Communicable diseases are caused by infectious agents that are transmitted between hosts. There are six links in the chain of disease transmission: the agent, its reservoir, its portal of exit, its mode of transmission, its portal of entry, and the susceptible human host. Diseases are transmitted either directly from person to person or indirectly through vectors or fomites. The interaction between the infectious agent, host factors, and environmental conditions determines whether a person develops disease. Models like the epidemiological triangle and web of causation are used to illustrate the complex interplay between these factors in disease causation.

1. Communicable diseases
Epidemiology
2
1

2. 2
Communicable disease (infectious disease)
 Is an illness due to a specific infectious agent or
its toxic products that arises through transmission
of that agent or its products from an infected
person, animal, or reservoir to a susceptible host,
either directly or indirectly through an
intermediate plant or animal host, vector, or the
inanimate environment.

3. The chain of disease transmission
3
•There are six links in the chain of infection

4. 4

5. 5
Components of the infectious process
 The infectious process of a specific disease can
be described by the following components,
which constitute of the chain of disease
transmission.
1. The Agent
2. Its reservoirs
3. Its portal of exits
4. Its mode of transmission
5. Its portals of entry
6. The human host

6. 6
I. The Agents
 The agents in the infectious process range from
viral particles to complex multi-cellular organisms
 Characteristics
– Size
– Chemical character
– Antigenic make up
– Ability to survive out side the host
– Ability to produce toxin

7. 7
Host -agent interaction
1. Infectivity
2. Pathogenicity
3. Virulence
4. Immunogenicty

8. 8
 Infectivity (infectiousness) -the ability of an agent to
invade and multiply in the susceptible host.
– Measured by the infection rate as
Number of infected X 100
Number of susceptible and exposed
 Pathogencity -The ability to produce clinically
apparent infection( diseases)
– Measured by clinical to subliminal ratio
Number of clinical cases
Number of sub clinical cases

9. 9
 Virulence -the proportion of clinical cases resulting
in severe clinical diseases
– Measured in different ways such as
– case fatality rate= number of fatal cases X 100
Total no of cases
hospitalization rate= number of hospitalized cases X 100
Total no of cases
 Immunogencity -the infection's ability to produce
specific immunity

10. 10
Class work
 One hundred people attended a wedding feast, and eighty
of them ate a piece of cake. Ten participant were latter
hospitalized .during investigation, It was found that the
weeding cake harbors the infectious agent .
Immunoglobulin class M antibodies an indicative of recent
infection were found in 60 of the 80 participants who had
eaten the cake, including the 10 hospitalized. Another 20
of the 60 participant with antibodies reported having
diarrhea but not serious to report health services
 From the data calculate
– Infectiousness
– Phathogenecity
– Virulence of infection

11. 11
Given
Total population ?
Number of exposed ?
Number of infected persons ?
Number clinical cases ?
Number of sub clinical ?

12. 12
Answer
Given
Total population =100
Number of exposed =80
Number of infected persons = 60
Number of ill ( clinical cases)
Sever cases (hospitalized) =10
Number of simple diarrhea =20
total 30
Number of sub clinical = infected – clinical cases
60-30= 30

13. 13
Solutions
 (infectiousness)
Number of infected X 100
Number of susceptible and exposed
60 X 100 = 75%
80
 Pathogencity
Number of clinical cases = 30 1:1
Number of sub clinical cases 30
 Virulence of infection
hospitalization rate= number of hospitalized cases X 100 = 10 X 100 = 33 %
Total no of cases 30

14. 14
 Factors which can changes the Infectivity
Pathogenicity, Virulence and Immunogenicty
– Dose
– Route of infection
– Host factor
» Age, race
» Nutritional status etc
– Environmental conditions

15. 15
II. Reservoirs
 A reservoir is an organism or habitat, in which an
infectious agent normally lives, transforms, develops
and/or multiplies. Reservoirs for infectious agents may
be humans, animals, plants or other inanimate objects.
 Some diseases with human reservoirs are:
– Most bacterial and viral respiratory diseases
– HIV/AIDS/Sexually Transmitted Infections (STIs), measles,
typhoid etc.
– Some diseases are transmitted to human beings from animals.
These diseases are called zoonoses.
– Examples: Rabies, anthrax, etc.

16. 16
III. Portal of Exit
 Portal of exit is the way the infectious agent
leaves the reservoir.
 Possible portals of exit include all body
secretions and discharges:
– Mucus, saliva, tears, breast milk, vaginal and
cervical discharges, excretions (feces and urine),
blood, and tissues.
 For example feces is the portal of exit for the
eggs of hook worm.

17. 17
IV. Mode of Transmission
 Modes of transmission include the various
mechanisms by which agents are conveyed to
other susceptible hosts.
 Transmission may be direct or indirect.

18. 18
1. Direct Transmission
1.1 Direct contact:
– Occurs when there is contact of skin, mucosa, or
conjunctiva with infectious agents directly from
person or vertebrate animal, via
» touching,
» kissing,
» biting,
» passage through the birth canal, or
» during sexual intercourse.
 Example: HIV/AIDS/STIs, rabies

19. 19
1. Direct Transmission…..
 1.2 Direct Projection: is transmission by
projection of saliva droplets during
– coughing,
– sneezing,
– singing,
– spitting or
– talking.
 Example: common cold

20. 20
1. Direct Transmission…..
1.3 Transplacental:
is transmission from mother to fetus through the
placenta.
 Example: syphilis, HIV/AIDS

21. 21
2. Indirect transmission
 The following are the different types of indirect
transmission
2.1. Vehicle-borne
2.2. Vector-borne
2.3. Airborne

22. 22
2. Indirect transmission…
 2.1 Vehicle-borne: Transmission occurs through
indirect contact with inanimate objects fomites:
– bed sheets,
– towels, toys, or
– surgical instruments;
– as well as through contaminated food, water, IV
fluids etc.

23. 23
2. Indirect transmission…
 2.2 Vector-borne: The infectious agent is
conveyed by an arthropod to a host.
 Vectors may be
1. biological or
2. mechanical.
 Biological vector: A vector is called biological
vector if the agent multiplies in the vector before
transmission.
 Example: anopheles mosquito is a biological
vector for malaria.

24. 24
2. Indirect transmission…
 Mechanical vector: A vector is called mechanical
vector if the agent is directly infective to other
hosts, without having to go through a period of
multiplication or development in the vector.
 The vector simply carries the agent by its body
parts (leg, proboscis etc) to convey it to
susceptible hosts.
 Example: Flies are mechanical vectors for the
transmission of trachoma.

25. 25
2. Indirect transmission…
2.3 Airborne: which may occur by dust or droplet nuclei
(dried residue of aerosols)
 Example: Tuberculosis.
 When pulmonary tuberculosis patients cough, they emit
many aerosols which consists the agents of tuberculosis
When these aerosols dry droplet nuclei will be formed.
 These droplet nuclei will remain suspended in the air for
some time. When another healthy susceptible individual
breaths he/she will inhale the droplet nuclei and become
infected with tuberculosis.

26. 26
V. Portal of entry.
 is the site where an infectious agent enters a
susceptible host.
 It may be
 Mucosa
Nasal --------------------common cold
Conjunctiva ------------trachoma, common cold
Respiratory -------------TBC
Vaginal------------------ STDs
Urethral
Anal
 Injury sites-------------- tetanus
 Skin ----------------------skin diseases

27. 27
VI. Susceptible human host
 The susceptible human host is the final link in the
infectious process.
 Host susceptibility or resistance can be seen at the
individual and at the community level.
 Host resistance at the community (population) level is
called herd immunity.
 Herd immunity can be defined as the resistance of a
population to the introduction and spread of an infectious
agent, based on the immunity of a high proportion of
individual members of the population, thereby lessening
the likelihood of a person with a disease coming into
contact with susceptible.

28. 28
Herd immunity
 Example - If 90 % of the children are vaccinated
for measles, the remaining 10 % of the children
who are not vaccinated might not become
infected with measles because most of the
children (90 %) are vaccinated. That means
transmission from infected person to other
susceptible children will not be easier.

29. 29
Conditions under which herd immunity best
functions
1. Single reservoir (the human host)
2. Direct transmission
3. Total immunity
4. No shedding of the agent by immune hosts
5. Uniform distribution of immunes
6. No overcrowding

30. 30
Disease Causation and Model

»Definition
»Principles of disease causation
Germ Theory
Ecological Approach
»Models of disease causation
Epidemiological Triangle Model
Web of Causation Model
The Wheel Model

31. 31
Definition
 Cause of disease: is an event, condition,
characteristic or a combination of these factors
which plays an important role in producing the
disease.
 any cause must precede a Diseases.

32. 32
Causes of diseases
 A necessary cause: - is a factor that must be present to
produce a disease ( the disease doesn’t develop in the
absence of this factor).
 A sufficient cause: - is a factor which inevitability
produces or initiates a disease
Types of Causal Relationships
There are four types of causal relationship in disease
causation.
1. Necessary and sufficient cause – without the factor,
disease never develops;
Factor A Disease
Example HIV infection

33. 33
Continued
2. Necessary but not sufficient cause – the factor in itself is
not enough to cause disease.
 Multiple factors including main factor are
required, usually in a specific temporal sequence
Example: development of tuberculosis required M.
tuberculosis and other factors such as malnutrition,
genetic factors, crowded housing poverty and so on.
Factor A +
Factor B +
Factor C
Disease

34. 34
Continued
3. Sufficient but not necessary cause – the factor
alone can cause disease, but so can other factors
in its absence.
Example: sun can cause burn without the presence of
the other factor such as fire
Factor A or
Factor B or
Factor C or
disease
Factor F &/or
Factor A &/or
Factor C &/or
Factor E &/or
Factor B &/or
Factor D &/or
Disease

35. 35
Continued…
4. Neither sufficient nor necessary cause– the factor
cannot cause disease on its own, nor it is the only factor
that can cause that disease.
 This is the probable model for chronic disease
relationships.
 Example: High fat diet and heart disease, hypertension,
diabetes and so on.

36. 36
Exercise
 If a particular disease is caused by any of the three
sufficient causes diagrammed in Figure below (but
only these three), which components are a necessary
cause?

37. 37
Principles of disease causation
Two principles
 Germ Theory & Ecological Approach
Germ theory- applied in infectious disease epidemiology
Koch’s postulated in 1877
 Set a rule for determining the cause
1. The organism must be present in every case-
 assuming all diseases are caused by micro organisms
2. The organism must be isolated and grown in culture
3. The organism must cause the specific disease when
inoculated into the susceptible animal
4. The organism must then be recovered from the infected
animal

38. 38
Ecological Approach
 Ecology –the study of the relation ship of organisms to each
other as well as to all other aspects of the environment.
 In the ecological view,
– an agent is considered to be necessary but not sufficient cause of
the disease b/c the condition of the host and the environment be
present for the disease to be to develop
 Etiology of disease : all factors that contribute the
occurrence of a disease
 These factors are related to the
– Agent
– Host
– Environment

39. 39
Agent
 Nutritive Element
– Excess = cholesterol
– Deficiency = vitamin , protein etc
 Chemical agents
– Poison = CO
 Physical agents
– Radiation
 Infectious agents
– Metazoans – hookworm
– Protozoa – amoeba
– Bacteria-M.TB
– Fungus- Candida
– virus –polio

40. 40
Host factor
 The state of the host at any given time influences
exposure, susceptibility or response to the agent
 Genetic factors: age, sex,
 Physiologic states: pregnancy, puberty, stress
 Immunologic Conditions:
– Active- prior to infection, immunization of measles
– passive after exposure, antibodies , Rabies vaccine
 Personality trait/human behavior
– Hygiene, Diet,

41. 41
Environmental Factors (Extrinsic)
 Influence the existence of the agent, exposure, or
susceptibility to the agent
 Classified as biologic, social and physical.
Biologic Environment.
(1) Infectious agents of Ds
(2) Reservoirs of infection (other human beings, animals,
and soil)
(3) Vectors that transmit Ds (e.g. flies and mosquitoes)
(4) Plants and animals (as sources of food, antibiotics, and
other drug principles or as antigens)

42. 42
Social Environment
 Socio economic & political organization of a
society affects
– the technical level of medical care
– The systems by which that care is delivered
– The extent of support for medical care
 The adequacy and level of enforcement of codes
and laws controlling health-related environmental
hazards (pollution, housing, occupational safety,
etc.)
 Social customs may affect health
» E.g. the types of foods eaten

43. 43
Physical Environment:
 The physical aspects of the environment include
» heat, light, air, water,
» Radiation
» chemical agents.
– E.g. air pollution has emerged as an urgent threat to
health.
– Long-term exposure to pollution contributes to higher
rates of chronic respiratory Ds in urban than rural
areas.

44. 44
N.B.
 The interaction of agent , host and environment
which determine whether or not a diseases
develops can be illustrated using different models
»Models of disease causation
Epidemiological Triangle Model
Web of Causation Model
The Wheel Model

45. 45
The epidemiological triangle
Host
EnvironmentAgent
-Was widely used for many years

46. 46
The epidemiological triangle …
 The epidemiologic triangle consists of three
components -host, environment, and agent.
 The model implies that each must be analyzed and
understood for comprehension and predictions of
patterns of disease.
 Disease depends on interaction of host, agent and
environment.
 A change in any of the components will alter an
existing equilibrium to increase or decrease the
frequency of the disease.

47. 47
The Web of Causation
 The essence of the concept is that
– disease never developed from single isolated
causes, but rather develops as the result of
chains of causation in which each link itself is
the result of "a complex genealogy of
antecedents.
 Disease is the result of a complex interaction
factors (chain of causation)

48. 48
The wheel
 Another approach to depicting human-environment
relations
 Consists of a hub (the host or human), which has
genetic make-up as its core, surrounded by the
environment, schematically divided into the three
sectors mentioned

49. 49
The wheel
 The relative size of the different components of the wheel
depend upon the specific Ds problem under consideration
 Hereditary Ds  genetic core is relatively large
 Measles  state of immunity of the host & biological sector
of the environment large
Genetic core
Social
environment
Physical
environment
Biological
environment
host

50. 50
The wheel…
Similarity with the web of causation
 The need to identify multiple etiologic factors of
Ds without emphasizing the agent of Ds
Difference with the web of causation
 Separate delineation of host and environmental
factors, a distinction useful for epidemiological
analyses

51. 51
Natural History of diseases and
Levels of Prevention
– Definition
– Stages in the Natural History of Diseases
– Levels of Prevention

52. 52
Natural history of disease
 The “natural history of disease” refers to the
progression of disease process in an individual
over time, in the absence of intervention.
 There are four stages in the natural history of a
disease. These are:
1. Stage of susceptibility
2. Stage of pre-symptomatic (sub-clinical) disease
3. Stage of clinical disease
4. Stage of disability or death

53. 53
1. Stage of susceptibility
 In this stage, disease has not yet developed, but
the groundwork has been laid by the presence of
factors that favor its occurrence.
 Example: unvaccinated child is susceptible to
measles.

54. 54
2. Stage of Pre-symptomatic
(sub-clinical) disease
 In this stage there are no manifestations of the
disease but pathologic changes (damages) have
started to occur in the body.
 The disease can only be detected through special
tests since the signs and symptoms of the disease
are not present.
Example
 Detection of antibodies against HIV in an
apparently healthy person.
 Ova of intestinal parasite in the stool of apparently
healthy children.

55. 55
 The pre-symptomatic (sub-clinical) stage may lead
to the clinical stage, or may sometimes end in
recovery without development of any signs or
symptoms.

56. 56
3. The Clinical stage
 At this stage the person has developed signs and
symptoms of the disease.
 The clinical stage of different diseases differs in
duration, severity and outcome.
 The outcomes of this stage may be recovery,
disability or death.
Examples:
 Common cold has a short and mild clinical stage
and almost everyone recovers quickly

57. 57
 Polio has a severe clinical stage and many patients
develop paralysis becoming disabled for the rest of
their lives
 Rabies has a relatively short but severe clinical
stage and almost always results in death.
 Diabetes Mellitus has a relatively longer clinical
stage and eventually results in death if the patient
is not properly treated.

58. 58
4. Stage of disability or death
 Some diseases run their course and then resolve
completely either spontaneously or by treatment.
 In others the disease may result in a residual
defect, leaving the person disabled for a short or
longer duration.
 Still, other diseases will end in death.
 Disability is limitation of a person's activities
including his role as a parent, wage earner, etc

59. 59
 Examples:
 Trachoma may cause blindness
 Meningitis may result in blindness or
deafness.
 Meningitis may also result in death.

60. 60

61. 61
Clinical cases
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As
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m
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ati
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Clinical threshold
Biological
Onset
Agent
Starts being
shed
First manifestation of
diseases
(Clinical stage)
Recovery Agent
Stops being
shed
Relapse
Chronic carrierAsymptomatic
carriers
B
A
Incubation period
Period of communicability
Time course of infectious diseases

62. 62
Time course of infectious diseases
1. Patent period- the time interval bn biological
onset and the point at which the infection can
first be detected (time of first shedding)
2. Incubation period
– The time interval between biological onset and
clinical onset
3. Communicable period- the time interval during
the agent is shed by the host
4. Latent period- the interval between recovery and
relapse in clinical cases

63. 63
Types of Carries
1. Incubatory carrier
– Transmission during incubation period from the first shedding
to clinical onset
– Eg measles, Mumps
2. Convalescent carriers
– Transmits from recovery to when shedding stops.
– Eg typhoid fever
3. Asymptomatic carriers
– transmission without manifestation
– ‘eg amoebiasis
4. Chronic carries
– Long period (indefinite transmission)
– Viral hepatitis B, typhoid fever

64. 64
Importance of carriers
– Carriers plays an important role in the transmission of diseases
– Their importance in disease transmission is attributed to the
following factors
1. Number
 They may outnumber cases and so may constitute a significant
reservoir
2. Difficulty in recognition
– Cases are easily recognized and treated and so can be removed
as a source of infection but not carries
3. Mobility
– cases care restricted to their beds by their illness and so can
only infect a limited number of contacts.
 Carriers freely moves around and so have many more contacts
4. Chronicity
– Chronic carriers can reportedly re introduce the diseases after it
has been apparently controlled

65. 65
Levels of Disease Prevention
 The major purpose in investigating the
epidemiology of diseases is to learn how to prevent
and control them.
 Disease prevention means to interrupt or slow the
progression of disease.
 Epidemiology plays a central role in disease
prevention by identifying those modifiable causes.

66. 66
There are three levels of prevention
1) Primary prevention:-
The main objectives of primary
 prevention are promoting health, preventing
exposure and preventing disease.
 Primary prevention keeps the disease process
from becoming established by eliminating causes
of disease or increasing resistance to disease.
 Primary prevention has 3 components.
1. promotion,
2. prevention of exposure, and
3. prevention of disease.

67. 67
 A. Health promotion:- consists of general non-
specific interventions that enhance health and the
body's ability to resist disease.
 Examples of health promotion.
– Improvement of socioeconomic status,
– provision of adequate food, housing, clothing, and
education

68. 68
 B. Prevention of exposure:- is the avoidance of
factors which may cause disease if an individual
is exposed to them.
 Examples can be provision of safe and adequate
water, proper excreta disposal, and vector control.

69. 69
C. Prevention of disease:-
 is the prevention of disease development after the
individual has become exposed to the disease causing
factors.
 Immunization is an example of prevention of disease.
 Immunization acts after exposure has taken place.
 Immunization does not prevent an infectious organism
from invading the immunized host, but does prevent it
from establishing an infection.
 If we take measles vaccine, it will not prevent the virus
from entering to the body but it prevents the
development of infection/disease.

70. 70
2) Secondary prevention:-
 The objective of secondary prevention is to stop
or slow the progression of disease so as to
prevent or limit permanent damage.
 Secondary prevention can be achieved through
detecting people who already have the disease as
early as possible and treat them.
 It is carried out before the person is permanently
damaged.

71. 71
Examples:
 Prevention of blindness from Trachoma
 Early detection and treatment of breast cancer to
prevent its progression to the invasive stage,
which is the severe form of the disease.

72. 72
3) Tertiary prevention:–
 is targeted towards people with permanent damage or
disability.
 Tertiary prevention is needed in some diseases because
primary and secondary preventions have failed, and in
others because primary and secondary prevention are not
effective.
 It has two objectives:
– Treatment to prevent further disability or death and
– To limit the physical, psychological, social, and financial
impact of disability, thereby improving the quality of life.
 This can be done through rehabilitation, which is the
retraining of the remaining functions for maximal
effectiveness

73. 73
Example: When a person becomes blind due to
vitamin A deficiency, tertiary prevention
(rehabilitation) can help the blind or partly blind
person learn to do profitable work and be
economically self supporting.

74. 74
Natural history of diseases and level of prevention
Levels of
prevention
Points of intervention Natural history of diseases
Primary
Health promotion
Prevention of exposure
Prevention of diseases
Latent period
Secondary Early detection and treatment
(prevention of clinical onset)
Early treatment
(prevention of permanent
damages)
Incubation period
Tertiary Limitation of disabilities
Rehabilitation (prevention of
deterioration in quality of life
Death
Exposure
Biological onset
Clinical onset
Permanent damages

75. 75
Infectious disease Epidemiology
 The study of circumstances under which both
infection and disease occur in a population and
the factors which influence their frequency,
spread and distribution of infectious diseases.

76. Infectious Disease Epidemiology:
Major Differences
 A case can also be an exposure
 Subclinical infections influence epidemiology
 Contact patterns play major role
 Immunity
 There is sometimes a need for urgency
76

77. Outcomes of exposure
1. No infection
2. Clinical infection resulting in death,
immunity, carrier or non-immunity
3. Sub-clinical infection resulting in
immunity, carrier or non-immunity
4. Carrier
77

78. Two or more populations
Humans
Infectious agents
Helminths, bacteria, fungi, protozoa, viruses, prions
Vectors
Mosquito (protozoa-malaria), snails (helminths-
schistosomiasis)
Blackfly (microfilaria-onchocerciasis) – bacteria?
Animals
Dogs and sheep/goats – Echinococcus
Mice and ticks – Borrelia
What is infectious disease
epidemiology?

79. A case is a risk factor …
Infection in one person can be transmitted to others
What is infectious disease epidemiology?

80. The cause often known
An infectious agent is a necessary cause
What is infectious disease epidemiology used for?
Identification of causes of new, emerging infections, e.g.
HIV, SARS
Surveillence of infectious disease
Identification of source of outbreaks
Studies of routes of transmission and natural history of
infections
Identification of new interventions
What is infectious disease epidemiology?

81. Transmission
81

82. Estimating the Transmission
Probability
 The probability that successful transfer of the
agent will occur so that the susceptible host
becomes infected
 Two common ways of estimating transmission
probability are:
1. Secondary attack rate
2. Binomial Model
82

83. Secondary Attack Rate
 is a measure of the frequency of new cases of a
disease among the contacts of known cases.
83
Secondary
Attack
Rate
Number of cases among contacts of
primary cases during the period
=
Total number of contacts
X 10n

84. Population Cases
Age
(yrs)
Total #
Individuals
# Susceptibles
before 1o cases
occurred
1o + 2o = Total
Cases
2-4 300 250 100 50 150
5-9 450 420 204 87 291
10-19 152 84 25 15 40
Mumps experience of 390 families each exposed to a
primary case within the family
Secondary attack rate for 2 - 4 year olds =
(Total # cases-1o) / (# Susceptible-1o)x100% =
(150–100=50) / (250–100=150) x 100% = 33%

85. Binomial Model of Transmission Probability
(TP)
 One of the most commonly used approaches used
for estimating the transmission probability.
 Used when susceptible make more than one
potentially infectious contact
The numerator is the same as secondary attack rate
85
TP
# of susceptible who become infected
=
total number of contacts with infective

86. Binomial Model (TP)
86

87. Example
 Study of HIV transmission was conducted in a
population of 100 steady sexual couples. At the
beginning, one couple was already infected. 25
became infected. The total number of sexual
contacts was 1500. what is probability of being
infected after 2 contacts.
– the probability being infected = 1-(1-p) n
– n=2
= 1-(1-p) 2
= 1-(1-25/1500) 2
= 1-(1-0.016) 2
=0.031 87

88. A measure of the potential for transmission
The basic reproductive number, R0, the mean number of individuals directly
infected by an infectious case through the total infectious period, when
introduced to a susceptible population
R0 = p • c • d
contacts per unit time
probability of transmission per contact
duration of infectiousness
Infection will ….. disappear, if R < 1
become endemic, if R = 1
become epidemic, if R > 1
Basic Reproductive Number, R0

89.  Useful summary statistic
 Definition: the average number of secondary
cases a typical infectious individual will cause in
a completely susceptible population
 Measure of the intrinsic potential for an
infectious agent to spread
Basic Reproductive Number, R0

90. Basic Reproductive Number, Ro
• If R0 < 1 then infection cannot invade a
population
» implications: infection control mechanisms unnecessary
(therefore not cost-effective)
• If R0 > 1 then (on average) the pathogen will
invade that population
» implications: control measure necessary to prevent (delay) an
epidemic
90

91. p, transmission probability per exposure – depends on the infection
 HIV, p(hand shake)=0, p(transfusion)=1, p(sex)=0.001
 interventions often aim at reducing p
 use gloves, screene blood, condoms
c, number of contacts per time unit – relevant contact depends on
infection
 same room, within sneezing distance, skin contact,
 interventions often aim at reducing c
 Isolation, sexual abstinence
d, duration of infectious period
 may be reduced by medical interventions (TB)
What determines R0 ?

92. Effective Reproductive Number, R
 R unlike Ro assumes that all contacts by the
infective case are not with susceptible
individuals
R= Ro X proportion of susceptible population
 Example , if Ro is 5 and 40% of the population is
immune , the susceptible 100% - 40%= 60%
Then , R= 5 X 0.6= 3 cases
– A case of disease will produce only 3 cases
92

93. 93

94. 94

95. Basic Calculation of VE
% reduction in attack rate of disease in vaccinated (ARV)
compared to unvaccinated (ARU) individuals
VE (%) = (ARU-ARV) X 100
ARU
Where
and
Consequently, VE = 1-RR (preventive fraction)
95
1
ARU
ARU ARV
ARU
 RR

96. 0,9 – 0,2
0,9
VE = = 78%
Vaccinated
IV = 2/10 = 0,2
IU = 9/10 = 0,9
Unvaccinated
Basic Calculation of VE
96

97. Example
 In an outbreak of varicella (chickenpox) in Oregon in
2002,
From CDC
http://www.cdc.gov/osels/scientific_edu/SS1978/Lesson
3/Section5.html
97

98. Incidence of varicella (chickenpox) Among
Schoolchildren in 9 Affected Classrooms —
Oregon, 2002
.
98
Varicella Non-case Total
Vaccinated a=18 b=134 152
Unvaccinated c=3 d=4 7
Total 21 138 159

99. Incidence of varicella (chickenpox)
 Risk among vaccinated children
= 18 ⁄ 152 = 0.118 = 11.8%
 Risk among unvaccinated children
= 3 ⁄ 7 = 0.429 = 42.9%
 RR= 0.118 ⁄ 0.429 = 0.28
99

100. Calculate vaccine effectiveness
100

101. VE (%) = (ARU-ARV) X 100
ARU
 VE = (42.9 − 11.8) ⁄ 42.9 = 31.1 ⁄ 42.9 = 72%
 Alternatively -VE = 1 − RR = 1 − 0.28 = 72%
So, the vaccinated group experienced 72% fewer
varicella cases than they would have if they had
not been vaccinated.
101

102. Herd Immunity
 A population may become immune to an infectious
agent after a large proportion of individuals have
become immune
– i.e. through past infections or vaccination
 Can occur when immune persons prevent the spread of
disease to unimmunized individuals and confers
protection to the population even though not every
single individual has been immunized
102

103. Effect of Herd Immunity on Spread of
Infection
-+
++ - +
+++ + +-- -
+
+ +
+ +
+
+
+
-
- -
- -
-
-
+
Absence of Herd
Immunity
Presence of 50%
Herd Immunity

104. Herd Immunity…
 The indirect protection from infection of
susceptible members of the population, and the
protection of the population as a whole, which
is brought about by the presence of immune
individuals
104

105. Herd Immunity…
 If an infection is to persist, each infected
individual must, on average, transmit that
infection to at least one other individual. If
this does not occur, the infection will
disappear progressively from the population
105

106. Calculating susceptibility of a cohort
(assuming 90% measles vaccine efficacy)
% cohort unprotected by vaccine
 % with 0 dose x 100%
 % with 1 dose x 10%
 % with 2 doses x 1%

107. Example – Calculating susceptibility
 (assuming 90% measles vaccine efficacy)
If 10% have 0 doses
20% have 1 dose
70% have 2 doses
 Then % susceptible
=0.10 x 100% + 0.2x 10% + 0.70% x 1%
= 10% + 2% + 0.70%
= 12.7%

108. Example - Calculating R
R = RoS
R = 15 (for measles) x 12.7%
R = 1.905
 Therefore measles will continue to spread with
this level of vaccination coverage

109. Why Herd immunity
 No vaccine is 100% effective e.g. measles
vaccine is 90- 95%
 Some people unable to receive live vaccines e.g
the immunocompromised
 Herd immunity is the most effective way of
protecting people who do not respond to
vaccines
109

110.  Judging the vaccination coverage of
Amhara region and epidemics of measles??
 Why clusters of measles epidemic
occurred?
110