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By zinabu D 1
Objective
At the end of this chapter the student should be
able to define
 Define Communicable Disease
 Explain common terms
 Describe chain of disease transmission
By zinabu D 2
Introduction to communicable diseases control
 What are a communicable diseases ?
Example:
 What are a non-communicable diseases?
Example:
By zinabu D 3
Communicable Diseases
 Is an illness due to specific infectious agent or its
products arises through transmission of that agent
or its products an infected person, animal or
inanimate reservoir to a susceptible host.
 The transmission may occur either directly or
indirectly through an intermediate host which can
be plant or animal or a non living thing, or in both
direct and indirect.
By zinabu D 4
Cont
Communicable Diseases control
It refers to the reduction of the incidence &
prevalence of diseases to level where it can not be
a major public health problem.
By zinabu D 5
DEFINITION OF COMMON TERMS
Transmission:- is the process by which an infectious
agent or its products passes from the source to the new
host.
Period of communicability:- the time during which the
infectious agent may be transferred from infected person
to another.
Incubation period:- The time interval between initial
contact with the infectious agent and the appearance of
the first sign or symptoms of the disease.
By zinabu D 6
Cont
Prodormal period:
The time interval between the onset of symptoms
of an infectious disease and the appearance of
characteristic manifestations.
E.g. In measles from the onset of fever and coryza
to the development of characteristic signs like
koplick’s spots and characteristic skin lesions.
By zinabu D 7
Cont
Prepatent period:
The period in people between the time of exposure to a
parasite and the time when the parasite can be detected
in blood or in stool.
Incubation period in a vector:
is the time between entrance of an organism in to the
vector and the time when that vector can transmit the
infection (extrinsic incubation period).
By zinabu D 8
Cont
Exposure:
The contact between the agent and susceptible host.
Infectivity:
The ability of an agent to invade and multiple in a host.
Pathogencity:
The ability of an agent to produce clinically apparent
disease, or the property of an infectious agent that
determines the extent to which overt dx is produced.
By zinabu D 9
Cont,
Virulence:
The ability of infectious agent to produce severe
disease among clinically infected persons.
Immunogenicity:
The ability of an agent to produce specific
immunity
Illness:
Individual or subjective feeling of discomfort.
By zinabu D 10
Cont
Infectious agent- an agent capable of causing
infection
Contamination – presence of living infectious
agent upon Articles
Infestation – presence of living infectious agent
on the exterior surface of the body
Infection - the entry and development or
multiplication of an infectious agent in the body
of man or animal
By zinabu D 11
Cont
Infectious: caused by microbes and can be
transmitted to other persons
Disease :a state of physiological or psychological
dysfunction.
Epidemics :the occurrence of any health related
condition in a given population in excess of the usual
frequency in that population.
Endemic :a disease that is usually present in a
population or in an area at a more or less stable level.
By zinabu D 12
Cont
Sporadic - a disease that does not occur in that
population, except at occasional and irregular
intervals.
Pandemic - an epidemic disease which occurs
worldwide
By zinabu D 13
Chain of disease transmission
This refers to a logical sequence of factors or
links of a chain that are essential to the
development of the infectious agent and
propagation of disease.
The six factors involved in the chain of disease
transmission are:
By zinabu D 14
Chain of diseases transmission
By zinabu D 15
Cont
 Infectious agent (aetiology or causative agent)
 Reservoir
 Portal of exit
 Mode of transmission
 Portal of entry
 Susceptible host
By zinabu D 16
Infectious Agent
An organism that is capable of producing infection or
infectious disease.
On the basis of their size, etiological agents are generally
classified into:
 Metazoa (multicellular organisms). (e.g. Helminths).
 Protozoa (Unicellular organisms) (e.g. Ameobae)
 Bacteria (e.g. Treponema pallidum, Mycobacterium
tuberculosis, etc.)
 Fungus (e.g. Candida albicans)
 Virus (e.g. Chickenpox, polio, etc.)
By zinabu D 17
Reservoir
 Any person, animal, arthropod, plant, soil or
substance (or combination of these) in which an
infectious agent normally lives and multiplies,
on which it depends primarily for survival and
where it reproduces itself in such a manner that
it can be transmitted to a susceptible host.
By zinabu D 18
Types of Reservoirs
Man:
 There are a number of important pathogens that
are specifically adapted to man, such as:
measles, smallpox, typhoid, meningococcal
meningitis, gonorrhea and syphilis.
 The cycle of transmission is from human to
human.
By zinabu D 19
Cont..
II. Animals:
 Some infective agents that affect man have their
reservoir in animals. The term “zoonosis” is applied
to disease transmission from animals to man under
natural conditions.
For example:
Bovine tuberculosis - cow to man
Brucellosis - Cows, pigs and goats to man
Anthrax - Cattle, sheep, goats, horses to man
Rabies - Dogs, foxes and other wild animals to
man
By zinabu D 20
Cont...
3.Non-living things as reservoir:
 Many of the agents are basically saprophytes living in soil and
fully adapted to live freely in nature.
 Biologically, they are usually equipped to withstand marked
environmental changes in temperature and humidity.
E.g.
Clostridium botulinum etiologic agent of Botulism
Clostridium tetani etiologic agent of Tetanus
Clostridium welchi etiologic agent of gas gangrene
By zinabu D 21
3. Portal of exit
This is the site through which the agent escapes from
the reservoir.
Examples include:
 GIT: typhoid fever, bacillary dysentery, amoebic
dysentery, cholera, ascariasis, etc
Respiratory: tuberculosis, common cold, etc.
Skin and mucus membranes: Syphilis
By zinabu D 22
4.Mode of transmission
 Refers to the mechanisms by which an infectious
agent is transferred from one person to another or
from a reservoir to a new host.
 Transmission may be direct or indirect.
1. Direct transmission:
 Consists of essentially immediate transfer of
infectious agents from an infected host or
reservoir to an appropriate portal of entry.
By zinabu D 23
Cont
This could be:
I. Direct Vertical
– Such as: transplacental transmission of syphilis, HIV, etc.
II. Direct horizontal
 Direct touching, biting, kissing, sexual intercourse,
droplet spread onto the conjunctiva or onto mucus
membrane of eye, nose or mouth during sneezing
coughing, spitting or talking; Usually limited to a
distance of about one meter or less.
By zinabu D 24
Cont
II. Indirect transmission
A.Vehicle-borne transmission:
Indirect contact through contaminated :
 Inanimate objects (fomites) like: Bedding, toys,
handkerchiefs, soiled clothes, cooking or eating utensils,
surgical instruments.
 Contaminated food and water.
 Biological products like blood, serum, plasma or IV-fluids or
any substance serving as intermediate means by which an
infectious agent is transported and introduced into a
susceptible host through a suitable portal of entry.
By zinabu D 25
Cont..
B. Vector-borne transmission:
Occurs when the infectious agent is conveyed by an
arthropod (insect) to a susceptible host.
1. Mechanical transmission:
 The arthropod transports the agent by soiling its feet
or proboscis, in which case multiplication of the
agent in the vector does not occur. (e.g.common
house fly.)
By zinabu D 26
Cont...
2. Biological transmission:
 This is when the agent multiplies in the arthropod
before it is transmitted, such as the transmission of
malaria by mosquito.
C. Air-borne transmission:
 Dissemination of microbial agent by air to a suitable
portal of entry, usually the respiratory tract. Two
types of particles are implicated in this kind of
spread: dusts and droplet nuclei.
By zinabu D 27
Cont...
Dust:
 Small infectious particles of widely varying size that may
arise from soil, clothes, bedding or contaminated floors
and be re-suspended by air currents.
Droplet nuclei :
 Small residues resulting from evaporation of fluid
(droplets emitted by an infected host). They usually
remain suspended in the air for long periods of time.
By zinabu D 28
5. Portal of entry
The site in which the infectious agent enters to the susceptible
host.
For example:
 Mucus membrane
 Skin
 Respiratory tract
 GIT
 Blood
By zinabu D 29
6.Susceptible host
 A person or animal lacking sufficient resistance to a
particular pathogenic agent to prevent disease if or
when exposed.
 occurrence of infection and its outcome are in part
determined by host factors.
 The term “immunity” is used to describe the ability of
the host to resist infection.
 Resistance to infection is determined by non-specific
and specific factors: By zinabu D 30
Cont..
Non-specific factors
 Skin and mucus membrane
 Mucus, tears, gastric secretion
 Reflex responses such as coughing and sneezing.
Specific factors
 Genetic-hemoglobin resistant to Plasmodium falciparum
 Naturally acquired or artificially induced immunity. Acquired
immunity may be active or passive
By zinabu D 31
Cont..
Active immunity:
Acquired following actual infection or
immunization.
Passive immunity:
pre-formed antibodies given to the host.
By zinabu D 32
Carrier and Its Type
 A carrier is an infected person or animal who does not
have apparent clinical disease but is a potential source
of infection to others.
A. Healthy or asymptomatic carriers:
These are persons whose infection remains unapparent.
For example, in poliovirus, meningococcus and
hepatitis virus infections, there is a high carrier rate.
By zinabu D 33
Cont...
B. Incubatory or precocious carriers:
 These are individuals or persons who excrete the
pathogen during the incubation period (i.e. before the
onset of symptoms or before the characteristic features
of the disease are manifested).
E.g. Measles, mumps, chickenpox and
hepatitis.
By zinabu D 34
Cont..
C. Convalescent Carriers:
 These are those who continue to harbor the infective
agent after recovering from the illness.
E.g. Diphtheria, Hepatitis B virus.
D. Chronic Carriers:
 The carrier state persists for a long period of time.
E.g. Typhoid fever, Hepatitis B virus infection
By zinabu D 35
Time Course of Infectious Diseases
 Incubation period: It is the interval of time
between infection of the host and the first
appearance of symptoms and signs of the disease.
 Prodormal period: It is the interval between the
onset of symptoms of an infectious disease and the
appearance of characteristic manifestations.
By zinabu D 36
For example, in a measles
 Patient, fever and coryza occur in the first three days
and
 Koplick spots in the buccal mucosa and
characteristics skin lesions appear on the fourth day.
By zinabu D 37
Cont..
Period of communicability:
 The period during which that particular
communicable disease (infectious agent) is
transmitted from the infected person to the
susceptible host.
By zinabu D 38
Levels of Prevention
Three levels of prevention: primary, secondary, and tertiary.
A.Primary prevention:
The objectives here are to promote health, prevent exposure,
and prevent disease.
 Health promotion .E.g. affordable and adequate housing, old-age pension
benefits; emotional and social support, education and vocational training etc
 Prevention of exposure E.g. provision of safe and adequate water, vector
control, proper excreta disposal, etc.
 Prevention of disease. This occurs during the latency period between
exposure and the biological onset of disease. E.g. Immunization
By zinabu D 39
Cont...
B. Secondary prevention:
 After the biological onset of disease, but before
permanent damage.
 The objective here 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)
By zinabu D 40
Cont...
C. Tertiary prevention: After permanent damage
has set in,
 The objective of tertiary prevention is to limit the
impact of that damage.
 The impact can be physical, psychological, social
(social stigma or avoidance by others), and
financial.
 Rehabilitation refers to the retraining of
remaining functions for maximum effectiveness.
By zinabu D 41
Communicable Disease Control
This refers to the reduction of the incidence and
prevalence of communicable disease to a level
where it cannot be a major public health problem.
Methods of Communicable Disease Control
I. Elimination of the Reservoir
II. Interruption of transmission
III. Protection of susceptible host
By zinabu D 42
I.Elimination of the reservoir
A. Man as reservoir:
When man is the reservoir, eradication of an infected
host is not a viable option. Instead, the following
options are considered.
Detection and adequate treatment of cases
 Isolation-separation of infected persons for a period of
communicability of the disease.
 Quarantine-limitation of the movement of apparently
well person who has been exposed to infectious diseases.
By zinabu D 43
Cont..
B. Animals as reservoir
Action will be determined by the usefulness of the animals,
how intimately they are associated to man and the feasibility of
protecting susceptible animals.
E.g:
Rabies: Pet dogs can be protected by vaccination but stray dogs
are destroyed.
 Infected animals used for food are examined and destroyed.
By zinabu D 44
Cont..
C. Reservoir in non-living things:
Possible to limit man’s exposure to the affected
area (e.g. Soil, water, forest, etc.).
By zinabu D 45
II.Interruption of transmission
This involves the control of the modes of
transmission from the reservoir to the potential
new host through:
 Improvement of environmental sanitation and
personal hygiene
 Control of vectors
 Disinfections and sterilization
By zinabu D 46
III.Protection of susceptible host
This can be achieved through:
 Immunization: Active or Passive
 Chemo-prophylaxis- (e.g. Malaria, meningococcal
meningitis, etc.)
 Better nutrition
 Personal protection. (e.g. wearing of shoes, use of
mosquito bed net, insect repellents, etc.)
By zinabu D 47
By zinabu D 48
UNIT TWO
FECO-ORAL TRANSMITED
DISEASES
By zinabu D 49
INTRODUCTION
 Causative agents are excreted in the stools
of infected persons.
 The portal of entry for these diseases is the
mouth.
By zinabu D 50
Cont,
 Thus the causative organisms have to pass through the
environment from the feces of an infected person to the
gastro-intestinal tract of a susceptible person
 This is known as the fece-oral transmission route
 This transmission occurs mostly through unapparent fecal
contamination of food, water and hands
 Food takes a central position; it can be directly or
indirectly contaminated via polluted water, dirty hands,
contaminated soil, or flies.
By zinabu D 51
By zinabu D 52
Five “fs” fecal oral diseases transmission
By zinabu D 53
Flies
Finger
Fomites
Fluid
Food Mouth
Feces
.
MANAGE A PATIENT
WITH FECO-ORAL
TRANSMITED
DISEASE
By zinabu D 54
TYPHOID FEVER
A systemic infectious disease characterized by high
continuous fever, malaise & involvement of
Lymphoid tissues.
Etiology:
 Salmonella typhi
 Salmonella enteritidis
By zinabu D 55
Epidemiology
Occurrence:
It occurs worldwide, particularly in poor socioeconomic
areas. Annual incidence is estimated at about 17 million
cases with approximately 600,000 deaths worldwide.
In endemic areas the disease is most common in
preschool and school aged children (5-19 years ofage).
By zinabu D 56
Cont,
Reservoir:
Human as a case or as a carrier.
Temporary carrier: that excretes the organisms for
at least 6-8 weeks.
Chronic carrier : which excretes the organisms for
at least 1 year.
In some cases, it can be life long.
By zinabu D 57
Mode of transmission
By water and food contaminated by feces and
urine of patients and carriers.
Flies may infect foods in which the organisms
then multiply to achieve an infective dose.
By zinabu D 58
Cont,
Incubation period –1-3 weeks
Period of communicability:
As long as the bacilli appear inexcreta, usually from the
first week throughout convalescence.
About 10% of untreated patients will discharge bacilli for
3 months after onset of symptoms,And 2%-5% become
chronic carriers.
By zinabu D 59
Susceptibility And Resistance
 Susceptibility is general and increased in
individuals with gastric achlorhydria or those
who are HIV positive.
By zinabu D 60
Clinical manifestation
First week:
 Mild illness characterized by:
 Fever rising stepwise(ladder type),
 Anorexia, lethargy, malaise and
 General aches.
 Dull and continuous frontal headache is prominent.
 Nose bleeding, vague abdominal pain and
 Constipation in 10% of patients.
By zinabu D 61
Second week:
 Sustained temperature (fever).
 Severe illness with weakness, mental delirium,
 Abdominal discomfort and distension.
 Diarrhea is more common than first
 week and feces may contain blood.
By zinabu D 62
Third week
 Patient continues to be febrile and increasingly
exhausted.
 If no complications occur, patient begins to
improve and temperature decreases gradually.
By zinabu D 63
Clinical manifestations suggestive of typhoid fever
 Fever: Sustained fever (ladder fashion)
 Rose spots:Small pallor, blanching, slightly raised
macules usually seen on chest and abdomen in the
firstweek in 25% of white people.
 Relative bradycardia:slower than would be
expected from the level of temperature.
 Leucopoenia: White cell count is less than 4000/mm3 of
blood.
By zinabu D 64
Diagnosis
 Based on clinical grounds but this is confused
with wide variety of diseases.
 Serological examination :Widal test (reaction)
against somatic and flagellar antigens(O or H)
reactive
 Blood, feces or urine culture :Golden Dx for TF
By zinabu D 65
Treatment
 Ciprofloxacin, 500mg P.O, BID for 10-14 days
Alternative
 Amoxicillin,1g, P.O.QID, for children: 20 –
40mg/kg/day P.O.in 3 divided doses for 14 days
OR
 Chloramphenicol, 500mg P.O QID, for 14 days:
 For children: 25mg/kg.
OR By zinabu D 66
Cont,
Sulfamethoxazole+trimethoprim, 800mg/160mg
P.O.BID for 14 days.
For children
 6 weeks– 5 months, 100/20mg;
 6 months – 5 yrs, 200/40mg;
 6 – 12 yrs, 400/80mg BID
For severe cases which are fluoroquinolone resistant:
By zinabu D 67
Cont,
Ceftriaxone, 1g QID as a single dose OR in 2 divided
doses I.M. OR I.V. for 7-10 days.
OR
Chloramphenicol, 1g, IV bolus QID until 48 hrs after
fever has settled, followed by 500mg P.O QID for a total
of 14 days.
For children: 25mg/kg, IV bolus QID, until 48 hrs
after fever has settled, followed by 25mg/kg P.O.QID for
a total of 14 days. By zinabu D 68
Cont,
Adjunct Corticosteroid treatment:
This is recommended only for patients with
evidences of CNS involvement (delirium, coma)
Shock.
By zinabu D 69
Cont,
First line
Dexamethasone, 3mg/kg IV initially, followed by
1mg/kg IV Q 6hrs for 48hrs total
(This is prefered in patients with severe disease)
OR
Prednisolone, 20-40mg P.O. (or equivalent) once
daily for the first three days of antibiotic treatment.
By zinabu D 70
Nursing care
 Maintain body temperature to normal.
Apply comfort measures.
Follow side effects of drugs.
Monitor vital signs.
Follow strictly enteric precautions:
 Wash hands
 Wear gloves
 Teach all persons about personal hygiene
By zinabu D 71
Cont,
Observe the patient closely for sign and symptoms of:
 Bowel perforation
 Erosion of intestinal ulcers
 Sudden pain in the lower right side of the abdomen
 Abdominal rigidity
 Sudden fall of temperature and blood pressure
Accurately record intake and output.
Provide proper skin and mouth care.
By zinabu D 72
Prevention and control
Treatment of patients and carriers
Education on handwashing, particularly food
handlers,patients and childcare givers
Sanitary disposal of feces and control of flies.
Provision of safe and adequate water
Safe handling of food.
By zinabu D 73
Cont,
Exclusion of typhoid carriers and patients from
handling of food and patients
Immunization for people at special risk (e.g
children &travelers to endemic areas)
Regular check-up of food handlers in food and
Drinking establishments
By zinabu D 74
Bacillary Dysentery (Shigellosis)
Is acute bacterial disease involving the large and
distal small intestine, caused by the bacteria of
the genus shigella.
Infectious agent
Shigella is comprised of four species or serotypes.
 Group A= Shigella dysentraie (most common cause)
 Group B= Shigella flexneri
 Group C= Shigella boydii
 Group D= Shigella sonnei
By zinabu D 75
Epidemiology
 Occurrence- It occurs worldwide, and is endemic
in both tropical and temperate climates.
 Outbreaks commonly occur under conditions of
crowding and where personal hygiene is
 poor, such as in jails, institutions for children, day
care centers, mental hospitals and refugee camps.
By zinabu D 76
Cont,
 It is estimated that the disease causes 600,000
deaths per year in the world.
 Two-thirds of the cases, and most of the
deaths, are in children under 10 years of age.
Reservoir- Humans
By zinabu D 77
Mode of transmission-
 Mainly by direct or indirect fecal-oral
transmission from a patient or carrier.
 Transmission through water and milk may occur
as a result of direct fecal contamination.
 Flies can transfer organisms from latrines to a
 non-refrigerated food item in which organisms
can survive and multiply.
By zinabu D 78
Cont,
 Incubation period- 12 hours-4 days (usually 1-3
days)
 Period of communicability:
During acute infection and until the infectious agent
is no longer present in feces, usually within four
weeks after illness.
By zinabu D 79
Susceptibility and resistance
Is general.
The disease is more severe in:
 Young
 Children,
 Elderly and the malnourished.
Breast-feeding is protective for infants and
Young children.
By zinabu D 80
Clinical Manifestation
 Fever, rapid pulse, vomiting and abdominal cramp are
prominent.
 Diarrhea usually appears after 48 hours with
dysentery supervening two days later.
 Generalized abdominal tenderness.
 Tenesmus is present and feces are bloody, mucoid and
Of small quantity.
 Dehydration is common and dangerous - it may cause
muscular cramp, oliguria and shock.
By zinabu D 81
Diagnosis
Based on clinical grounds
Stool microscopy (presence of pus cells)
Stool culture confirms the diagnosis
By zinabu D 82
Treatment
 Fluid and electrolyte replacement
 Co-trimoxazole 960 mg po bid for 10 day
 Doxaciclline 100mg po bid for 10 day
 Nalidixic acid, which is the most important especially
for children.
By zinabu D 83
Prevention and control
 Detection of carriers and treatment of the sick
will interrupt an epidemic.
 Hand washing after toilet and before handling or eating food.
 Proper excreta disposal especially from patients,
convalescent and carriers.
 Adequate and safe water supply.
 Control of flies.
 Cleanliness in food handling and preparation.
By zinabu D 84
Amoebiasis (Amoebic Dysentery)
An infection due to a protozoan parasite that
Causes intestinalor extra-intestinal disease.
Infectious agent
Entamoeba histolytica
By zinabu D 85
Epidemiology
Occurrence:
 Worldwide but most common in the tropics
and sub-tropics.
 Prevalent in areas with poor sanitation, in mental
institutions and homosexuals. Invasive amoebiasis is
mostly a disease of young people (adults).
 Rare below 5 years of age, especially below 2 years.
By zinabu D 86
Mode of transmission
Fecal-oral transmission by ingestion of food or
water contaminated by feces containing the cyst.
Acute amoebic dysentery poses limited danger.
Incubation period:
Variable from few days to several months
or years; commonly 2-4 weeks
By zinabu D 87
Cont,
Period of communicability
 During the period of passing cysts of
E.histolytica, which may continue for years.
Susceptibility and resistance:
 General
By zinabu D 88
Life cycle
..
By zinabu D 89
TRANSMISSION
1.Cysts ingested in
Food, water Or from
hands contaminated
with feces
Environment.
6.Feces containing infective
cysts contaminate the
environment.
HUMAN HOST
2. Cysts excyst, forming trophozoites
3. Multiply in intestine
4. Trophozoites encyst.
5. Infective cysts passed in feces.*
* trophozoites passed in feces disintegrate
Clinical Manifestation
 Starts with a prodormal episode of :
Diarrhea
Abdominal cramps
Nausea, vomiting and tenesmus.
 With dysentery, feces are generally watery,
Containing mucus and blood.
By zinabu D 90
Diagnosis
Lab :
Stool examination:
Etamoeba histolytica cyst or trophozoite
Treatment
Metronidazole 500mg po tid for 07 day
or
Tinidazole 2gm po bid for 02 day
By zinabu D 91
Prevention and control
 Adequate treatment of cases
 Provision of safe drinking water
 Proper disposal of human excreta (feces) and
hand washing following defecation.
 Cleaning and cooking of local foods (e.g. raw
vegetables) to avoid eating food contaminated
with feces. By zinabu D 92
Giardiasis
A protozoan infection principally of the upper
small intestine associated with symptoms of
chronic diarrhea, steatorrhea, abdominal
cramps, bloating, frequent loose and pale greasy
stools, fatigue and weight loss.
Infectious agent
Giardia lamblia
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Epidemiology
 Occurrence- Worldwide distribution. Children are more affected
than adults.
 The disease is highly prevalent in areas of poor sanitation.
Reservoir- Humans
Mode of transmission
Person to person transmission occurs by hand to mouth transfer of
cysts from feces of an infected individual especially in institutions
and day Care centers.
By zinabu D 94
Period of communicability
 Entire period of infection, often months.
Susceptibility and resistance :
Asymptomatic carrier rate is high. Infection is
frequently self-limited.
 Persons with AIDS may have more serious and
prolonged infection.
By zinabu D 95
Life cycle
• .
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TRANSMISSION
1. Cysts ingested in food,
water or from hands
contaminated with feces.
HUMAN HOST
2 cysts excyst,forming trophozoites
3. Multiply in intestine
4. Trophozoites encyst.
5. Infective cysts passed in feces. *
* trophozoites passed in feces
disintegrate.
ENVIRONMENT
6. Feces containing infective
cysts contaminate the
environment.
Clinical Manifestation
 Asymptomatic
 Severe failure to thrive and mal-absorption.
 Children usually have diarrhea but
abdominal distension and bloating are frequent.
 Adults have :
Abdominal cramps, diarrhea,
Anorexia,nausea, malaise,
Bloating, many
Patients complain of sulphur testing (belching).
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Diagnosis
Stool examination:
 Cyst :Diagnostic stage
 Trophozoite :Rx in stage
Treatment
First Lline
 Tinidazole, single oral dose of 2g
 For children, 50-75mg/kg as a single dose
Alternative
 Metronidazole, 250-500mg P.O., TID for five days
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Prevention and control
Good personal hygiene, and handwashing
before food and following toilet use
Sanitary disposal of feces
Protection of public water supply from
contamination of feces
Case treatment
Safe water supply
By zinabu D 99
Cholera
An acute illness caused by an enterotoxin
elaborated by vibrio cholerae.
Infectious agent
 Vibrio cholerae
Epidemiology
Occurrence: has made periodic outbreaks in
different parts of the world and given rise to
pandemics. Endemic predominantly in children.
By zinabu D 100
Cont,
Reservoir- Humans
Mode of transmission- by ingestion of food or
water directly or indirectly contaminated with
feces or vomitus of infected person.
Incubation period- from a few hours to 5 days,
usually 2-3 days.
By zinabu D 101
Period of communicability
For the duration of the stool positive stage,
usually only a few days after recovery.
Antibiotics shorten the period of communicability.
Susceptibility and resistance
Gastric Achlorhydria increases risk of illness.
Breast-fed infants are protected.
By zinabu D 102
Clinical Manifestation
 Abrupt painless watery diarrhea; the diarrhea looks like rice
water.
 In severe cases, several liters of liquid may be lost in
few hours leading to shock.
 Severely ill patients are :
 Cyanotic,
 Have sunken eyes and cheeks,
 Scaphoid abdomen, poor skin turgor, and
 Thready or absent pulse.
 Loss of fluid continues for 1-7 days
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Diagnosis
Based on clinical grounds
Lab :
 Culture (stool) confirmation
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Treatment
Objectives:
 Replace volume deficit and ongoing losses –
 Decrease duration of diarrhoea .
For dehydration in mild cases:
 Give ORS, for children: < 2yrs: 50-100ml
 2-10 years: 100-200ml after each loose stool.
For severe cases
 Ringer lactate IV infusion (alternatively Normal
saline) should be given 50-100ml/min until shock is reversed .
 KCl solution 20-40mmol/litre may be added as required.
By zinabu D 105
Pharmacologic
First line
 Doxycycline, 100mg, P.O., BID for 3 days.
 For children: 6mg/kg daily for 3 days.
 Alternatives
 Tetracycline, 500mg P.O., QID for 3-5 days
Sulfamethoxazole+trimethoprim,
 Children 6 weeks – 5 months: 100/20mg
 Children 6 months – 5 yrs: 200/40mg
 Children 6 – 12 yrs: 400/80mg BID for 5 days
 Adults: 800mg/160mg P.O., BID for 5 days.
OR
Ciprofloxacin, 500mg P.O., BID, for 3-5 days
By zinabu D 106
Nursing care
 Wear gown and glove.
 Wash your hands.
 Monitor output including stool output.
 Protect the patient family by administering
Tetracycline.
 Health education
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Prevention and control
 Case treatment
 Safe disposal of human excreta and control of
flies
 Safe public water supply
 Hand washing and sanitary handling of food
 Control and management of contact cases
By zinabu D 108
Managing viral hepatitis
An acute viral disease characterized by abrupt
onset of:
 Fever,malaise
 Anorexia, nausea and
 Abdominal discomfort followed within a few days by
 Jaundice
Infectious agent
Type A, B, C, D & E virus
Type :A is Epidemic hepatitis
By zinabu D 109
Epidemiology
Occurrence:
Worldwide distribution in sporadic and Epidemic
forms.
Infection is common where environmental
Sanitation is poor and occurs at an early age.
Reservoir- Humans.
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Mode of transmission
Person to person by fecal-oral route.
Through contaminated water and food
contaminated byinfected food handlers.
Incubation period:
15-55 days, average 28-30 days.
By zinabu D 111
Period of communicability
High during the later half of the incubation
period continuing for few days following onset of
jaundice.
Most cases are non-infectious following first week
of jaundice.
Susceptibility and resistance:
General.Immunity following infection probably
lasts for life.
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Clinical manifestation
Abrupt onset of :
 Fever, malaise
 Anorexia, nausea and
 Abdominal discomfort, followed in few days by
jaundice.
Complete recovery without sequel or recurrence as
a rule.
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Diagnosis
Based on clinical and epidemiological grounds
Demonstration of IgM (IgM anti-HAV) in the
serum of acutely or recently ill patients.
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Treatment
Symptomatic:
 Rest
 High carbohydrate diet with low fat and protein
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Prevention and control
 Public education about good sanitation and personal
hygiene, with special emphasis on careful handwashing
and sanitary disposal of feces.
 Proper water treatment and distribution systems and sewage
disposal.
 Proper management of day care centers to minimize possibility of
fecal-oral transmission.
 HA vaccine for all travelers to intermediate or highly endemic
areas.
 Protection of day care centers’ employees by vaccine.
By zinabu D 116
Hepatitis B
Inflammation of liver caused by hepatitis B virus (HBV).
WHO estimates above 2 billion person infected world wide
with HBV of which 350 million are chronically infected
and 1 million die per year.
Etiology
Hepatitis B virus (HBV)
Reservoir
• Human By zinabu D 117
Mode of transmission
Blood born transmission
 Sharing needles, toothbrush, razor blades,
exposure to infected blood (transfusion), towels
and close contact.
 Sexual transmission: - saliva, semen & vaginal
fluid during kissing and sexual intercourse.
By zinabu D 118
Cont,
From mother to child: - at birth (mostly), during
breast-feeding and intra-utero transmission.
 No faeco- oral transmission.
 No air borne transmission.
 Urine is not infective unless it contains blood.
N.B: HBV is highly transmitted through parental
way than HIV /AIDS.
By zinabu D 119
Cont,
Incubation period
• 45 – 160 days
Period of communicability
Extends over the period of acute illness that
means it may last from few years to lifetime.
10% of patients become carriers.
By zinabu D 120
Clinical manifestations
 Anorexia, nausea & vomiting
 Abdominal discomfort
 Arthralgia and rash
 Jaundice
 Chronically infected individuals may develop
hepatoma (liver cancer), cirrhosis or chronic
liver disease
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Diagnosis
Detection of hepatitis B surface antigen
(HBSAG), which
is present when the virus is in the blood in the
acute stage &
chronic carrier stage.
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Treatment
Drugs used in the treatment of hepatitis B include;
 Adefovir dipivoxil
 Interferon alfa- 2b,
 Pegylated interferon alfa- 2a,
 Lamivudine
 Entecavir
Liver transplants may be beneficial to infected
patients, but the virus remains in the body after
transplantation surgery and may eventually attack the
new liver.
 Alcohol is strictly for bidden because it increases the risk of
cirrhosis.
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Feces Mainly in Soil
The diseases in this category are mainly
transmitted through :
 Fecal contamination of soil.
These infections are acquired through man’s
exposure to focally contaminated soil.
By zinabu D 124
Ascariasis
A helminthic infection of the small intestine generally
associated with few or no symptoms
Infectious agent
Ascaris lumbricoides.
Epidemiology
Occurrence:
The most common parasite of humans wheresanitation
is poor.
School children (5-10 years of age) are most affected.
Highly prevalent in moist tropical countries 125
Cont,
Reservoir: Humans ascarid eggs in soil.
Mode of transmission:
 Ingestion of infective eggs from soil
contaminated with human feces or uncooked
Produce contaminated with soil containing
infective eggs but not directly from person to
person or from fresh feces.
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Cont,
Incubation period- 4-8 weeks
Period of communicability:
As long as mature fertilized female worms live
in the intestine.
Usual life span of the adult worm is 12 months.
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Cont,
Susceptibility and resistance:
Is general
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Life Cycle
• .
By zinabu D 129
TRANSMISSION
1.Infective eggs ingested in
food or from contaminated
hands
HUMAN HOST
2. Larvae hatch.Migrate through liver
and lungs.
3. Pass up trachea and are swallowed
4. Become mature worms in small
intestine
5. Eggs produced and passed in feces.
ENVIRONMENT
6. Eggs become infective
(embryonated) in soil in 30-40 days.
7. Infective eggs contaminate
theenvironment.
Clinical Manifestation
Most infections go unnoticed until large worm is
passed in feces and occasionally the mouth and nose.
Migrant larvae may cause:
 Itching, wheezing
 Dyspnea,fever and
 productive cough with bloody sputum may occur.
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Cont,
Abdominal pain may arise from intestinal or
duct (biliary,pancreatic) obstruction.
Serious complications include:
 Bowel obstruction due to
knotted/intertwined worms.
By zinabu D 131
Diagnosis
 Microscopic identification of eggs in a stool
sample
 Adult worms passed from anus, mouth or nose.
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Treatment
First line:
 Albendazole, 400mg P.O. as a single dose, for
children: 1 – 2 years, 200mg as a single dose.
 Mebendazole, 100mg P.O.BID for 3 days or
500mg, once
Alternative (pregnant women)
Pyrantel pamoate, 700mg P.O as a single dose
By zinabu D 133
Prevention and control
 Treatment of cases
 Sanitary disposal of feces
 Prevent soil contamination in areas where
children play
 Promote good personal hygiene(handwashing).
By zinabu D 134
Trichuriasis
A nematode infection of the large intestine, usually
asymptomatic in nature.
Infectious agent
Trichuris trichuria (whip worm)
Found in (adult) caecum and vermiform appendix
Epidemiology
Occurrence:
Worldwide, especially in warm moist regions.
Common in children 3-11 years of age.
By zinabu D 135
Cont,
Reservoir- Humans
Mode of transmission:
Indirect, particularly through pica or ingestion of
contaminated vegetables.
Incubation period:
• Indefinite
Period of communicability:
 Several years in untreated carriers.
Susceptibility and resistance:
Is universal
By zinabu D 136
Life Cycle
• .
By zinabu D 137
TRANSMISSION
1. Infective eggs ingested in food
or from contaminated hands
HUMAN HOST
2. Larvae hatch.
Develop in small intestine.
Migrate to caecum.
3. Become mature worms.
4. Eggs produced and passed
in feces.
ENVIRONMENT
6. Eggs become infective
(embryonated) in soil after 3weeks.
7. Infective eggs contaminate the
environment
Clinical manifestation
Severity is directly related to the number of
infecting worms.
Most infected people are asymptomatic.
Abdominal pain, tiredness, nausea and
vomiting, diarrhea or constipation are complaints
by patients.
Rectal prolapse may occur in heavily infected
very young children
By zinabu D 138
Diagnosis
Demonstration of eggs in feces
Treatment
Mebendazole, 500mg P.O., single dose OR
Albendazole, 400mg,P.O. for three days
By zinabu D 139
Prevention and control
 Sanitary disposal of feces
 Maintaining good personal hygiene (i.e.
washing hands and vegetables and other soil
contaminated foods)
 Cutting nails especially in children
 Treatment of cases.
By zinabu D 140
Entrobiasis
A common intestinal helminthic infection that is
often asymptomatic.
Infectious agent
 Entrobius vermicularis
(Oxyuriasis, pinworm infection)
By zinabu D 141
Epidemiology
Occurrence :
 Worldwide, affecting all socio-economic classes with high
rates in some areas.
 Prevalence is highest in school-aged children, followed by
preschools and is lowest in adults except for mothers of
infected children. Prevalence is often high in domiciliary
institutions.
 Infection usually occurs in more than one family member.
By zinabu D 142
Cont,
Reservoir- Human
Mode of transmission- Direct transfer of
infective eggs by hand from anus to mouth of
the same or another person or indirectly
through clothing, bedding, food or other articles
contaminated with eggs of the parasite.
By zinabu D 143
Cont,
Incubation period: 2-6 weeks
Period of communicability:As long as gravid
females are discharging eggs on perianal skin.
Eggs remain infective in an indoor environment
for about 2 weeks.
Susceptibility and resistance: universal.
By zinabu D 144
Life Cycle
• .
By zinabu D 145
Adult worms
in Caecum
Gravid females migrate through the anus
to the perianal skin and deposit eggs
(usually during the night)
Eggs become infective in a few
hours in perianal area
Migrate down
To caecum
Ingestion of eggs by Man
Larvae hatch in
duodenum
2-3
weeks
Clinical manifestation
 Perianal itching,
 Disturbed sleep, irritability and
some times secondary infection of the scratched
skin.
By zinabu D 146
Diagnosis
Stool microscopy for eggs or female worms.
Treatment
First line-options
 Mebendazole, 100mg P.O. BID for 3 days OR
 Albendazole, 400mg P.O. as a single dose
Alternative
Piperazine, 4g in a single dose.
By zinabu D 147
Prevention and control
Educate the public about hygiene (i.e. hand
Washing before eating or preparing food,
keeping nails short and discourage nail biting).
Treatment of cases
Reduce overcrowding in living accommodations.
Provide adequate toilets.
By zinabu D 148
Strongyloidiasis
An often asymptomatic helminthic infection of
the duodenum and upper jejunum.
Infectious agent
Strongyloides stercolaris
Epidemiology
Occurrence:
Commonly occurs as opportunistic infection
In tropical and temperate areas.
More common in warm and wet regions.
By zinabu D 149
Cont
Reservoir- Human
Mode of transmission- Infective (filariform)
larvae penetrate the skin and enter the venous
circulation.
By zinabu D 150
Cont,
Incubation period- 2-4 weeks (from skin
penetration up towhen rhabditi form larvae
appear in the feces).
Period of communicability- As long as living
worms remain in the intestine; up to 35 years in
cases of auto-infection.
By zinabu D 151
Cont,
Susceptibility and resistance: is universal.
Patients with AIDS or on immuno-suppressive
medication are at risk of dissemination.
By zinabu D 152
Life Cycle
• .
By zinabu D 153
TRANSMISSION
1. Infective filariform
larvaepenetrate skin, e.g.
feet.
Autoinfection also occurs.
HUMAN HOST
2. Larvae migrate, pass up trachea and are
swallowed.
3. Become mature worms in small intestine
4. Eggs laid. Hatch rhabditiform larvae in
intestine.
5. Rhabditiform larvae:
- Passed in feces, or
- Become filariform larvae in intestine, causing
atutoinfection..
ENVIRONMENT
6. In soil larvae become freeliving
worms produce more
rhabditiform larvae*
* Free-living cycle can be
repeated several times
7. Become infective filariform
larvae in the soil
Clinical Manifestation
 Pneumonia occurs during heavy larval migration.
 Mild peptic ulcer like epigastric discomfort to
Severe watery diarrhea.
 Heavy infection may result in malabsorption
syndrome.
By zinabu D 154
Cont,
Diagnosis
Identification of larvae in stool specimen.
Treatment
First line
Ivermectin, 200mg/kg daily for 2 days.
Alternatives
Albendazole 400mg P.O.BID for three consecutive
days.
OR
Thiabendazole, 1500mg, P.O. BID,for 3day
for children: 25mg/kg p.o. for three consecutive days.
By zinabu D 155
Prevention and control
 Proper disposal of human excreta (feces)
 Personal hygiene including use of footwear.
 Case treatment.
By zinabu D 156
Hookworm disease
A common chronic parasitic infection with a
variety of symptoms usually in proportion of the
degree of anemia.
Infectious agent
Nematode of Intestine
Ancyclostoma duodenale- less common than N. Americans
Necator Americanus:
• Common in western hemisphere
• In all parts of tropics like Far East, South Asia, Tropical
Africa (like Ethiopia)
By zinabu D 157
Epidemiology
Occurrence- Widely endemic in tropical and
subtropical countries where sanitary disposal of
human feces is not practiced and the soil moisture
and temperature conditions favor development of
Infective larvae.
Reservoir- Humans
By zinabu D 158
Cont.
Mode of transmission-
 Through skin penetration by infective larvae
 Ingesting filariform larvae
Incubation period- Symptoms may develop
after a few weeks to many months depending
on intensity of infection and iron intake of the
host.
By zinabu D 159
Cont,
Period of communicability- Infected people can
Contaminate the soil for several years in the
absence of treatment.
Susceptibility and resistance-
Is universal.
No evidence that immunity develops with infection.
By zinabu D 160
Life cycle
• .
By zinabu D 161
TRANSMISSION
1. Infective filariform larvae
penetrate theskin, e.g. feet.
A. duodenale also transmitted by
ingestion of larvae
HUMAN HOST
2. Larvae migrate. Pass up trachea
and are swallowed.
3. Become mature worms in small
intestine (attach to wall and suck
blood).
4. Eggs produced and passed in
feces.
ENVIRONMENT
5. Eggs develop; Rhabditiform
larvae hatch. Feed in soil.
6. Develop into infective filariform
larvae in about 1 week.
7. Filariform larvae contaminate
soil.
Clinical Manifestation
The clinical manifestation is related to:
 Larval migration of the skin
Produces transient, localized maculo papular
rash associated with itching called ground itch.
 Migration of larva to the lungs.
Produces cough, wheezing and transient
pneumonitis.
By zinabu D 162
Cont,
Blood sucking
 Light infection-no symptoms
Heavy infection-result in symptoms of peptic
ulcer disease like epigastric pain and tenderness.
Further loss of blood leads to anemia manifested
by exertional dyspenea, weakness and light-
headedness.
By zinabu D 163
Cont
Diagnosis
Demonstration of eggs in stool specimen
Treatment
First line-options
Mebendazole, 100mg P.O. BID for 3 days or 500mg
stat
OR
Albendazole, 400mg P.O. as a single dose.
Alternatives:
Pyrantel pamoate, 700mg P.O. as a single dose
By zinabu D 164
Prevention and control
 Sanitary disposal of feces
 Wearing of shoes
 Case treatment.
By zinabu D 165
Direct Contact with Feces
Are diseases transmitted mainly through
direct contact with feces of the infected person.
Poliomyelitis
A viral infection most often recognized by the
acute onset of flaccid paralysis.
Infectious agent
Polio viruses (type I, II and III)
By zinabu D 166
Epidemiology
Occurrence – Worldwide prior to the advent
of immunization.
Cases of polio occur both sporadically and in
epidemics.
Primarily a disease of infants and young children.
70-80% of cases are less than three years of age.
More than 90% of infections are unapparent.
Flaccid paralysis occurs in less than 1% of
infections.
By zinabu D 167
Cont,
Reservoir – humans, especially children
Mode of transmission- Primarily person-to-
person, spread principally through the fecal-oral
route. In rare instances, milk, food stuffs and other
materials contaminated with feces have been
incriminated as vehicles.
By zinabu D 168
Cont
Incubation period- commonly 7-14 days
Period of communicability – not precisely
known, buttransmission is possible as long as the
virus is excreted.
Susceptibility and resistance-
Is common in children but paralysis rarely
occurs. Infection confers permanent immunity.
By zinabu D 169
Clinical manifestation
 Usually asymptomatic or non-specific fever is
manifestedin 90% of cases.
If it progresses to major illness, severe muscle pain, stiff
neck and back with or without flaccid paralysis may occur.
Paralysis is asymptomatic and occurs within three to fourd ays of
illness.
The legs are more affected than other part of the body.
Paralysis of respiratory and swallowing muscles is life
threatening.
By zinabu D 170
Cont,
Diagnosis
Based on clinical and epidemiological grounds
Treatment
Symptomatic
Prevention and control
 Educate public about the advantage of immunization
in early childhood.
 Trivalent live attenuated vaccine (OPV) at birth.
 Safe disposal of human excreta (feces).
By zinabu D 171
Hydatid Disease (Echinococcosis)
The tapeworm Echinococcus granulosus is the
most common species of Echinococcus and causes
cystic hydatid disease.
Infectious agent
Echinococcus granulosus, a small tapeworm of dog
By zinabu D 172
Epidemiology
Occurrence – occurs on all continents except
Antarctica. Especially common in grazing
countries where dogs consume viscera
containing cysts.
Reservoir- Domestic dogs are definitive hosts; they
may harbor thousands of adult tapeworms in their
intestines without signs of
infection.
Sheep act as intermediate hosts.
By zinabu D 173
Cont,
Mode of transmission – directly with hand to
mouth transfer of eggs after association with
infected dogs or indirectly through contaminated
food, water, soil or fomites.
By zinabu D 174
Cont,
• Incubation period – variable from 12 months
to many years, depending on the number and
location of cysts and how rapidly they grow.
• Period of communicability – Infected dogs
begin to pass eggs approximately 7weeks after
infection. Most canine infections resolve
spontaneously by six months.
By zinabu D 175
Cont,
Susceptibility and resistance :
Children are more likely to be exposed to
infection because they are more likely to have
close contact with infected dogs.
By zinabu D 176
Clinical manifestations
The signs and symptoms vary according to
location of the cyst and number.
 Ruptured or leaking cysts can cause severe
anaphylactic reactions.
 Cysts are typically spherical, thick walled and
unilocular and are most frequently found in the
liver and lungs.
By zinabu D 177
Diagnosis
 History of residence in an endemic area along
with association with canines
 Sonography and CT scan
 Serologic test
By zinabu D 178
Treatment
 Multi cyst not amenable to surgery may respond
to:
 Flumebendazol 2gm daily for 10-12 months
or
 Prolonged Albendazole therapy,
 Surgical resection of isolated cysts is the most
common treatment.
By zinabu D 179
Prevention and control
 Educate the public at risk to avoid exposure to
dog feces.
 Handwashing should be emphasized.
 Interrupt transmission from intermediate to
definitive hosts by preventing dogs’ access to
uncooked viscera.
 Safe disposal of infected viscera.
 Periodical treatment of high-risk dogs.
By zinabu D 180
Quiz
1.What does fecal-oral transmission mean?
2.Mention some of the diseases transmitted through
unapparent fecal contamination of food, water
and hands.
3.State some of the common preventive and control
measures of oral-fecal transmitted diseases.
By zinabu D 181
By zinabu D 182
CHAPTER 3
AIR-BORNE
DISEASES
Zinabu D(Bsc)
Learning Objectives
At the end of this chapter, students will be able to:
List common air-borne diseases.
Identify the common modes of air-borne
diseases transmission.
Participate in diagnosis and treatment of common air
borne diseases.
Apply preventive and control methods for air-
borne diseases.
INTRODUCTION
The organisms causing the diseases in the air-
borne group enter the body via the respiratory
tract.
When a patient or carrier of pathogens talks,
coughs, laughs, or sneezes, he/she discharges fluid
droplets.
Cont,
The smallest of these remain up in the air for
some time and may be inhaled by a new host.
Droplets with a size of 1-5 microns are quite
easily drawn in to the lungs and retained there.
Cont,
Droplets that are bigger in size will not remain air
borne for long but will fall to the ground.
Here, however, they dry and mix with dust.
When they contain pathogens that are able to survive
drying, these may become air-borne again by wind or some
thing stirring up the dust, and they can then be inhaled.
Cont,
Air-borne diseases, obviously, will spread more easily
when there is overcrowding, as in overcrowded class
rooms, public transport, canteens, dance halls, and
cinemas.
Good ventilation can do much to counteract the effects
of overcrowding.
Air-borne diseases are mostly acquired through the
respiratory tract.
1.Common Cold
An acute catarrhal infection of the upper respiratory tract.
Infectious agent
Rhino viruses (100 serotypes) are the major causes in
adults.
Parainfluenza viruses, respiratory syncytial viruses (RSV)
Influenza, and Adeno viruses cause common cold-like
illnesses in infants and children.
Epidemiology
 Occurrence- Worldwide both in endemic and
epidemic forms.
 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.
Cont,
Reservoir- Humans
Mode of transmission- by direct contact or
inhalation of airborne droplets. Indirectly by
hands and articles freshly soiled by discharges
of nose and throat of an infected person.
Cont,
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- is universal.
Repeated infections (attacks) are most likely due
to multiplicity of agents.
Clinical Manifestation
Coryza, sneezing, lacrimation, pharyngeal or
nasal irritation, chills and malaise dry or painful
throat.
Diagnosis
Based on clinical grounds
Treatment
No effective treatment but supportive measures
Like:
 Bed rest
 Steam inhalation
 High fluid intake
 Anti pain
 Balanced diet intake
Prevention and Control
I.Educate the public about the importance of:
 Handwashing
 Covering the mouth when coughing and
sneezing
 Sanitary disposal of nasal and oral discharges
II,Avoid crowding in living and sleeping quarters
especially in institutions
III.Provide adequate ventilation
2.Measles
An acute highly communicable viral disease
Infectious agent
Measles virus
Epidemiology
Occurrence :Prior to widespread immunization,
measles was common in childhood so that more
than 90% of people had been infected by age
20; few went through life without any attack.
Cont,
 Reservoir- Humans
 Mode of transmission- Airborne by droplet spread,
direct contact with nasal or throat secretions of
infected persons and less commonly by articles
freshly solid with nose and throat secretion.
 Greater than 94% herd immunity may be needed
to interrupt community transmission.
Cont,
 Incubation period- 7-18 days from exposure to
onset of fever.
 Period of communicability- slightly before the
prodromal period to four days after the
appearance of the rash and minimal after the
second day of rash.
Cont
 Susceptibility and resistance- All those who
are non vaccinated or have not had the disease
are susceptible.
 Permanent immunity is acquired after natural
infection or immunization.
Clinical Manifestation
 Prodromal fever, conjunctivitis, coryza, cough and Koplik
spots on the buccal mucosa
 A characteristic red blotchy rash appears on the third to seventh
day, beginning on the face, gradually becoming generalized,
lasting 4-7 days.
 Leucopoenia is common.
 Complications like otitis media, pneumonia, diarrhea,
encephalitis, croup (Laryngo tracheo bronchitis) may
result from viral replication or bacterial super infection.
Cont,
Diagnosis
Based on clinical and epidemiological grounds
Treatment
 No specific treatment
 Treatment of complications
 Vitamin A provision
Cont,
Nursing care
 Advise patient to have bed rest.
 Relief of fever.
 Provision of non-irritant small frequent diet.
 Shorten the fingernails.
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 months of age.
Initiate measles vaccination at 6 months of age
during epidemic and repeat at 9 months of age.
3.Influenza
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 outbreaks.
Reservoir- Humans are the primary reservoirs
for human infection.
Cont,
Mode of transmission- Airborne spread
predominates among crowded populations in
closed places such as school buses.
Incubation period- short, usually 1-3 days
Cont
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.
Clinical Manifestation
Fever, head ache, mayalgia, prostration, sore
throat and cough
Cough is often severe and protracted, but
other manifestations are self-limited with
recovery in 2-7days
Diagnosis
Based on clinical ground
Treatment
Same as common cold, namely:
Anti-pain and antipyretic
High fluid intake
Bed rest
Balanced diet intake
Prevention and control
I. Educate the public in basic personal hygiene,
especially the danger of unprotected coughs and
sneezes and hand to mucus membrane
transmission.
II. Immunization with available killed virus
vaccines may provide 70-80% protection.
III. Amantadize hydrochloride is effective in the
chemprophylaxis of type A virus but not others
4.Diphtheria
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
Epidemiology
Occurrence- 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. Unapparent, cutaneous and wound
diphtheria cases are much more common in the
tropics.
Cont,
Reservoir- Humans
Mode of transmission- contact with a patient
of carrier. i.e.with oral or nasal secretions or
infected skin.
Incubation period- usually 2-5 days
Period of communicability- variable, until
virulent bacilli have disappeared from
discharges and lesion; usually 2 weeks or less.
Cont,
Susceptibility and resistance-
Is universal.
Infants borne to immune mothers are relatively immune, but
protection is passive and usually lost before months.Recovery
from clinical disease is not always followed by lasting
immunity. Immunity is often acquired through unapparent
infection. Prolonged active immunity can be induced by
diphtheria toxoid.
Clinical Manifestation
Characteristic lesion marked by a patch or
patches of an adherent grayish membrane with a
surrounding inflammation (pseudo membrane).
 Throat is moderately sore in pharyngo
tonsillar diphtheria,with cervical lymph nodes
somewhat enlarged and tender; in severe cases,
there is marked swelling and edema of neck.
Cont
Late effects of absorption of toxin appearing
after 2-6 weeks, including cranial and peripheral,
motor and sensory nerve palsies and myocarditis
(which may occur early) and are often severe.
Diagnosis
Based on clinical and epidemiological grounds
Bacteriologic examination of discharges from
lesions.
Treatment
 Diphtheria antitoxin
 Erythromycin for 2 weeks but 1 week for cutaneous form
or
 Procaine penicillin for 14 days or single dose of
 Benzathin penicillin
Primary goal of antibiotic therapy for patients or carriers
is to eradicate C. diphtheriae and prevent transmission from
the patient to susceptible contacts.
Prevention and control
 Educate the public, and particularly the parents of young
children, of the hazards of diphtheria and the necessity for active
immunization.
 Immunization of infants with diphtheria toxoid.
 Concurrent and terminal disinfection of articles in contact with
patient and soiled by discharges of patient.
 Single dose of penicillin (IM) or 7-10 days course of
 Erythromycin (PO) is recommended for all persons exposed to
diphtheria.
5.Pertusis (whooping cough)
An acute bacterial disease involving the respiratory tract.
Infectious agent
Bordetella pertusis
Epidemiology
Occurrence- An endemic disease common to children especially
young children everywhere in the world. A marked decline has
occurred in incidence and mortality rates during the past four
decades. Outbreaks occur periodically. Endemic in developing world
and 90% of attacks occur in children under 6 years of age.
Cont,
Reservoir- Humans
Mode of transmission- Primarily by direct
contact with discharges from respiratory mucus
membranes of infected persons by airborne route,
probably by droplets. Indirectly by handling objects
freshly solid with nasopharyngeal secretions.
Cont,
Incubation period- 1-3 weeks
Period of communicability:
Highly communicable in early catarrhal stage before the
paroxysmal cough stage. The most contagious disease with
an attack rate of 75-90%. Gradually decreases and becomes
negligible in about 3 weeks.
When treated with erythromycin, infectiousness is usually 5
days orless after onset of therapy.
Cont,
Susceptibility and resistance:
Susceptibility to non immunized individuals is
universal. One attack usually confers
prolonged immunity but may not be lifelong.
Clinical manifestation
The disease has insidious onset and 3 phases:
I. Catarrhal phase
 Lasts 1-2 weeks
 Cough and rhinorrhea
II Paroxysmal phase
 Explosive, repetitive and prolonged cough
 Child usually vomits at the end of paroxysm
 Expulsion of clear tenacious mucus often followed by
vomiting
Cont,
 Whoop (inspiratory whoop against closed
glottis) between paroxysms.
 Child looks healthy between paroxysms
 Paroxysm of cough interferes with nutrition
 Cyanosis and sub conjunctiva hemorrhage due
to violent cough.
Cont,
III.Convalescent phase
 The cough may diminish slowly or may last
long time.
 After improvement the disease may recur.
Diagnosis
 History and physical examination at phase two
(paroxysmal phase) ensure the diagnosis.
 Marked lymphocytosis.
Treatment
1.Erythromycin- to treat the infection in phase one but to
decrease transmission in phase two
2. Antibiotics for super infections like pneumonia
because of bacterial invasion due to damage to cilia
Nursing care
 Proper feeding of the child.
 Encourage breastfeeding immediately after an
attack(each paroxysm).
 Proper ventilation- continuous well humidified
oxygen administration.
 Reassurance of the mother (care giver),
Prevention and control
I. Educate the public about the dangers of
whooping cough and the advantages of initiating
immunization at 6 weeks of age.
II. Consider protection of health workers at high
risk of exposure by using erythromycin for 14
days.
6.Pneumococcal pneumonia
An acute bacterial infection of the lung tissue
and bronchi
Infectious agent
Streptococcus pneumoniae (pneumococcus)
Epidemiology
Occurrence- Endemic particularly in infancy, old age and persons with
underlying medical conditions. Epidemics can occur in institutions,
barracks and on board ship where people are living and sleeping in close
quarters. Common in lower socio-economic groups and developing
countries.
Cont,
Reservoir- Humans :
Pneumococci are usually found in the
URT of healthy people throughout the world.
Mode of transmission
Droplet spread, direct oral contact or indirectly through
articles freshly soiled with respiratory discharges.
Person to person transmission is common.
Incubation period- not well determined, may be as
short as 1-3 days.
Period of communicability-
Until discharges of mouth and nose no longer contain virulent
pneumococci in significant number.
Cont,
Susceptibility and resistance:
 Susceptibility is increased by influenza, pulmonary edema of
any cause, aspiration following alcohol intoxication, chronic
lung disease, &exposure to irritants in the air.
 Malnutrition and low birth weight are important risk factors in
infants and young children in developing countries.
 Immunity following an attack may last for years.
Clinical Manifestation
Sudden onset of chill, fever, pleural pain,
 Dyspnea,tachypnea, a
 Cough productive of rusty
 Sputum,chest indrawing, shallow and
 Rapid respiration in infants and young children.
 Vomiting and convulsion may occur in infants
and young children.
Diagnosis
Based on clinical grounds
Chest X-ray- reveals consolidation of the
affected lung tissue but not in children.
Sputum gram stain- reveals gram negative
diplococci.
Treatment
Community acquired ambulatory patients (Mild Pneumonia):
Clarithromycin, 500mg P.O. BID for 5-7 days OR
Azitromycin, 500mg P.O first day then 250mg P.O., for 4d.
PLUS
Amoxicillin, 1000mg P.O., TID for 5 to 7 days.
OR
Amoxicillin-clavulanate, 625mg P.O., TID for 5-7days
Or
Doxycycline, 100mg P.O., BID for 7-10 days (Not ordered for PW)
Cont,
Community acquired hospitalized patients (Severe Pneumonia)
Ceftriaxone, 1g I.V. OR I.M every 12-24 hours for 7 days.
OR
Benzyl penicillin, 2-3 million IU I.V. QID for 7-10 days.
PLUS
Azithromycin, 500mg on day 1 followed by 250mg/day on
days 2 – 5day or
Clarithromycin, 500mg P.O., BID for 7-10 days
Empiric treatment for commonly suspected etiologies of HAP
First line
Ceftazidime, 1gm I.V. TID for 10-14days
PLUS
Vancomycin 1g I.V. BID for 10-14 days
Alternatives
Ceftriaxone, 1-2g I.V. OR I.M. BID for 7 days.
PLUS
Gentamicin, 3-5mg/kg I.V. QDdaily in divided doses for 7 days.
OR
Ciprofloxacin, 500mg P.O./I.V. BID every 12 hours for 7 days.
Nursing care
 Monitor vital signs especially of children.
 Maintain high body temperature to normal.
 Intermittent administration of humidified oxygen
if indicated especially for young children.
 Timely administration of ordered medication.
Prevention and control
 Treatment of cases
 Treatment of other underlying medical conditions
 Improved standard of living (adequate and
ventilated housing and better nutrition)
 Avoid overcrowding.
7.Meningococcal Meningitis
What is meningitis?
Cont,
An inflammation of the tissue of the meninges
An acute bacterial disease that causes
inflammation of the pia and arachnoid space.
A general name for inflammation of
a ) m e n i n g e s
sheaths that cover the
brain and spinal cord.
b ) c e r e b r o s p i n a l
f l u i d
The fluid that circulates in the
spaces in and around the brain
and spinal cord.
Cont,
Types of Meningitis
 Caused by virus.
 Less severe
 Resolves without specific
treatment within a week or 2 week
Also called as aseptic meningitis
Eg : Enteroviruses coxsackie virus,
echovirus, HSV-2, etc
Caused by bacteria
 Quite severe and may
result in
a) brain damage
b) hearing loss
c) learning disability
 It would also causes
death!
Cont,
Etiologic agent
 Bacterial
 Viral
 Fungus
1.Neisseria meningitis ( meningococcous) Common in adults and
children
2. Streptococcous pneumonia ( pneumoccous) Common in adults
3. Hemophilus influenza Common under 5 years of age
Epidemiology
Occurrence- Greatest incidence occurs during
winter and spring.
 Epidemics occur irregularly.
 Common in children and young adults.
 It is also common in crowded living conditions.
Cont,
Reservoir- Humans
Mode of transmission- Direct contact with
respiratory droplets from nose and throat of
infected person.
Risk factors
 Sero-type -subgroup A cause historically epidemic
meningitis
 Nasopharyngeal carriage
 Low humidity (dry) and dust enhance transmission
 Travel , migration and gathering together
 Poor living condition
Cont,
 Incubation period- 2-10 day, commonly 3-4
days.
 Period of communicability- as long as the
bacteria is present in the discharge.
 Susceptibility and resistance
Susceptibility is low and decreases with age
Cont,
Symptoms are result from infection and
increased intracranial pressure(IICP)
 Fever
 Altered consciousness, irritability,
photophobia
 Seizures 20 - 30% of the cases
 Bulging fontanel 30%
Cont,
Sign are result from infection and increased
intracranial pressure(IICP)
 Change in vital sign (Cushing’s triad (HTN, brady
cardia, irreg resp) )
 Headache
 Projectile Vomiting, poor appetite
 Decreased level of consciousness
 Cranial nerve palsies
 Coma
Cont,
Cont,
N.B Meningismus (stiff neck + Brudzinski + Kernig signs)
 Positive Brudzinski sign –flex the neck while
the patient in supine position with extremities
extended.
 Patient neck is flexed , involuntary flexion of
leg & knees occur or passive flexion of leg cause
similar movement of the other
Cont,
Positive Kernig sign – in a supine patient flex
the hip to 90 while the knee is flexed at 90 , an
attempt to further extend of the knees produce pain
in the hamstrings back or neck and resistance to
further extension.
Cont,
Diagnosis
 Clinical and epidemiological ground
 CSF analysis – the corner stone in the the diagnosis of meningitis is
examination of the CSF
 In general , whenever the diagnosis of meningitis is strongly considered
, promptly perform a Lumbar puncture
 Measure the opening pressure and send the fluid for cell count (and
differential count ) ,chemistry (i.e CSF glucose,and protien ), and
microbiology (i.e gram stain and culture )
 CT scan of the brain may be done prior to lumbar puncture in some
patients with a high risk of herniation
Cont,
 Needle with stylet inserted into the
subarachnoid space between L3-4 or L4-5.
 Styleted needle used so as to not introduce a
plug of epidermal cells into the space which
may later grow into a cord-compressing
epidermoid tumor.
lumbar puncture
Contraindications to Lumbar Puncture
 Respiratory distress (positioning)
  ICP reported to increase risk of herniation
 Cellulitis at area of tap
 Bleeding disorder
CSF evaluation
Condition WBC L
Protein
(mg/dL)
Glucose
(mg/dL)
Normal
<7, lymphs
mainly
5-45 >50
Bacterial, acute 100 – 60 100-500 Low
Bacterial 1 – 10,000 100+ Low to normal
TB 10 – 500 100-500 <50
Fungal 25 – 500 25-500 <50
Viral <1000 50-100 Normal
Cont,
Treatment
A.Community acquired, bacterial etiology unknown
First line
Ceftriaxone, 4g/day, I.V., divided in 2 doses for 10-14 days
PLUS
Vancomycin, 1gm IV BID for 10-14days
Alternative
Benzyl penicillin, 20-24 million IU/day I.V. in 4-6 divided
doses for 7 –10 days.
PLUS
Chloramphenicol, 500mg I.V. QID. In severe infections,
up to 100mg/kg/day in 4 divided doses, may be used
for 7 days
B.Empiric treatment, hospital acquired meningitis, related to post-
neurosurgery lumbar catheter &penetrating trauma
First line
Vancomycin, 15mg/kg IV Q8h
PLUS
Ceftazidime, 2g IV q8h
Alternative
Vancomycin, 15mg/kg IV Q8h
PLUS
Meropenem, 2gm IV Q8hr
C. Immunosuppressed (HIV positive, uncontrolled
diabetes, patients taking high dose
 Dexamethasone, 10mg IV QID for 4 days
PLUS
 Ceftazidime, 2g IV q8h
PLUS
 Vancomycin, 15mg/kg IV Q8h
PLUS
 Ampicillin, 2g IV q4h
PLUS
 Acyclovir 10mg/kg (infuse over 1h) Q8h for 14-21d
Complications of Meningitis
 One of the most common problems resulting
from meningitis is hearing loss.
 Anyone who has had meningitis should take a
hearing test.
Young children:
 Babyish behavior
 Forgetting recently learned skills
 Reverting to bed-wetting
 Babyish behavior
Cont,
Older people:
 Lethargy
 Recurring headaches
 Difficulty in concentration
 Short-term memory loss
 Balance problems
 Depression
Serious complications
I. Brain damage
I. Epilepsy
II. Changes in eye sight
Nursing care
 Maintain fluid balance (input and output)
 Maintain body temperature to normal
 Timely administration of antibiotics
 Monitor vital signs.
Prevention and control
I. Educate the public on the need to reduce direct
contact and exposure to droplet infection.
I. Reduce overcrowding in work places,
schools,& camps,
I. Vaccines containing group A,C and Y strains.
II. Chemotherapy of cases.
III. Chemo prophylaxis (e.g.Rifampin for 2 days)
IV. Report to the concerned health authorities.
8.Tuberculosis
Tuberculosis
A chronic and infectious mycobacterial disease
important as a major cause of illness and death
in many parts of the world.
Is an air borne communicable disease caused
by bacteria from Mycobacterium tuberculosis
complex.
Cont,
Infectious agent
 Mycobacterium tuberculosis- human tubercle
bacilli (commonest cause)
 Mycobacterium bovis- cattle and man infection
 Mycobacterium avium- infection in birds and man.
Epidemiology
Occurrence
Worldwide, however underdeveloped areas are more affected. Affects
all ages and both sexes. Age groups between 15-45 years are mainly
affected. According to the WHO 1995 report, 9 million cases and 3
million deaths have occurred. According to the Ministry of Health
report in 1993 E.C, tuberculosis was a leading cause of outpatient
morbidity (ranked 8th with 2.2%), leading cause of hospitalization
(ranked 3rd with 7.8%) and leading cause of hospital death (ranked
1st with 10.1%).
Cont,
Tuberculosis has two major clinical forms. Pulmonary
(80%) primarily occurs during childhood and
secondarily 15-45 years or later. The other is extra
pulmonary, which affects all parts of the body.
Most common sites are lymph nodes, pleura,
genitourinary tract, bone and joints, meninges and
peritoneum.
Cont,
Mode of transmission-
 Through aerosolized droplets mainly from persons with active
ulcerative lesion of lung expelled during talking, sneezing,
singing, or coughing directly.
 Untreated pulmonary tuberculosis positive (PTB+) cases are the
source of infection. Most important is the length of time of
contact an individual shares volume of air with an infectious
case.
 That is intimate, prolonged or frequent contact is required.
Cont,
 Transmission through contaminated fomites
(clothes, personal articles) is rare.
 Ingestion of unpasteurized milk transmits bovine
tuberculosis.
 Overcrowding and poor housing conditions favor
the disease transmission.
Incubation period- 4-12 weeks
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 immuno suppressed are susceptible.
Everyone who is non-infected or non-vaccinated can be
infected.HIV is an important risk factor for the development
of HIV associated tuberculosis by facilitating:
 Reactivation or
 Progression of recent infection or
 Reinfection
Pathogenesis
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 extrapulmonary
TB.
Cont,
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. While in few patients, the multiplication
continues and directly progress to active disease
(primary TB), mainly in person with compromised
immunity.
Cont,
 The latent infection may be reactivated into active TB
(secondary TB) later in life, if the person encounters
conditions that compromise cell-mediated immunity.
 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).
Evolution of latent and active TB
Latent TB Infection (LTBI): refers to the stage
whereby the immune system of the person halt the
multiplication of the bacilli and tissue damage, and
hence, no symptoms presents.
Active TB disease refers :to the conditions whereby
the person with TB infection starts to present with
clinical presentation of TB that requires full course
multi-drug chemotherapy.
Cont,
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 immuno suppressed individuals
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.
Differences between latent TB infection and active TB disease
Characteristics Latent TB Infection Active TB Disease
M. tuberculosis in the body Yes Yes
Tuberculin skin test reaction Positive Positive
Symptoms No Yes
Chest x-ray Normal Abnormal if pulmonary
Sputum smears and cultures Negative *Positive
Infectiousness Not Pulmonary TB is
infectious
A case of TB No Yes
Risk factors/ conditions for developing active TB
I.Host immunity
 HIV infection(risk:20-40 time fold)
 Diabetes mellitus (risk: 3-5time fold)
 Malnutrition
 Extremes of Age (under-five and elderly)
 Prolonged steroid therapy
 Severe kidney disease
 Malignancies(Ex:leukemia, lymphoma…)
 Alcoholism
Cont,
II. Conditions that damages the lung:
 Tobacco smoking
 Silicosis
III. Intensity of exposure:
 Resident or workers in high-risk congregate settings
 Degree of infectiousness
 Household or other closed space contacts
 Time elapsed since exposure/infection:
 Infection within one year
Clinical Manifestation
Pulmonary tuberculosis
 Persistent cough for 2 weeks or more
 Productive cough with or without blood-stained
sputum
 Shortness of breath and chest pain
 Intermittent fevers, night sweats, loss of weight,
 loss of appetite, fatigue and malaise.
Extra-pulmonary TB
Patients may present with non-specific symptoms
such as unintentional weight loss, night sweats and
fever for more than 2 weeks. other symptoms
depend on the site or organ affected. The most
common types of extra-pulmonary tuberculosis are
Cont,
Tuberculous lymphadenitis :
Caused by lymphatic spread of the organism, is
one of the commonest forms of extra-pulmonary TB.
Involvement of the lymph nodes is common in
children and in person in the later stages of HIV
infection.
Cont,
Slowly developing painless cervical lymph
node enlargement (regardless of HIV infection)
is the commonest sites of involvement, though
axillary and intra-abdominal lymph nodes may
be affected.
Clinical presentations
 Overlying skin may breakdown
 Abscesses and chronic discharging sinuses which
heal with scarring
Tuberculous pleural effusion
Is the commonest cause of a unilateral pleural effusion.
It is also the commonest form of HIV-related extra-
pulmonary disease.
Clinical features
Presentation is most often acute with:
 Non-productive cough,
 Chest pain, shortness ofbreath and
 High temperature.
Findings on clinical examination may include:
 Tracheal and mediastinal shift away from the side of the
effusion
 Decreased chest movement
 Stony dullness on percussion on the side of the effusion.
TB of bones
 Localized pain and/or swelling, discharging of pus, muscle
weakness, paralysis and stiffness of joints. can affect any bone but
most commonly affects the vertebral column.
Involvement of the thoracic vertebrae causes localized
 Back pain,deformity of the spine, and
 Angulated kyphosis (gibbus)
 Paravertebral tissue abscess
Intestinal TB
Loss of weight and appetite
Abdominal pain, diarrhea and constipation
Mass in the abdomen
Fluid in the abdominal cavity (ascites)
Miliary Tuberculosis
Presents with constitutional features rather than
respiratory symptoms.
Early symptoms are :
 Vague and lack specificity.
 Lassitude, anorexia, failure to thrive and
 Prolonged unexplained fever are common.
TB meningitis is the commonest cause of death if miliary
TB is untreated.
CNS TB( including TB meningitis)
The patient may present with constitutional features
and chronic meningitis and there is:
 Gradual onset and progression of headache and
 Decreased consciousness.
It is most common in children between 6 month and
4 years of age.
Tuberculosis diagnostic methods
Clinical manifestations
Bacteriologic confirmation using
 Identification of the bacillus on ZN/FM
microscopic examination(AFB)
 Identification of bacillary genetic material
using molecular techniques like xpert MTB
 Culture media
Cont,
Clinical decision of expert clinician by analyzing
the supportive evidences from:
 Medical imaging of the affected organs eg. X-ray,
Ultra sound,etc.
 Histo-pathologic studies of sample obtained from body
tissue or fluid
 Biochemical analysis of body fluids: glucose, cell
counts,& protein.
 Heamatology tests: Complete blood cell count, ESR
TB CASE DEFINITIONS
Presumptive Tuberculosis:
Refers to a patient who presents with symptoms
or signs suggestive of TB, in particular cough of two
weeks or more duration.
Bacteriologically confirmed TB case:
Refers to a patient from who has at least one Positive
result either by smear microscopy, culture or Xpert
MTB/RIF assay
Cont,
Clinically diagnosed TB case:
Refers to a patient who does not fulfill the criteria for
bacteriological confirmation but has been diagnosed with active
TB by a clinician and decided to treat with a full course of TB
treatment. includes cases diagnosed on the basis of X-ray
abnormalities or suggestive histopathology and Extra
pulmonary TB cases diagnosed without laboratory
identification of the mycobacterium.
Patient registration groups for drug susceptible TB
 Relapse patients: patients that have previously been
treated for TB were declared cured or treatment completed
at the end of their most recent course of treatment, and is
now diagnosed with a recurrent episode of TB (either a
true relapse or a re infection).
 Treatment after failure: patients are those who have previously
been treated for TB and whose treatment failed (: smear positive
results after fifth month during treatment) at the end of their most
recent course of treatment.
Cont,
New TB cases: refers to patients have never been
treated for TB or have taken anti-TB drugs for
less than 1 month.
Previously treated TB case: refers to patients
that have received 1 month or more of anti-TB
drugs in the past.
Classifications based on drug resistance
 Mono-drug resistance: resistance to one first
line anti-TB drug only.
 Poly-drug resistance: resistance to more than
one first-line anti-TB drug (other than both Isoniazid
and Rifampicin).
 Multidrug resistance (MDR-TB): resistance to at
least both Isoniazid and Rifampicin.
Cont,
Extensive drug resistance (XDR-TB):
resistance to any fluoroquinolone and to at least
one of three second-line injectable drugs
(Capromycin, Kanamycin and Amikacin), in
addition to multidrug resistance (- Isoniazid and
Rifampicin).
Treatment
 Streptomycin (s) daily IM injection
 Ethambutol(E)
 Rifampin (R)
 Isoniazid (H)
 Pyrazinamide (Z)
Drug regimens (prescribed course of therapy)
I.Short course chemotherapy regimen (DOTS)
 Intensive phase 2(RHZE) for two months
 Continuation phase 4(RH)for the next 4 months.
II.Long course chemotherapy regimen.
 Intensive phase 2(RHZE) for 2 months
 Continuation phase 10 (RH)for the next 10 months
Treatment
TB Patient
type
Standard Regimen TB types receiving the
regimen
Intensive phase Continuation phase
Drug
susceptible TB
case
2(RHZE) 4(RH) All pulmonary TB cases
Most Extrapulmonary TB
cases
2(RHZE) 10 (RH) Extrapulmonary TB patients
involving:
CNS ( meningitis,
tuberculoma)
 vertebra and Osteoarticular
space
Drug Resistant
TB( at least to
rifampicin)
Second line anti-TB drugs Confirmed or clinically
diagnosed DR-TB
cases
Cont,
Nursing care
 Educate the patient how and when to take the prescribed
medication.
 Tell the patient not to stop the medication unless he/she
is told to do so.
 Tell the patient to come to the health institution if he/she
develops drug side effects.
 Advice the patient on the importance of taking adequate
and balanced diet and to eat what is available at home.
Prevention and control
 Chemotherapy of cases
 Chemoprophylaxis for contacts:
INH (Isoniazid) for adults and children who have close
contact with the source of infection
 Immunization of infants with BCG
 Educate patients with TB about the mode of disease
transmission and how to dispose their sputum and cover
their mouth while coughing,& sneezing.
Cont,
Public health education about the modes of
disease transmission and methods of control
 Improved standard of living
 Adequate nutrition
 Health housing
 Environmental sanitation
 Personal hygiene; etc.
 Active case finding and treatment
Leprosy (Hansen’s disease)
A chronic bacterial disease of the skin, peripheral
nerves and,in lepromatous patients, the upper
airway.
Infectious agent
Mycobacterium leprae
Epidemiology
Occurrence:
Although common in rural tropics and subtropics,
socio-economic conditions may be more important
than climate itself. Endemic in south and southeast
Asia,tropical Africa and Latin America.
Reservoir- Humans
Mode of transmission
 Not clearly established. Householdand prolonged close contact
appear to be important. Millions of bacilli are liberated daily in the
nasal discharges of untreated lepromatous patients.
 Cutaneous ulcers in lepromatous patients may shed large number
of bacilli.
 Organisms probably gain access (entrance) through the URT and
possibly through broken skin.
 In children less than one year of age, transmission is presumed to
be transplacental.
Cont,
Incubation period- 9 months to 20 years.
Period of communicability- Infectiousness is lost
in most instances within 3months of continuous
and regular treatment with dapsone or clofazamin
or within 3 days of rifampicin treatment.
Cont,
Susceptibility and resistance- The presence and
form of leprosy depend on the ability to develop
effective cell mediated immunity.
Clinical Manifestation
Clinical manifestations vary between two polar forms:
lepromatous and tuberculoid leprosy.
Lepromatous (Multibacillary form)
Nodules, papules, macules and diffused
infiltration are bilaterally symmetrical and usually
numerous and extensive.
Involvement of the nasal mucosa may lead to
crusting,obstructed breathing and epistaxis.
Occular involvement leads to iritis and keratitis.
Tuberculoid (Paucibacillary form)
Skin lesions are single or few, sharply
demarcated, anesthetic or hyperesthetic and
bilaterally symmetrical.
Peripheral nerve involvement tends to be severe.
Cont,
Borderline
Has features of both polar forms and is more
liableto shift toward the lepromatous form in
untreated patients and toward
the tuberculoid form in treated patients.
Diagnosis
Complete skin examination (hyperesthesia,
anesthesia, paralysis, muscle wasting or trophic ulcer which
are signs of peripheral nerve involvement) with bilateral
palpation of peripheral nerves (ulnar nerve at the elbow,
Peroneal nerve at head of fibula and the
great auricular nerve) for enlargement and tenderness.
Cont,
Skin lesion are tested for sensation (light touch,
Pink prick, temperature discrimination).
Demonstration of AFB in skin smears made by
scraped incision method.
Skin biopsy confined to the affected area should
be sent to the experienced pathologists in leprosy
diagnosis.
Treatment
Dapsone three drugs for 12 months and then
Refampicin dapsone alone for the next 12 months.
Clfazamin
Aspirin for mild reactions and inflammation
Severe reaction can be treated with corticosteroids
Review Questions
1.What do you understand by air-borne disease
transmission?
2.Which airborne disease occurrence should be reported immediately to
the concerned health authorities for their prompt action?
a. Pneumonia
b. Tuberculosis
c. Leprosy
d. Meningococcal meningitis
Cont,
3.Select diseases which cause chronic illness:
a. Tuberculosis
b. Leprosy
c. Measles
d. Infection hepatitis
4.State some of the preventive and control methods for
tuberculosis.
UNIT FOUR
Manage a patient
with arthropod
borne disease
323
Zinabu D
Objectives
At the end of this chapter, the student will be able to:
 Describe what arthropod borne disease means.
 Identify common vectors which transmit disease to man
 List the common vector-borne diseases.
 Participate in diagnosis and treatment of vector-borne
diseases.
 Implement the common preventive and control methods of
vector-borne diseases.
324
Zinabu D
Introduction
Vector is any carrier of disease
But in the case of the ‘vector-borne diseases’ it is
Those invertebrate hosts (insects or snails),
which are an essential part of the life cycle of
the disease organism.
A period of development of pathogen inside the
vector is called the extrinsic incubation period
325
Zinabu D
Common vector borne disease includes
 Malaria
 Flariasis
 Endemic typhus
 Relapsing fever
 Schistosomiasis
 Guinea worm
326
Zinabu D
327
1.Malaria
An acute infection of the blood caused by
protozoa of the genus plasmodium inoculated
into the human host by feeding female annoplin
mosquito
The most serious and life-threatening disease
occurs from Plasmodium Falciparum infection.
Zinabu D
Infectious agent
Plasmodium falciparum /malignant tertian
– Invades all ages of red blood cells
– Red blood cell cycle is 48 hours
Plasmodium Vivax /benign tertian
– Invades reticulocytes only&
– Red blood cell cycle is 48 hours
Plasmodium ovale/tertian
– Invades reticulocytes only &Red blood cell cycle is 48 hours
Plasmodium Malariae/Quartan malaria
– Invades reticulocytes only&Red blood cell cycle is 72 hours
328
Zinabu D
Epidemiology
• Endemic in tropical and sub-tropical countries of the
world
• Affects 40% of the world population, Children less 5
years of age, pregnant women and travelers to
endemic areas are risk groups
• Plasmodium falciparum 60% and Vivax 40% are
common in Ethiopia
329
Zinabu D
Cont,
Predisposing factors are:
• Environment- physical environment for the
propagation, Patient source, Susceptible recipients
• Anopheles capable to transmit the parasite
• Socio-economic factors like immigration, war,
poverty, ignorance, agricultural irrigation farms, etc.
Reservoir- Humans
330
Zinabu D
Mode of transmission
By the bite of an infective female anopheles
mosquito
Blood transfusion
Hypodermic needles
Organ transplantation and mother to fetus
331
Zinabu D
Cont,
Incubation period- Varies with species
I. Plasmodium falciparum 7-14 days
II. Plasmodium virvax 8-14 days
III. Plasmodium ovale 8-14 days
IV.Plasmodium Malariae 7-30 days
332
Zinabu D
Period of communicability
Mosquitoes are infective as long as infective
gametocytes are present in the blood of patients
Once infected, mosquito remains infective for life
Susceptibility and resistance
Susceptibility is universal except in some host-
resistance factors
333
Zinabu D
Non specific factors
 Increased splenic clearance reaction
 Hyperpyrexia- which is said to be schizontcidal
 Sickle cell traits are resistant to plasmodium falciparum
 Duffy blood group deficiency (Duffy antigen negative red
blood cells) lack receptor for plasmodium vivax.
 Because of passive immunity infants are resistant in early
life
334
Zinabu D
Cont,
Specific factors
–This is a humoral and cell mediated
immunity that is species and strain specific,
and hard-won after repeated infection
335
Zinabu D
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  • 2. Objective At the end of this chapter the student should be able to define  Define Communicable Disease  Explain common terms  Describe chain of disease transmission By zinabu D 2
  • 3. Introduction to communicable diseases control  What are a communicable diseases ? Example:  What are a non-communicable diseases? Example: By zinabu D 3
  • 4. Communicable Diseases  Is an illness due to specific infectious agent or its products arises through transmission of that agent or its products an infected person, animal or inanimate reservoir to a susceptible host.  The transmission may occur either directly or indirectly through an intermediate host which can be plant or animal or a non living thing, or in both direct and indirect. By zinabu D 4
  • 5. Cont Communicable Diseases control It refers to the reduction of the incidence & prevalence of diseases to level where it can not be a major public health problem. By zinabu D 5
  • 6. DEFINITION OF COMMON TERMS Transmission:- is the process by which an infectious agent or its products passes from the source to the new host. Period of communicability:- the time during which the infectious agent may be transferred from infected person to another. Incubation period:- The time interval between initial contact with the infectious agent and the appearance of the first sign or symptoms of the disease. By zinabu D 6
  • 7. Cont Prodormal period: The time interval between the onset of symptoms of an infectious disease and the appearance of characteristic manifestations. E.g. In measles from the onset of fever and coryza to the development of characteristic signs like koplick’s spots and characteristic skin lesions. By zinabu D 7
  • 8. Cont Prepatent period: The period in people between the time of exposure to a parasite and the time when the parasite can be detected in blood or in stool. Incubation period in a vector: is the time between entrance of an organism in to the vector and the time when that vector can transmit the infection (extrinsic incubation period). By zinabu D 8
  • 9. Cont Exposure: The contact between the agent and susceptible host. Infectivity: The ability of an agent to invade and multiple in a host. Pathogencity: The ability of an agent to produce clinically apparent disease, or the property of an infectious agent that determines the extent to which overt dx is produced. By zinabu D 9
  • 10. Cont, Virulence: The ability of infectious agent to produce severe disease among clinically infected persons. Immunogenicity: The ability of an agent to produce specific immunity Illness: Individual or subjective feeling of discomfort. By zinabu D 10
  • 11. Cont Infectious agent- an agent capable of causing infection Contamination – presence of living infectious agent upon Articles Infestation – presence of living infectious agent on the exterior surface of the body Infection - the entry and development or multiplication of an infectious agent in the body of man or animal By zinabu D 11
  • 12. Cont Infectious: caused by microbes and can be transmitted to other persons Disease :a state of physiological or psychological dysfunction. Epidemics :the occurrence of any health related condition in a given population in excess of the usual frequency in that population. Endemic :a disease that is usually present in a population or in an area at a more or less stable level. By zinabu D 12
  • 13. Cont Sporadic - a disease that does not occur in that population, except at occasional and irregular intervals. Pandemic - an epidemic disease which occurs worldwide By zinabu D 13
  • 14. Chain of disease transmission This refers to a logical sequence of factors or links of a chain that are essential to the development of the infectious agent and propagation of disease. The six factors involved in the chain of disease transmission are: By zinabu D 14
  • 15. Chain of diseases transmission By zinabu D 15
  • 16. Cont  Infectious agent (aetiology or causative agent)  Reservoir  Portal of exit  Mode of transmission  Portal of entry  Susceptible host By zinabu D 16
  • 17. Infectious Agent An organism that is capable of producing infection or infectious disease. On the basis of their size, etiological agents are generally classified into:  Metazoa (multicellular organisms). (e.g. Helminths).  Protozoa (Unicellular organisms) (e.g. Ameobae)  Bacteria (e.g. Treponema pallidum, Mycobacterium tuberculosis, etc.)  Fungus (e.g. Candida albicans)  Virus (e.g. Chickenpox, polio, etc.) By zinabu D 17
  • 18. Reservoir  Any person, animal, arthropod, plant, soil or substance (or combination of these) in which an infectious agent normally lives and multiplies, on which it depends primarily for survival and where it reproduces itself in such a manner that it can be transmitted to a susceptible host. By zinabu D 18
  • 19. Types of Reservoirs Man:  There are a number of important pathogens that are specifically adapted to man, such as: measles, smallpox, typhoid, meningococcal meningitis, gonorrhea and syphilis.  The cycle of transmission is from human to human. By zinabu D 19
  • 20. Cont.. II. Animals:  Some infective agents that affect man have their reservoir in animals. The term “zoonosis” is applied to disease transmission from animals to man under natural conditions. For example: Bovine tuberculosis - cow to man Brucellosis - Cows, pigs and goats to man Anthrax - Cattle, sheep, goats, horses to man Rabies - Dogs, foxes and other wild animals to man By zinabu D 20
  • 21. Cont... 3.Non-living things as reservoir:  Many of the agents are basically saprophytes living in soil and fully adapted to live freely in nature.  Biologically, they are usually equipped to withstand marked environmental changes in temperature and humidity. E.g. Clostridium botulinum etiologic agent of Botulism Clostridium tetani etiologic agent of Tetanus Clostridium welchi etiologic agent of gas gangrene By zinabu D 21
  • 22. 3. Portal of exit This is the site through which the agent escapes from the reservoir. Examples include:  GIT: typhoid fever, bacillary dysentery, amoebic dysentery, cholera, ascariasis, etc Respiratory: tuberculosis, common cold, etc. Skin and mucus membranes: Syphilis By zinabu D 22
  • 23. 4.Mode of transmission  Refers to the mechanisms by which an infectious agent is transferred from one person to another or from a reservoir to a new host.  Transmission may be direct or indirect. 1. Direct transmission:  Consists of essentially immediate transfer of infectious agents from an infected host or reservoir to an appropriate portal of entry. By zinabu D 23
  • 24. Cont This could be: I. Direct Vertical – Such as: transplacental transmission of syphilis, HIV, etc. II. Direct horizontal  Direct touching, biting, kissing, sexual intercourse, droplet spread onto the conjunctiva or onto mucus membrane of eye, nose or mouth during sneezing coughing, spitting or talking; Usually limited to a distance of about one meter or less. By zinabu D 24
  • 25. Cont II. Indirect transmission A.Vehicle-borne transmission: Indirect contact through contaminated :  Inanimate objects (fomites) like: Bedding, toys, handkerchiefs, soiled clothes, cooking or eating utensils, surgical instruments.  Contaminated food and water.  Biological products like blood, serum, plasma or IV-fluids or any substance serving as intermediate means by which an infectious agent is transported and introduced into a susceptible host through a suitable portal of entry. By zinabu D 25
  • 26. Cont.. B. Vector-borne transmission: Occurs when the infectious agent is conveyed by an arthropod (insect) to a susceptible host. 1. Mechanical transmission:  The arthropod transports the agent by soiling its feet or proboscis, in which case multiplication of the agent in the vector does not occur. (e.g.common house fly.) By zinabu D 26
  • 27. Cont... 2. Biological transmission:  This is when the agent multiplies in the arthropod before it is transmitted, such as the transmission of malaria by mosquito. C. Air-borne transmission:  Dissemination of microbial agent by air to a suitable portal of entry, usually the respiratory tract. Two types of particles are implicated in this kind of spread: dusts and droplet nuclei. By zinabu D 27
  • 28. Cont... Dust:  Small infectious particles of widely varying size that may arise from soil, clothes, bedding or contaminated floors and be re-suspended by air currents. Droplet nuclei :  Small residues resulting from evaporation of fluid (droplets emitted by an infected host). They usually remain suspended in the air for long periods of time. By zinabu D 28
  • 29. 5. Portal of entry The site in which the infectious agent enters to the susceptible host. For example:  Mucus membrane  Skin  Respiratory tract  GIT  Blood By zinabu D 29
  • 30. 6.Susceptible host  A person or animal lacking sufficient resistance to a particular pathogenic agent to prevent disease if or when exposed.  occurrence of infection and its outcome are in part determined by host factors.  The term “immunity” is used to describe the ability of the host to resist infection.  Resistance to infection is determined by non-specific and specific factors: By zinabu D 30
  • 31. Cont.. Non-specific factors  Skin and mucus membrane  Mucus, tears, gastric secretion  Reflex responses such as coughing and sneezing. Specific factors  Genetic-hemoglobin resistant to Plasmodium falciparum  Naturally acquired or artificially induced immunity. Acquired immunity may be active or passive By zinabu D 31
  • 32. Cont.. Active immunity: Acquired following actual infection or immunization. Passive immunity: pre-formed antibodies given to the host. By zinabu D 32
  • 33. Carrier and Its Type  A carrier is an infected person or animal who does not have apparent clinical disease but is a potential source of infection to others. A. Healthy or asymptomatic carriers: These are persons whose infection remains unapparent. For example, in poliovirus, meningococcus and hepatitis virus infections, there is a high carrier rate. By zinabu D 33
  • 34. Cont... B. Incubatory or precocious carriers:  These are individuals or persons who excrete the pathogen during the incubation period (i.e. before the onset of symptoms or before the characteristic features of the disease are manifested). E.g. Measles, mumps, chickenpox and hepatitis. By zinabu D 34
  • 35. Cont.. C. Convalescent Carriers:  These are those who continue to harbor the infective agent after recovering from the illness. E.g. Diphtheria, Hepatitis B virus. D. Chronic Carriers:  The carrier state persists for a long period of time. E.g. Typhoid fever, Hepatitis B virus infection By zinabu D 35
  • 36. Time Course of Infectious Diseases  Incubation period: It is the interval of time between infection of the host and the first appearance of symptoms and signs of the disease.  Prodormal period: It is the interval between the onset of symptoms of an infectious disease and the appearance of characteristic manifestations. By zinabu D 36
  • 37. For example, in a measles  Patient, fever and coryza occur in the first three days and  Koplick spots in the buccal mucosa and characteristics skin lesions appear on the fourth day. By zinabu D 37
  • 38. Cont.. Period of communicability:  The period during which that particular communicable disease (infectious agent) is transmitted from the infected person to the susceptible host. By zinabu D 38
  • 39. Levels of Prevention Three levels of prevention: primary, secondary, and tertiary. A.Primary prevention: The objectives here are to promote health, prevent exposure, and prevent disease.  Health promotion .E.g. affordable and adequate housing, old-age pension benefits; emotional and social support, education and vocational training etc  Prevention of exposure E.g. provision of safe and adequate water, vector control, proper excreta disposal, etc.  Prevention of disease. This occurs during the latency period between exposure and the biological onset of disease. E.g. Immunization By zinabu D 39
  • 40. Cont... B. Secondary prevention:  After the biological onset of disease, but before permanent damage.  The objective here 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) By zinabu D 40
  • 41. Cont... C. Tertiary prevention: After permanent damage has set in,  The objective of tertiary prevention is to limit the impact of that damage.  The impact can be physical, psychological, social (social stigma or avoidance by others), and financial.  Rehabilitation refers to the retraining of remaining functions for maximum effectiveness. By zinabu D 41
  • 42. Communicable Disease Control This refers to the reduction of the incidence and prevalence of communicable disease to a level where it cannot be a major public health problem. Methods of Communicable Disease Control I. Elimination of the Reservoir II. Interruption of transmission III. Protection of susceptible host By zinabu D 42
  • 43. I.Elimination of the reservoir A. Man as reservoir: When man is the reservoir, eradication of an infected host is not a viable option. Instead, the following options are considered. Detection and adequate treatment of cases  Isolation-separation of infected persons for a period of communicability of the disease.  Quarantine-limitation of the movement of apparently well person who has been exposed to infectious diseases. By zinabu D 43
  • 44. Cont.. B. Animals as reservoir Action will be determined by the usefulness of the animals, how intimately they are associated to man and the feasibility of protecting susceptible animals. E.g: Rabies: Pet dogs can be protected by vaccination but stray dogs are destroyed.  Infected animals used for food are examined and destroyed. By zinabu D 44
  • 45. Cont.. C. Reservoir in non-living things: Possible to limit man’s exposure to the affected area (e.g. Soil, water, forest, etc.). By zinabu D 45
  • 46. II.Interruption of transmission This involves the control of the modes of transmission from the reservoir to the potential new host through:  Improvement of environmental sanitation and personal hygiene  Control of vectors  Disinfections and sterilization By zinabu D 46
  • 47. III.Protection of susceptible host This can be achieved through:  Immunization: Active or Passive  Chemo-prophylaxis- (e.g. Malaria, meningococcal meningitis, etc.)  Better nutrition  Personal protection. (e.g. wearing of shoes, use of mosquito bed net, insect repellents, etc.) By zinabu D 47
  • 50. INTRODUCTION  Causative agents are excreted in the stools of infected persons.  The portal of entry for these diseases is the mouth. By zinabu D 50
  • 51. Cont,  Thus the causative organisms have to pass through the environment from the feces of an infected person to the gastro-intestinal tract of a susceptible person  This is known as the fece-oral transmission route  This transmission occurs mostly through unapparent fecal contamination of food, water and hands  Food takes a central position; it can be directly or indirectly contaminated via polluted water, dirty hands, contaminated soil, or flies. By zinabu D 51
  • 53. Five “fs” fecal oral diseases transmission By zinabu D 53 Flies Finger Fomites Fluid Food Mouth Feces
  • 54. . MANAGE A PATIENT WITH FECO-ORAL TRANSMITED DISEASE By zinabu D 54
  • 55. TYPHOID FEVER A systemic infectious disease characterized by high continuous fever, malaise & involvement of Lymphoid tissues. Etiology:  Salmonella typhi  Salmonella enteritidis By zinabu D 55
  • 56. Epidemiology Occurrence: It occurs worldwide, particularly in poor socioeconomic areas. Annual incidence is estimated at about 17 million cases with approximately 600,000 deaths worldwide. In endemic areas the disease is most common in preschool and school aged children (5-19 years ofage). By zinabu D 56
  • 57. Cont, Reservoir: Human as a case or as a carrier. Temporary carrier: that excretes the organisms for at least 6-8 weeks. Chronic carrier : which excretes the organisms for at least 1 year. In some cases, it can be life long. By zinabu D 57
  • 58. Mode of transmission By water and food contaminated by feces and urine of patients and carriers. Flies may infect foods in which the organisms then multiply to achieve an infective dose. By zinabu D 58
  • 59. Cont, Incubation period –1-3 weeks Period of communicability: As long as the bacilli appear inexcreta, usually from the first week throughout convalescence. About 10% of untreated patients will discharge bacilli for 3 months after onset of symptoms,And 2%-5% become chronic carriers. By zinabu D 59
  • 60. Susceptibility And Resistance  Susceptibility is general and increased in individuals with gastric achlorhydria or those who are HIV positive. By zinabu D 60
  • 61. Clinical manifestation First week:  Mild illness characterized by:  Fever rising stepwise(ladder type),  Anorexia, lethargy, malaise and  General aches.  Dull and continuous frontal headache is prominent.  Nose bleeding, vague abdominal pain and  Constipation in 10% of patients. By zinabu D 61
  • 62. Second week:  Sustained temperature (fever).  Severe illness with weakness, mental delirium,  Abdominal discomfort and distension.  Diarrhea is more common than first  week and feces may contain blood. By zinabu D 62
  • 63. Third week  Patient continues to be febrile and increasingly exhausted.  If no complications occur, patient begins to improve and temperature decreases gradually. By zinabu D 63
  • 64. Clinical manifestations suggestive of typhoid fever  Fever: Sustained fever (ladder fashion)  Rose spots:Small pallor, blanching, slightly raised macules usually seen on chest and abdomen in the firstweek in 25% of white people.  Relative bradycardia:slower than would be expected from the level of temperature.  Leucopoenia: White cell count is less than 4000/mm3 of blood. By zinabu D 64
  • 65. Diagnosis  Based on clinical grounds but this is confused with wide variety of diseases.  Serological examination :Widal test (reaction) against somatic and flagellar antigens(O or H) reactive  Blood, feces or urine culture :Golden Dx for TF By zinabu D 65
  • 66. Treatment  Ciprofloxacin, 500mg P.O, BID for 10-14 days Alternative  Amoxicillin,1g, P.O.QID, for children: 20 – 40mg/kg/day P.O.in 3 divided doses for 14 days OR  Chloramphenicol, 500mg P.O QID, for 14 days:  For children: 25mg/kg. OR By zinabu D 66
  • 67. Cont, Sulfamethoxazole+trimethoprim, 800mg/160mg P.O.BID for 14 days. For children  6 weeks– 5 months, 100/20mg;  6 months – 5 yrs, 200/40mg;  6 – 12 yrs, 400/80mg BID For severe cases which are fluoroquinolone resistant: By zinabu D 67
  • 68. Cont, Ceftriaxone, 1g QID as a single dose OR in 2 divided doses I.M. OR I.V. for 7-10 days. OR Chloramphenicol, 1g, IV bolus QID until 48 hrs after fever has settled, followed by 500mg P.O QID for a total of 14 days. For children: 25mg/kg, IV bolus QID, until 48 hrs after fever has settled, followed by 25mg/kg P.O.QID for a total of 14 days. By zinabu D 68
  • 69. Cont, Adjunct Corticosteroid treatment: This is recommended only for patients with evidences of CNS involvement (delirium, coma) Shock. By zinabu D 69
  • 70. Cont, First line Dexamethasone, 3mg/kg IV initially, followed by 1mg/kg IV Q 6hrs for 48hrs total (This is prefered in patients with severe disease) OR Prednisolone, 20-40mg P.O. (or equivalent) once daily for the first three days of antibiotic treatment. By zinabu D 70
  • 71. Nursing care  Maintain body temperature to normal. Apply comfort measures. Follow side effects of drugs. Monitor vital signs. Follow strictly enteric precautions:  Wash hands  Wear gloves  Teach all persons about personal hygiene By zinabu D 71
  • 72. Cont, Observe the patient closely for sign and symptoms of:  Bowel perforation  Erosion of intestinal ulcers  Sudden pain in the lower right side of the abdomen  Abdominal rigidity  Sudden fall of temperature and blood pressure Accurately record intake and output. Provide proper skin and mouth care. By zinabu D 72
  • 73. Prevention and control Treatment of patients and carriers Education on handwashing, particularly food handlers,patients and childcare givers Sanitary disposal of feces and control of flies. Provision of safe and adequate water Safe handling of food. By zinabu D 73
  • 74. Cont, Exclusion of typhoid carriers and patients from handling of food and patients Immunization for people at special risk (e.g children &travelers to endemic areas) Regular check-up of food handlers in food and Drinking establishments By zinabu D 74
  • 75. Bacillary Dysentery (Shigellosis) Is acute bacterial disease involving the large and distal small intestine, caused by the bacteria of the genus shigella. Infectious agent Shigella is comprised of four species or serotypes.  Group A= Shigella dysentraie (most common cause)  Group B= Shigella flexneri  Group C= Shigella boydii  Group D= Shigella sonnei By zinabu D 75
  • 76. Epidemiology  Occurrence- It occurs worldwide, and is endemic in both tropical and temperate climates.  Outbreaks commonly occur under conditions of crowding and where personal hygiene is  poor, such as in jails, institutions for children, day care centers, mental hospitals and refugee camps. By zinabu D 76
  • 77. Cont,  It is estimated that the disease causes 600,000 deaths per year in the world.  Two-thirds of the cases, and most of the deaths, are in children under 10 years of age. Reservoir- Humans By zinabu D 77
  • 78. Mode of transmission-  Mainly by direct or indirect fecal-oral transmission from a patient or carrier.  Transmission through water and milk may occur as a result of direct fecal contamination.  Flies can transfer organisms from latrines to a  non-refrigerated food item in which organisms can survive and multiply. By zinabu D 78
  • 79. Cont,  Incubation period- 12 hours-4 days (usually 1-3 days)  Period of communicability: During acute infection and until the infectious agent is no longer present in feces, usually within four weeks after illness. By zinabu D 79
  • 80. Susceptibility and resistance Is general. The disease is more severe in:  Young  Children,  Elderly and the malnourished. Breast-feeding is protective for infants and Young children. By zinabu D 80
  • 81. Clinical Manifestation  Fever, rapid pulse, vomiting and abdominal cramp are prominent.  Diarrhea usually appears after 48 hours with dysentery supervening two days later.  Generalized abdominal tenderness.  Tenesmus is present and feces are bloody, mucoid and Of small quantity.  Dehydration is common and dangerous - it may cause muscular cramp, oliguria and shock. By zinabu D 81
  • 82. Diagnosis Based on clinical grounds Stool microscopy (presence of pus cells) Stool culture confirms the diagnosis By zinabu D 82
  • 83. Treatment  Fluid and electrolyte replacement  Co-trimoxazole 960 mg po bid for 10 day  Doxaciclline 100mg po bid for 10 day  Nalidixic acid, which is the most important especially for children. By zinabu D 83
  • 84. Prevention and control  Detection of carriers and treatment of the sick will interrupt an epidemic.  Hand washing after toilet and before handling or eating food.  Proper excreta disposal especially from patients, convalescent and carriers.  Adequate and safe water supply.  Control of flies.  Cleanliness in food handling and preparation. By zinabu D 84
  • 85. Amoebiasis (Amoebic Dysentery) An infection due to a protozoan parasite that Causes intestinalor extra-intestinal disease. Infectious agent Entamoeba histolytica By zinabu D 85
  • 86. Epidemiology Occurrence:  Worldwide but most common in the tropics and sub-tropics.  Prevalent in areas with poor sanitation, in mental institutions and homosexuals. Invasive amoebiasis is mostly a disease of young people (adults).  Rare below 5 years of age, especially below 2 years. By zinabu D 86
  • 87. Mode of transmission Fecal-oral transmission by ingestion of food or water contaminated by feces containing the cyst. Acute amoebic dysentery poses limited danger. Incubation period: Variable from few days to several months or years; commonly 2-4 weeks By zinabu D 87
  • 88. Cont, Period of communicability  During the period of passing cysts of E.histolytica, which may continue for years. Susceptibility and resistance:  General By zinabu D 88
  • 89. Life cycle .. By zinabu D 89 TRANSMISSION 1.Cysts ingested in Food, water Or from hands contaminated with feces Environment. 6.Feces containing infective cysts contaminate the environment. HUMAN HOST 2. Cysts excyst, forming trophozoites 3. Multiply in intestine 4. Trophozoites encyst. 5. Infective cysts passed in feces.* * trophozoites passed in feces disintegrate
  • 90. Clinical Manifestation  Starts with a prodormal episode of : Diarrhea Abdominal cramps Nausea, vomiting and tenesmus.  With dysentery, feces are generally watery, Containing mucus and blood. By zinabu D 90
  • 91. Diagnosis Lab : Stool examination: Etamoeba histolytica cyst or trophozoite Treatment Metronidazole 500mg po tid for 07 day or Tinidazole 2gm po bid for 02 day By zinabu D 91
  • 92. Prevention and control  Adequate treatment of cases  Provision of safe drinking water  Proper disposal of human excreta (feces) and hand washing following defecation.  Cleaning and cooking of local foods (e.g. raw vegetables) to avoid eating food contaminated with feces. By zinabu D 92
  • 93. Giardiasis A protozoan infection principally of the upper small intestine associated with symptoms of chronic diarrhea, steatorrhea, abdominal cramps, bloating, frequent loose and pale greasy stools, fatigue and weight loss. Infectious agent Giardia lamblia By zinabu D 93
  • 94. Epidemiology  Occurrence- Worldwide distribution. Children are more affected than adults.  The disease is highly prevalent in areas of poor sanitation. Reservoir- Humans Mode of transmission Person to person transmission occurs by hand to mouth transfer of cysts from feces of an infected individual especially in institutions and day Care centers. By zinabu D 94
  • 95. Period of communicability  Entire period of infection, often months. Susceptibility and resistance : Asymptomatic carrier rate is high. Infection is frequently self-limited.  Persons with AIDS may have more serious and prolonged infection. By zinabu D 95
  • 96. Life cycle • . By zinabu D 96 TRANSMISSION 1. Cysts ingested in food, water or from hands contaminated with feces. HUMAN HOST 2 cysts excyst,forming trophozoites 3. Multiply in intestine 4. Trophozoites encyst. 5. Infective cysts passed in feces. * * trophozoites passed in feces disintegrate. ENVIRONMENT 6. Feces containing infective cysts contaminate the environment.
  • 97. Clinical Manifestation  Asymptomatic  Severe failure to thrive and mal-absorption.  Children usually have diarrhea but abdominal distension and bloating are frequent.  Adults have : Abdominal cramps, diarrhea, Anorexia,nausea, malaise, Bloating, many Patients complain of sulphur testing (belching). By zinabu D 97
  • 98. Diagnosis Stool examination:  Cyst :Diagnostic stage  Trophozoite :Rx in stage Treatment First Lline  Tinidazole, single oral dose of 2g  For children, 50-75mg/kg as a single dose Alternative  Metronidazole, 250-500mg P.O., TID for five days By zinabu D 98
  • 99. Prevention and control Good personal hygiene, and handwashing before food and following toilet use Sanitary disposal of feces Protection of public water supply from contamination of feces Case treatment Safe water supply By zinabu D 99
  • 100. Cholera An acute illness caused by an enterotoxin elaborated by vibrio cholerae. Infectious agent  Vibrio cholerae Epidemiology Occurrence: has made periodic outbreaks in different parts of the world and given rise to pandemics. Endemic predominantly in children. By zinabu D 100
  • 101. Cont, Reservoir- Humans Mode of transmission- by ingestion of food or water directly or indirectly contaminated with feces or vomitus of infected person. Incubation period- from a few hours to 5 days, usually 2-3 days. By zinabu D 101
  • 102. Period of communicability For the duration of the stool positive stage, usually only a few days after recovery. Antibiotics shorten the period of communicability. Susceptibility and resistance Gastric Achlorhydria increases risk of illness. Breast-fed infants are protected. By zinabu D 102
  • 103. Clinical Manifestation  Abrupt painless watery diarrhea; the diarrhea looks like rice water.  In severe cases, several liters of liquid may be lost in few hours leading to shock.  Severely ill patients are :  Cyanotic,  Have sunken eyes and cheeks,  Scaphoid abdomen, poor skin turgor, and  Thready or absent pulse.  Loss of fluid continues for 1-7 days By zinabu D 103
  • 104. Diagnosis Based on clinical grounds Lab :  Culture (stool) confirmation By zinabu D 104
  • 105. Treatment Objectives:  Replace volume deficit and ongoing losses –  Decrease duration of diarrhoea . For dehydration in mild cases:  Give ORS, for children: < 2yrs: 50-100ml  2-10 years: 100-200ml after each loose stool. For severe cases  Ringer lactate IV infusion (alternatively Normal saline) should be given 50-100ml/min until shock is reversed .  KCl solution 20-40mmol/litre may be added as required. By zinabu D 105
  • 106. Pharmacologic First line  Doxycycline, 100mg, P.O., BID for 3 days.  For children: 6mg/kg daily for 3 days.  Alternatives  Tetracycline, 500mg P.O., QID for 3-5 days Sulfamethoxazole+trimethoprim,  Children 6 weeks – 5 months: 100/20mg  Children 6 months – 5 yrs: 200/40mg  Children 6 – 12 yrs: 400/80mg BID for 5 days  Adults: 800mg/160mg P.O., BID for 5 days. OR Ciprofloxacin, 500mg P.O., BID, for 3-5 days By zinabu D 106
  • 107. Nursing care  Wear gown and glove.  Wash your hands.  Monitor output including stool output.  Protect the patient family by administering Tetracycline.  Health education By zinabu D 107
  • 108. Prevention and control  Case treatment  Safe disposal of human excreta and control of flies  Safe public water supply  Hand washing and sanitary handling of food  Control and management of contact cases By zinabu D 108
  • 109. Managing viral hepatitis An acute viral disease characterized by abrupt onset of:  Fever,malaise  Anorexia, nausea and  Abdominal discomfort followed within a few days by  Jaundice Infectious agent Type A, B, C, D & E virus Type :A is Epidemic hepatitis By zinabu D 109
  • 110. Epidemiology Occurrence: Worldwide distribution in sporadic and Epidemic forms. Infection is common where environmental Sanitation is poor and occurs at an early age. Reservoir- Humans. By zinabu D 110
  • 111. Mode of transmission Person to person by fecal-oral route. Through contaminated water and food contaminated byinfected food handlers. Incubation period: 15-55 days, average 28-30 days. By zinabu D 111
  • 112. Period of communicability High during the later half of the incubation period continuing for few days following onset of jaundice. Most cases are non-infectious following first week of jaundice. Susceptibility and resistance: General.Immunity following infection probably lasts for life. By zinabu D 112
  • 113. Clinical manifestation Abrupt onset of :  Fever, malaise  Anorexia, nausea and  Abdominal discomfort, followed in few days by jaundice. Complete recovery without sequel or recurrence as a rule. By zinabu D 113
  • 114. Diagnosis Based on clinical and epidemiological grounds Demonstration of IgM (IgM anti-HAV) in the serum of acutely or recently ill patients. By zinabu D 114
  • 115. Treatment Symptomatic:  Rest  High carbohydrate diet with low fat and protein By zinabu D 115
  • 116. Prevention and control  Public education about good sanitation and personal hygiene, with special emphasis on careful handwashing and sanitary disposal of feces.  Proper water treatment and distribution systems and sewage disposal.  Proper management of day care centers to minimize possibility of fecal-oral transmission.  HA vaccine for all travelers to intermediate or highly endemic areas.  Protection of day care centers’ employees by vaccine. By zinabu D 116
  • 117. Hepatitis B Inflammation of liver caused by hepatitis B virus (HBV). WHO estimates above 2 billion person infected world wide with HBV of which 350 million are chronically infected and 1 million die per year. Etiology Hepatitis B virus (HBV) Reservoir • Human By zinabu D 117
  • 118. Mode of transmission Blood born transmission  Sharing needles, toothbrush, razor blades, exposure to infected blood (transfusion), towels and close contact.  Sexual transmission: - saliva, semen & vaginal fluid during kissing and sexual intercourse. By zinabu D 118
  • 119. Cont, From mother to child: - at birth (mostly), during breast-feeding and intra-utero transmission.  No faeco- oral transmission.  No air borne transmission.  Urine is not infective unless it contains blood. N.B: HBV is highly transmitted through parental way than HIV /AIDS. By zinabu D 119
  • 120. Cont, Incubation period • 45 – 160 days Period of communicability Extends over the period of acute illness that means it may last from few years to lifetime. 10% of patients become carriers. By zinabu D 120
  • 121. Clinical manifestations  Anorexia, nausea & vomiting  Abdominal discomfort  Arthralgia and rash  Jaundice  Chronically infected individuals may develop hepatoma (liver cancer), cirrhosis or chronic liver disease By zinabu D 121
  • 122. Diagnosis Detection of hepatitis B surface antigen (HBSAG), which is present when the virus is in the blood in the acute stage & chronic carrier stage. By zinabu D 122
  • 123. Treatment Drugs used in the treatment of hepatitis B include;  Adefovir dipivoxil  Interferon alfa- 2b,  Pegylated interferon alfa- 2a,  Lamivudine  Entecavir Liver transplants may be beneficial to infected patients, but the virus remains in the body after transplantation surgery and may eventually attack the new liver.  Alcohol is strictly for bidden because it increases the risk of cirrhosis. By zinabu D 123
  • 124. Feces Mainly in Soil The diseases in this category are mainly transmitted through :  Fecal contamination of soil. These infections are acquired through man’s exposure to focally contaminated soil. By zinabu D 124
  • 125. Ascariasis A helminthic infection of the small intestine generally associated with few or no symptoms Infectious agent Ascaris lumbricoides. Epidemiology Occurrence: The most common parasite of humans wheresanitation is poor. School children (5-10 years of age) are most affected. Highly prevalent in moist tropical countries 125
  • 126. Cont, Reservoir: Humans ascarid eggs in soil. Mode of transmission:  Ingestion of infective eggs from soil contaminated with human feces or uncooked Produce contaminated with soil containing infective eggs but not directly from person to person or from fresh feces. By zinabu D 126
  • 127. Cont, Incubation period- 4-8 weeks Period of communicability: As long as mature fertilized female worms live in the intestine. Usual life span of the adult worm is 12 months. By zinabu D 127
  • 128. Cont, Susceptibility and resistance: Is general By zinabu D 128
  • 129. Life Cycle • . By zinabu D 129 TRANSMISSION 1.Infective eggs ingested in food or from contaminated hands HUMAN HOST 2. Larvae hatch.Migrate through liver and lungs. 3. Pass up trachea and are swallowed 4. Become mature worms in small intestine 5. Eggs produced and passed in feces. ENVIRONMENT 6. Eggs become infective (embryonated) in soil in 30-40 days. 7. Infective eggs contaminate theenvironment.
  • 130. Clinical Manifestation Most infections go unnoticed until large worm is passed in feces and occasionally the mouth and nose. Migrant larvae may cause:  Itching, wheezing  Dyspnea,fever and  productive cough with bloody sputum may occur. By zinabu D 130
  • 131. Cont, Abdominal pain may arise from intestinal or duct (biliary,pancreatic) obstruction. Serious complications include:  Bowel obstruction due to knotted/intertwined worms. By zinabu D 131
  • 132. Diagnosis  Microscopic identification of eggs in a stool sample  Adult worms passed from anus, mouth or nose. By zinabu D 132
  • 133. Treatment First line:  Albendazole, 400mg P.O. as a single dose, for children: 1 – 2 years, 200mg as a single dose.  Mebendazole, 100mg P.O.BID for 3 days or 500mg, once Alternative (pregnant women) Pyrantel pamoate, 700mg P.O as a single dose By zinabu D 133
  • 134. Prevention and control  Treatment of cases  Sanitary disposal of feces  Prevent soil contamination in areas where children play  Promote good personal hygiene(handwashing). By zinabu D 134
  • 135. Trichuriasis A nematode infection of the large intestine, usually asymptomatic in nature. Infectious agent Trichuris trichuria (whip worm) Found in (adult) caecum and vermiform appendix Epidemiology Occurrence: Worldwide, especially in warm moist regions. Common in children 3-11 years of age. By zinabu D 135
  • 136. Cont, Reservoir- Humans Mode of transmission: Indirect, particularly through pica or ingestion of contaminated vegetables. Incubation period: • Indefinite Period of communicability:  Several years in untreated carriers. Susceptibility and resistance: Is universal By zinabu D 136
  • 137. Life Cycle • . By zinabu D 137 TRANSMISSION 1. Infective eggs ingested in food or from contaminated hands HUMAN HOST 2. Larvae hatch. Develop in small intestine. Migrate to caecum. 3. Become mature worms. 4. Eggs produced and passed in feces. ENVIRONMENT