University of Gondar

College of Medicine and Health Sciences

Institute of Public Health

Department of Epidemiology and Biostatistics

EPIDEMOLOGY INDIVIDUAL ASSIGNMENT

By: Shimels Derso (Section B, HI Department)

Submitted to: Ejigu Gebeye (MPH, Associate Professor)

February 22, 2021
Table of Contents
Historical Evolution of Epidemiology ................................................................................................... 2
Branches of Epidemiology ................................................................................................................... 3
Epidemiologic transition...................................................................................................................... 4
Disease Control, Elimination, Eradication and Extinction..................................................................... 5
Parameters to label a disease public health important in surveillance system ......................................... 5
Why Measles vaccine don't given before 9 month, is there a scenario given before 9 month? .................. 5
References ........................................................................................................................................ 6
Historical Evolution of Epidemiology
Although epidemiology as a discipline has blossomed since World War II, epidemiologic thinking has been traced
from Hippocrates through John Graunt, William Farr, John Snow, and others. The contributions of some of these
early and more recent thinkers are described below.

Circa 400 B.C

Hippocrates attempted to explain disease occurrence from a rational rather than a supernatural viewpoint. In his
essay entitled “On Airs, Waters, and Places,” Hippocrates suggested that environmental and host factors such as
behaviors might influence the development of disease.

1662
Another early contributor to epidemiology was John Graunt, a London haberdasher and councilman who
published a landmark analysis of mortality data in 1662. This publication was the first to quantify patterns of
birth, death, and disease occurrence, noting disparities between males and females, high infant mortality,
urban/rural differences, and seasonal variations.

1800
William Farr built upon Graunt’s work by systematically collecting and analyzing Britain’s mortality statistics.
Farr, considered the father of modern vital statistics and surveillance, developed many of the basic practices used
today in vital statistics and disease classification.

1854
In the mid-1800s, an anesthesiologist named John Snow was conducting a series of investigations in London that
warrant his being considered the “father of field epidemiology.” Twenty years before the development of the
microscope, Snow conducted studies of cholera outbreaks both to discover the cause of disease and to prevent its
recurrence.

Snow conducted one of his now famous studies in 1854 when an epidemic of cholera erupted in the Golden
Square of London.(5) He began his investigation by determining where in this area persons with cholera lived and
worked.

19th and 20th centuries

In the mid- and late-1800s, epidemiological methods began to be applied in the investigation of disease
occurrence. At that time, most investigators focused on acute infectious diseases. In the 1930s and 1940s,
epidemiologists extended their methods to noninfectious diseases. During the 1960s and early 1970s health
workers applied epidemiologic methods to eradicate naturally occurring smallpox worldwide. In the 1980s,
epidemiology was extended to the studies of injuries and violence. In the 1990s, the related fields of molecular
and genetic epidemiology took root. Beginning in the 1990s and accelerating after the terrorist attacks of
September 11, 2001, epidemiologists have had to consider not only natural transmission of infectious organisms
but also deliberate spread through biologic warfare and bioterrorism.
Today, public health workers throughout the world accept and use epidemiology regularly to characterize the
health of their communities and to solve day-to-day problems, large and small.
Branches of Epidemiology
1. Molecular Epidemiology
This branch of epidemiology is concerned with the application of molecular biology to study various
epidemiologic problems.
Various molecular biology techniques such as DNA cloning, nucleic acid analysis, polymerase chain
reaction, etc. are applied in this study.
2. Disaster Epidemiology
It is a branch of epidemiology that studies the factors that cause disasters.
It is also concerned with the study to find mechanisms in order to reduce the negative health effects of
that disaster.
Its main objective is to generate information so that the disaster relief workers could be aware about the
situation. It uses techniques such as identification of potential diseases, establishment of surveillance
systems, etc.
3. Forensic Epidemiology
It contains the mixture of principles and practices common to both forensic medicine and epidemiology.
It is involved in formulation of evidence-based probabilistic conclusions about the type and quantity of
causal association between an antecedent harmful exposure and an injury or disease outcome in both
populations and individuals. The conclusions resulting from analysis can support legal decision-making
regarding guilt or innocence in criminal actions, and provide an evidentiary support for findings of causal
association in civil actions.
4. Environmental Epidemiology
Environmental epidemiology is a branch of epidemiology concerned with determining how
environmental exposures impact human health.
This field seeks to understand how various external risk factors may predispose to or protect against
disease, illness, injury, developmental abnormalities, or death.
5. Travel Epidemiology
It is a specific branch of epidemiology that is concerned with the health risks associated with travelling.
One of the main purposes of travel epidemiology is to provide necessary health-related information so
that the travellers can plan a safe journey. For example, in high altitude regions health issues like snow
blindness, heat exhaustion, dehydration, frostbite, etc. is possible.
6. Occupational Epidemiology
Occupational epidemiology is a sub-discipline of epidemiology that focuses on investigations of workers
and the workplace. Occupational epidemiologic studies examine health outcomes among workers, and
their potential association with conditions in the workplace including noise, chemicals, heat, or radiation,
or work organization such as schedules. Occupational epidemiological research can inform risk
assessments; development of standards and other risk management activities; and estimates of the co-
benefits and co-harms of policies designed to reduce risk factors or conditions that can affect human
health.
Epidemiologic transition
It’s the process by which the pattern of mortality and disease in a population is transformed from one of
high mortality among infants and children and episodic famine and epidemics affecting all age groups to
one of degenerative and human-made diseases (such as those attributed to smoking) affecting principally
the elderly.

Omran divided the epidemiological transition of mortality into three phases, in the last of which chronic
diseases replace infection as the primary cause of death. These phases are:

1. The Age of Pestilence and Famine: Mortality is high and fluctuating, precluding sustained
population growth, with low and variable life expectancy vacillating between 20 and 40 years. It is
characterized by an increase in infectious diseases, malnutrition and famine, common during the
Neolithic age. Before the first transition, the hominid ancestors were hunter-gatherers and foragers,
a lifestyle partly enabled by a small and dispersed population. However, unreliable and seasonal
food sources put communities at risk for periods of malnutrition.
2. The Age of Receding Pandemics: Mortality progressively declines, with the rate of decline
accelerating as epidemic peaks decrease in frequency. Average life expectancy increases steadily
from about 30 to 50 years. Population growth is sustained and begins to be exponential.
3. The Age of Degenerative and Man-Made Diseases: Mortality continues to decline and eventually
approaches stability at a relatively low level. Mortality is increasingly related to degenerative
diseases, cardiovascular disease (CVD), cancer, violence, accidents, and substance abuse, some of
these due primarily to human behavior patterns. The average life expectancy at birth rises gradually
until it exceeds 50 years. It is during this stage that fertility becomes the crucial factor in population
growth.

In 1998 Barrett et al. proposed two additional phases in which cardiovascular diseases diminish as a
cause of mortality due to changes in culture, lifestyle and diet, and diseases associated with aging
increase in prevalence. In the final phase, disease is largely controlled for those with access to education
and health care, but inequalities persist.

1. The Age of Declining CVD Mortality, Aging and Emerging Diseases: Technological advances in
medicine stabilize mortality and the birth rate levels off. Emerging diseases become increasingly
lethal due to antibiotic resistance, new pathogens like Ebola or Zika, and mutations that allow old
pathogens to overcome human immunity.
2. The Age of Aspired Quality of Life with Persistent Inequalities: The birth rate declines as lifespan
is extended, leading to an age-balanced population. Socioeconomic, ethnic, and gender inequalities
continue to manifest differences in mortality and fertility.

The epidemiological transition occurs when a country undergoes the process of transitioning from
developing nation to developed nation status. The developments of modern healthcare and medicine,
such as antibiotics, drastically reduce infant mortality rates and extend average life expectancy which,
coupled with subsequent declines in fertility rates, reflects a transition to chronic and degenerative
diseases as more important causes of death
Disease Control, Elimination, Eradication and Extinction
Although definitions outlined below were developed for infectious diseases, those for control and elimination
apply to noninfectious diseases as well.

● Control: The reduction of disease incidence, prevalence, morbidity or mortality to a locally acceptable
level as a result of deliberate efforts; continued intervention measures are required to maintain the
reduction. Example: diarrheal diseases.
● Elimination of disease: Reduction to zero of the incidence of a specified disease in a defined geographical
area as a result of deliberate efforts; continued intervention measures are required. Example: neonatal
tetanus.
● Elimination of infections: Reduction to zero of the incidence of infection caused by a specific agent in a
defined geographical area as a result of deliberate efforts; continued measures to prevent re-establishment
of transmission are required. Example: measles, poliomyelitis.
● Eradication: Permanent reduction to zero of the worldwide incidence of infection caused by a specific
agent as a result of deliberate efforts; intervention measures are no longer needed. Example: smallpox.
● Extinction: The specific infectious agent no longer exists in nature or in the laboratory. Example: none.

Parameters to label a disease public health important in surveillance system

Public health importance of the problem:

• incidence, prevalence,
• severity, sequela, disabilities,
• mortality caused by the problem,
• socioeconomic impact,
• communicability,
• potential for an outbreak,
• public perception and concern, and
• international requirements.

Why Measles vaccine don't given before 9 month, is there a scenario given before 9
month?
Measles vaccine immunogenicity and effectiveness are lower at 6 months than at later ages, and there
are concerns about the long-term effectiveness of an early 2-dose schedule and its potential for later
blunting of immunity.
Antibody avidity to measles virus is generally lower in children vaccinated at 6 or 9 months of age
compared with the avidity obtained in children vaccinated at age 12 months. Therefore, the
recommended age at vaccination must balance the risk of primary vaccine failure, which decreases with
increasing age, with the risk of measles virus infection prior to vaccination which increases with age. As
some individuals do not mount a protective immune response to MCV1, especially when it is given
before 12 months of age, a single dose may not lead to protection
Vaccinating infants before or at the age of 6 months often fails to induce seroconversion due to the
immaturity of the immune system as well as the presence of neutralizing maternal antibodies. The
median vaccine effectiveness of a single dose of MCV administered at 9–11 months and greater
than 12 months of age is 84%(interquartile range (IQR), 72–95%) and 92.5% (IQR, 84.8–97%),
respectively.
However, a new study (published on 2019) revealed that MCV1 administered to infants younger than 9
months induces a good immune response, whereby the proportion of infants seroconverted increases
with increased age at vaccination. A large proportion of infants receiving MCV1 before 9 months of
age are protected and the vaccine is safe, although higher antibody titres and vaccine
effectiveness are found when MCV1 is administered at older ages. Recommending MCV1
administration to infants younger than 9 months for those at high risk of measles is an important
step towards reducing measles-related mortality and morbidity.
scenario that measles given before 9 months
A supplementary dose of MCV should be given to infants from 6 months of age:
✓ during a measles outbreak as part of intensified service delivery;
✓ during campaigns where the risk of measles among infants < 9 months of age is high;
✓ for internally displaced populations, refugees, and populations in conflict zones;
✓ for individual infants at high risk of contracting measles;
✓ for infants travelling to countries experiencing measles outbreaks;
✓ for infants known to be HIV-infected or exposed

References
1. Principles of Epidemiology | Lesson 1 - Section 2. 11 May 2020,
https://www.cdc.gov/csels/dsepd/ss1978/lesson1/section2.html
2. “Branches of Epidemiology | Epidemiology.” Microbe Notes, 2 Jan. 2020,
https://microbenotes.com/branches-of-epidemiology/.
3. Britannica, The Editors of Encyclopaedia. "Epidemiologic transition". Encyclopedia Britannica,
Invalid Date, https://www.britannica.com/topic/epidemiologic-transition. Accessed 31 January
2021.
4. Epidemiological Transition.” Wikipedia, 11 Dec. 2020. Wikipedia,
https://en.wikipedia.org/w/index.php?title=Epidemiological_transition&oldid=99355778

5. The Principles of Disease Elimination and Eradication.

https://www.cdc.gov/mmwr/preview/mmwrhtml/su48a7.htm. Accessed 11 Feb. 2021.
6. Principles of Epidemiology: Lesson 5, Section 3|Self-Study Course SS1978|CDC. 11 May 2020,
https://www.cdc.gov/csels/dsepd/ss1978/lesson5/section3.html.
7. WHO Position Paper on Vaccines against measles virus April 2017
8. Nic Lochlainn, Laura M., et al. “Immunogenicity, Effectiveness, and Safety of Measles Vaccination in
Infants Younger than 9 Months: A Systematic Review and Meta-Analysis.” The Lancet Infectious
Diseases, vol. 19, no. 11, Nov. 2019, pp. 1235–45. DOI.org (Crossref), doi:10.1016/S1473-
3099(19)30395-0.
9. Basic Epidemiology Module. First Edition, 2017.
Assignment on Screening
1. A new test was developed for screening of breast cancer. This new test was applied on 750 women known
early cases of breast cancer and 900 women free from cervical cancer on the gold standard test. The new
test was positive for 600 women with breast cancer and 60 women without breast cancer

Answer
A. Construct a two-by-two table showing the above screening test results and disease status

Gold standard
Positive Negative Total
Screening Positive 600 (TP) 60 (FP) 660
test Negative 150 (FN) 840 (TN) 990
Total 750 900 1650
B. Calculate Sensitivity
𝑇𝑃 600
Sn= 𝑇𝑃+𝐹𝑁 = 600+150 *100%=80%
C. Calculate Specificity
𝑇𝑁 840
Sp = = *100%=93.3%
𝑇𝑁+𝐹𝑃 840+60
D. Calculate Positive predictive value (PPV)
𝑇𝑃 600
PPV=𝑇𝑃+𝐹𝑃 =600+60*100%=90.9%
E. Calculate Negative predictive value (NPV)
𝑇𝑁 840
NPV = = *100%=84.8%
𝑇𝑁+𝐹𝑁 840+150
F. Calculate yield
𝑇𝑃 600
Yield=𝑇𝑃+𝐹𝑃+𝑇𝑁+𝐹𝑁 =600+60+840+150*100% = 36.36%

2. A researcher conducted a study to see the validity of abdominal ultrasound in the diagnosis of
acute appendicitis by comparing it with intra-operative findings. There were a total of 500
patients out of whom 300 were confirmed to have acute appendicitis by surgery. Ultrasound
has detected only 100 of the 300. On the other hand, ultrasound wrongly labeled 50 persons as
appendicitis patients (while they were proved by surgery to have no appendicitis). Based on
the case answer from Q A-G
Answer

A. Prepare a 2X2 table

surgery
Positive Negative Total
abdominal Positive 100 (TP) 50 (FP) 150
ultrasound Negative 200 (FN) 150 (TN) 350
Total 300 200 500
B. Calculate Sensitivity
 𝑇𝑃 100
Sn= 𝑇𝑃+𝐹𝑁 = 100+200
*100%=33.33%

C. Calculate Specificity
𝑇𝑁 150
Sp = 𝑇𝑁+𝐹𝑃 = 150+50
*100%=75%
D. Calculate Positive predictive value (PPV)
𝑇𝑃 100
PPV=𝑇𝑃+𝐹𝑃 =100+50*100%=66.66%
E. Calculate Negative predictive value (NPV)
𝑇𝑁 150
NPV =𝑇𝑁+𝐹𝑁 =150+200*100%=42.85%
F. Accuracy : accuracy is also known as overall agreement so it’s given by
𝑇𝑃+𝑇𝑁 100+150
=
𝑇𝑃+𝐹𝑃+𝑇𝑁+𝐹𝑁 100+50+150+200
=250/500*100%= 50%
G. Calculate yield
𝑇𝑃 100
Yield=𝑇𝑃+𝐹𝑃+𝑇𝑁+𝐹𝑁 =100+50+150+200*100% = 20%
3. Two radiologists were asked to classify 100 chest x-rays as abnormal or normal independently.
The comparison of their classification is shown in the following table:

Answer

A. Kappa is a widely used test of inter or intra-observer agreement (or reliability) which corrects for chance
agreement
Defined as fraction of observed agreement not due to chance
B. Calculate Kappa agreement and comment on the result
𝑃(𝑂) − 𝑃(𝐸)
𝐾=
1 − 𝑃(𝐸)
Observed agreement= 40+30/100 = 0.7
Chance agreement for Normal-Normal cell=40*50/100 =20
Chance agreement for Abnormal-Abnormal cell=60*50/100 =30
Total Chance agreement=20+30/100=0.5
0.7−0.5)
𝐾= 1−0.5
=0.4
The kappa coefficient (K) 0.4 indicates fair agreement between the two radiologist’s measurement.
4. A school nurse examined a population of 2,000 school children in an attempt to detect
(preclinical) heart disease. Assume that the prevalence of heart disease in this school age
population is known to be 10%. The sensitivity of the nurse’s examination is 80% and
specificity is 80%. All school children who are labeled as positive (that is suspected of having
heart disease) by the school nurse are later sent for examination by a physician. The sensitivity
of the physician’s examination is 90%, and its specificity is also 90%.
 Answer

A. Complete a 2x2 table of nurse’s diagnosis by heart disease status

Gold standard
Sn1=0.8 Positive Negative Total
Sp1=0.8 nurse Positive 160 (TP) 360 (FP) 520
exam Negative 40 (FN) 1440 (TN) 1480
Total 200 1800 2000
B. How many children were labeled “positive” by the school nurse?
520
C. Of those sent to the physician, how many children were labeled “positive”? 180

Sn2=0.9
Positive Negative Total
Sp2=0.9
Physician Positive 144 (TP) 36 (FP) 180
exam Negative 16 (FN) 324 (TN) 340
Total 160 360 520
D. What is the net sensitivity of both examinations combined?
144/200=0.72 (OR)
Net Sn=Sn1*Sn2=0.8*0.9=0.72

E. What is the net specificity of both examinations combined?

1440+324/1800 =0.98 (OR)
Net Sp=Sp1+Sp2-(Sp1 * Sp2) =0.9+0. 8-(0.9*0.8) =1.7-0.72=0.98

5. Screening test of cancer ,Comparison with the gold standard of biopsy provided the following
results

Answer
A. What is the prevalence of cancer in this example?
𝑇𝑜𝑡𝑎𝑙 𝑑𝑖𝑠𝑒𝑎𝑠𝑒𝑑 350
Prevalence=𝑇𝑜𝑡𝑎𝑙 𝑝𝑜𝑝𝑢𝑙𝑎𝑡𝑖𝑜𝑛 ∗ 100% = 5600*100%=6.25%
B. Calculate and interpret the specificity and sensitivity.
 Sn= 325/350
Sp=4800/5250
C. Calculate and comment on the positive and negative predictive values
PPV=325/775
NPV=4800/4825
D. Calculate and comment on yield of the screening test
Yield=325/5600

6. Suppose that two different doctors examine 100 patients for dyspnea in a respiratory-disease
clinic and that doctor A diagnosed 15 patients as having dyspnea, doctor B diagnosed 10
patients as having dyspnea, and both doctor A and doctor B diagnosed 7 patients as having
dyspnea.
Answer

Doctor B
Positive Negative Total
Doctor Positive 7 8 15
A Negative 3 82 85
Total 10 90 100
A. Compute the Kappa statistic and its standard error regarding reproducibility of the
diagnosis of dyspnea in this clinic.

𝑃(𝑂) − 𝑃(𝐸)
𝐾=
1 − 𝑃(𝐸)
Observed agreement=7+82/100 =0.89
Chance agreement for positive-positive cell=15*10/100 =1.5
Chance agreement for negative-negative cell=85*90/100 =76.5
Total chance agreement= 1.5+76.5/100 =0.78
𝑃(𝑂)−𝑃(𝐸) 0.89−0.78
𝐾= = = 0.5
1−𝑃(𝐸) 1−0.78

➢ The standard error of is given by: (Cohen, J. (1960))

𝑃(𝑜)(1 − 𝑃(𝑜))
𝑆𝐸(𝑘) = √
𝑛(1 − 𝑃(𝐸))2

0.89 ∗ (1 − 0.89)
𝑆𝐸(𝑘) = √
100 ∗ (1 − 0.78)2
𝑆𝐸(𝐾) = 0.14

95% confidence interval for K is

[k-(1.96*SE(k)) to k+(1.96*SE(k))] = 0.5-(1.96*0.14), 0.5+(1.96*0.14)
0.36 to 0.64