T4-T2.
E. BIASES IN THE INTERPRETATION OF SCREENING RESULTS
Correct interpretation of the screening results requires appreciation of lead-time bias, length bias, selection bias, over diagnosis bias, and overtreatment bias. Lead time is amount of time by which the diagnosis is early. Earlier diagnosis of disease does not change the natural history of the disease but could give an apparent picture of better survival for screen-detected cases. The earlier detection of disease leads to a longer period of morbidity. This may not be accompanied by any change in survival had the disease been detected clinically. Some screen-detected cases may not develop into clinical disease because they are biologically different. Their detection causes morbidity, worry and anxiety. It leads to further diagnostic work-up and therapeutic procedures that could be risky but are yet unnecessary. Length bias could give a false picture of better survival in screen-detected cases because prevalent cases with slower-growing lesions are detected by screening more than incident cases with rapidly-growing lesions that are more easily detected clinically. Selection bias occurs when cases with a good prognosis are more likely to be screened than those with a bad prognosis. Overdiagnosis bias or overtreatment arise when lesions that are histologically malignant are treated whereas they would have never progressed to invasive disease.
9.5.3 EPIDEMIOLOGIC EVALUATION OF SCREENING PROGRAMS
A. FACTORS OF SCREENING PROGRAM EFFECTIVENESS
The effectiveness of the screening program is affected by the test used, the attendance or coverage, the screening interval, and success of referral for diagnostic confirmation. Effects of a single screen are different from those of repeated screening. After a single screen, incidence increases dramatically due to detection of pre-clinical cases. The incidence then falls to below pre-screen levels and gradually build up to the pre-screen levels (see figure below). Care must be taken in interpreting this data because death may be just postponed if the early treatment following screening removes tumor bulk but does not eradicate disease. Some cases die of competing causes of death during the period of postponement. Repeated screening results in lower average disease-specific death rates and increase in the number of years of life gained.
B. PROCESS EVALUATION
The various parameters of accuracy, validity, and predictability give an indication on the test. Other process measures that can be used are the number referred for screening, the number whoi received at least one screening, the number who receib=ved multiple screenings, the number screened as a proportion of the target population, number found positive, number of pre-clinical cases detected, number of cases confirmed, number referred for diagnostic work-up, total cost of the program, cost per case detected by screening.
C. OUTCOME EVALUATION
It is easy to tell whether screening has benefited an individual if his or her disease is discovered early and is treated. Longer survival of screen-detected cases compared to normally-detected cases is a useful outcome measure. It is not easy to tell whether a screening program has made a difference in morbidity and mortality for the general population. Controversy is over whether risk and costs borne by the individual are commensurate with the benefit that is measurable only for the whole population. Selection bias, over-diagnosis bias, length bias, and lead-time bias complicate the interpretation of morbidity and mortality data. Selection bias occurs in the form of referral bias or volunteer bias. It is the situation in which the screened population does not have the same characteristics as the unscreened. For example volunteers are healthier and more health-conscious than non-volunteers. Over diagnosis bias arises due to higher diagnostic enthusiasm due to the screening program. Length bias, a type of prognostic bias, is a situation in which screen-detected cases have grow more slowly and are easy to detect by screening and have a better prognosis. Lead-time bias arises when screen-detected cases appear to have improved survival when actually screening made no difference to the time of death but increased the time they were under observation. Lead-time bias could be the reason for false 5-year survival rates.
Outcome measures are decrease in mortality, decrease of case fatality, decrease in site-specific mortality, increase in the proportion of early diagnosis, stage distribution of screening-detected cases, decrease in complications, decrease in recurrence, and improved quality of life. Three approaches are available for assessing outcome. The outcome in the screened population could be compared to data in the same population before the screening program or could be compared to data of similar populations in an ecologic study. This is fraught with a lot of interpretive complications because of confounding bias. A case control study could be set up in which morbidity and mortality are compared among screened and non-screened individuals. This may however not assess the whole program because there are parameters in the general population that affect outcome but may not be measured by the case control study. The best approach is to select a study population and randomize subjects to the screening or non-screening groups. Morbidity and mortality are then compared after a suitable duration of the study.
D. EVALUATION OF BREAST CANCER SCREENING PROGRAMS
Case Control Studies: In the case control design, cases are selected as subjects with advanced disease. Controls are selected as a sample of healthy people from the population. The study exposure is the screening program. Four examples of case control studies of breast cancer screening were cited (Douglas S Reintgen and Robert Clark (eds): Cancer Screening. Mosby New York Netherlands Nijmegen study in the Netherlands UK Florence
Randomized Controlled Studies: In the randomized design, a population is randomly allocated to the screen and non-screen group. The most famous example of a randomized study was the study of the Health Insurance Plan of New York in 1963 in which 62,000 women aged 40-64 were randomized to screening (31,000) and non screening groups (31,000). The total number of women analyzed for the study ended up as 60, 995. The screening group had an initial screening followed by annual screening using physical examination (clinical breast examination), 2-view mammography, and interview. The screening interval was 12 months with a total of 4 screening rounds. Follow-up was for 10 years extended to 18 years. Thirty nine (39) cases were detected in the screened group (IR = 2.6/100,000) and 63 cases were detected in the unscreened group (IR = 4.1/100,00). The study found a relative risk of 0.71 (0.55-0.93) for women of all ages and 0.77(0.50-1.16) for women aged less 50 years. Among the screened group, case fatality was higher among cases detected in the interval between screens rather than at the scheduled screening. Other randomized studies were described by (Douglas S Reintgen and Robert Clark (eds): Cancer Screening. Mosby New York ?date) as follows: studies in Sweden at Kopparberg, Ostergotland, Malmo , Stockholm UK at Edinburgh , and 2 studies in 2 Canada
The Ostergotland study started in 1977, enrolled women aged 40-74 who underwent 6 screening rounds using 1-view mammographic examination at screening intervals of 24-33 months and for a duration of 12 years. It found a relative risk of 0.82(0.64-1.05) for women of all ages and 1.28(0.76-2.33) for women aged below 50 years. The Malmo Stockholm Edinburgh
Apparent lack of benefit from a screening program could be due to two reasons. The disease may have no detectable pre-clinical phase. The therapeutic intervention may not be effective.
EVALUATION OF CERVICAL CANCER SCREENING PROGRAMS
EVALUATION OF LUNG CANCER SCREENING PROGRAMS (Douglas S Reintgen and Robert Clark (eds): Cancer Screening. Mosby New York
Early non-randomized Studies: In the 1950s several non-randomized studies were carried out. Studies reported in 1959 from London and Philadelphia
Prospective non-randomized studies: In the 1970s lung cancer prospective screening trials were carried out at Johns Hopkins, the Mayo Clinic, and Memorial-Sloan Kettering Cancer Center
EVALUATION OF COLON
(Douglas S Reintgen and Robert Clark (eds): Cancer Screening. Mosby New York
Case Control Studies: Three case control studies are described: The Kaiser Permanente Study, The Marshfield Study, and The Puget Sound Study. The Kaiser Permanente Study involved cases selected as members in Northern California aged 50 or more diagnosed with colon cancer in the period 1981-1987 and subsequently died of the disease before December 1998. One control from the plan membership was matched to each case by age, sex, and date of entry into the health plan. Outpatient records were reviewed for both cases and controls for the past 10 years for evidence of FOBT screening. An adjusted odds ratio with 95% confidence intervals was found as 0.69(0.52-091) for exposure to at least 1 screening in the past 5 years. This indicated that FOBT screening reduced colo-rectal cancer mortality by 31%. A population-based case control study in Saarland in Germany Marshfield Puget sound case control study recruited cases who were members of an HMO and subsequently died of colorectal adenocarcinoma. Controls were randomly selected from the HMO list and were matched to cased based on year of birth, gender, and year of enrolment. The odds ratio for those screened with FOBT before age 75 was 0.95(0.67-1.36) and for those screened after age 75 it was 0.98(0.49-1.96). These studied show that FOBT screening is of benefit.
Randomized Controlled Trials: Three randomized studies were reported from Minnesotta, Goteborg , Nottingham , and Funen. The Minnesota Goteborg Nottingham study started in 1981 and enrolled 144,103 subjects aged 50-74 screened by Hemoccult biannually and diagnostic examination was carried out by colonoscopy. The study has sensitivity 68%, specificity 98%, and predictive value 11.5%. The Funen study started in 1985 and enrolled 61,308 subjects aged 45-75 screened by Hemoccult II binannually and diagnostic examination was by colonoscopy. The study has sensitivity 48%, specificity 99%, and predictive value 8.2%.
IMPROVING SCREENING PROGRAMS
The following measures can be used to improve screening program effectiveness: selective screening, optimal screening frequency, multi-phase screening, and sequential screening. Selective screening can be by age, gender, and high risk groups. More frequent screening will detect more cases and earlier but is expensive and could discourage people from participation. Long intervals between screens may miss many cases. Multi-phase screening or multiple screening: screening for more than one disease. Sequential screening: screening can be carried out in 2 stages starting with a cheaper test and then applying a more expensive test.
9.5.4 COST BENEFIT ANALYSIS OF SCREENING PROGRAMS
A. FINANCIAL COSTS
This includes the cost of screening and the cost of further diagnostic work-up and treatment of screen-detected cases. There are also financial costs to the screened subjects themselves because they have to leave work and go for screening. The cost are relatively higher if they screen negative. False positive and false negative screens are an additional cost. Rehabilitation of detected cases is an additional health cost. Death is a cost to the family and the estate.
B. HUMAN COSTS
The human costs of screening programs include: (a) inappropriate reassurance for false negatives. (b) anxiety in the positives (c) false morbidity in the false positive (d) generation of true morbidity and problems eg SCD screening revealing illegitimacy (e) opportunity costs
C. BENEFITS
The benefits of screening programs include: (a) prevention of disease, disability, and handicap. This benefit is quantified by the number of cancers detected, Quality adjusted life years (QUALY) and healthy years equivalent (HYE). (b) patient concerns are alleviated by early diagnosis (c) genetic counseling is possible (d) service provision/access to services (e) decrease of health service expenditure by early detection and treatment. For regular participants in screening programs two types of cancer can be detected: screen detected cancer and interval cancer that is detected in the routine way.
D. HAZARDS OF SCREENING:
E. RECOMMENDED SCREENING SCHEDULES FOR DIFFERENT DISEASES IN ASYMPTOMATIC CASES (US) Jekel et al Epidemiology, Biostatistics, and Preventive Medicine WB Saunders Philadelphia ? year)
Cancers: Annual breast examination is recommended for all women 40 years and above. Mammography is recommended every 1-2 years for women 50-75 years. Papanicolaou testing is recommended every 3 years for women of all ages who are sexually active. FOBT and colonoscopy for colon cancer are recommended for those aged 50, or have a family history of colon cancer, or have a family history of polyposis. Routine screening is not recommended for lung cancer by sputum cytology, ovarian cancer, pancreatic cancer, or prostate cancer. Screening for oral cancer and testicular cancer is done for those with specific risk factors.
Congenital Conditions: Amniocentesis for karyotyping is offered to all women aged 35 years and higher. Alpha feto-protein levels should be measured at weeks 16-18. Routine ultrasound examination is not recommended
Perinatal conditions: For fetal distress, heart monitoring by auscultation is sufficient. Electronic monitoring is carried out only for women at very high risk. Ultrasound examination is carried out for women whose fetuses are at high risk for intra-uterine growth retardation. Blood pressure monitoring during pregnancy and labor is carried out for pre-ecclampsia.
Hematological conditions: Hemoglobin determination for anemia is carried out in pregnant women and infants in the first year of life. Hemoglobinopathy analysis is recommended for newborns of African, Mediterranean , and south-east Asian origin. Screening for Rh compatibility is carried out in the first pre-natal visit by testing for ABO and Rh status. Unsensitized women should be given Rh(D) immune globulin at 23-29 weeks of gestation.
Infectious Diseases: Periodic dipstick urine testing is recommended for diabetic patients and pregnant women. Culture for genital herpes infection is recommended for pregnant women with a history of infection or whose partners have had lesions. Pregnant women should have an endocervical culture for gonorrhea and chlamydial infections. Pregnancy women should be tested for HBV infection in the 3rd trimester. Persons with multiple sexual partners or those who use intravenous drugs should be tested for HIV. Serological testing for rubella is recommended for all women in the child bearing age. Pregnantb women should be tested for syphilis at the first pre-natal visit. Persons at high risk of tuberculosis should undergo tuberculin testing.
Metabolic and genetic diseases: Routine testing for hyperglycemia is recommended in high risk groups and pregnant women at 24-28 weeks of gestation. Periodic height and weight determinations are recommended in children and adults to detect obesity. Routine x-rays for osteoporosis are not recommended. Phenylketonuria testing of all newborns is recommended. Newborns are screened for hypothyroidism in the first week of life.
Vascular diseases: Screening for cerebrovascular disease and coronary heart disease is based on screening for its risk factors (diet, exercise, smoking, and hypertension). Periodic testing for serum cholesterol is recommended in the middle aged. Regular measurement of blood pressure for hypertension is recommended for all persona aged 3 years and over. No routine screening for peripheral artery disease is recommended.
OTHER DISEASES
Alcohol and drug abuse: Routine biochemical screening is not recommended
Dementia: Routine screening of asymptomatic persons is not recommended
Depression and suicide: Routine screening is not recommended
Vision: Routine screening is carried out in the pre-school period at ages 3 or 4.
Glaucoma screening is done only for people aged 65 and over
Hearing impairment: children at high risk of hearing impairment should be screened before the age of 3 years. There is no recommended routine screening for low back injury.
9.5.5 ETHICAL ISSUES
A. BENEFIT vs HARM
In general the benefit of screening must outweigh the harm.
B. EFFICACY
It is unethical to offer a screening program whose efficacy has not been proved in a proper trial. Definitive evidence of efficacy is available only for breast cancer and cervical cancer.
C. ADVERSE SOCIAL CONSEQUENCES
The results of genetic screening may have several adverse consequences such as stigmatization, discrimination, abortion, and psychological stress.
D. FALSE POSITIVE and FALSE NEGATIVE RESULTS
False positive results create unnecessary distress. False negative results create a false sense of security. True negative results may cause complacency. True positive results lead to worry and anxiety.
E. OTHERS
Screening programs may create an ethical issue by diverting resources away from other health programs. Failure to obtain informed consent is a serious ethical violation.