The document provides an overview of communicable diseases, including their definitions, transmission methods, and common terms associated with them. It details the chain of disease transmission involving infectious agents, reservoirs, portals of exit and entry, and susceptible hosts, along with preventive measures and levels of prevention. Specific examples of diseases such as typhoid fever and the fecal-oral transmission route are also discussed.

1. By zinabu D 1

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:
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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.
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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.
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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
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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:
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15. Chain of diseases transmission
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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.)
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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.
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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
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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
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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.
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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.
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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.
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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.
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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.
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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
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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
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32. Cont..
Active immunity:
Acquired following actual infection or
immunization.
Passive immunity:
pre-formed antibodies given to the host.
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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.
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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.
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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
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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.
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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.
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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.
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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
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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)
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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.
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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
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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.
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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.
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45. Cont..
C. Reservoir in non-living things:
Possible to limit man’s exposure to the affected
area (e.g. Soil, water, forest, etc.).
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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
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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.)
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48. By zinabu D 48

49. UNIT TWO
FECO-ORAL TRANSMITED
DISEASES
By zinabu D 49

50. INTRODUCTION
 Causative agents are excreted in the stools
of infected persons.
 The portal of entry for these diseases is the
mouth.
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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.
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52. By zinabu D 52

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
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55. TYPHOID FEVER
A systemic infectious disease characterized by high
continuous fever, malaise & involvement of
Lymphoid tissues.
Etiology:
 Salmonella typhi
 Salmonella enteritidis
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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).
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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.
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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.
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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.
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60. Susceptibility And Resistance
 Susceptibility is general and increased in
individuals with gastric achlorhydria or those
who are HIV positive.
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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.
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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.
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63. Third week
 Patient continues to be febrile and increasingly
exhausted.
 If no complications occur, patient begins to
improve and temperature decreases gradually.
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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.
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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.
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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.
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82. Diagnosis
Based on clinical grounds
Stool microscopy (presence of pus cells)
Stool culture confirms the diagnosis
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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
6. Eggs become infective
(embryonated) in soil after 3weeks.
7. Infective eggs contaminate the
environment

138. 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

139. 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

140. 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

141. Entrobiasis
A common intestinal helminthic infection that is
often asymptomatic.
Infectious agent
 Entrobius vermicularis
(Oxyuriasis, pinworm infection)
By zinabu D 141

142. 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

143. 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

144. 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

145. 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

146. Clinical manifestation
 Perianal itching,
 Disturbed sleep, irritability and
some times secondary infection of the scratched
skin.
By zinabu D 146

147. 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

148. 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

149. 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

150. Cont
Reservoir- Human
Mode of transmission- Infective (filariform)
larvae penetrate the skin and enter the venous
circulation.
By zinabu D 150

151. 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

152. Cont,
Susceptibility and resistance: is universal.
Patients with AIDS or on immuno-suppressive
medication are at risk of dissemination.
By zinabu D 152

153. 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

154. 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

155. 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

156. Prevention and control
 Proper disposal of human excreta (feces)
 Personal hygiene including use of footwear.
 Case treatment.
By zinabu D 156

157. 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

158. 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

159. 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

160. 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

161. 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.

162. 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

163. 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

164. 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

165. Prevention and control
 Sanitary disposal of feces
 Wearing of shoes
 Case treatment.
By zinabu D 165

166. 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

167. 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

168. 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

169. 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

170. 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

171. 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

172. 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

173. 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

174. 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

175. 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

176. 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

177. 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

178. Diagnosis
 History of residence in an endemic area along
with association with canines
 Sonography and CT scan
 Serologic test
By zinabu D 178

179. 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

180. 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

181. 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

182. By zinabu D 182

183. CHAPTER 3
AIR-BORNE
DISEASES
Zinabu D(Bsc)

184. 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.

185. 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.

186. 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.

187. 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.

188. 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.

189. 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.

190. 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.

191. 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.

192. 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.

193. Clinical Manifestation
Coryza, sneezing, lacrimation, pharyngeal or
nasal irritation, chills and malaise dry or painful
throat.
Diagnosis
Based on clinical grounds

194. Treatment
No effective treatment but supportive measures
Like:
 Bed rest
 Steam inhalation
 High fluid intake
 Anti pain
 Balanced diet intake

195. 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

196. 2.Measles
An acute highly communicable viral disease
Infectious agent
Measles virus

197. 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.

198. 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.

199. 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.

200. 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.

201. 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.

202. Cont,
Diagnosis
Based on clinical and epidemiological grounds
Treatment
 No specific treatment
 Treatment of complications
 Vitamin A provision

203. Cont,
Nursing care
 Advise patient to have bed rest.
 Relief of fever.
 Provision of non-irritant small frequent diet.
 Shorten the fingernails.

204. 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.

205. 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.

206. Cont,
Mode of transmission- Airborne spread
predominates among crowded populations in
closed places such as school buses.
Incubation period- short, usually 1-3 days

207. 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.

208. 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

209. Treatment
Same as common cold, namely:
Anti-pain and antipyretic
High fluid intake
Bed rest
Balanced diet intake

210. 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

211. 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

212. 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.

213. 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.

214. 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.

215. 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.

216. 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.

217. Diagnosis
Based on clinical and epidemiological grounds
Bacteriologic examination of discharges from
lesions.

218. 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.

219. 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.

220. 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.

221. 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.

222. 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.

223. Cont,
Susceptibility and resistance:
Susceptibility to non immunized individuals is
universal. One attack usually confers
prolonged immunity but may not be lifelong.

224. 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

225. 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.

226. Cont,
III.Convalescent phase
 The cough may diminish slowly or may last
long time.
 After improvement the disease may recur.

227. 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

228. 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),

229. 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.

230. 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.

231. Cont,
Reservoir- Humans :
Pneumococci are usually found in the
URT of healthy people throughout the world.

232. 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.

233. 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.

234. 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.

235. 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.

236. 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)

237. 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

238. 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.

239. 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.

240. 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.

241. 7.Meningococcal Meningitis
What is meningitis?

242. 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.

243. Cont,

244. 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!

245. 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

246. 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.

247. 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

248. 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

249. 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%

250. 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

251. Cont,

252. 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

253. 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.

254. Cont,

255. 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

256. 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.

257. lumbar puncture

258. Contraindications to Lumbar Puncture
 Respiratory distress (positioning)
  ICP reported to increase risk of herniation
 Cellulitis at area of tap
 Bleeding disorder

259. 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

260. Cont,

261. 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

262. 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

263. 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

264. 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

265. Cont,
Older people:
 Lethargy
 Recurring headaches
 Difficulty in concentration
 Short-term memory loss
 Balance problems
 Depression

266. Serious complications
I. Brain damage
I. Epilepsy
II. Changes in eye sight

267. Nursing care
 Maintain fluid balance (input and output)
 Maintain body temperature to normal
 Timely administration of antibiotics
 Monitor vital signs.

268. 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.

269. 8.Tuberculosis

270. 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.

271. Cont,
Infectious agent
 Mycobacterium tuberculosis- human tubercle
bacilli (commonest cause)
 Mycobacterium bovis- cattle and man infection
 Mycobacterium avium- infection in birds and man.

272. 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%).

273. 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.

274. 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.

275. 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

276. 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

277. 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.

278. 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.

279. 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).

280. 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.

281. 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.

282. 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

283. 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

284. 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

285. 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.

286. 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

287. 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.

288. 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.

289. 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.

290. 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.

291. 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

292. Intestinal TB
Loss of weight and appetite
Abdominal pain, diarrhea and constipation
Mass in the abdomen
Fluid in the abdominal cavity (ascites)

293. 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.

294. 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.

295. 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

296. 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

297. 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

298. 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.

299. 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.

300. 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.

301. 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.

302. 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).

303. Treatment
 Streptomycin (s) daily IM injection
 Ethambutol(E)
 Rifampin (R)
 Isoniazid (H)
 Pyrazinamide (Z)

304. 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

305. 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

306. Cont,

307. 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.

308. 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.

309. 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

310. Leprosy (Hansen’s disease)
A chronic bacterial disease of the skin, peripheral
nerves and,in lepromatous patients, the upper
airway.
Infectious agent
Mycobacterium leprae

311. 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

312. 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.

313. 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.

314. 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.

315. 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.

316. Tuberculoid (Paucibacillary form)
Skin lesions are single or few, sharply
demarcated, anesthetic or hyperesthetic and
bilaterally symmetrical.
Peripheral nerve involvement tends to be severe.

317. 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.

318. 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.

319. 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.

320. 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

321. 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

322. 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.

323. UNIT FOUR
Manage a patient
with arthropod
borne disease
323
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324. 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
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325. 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
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326. Common vector borne disease includes
 Malaria
 Flariasis
 Endemic typhus
 Relapsing fever
 Schistosomiasis
 Guinea worm
326
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327. 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

328. 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
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329. 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
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330. 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
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331. Mode of transmission
By the bite of an infective female anopheles
mosquito
Blood transfusion
Hypodermic needles
Organ transplantation and mother to fetus
331
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332. 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
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333. 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
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334. 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

335. Cont,
Specific factors
–This is a humoral and cell mediated
immunity that is species and strain specific,
and hard-won after repeated infection
335
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336. Life cycle
.
TRANSMISSION
1. Sporozoites inoculated when Anopheles
mosquito takes a blood meal.
HUMAN HOST
2. Sporozoites infect liver cells. Multiplyby
schizogony.
Note: some sporozoites of P.vivax and p.ovale
become
dormant hypnozoites in liver. Become active after
several months.
3. Liver schizonts rupture. Merozoites enter red cells,
become trophozites.Multiply by schizogony.*
* with P. falciparum, schizogony occurs in capillaries
of body organs.
4. Schizonts rupture. Merozoites infect new red cells.
5. Some merozoites develop into male and female
gametocytes.
MOSQUITO
6. gametocytes ingested by
mosquito.
7. Male and female gametes
fuse. Zygote oocyst in
stomach wall.
8. Sporozoites form in oocyst.
9. Oocyst ruptures.
Sporozoites reach salivary
glands of mosquito
336
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337. Clinical feature: uncomplicated malaria
 Fever, Chills, Rigors, Sweating, Severe
Headache, Generalized body and joint pain
 Nausea and or vomiting, Loss of appetite,
Abdominal pain (especially in children)
 Irritability and refusal to feed (in infants), flu-
like symptoms, fever above 38°C
 Splenomegaly, Pallor
337
Zinabu D

338. Complicated P. Falciparum malaria
 Inability to take in fluids (or breast milk in children),
Repeated profuse vomiting,
 Haemoglobinuria(Dark or 'cola-coloured' urine), Passing of
very little urine
 Difficulty in breathing, Generalized weakness, inability to
walk or sit without assistance
 Repeated generalized convulsions
 Altered consciousness, confusion, delirium, coma
 Tachypnea, respiratory distress and/or cyanosis
338
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339. Cont,
 Hypoglycemia
 Severe anaemia (Hb < 6 g/dL)
 Hyperpyrexia (axillary temperature >38.5°C)
 Circulatory collapse or shock (cold limbs, weak
rapid pulse)
 Spontaneous unexplained heavy bleeding
(disseminated intravascular coagulation)
339
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340. Diagnosis
Clinical manifestation and epidemiological
grounds
 Blood film for hemoparasite(thin & thick)
 Rapid diagnostic tests (RDT)-if microscopy
is unavailable
340
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341. Treatment of malaria
341
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342. Objectives of treatment
 Treat the patient and restore quality of life and
productivity
 Prevent uncomplicated malaria from progressing
to severe and fatal illness
 Prevent death from malaria complication
 Prevent the development and transmission of
medicine resistance
 Decrease malaria transmission to others
342
Zinabu D

343. Treatment of uncomplicated P. Falciparum
malaria
First line
 Artemether + Lumefantrine, 20mg + 120mg in
a fixed dose combination
Alternative
 Quinine dihydrochloride, 10mg quinine
sulphate salt/kg TID for 7 days
343
Zinabu D

344. Dose regimens of artemether-lumfantrine
Weight (KG) AGE DOSE
5-14KG
From 4 months to 2
years
1 tablet bid for 3 days
15-24KG
From 3 years to 7 years 2 tablets bid for 3 days
25-34KG
From 8 years to 10 years 3 tablets bid for 3 days
>34KG
10 years & above 4 tablets bid for 3 days
344
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345. Treatment of uncomplicated P. Vivax malaria
First line
 Chloroquine phosphate, 1 g, then 500mg in 6 hours followed by
500mg P.O., QD for 2 days
Followed by
 Primaquine, 15mg base P.O., QID for 14 days.
Alternatives
 Artemether + Lumefantrine, 20mg + 120mg in a fixed dose
combination OR
 Quinine dihydrochloride, 10mg quinine sulphate salt/kg TID for 7
days
345
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346. Treatment of Severe and complicated
P. falciparum malaria
First line
 Artesunate, 2.4mg/Kg IV or IM given on
admission (time = 0), then repeat at 12 hours, and
24 hours, then once a day for up to 5 days.
Alternatives
 Artemether, IM 3.2mg/kg loading dose on the
first day followed by 1.6mg/kg daily for five days
346
Zinabu D

347. Treatment of Severe and complicated
P. falciparum malaria
Quinine dihydrochloride:
Loading dose: 20mg/kg in 500ml of isotonic
saline or 5% dextrose over 4 hours (4ml/minute).
The pediatric dose is the same but the fluid
10ml/kg replacement must be based on body
weight.
347
Zinabu D

348. Cont,
Maintenance dose:
should be given 8 hours after the loading dose at
a dose of 10mg /kg and it should be given 8
hourly diluted in 500 ml of isotonic saline or 5%
dextrose over 4 hours
348
Zinabu D

349. Prevention and control
Chemoprophylaxis
 Those who traveling to endemic areas
 Under-five children and pregnant mothers
Vector control
 Avoiding mosquito breeding sites
 Chemicals
 Personal protection against mosquito bite (use of bed
nets, etc.)
349
Zinabu D

350. 2.Filariasis
 A disease caused by the reaction of the body to
the presence of worms in the lymphatic system
 It results from infection with vector borne
tissue-dwelling worm called filarae.
350
Zinabu D

351. Infectious agent:
Three species of lymphatic dwelling filarial worms:
I. Wucheriria bancrofti (vectors are culex,
Anopheles and Aedes species)
II. Brugia malayi (vector is mansonia species)
III. Brugia timori (vector is Anopheles)
 Causes lymphatic Flariasis in humans
351
Zinabu D

352. Epidemiology
Widely prevalent in tropical and subtropical areas of
Africa, Asia, Pacific Region, Central and South
America
Found in Gambella region (western Ethiopia)
Particularly endemic in areas of hot and humid
climate.
It is estimated that at least 128 million people are
infected globally.
352
Zinabu D

353. Reservoir
 Humans are definitive hosts.
Mode of transmission
 By bite of mosquito harboring infective larvae
353
Zinabu D

354. Life cycle
.
TRANSMISSION
1. Infective larvae penetrate skin
when a mosquito takes a blood
meal.
HUMAN HOST*
2. Larvae become adult worms in
the lymphatics.
3. Females produce sheathed
Microfilariae which pass in to
blood.* Animal hosts may be
important for B. Malayi.
MOSQUITO
4. Microfilariae ingested
by mosquito.
5. Microfilariae lose
sheath.Develop into
infective larvae
in thoracic muscles.
6. Infective larvae
(sheathed) migrate to
mouth parts.
354
Zinabu D

355. Incubation period
One month, while allergic inflammatory
manifestations may appear.
355
Zinabu D

356. Period of communicability-
 Humans may infect mosquitoes when microfilariae are
present in the peripheral blood
 Microfilaremia may persists for 5-10 years or longer
 The mosquito becomes infective about 12-14 days after an
infective blood meal
Susceptibility and resistance
 Universal. Susceptibility to infection is probable
356
Zinabu D

357. Clinical Manifestation
 The presence of worms in the lymph vessels
gives rise to a foreign-body reaction
 After the death of the worm, more proteins are
released; the reaction then is even more severe
357
Zinabu D

358. Cont,
Three phases may be distinguished
Acute phase:
 Starts within a few months after infection
 Lymphadenopathy and Fever
 Eosinophilia
 Microfilariae are not demonstrable in the peripheral blood
because the worms are not yet mature
 The acute phase is mainly due to a hypersensitivity reaction
358
Zinabu D

359. Subacute phase:
 This occurs after about one year following acute phases
 Worms are matured and microfilariae are present in the
peripheral blood
 Reactions to the adult worms cause attacks of fever with
lymphangitis, funiculitis or Epididymitis
 Recurrent attacks will sooner or later lead to hydrocele
 Lesions caused by microfilariae are less common and are
associated with hyper eosinophilia and lung symptoms
(tropical pulmonary eosinophilia syndrome). 359
Zinabu D

360. Chronic phase:
 After many years of repeated attacks, lymph glands
and lymph vessels become obstructed; as a result
lymph edema develops
 Lymph edema most commonly seen in the legs or
scrotum (elephantiasis) but may also be present in
vulva, breasts, or arms
 Since the adult worms have usually died,
microfilariae are not seen in the blood
360
Zinabu D

361. Filariasis…
361
Zinabu D

362. Scrotum
362
Zinabu D

363. Cont
Gross scrotal enlargement or
wheelbarrow scrotum 363
Zinabu D

364. Penis
364
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365. Leg
365
Zinabu D

366. Arm
366
Zinabu D

367. Breast
367
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368. N:B
 Studies showed that elephantiasis of the lower legs is not
encountered in Ethiopia.
 But there is elephantiasis of the foot called the big foot
disease (elephantiasis of lower leg) as a result of
accumulation of silica and other minerals in the leg
(lymphatics) mostly occurring in bare-footed individuals.
 This big foot disease is named podoconiosis, which is
common in the eastern high lands of Ethiopia (Wolayita,
Gojjam, Gondar, Gedeo, Sidamo, etc.)
368
Zinabu D

369. 369
Diagnosis
 Clinical and epidemiological grounds
 Obstructive signs with history and travel to and
residence in endemic areas
 Best established by identifying microfilariae in the
peripheral blood (blood film)
 Mazoti test (by adminstering Single dose of
Diethylcarbamazin Citrate (DEC) causes the sequestered
microfilaria to emerge to blood 45-60 minutes later.
Zinabu D

370. Cont.
Before taking blood sample one should know
the periodicity of microfilariae that is,
microfilariae appear in the peripheral blood
during the night (nocturnal) in most parts of
the world and during day (diurnal) in the South
Pacific region
370
Zinabu D

371. Treatment
 Diethyl carbamazin Citrate (DEC) results in
rapid disappearance of most microfilariae from
blood but may not destroy the adult worm.
Because of this, we need to repeat DEC
annually for some years.
 Refer the patient for surgical treatment of
hydrocele
371
Zinabu D

372. Prevention and control
 Reducing the vector population
 Mass and selective treatment
 Personal protection against mosquito bite.
372
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373. 3.Schistosomiasis
It is a blood fluke (trematode) infection with adult worms
living within mesenteric or vesicle veins of the host over a
life span of many years.
Infectious agent
 Schistosoma mansoni
 Schistosoma Japonicum
 Schistosoma Hematobium
Most prevalent species in Africa are S. mansoni and S.
hematobium.
373
Zinabu D

374. Epidemiology
 S. mansoni is found in South America, Caribbean
Islands, Africa and the Middle East
 S. hematobium is found in Africa and the Middle East.
 S. Japonicum is found in the far East
 The disease occurs worldwide and 2 million people
are expected to be infected; however, most infected
individuals show few or no signs and symptoms, and
only a small minority develop significant disease
374
Zinabu D

375. Reservoir
 The principal reservoir for S. mansoni, and S.
haematobium is man
 Other animals, like dog, cat, pig, cattle, water buffalo,
horse and wild rodents, are hosts for S. japonicum
Mode of transmission
Infection is acquired from water containing free-
swimming larval forms (cercariae) that have developed in
snails
375
Zinabu D

376. Incubation period
 Acute systemic manifestations (katayama fever) may
occur in primary infections 2-6 weeks after exposure,
immediately before and during initial egg deposition
 The infection in humans can persist up to 10 years
 Snails release cercariae as long as they live (from several
weeks to 3 months).
Susceptibility and resistance
 Susceptibility is universal.
 Resistance is poorly defined.
376
Zinabu D

377. Life cycle
• .
Zinabu D 377
TRANSMISSION
1. Cercariae penetrate skin when
person in contact with contaminated
water
HUMAN HOST*
2. Cercariae I Schistosomula.Migrate through lungs
and liver.
3. Become mature flukes inportal venous system.
Flukes pair.
4. Migrate to veins of lower large intestine (S.
haematobium to veins of bladder)
5. Eggs laid in venules. Burrow through into
intestine (eggs of S. haematobium into bladder)
6. Eggs passed in feces. (S.haematobium in urine).
*S. japonicum also infects animals.
FRESH WATER
7. Eggs reach water.
Miracidia hatch
Snail host
8. Miracidia penetrate snail.
Become sporocysts and
multiply (2 generations).
Sporocysts Î cercariae.
9. Cercariae leave snail.
(S.Japonicum attaches to
water vegetation).

378. Zinabu D 378

379. Clinical Manifestation
The stages of schistosomiasis are:
I. Invasion
II. Maturation
III. Established infection and
IV. Late stage
379
Zinabu D

380. Cont,
I. Invasion stage
– Cercariae penetrate skin
– Cercarial dermatitis with itching papules and local
edema
– Cercariae remain in skin for 5 days before they
enter the lymphatic system and reach the liver.
380
Zinabu D

381. II.Maturation
 Schistosoma mature in the liver.
 Fever, eosinophilia, abdominal pain and transient
generalized urticaria (known as katayama syndrome)
 Worms descend the portal vein. S. manson; migrates
to mesenteric veins in the intestinal wall and S.
haematobium to bladder plexus.
 This stage may be diagnosed as clinical malaria or
may pass unnoticed.
381
Zinabu D

382. III.Established infection
 This is a stage of egg production and eggs reach to the
lumen of bladder and bowel.
 Some eggs penetrate the tissue, reach the bladder and
intestinal wall are discharged with urine and feces.
 Eggs that could not penetrate the tissue are carried
with blood to the liver and lungs.
382
Zinabu D

383. Cont,
 Other eggs that fail to reach the lumen of the
bladder or bowel provoke an inflammatory reaction.
 The inflammatory reaction, resulting in fibrosis,
causes signs and symptoms of schistosomiasis.
 Sign of colitis with bloody diarrhea and cramps in
S. mansoni infection. Terminal hematuria and
dysuria in S. haematobium infection.
383
Zinabu D

384. IV.Late stage
 This is the stage of fibrosis, which occurs where there are
eggs in the tissues.
Around the bladder this may result in:
 Stricture of urethra leading to urine retention or fistula.
 Dilatation of ureters (hydroureter) and kidney
(hydronephrosis) possibly leading to kidney failure
 Calcification of bladder.
384
Zinabu D

385. Cont,
 In the liver portal hypertension leads to
hypersplenism and anemia, eosophageal varices
and bleeding.
 In the lungs fibrosis results in pulmonary
hypertension, which leads to congestive cardiac
failure
385
Zinabu D

386. Diagnosis
 Demonstration of ova in urine or feces,
 Biopsy of urine and feces are repeatedly negative
(rectal snip, liver biopsy, bladder biopsy).
Treatment
 Praziquantel and oxamniquine are the drugs of
choice but in
 Africa praziquantel is best because of resistance
strain of oxamniquine.
386
Zinabu D

387. Prevention and control
 Treatment of cases
 Intermittent irrigation
 Drainage of water bodies
 Clearing of vegetation in water bodies to deprive
snails of food and resting place
 Flooding
 Straightening and deepening margins of water
bodies
 Educating the public about the mode of
transmission and ways of prevention
 Proper disposal of human feces and urine
 Avoid swimming in water bodies known to have
the infection
 Use rubber boots to prevent exposure to
contaminated water.
387
Zinabu D

388. 388
4.Guinea Worm Infection
 An infection of the subcutaneous and deeper tissues by
large nematode.
Infections agent
 Dracunculus medinensis, a nematode
Reservoir- Humans
Zinabu D

389. Cont,
Zinabu D 389

390. Epidemiology
 In Africa (16 countries south of the Sahara)
and in Asia (India and Yemen) especially in
regions with dry climates
 Local prevalence varies greatly
 In some locales, nearly all inhabitants are
infected, in others, few, mainly young adults
390
Zinabu D

391. Mode of transmission
 Larvae discharged by the female worm into
stagnant fresh water are ingested by minute
crustacean copepods, Cyclops or water fleas
 In about 2 weeks the larvae develop into the
infective stage
 People swallow the infected copepods in drinking
water from infested step wells and ponds.
391
Zinabu D

392. Cont,
 The larvae are liberated in the stomach, cross the
duodenal wall, migrate through the viscera and
become adults.
 The female, after mating, grows and develops to full
maturity, then migrates to the subcutaneous tissues
(most frequently of the legs).
392
Zinabu D

393. Cont.
Incubation period- About 12 months
Period of communicability
 From rupture of vesicle until larvae have been completely
evacuated from the uterus of the gravid worm, usually 2-3
weeks
 In water, the larvae are infective for the copepods for about 5
days
 After ingestion by copepods, the larvae become infective for
people after 12-14 days at temperatures >25oc and remain
infective in the copepods for about 3 weeks.
393
Zinabu D

394. Cont,
Susceptibility and resistance
 Susceptibility is universal.
 No acquired immunity; multiple and repeated
infections may occur in the same person
394
Zinabu D

395. Clinical Manifestation
 Few or no clinical manifestations are evident until just
before the blister forms.
 Fever and generalized allergic symptoms, including
periorbital edema, wheezing, and urticaria.
 The emergence of the worm is associated with local
pain and swelling.
 When the blister ruptures, the adult worm releases
larva-rich fluid and this is associated with a relief of
symptoms.
 The shallow ulcer surrounding the emerging adult worm
heals over weeks to months.
Diagnosis
 Based on clinical and epidemiological grounds
395
Zinabu D

396. Treatment
 Gradual extraction of the worm by winding of a few
centimeters on a stick each day remains the common
and effective practice.
 Worms may be excised surgically.
 Administration of thiabendazole and mebedadazol
may relive symptoms but has no proven activity
against the worm
396
Zinabu D

397. Prevention and control
I. Provide health education programs in endemic
communities to covey three messages:
 The guinea-worm infection comes from their drinking water
 Villagers with blisters or ulcers should not enter any source of
drinking water and
 That drinking water should be filtered through fine mesh cloth
to remove copepods
II. Provision of safe drinking water
397
Zinabu D

398. 5.Endemic Typhus (Flea-borne typhus)
A rickettsial disease whose course resembles that
of louse borne typhus, but is milder
Infectious agent:
Rickettsia typhi (Rickettsia mooseri)
398
Zinabu D

399. Epidemiology
Worldwide, found in areas where people and rats
occupy the same buildings and where large numbers
of mice live. Occurs sporadically.
Reservoir:
Rats, mice and possibly other small animals.
Infection is maintained in nature by a rat-flea-rat cycle
where rats are reservoirs
399
Zinabu D

400. Mode of Transmission-
 Infective rat fleas defecate rickettsia while sucking
blood, contaminating the bite site and other fresh
skin wounds.
 An occasional case may follow inhalation of dried
infective flea feces.
400
Zinabu D

401. Pathogenesis
• Rickettsia is intracellular, gram-ve organism parasitize intestinal of
arthropods
• Rickettsia from the blood of a human case are ingested by a biting
louse and multiply in the gut of the insect
• Its faces are heavily infected
• Scratching of subsequent bite inoculate the organism
• It can also enter the body through rubbing the conjunctiva
membrane
• Infected lice may die from the disease
• It can transmit the rickettsia to other lice through ingestion of faces
Zinabu D 401

402. Cont,
• Trans ovarian (vertical transmission) doesn’t occur
• Infection is usually conveyed to human beings through the skin from
the excreta of arthropods
• The organism multiply in capillary endothelial cells
• It produce lesion of the skin, central nervous system, heart, lung,
kidney and skeletal muscles
• Endothelial proliferation associated to perivsular reaction
• It cause thrembosis and small haemorrhage
• Brain and cardiovascular systems are the affected areas.
Zinabu D 402

403. Cont,
Incubation period-
 From 1 to 2 weeks; commonly 12 days
Zinabu D 403

404. Period of communicability
Not directly transmitted from person to person.
Once infected, fleas remain so for life.
Susceptibility and resistance
Susceptibility is general. One attack confers
immunity.
404
Zinabu D

405. 405
Clinical Manifestation
 Prodromal symptoms of headache, myalgia, arthralgia,
nausea, and malaise developing 1 to 3 days before the
abrupt onset of chills and fever
 Nearly all patients experience nausea and vomiting
early in the illness
 The duration of untreated illness averages 12 days.
 Rash is present in only 13% of patients
 Pulmonary involvement: non-productive cough and
pneumonia
Zinabu D

406. Complication
Delirium
Epistaxis
Constipation and paralytic ileus may occur
In up to 50% of sever cases meningoencephalitis with
meningism, tinnitus followed by deafness, dysphrgia
Other problems include broachopneumonia supportive
parotitis or Otitis media, peripheral blood vessel
occlusion resulting in leg vein thrombosis
Myocarditis
Hypotension
Cariac failure
Zinabu D 406

407. Differential Diagnosis
Typhoid Fever
Measles
Viral haemorrhgic fever
Meningococcal septicaemia
Zinabu D 407

408. Diagnosis
 Epidemiological ground
 Weil-Felix test OX-19 and OX-2 strain
antibody
Treatment
 Doxycyclin or
 Chloramphenicol
Prevention and control
 Destroy rats from burrows and harborages.
 Use insecticides to abolish flea from living
quarters.
 Treatment of patients.
408
Zinabu D

409. 6.Relapsing Fever
 An acute infectious bacterial disease characterized
by alternating febrile periods (recurrent pyrexial
attacks)
Infectious agent
 Borrelia recurrentis- cause of louse-borne relapsing
fever
 Borrelia duttoni-cause of tick-borne relapsing fever
409
Zinabu D

410. Epidemiology
 Occurs in Asia, eastern Africa (Ethiopia and
Sudan), the highland areas of central Africa and
South America
 It occurs in epidemic form when it is spread by
lice and in endemic form when spread by ticks
410
Zinabu D

411. Reservoir
 Humans for Borrelia recurrentis
 Wild rodents and soft ticks through trans ovarian
transmission for tick borne relapsing fever
Mode of transmission
 vector-borne:- Acquired by crushing an infected
louse so that it contaminates the bite wound or an
abrasion of the skin.
411
Zinabu D

412. Incubation period-
 5-10 days usually 8 days.
Period of communicability-
 Louse becomes infective 4-5 days after
ingestion of blood from an infected person
and remains so for life (20-40 days)
412
Zinabu D

413. Cont,
Susceptibility and resistance
 Susceptibility is general.
 Duration and degree of immunity after
clinical attack are unknown; repeated
infection may occur.
413
Zinabu D

414. Clinical Manifestation
 Sudden onset of illness with chills, fever and
prostration, headache, mayalgia and arthralgia
 There may be nausea and vomiting, jaundice and liver
swelling
 After 4-5 days the temperature comes down, the patient
stays free for 8-12 days and then a relapse follows with
the same signs but less intense
 In untreated cases there may be up to ten relapses
414
Zinabu D

415. Diagnosis
 Clinical and epidemiological grounds
 Giemsa or Wright stain (blood film)
 Dark field microscopy of fresh blood.
Treatment
 Admit the patient.
 Open vein before administering penicillin.
 Administer 400,000-600,000 IU procaine penicillin IM stat
 Tetracycline during discharge for 3 days
 Chloramphenicol in infants and children can be used in place of
tetracycline. 415
Zinabu D

416. Nursing care
Maintain body temperature to normal.
Close vital sign monitoring for 3 hours after medication.
Check whether there is reaction or not and report.
Comfort the patient by providing antipain.
Shaving of hair, and delousing of clothes.
Prevention and control
Control of vectors (louse)
Personal hygiene
Health education about hygiene and modes of disease transmission
Delousing of patient’s clothes and his/her family
Chemotherapy of cases and Chemoprophylaxis for contacts.
416
Zinabu D

417. .
Thank you !!!
Zinabu D 417

418. 5/11/2024 418

419. Objectives
5/11/2024 419
At the end of this session the students will able to:-
Define STIs and Syndromic approach to manage STI
Recognize causative agents
Describe the epidemiology of STIs and risk factors.
Explain mode of transmission
Describe Clinical manifestation & incubation period
Discuss the ways & principles of prevention & control.
BY Zinabu Dawit(PBsc)

420. DEFINITION
5/11/2024 420
 It is an infection passed from person to person through
sexual contact(most common).
 Mother- to- child
I. During pregnancy (HIV, syphilis)
II. At delivery(Gonorrhea,chlamydia, genital
herpes and HIV)
III. Through breast feeding(HIV)
 Unsafe injections/contact with blood products(syphilis,
HIV and hepatitis) BY Zinabu Dawit(PBsc)

421. Epidemiology
5/11/2024 421
 According to WHO globally as many as 340 million new cases of
curable STI occur each year with the largest proportion in the
regions of south & south east Asia followed by the sub-Saharan
African countries and Latin American & Caribbean
countries(WHO,2001).
 There is little information on the incidence and prevalence of STIs
in Ethiopia, except for adult prevalence of HIV(3.5%) and
syphilis(2.7%) (MOH,2006)
BY Zinabu Dawit(PBsc)

422. Cont..
5/11/2024 422
 There are a number of factors that increases the risk
of transmission of STIs, including biological,
behavioral and socio-cultural factors.
 Prevalence tends to be higher in urban than rural.
 STI occur most frequently among females between
the 14-19,where as after the age of 19 it is slightly
more frequent among males.
BY Zinabu Dawit(PBsc)

423. Infectious agents
5/11/2024 423
 STIs are a major public health problem in all
countries, but are especially so in developing
countries.
 More than 30 bacterial, fungal, viral, protozoal
(trichomonias vaginalis )and parasitic( pubic lice)
pathogens are transmitted sexually.
BY Zinabu Dawit(PBsc)

424. 1.Bacterial infection
5/11/2024 424
BY Zinabu Dawit(PBsc)

425. 2.Viral infections
5/11/2024 425
BY Zinabu Dawit(PBsc)

426. Viral infections…
5/11/2024 426
 CMV (Human Cytomegalovirus):- saliva, venereal fluids,
blood, organ transplant, urine, pregnancy, childbirth, breast
milk
 Hepatitis B virus:-saliva, venereal fluids.
(Note: Hepatitis A and Hepatitis E are transmitted via
the fecal-oral route, Hepatitis C is rarely sexually
transmittable.
 Herpes simplex virus( type I&II) skin and mucosal,
transmissible with or without visible blisters.
BY Zinabu Dawit(PBsc)

427. 5/11/2024 427
Cont,
3. Fungal
 Candidiasis (yeast infection)
4. Parasites
 Crab louse or "pubic lice"
 Scabies (Sarcoptes scabiei)
5. Protozoal
– Trichomoniasis (Trichomonas vaginalis)

428. Other causes
5/11/2024 428
BY Zinabu Dawit(PBsc)

429. Mode of transmission
5/11/2024 429
 Person to person through sexual contact and mucosal
contact
 Factors affecting the transmission
1.Biological (age, sex& immune status)
Age:-
Young(immature and cervical ectopy) and sexually active
post menopausal women(atrophy and loss of elasticity of
the vagina ) are vulnerable.
BY Zinabu Dawit(PBsc)

430. Cont…
5/11/2024 430
Sex:-
 Infective agents enter the body most easily through a
mucosal surface such as the lining of the vagina, so a
women are more infected than men.
Immune status:-
 Certain STIs increase the risk of transmission of HIV.
 HIV in turn facilitates the transmission of STIs and
worsens the complications
BY Zinabu Dawit(PBsc)

431. Cont…
5/11/2024 431
2. Behavioral factors
 Changing sexual partner more frequently
Having more than one sexual partner
Having sex with casual partners, commercial sex
workers or their clients.
Use of alcohol or other drugs before or during sex.
BY Zinabu Dawit(PBsc)

432. Cont…
5/11/2024 432
3. Socio-cultural factors
Little decision making power of women over sexual
practices and choices
Women tend to economically dependent on their male
partners and are therefore more likely to tolerate men’s
risky behavior.
Sexual violence tends to be directed more towards women
by men.
BY Zinabu Dawit(PBsc)

433. Cont…
5/11/2024 433
 Early marriage to an adult male
 Permissive attitude is taken towards men
allowing them to have more than one sexual
partner.
 Harmful traditional practices (skin-piercing,
circumcision using shared items).
BY Zinabu Dawit(PBsc)

434. Incubation period
5/11/2024 434
 It differs with the specific causative agent
Syphilis : 10 days - 12 wks( usually 3 wks )
Chancroid : 3-14 days
Gonorrhoea: 2 -7 days
Chlamydia: 7 -14 days
LGV:3-30 days
Herpes genitalia:2 – 12 days
Candidiasis :variable.
Trichomoniasis :4 - 20 days, average 7days
BY Zinabu Dawit(PBsc)

435. Approaches to STIs management
5/11/2024 435
1. Classical Approach
I. Etiological approach
II. Clinical approach
 Etiological approach: uses laboratory tests to
identify the causative agent.
 Clinical approach: uses clinical experience to
identify symptoms which are typical for a
specific STI.
BY Zinabu Dawit(PBsc)

436. Cont…
5/11/2024 436
Advantages of etiologic approach
 Patient satisfaction
 Asymptomatic screening
 Important for syphilis case-finding in pregnant.
BY Zinabu Dawit(PBsc)

437. Disadvantage of Etiological approach
5/11/2024 437
 Requires skilled personnel and sophisticated
equipment
 Laboratory tests for diagnosis are expensive(E.g.
chlamydia trachomatis)and time-consuming.
 Treatment does not begin until the results are
obtained.
 Testing facilities are not available at the primary
health care level.
BY Zinabu Dawit(PBsc)

438. Disadvantage of clinical approach
5/11/2024 438
 Only accurate for 50% of STI cases.
 Mixed infections are common and the clinician
may diagnosis only one of them.
 Different STIs cause similar symptoms, so
clinician may pick the wrong to treat
 Miss-treated or untreated infections can lead to
complications and continued transmission.
BY Zinabu Dawit(PBsc)

439. 2. Syndrome approach
5/11/2024 439
 Syndrome is a group of symptoms that patients
describe, combined with classic signs the providers
observe during physical examination..
 A number of different organisms that causes STIs
give rise to limited number of syndrome.
 Giving treatment targeting all the locally known
pathogens which can cause the syndrome.
BY Zinabu Dawit(PBsc)

440. 5/11/2024 440
Cont,
 Developed by WHO
 Does not require laboratory tests
 Tested in many countries since 1970’s
 STIs grouped into 7 main categories,
according to symptoms and signs
BY Zinabu Dawit(PBsc)

441. Principles of syndrome management
5/11/2024 441
 Recognize the syndrome
 The syndrome could be caused by one or more of a
number of organisms
 Treat with a combination of drugs
 Drugs should cover the common organisms
potentially responsible for the syndrome
 Organisms must be sensitive to the drugs
BY Zinabu Dawit(PBsc)

442. The four steps in syndrome STIs management
5/11/2024 442
1. History taking and physical examination
2. Syndrome diagnosis and treatment, using
flow charts
3. Education and counseling on HIV testing
and safer sex, including condom promotion
and provision.
4. Management of sexual partner.
BY Zinabu Dawit(PBsc)

443. Advantage of syndrome approach
5/11/2024 443
 Treatment covers the most common organisms
potentially responsible for the syndrome
 Simple, rapid and inexpensive
 Complete care offered at first visit
 Patients are treated for possible mixed infections
BY Zinabu Dawit(PBsc)

444. Cont…
5/11/2024 444
 Can be used at all levels of the health system
 Accessible to a broad range of health workers
 Promotes standardization
 Avoids unnecessary referrals to hospitals
 Does not require laboratory tests
BY Zinabu Dawit(PBsc)

445. Cont…
5/11/2024 445
Disadvantages
 Asymptomatic infections are missed
 Overuse of drugs(Over-treatment): costs, side effects,
resistance
 Lack of acceptance by clinicians
BY Zinabu Dawit(PBsc)

446. Common STI Syndromes
5/11/2024 446
I. Urethral discharge
II. Abnormal Vaginal discharge
III. Genital ulcer
IV. Lower abdominal pain
V. Scrotal swelling
VI. Inguinal bubo
VII.Neonatal Conjunctivitis
BY Zinabu Dawit(PBsc)

447. SIGNS AND SYMPTOMS OF THE MAIN STIs SYNDROMES AND THEIR CAUESES
SYNDROME SYMPTOMS SIGN MOST COMMON CAUSES
1. Vaginal
discharge
 Unusual
vaginal
discharge
 vaginal itching
 Dysuria
 Dyspareunia
Abnormal vaginal
discharge
Vaginitis
Trichomoniasis,
candidiasis
Bacterial vaginosis
Gerdenella vaginalis
Cervicitis
 Gonorrhea
 Chlamydia
2. Urethral discharge  Urethral
discharge
 Dysuria
 Frequent
urination
 Urethral
discharge
(if necessary ask
patient to milk
urethra)
Gonorrhea
chlamydia
3. Genital ulcer  Genital sore  Genital ulcer Syphilis
Chancroid
Genital herpes
5/11/2024 447
BY Zinabu Dawit(PBsc)

448. Cont..
5/11/2024 448
4.Lower
abdominal
pain
 Lower
abdominal
pain
 Dyspareunia
Vaginal discharge
Lower abdominal
tenderness on
palpation
Temperature>380c
 Gonorrhea
 Chlamydia
 Mixed anaerobes
5. Scrotal
swelling
 Scrotal pain
and swelling
 Scrotal swelling  Gonorrhea
 Chlamydia
6. Inguinal
bubo
 Painful
enlarged
inguinal
lymph nodes
 Enlarged inguinal
lymph nodes
 Fluctuation
 Abscess or
fistulae
 LGV
 chancriod
7. Neonatal
conjunctivitis
 Swollen
eyelids
 Discharge
 Baby cannot
open eyes
 Oedema of the
eyelids
 Purulent
discharge
 Gonorrhea
 Chlamydia
BY Zinabu Dawit(PBsc)

449. GENITAL ULCER
5/11/2024 449
 The common ulcerative lesions of the genitalia in men
and women are:-
Primary syphilis(T.pallidum)(Hard chancre)
Genital herpes(HSV-2)
Chancroid (Haemophilus ducreyi) (soft chancre)
Lymphogranuloma venereum(LGV)( chlamydia
trachomatis serovars L1,L2 or L3.
Granuloma inguinale also known as Donovanosis,
caused by bacterium klebsiella granulomatis
BY Zinabu Dawit(PBsc)

450. Genital ulcer
5/11/2024 450
BY Zinabu Dawit(PBsc)

451. Genital warts, HPV infection, cervical cancer
5/11/2024 451
BY Zinabu Dawit(PBsc)

452. Genital Ulcer Syndrome
5/11/2024
452
Patient complains of genital ulcer
Take history & examine
Vesicles or recurrence
Treat for HSV,
Treat for syphilis if indicated
•Educate and counsel
•Promote and provide condoms
•Offer VCT
•Ask the patient to return in 7 days
Ulcers healed
Educate and counsel
Promote and provide condoms
Offer VCT
Partner management
Ulcers and sores
Treat for syphilis,
chancroid and HSV
•Educate
•Promote and
provide
condoms
•Offer VCT
Ulcers improving Refer
Continue treatment for further 07 days
No
No
Yes
Yes
Yes
Yes
No No
Patient complains of genital ulcer
Take history & examine
Vesicles or recurrence
Treat for HSV,
Treat for syphilis if indicated
•Educate and counsel
•Promote and provide condoms
•Offer VCT
•Ask the patient to return in 7 days
Ulcers healed
Educate and counsel
Promote and provide condoms
Offer VCT
Partner management
Ulcers and sores
Treat for syphilis,
chancroid and HSV
•Educate
•Promote and
provide
condoms
•Offer VCT
Ulcers improving Refer
Continue treatment for further 07 days
No
No
Yes
Yes
Yes
Yes
No No

453. Genital Ulcer Disease Treatment
5/11/2024
453
 Recommended treatment for non-vesicular genital ulcer
 Benzanthine penicilline 2.4 million units IM stat or
 Doxycycline 100 mg bid for 15 days plus Ciprofloxacin
500mg, po, bid for 3 days or
 Erythromycin 500 mg, po, QID for 7 days
 Recommended treatment for vesicular or recurrent genital ulcer
 Acyclovir 200 mg five times per day for 5 days, or
 Acyclovir 400 mg TID for 5 days
BY Zinabu Dawit(PBsc)

454. Cont
5/11/2024 454
Recommended treatment for vesicular, multiple first episode genital
ulcer.
 Acyclovir 400mgTID for 10 days/ 200mg five times per day for 10
days.
 Alternatives
For syphilis For chancroid For LVG
Procain penicillin Ceftriaxone Tetracycline
Benzylpencillin
Tetracycline
BY Zinabu Dawit(PBsc)

455. Urethral discharge
5/11/2024 455
 N. gonorrhea and C. trachomatis are generally
the most common cause.
 Trichomonas vaginalis is the 2nd most common
cause in Ethiopia, exceeds C.trachomatis and is
responsible for persistent or recurrent urethral
discharge.
 Mycoplasma genitalium and ureaplama
BY Zinabu Dawit(PBsc)

456. Cont…
5/11/2024 456
Sign and symptoms
 Large amount of purulent urethral discharge.
 Pruritis( burning sensation on urination)
 Dysuria
 Anal discharge and rectal bleeding (proctatis)
BY Zinabu Dawit(PBsc)

457. Urethral discharge
5/11/2024 457
BY Zinabu Dawit(PBsc)

458. milking penis
5/11/2024 458
BY Zinabu Dawit(PBsc)

459. Urethral Discharge Syndrome
5/11/2024
459 BY Zinabu Dawit(PBsc)

460. complains of urethral discharge or dysuria
Take history & Examine [Milk urethra if necessary]
Discharge present? Other
STIs?
No
Yes
Use appropriate flow chart
Yes
Urethral discharge
• Educate on RR
• Offer CTP
• Promote &
provide condoms
Treat for CT
•Educate on risk reduction
•Offer HCT
•Promote & provide condoms
• Partner management
• Advise to return in 7 days if symptoms persist
Figure 1
5/11/2024 460
BY Zinabu Dawit(PBsc)

461. Persistent or Recurrent Urethral
Discharge in Men
Take history
and examine
Does history
confirm reinfection
or poor compliance?
Treat for trichomonas
vaginalis
•Educate/counsel
•Promote and provide condoms
•Return in 7 days
Improved
Discharge confirmed
Patient complains of
persistent/ recurrent
urethral discharge or dysuria
Other STIs
present
Use appropriate
flow chart
Repeat
urethral discharge
treatment
Refer
•Educate/counsel
•Promote and provide condoms
• Offer VCT
Yes
No
No
Yes
Yes
•Educate/counsel
•Promote and
provide condoms
• Offer VCT
No
Yes
No
5/11/2024 461
BY Zinabu Dawit(PBsc)

462. Recommended Treatment for Urethral Discharge
and Burning on Urination
5/11/2024
Ciprofloxacin 500 mg po stat, or
Spectinomycin 2g IM stat
Plus
Doxycycline 100 mg po BID for 7 days, or
Tetracycline 500 mg po QID for 7 days, or
Erythromycin 500 mg po QID for 7 days
BY Zinabu Dawit(PBsc)

463. Recommended treatment for persistent
/recurrent urethral discharge
5/11/2024 463
Metronidazole 2mg single dose
Plus
Erythromycin base 500mg qid X7 days or
Erythromycin ethylsuccinate 800mg qid x 7days.
For infection with T. vaginalis
– Metronidazole 2mg PO stat , avoid alcohol while
taking.
BY Zinabu Dawit(PBsc)

464. Abnormal Vaginal Discharge
5/11/2024 464
• Common causes:
N. gonorrhea
Chlamydia trachomatis sexually acquired
Trichomonas vaginalis
Gardnerella vaginalis
Candida albicans endogenous infection
BY Zinabu Dawit(PBsc)

465. Differences Between Vaginitis and Cervicitis
5/11/2024 465
Vaginitis Cervicitis
Caused by trichomoniasis,
Candidiasis and bacterial
vaginosis
Caused by gonorrhea and
Chlamydia
 Most common cause of
vaginal discharge
Less common cause of
vaginal discharge
Easy to diagnose Difficult to diagnose
Treatment of partner not
necessary
Need to treat partner
BY Zinabu Dawit(PBsc)

466. vaginal discharge
5/11/2024 466
© Teaching-aids at low cost
BY Zinabu Dawit(PBsc)

467. 5/11/2024
467
Patient complains
of vaginal discharge or
vulval itching/ burning
Abnormal discharge present
Take history, examine patient
(external speculum and bimanual)
and assess risk
Lower abdominal tenderness
or cervical motion tenderness
Was risk assessment positive?
Is discharge from the cervix?
Vulval edema/curd like discharge
Erythema excoriation present
Treat for bacterial vaginosis
and trichomoniasis
Treat for chlamydia, gonorrhea,
bacterial vaginosis and trichomoniasis
Use flow chart for lower abdominal pain
Educate
Counsel
Promote and provide condoms
Offer VCT
Educate
Counsel
Promote and provide condoms
Offer VCT
Treat for
candida albicans
No
Yes
Yes
Yes
No
No
No
Yes
Vaginal
Discharge
BY Zinabu Dawit(PBsc)

468. Risk assessment:
5/11/2024 468
 Multiple sexual partners
 Recent unprotected sex
 Age < 25 yrs
 New partner
BY Zinabu Dawit(PBsc)

469. Recommended Treatment for
Vaginal Discharge
469
Metronidazole 500mg PO BID for 7
days
plus
Clotrimazole vaginal tabs 200mg at
bed time for 3 days
Ciprofloxacin 500mg PO stat or
Spectinomycin 2gm IM stat
plus
Doxycycline 100mg PO BID for 7
days
plus
Metronidazole 500mg BID for 10
days
Risk Assessment Negative for STI
Risk Assessment Positive for STI

470. Recommended regimens for pregnant women
5/11/2024 470
 Metrondazole use in first trimester pregnancy is not
recommended ,but lower dose or single dose rather
than a long course use when early treatment has
chance of preventing adverse pregnancy out comes.
 Metrondazole 2g po as single dose, if treatment is
imperative during the first trimester.
 Metrondazole 200/250mg TIDx 7days after 1st
trimester
BY Zinabu Dawit(PBsc)

471. Lower Abdominal Pain (PID)
5/11/2024 471
 PID is ascending infection of the upper genital
tract (cervix, uterus, tubes, ovaries or pelvic
cavity) and is associated with polymicrobial
organisms.
 The morbidity from PID causes a 7-10 fold
increase in ectopic pregnancy, chronic pelvic
pain and infertility(15-75%)
BY Zinabu Dawit(PBsc)

472. PID…
5/11/2024 472
Common etiologies
 Sexually transmitted:
I. Neisseria gonorrhea,
II. Chlamydia trachomatis
III. Mycoplasma hominis
 Others (non-STI):
I. Streptococci
II. E. coli
III. H. influenza
IV. IUCD/endometrial biopsy
BY Zinabu Dawit(PBsc)

473. Micro-organisms
originating in the
endocervix
Ascend into the
endometrium,
fallopian tubes, and
peritoneum causing
PID (endometritis,
salpingitis,
oophoritis,
peritonitis)
5/11/2024 473
BY Zinabu Dawit(PBsc)

474. Cont…
5/11/2024 474
Signs and symptoms
 Lower abdominal pain and lower abdominal
tenderness
 cervical motion tenderness
 Increased Vaginal discharge
 Pain during intercourse
 Painful urination
 Dysmenorrhea
BY Zinabu Dawit(PBsc)

475. Differential diagnosis
5/11/2024 475
 Acute appendicitis
 Ectopic pregnancy
 Endometriosis
 Acute hemorrhage from an ovarian cyst
 Septic incomplete abortion
 Cholecystitis
BY Zinabu Dawit(PBsc)

476. 5/11/2024
476
Lower Abdominal Pain
Patient complains of
lower abdominal pain
Take history including gynecological
And examine (abdominal and vaginal)
Any of the following present
•Missed overdue period
•Recent delivery/ abortion
•Miscarriage
•Abdominal guarding
•And/or rebound tenderness
•Abdominal mass
•Abnormal vaginal bleeding
Refer the patient for surgical or
gynecological opinion
and assessment
Before referral set up
an IV line and resuscitate
if required
Is there cervical excitation tenderness
Or lower abdominal tenderness
And vaginal discharge
Manage for PID
Review in three days
Continue treatment until completed
•Educate and counsel
•Offer VCT
•Promote and provide condom
•Ask patient to return if necessary
Patient has improved Refer patient
Manage
appropriately
Any other
illness found
Yes
No
Yes
Yes
No
No
Yes

477. Recommended Treatment for PID
Out patient Inpatient
Ciprofloxacin 500mg PO bid for
7 days, OR
Spectinomycin 2gm IM stat
plus
Doxycycline 100mg BID for 14
days
plus
Metronidazole 500mg BID for
14 days
Ceftriaxone 250mg IV BID, OR
Spectinomycin 2gm IM BID
plus
Doxycycline 100mg BID for 14
days
plus
Metronidazole 500mg BID for
14 days, OR Chloramphenicol
500mg IV QID
477

478. Scrotal Swelling
5/11/2024 478
 Common causes of scrotal swelling depends on age of patient.
– Age <35 yrs
-Neisseria gonorrhea
-Chlamydia trachomatis
– Age > 35yrs commonly caused by other organisms if the patient has not been
involved in unsafe sex.
-Mumps
-Onchocerciasis
-TB
-Inguinal hernia
-Testicular torsion
BY Zinabu Dawit(PBsc)

479. Cont…
5/11/2024 479
• Pre-pubertal children
- coliform
- Pseudomonas
- Mumps virus
BY Zinabu Dawit(PBsc)

480. 5/11/2024
480
Scrotal Swelling
Patient complains of
scrotal swelling or pain
Take history, examine,
offer HIV test
Scrotal swelling or
pain present?
History of trauma or testis
elevated or rotated?
or
Diagnosis in doubt?
Refer patient to
hospital
Signs of other
STI present?
Reassure patient, educate,
counsel, provide condoms.
Review if symptoms persist
Treat according to
appropriate flowchart
Treat for chlamydia
and gonorrhea.
Review in 7 days
Patient has improved? Complete treatment course,
reinforce education and counseling
Review if symptoms persist
Yes
Yes
No
Yes
No
No
Yes
No

481. Scrotal Swelling
Recommended Therapy
5/11/2024
481
 Ciprofloxacin 500mg PO stat,
or
 Spectinomycin 2gm IM stat
plus
 Doxycycline 100mg PO BID for 7 days, or
 Tetracycline 500mg BID for 7 days
BY Zinabu Dawit(PBsc)

482. Inguinal Bubo
5/11/2024
482
 Painful, fluctuant Swelling of inguinal lymph nodes
in groin.
Common causes:
Chlamydia trachomatis(serovar L1, L2 &L3)
(LGV)
Homophiles ducreyi (chancroid)
Calymatobacterium granulomatis (granuloma
inguinale)
T.pallidum(some times)
BY Zinabu Dawit(PBsc)

483. Inguinal Bubo
5/11/2024
483
Courtesy of CDC/ Susan Lindsley
BY Zinabu Dawit(PBsc)

484. Sign and symptoms
5/11/2024 484
• Produces necrosis and abscess in the lymph
nodes( except syphilis)
• Fluctuant bubo
• Enlarged lymph nodes usually painful
• Warm, tender and discharging pus on P/E
BY Zinabu Dawit(PBsc)

485. 5/11/2024
485
Inguinal Bubo
Patient complaining of
inguinal swelling
Take history
and examine
Inguinal/femoral
bubo present?
Ulcers
present
Treat for LGV, GI and chancroid
•Aspirate if fluctuant
•Educate on treatment compliance
•Counsel on risk reduction
•Promote and provide condoms
•Partner management
•Offer VCT if available
•Advise to return in 07 days
•Refer if no improvement
Any other STI present
Use appropriate flow chart
•Educate
•Counsel
•Offer VCT
•Promote and provide condoms
Use genital ulcer flow chart
No No
Yes
Yes
No
BY Zinabu Dawit(PBsc)

486. Inguinal Bubo
5/11/2024
486
Recommended treatment:
• Ciprofloxacin 500mg PO BID for 3 days
and
• Erythromycin 500mg PO QID for 14 to 21
days
or
• Doxycycline 100 mg 14 days.
BY Zinabu Dawit(PBsc)

487. Neonatal Conjunctivitis(Ophthalmia neonatorum)
5/11/2024
487
Neonatal conjunctivitis is swelling (inflammation) or
infection of the tissue lining the eyelids in a newborn, in
a less than one month of age, as a result of genital
infection of the mother, transmitted during birth.
Causes:
Neisseria gonorrhea(blindness may follow)
Chlamydia trachomatis
Gonorrhea accounts for 20 -75% and Chlamydia for
15- 35% of cases in developing countries.
BY Zinabu Dawit(PBsc)

488. Symptoms
5/11/2024 488
• Infected newborn infants develop drainage
from the eyes within 1 day to 2 weeks after
birth.
• The eyelids become puffy, red and tender.
• There may be watery, bloody or thick pus-
like drainage from the infant's eyes.
BY Zinabu Dawit(PBsc)

489. Ophthalmia neonatorum
For babies older than one month the cause is unlikely to be an STIs.
5/11/2024 489
BY Zinabu Dawit(PBsc)

490. 5/11/2024
490
Neonatal Conjunctivitis
Neonate presents with eye discharge
Take history and examine child
Purulent conjunctivitis present?
Complete treatment course,
reinforce education and counseling
Review if necessary
Treat baby for gonococcal and
chlamydial opthalmia
AND
Treat mother and partner for gonorrhoea
and chlamydia
Educate and counsel
Review baby in 7 days or sooner
if symptoms worsen
Signs of other illness
present?
Treat appropriately
Reassure mother,
educate parents
Review if symptoms persist
Eye infection cleared?
No No
Yes
Yes
Review in
7 days
Yes
Refer for specialist opinion
and management
No
BY Zinabu Dawit(PBsc)

491. Treatment
5/11/2024 491
 Spectinomycin 25mg/kg IM stat max.dose
75mg. or ceftriaxone 50mg/kg max.dose
125mg IM stat
plus
 Erythromycin 50mg/kg PO in 4 divided doses
for 14 days
 May lead to blindness if not treated properly
BY Zinabu Dawit(PBsc)

492. Prevention of Neonatal conjuctivitis
5/11/2024 492
 As soon as the baby is born, carefully wipe both eyes
with dry, clear cotton wool.
 Then apply 1% silver nitrate solution or
1% TTC eye ointment or
 0.5%Erythromycin ointment or 2.5% povidone iodine
solution.
NB. The baby’s eyes are usually swollen after birth and
may be difficult to open, so open the eyes and apply the
eye ointment on the lower conjuctival and not on
eyelids.
BY Zinabu Dawit(PBsc)

493. Principles of prevention and control of STIs
5/11/2024 493
• Reduction of the average rate of sexual
exposure.
• Reduction of the efficiency of transmission.
• Shortening the duration of infectivity of
STI(early detection & treatment).
BY Zinabu Dawit(PBsc)

494. Prevention of STIs
5/11/2024 494
 Primary prevention:-
 Aims to prevent people from being infected with STIs.
Safer sexual behavior:
 ABC
 Non penetrative sex: masturbation
 Secondary prevention :-
Promoting STI care-seeking behavior, through:
-public education campaigns
-providing non-stigmatizing and non-
discriminatory health services
BY Zinabu Dawit(PBsc)

495. 5/11/2024 495
Providing quality STIs care
 Ensuring a continuous supply of highly effective drugs and
condoms.
 Rapid and effective treatment of people with STI, through
comprehensive case management of STIs w/c includes:
 Correct diagnosis
 Correct therapy
BY Zinabu Dawit(PBsc)

496. Cont.
5/11/2024 496
 Educate on the nature of infection, safer sexual
behavior & risk reduction
 Educate on treatment compliance
 Demonstrate the correct use of condoms & provision
of condoms
 Advise on partner treatment
BY Zinabu Dawit(PBsc)

497. .
5/11/2024 497
BY Zinabu Dawit(PBsc)

498. HIV/ AIDS
5/11/2024 498
 HIV:-human immune deficiency virus
 AIDS:-Acquired immunodeficiency syndrome
 was first reported by the US CDC in 1981GC.
 By 1984GC. HIV was identified as the causative agent
for AIDS by Luc Montanier (Pasteur Institute, Paris)
and Robert Gallo.
 HIV is an enveloped and special family of retroviruses,
a class of RNA virus.
BY Zinabu Dawit(PBsc)

499. HIV AND THE IMMUNE SYSTEM
5/11/2024 499
 The WBC play an important role to defend the body
against all kinds of diseases.
 The CD4 is a special type of lymphocyte(T-cells) with a
marker on its surface called CD4.
 In order for the cell to be infected by HIV, there must be
CD4 receptors which are occur on T- helper
lymphocytes, monocytes and macrophages cell lines.
BY Zinabu Dawit(PBsc)

500. Cont…
5/11/2024 500
 Although helper T cells seem to be the main
target for HIV, other cells become infected as
well(monocytes,macrophages)
 HIV destroys CD4 cells and consequently the
body is exposed to conditions called
opportunistic infections( OI).
 These CD4 cells can be compared like army
BY Zinabu Dawit(PBsc)

501. The immune system and HIV
5/11/2024 501
Immune system
Innate immunity
• Fast/immediate
• Short-lived
(E.G., Skin as a mechanical
barrier, and the acid in the
stomach)
Humeral immunity
(antibody-mediated)
Adaptive immunity
• slow but progressive
• long-lived memory
Cellular immunity
(T-cell-mediated)
BY Zinabu Dawit(PBsc)

502. VIRAL STRUCTURE
5/11/2024 502
 The outer envelope includes two major
glycoproteins, gp120 and gp41
 The viral core has two copies of HIV RNA,
core protien(P24), matrix protein( P17) &
three enzymes(reverse transcriptase,
integrase & protease).
BY Zinabu Dawit(PBsc)

503. 5/11/2024 503
BY Zinabu Dawit(PBsc)

504. There are 8 major steps in
the virus life cycle.
5/11/2024 504
HIV LIFE CYCLE
BY Zinabu Dawit(PBsc)

505. Step 1: Binding/ Fusion
5/11/2024 505
 The virus locks onto a special receptors on
the surface of the cell
 The gp120 has specific affinity and binding
of the viral gp120 leads to conformational
changes of viral envelope
 Expose gp41 to initiate the fusion process.
BY Zinabu Dawit(PBsc)

506. Step2: Penetration and uncoating
5/11/2024 506
 Internalization to the cytoplasm of the host
cell
 uncoating/releasing of the viral core proteins
(proteins, RNA& enzymes)
BY Zinabu Dawit(PBsc)

507. Step3: Reverse transcription
5/11/2024 507
 The enzyme Reverse transcriptase makes a
DNA copy of the viral RNA.
 The new DNA is called “ proviral DNA”.
BY Zinabu Dawit(PBsc)

508. Step4: Integration
5/11/2024 508
 The new DNA(HIV genes) enters the nucleus
and becomes part of the cell’s DNA.
 The integrated viral DNA may persist in a
latent state for some time or will be active.
BY Zinabu Dawit(PBsc)

509. Step 5: Transcription
5/11/2024 509
• Transcription of viral DNA to mRNA
(instructions for making new HIV proteins,
with the help of RNA polymerase).
• When the host cell tries to make new proteins ,
it will start producing new HIV proteins using
the cell’s “ machinery”.
BY Zinabu Dawit(PBsc)

510. Step 6: Translation
5/11/2024 510
 The mRNA leaves to the cytoplasm and carries
instructions for making new viral proteins.
 Structural proteins, regulatory proteins,
accessory proteins & other genetic materials
for the new virions.
BY Zinabu Dawit(PBsc)

511. Step7: Viral assembly & maturation
5/11/2024 511
• Protease process the new proteins into their
functional forms
• Assemble together to form mature virion at the
inner surface of the host cell membrane.
• Soon each copy of RNA(HIV genes) is
packaged in a protective shell.
BY Zinabu Dawit(PBsc)

512. Step8: Budding
5/11/2024 512
• The virus acquires a lipid coat from the host
cell
• Thousands of viruses break out of the cell &
released as new viruses and go on to infect
other cells.
BY Zinabu Dawit(PBsc)

513. 5/11/2024 513
BY Zinabu Dawit(PBsc)

514. Classification of HIV
5/11/2024 514
 HIV-1 :-
Was described in 1983
Responsible for the global pandemic.
Three distinctive hiv-1 virus groups, m, o &
n.
 HIV-2:-
Was described in 1985
Limited to west africa
Causes AIDS much more slowly than HIV-1
BY Zinabu Dawit(PBsc)

515. MODES OF TRANSMISSION OF HIV
5/11/2024 515
 Sexual relations (anal, vaginal and oral sex).
 Transfusion with contaminated blood or blood
products
 The use of needles, syringes and cutting or
perforating objects contaminated by HIV infected
blood
 Transmission from mother to child
BY Zinabu Dawit(PBsc)

516. HIV IS NOT TRANSMITTED
5/11/2024 516
 Body fluids like tears, saliva,sweat and urine
 Personal contacts: kisses on mouth, hugging, hand
shakes
 Social contacts: During work, in the school , cinema,
restaurant and sauna
 Air or water sneezing, coughing, swimming
 Contact with common items: pens, toilets, towels
sheets, soap BY Zinabu Dawit(PBsc)

517. Spectrum of HIV tests
5/11/2024 517
 HIV diagnosis(antibody/ antigen testing)
• Enzyme-linked immunosorbent assay(ELISA)
• Rapid tests
• Western blot
 Early diagnosis in infants
• DNA PCR
 Initiation and monitoring of ART
• CD4 count(start HAART if CD4 counts <200 cells/mm3).
• Viral load(start HAART if a viral load >100,000 copies/mL)
BY Zinabu Dawit(PBsc)

518. THE CLINICAL COURSE OF HIV
5/11/2024 518
 During the process of sero-conversion often patients
develop non-specific flu- like symptoms.
 These symptoms include:
– Fever
– Fatigue
– Pharyngitis
– Lymphadenopathy
– Rash
BY Zinabu Dawit(PBsc)

519. Cont…
5/11/2024 519
Three types of progression are noted.
1. Typical progressors
 Account for 90% of individuals who can stay
for 7 -10 years before developing symptoms.
 The viral set point is medium in this group
2. Rapid progressors
 Account for 5%, they develop AIDS with in 3
years
-patients have high viral set point.
BY Zinabu Dawit(PBsc)

520. Cont…
5/11/2024 520
3. Long term non- progressors
 Account for <10%,have stable CD4 count for
more than 10 -15 years
 This group has remarkably low viral set point.
BY Zinabu Dawit(PBsc)

521. Patterns of HIV Disease Progression
5/11/2024 521
.
HIV
Infection
Long-term
Non-progressors
Rapid Progressors
Typical Progressors
<3 years
7-10 years
>10-15 yr
Normal, Stable CD4
90 %
<5 %
<10 %
BY Zinabu Dawit(PBsc)

522. OPPORTUNISTIC INFECTIONS(OIs)
5/11/2024 522
• People with good immune systems have CD4
counts between 450 and 1500cells/mm3.
• As CD4 level declines the risk of getting
opportunistic infections increases.
• When the number of CD4 has decreased below
450cells/mm3 , the person will start to have some
opportunistic infections
• When the CD4 count has decreased below
BY Zinabu Dawit(PBsc)

523. Overview of Aetiologies
5/11/2024 523
Bacterial infection: Streptococcus aureus, streptococcus
species, Treponema pallidum,
 Bartonella species

 Mycobacterial infection: M. tuberculosis, M. Avium complex
 Viral infection: Herpes simplex and zoster virus,
molluscum contagiosum, condylomata
accuminata

 Infestations: Scabies
 Fungal infection: seborrheic dermatitis, tinea corporis,
pityriasis versicolor, Cryptococcus
neoformans, Histoplasma
capsulatum, Candida species
BY Zinabu Dawit(PBsc)

524. OI PROPHYLAXIS
5/11/2024 524
1. Cotrimoxazole prophylaxis
 is the most commonly used for:-
Pneumocystis pneumonia
Toxoplama brain abscess
Isospro belli
Non-typhodal salmonella species
Pneumonia from s.Pneumonia
P. Falciparum malaria
BY Zinabu Dawit(PBsc)

525. Cont…
5/11/2024 525
Indication
WHO-clinical stage 2,3 & 4 in the absence of
CD4 count
WHO – clinical stage 3 & 4 irrespective of the
level of CD4 count.
Patients with CD4 count of ≤ 350/mm3
People with TB and HIV co- infection.
Dose: cotrimoxazole 480mg two tablets or 960
BY Zinabu Dawit(PBsc)

526. Cont…
5/11/2024 526
2. Fluconazole prophylaxis
(200mg/day)
• after full treatment of cryptococcal meningitis
• when on ART, stop when CD4 has been greater
than 100 for 6 months after at least 6 months
treatment.
3. INH prophylaxis
• prevention of TB which is common in patients
with HIV.
BY Zinabu Dawit(PBsc)

527. WHO CLINICAL STAGING
5/11/2024 527
• Used for assessment at baseline or entry into HIV
care
• Provide simple guidance to assist clinical care
providers on when to start or substitute ART
• used to assess current clinical status of individuals in
HIV care, either on or off ART
BY Zinabu Dawit(PBsc)

528. Cont…
5/11/2024 528
• Encourage clinical care providers to offer
diagnostic testing for HIV
• Be used to guide clinicians in assessing the
response to ART.
• New or recurrent OIs after ART may suggest an
inadequate response to treatment
• Clinical events in the first three months after ART
has begun may be caused by immune restoration
BY Zinabu Dawit(PBsc)

529. WHO clinical staging for HIV
5/11/2024 529
Primary HIV Infection
Stage 1 - Asymptomatic
Stage 2 - Mild disease
Stage 3 - Moderate disease
Stage 4 – Severe disease (AIDS)
BY Zinabu Dawit(PBsc)

530. Primary HIV infection
5/11/2024 530
• Asymptomatic
• Acute retroviral syndrome( non-specific
symptoms)
• Fever
• Fatigue
• Pharyngitis
• Rash
BY Zinabu Dawit(PBsc)

531. Clinical stage 1
5/11/2024 531
• Asymptomatic
• Persistent generalized lymphadenopathy
(PGL)
• PGL is swollen or enlarged lymph nodes >
1cm in 2 or more non-contiguous extra-
inguinal sites in absence of known cause
BY Zinabu Dawit(PBsc)

532. Clinical stage 2
5/11/2024 532
• Moderate unexplained weight loss(<10%)
• Recurrent respiratory tract infections
• Herpes zoster
• Angular cheilitis
BY Zinabu Dawit(PBsc)

533. Cont…
5/11/2024 533
 Recurrent oral ulcerations
 Papular pruritic eruptions
 Seborrhoeic dermatitis
 Fungal nail infections of fingers
BY Zinabu Dawit(PBsc)

534. Papular Pruritic Eruption (PPE)
5/11/2024 534
• Hyperpigmented papules
and nodules (up to 1 cm)
with severe itching. Often
ulcerations and scars
because of scratching
• Most frequently on
extensor side of arms and
legs
BY Zinabu Dawit(PBsc)

535. PPE treatment
5/11/2024 535
• Antihistamines
• Potent topical
steroids
• Calamine lotion
• ART
BY Zinabu Dawit(PBsc)

536. Impetigo
5/11/2024 536
•Local antiseptics
•Cloxacilline 500 mg
4x/d for 10 days
BY Zinabu Dawit(PBsc)

537. Scaly skin eruption on the border between face and hair
and side of the nose, scalp or chest
These are often greasy scales and redness. It also common in non-HIV.
5/11/2024 537
Seborrhoeic dermatitis
BY Zinabu Dawit(PBsc)

538. Seborrhoeic Dermatitis
5/11/2024 538
•Whitfields ointment bd OR
•Ketoconazole ointment bd
OR
•Miconazole cream bd
•Local steroid cream added if
severe and lots of
inflammation
BY Zinabu Dawit(PBsc)

539. Tinea Pedis
5/11/2024 539
• Interdigital itching, scaling,
fissures and maceration,
sometimes redness.
• Rx: antifungal
BY Zinabu Dawit(PBsc)

540. Clinical stage 3
5/11/2024 540
• Severe weight loss (>10%)
• Unexplained chronic diarrhea for longer
than one month
• Unexplained persistent fever (intermittent
or constant for longer than one month)
• Oral candidiasis
• Oral hairy leukoplakia
BY Zinabu Dawit(PBsc)

541. Cont…
5/11/2024 541
• Pulmonary tuberculosis (TB) diagnosed in last two years
• Severe presumed bacterial infections
• Acute necrotizing ulcerative stomatitis, gingivitis or
periodontitis
• Unexplained anemia (< 8 g/dl) and neutropenia (<500/mm3)
and
• Thrombocytopenia (<50 000/ mm3) for more than one month
BY Zinabu Dawit(PBsc)

542. Necrotising Gingivitis
• Inflammation of the
gums
• Extensive and necrotic
• Tooth loss
• Anaerobic infection
• Rx: penicillin,
clindamycin, or
metronidazole
5/11/2024 542
Gingivitis
BY Zinabu Dawit(PBsc)

543. ORAL HAIRY LEUKOPLAKIA (OHL)
• Non-removable
• Vertical white/gray
patches/folds on lingual
lateral margins (+/- dorsal or
ventral surface of tongue)
• Not painful
• No treatment
• Sign of immune suppression
5/11/2024 543
Caused by Epstein-Barr virus
(EBV) replication in the
epithelium of the surface of
the tongue
BY Zinabu Dawit(PBsc)

544. Oral Thrush
• 60% of patients per year
with CD4 < 100
• 10-20% associated with
oesophageal candidiaisis
• White painless plaques on
the buccal or pharyngeal
mucosa or tongue surface
that can easily be scraped
off
5/11/2024 544
Candida albicans is an
endogenous yeast
Oral thrush
BY Zinabu Dawit(PBsc)

545. Clinical stage 4
5/11/2024 545
• HIV wasting syndrome
• Pneumocystis carnii pneumonia
• Chronic herpes simplex infection (orolabial, genital or anorectal of
more than one month’s duration)
• Cytomegalovirus (CMV) infection
• Recurrent non-typhoidal salmonella septicaemia
• Lymphoma (cerebral or B cell non-Hodgkin)
• Invasive cervical carcinoma
• Visceral leishmaniasis
BY Zinabu Dawit(PBsc)

546. Cont…
5/11/2024 546
• Oesophageal candidiasis
• Extra pulmonary TB
• Kaposi’s sarcoma
• Central nervous system (CNS) toxoplasmosis
• HIV encephalopathy
• extra pulmonary cryptococcosis including
BY Zinabu Dawit(PBsc)

547. HIV
wasting
syndrome
Patient is extremely thin(lost >10% of body weight)
with chronic fever and/or chronic diarrhea> 1 month
5/11/2024 547
BY Zinabu Dawit(PBsc)

548. HIV wasting syndrome
.
5/11/2024 548
BY Zinabu Dawit(PBsc)

549. Chronic Mucocutaneous HSV
5/11/2024 549
• Genital herpes may become
chronic, persisting for
months, ulcerating and may
cover large parts of the
genitals and surrounding
skin, causing severe pain
and disability.
• Spread by direct contact.
Contagious when lesions
are visible and people shed
virus even when there are
no symptoms.
BY Zinabu Dawit(PBsc)

550. Chronic Mucocutaneous Herpes Simplex: treatment
5/11/2024 550
• Acyclovir 200-400 mg
5x/d till resolution
• Analgetics
• Suppressive therapy if >6
recurrences/year
(acyclovir 200 mg 2x/d)
• Betadine or potassium
permanganate solution
sit baths 3 times daily.
• Zinc oxide to soothe.
Alternatively betadine
ointment or
oxytetracycline ointment
3 times daily
BY Zinabu Dawit(PBsc)

551. CMV oral Ulcerations
5/11/2024 551
May be the first
clue to
disseminated
disease
Responds to
ganciclovir
Requires biopsy
for diagnosis
Expensive!
BY Zinabu Dawit(PBsc)

552. 5/11/2024 552
Kaposis Sarcoma
BY Zinabu Dawit(PBsc)

553. Cont...
5/11/2024 553
Kaposis Sarcoma
BY Zinabu Dawit(PBsc)

554. 5/11/2024 554
Lymphoma
BY Zinabu Dawit(PBsc)

555. Lymphoma
.
5/11/2024 555
BY Zinabu Dawit(PBsc)

556. Presentation of TB Lymphadenopathy
5/11/2024 556
Usual course of TB lymph nodes:
firm discrete nodes
fluctuant nodes
 skin breakdown, abscesses, sinuses
 healing with scarring
IN ADVANCED HIV, TB LYMPHADENOPATHY
MAY BE ACUTE
AND RESEMBLE
ACUTE PYOGENIC LYMPADENITIS
70% sensitivity
of AFB
on aspirate
Look also
at aspirate:
caseation?
Can occur even
at a relatively high CD4
BY Zinabu Dawit(PBsc)

557. Cryptococcal Skin Lesions
5/11/2024 557
 Sign of disseminated
cryptococcosis
 Nodular, papular, follicular
 May resemble molluscum!
 Usually on face, neck, scalp
BY Zinabu Dawit(PBsc)

558. IMMUNOLOGICAL STAGING OF HIV INFECTION
5/11/2024 558
 Clinical staging can be used effectively without access to CD4 or
other laboratory testing.
 CD4 testing is useful for determining the degree of
immunocompromise and serves as the major laboratory indicator
of immune function in patients.
 It is one of the key factors in determining both the urgency of
antiretroviral therapy (ART) initiation and the need for prophylaxis
for opportunistic infections.
 It is also the strongest predictor of subsequent disease progression
and survival
BY Zinabu Dawit(PBsc)

559. Cont…
5/11/2024 559
CD4 LEVELS IN RELATION TO THE SEVERITY OF IMMUNOSUPPRESSION
1. Not significant immunosuppression
2. Mild immunosuppression
3. Advance immunosuppression
4. Severe immunosuppression
>500/mm3
350 −499/mm3
200−349/mm3
<200/mm3
BY Zinabu Dawit(PBsc)

560. CRITERIA FOR INITIATING ART
5/11/2024 560
Clinical stage ART Treatment options
4 treat
3
Consider treatment: CD4, if available, can guide the urgency with which ART
should be started
1 or 2 Only if CD4 <200/mm3.
BY Zinabu Dawit(PBsc)

561. ANTIRETROVIRAL DRUGS
5/11/2024 561
 Standard ART consists of the combination of at least three drugs, which
introduced in 1996 G.C.
 Typically three are taken in combination the approach is known as
Highly Active Antiretroviral Therapy (HAART).
 In general, three-drug regimens that include three drugs from the same
class (ie, nucleoside analogs) are not as effective as regimens that
combine drugs from different classes and are not recommended.
 The optimal time to initiate treatment is influenced by the benefits and
the risks of drug toxicity, potential emergence of viral drug resistance,
and the need for lifetime therapy.
BY Zinabu Dawit(PBsc)

562. Goals of therapy
5/11/2024 562
o Durable suppression of HIV viral load to less than
50 copies/mL
o Restoration of immune function (as indicated by
the CD4 cell count)
o Prevention of HIV transmission
o Prevention of drug resistance
o Improvement in quality of life
BY Zinabu Dawit(PBsc)

563. Cont…
5/11/2024 563
Why we have to use the combination of three ART drugs.
• To have sustained viral suppression for long period of
time.
• To attack the virus at different life cycle of the virus
• To overcome or delay resistance because HIV changes
its structure to make ARV less effective.
BY Zinabu Dawit(PBsc)

564. HAART
5/11/2024 564
BY Zinabu Dawit(PBsc)

565. Classes of ARV
5/11/2024 565
Drug selection is becoming increasingly complex, with more than 20
antiretroviral medications available in six major classes
1. Fusion inhibitors (FIs)
2. CCR5 antagonists
3. Nucleoside (and nucleotide) reverse transcriptase
inhibitors (NRTIs)
4. Nonnucleoside reverse transcriptase inhibitors (NNRTIs)
5. Protease inhibitors (PIs)
6. Integrase strand transfer inhibitors (INSTIs)
BY Zinabu Dawit(PBsc)

566. Fusion inhibitors
5/11/2024 566
 Were the first class of antiretroviral medications to target the
HIV replication cycle extracellularly.
 Currently, enfuvirtide (Fuzeon) is the only product
marketed in this class.
 Act extracellularly to prevent the fusion of HIV to the CD4
or other target cell.
 Enfuvirtide binds to gp41 and interferes with its ability to
approximate the two membranes.
BY Zinabu Dawit(PBsc)

567. Nucleoside (and nucleotide) reverse
transcriptase inhibitors (NRTIs)
5/11/2024 567
 Less potent against HIV than NNRTIs and Pis, but have had a central
role in antiretroviral treatment and remain part of the current standard
of care.
 Are structurally similar to the DNA nucleoside bases interrupt the
HIV replication cycle via competitive inhibition of HIV reverse
transcriptase and termination of the DNA chain.
 Tenofovir, lamivudine, and emtricitabine exhibit activity against
hepatitis B virus (HBV) in addition to HIV and are frequently
incorporated into antiretroviral regimens for patients with HIV and
HBV coinfection.
BY Zinabu Dawit(PBsc)

568. Cont…
5/11/2024 568
A total of 7 drugs make up the NRTI class.
Abacavir (ABC, Ziagen)
Didanosine (ddI, Videx)
Emtricitabine (FTC, Emtriva)
Lamivudine (3TC, Epivir)
Stavudine (d4T, Zerit)
Tenofovir (TDF, Viread)
Zidovudine (ZDV, Retrovir; formerly
azidothymidine (AZT)
BY Zinabu Dawit(PBsc)

569. Non-nucleoside Reverse Transcriptase
Inhibitors
5/11/2024 569
 HIV reverse transcriptase is a heterodimer composed of 2
subunits (p66 and p51).
 NNRTIs bind the p66 subunit at a hydrophobic pocket distant
from the active site of the enzyme.
 This noncompetitive binding induces a conformational change in
the enzyme that alters the active site and limits its activity.
 Exhibit potent activity against HIV-1 and are part of preferred
initial regimens.
BY Zinabu Dawit(PBsc)

570. NNRTIs cont…
5/11/2024 570
First-generation NNRTIs include delavirdine
(Rescriptor), efavirenz(Sustiva) and nevirapine
(Viramune).
Second-generation NNRTIs currently include
etravirine(Intelence) and rilpivirine(Edurant).
BY Zinabu Dawit(PBsc)

571. Protease inhibitors(PIs)
5/11/2024 571
 HIV protease is a 99-amino-acid, aspartic acid protein and is
responsible for maturation of virus particles late in the viral
life cycle.
 HIV protease inhibitors function as competitive inhibitors that
directly bind to HIV protease and prevent subsequent
cleavage of polypeptides.
 They exhibit activity against clinical isolates of both HIV-1
and HIV-2.
BY Zinabu Dawit(PBsc)

572. PIs cont…
5/11/2024 572
A total of 8 compounds are approved for use
 Atazanavir(Reyataz)
 Darunavir (Prezista)
 Fosamprenavir (Lexiva)
 Indinavir(Crixivan)
 Lopinavir/ritonavir (Kaletra)
 Nelfinavir(Viracept)
 Saquinavir(Invirase)
 Tipranavir(Aptivus)
NB:- Ritonavir is used as a helper for another
PI in adults in to make the effect of other PI stronger.
BY Zinabu Dawit(PBsc)

573. Integrase Inhibitors
5/11/2024 573
 The integrase enzyme combines with viral DNA and other
cellular cofactors to form the preintegration complex (PIC).
 These drugs prevent or inhibit the binding of the pre-integration
complex to host cell DNA, thus terminating the integration step
of HIV replication.
 The one currently approved integrase inhibitor, raltegravir, and
the investigational agent, elvitegravir, both target the strand
transfer step of viral DNA integration, and are sometimes
referred to as “INSTI” (Integrase Strand Transfer Inhibitor)
drugs.
BY Zinabu Dawit(PBsc)

574. FIRST LINE ART REGIMEN
5/11/2024 574
Will be used in a patient who has no prior ART
experience.
D4t-3TC-NVP (1A)
D4t-3tc-efv (1B)
AZT- 3TC-NVP (1C)
AZT-3TC-EFV (1D)
BY Zinabu Dawit(PBsc)

575. Special first line Regimen.
5/11/2024 575
At times when AZT or d4t cannot used,
abacavir(ABC) or tenofovir(TDF) can be used
as the first line drugs
TDF-3TC-EFV or NVP
ABC -3TC –NVP or EFV
But currently used drug is TDF+3TC+EFV
BY Zinabu Dawit(PBsc)

576. Second- line regimen
5/11/2024 576
 The first line therapy can fail if the drugs are not taken
correctly and used for treatment failure
 it consists of 2NRTIs and 1PI.
 stronger because the virus has not yet developed a way
to avoid the drugs.
 DDI or TDF +ABC+LPV/r or SQV/r or IND/r or NFV
BY Zinabu Dawit(PBsc)

577. QUIZ
5/11/2024 577
1. Write the principles synderomic management of of STIs?(1%)
2. List and discuses the approaches to STIs management(2%)
3 List and discuses some factors that affects the transmutations of
STIs (2%)
BY Zinabu Dawit(PBsc)

578. Individual assignment for 2nd year BSC nursing
student 20%
1. Describe chain of disease transmission
2. Explain Five “fs” fecal oral diseases transmission
3. Describe at list the three most common arthropod
borne disease
4. Define STIs and Syndromic approach to manage STI
5. Describe the epidemiology of STIs and risk factors.
By zinabu D 578

579. Any Questions
5/11/2024 579
BY Zinabu Dawit(PBsc)