Communicable Disease Control Guide

DREAM SCIENCE AND
TECHNOLOGY COLLEGE
COMMUNICABLE DISEASE CONTROL(CDC)
By: Gebeyaw B. (BSc, MSc)
February, 2022
1

UNIT ONE
INTRODUCTION TO
COMMUNICABLE DISEASE
CONTROL (CDC)
2

Objective
At the end of this session students will be able to;
- Define common terminologies
- Overview of communicable disease
- Classify communicable disease
3

Definitions of basic terms
Infection: the entry, development and multiplication of
an infectious agent in the body of human beings.
Infestation: presence of living infectious agent on the
exterior surface of the human body
Host: person or animal that affords survival or lodgment
to an infectious agent under natural conditions.
Disease: a state of physiological or psychological
dysfunction.
4

Infectious agent: an organism capable of
causing infection.
Infectious disease: a clinically manifest
disease of a man or animal resulting from an
infection.
Contagious disease: a disease that can be
transmitted through contact.
5

Epidemic: unusual occurrence of disease , specific
health related behavior or events clearly in excess of
expected occurrence in a community or region.
Endemic: constant presence of a disease or infectious
agent within a given geographic area or population
group; without importation from outside.
- A disease that is usually present in a population or
in an area at a more or less stable level.
6

Sporadic: cases occur irregularly, randomly from
time to time and generally infrequent. E.g. polio,
tetanus, herpes zoster.
Pandemic: an epidemic affecting a large proportion
of the population occurring over a wide geographic
area
Zoonosis: an infection transmissible under natural
conditions from animals to man.
7

Nosocomial infection: infection originating in a
patient while in hospital or other health care facility.
Opportunistic infection: an infection by organisms
that take the opportunity of defect in the host defense
to infect the host and cause disease.
Iatrogenic disease: any unpleasant or adverse
consequence of preventive, diagnostic or therapeutic
regimen or procedure that causes impairment,
handicap, disability or death resulting from clinicians
professional activity.
8

Surveillance: continuous study of the factors
that determine the occurrence and distribution
of disease and other conditions of health.
Monitoring: continuous follow up of activities
to ensure that they are proceeding according to
plan.
Control: ongoing operation aimed at reducing
incidence, duration and effects of disease.
9

 Elimination: refers to the reduction to zero (very low
defined target rate) of new cases in a defined geographical
area.
Eradication: complete and permanent worldwide reduction
to zero new cases of the disease through deliberate efforts.
If a disease has been eradicated, no further control
measures are required.
Extinction: eradication of infectious agent including in the
lab.
10

Overview of Communicable Disease
11
Communicable disease
 An illness due to a specific infectious agents or its
toxic products capable of being directly or indirectly
transmitted from man to man, animal to animal or
from environment to man or animal.
 Communicable diseases are the major cause of
suffering, disability and death in the world
Particularly in developing countries.

Overview of Communicable Disease
Disease: is a state of discomfort in which the normal
functioning of the body is disturbed (e.g. Malaria, typhoid,
chickenpox).
• Diseases can be classified according to two major
dimensions.
- time course & cause .
1. Time course:
- Acute (characterized by a rapid onset and a short duration),
- Chronic (characterized by prolonged duration).
12

2. Based on the cause, broadly categorized as:
 Infectious or communicable disease: caused by living
parasitic organisms such as viruses, bacteria, parasitic
worms, insects, etc.) which is transmit from one person to
the other.
 Non-communicable disease: caused by something other
than a living parasitic organism, which is not spread from
one person to another.
 However, most of the common diseases in Africa are
environmental diseases (infectious) due to different reasons.
13

Cont’d...
Communicable diseases are common in
developing countries because:
 Poor socio-economic status,
 Low educational status,
 Lack of access to modern health care service.
14

Classification of Communicable Disease
1. Clinical classification
Diarrheal diseases
Respiratory diseases
CNS infection…..
2. Microbiological
Bacterial
Viral
Fungal
Protozoan
15

Classification con.....
3. Epidemiological classification
a. Based on Means of transmission
Contact (Direct or indirect)
Food/water borne
Airborne
Vector-born
b. Based on reservoir
Human
Animal(zoonosis)
Soil
Water
16

Epidemiology and scope
Why we study CD Epidemiology?
Changes in the pattern of infectious
diseases.
 Discovery of new infections.
 The possibility that some chronic
diseases have an infective origin.
17

 Incidence of CD fall during the past 70 years due to:
• Immunization
• Chemotherapy
• Improved nutrition
• Improved socio-economic condition (housing,
sanitation …..)
 However, it has remained the leading cause of
mortality and morbidity in developing countries.
18

Global factor for the emerging of CD
Dramatic societal and environmental changes,
Explosive population growth,
 Expanding poverty and urban migration,
 International travel and commerce are increasing,
Technology is rapidly changing and increases the risk
of exposure,
Climatic change,
19

20
 Infectious agents are still being discovered e.g. Ebola,
HIV, influenza, COVID-19.
 Role of infectious diseases for chronic disease
E.g - H. Pylori in peptic ulcer disease, gastrointestinal
malignancy;
- EBV, malaria – Burkitt’s Lymphoma; HHV8 – Kaposi's
sarcoma
 Antibiotic resistance rate is increasing
 Immune compromised host is increasing

UNIT TWO
Chain of disease transmission
Objective
At the end of the unit you are able to;
 Define chain of disease transmission
 Describe the disease transmission cycle
 Describe the natural history of a disease
 Define carrier and identify its type
21

Chain of disease transmission
 Is a logical sequence of factors or links of a chain that are essential
for the development of the infectious agent and propagation of
disease.
 The six factors involved in the chain of disease transmission are:
 Infectious agent (etiology or causative agent)
 Reservoir
 Portal of exit
 Mode of transmission
 Portal of entry
 Susceptible host
22

1. Reservoir/source of infection
The starting point for the occurrence of a CD
 Reservoir: Any person, animal, arthropod, plant or soil
or substance (or combination of these) in which an
infectious agent normally lives, transforms, develops
and /or multiplies.
 `Primarily for survival and where it reproduces itself in
such a manner that it can be transmitted to a susceptible
host. It is the natural habitat of the infectious agent.
24

Cont’d....
Common reservoir
Human being (STI, polio, measles…)
Animals
 Vertebrate animals ( rabies, anthrax)
 Invertebrate animals (tick, flea, louse)
Non living reservoir ( plants, soil, water)
25

Human as a reservoir
Case: is defined as “a person in the population or
study group identified as having the particular
disease, health disorder, or condition under
investigation”
Carriers: A carrier is an infected person or animal
who does not have an apparent clinical disease but
is a potential source of infection to others.
26

Carriers….
27
 Asymptomatic carriers: persons whose infection
remains unapparent.
 Incubatory carriers: persons who excrete the
pathogen during the incubation period.
 Convalescent Carriers: These are those who
continue to harbor the infective agent after
recovering from the illness..
 Chronic Carriers: carrier state persists for a long
period of time.

Animal as reservoirs/ zoonosis: is an infection that is
transmissible under natural conditions from vertebrate
animals to man, e.g. rabies, plague, bovine tuberculosis
 Non-living things as Reservoir
Soil and inanimate matter can also act as reservoir of
infection.
E.g. Soil may harbor agents that causes tetanus,
anthrax, and coccidiomycosis.
28

2. Infectious agent
 Is pathogen that cause infection/disease.
 Can be virus, bacteria, parasite or other microbes.
 The agent causes infection and disease depending on
its basic biological characteristics:
o Infectiousness,
o Pathogenicity,
o Virulence,
o Immunogenicity
29

Infectiousness (infectivity)
The ability of an infectious agent to cause
infection in an exposed human host.
Infectivity is measured by Infection Rate (IR):
Infectivity = number of infected persons X100
number of exposed persons
30

Pathogenicity
─ The ability of an infectious agent to cause clinical
disease among infected human hosts.
─ It is measured by clinical to sub-clinical ratio or
proportion of clinical cases among infected human hosts
Examples:
o High pathogenicity: HIV, Rabies, Measles… etc.
o Moderate pathogenicity: Mumps virus and Rhino virus
o Highly infectious but less pathogenic: Poliovirus
31

Virulence
 It is the ability of an infectious agent to cause severe
clinical disease or death among the clinical cases.
 Virulence of the infectious agent can be measured by:
o Case fatality Rate (CFR)
o Hospitalization Rate (HR)
CFR = Number of fatal cases X100
total number of cases
HR = Number of hospitalized cases X100
total number of cases
32

Immunogenicity
The infection’s ability to produce specific immunity.
 It is defined as the ability of a pathogen or a vaccine
to inducing an immune response after an infection or
a vaccination respectively
 It may lead to protection against re-infection or re-
activation with the same or similar pathogen in the
future
33

Immunity
Immunity after infection may or may not be
protective against re-infection or may last for variable
periods of time.
o some infectious diseases confer lifelong immunity
o Others confer partial immunity against severe
symptomatic infection, but much less against sub-
clinical infection
o Some confer no or negligible immunity.
34

Immunity......
o Immunity can be acquired either after natural infection or
indirectly.
o Maternal antibodies protect the newborn child against
many infections in the first few months of life.
o Vaccine-induced immunity can be lifelong or temporary
o For temporary immunity, repeated booster vaccinations
are necessary to ensure protection against the infection
Example: TT vaccine
35

Immunity......
Individuals gain protective antibodies in two ways:
1) They develop antibodies in response to infection,
vaccine, or toxoid; immunity developed in these ways
is called active immunity
2) They acquire their mothers’ antibodies before birth
through the placenta or they receive injections of
antitoxins or immune globulin; immunity that is
acquired in these ways is called passive immunity
36

Cont’d....
Other factors that influence disease development:
o Strain of agent, Dose of agent
o Route of infection
o Influence of human host age
o Influence of human host nutritional status
o Influence of human host immune response
o Influence of treatment
o Influence of seasonal variation, etc…
38

Factors influencing disease
transmission
39

Toxigenecity
 Capacity of agent to produce a toxin or
poison.
 Toxin produced by the microorganism
causes diseases rather than microorganism
itself (such as botulism )
40

On the basis of their size, etiological agents are
generally classified into:
1.Metazoa (multicellular organisms e.g. Helminths).
2.Protozoa (Unicellular organisms e.g. Amoeba)
3. Bacteria (Treponema pallidum, Mycobacterium
tuberculosis, etc.)
4. Fungus (e.g. Candida albicans)
5. Virus (e.g. Chickenpox, polio, etc.)
41

3. Portal of Exit
 The route by which the infectious agent leaves
the infectious hosts or reservoirs.
 Many diseases have multiple reservoirs.
 The most common portals of exit are respiratory
tract, genitourinary tract, gastrointestinal tract,
through skin, etc…
42

Portal of exit includes
—Body secretions and discharges (mucus, saliva tears,
breast milk, urethral secretion, semen, vaginal
secretion, pus, cervical secretion, exudates etc…)
—Excretions (feces, urine, blood and tissues including
placenta , etc
e.g. Flu /cold - mucous secretions
Hepatitis A - stool
43

4. Modes of Transmission
 Mode of transmission is the mechanism by
which the infectious agent escapes from a
reservoir and enters into a susceptible human
host.
 There are 2 major mechanisms of transmission
I. Direct transmission
II. Indirect Transmission
44

 The immediate transfer of infectious agents from an
infected host or reservoir to the appropriate portal of
entry on the susceptible host.
a) Transmission by direct contact
b) Transmission by direct projection
c) Trans-placental transmission
d) Blood transfusion
e) Organ transplantation
I. Direct transmission
45

a) Transmission by direct contact
 Transmission by contact of skin, mucosa, or
conjunctiva with infectious agents directly transferred
from another person or vertebrate animal including:
 Touching: Trachoma. Common cold, Shigellosis,
Viral hepatitis and HIV (through breaks in skin)
 Sexual intercourse: HIV/AIDS
Kissing: mononucleosis
 Passing through birth canal: Gonorrhea
46

b) Transmission by direct projection
Transmission by direct projection of saliva
droplets created by expiratory activities such as
breathing, coughing, sneezing, spitting, talking,
singing etc…
Example: common cold, Tuberculosis
47

c) Trans-placental transmission
 Trans-placental transmission of infectious
agent is transmission from mother to fetus via
the placental membrane
Examples:
oHIV/AIDS
oSyphilis
oToxoplasmosis
oMalaria etc...
48

d) Blood transfusion
o It is the transmission of disease through blood
and blood products
E. g. HIV and Hepatitis-B viruses
e) Organ transplantation
 It may include kidney, liver and cardiac transplantation
which transmit some communicable diseases from the
donors to the receivers.
49

a) Airborne transmission
—It is the transmission or dissemination of infectious
agents by either suspended dust, particle or droplet
nuclei, usually through respiratory tract.
 Microbial aerosols are suspensions of particles in the
air consisting of partially or wholly of microorganisms
—Particles in the 1-5 micro meter range are easily drawn
into the alveoli
Examples: Tuberculosis, Brucellosis
50
II. Indirect transmission

b) Vehicle borne transmission
 It is the transmission of infectious agents by a vehicle
 Examples: Food, milk, water, soil, biological products, fomites
(cooking utensils, towels, bed sheets, clothing, syringe, beddings,
etc…)
51

c) Vector borne transmission
It is the transmission of infectious agents by a vector
 A vector is responsible for introducing the agent into
the susceptible human host through a suitable portal of
entry
—Biological vector: malaria transmission (by mosquito)
—Mechanical vector: trachoma by common fly
Vector: is an organism usually an arthropod, such as
insect, tick, mite, which transports an infectious agent to a
susceptible human host or to a suitable vehicle
52

Vector borne transmission
Biologic transmission: when the agent undergoes
physiologic changes within the vector, the vector is
serving as both an intermediate host and a mode of
transmission.
o An agent undergoes part of its life cycle inside a vector
before being transmitted to a new host
 Mechanical transmission - the agent does not multiply
or undergo physiologic changes in the vector
53

d) non-vector intermediate host
—These are hosts which are important for
development of the infectious agent but don’t
play an active role in transporting the agent to
the susceptible human host
Example: Aquatic snail for schistosomiasis
54

A disease may often have several modes of
transmissions
 It is vital to distinguish the predominant mode or
modes of transmission so as to target preventive
activities
 Example: malaria can be transmitted by blood
transfusion, trans-placental or by vector.
55

5. Portal of Entry
─The route through which microorganism enters
into the susceptible human host
─ Whether an agent will establish infection
depends on the suitable portal of entry
Example: No harm in ingesting the Clostridium
tetani.
56

Portal of entry includes
─ Conjunctiva (trachoma, common cold)
─ Nasal or upper respiratory tract (common cold,
diphtheria)
─ Lower respiratory tract (TB)
─ Percutaneous (tetanus, hookworm)
─ GIT (typhoid fever)
─ Viginal (STDs/HIV/AIDS)
─ Anal (STDs/HIV/AIDS) etc…
57

6. Susceptible Human Host
 Host factors influence individual's exposure, susceptibility or
response to infectious agent
 The susceptible human host is the final link in the infectious
disease transmission process
 The susceptibility of the human host depends on:
o Genetic factors (including sex, blood group, ethnicity,…)
o Immunity due past infection or immunization
o Nutritional status
o Personal behaviors like drinking, smoking etc
o Anti-microbial or antibiotics availability & effectiveness
58

Natural history of a disease
It is the course of a disease without any intervention
/treatment.
Intervention modify the natural history of a disease.
Each disease has its own natural history.
Used to understand the progress of each disease and
helps to take appropriate intervention at each stage
60

Stages for disease development
1. Stage of susceptibility (stage of exposure)
 The disease has not yet developed but the presence of
risk factor increase the probability of its occurrence.
Ex. Traveling to malaria endemic area.
2. Stage of sub-clinical/pre-symptomatic
 The disease process is already begun inside the body but
there is no recognizable sign and symptom.
 It may be detected by laboratory investigation.
61

Cont’d...
 This stage include
 Biological onset of disease-initiation or induction
of the disease process within the body.
3. Stage of clinical disease:
- recognizable s/s appear
4. Stage of disability/death
- the disease left over damage to the body or ends
with death
62

The time course of infectious disease
1.Incubation period: time from exposure to development of
disease. Or between invasion by an infectious agent and the
appearance of the first sign or symptom of the disease.
2.Prodromal period: short, mild symptoms following incubation
period or the appearance of characteristic manifestations.
- between the onset of symptoms of an infectious disease and the
appearance of characteristic manifestations.
3. Period of illness: acute phase, between most severe signs and
symptoms & the immune system either overcomes pathogen or
person dies.
63

Cont’d....
4. Communicable period: the period during which an
infected host can transmit the infection to other host
 It can be measured by the time interval during which the
agent is shed by the host
5. Latent period: It is the time interval between recovery
and the occurrence of a relapse in clinical disease. Eg:
Typhus and malaria
6. Period of decline : signs and symptoms begin to subside.
7. Period of convalescence: host returns to pre-disease
64

8. Pre-patent period
It is the time interval between infection and the time of
first shedding of the agent by the human host
For some diseases the time when the agent can first be
detected and the time of the first shedding do have
difference- i.e. the detection might not be possible at the
beginning of the shedding of infectious agents
E.g. Window period of HIV/AIDS
65

Prevention and control of CD
Stopping the disease before it starts to occur
OR
Interrupting/slowing the progress of disease after
exposure
OR
 Prevents further disability or damage.
66

Level of prevention
A. Primary prevention
 Preventing disease before it starts to occur&
includes:
1. Health promotion: general non-specific interventions that
enhance health and the body’s ability to resist disease,
such as measures aimed at the improvement of socio-
economic status through the provision of nutrition,
affordable and adequate housing, clothing; emotional and
social support, relief of stress, etc.
67

Level of prevention …. cont’d
it is any intervention that promotes a healthier and
happier life such as :
- Breast feeding
- balanced nutrient
- physical exercise..
68

Level of prevention......
2. Prevention of exposure
ex. Provision of safe water supply
- environmental sanitation
- proper excreta disposal
- vector control..
- safe environment at home (e.g., proper storage of insecticides &
medicines, out of children’s reach), at school and at work (e.g.,
proper ventilation, - monitoring of harmful substances in factories),
and on the streets (e.g., driver licensing laws).
69

B. Secondary prevention
After the biological onset of disease, but before
permanent damage sets in.
The objective is to stop or slow the progression of disease
so as to prevent or limit permanent damage, through the
early detection and treatment of disease. e.g.
breast cancer (prevention of the invasive stage of the
disease),
 trachoma (prevention of blindness), &
 syphilis (prevention of tertiary or congenital syphilis)
70

C. Tertiary prevention
 limitation of disability and rehabilitation.
limit the physical, psychological, social and economical impact of
disability.
Tertiary prevention activities involve:
 The care of established disease, with attempts made to restore to
highest function, minimize the negative effects of disease, and
prevent disease-related complications.
 Adjust individual to live with disability
Ex: rehabilitation after stroke, polio, blindness….
71

Principle of CD control
1. Measure directed against the reservoir
 If reservoir is human being - early Dx and Rx
 Isolation: Keeping infected persons or animals in separate
places or under certain conditions for as long as they can
transmit disease.
 Quarantine: limitation of the movement of apparently well
person or animal who has been exposed to infectious disease
for a duration of the maximum incubation period of the
disease.
 If reservoir is animal –eradication is possible.
72

Principle.....
2.Interrupting the chain of transmission
 Environmental sanitation
 Personal hygiene/PPE
 Vector control
 Disinfection and sterilization
3. Reducing host susceptibility
 Immunization
 Prophylaxis
 Health education
 Personal protection
73

74
 Learning objectives
- Define surveillance
- Describe types of surveillance
Unit 3
Surveillance

Surveillance
 A systematic collection, analysis, interpretation and
dissemination of relevant health data for monitoring
the occurrence and trends of disease in human
population.
 It is continuous (ongoing) study of the factors that
determine the occurrence and distribution of diseases
and other health related events through a systematic
collection of data.
 Surveillance data provides information for action.
75

Purpose of surveillance
 Early detection of problems E.g. Epidemic
 Provide scientific baseline data for priority setting, planning,
implementing and evaluating disease control programs.
 Define the magnitude and distribution of diseases by time,
person and place dimension.
 Identification of seasonal and long-term trends of Disease in
the area.
76

Public Health
Approach
77
Problem Response
Surveillance:
What
is the
problem?
Risk Factor
Identification:
What is the
cause?
Intervention
Evaluation:
What
works?
Implementation:
How do you
do it?

Activities in Surveillance
 Data collection and recording
 Data compilation, analysis and interpretation
 Reporting and notification
 Dissemination of information
78

Types of surveillance
There are three major types of surveillance:
1. Passive Surveillance
2. Active Surveillance
3. Sentinel Surveillance
79

1. Passive surveillance
 Defined as a mechanism for routine survey based on
passive case detection and on the routine recording and
reporting system.
 The information provider comes to the health
institutions for help, be it medical or other non medical.
 It involves collection of data as part of routine
provision of health services.
80

Advantages
Covers a wide range of problems
Does not require special arrangement
Is relatively cheap
Covers a wider area
81

Disadvantages
 The information is to a large extent unreliable,
incomplete and inaccurate.
 Lacks timeliness.
 Desired information may not be there.
 Lacks representativeness.
 No feed back system.
82

2. Active surveillance
Data collection usually on a specific disease, for
relatively limited period of time through:
 House-to-house surveys or
 Mobilizing communities to some central point where
data can be collected.
Example: Investigation of out-breaks
83

Active surveillance is appropriate for:
 Periodic evaluation of an ongoing program
 Programs with limited time of operation
 Unusual situations such as:
- New disease discovery
- New mode of transmission
- When a high-risk season/year is recognized.
- When a disease is found to affect a new subgroup
- When a previously eradicated disease reappears.
84

 Advantages
 Data are Complete, Accurate, and Timely
Disadvantages:
 It requires good organization,
 It is expensive,
 Requires skilled human power,
 It is for short period of time,
 It is directed towards specific disease conditions,
85

3. Sentinel Surveillance
 It uses a pre-arranged sample of reporting sources to report
all cases of one or more conditions.
This is carried out by:
 Selecting sample sources most likely to see cases of the
specified condition.
 Identifying institutions that serve the population subgroups and
that can obtain data regarding the condition of interest.
 It provides a practical alternative to population-based
surveillance, in developing countries.
86

Advantages
 Relatively inexpensive
 Provides a practical alternative to population-based
surveillance
 Can use of data collected for other purposes
Disadvantages
 The selected population may not be representative of the
whole population
 Use of secondary data may lead to data of lesser quality and
timeliness
87

Steps in Planning surveillance
 Establish objectives
 Develop case definitions
 Determine data source
 Develop data collection instruments
 Collection of Data
 Compilation and Analysis of Data
 Formulation of Recommendation
 Dissemination of Information to the concerned bodies
88

Criteria for identifying disease for surveillance
Frequency
 Incidence
 Prevalence
Severity
 Case fatality ratio/Mortality
 Hospitalization rate
 Disability rate
89

Criteria cont’d…
 Cost/affordability
 Preventability
 Communicability
 Public Interest (community concern)
90

Data Collection and recording
Basic techniques of data collection include the
following:
 Record review,
 Interviews,
 Surveys using questionnaires, and recording,
 Observation.
91

Sources of data for surveillance
The major sources summarized by the WHO in
1968 are:
 Mortality registration
 Morbidity registration
 Epidemic reporting
 Reports of laboratory utilization
92

Source of data …
93
 Reports of individual case investigations
 Reports of epidemic field investigations
 Special surveys
 Information on animal reservoir and vector
distribution
 Report of biologics and drug utilization
 Knowledge of the population and environment

Data compilation, analysis and interpretation
 Data should be collected at each level of health care delivery
system.
 Quality of data should be accurate, complete, reliable, and
submitted on time.
 Surveillance data is analyzed in terms of time, place and person
 Analysis of data must be made at every level of the health delivery
system.
 Analysis at the health facility level helps to recognize problems
timely and to take appropriate action immediately.
94

Data analysis cont’d…
 Proper analysis of surveillance data includes
determination of both numbers and rates.
The interpretation: Is the change a true change?
Apparent changes can occur as a result of:
• Change in the population size,
• Improvement in the diagnostic capability,
• Improved reporting, duplicate reporting
• Improved health service coverage, etc.
95

Reporting and notification
 Reporting formats must be clear and easy to use.
 Any report must be clear and answer questions like
what, where, when, to whom, for what and why.
Types of reports
 Oral
 Radio or telephone
 Written
96

Dissemination of information
 To ensure motivation and active involvement there
must be:
 Preparation of regular weekly, monthly, quarterly and
annual reports.
 Regular feedback from higher levels.
 Publication of newsletters.
97

Link to public health action
 “information for action” implies that surveillance
systems should be functionally linked with public health
programs.
 In Ethiopia the Ministry of health and Regional Health
Bureaus are responsible for both surveillance and
program action.
 A communicable disease outbreak usually leads to an
investigation and appropriate public health action.
98

Features of a good surveillance system
 Using a combination of methods,
 Timely notification,
 Timely and comprehensive action taken,
 Availability of a strong laboratory service.
99

Limitations of existing surveillance system in Ethiopia
 Deficiencies in data collection
 Lack of diagnostic accuracy
 Lack of completeness
 Lack of representativeness
 Deficiencies in reporting/notification
 Multiplicity of case reporting forms
 Lack of compliance/continuity
 Lack of timeliness
100

Limitations……
101
 Deficiencies in data analysis
 Carried out at the central rather than local level
 Results in national indicators of health status rather than
local indicators
 Deficiencies in dissemination
 Aggregate information which is not useful at the local
level
 No feedback system
 Lack of follow-up for action

List of Priority Diseases in Ethiopia
Epidemic-prone diseases
1.Cholera
2.Diarrhea with blood
(Shigellosis)
3.Measles
4.Meningitis
5.Plague
6.Viral hemorrhagic fever
7.Yellow fever
8.Typhoid fever
9.Relapsing fever
10.Epidemic typhus
11.Malaria
Diseases targeted for eradication
12. Acute flaccid paralysis (Polio)
13. Dracunculiasis (Guinea worm)
14. Leprosy
15. Neonatal Tetanus
Other diseases of public health
importance
16. Pneumonia in children
17. Diarrhea in children
18. New AIDS cases
19. Onchocerciasis
20. Sexually transmitted diseases
21. Tuberculosis
22. Rabies
23. Maternal mortality
102

List of reportable disease in Ethiopia
Immediately reportable disease
1. Acute Flaccid Paralysis (AFP)/Polio
2. Anthrax
3. Avian Human Influenza
4. Cholera
5. Dracunculiasis / Guinea worm
6. Measles
7. NNT
8. Pandemic Influenza A
9. Rabies
10. Smallpox
11. SARS
12. Viral hemorrhagic fever (VHF)
13. Yellow fever
Weekly reportable disease
14. Dysentery
15. Malaria
16. Meningitis
17. Relapsing fever
18. Severe Malnutrition
19. Typhoid fever
20. Typhus
103

Investigation and management of Epidemic
Levels of disease occurrence
 Diseases occur in a community at different levels at a
particular point in time.
 Some diseases are usually present at a predictable
level/expected level (examples; endemic and hyper
endemic).
 But sometimes they occur in excess of what is expected
(Outbreak, Epidemic, and Pandemic)
104

Definition of terms related to the level of
occurrence of disease
1. Endemic: Presence of a disease at more or less stable
level.
 Malaria is endemic in the lowland areas of Ethiopia.
2. Hyper endemic: Persistently high level of disease
occurrence.
3. Sporadic: Occasional or irregular occurrence of a
disease. When diseases occur sporadically they may occur
as epidemic.
105

Definition of terms …
4. Epidemic: The occurrence of disease or other
health related condition in excess of the usual
frequency in a given area or among a specific
group of people over a particular period of time
5. Outbreak: Epidemics of shorter duration covering
a more limited area.
6. Pandemic: An epidemic involving several
countries or continents affecting a large number
of people.
For example the worldwide occurrence of
106

Epidemics
Three points to be kept in mind
1. Epidemic refers to
 Acute and chronic infection
 Infectious diseases/communicable
disease
 Other related conditions
2. No minimum number
3. Knowledge of the usual frequency
107

Types of epidemics
Epidemics (outbreaks) can be classified according to
 The method of spread or propagation,
 Nature and length of exposure to the infectious
agent, and duration.
108

Types of epidemics….
1. Common Source Epidemics:
 Disease occurs as a result of
- exposure of a group of susceptible persons to a
common source of a pathogen,
- often at the same time or within a brief time
period.
 When the exposure is simultaneous, the
resulting cases develop within one incubation
period of the disease and this is called a point
109

110
Number of
cases
Time
Usual rate
Epidemic
Fig. the epidemic curve for point source epidemic
Characteristics:
•Sharp rise and fall
•Unimodal peak
•Short duration

Common Source Epidemics….
 If the exposure to a common source continues over
time it will result in a continuous common source
epidemic.
E.g. A waterborne outbreak that spreads through a
contaminated community water supply.
 The epidemic curve may have a wide peak because of
the range of exposures and the range of incubation
periods.
111

112
Usual rate
Number of
cases
Time
Epidemic
Pattern of a continuous common source epidemic
Flat top

2. Propagated/ Progressive Epidemics
 The infectious agent is transferred from one host to
another.
 It can occur through direct person to person
transmission or it can involve more complex cycles
in which the agent must pass through a vector. e.g.
outbreak of malaria
 Propagated spread usually results in an epidemic
curve with a relatively gentle upslope and
somewhat steeper tail.
113

114
Time
Pattern of a propagated type epidemic
Usual rate
Number of
cases
Epidemic
Characteristics:
•Slow increase
•Several peaks
•Sharp fall

3. Mixed Epidemics
 The epidemic begins with a single, common source
of an infectious agent with subsequent propagated
spread.
 Many food borne pathogens result in mixed
epidemics.
115

Investigation of an Epidemic
Purpose:
 To determine the specific cause or causes of the
outbreak at the earliest time.
 To take appropriate measure directed at controlling
the epidemic and preventing future occurrence.
116

Questions should be answered when investigating an epidemic.
1. What is the etiological agent responsible for the epidemic?
2. What is/are the predominant modes of transmission?
3. What specific source/s of disease can be identified?
E.g. human carriers, breeding sites for vectors, etc.
4. What specific practices or environmental deficiencies have
contributed to the outbreak?
E.g. improper food handling, human made breeding sites for mosquitoes.
5. What is the chain of events that led to the outbreak?
E.g. accumulation of susceptible hosts in an area.
117

Steps in epidemic investigation
1. Prepare for fieldwork.
 Before leaving for the field you should be well
prepared to under take the investigation.
 Preparations can include:
a. Investigation-
– appropriate scientific knowledge,
– supplies, and equipment to carry out the investigation
b. Administration, and
c. Consultation.
118

Steps in epidemic investigation….
2. Verify (confirm) the existence of an epidemic
 This initial determination is often made on the
basis of available data.
 Compare the number of cases with the past levels
to identify whether the present occurrence is in
excess of its usual frequency.
 Instead of comparing absolute numbers it is
advisable to compare rates like incidence rate
119

3. Verify (confirm the diagnosis).
 Always consider whether initial reports are correct.
 Carry out clinical and laboratory investigations on the
reported cases. It is important to investigate the index
case (the first case that comes to the attention of health
authorities) and other early cases.
 The sooner the index case and other early cases are
investigated, the greater the opportunity to arrest the
outbreak at earliest stage possible.
120

4. Establishing case definition
 Remember excess may be due to changes in local reporting
producers, changes in case definition, or change in diagnostic tool
 A standard case definition is required to differentiate cases & non
cases
 Confirmed / definite: a case with clinical features and
laboratory investigation
 Probable: a case with typical clinical features without
laboratory confirmation ,
 Possible: a case with fewer of typical clinical features.
121

5. Describe the epidemic with respect to person, place
and time
 Each case must be defined according to standard
epidemiologic parameters:
- The date of onset of the illness,
- The place where the person lives or became ill, and
- Socio-demographic characteristics (age, sex, education
level, occupation).
 The tools to be used when characterizing the epidemic are
 Epidemic curve, Spot map, and Attack rates
122

 Epidemic curve is an important tool for the
investigation of disease outbreaks.
 In epidemic curve the distribution of cases is plotted
over time, usually in the form of histogram,
- with the date of onset of cases on the horizontal axis,
and
- the number of cases corresponding to each date of
onset on the vertical axis.
123

 Spot map is a map of locality where the outbreak has
occurred, on which the location of cases is plotted.
- Mapping disease can be done at kebele, woreda, regional,
and national level.
- One limitation of spot map is that it does not take into
account underlying geographic differences in population
density.
- Thus the spot map needs to be supplemented by calculation
of place specific attack rates.
124

6. Formulate hypothesis
 The hypothesis should addressed
 Source of the agent
 Exposure that cause the disease
 All factors that can contribute to the occurrence of
the epidemic should be assessed.
125

126
 The epidemic investigating team should try to answer
questions like:
 Why did this epidemic occur?
 Are there many susceptible individuals?
 Is the temperature favorable for the transmission of
the diseases?
 Are there breeding sites for the breeding of vectors?

Developing Hypothesis
How do we Generate Hypotheses?
1. Subject-matter knowledge
2. Descriptive epidemiology
3. Talking with patients
4. Talking with local officials
127

7. Search for additional cases
 Using active and passive case detection
 Investigation of unapparent asymptomatic person
8. Analyze the data - interpret findings
9. Make a decision on the hypothesis tested
10. Intervention and follow up
 Intervention must be as soon as possible
 Control
 Destroying contaminated food
 Sterilizing
128

11. Reporting
 Comprehensive report to concerned agencies
- Factor leading to epidemics
- Evaluation of measures
- Recommendation for prevention of similar
episodes
129

Epidemic management
 Management of epidemics requires an urgent and
intelligent use of appropriate measures against the
spread of the disease.
 Action to be taken is dependent on
- the type of the disease
- the source of the outbreak.
130

Epidemic management….
1. Measure directed against the reservoir
Domestic animals as reservoir:
- Immunization. Example – giving anti-rabies
vaccine for dogs
- Destruction of infected animals e.g. anthrax
Wild animals as reservoir:
 post-exposure prophylaxis for human beings-
Example: rabies
131

Epidemic management….
Humans as reservoir:
A . Isolation of infected persons- separation of infected persons
from non-infected for the period of communicability.
B. Treatment to make them noninfectious- e.g., tuberculosis.
C. Quarantine- is the limitation of freedom of movement of
apparently healthy persons or animals who have been
exposed to a case of infectious disease.
 Usually imposed for the duration of the usual maximal
incubation period of the disease.
132

Quarantine…….
 The three internationally quarantinable diseases by
international agreement:
- Cholera
- Plague and
- Yellow fever
 Now quarantine is replaced in some countries by
active
surveillance of the individuals;
- maintaining close supervision over possible contacts
of ill persons to detect infection or illness promptly;
- their freedom of movement is not restricted.
133

2. Measures that interrupt the transmission of
organisms
 Action to prevent transmission of disease by ingestion:
i. Purification of water
ii. Pasteurization of milk
iii. Inspection procedures to ensure safe food supply.
IV. Improve housing conditions.
V. Sanitation and hygiene
134

3. Measures that reduce host susceptibility
 Immunization
- Active immunization – antigen
- Passive immunization- antibody e.g. TAT
 Chemoprophylaxis: for example, use of chloroquine to
persons traveling to malaria endemic areas.
 After the epidemic is controlled, strict follow up
mechanisms should be designed so as to prevent similar
epidemics in the future.
135

Unit 4
Feco-orally transmitted disease
Learning Objective :
 List diseases that spread with contaminated food and water.
 Describe the epidemiologic distribution of each disease.
 Describe the clinical manifestations and diagnosis modalities
of each disease.
 Describe and able to treat and prevent this infections .
136

1.Typhoid/enteric fever
 Bacteria of the genus Salmonella are highly
adapted for growth in both humans and animals
and cause a wide spectrum of systemic disease
 Salmonella spp. > 2400 serotypes
 Motile, Non-spore forming Gram-ve bacilli
 Infectious agent: S.typhi and S.paratyphi are
restricted to human host causing enteric
fever
137

Typhoid fever…
Reservoir
Human hosts and animals, including mammals, reptiles,
birds, and insects.
Epidemiology
17 million cases annually with 600,000 deaths
In Ethiopia common in the highland areas in the cool
seasons.
Mode of transmission:
Ingestion of contaminated food and water (inoculums dose
103-106) by susceptible host.
138

139
Susceptible host
 Stomach acidy, Achlorhydric diseases,
 Antiacid ingestion,
 Age <1yr
 Decreased in Intestinal integrity
 IBD
 GI Surgery
 Broad spectrum antibiotic use
Typhoid fever…

Pathophysiology
 Penetration of gut mucosal layer and infection
of payer’s patches (phagocytosed by
macrophages).
 Dissemination throughout the body via
lymphatics and colonize RES  Re infection
of intestine as well as other body parts via
hematogenous dissemination.
140

Cont’d ...
 Incubation Period (IP): 3-21 days
 Period of communicability:
As long as the bacilli appears in excreta
10% untreated cases will discharge bacilli for 3
month After onset of symptoms.
141

Clinical presentation
Step ladder pattern fever (75%)
Relative bradycardia
Abdominal pain (20-40%)
GI symptoms: diarrhea (AIDS patients, Age <1
yr)/constipation
Rose spots: Maculopapular blanching rash over the
trunk and chest.
Hepatosplenomegaly, Epistaxis
Delirium/coma
142

Diagnosis
• 15-25% of cases → leukopenia and neutropenia;
• The majority of cases → normal WBC count despite high
fever.
• Moderately elevated LFT.
 Dx “gold standard”- a culture positive for S.typhi or
S.paratyphi
• Blood culture (yield) -1st week: 90%, 3rd week: 50%
• Bone marrow cultures remain 90% sensitive despite < 5
days antibiotic therapy .
143

 Stool cultures: negative in 1st week in 60 to70% of
cases; can become positive during the third week in
untreated patients.
 90% of patients clear bacteria from the stool by the
eight week.
 Serology: Widal test – high rates of false positivity and
false negativity → clinically not useful.
144
Diagnosis…

Treatment
 Quinolones or 3rd generation cephalosporin
Ciprofloxacin 500mg po bid for 7- 10days
Ceftriaxone 1 to 2 gram iv or im for 10 to14 days.
Alternatives
Ampicillin -1gram orally every 6 hrs
TMP-SXZ: one double strength tablet twice
daily.
Azithromycin (1 g orally once followed by 500 mg once daily
for 5 days
Chloramphenicol 2 to 3 g per day orally in four divided doses
for 14 day.
145

Severe typhoid fever (fever; delirium; obtundation;
stupor; coma; or septic shock; and a positive culture for
S.typhi or S.paratyphi) → Dexamethasone: a single dose
of 3mgkg followed by eight doses of 1mgkg; given
every 6 hrs).
 Chronic carriers (1 to 4 %) of salmonella → treatment
for six weeks with oral Amoxicillin, TMP-SXZ,
Ciprofloxacin or Norfloxacin→ 80% effective in
eradicating chronic carriage.
146

 Chronic carriage — an excretion of the organism in stool or urine
>12 months after acute infection.
 In general, chronic carriers do not develop recurrent
symptomatic disease.
 They appear to reach an immunologic equilibrium in
which they are chronically colonized and may excrete
large numbers of organisms,
 Have a high level of immunity and do not develop
clinical disease
 Rates of chronic carriage after S. typhi infection range from 2- 6%
147

Complication
 Intestinal perforation /bleeding
 Hepatic/splenic abscesses
 Meningoencephalitis
 Nephritis, Arthritis /osteomyelitis
Relapse rate despite Rx =10%
Chronic carriers
High incidence in women, individuals with biliary
tract abnormalities (stone /tumor) and GI malignancy
148

Prevention and control methods
 Proper sanitation and personal hygiene
 Educate the public food handlers
 Protect and purify public water
 Control flies
 Use thorough cleanliness in food preparation and handling
 Encourage breast feeding infancy period and boil water and
milk used for feeding
 Treat cases and source of infection
 Typhoid vaccines (Travelers to endemic areas, People
with close contact with chronic carrier )
149

2. Amoebiasis
o Is an infection with a protozoan parasite that exists in two
forms (cyst and Trophozoites)
o Infectious agent: Entamoeba histlolytica
o Epidemiology: higher in areas of poor sanitation, 2-10%
prevalence in Ethiopia.
o MOT: ingestion of fecally contaminated food or water
o IP: 2-4 weeks
o Period of communicability: during the period of E.
histlolytica cyst passed.
150

Trophozoite:
 Any stage in a protozoan’s life cycle which can ingest food.
 This is the motile form of the bacteria.
Cyst:
 The non motile form which is protected by a distinct
membrane or cyst wall.
 This is an infective stage of the parasite
Excystation:
 The process of emergence of the trophozoites from the cyst
(vs. encystations)
151

Pathophysiology
E. histolytica acquired by the ingestion of infectious
viable cysts from feces contaminated water, food or hands
 Release of motile Trophozoites from cysts in small
intestine 
Large bowel mucosa invasion with sub mucosal extension
 Inoculation of amoebas in to the portal system
distant metastatic abscess in liver /lung/brain 
Encystation of trophozoites and/or motile trophozoites
passage in stool.
152

Amoebic dysentery
Intestinal amoebiasis
 Mostly asymptomatic cyst passage (90%)
 Symptomatic cases (10%):
 Presentation
 - Bloody, mucoid diarrhea
 - Fever< 40 %, chills
 - lower Abdominal pain
Diagnosis
 Amoebic (hematophagous trophozoites) in stool (repeated
stool exam increases the yield)
 Mixed WBCs in stool
 Patchy inflammation seen on colonoscopy
 Stool PCR or antigen capture
154

155
 Amebomas
- A rare complication of intestinal disease
- Are granulomatous mass lesions protruding into the
bowel lumen, with a thickened edematous and
hemorrhagic bowel wall that can cause obstructive
symptoms.

Presentation
1. Persisting fever
2. RUQ or epigastric pain and/or shoulder pain
3. Rarely diarrhea
Diagnosis
1. Ultrasound (u/s)
2. Raised WBC
3. Serology
4. Aspirate microscopy
5. Response to metronidazole
Amoebic liver abscess

Treatment of Amebiasis
Disease Tissue agent Luminal agent
Amebic liver
abscess
Metronidazole
750mg po tid X
10d
Or
Tinidazole 2g
po/d X 5 d
Paromomycin
10mg/kg/d po tid
X 5-10 d
Or
Diloxanide
furoate 500 mg
po tid X 10d
Amebic Colitis Metronidazole
750mg po tid X
5-10d
As above
157

3. Giardiasis
o A protozoan infection principally affects the upper small
intestine.
o Infectious agent: Giardia lambli, also known as G.
duodenalis or G. intestinalis
 Reservoirs: zoonosis – human and found in most mammals
esp. beaver (“beaver fever”), cattle, cats, dogs…
 IP: usually 3-25 days
 Period of communicability: months during entire infection.
158

159
 Ingestion of 10 to 25 cysts can lead to giardiasis;
 Hypochlorhydria predisposes to infection
 Following cyst ingestion, excystation occurs in the
proximal small bowel with release of trophozoites
Fecal oral spread
Prevalence 30-40% carrier rate, more in children, and
seasonal (increase during rainy seasons).
Most common in HIV patients
Giardiasis

Symptoms of chronic giardiasis
161
 Loose stools but usually not diarrhea
 Steatorrhea
 Profound weight loss (10 to 20 percent of
body weight)
 Malabsorption
 Malaise
 Fatigue
 Depression
 Abdominal cramping
 Flatulence

Treatment
 Metronidazole 250-750 mg tid x 7-10 days
 Tinidazole: Tinidazole 2g po/d X 5 d
 Nitazoxanide: 500 mg every 12 hours for 3 days.
 Paromomycine:
 Hepatic coma: Oral: 4 g daily in divided doses (at regular intervals)
for 5 to 6 days
 Intestinal amebiasis: Oral: 25 to 35 mg/kg/day in 3 divided doses
for 5 to 10 days
 Furazolidone: oral: 100 mg 4 times/day
162

 Proper sanitation and personal hygiene
 Educate the public in sanitary disposal of feces and hand
washing before handling food
 Protect and purify public water against contamination of
human and animal feces
 Supervise the cleanliness of food preparation and handling
 Treat cases and source of infection
 Boil emergency water supplies
163

4.Cholera
o An acute diarrheal disease that can result progressive
dehydration and death rapidly .
o Causes secretory form of diarrhea
o It is toxin mediated disease
o Infectious agent :V. cholerae serogroup O1 or O139
o Epidemiology: periodic outbreak in different parts of the
world, Which causes 120,000 deaths/year
o Prevalent in 75 countries.
o Reservoir: human colon, invertebrate animal
contaminations (shell fish) and environment.
164

Cholera….Cont’d
o MOT: Ingestion of contaminated meal or water.
o IP: 12-48hrs.
o Period of communicability: as long as stool is
positive even after recovery and months in carrier
state.
 Risk groups: achlorhyrdia (use of antiacid or
food buffering), children, blood group O.
165

Clinical manifestation
o Abrupt, painless watery diarrhea
 Stool (non bilious, gray, cloudy, with flecks of
mucus, no blood, sweet, non offensive odour)
o Significant weight loss, vomiting
o Postural hypotension, weakness, tachycardia & ↓skin turgor,
shock and death.
o No fever
o CFR exceeds 50% in severe untreated cases
o If proper treatment with rehydration it will reduced to 1%.
166

Diagnosis
 Clinical presentation
 Stool examination /wet mount, dark field microscopy/
Stool culture
Treatment
Patients with suspected cholera need to be
treated prior to laboratory confirmation.
Fluid +electrolyte replacement, IV fluid
167

Treatment…
168
 Adequate replacement of fluid and electrolytes
- ORS (Na+ 90mmol/l, K+ 20, Cl 80, citrate 10, glucose
110)
 Antibiotics: TTC 2gm stat, Doxycycline 300mg stat
 Alternatives: ciprofloxaciline, erythromycin,
Cotrimoxazole
 Prevention safe water supply and sanitary disposal of
feces
 Vaccines under development.

o Health education about preparation and utilization of
foods.
o Wash hand and protect food from flies
o Personal hygiene
o Food safety
o Safe drinking water
o Sanitation (safe disposal of human excreta )
169

Prevention .....
o Preventing spread in health facility
o Disinfecting
o Breast feeding and proper nutrition.
o Isolation
o Investigation and management of contacts.
o Specific treatments.
o Report cases to nearby authority.
170

5. Shigellosis (bacillary dysentery)
 Shigellosis is an acute infectious inflammatory colitis
due to shigella spp.
Infectious agent :Gram-ve bacilli of shigella
Four species 1.S.dysentry
2.S.flexneri
3.S.boydi and
4.S.sonnei
171

Epidemiology
o Endemic in developing countries and causing bloody
diarrhea world wide.
o Causes more than 80 million cases and 700, 000
death each year globally.
o 95% cases occur in developing countries 70 % of
cases occur among children.
o Affects around 63,000 each year in Ethiopia.
172

Reservoir : human
MOT:
• Ingestion of contaminated food or drinking
contaminated water.
• Flies can transmit the infection.
• Highly infectious with low dose of bacilli (200
viable organism)
IP:1-4 days
173

 Period of communicability:
 During an acute infection and up to 4wks after illness.
 Clinical manifestation
 Bloody diarrhea/frequent dysentery (10-30 times per
day) of small volume bloody
 mucoid and pusy diarrhea
 abdominal cramp, fever
 tenesmus (Complicated by rectal prolapse in young
children)
 Diagnosis: Stool examination, Stool culture
 Treatment:
 Fluid and electrolyte replacement
 Ciprofloxacin 500mg PO bid for 7-10 days , Ceftriaxone,
174

Complications
175
 Toxic mega colon
 Colonic perforation
 Dehydration + electrolyte imbalance
 Protein losing enteropathy with extensive colonic
involvement - PEM in poorly nourished children
 Reactive arthritis (Reiter’s syndrome)-S.flexneri
infection, weeks to months after diarrheal illness
 Hemolytic-Uremic syndrome- 20 to S.dysentriae type
1 infection: Usually occurs in the end of 1st week of
shigellosis.

 Health education about preparation and utilization of
foods
 Wash hand and protect food from flies
 Personal hygiene
 Food safety
 Safe drinking water
 Sanitation (safe disposal of human excreta )
 Preventing spread in health facility
176

Cont’d ....
 Disinfecting
 Breast feeding and proper nutrition
 No licensed vaccine against shigella
Isolation
Investigation and management of contacts
Specific treatments
Report cases to nearby authority
177

6. Poliomyelitis
 Caused by poliovirus.
 The polioviruses are
- Non enveloped, single-stranded RNA viruses
- include 3 antigenically distinct serotypes (types 1, 2, and
3).
 Polioviruses spread from the intestinal tract to the
central nervous system (CNS), where they cause
aseptic meningitis and poliomyelitis, or polio.
178

Cont’d...
MOT
 Poliovirus is transmitted by oral-fecal contact.
 During epidemics, it also may be transmitted by
pharyngeal spread.
 IP: 8-12 days with a range of 5-35 days.
• Humans are the only known reservoir.
 Poliovirus has been isolated from feces for >2 wk before
paralysis to several weeks after the onset of symptoms.
179

Clinical manifestations
Poliovirus infections may follow 1 of several
courses:
1. Inapparent infection
 occurs in 90–95% of cases and causes no
disease and no sequelae;
2. Abortive poliomyelitis;
In about 5% of patients
a nonspecific influenza-like syndrome occurs 1–
2 wk after infection.
180

C/m....
3. Minor illness like
Fever, malaise, anorexia, and headache are
prominent features, and there may be sore
throat and abdominal or muscular pain
illness is short lived, up to 2–3 days
Recovery is complete, and no neurologic
signs or sequelae develop.
181

C/m....
4.Nonparalytic poliomyelitis
 In about 1% of patients infected with wild-type
poliovirus.
 More intense headache, nausea, and vomiting, as
well as soreness and stiffness of the posterior
muscles of the neck, trunk, and limbs.
 Nuchal and spinal rigidity are the basis for the
diagnosis of nonparalytic poliomyelitis
5. Paralytic poliomyelitis 0.1 –1%
182

183
 The mechanism of spread of poliovirus to the
central nervous system is not well understood.
- It may occur by direct passage of the virus from
blood by crossing the blood-brain barrier, or
- may occur by retrograde axonal transport from
muscle to spinal cord and brain.
 Proximal muscles usually are affected more than
distal muscles
 legs more commonly than arms.
 Reflexes are decreased or absent.
 The sensory examination is normal.

Con...
DX:
1. Clinically 2.Viral isolation
3. Serology 4. Histology
5. CSF-pleocytosis initially characterized by polymorphonuclear
leukocytes, followed by a shift to lymphocytes, protein is usually
elevated.
Treatment
 There is no specific antiviral treatment for poliomyelitis.
 Management is supportive
 Because there are no effective treatments to restore motor neuron
function after paralytic polio, prevention has been a mainstay of clinical
and research efforts
184

Prevention
 Vaccination is the only effective method of preventing poliomyelitis.
 Vaccines – IPV / OPV
- In areas of the world where polio is endemic, primary immunization is
still performed with OPV.
- because OPV causes polio in one out of 2.5 million cases, it has been
replaced by the IPV in countries without polio, including the United
States and most of Europe.
 Polio eradication – planned by WHO by 2000, then 2008
 Strategies
• routine immunization,
• National Immunization Days (NIDs),
• acute flaccid paralysis surveillance
185

7. Infectious hepatitis
Hepatitis is an inflammation of the liver
Hepatitis viruses are the most common cause of hepatitis
Hepatitis A and E are typically cause the acute form of
hepatitis.
HEV is a common cause of hepatitis outbreaks in
developing parts of the world.
IP:1wks-64 days
186

Classification of Hepatitis Viruses
*linear, single strand; ** circular, double strand; *** circular, single strand
Virus
HAV
HBV
HCV
HDV
HEV
DNA or RNA
RNA*
DNA**
RNA*
RNA***
RNA*
Family
Picornaviridae
Hepadnaviridae
Flaviviridae
Deltavirus (genus)
?
Envelope
no
yes
yes
yes
no
(Previously classified as a
calicivirus)

Basic Features of Hepatitis Viruses
Virus
A
B
C
D
E
Incubation
Period(week)
4 (2-6)
8-12 (6-24)
6-9 (2-24)
(2-10)
4-5 (2-9)
Transmission
fecal-oral
parenteral
parenteral
parenteral
fecal-oral
Chronic
Infection
No
Yes
Yes
Yes
No

Viral Hepatitis -
Overview
* Blood and blood-derived body fluids **Prevention of Hep B with vaccine
Source of
virus
Route of
transmission
Chronic
infection
Vaccine
Pre/Post
prophylaxis
A
Feces
fecal-oral
no
yes
pre/post
(IG)
B
Blood*
Percut-
aneous
yes
yes
post
(HBIG)
C
Blood*
Percut-
anous
yes
no
no
D
Blood*
Percut-
aneous
yes
yes**
no
E
Feces
fecal-
oral
no
no
no

Cont’d...
 Reservoir :human and animals
 MOT : ingestion of contaminated food or water
 Asymptomatic or symptomatic ± Jaundice , dark urine, extreme
fatigue, nausea, vomiting and abdominal pain
DX:
 Epidemiologically
 Serology test for IGM anti-A or E
Treatment
 Supportive management
 Vaccine
Prevention
 Proper handling of food and water
 Vaccine
190

Helmenthiasis (faces mainly in soil)
1. Ascariasis/Ascaris lumbricoides (roundworm)
 The prevalence of ascariasis is highest in tropical
countries where warm, wet climates favor year-round
transmission of infection.
 In dry areas, transmission occurs predominantly during
the rainy months.
 The prevalence is greatest in areas where suboptimal
sanitation practices lead to increased contamination of soil
and water.
191

Ascariasis
Ascaris lumbricoides
(roundworm)
Risk………… Fecal oral/soil
Presentation …… small intestine
12-40 cm

Life Cycle
Adult worms live in the lumen of the small intestine.
Mature female Ascaris worms are extraordinarily
lay up to 240, 000 eggs a day which are passed with
the feces.
Ascarid eggs are resistant to environmental stresses.
 Become infective after several weeks of maturation
in the soil and can remain infective for years.
193

Life cycle ...
 Infective eggs swallowed => larvae hatched in the
intestine, invade the mucosa => carried via the portal
circulation, then systemic circulation to the lungs,
 The larvae mature further in the lungs (10 to 14 days)
penetrate the alveolar walls, ascend the bronchial tree to the
throat, and are swallowed.
 Upon reaching the small intestine, they develop into adult
worms which can live 1 to 2 years.
194

Manifestations
 Asymptomatic
 Pneumonitis
 Abdominal pains
 Malnutrition
 Small intestine obstruction
 Biliary tree obstruction
 Perforation of intestine suture
195

Diagnosis
Stool microscopy for eggs and
Sometimes adults may be seen by naked eye.
Treatment
Albendazole (400 mg once), or
 Mebendazole (100 mg twice daily for 3 days or 500 mg
once), or
 Ivermectin (150–200 mg/kg once) is effective.
 Pyrantel pamoate (11 mg/kg once; maximum, 1 g) is safe in
pregnancy.
196

2. Trichuriasis
Trichuris trichuria
(whipworm)
Geography... tropical esp. SE Asia,
Philippines,
Risk... Fecal/soil oral transmission
Presentation ... colon
3-5 cm
head
tail

Trichuris trichuria……
198
 The life cycle for trichuriasis begins with passage of
unembryonated eggs in the stool, become infective in 15 to 30
days.
 After ingestion via food or hands contaminated with soil, the eggs
hatch and release larvae that mature into adults worms which
become established in the colon after two to three months
 Unlike the Ascaris trichuriasis has no heart lung migration

Trichuriasis….
 Manifestations: worm load dependent
- Asymptomatic (Most ) (<5000 eggs)
- Diarrhea, Dysentery
- Nocturnal stooling is common
- Prolapsed rectum (setting of heavy infection)
- Iron deficiency anemia, eosinophilia
 Diagnosis: Stool examination (finding the eggs).
 Treatment: Albendazole (400 mg daily for 3 doses), (500 mg
once) is the treatment of choice.
199

3. Enterobiasis
Enterobius vermicularis (pinworm)
Geography = > universal
Risk => small children
Presentation => colon, anus
 adult female lives 2-3 months
 eggs laid by adult after 2 months in colon
 lays eggs at night in perianal folds
 eggs become infective in 4-6 hours
 eggs can survive in carpet for 2 weeks
200

201
 Most common symptom of enterobiasis is perianal
itching.
 This is caused by an inflammatory reaction to the
presence of adult worms and eggs on the perianal skin
and occurs predominantly at night.
 Scratching leads to lodging of eggs beneath the
fingernails, facilitating subsequent autoinfection,
and/or person-to-person transmission.

C/m…
202
 Secondary bacterial infections can result if the
excoriation is severe.
 Nocturnal pruritus can also lead to difficulty sleeping
 Occasionally, abdominal pain, nausea, and vomiting.
 Adult pinworms may be found in normal and
inflamed appendices following surgical removal, but
whether or not they cause appendicitis is still debated

Diagnosis
Since pinworm eggs are not released in feces, the
diagnosis cannot be made by conventional fecal ova
and parasite tests.
Instead, eggs are detected by the application of clear
cellulose acetate tape to the perianal region in the
morning = "scotch tape" test.
The yield is greatest if the test is performed at night or
in the morning, prior to bathing.
203

Treatment
Mebendazole (100 mg once) or
 Albendazole (400 mg once) or
 Pyrantel pamoate (11 mg/kg once; maximum, 1 g),
with the same treatment repeated after 2 weeks.
NB: treatment of household members is advocated to
eliminate asymptomatic reservoirs of potential
reinfection.
204

4. Ancylostomiasis (Hookworm infection)
 Ancylostoma duodenale
(in Mediterranean countries, Iran, India, Pakistan, and
the Far East)
 Necator americanus
(in North and South America, Central Africa, Indonesia,
islands of the South Pacific, and parts of India
 Risk ….. Contact with feces contaminate soil.
205

 Dermal penetration by infecting larvae: Infective larvae
(filariform larva) may provoke pruritic maculopapular
dermatitis ("ground itch") at the site of skin penetration.
 Trans pulmonary passage: asymptomatic, mild cough and
pharyngeal irritation.
 Acute gastrointestinal symptoms: minor abdominal pains,
Nausea, diarrhea, vomiting,
 Chronic nutritional impairment: iron deficiency anemia,
malnutrition.
206

Diagnosis
 Clinical/history of skin exposure to potentially
contaminated soil.
 Hookworm eggs in the faeces.
 Unexplained blood eosinophilia
Treatment
 Albendazole (400 mg once),or
 Mebendazole (500 mg once)
 Iron replacement and nutrition
207

208
 Is caused by infection with Strongyloides stercoralis.
 Endemic in tropical and subtropical regions
 Manifestations of infection can range from
- Asymptomatic eosinophilia in the immunocompetent
host to
- Disseminated disease with septic shock in the
immunocompromised host.
5. Strongyloidiasis/Strongyloides, threadworm

Life cycle
209
 The infection begins when human skin contacts filariform
larvae (the infective larval stage) of S. stercoralis, which are
found in soil or other materials contaminated with human
feces.
 The filariform larvae penetrate the skin and migrate
hematogenously to the lungs where they penetrate into the
alveolar air sacs.
 The larvae then ascend the tracheobronchial tree and are re-
swallowed.

Life cycle…
210
 The larvae mature into adult worms that burrow into the
mucosa of the small intestine (duodenum and jejunum).
 Adult worms may live for up to five years.
 The adult female produces eggs, from which noninfectious
larvae (rhabditiform larvae) develop within the lumen of
the gastrointestinal tract.
 The rhabditiform larvae are generally passed in the feces.
 The cycle from dermal penetration to appearance of larvae
in the stool requires approximately three to four weeks

Autoinfection
211
 In contrast to other helminthic parasites, S. stercoralis can
complete its life cycle entirely within the human host
 So, the burden of adult worms in infected humans can increase.
 During autoinfection, the rhabditiform larvae mature into
filariform larvae within the gastrointestinal tract.
 The filariform larvae can then penetrate the perianal skin or
colonic mucosa to complete the cycle of autoinfection.
 Larval transformation within the gastrointestinal tract may also
be accelerated by constipation, diverticula, other conditions that
reduce bowel motility, and steroid use.

Clinical presentations
212
 Asymptomatic
 Dyspepsia
 Cutaneous larva currens
 Eosinophilia
 Disseminated strongyloides
 Chronic diarrhea, Weight loss
Diagnosis
 Detecting rhabditiform larvae in concentrated stool or via
serologic methods.

Treatment
213
 Ivermectin - 200 mcg/kg/day for 2 or 3 days, or
Thiabendazole, 50 mg/kg/day in two doses (maximum
3 g/day) for 2 days, is the treatment of choice.
 Albendazole - 400 mg PO twice daily for 3-7 days
 Prevention - Prevention of disease is mainly achieved
by wearing shoes in endemic areas to avoid contact
with infected soil.

UNIT 5: Air borne diseases
Are a group of diseases that are transmitted by inhalation
of infected air droplets.
The organisms causing these diseases enter the body via
the respiratory tract.
When a patient or carrier of pathogens talks, coughs,
laughs, or sneezes, he/she discharges fluid droplets.
The smallest of these remain up in the air for some time
and may be inhaled by a new host.
214

Cont’d...
 Droplets with a size of 1-5 microns are quite easily
drawn in to the lungs and retained there.
 Air borne diseases, obviously will spread more easily
when there is overcrowding as in overcrowded class
rooms, public transport, cafeteria, dance halls,
and cinemas.
 Good ventilation can do much to counteract the
effects of overcrowding.
215

1. Common cold (Acute viral rhinitis)
It is an acute catarrhal infection of the upper respiratory
tract.
Infectious agent
 Rhino viruses (100 serotypes): are the major causes in
adults.
 Para influenza viruses, respiratory syncytial viruses (RSV),
Influenza, Adeno viruses- cause common cold like illnesses
in infants and children.
216

Cont’d...
 Many people have one to six colds per year.
 Greater incidence in the highlands.
 Incidence is high in children under 5 years and gradually
declines with increasing age.
 Reservoir- Humans
 Mode of transmission-by direct contact or inhalation of air
droplets.
 Indirectly by hands and articles freshly soiled by discharges
of nose and throat of an infected person.
217

Cont’d...
 Incubation period- between 12 hours and 5 days,
usually 48 hours, varying with the agent.
 Period of communicability - 24 hours before onset
and for 5 days after onset.
 Susceptibility and resistance: Susceptibility is
universal.
 Repeated infection (attack) are most likely due to
multiplicity of agents.
218

Cont’d...
 Coryza, sneezing, lacrimation, pharyngeal or nasal
irritation, chills and malaise
 Dry or painful throat.
Diagnosis
 Based on clinical grounds
219

Treatment
 No effective treatment but supportive measure like:
 Bed rest
 Steam inhalation
 High fluid intake
 Anti pain and antipyretic
 Intake of balanced diet
220

2. Measles (Rubeola)
 It is an acute highly communicable viral disease.
 Infectious agent: Measles virus
Occurrence
 Prior wide spread immunization, measles was
common in childhood.
 Few went through life with out any attack.
 It is able to cause acute infection in individual only
once in life time.
221

Epidemiology
 Approximately 30 million measles cases are
reported annually to World Health Organization.
 Most reported cases are from Africa.
 Measles epidemics occur every 2-3 years in
population with large susceptible groups.

Risk factors
 Young age
 Malnutrition
 Lack of immunization
 Low maternal immunity
Reservoir- Humans

 Mode of transmission-
- Air borne by droplet spread, direct contact with nasal or throat
secretions of infected persons.
 Patients are infectious from 3 days before the rash up to 4–6 days
after its onset.
 Approximately 90% of the exposed susceptible individuals
develop measles.
- Greater than 94% herd immunity may be needed to interrupt
community transmission.
 Incubation period- 7-18 days from exposure to onset of fever.
224

Clinical presentation
 Fever and malaise followed by cough, coryza, and
conjunctivitis.
 Koplik's spots develop on the buccal mucosa 2 days before the
rash appears.
 The characteristic rash of measles begins 2 weeks after infection,
when the clinical manifestations are most severe, and signal the
host's immune response to the replicating virus.
 Headache, abdominal pain, vomiting, diarrhea, and myalgia may
be present.
225

Cont’d...
 Koplik's spots are pathognomonic of measles and consist
of a clustered bluish white lesions/dots 1 mm in diameter
surrounded by erythema.
 The lesions appear first on the buccal mucosa.
 The rash of measles begins as erythematous macules
behind the ears and on the neck and hairline.
 Reddish (erythematous), maculopapular rash typically
occurs in cephalocaudal progression.
226

 With the onset of the rash, symptoms begin to subside and
the rash fades over about 7 days in the same progression as
it evolved, often leaving a fine desquamation of skin .
 Of the major symptoms of measles, the cough lasts the
longest, often up to 10 days.
 In more severe cases, generalized lymphadenopathy may
be present, with cervical and occipital lymph nodes
especially prominent.
Cont’d…

Complications
 Otitis media
 Pneumonia
 Vit A deficiency
 Gastroenteritis
 Croup (Laryngo tracheo bronchitis) may result
from viral replication or bacterial super infection.
229

Complications….
230
 Mouth ulceration
 Acute glomerulonephritis
 Acute renal failure
 Severe Protein energy malnutrition
 Encephalitis

Diagnosis
 Based on clinical and epidemiological grounds
Treatment
No specific treatment
Treatment of complications
Vitamin A provision
Measles cases are hospitalized when:
 They have severe and complicated measles.
 Unsatisfactory home condition or not possible to arrange proper
Nursing care.
231

Vitamin A Prophylaxis
 Less than 6 months: 50,000 IU
 6 – 12 months: 100,000 IU
 12 months to 5 years: 200,000 IU given orally
- Reduced morbidity and mortality (recent study
showed) in malnourished African children with
severe measles.

Prevention and control
Educate the public about measles immunization.
Immunization of all children (less than 5 years of age)
who had contact with infected children.
Provision of measles vaccine at nine month.
Initiate measles vaccination at 6 months of age during
epidemic and repeat at 9 month of age.
233

3. Influenza
 It is an acute viral disease of the respiratory tract.
Infectious agent
 Three types of influenza virus (A, B and C)
Epidemiology
 Occurrence- In pandemics, epidemics and localized
out breaks.
Reservoir-
 Humans are the primary reservoirs
234

Cont’d...
 Mode of transmission- Air borne spread predominates
among crowded populations in closed places.
 Incubation period- short, usually 1-3 days
 Period of communicability- 3-5 days from clinical onset in
adults up to 7 days in young children
 Susceptibility and resistance- when a new sub type
appears all children and adults are equally susceptible.
 Infection produces immunity to the specific infecting agent.
235

Cont’d...
Clinical Manifestation
 Fever, headache, myalgia, prostration, sore throat
and cough.
 Cough is often sever and protracted, but other
manifestations are self limited with recovery in 2-
7days.
Diagnosis
 Based on clinical ground
236

Treatment
Symptomatic:
 Anti pain and antipyretic
 High fluid intake
 Bed rest
 Balanced diet intake
237

4. Diphtheria
It is an acute bacterial disease involving primarily
tonsils, pharynx, nose, occasionally other mucus
membranes or skin and sometimes the conjunctiva or
genitalia.
Infectious agent;
Corynebacterium diphtheriae (Gm tve bacilli)
238

Epidemiology
 Disease of colder months in temperate zones.
 Involving primarily non-immunized children under
15 years of age.
 It is often found among adult population groups
whose immunization was neglected.
 MOT: contact with a patient or carrier. i.e. with oral
or nasal secretions or infected skin.
239

Cont’d...
 IP: usually 2-5 days
 Period of communicability: variable, until virulent
bacilli have disappeared from discharges and lesion,
usually 2 weeks or less.
 Susceptibility and resistance.
 Immunity is often acquired through inapparent infection.
 Prolonged active immunity can be induced by diphtheria
toxoid.
240

Onset of symptoms is typically gradual.
The most common presenting symptoms are;
 Sore throat, painful swallowing
 Cervical lymphadenopathy
 Low grade fever
 Diffuse neck swelling ("bull-neck")
 Initially mild erythema, which can progress to
isolated spots of gray and white exudate.
241

Diagnosis
 Based on clinical and epidemiological grounds
 Bacteriologic examination of discharges from lesions.
Treatment
 Diphtheria antitoxin (early)
 Erythromycin (500mg PO QID) for 2 weeks Rx of choice.
 Penicillin G (25-50,000unit/kg Iv BID till pt can take oral.
and for contacts Benzathin penicillin (600,000 IU IM for <6
yrs and 1.2million IU for ≥6 yrs.
242

Prevention
 Immunization of infants with diphtheria toxoid.
 Disinfection of articles in contact with patient and
soiled by discharges of patient.
 Management of contacts.
243

5. Pertusis (whooping cough)
 Highly contagious, acute respiratory illness caused by
Bordetella pertussis (Gm tve coccobacillus).
 MOT: Primarily by direct contact with discharges
from respiratory mucus membranes of infected
persons by air borne route, probably by droplets.
244

Epidemiology
 There are 60 million cases of pertussis each year
worldwide, resulting in >500,000 deaths
 Pertussis is extremely contagious, with attack rates as
high as 100% in susceptible individuals exposed to
aerosol droplets at close range.
 B. pertussis does not survive for prolonged periods in the
environment.

Cont’d...
 Indirectly by handling objects freshly soiled with
nasopharyngeal secretions.
 IP:1-3 weeks.
Period of communicability- Highly communicable in
early catarrhal stage before the paroxysmal cough
stage.
246

Three phases
1. Catarrhal phase: common cold like
symptoms/non specific presentations;
 Coryza
 Lacrimation
 Mild cough
 Low-grade fever, and malaise.
 Lasts 1-2 weeks
247

Phases.....
2. Paroxysmal phase
Explosive, repetitive and prolonged cough (5–10
coughs after single expiration) .
Child usually vomits at the end of paroxysm vomiting
(“Posttussive vomiting” ).
Expulsion of clear tenacious mucus often followed
by, Whoop (inspiratory whoop) between paroxysms.
248

Phase 2.......
 Child looks healthy between paroxysms
 Paroxysm of cough interferes with nutrition.
 Cyanosis and sub conjunctiva hemorrhage due to violent
cough.
3. Convalescent phase;
 Gradual reduction in the frequency and severity of cough.
 It usually lasts one to two weeks, but may be prolonged.
 The total duration of all 3 phases is often about 3 months.
249

Diagnosis
 Difficult to distinguish it from other URTI
 Case definition: Who has a cough illness lasting at least two
weeks with one of the following:
 Paroxysms of coughing,
 Inspiratory "whoop," or posttussive vomiting, and without
other apparent cause (as reported by a health professional).
 History and physical examination at phase two (paroxysmal
phase) ensure the diagnosis.
- Marked lymphocytosis (catarrhal stage)
250

Treatment
Macrolides are highly effective at eradicating B.
pertussis from the nasopharynx.
 Azithromycin for five days (500 mg day one,
followed by 250 mg 2-5day) or
 Clarithromycin 500 mg BID for seven days.
Antibiotics for super infections like pneumonia
because of bacterial invasion due to damage to cilia.
251

Isolation
 Patients with suspected pertussis are placed in
respiratory isolation with use of masks by all health
care personnel entering the room.
 Screening for cough should be performed upon
entrance of patients to emergency departments,
offices, and clinics to begin isolation immediately and
until 5 days after initiation of macrolide therapy.
 Prevention-Vaccination at childhood.

6. Meninigococeal infections
 Neisseria meningitidis cause meninigitis and
meningococcemia (URTI).
 Gram negative, kidney-bean shaped diplococci.
 Serotype (A, B, C, Y, W-135).
 Serogroup A – major epidemics in sub-Saharan during
dry seasons.
253

254
 Meningococcal disease occurs as sporadic, Endemic,
out breaks or epidemics.
 Annual incidence of meningococcal disease
a. Sporadic disease 1-2/100,000/yr
b. Out breaks 5-10/100,000/yr
c. Epidemics >10/100,000/yr

Cont’d...
 Reservoirs: human nasopharynx (5-10%) .
 Transmission: respiratory droplets, oropharyngeal
colonization, hematogenous dissemination to the
meninges.
 Only small percentage of colonized individuals become
diseased.
 Attack rates are peak in teenagers and young adults
during epidemics
255

Predisposing factors
 Overcrowding and close contacts.
 Tobacco smoking (active or passive).
 Preceding recent viral respiratory illness.
256

Respiratory infections
 Meningococcal pneumonia
 Sinusitis
 Tracheobronchitis
 Conjunctivitis.
Meningococcemia
o Fever, Chills, Vomiting, Myalgia
o Petical Rash, purpural rash
257

C/M of Meningitis
Nausea
Vomiting
Headache
Neck stiffness
Lethargy or confusion
Petechial or purpuric skin lesions, + concomitant
meningococcemia.
258

Complications
CN palsy
Cerebral edema; Subdural effusions (in children)
Permanent sequelae: Mental retardation, Deafness,
Hemiparesis.
Loss of skin/limbs/digits in fulminant
meningococcemia 20 to ischemic necrosis /infarction.
259

Diagnosis
Clinical findings and isolation of micro-organism/its Ag /DNA
from sterile body fluids (blood/CSF/synovial fluid /skin lesion).
CSF findings:
 Hypoglycorrhachia (low CSF glucose)
 Increased Protein concentration
 Neutrophilic leukocytosis
 Gm stain (kidney shaped gm –ve diplococci).
260

Treatment
 Ceftriaxone (2g IV BID for one weeks).
 Penicillin for penicillin susceptible N. meningitidis
 CAF in out breaks in developing countries – single injection.
Management of contacts:
 Rifampin 600mg po BID for two days
 Ceftriaxone 250mg IM stat.
Prevention
 Meningococcal polysaccharide quadrivalent vaccine (A, C, Y,
W135)
 Efficacy 80-95% immunocompetent adults;
261

7. Tuberculosis (TB)
TB is an infectious disease primarily affects the lung
parenchyma (85%).
Also transmits to other parts of the body, including the
meninges, kidneys, bones, and lymph nodes.
Epidemiology:
TB is a worldwide public health problem that is closely
associated with poverty, malnutrition, overcrowding,
substandard housing, and inadequate health care.
262

Epidemiology
263
 About a third of the world‘s population is estimated to
be infected with tubercle bacilli.
 Ethiopia is among the 30 High TB, HIV and MDR-TB
Burden Countries.
 National DR-TB sentinel report in 2016 shows the
MDR-TB prevalence of 2.7% among new TB cases and
14% among previously treated TB cases.
 IP: 4-12 weeks.

Cont’d...
Period of communicability: as far as the bacilli is
present in the sputum.
Susceptibility and resistance- under 3 years old
children, adolescents, young adults, the very old and
the immune suppressed are susceptible.
o Etiology: Mycobacterium tuberculosis complex, is an
acid-fast aerobic rod that grows slowly and is sensitive
to heat and ultraviolet light.
264

Transmission
 Airborne transmission, droplet nuclei (usually
particles 1 to 5 mm in diameter) released through
talking, coughing, sneezing, laughing or singing.
 Larger droplets settle; smaller droplets remain
suspended in the air and are inhaled by a susceptible
person.
 Consumption of raw milk containing M. bovis.
265

Risk factors for transmission
 Exposure / Proximity, frequency, and duration of contact.
 Environment/Poor ventilation
 Infectiousness/Bacteriological status of patient.
 Susceptibility/Immunocompromised status (HIV
infection, cancer, transplanted organs, and prolonged
high dose corticosteroid therapy)
266

Risk factors....
 Substance abuse (IV/injection drug users and alcoholics,
drugs, tobacco).
 Pre-existing medical conditions or special treatment
(diabetes, chronic renal failure, malnourishment, selected
malignancies, hemodialysis, transplanted organ).
 The risk of transmission and infecting a susceptible
individual is therefore highest in close, prolonged, indoor
exposure with sputum smear-positive pulmonary TB.
267

Pathogenesis
268
 Infection establishes when the bacillus is recognized by the
immune cells of the susceptible individual.
 Once the bacilli start multiplication, it spreads through the
blood stream and seeds in multiple organs, which later may
evolve into extra pulmonary TB.
 After 6-8weeks, the immune system starts to contain the
multiplication and in most instances manages to stop
further multiplication and remain as latent infection.

Pathogenesis
269
 In few patients, the multiplication continues and directly
progress to active disease mainly in person with
compromised immunity.
 Latent infection may be reactivated into active TB (
secondary TB) later in life.
 Disease usually occurs in the lungs (pulmonary TB).
However, haematogenic dissemination can cause it also to
occur in other parts of the body (extra-pulmonary TB).
 If massive haematogenic dissemination occurs, all organs
can be affected (miliary TB).

Pathogenesis
 Majority (90-95%) of persons got infected with MTB,
but the immunological defense either kills or suppresses
the inhaled bacteria causing latent TB infection.
- The immune system of the person halt the multiplication
of the bacilli and tissue damage, and hence, no
symptoms presents.
 Only about 5-10% of such persons (with primary
infection) develop active TB.
270

Active TB disease
271
 TB patient who present with clinical presentation
A. Primary TB: occurs in 5-10% of case when active TB
develops immediately after infection usually within 1-2
years after exposure.
- Common in children and other immunosuppressed
individuals
B. Post-primary/secondary TB: refers to active TB that is a
result of reactivation of endogenous latent foci, which
remained dormant since the initial infection of TB.

Module 1 – Transmission and Pathogenesis
of Tuberculosis
272
LTBI vs. TB Disease
Latent TB Infection (LTBI) TB Disease (in the lungs)
Inactive, contained tubercle bacilli
in the body
Active, multiplying tubercle bacilli
in the body
Skin test or blood test results
usually positive
Skin test or blood test results
usually positive
Chest x-ray usually normal Chest x-ray usually abnormal
Sputum smears and cultures
negative
Sputum smears and cultures may
be positive
No symptoms Symptoms such as cough, fever,
weight loss
Not infectious Often infectious before treatment
Not a case of TB A case of TB

Natural history of TB
 If untreated TB leads to
- deaths within 2-3 years in at least half of the patients.
- Without treatment about 20-25% would have natural
healing.
- 25-30% would remain chronically ill, thus continuing
to spread the diseases in the community.
o Incubation Period
 2 to 12 weeks after exposure.
273

Clinical Manifestations
General symptoms
 Fever
 Night sweating
 Weight loss
 Fatigue
 loss appetite/anorexia
 Pulmonary symptoms
 Cough (usually
productive).
 Chest pain.
 Dyspnea.
 Hemoptysis.
274

C/m of extra pulmonary TB (ExPTB)
o C/m of ExPTB depend on its site of involvement.
TB lymphadenitis: slowly developing and painless
enlargement of lymph nodes eventually drainage of
pus.
TB meningitis: headache, fever, vomiting, neck
stiffness, mental status change.
Intestinal TB: loss of appetite and weight, abdominal
pain, diarrheal.
275

Tuberculous pleural effusion
276
 Tuberculous is the commonest cause of a unilateral
pleural effusion.
 It is also the commonest form of HIV-related extra-
pulmonary disease.
 Non-productive cough,
 Chest pain, shortness of breath.
 High temperature.

277
TB of bones
 Commonly affects the vertebral column.
 In many cases more than one intervertebral disc is
involved.
 It is characterized by loss of bone density and slow bone
erosion
 Involvement of the thoracic vertebrae causes localized
back pain, deformity of the spine, and in extreme cases an
angulated kyphosis

278
TB meningitis
 Gradual onset and progression of headache and
decreased consciousness.
 It is most common in children between 6 month and
4 years of age.
 More commonly, the signs and symptoms progress
slowly over several weeks

Diagnostic Methods
A. Bacteriological Methods
 Direct Light Smear Microscopy (conventional
microscopy)
 Light Emitting Diode (LED) Fluorescent Microscopy
 Culture
B. Molecular Tests for TB Diagnosis
 Line Probe Assay (LPA)
 GeneXpert MTB/RIF
C. Radiological Examination
D. Tuberculin Skin Test -false positivity
279

Smear Microscopy
280
 Is a bacteriologic confirmatory technique used to diagnose
infectious TB cases and monitor treatment response.
 Two samples (spot-spot)????
 Three samples yield high accuracy diagnosis (spot-early
morning-spot)
 It is cheap, simple, produces rapid results.
 Has low sensitivity (40-60%)
 Requires 5,000-10,000 bacilli per ml of sputum to get
positive results.

Culture
281
 Is a bacteriologic confirmatory test for MTB.
 It is highly sensitive technique that can detect 10 to 100
viable bacilli per ml of sputum.
 It allows species identification and drug susceptibility
testing and it is used to monitor treatment response for drug
resistance TB patient.
 More expensive, requires higher biosafety level setup, well
trained laboratory personnel and results takes longer
turnaround time.

GeneXpert MTB/RIF
282
 Automated genotypic technique used to detect MTB and
screen for Rifampicin resistance directly from the sputum
 Highly sensitive to detect MTB even in smear negative
cases.
 Preferred initial test for patients who are children and/or
people living with HIV .
 It produces results in two hours
 Does not require sophisticated bio-safety precautions
 But Requires continuous electrical supply.

GeneXpert MTB/RIF assay as initial bacteriologic tests
for:
283
 HIV positives/unknown with presumptive TB
 Children with presumptive TB
 Presumptive DR-TB cases,
 Presumptive extra-pulmonary TB,
 Patient from congregated setting, health facility or
other high MDRTB prevalent settings

Histo-Pathological Examination
284
 Multiplication of tubercle bacilli in any site of the human
body causes a specific type of inflammation,
 With formation of characteristic granuloma
 Fine needle aspiration from accessible mass like peripheral
enlarged lymph nodes
 Aspiration of effusions from serous membranes; serous fluid
 Tissue biopsy from any body tissues such as serous
membranes, skin, endometrium as well as bronchial, pleural,
gastric or liver tissue

Radiological Examination
285
 Chest X-ray is a rapid and convenient method to evaluate patients
who cannot produce sputum or who have negative results from
bacteriologic tests.
 To diagnose extra pulmonary TB (such as pleural effusions and
pericardial TB).
 x-ray findings must be interpreted in the light of the patient‘s history
and clinical findings

Classification of TB
1. Based on the anatomical site of TB disease
 Pulmonary tuberculosis (PTB): refers to a case of
TB involving the lung parenchyma.
 Extra pulmonary tuberculosis (ExPTB): TB
involving organs other than the lungs.
 A patient with both pulmonary and extra pulmonary
TB should be classified as a case of pulmonary TB.
286

Cont’d...
2. Bacteriologic classification
 Bacteriology refers to the smear status of pulmonary
cases and the identification of MTB for any cases by
culture or newer methods.
 Smear positive cases are the most infectious and most
likely to transmit the disease in their surroundings
and therefore are the focus of infection control
measures.
287

Communicable Disease Control Guide

Communicable Disease Control Guide

Recommended

Recommended

More Related Content

What's hot

What's hot (19)

Similar to Communicable Disease Control Guide

Similar to Communicable Disease Control Guide (20)

Recently uploaded

Recently uploaded (20)

Communicable Disease Control Guide