The Nurse and the Communicable Diseases

GERARDO A. NICOLAS RN, RM, RPT, MAN

 COMMUNICABLE DISEASE
Cause: infectious agent or its
toxic products
transmitted directly or indirectly
to a well person
through an agency, vector,
inanimate object.
endogenous or exogenous
 2 TYPES OF COMMUNICABLE DISEASE

CONTAGIOUS DISEASE INFECTIOUS DISEASE

spread by direct
not only by ordinary
contact w/ infectious
contact
agents causing the
disease. requires direct
inoculation of
easily transmitted from organism through a
1 person to another
break on the skin
through direct or
or mucous
indirect means
membrane
Infection – invasion of the body tissue by
microorganisms and their proliferation
Carrier- a person who without apparent symptoms
of a disease, harbors and spread the specific with
microorganisms.
Contact- any person or animal known to have been
in such association an infected person or animal
exposed to infection
Communicable period- the period which etiologic
agent may be transferred directly or indirectly from
the body of the infected person to the body of
another person
Sterilization- destruction of pathogens even the spores.
Contamination- invasion of surface (wound) or
article (handkerchief) or matter (water and
milk) implies the presence of undesirable substance
which may contain pathogenic microorganisms
Disinfection- destruction of the vitality of pathogens
microorganisms by chemical or physical
means directly applied.
Concurrent disinfection – ongoing practices that
are observed in the care of the client, his supplies,
environment and control of microorganisms.
Terminal disinfection – practices to
remove pathogens
from the client’s belongings and
environment after his illness is no
communicable. longer
Disinfectant – substance for inanimate objects that
destroys pathogens and the spores.
Antiseptic – substance intended for persons that
inhibit the growth of pathogens but not necessarily
destroy them
Bactericidal – chemical that kills microorganisms
Bacteriostatic – chemical that prevents
the multiplication but does not kill all forms of
microbes Asepsis – absence of disease-producing
microorganisms; free from infection
Sepsis – presence of infection
Medical asepsis – practices to reduced the number
and transfer of microorganisms; clean technique.
Surgical asepsis – practices that render and keep
objects & areas free from pathogens; sterile technique
Etiology - the study of causes
Virulence- the vigor with which the organism can
grow and multiply; refers to the degree or intensity
of disease produced
Nosocomial Infection- infections associated with
the delivery of health care services in a health care
facility
Opportunistic pathogen- causes disease in a
susceptible person
Resident flora- microorganisms that are always
present in specific areas of the body; normally lives
on a person’s skin.
Transient flora- microorganisms picked up by the
skin as a normal activities that can be removed
easily.
Pathogens – a disease producing-microorganism
Pathogenecity- the ability to produce a disease; the
ability of microbes to overcome the defensive powers
of the host to induce disease
Quarantine- limitation of freedom of movement of
such susceptible persons or animals as have been
exposed to communicable diseases
Colonization- a process by which strains of
microorganisms become resident flora, but their
presence does not cause disease
Fumigation- any process by which destruction of
insects, fleas, bugs, etc. and is accomplished by the
employment of gaseous agents
Isolation- the separation for the period of
communicability of infected persons.
 • Sporadic
• Endemic
Based on •
Epidemic
occurrence
•Pandemic
 Intermittent occurrence of few
isolated unrelated cases in
given locality
 Disease occurs occasionally

irregularly, no specific pattern

 Examples are cancers,

degenerative
diseases
 Continuous occurrence throughout a
period of time, of usual number of
cases in a given locality
 Constantly present in population,

community or country.
 Examples are STD’s, diarrheal

diseases, PTB, Influenza, different

types of pneumonia,
Schistosomiasis, Malaria, Filariasis
 Occurrence is of

unusually large # of cases in
a relatively short period of
time
 Examples are dengue fever,

leptospirosis, mumps, chicken

pox, measles
 Epidemic disease that occurs
worldwide
Simultaneous occurrence of
epidemic of same disease
in several countries
 Examples are HIV-AIDS, MERS-COV,
SARS
Based on severity or duration of disease

Acute Disease
 Develops rapidly (rapid onset) but lasts only a

short time
 Ex. Measles, Mumps, Influenza

Chronic disease
 Develops more slowly but lasts for a long

period
 Ex. TB, Leprosy
Sub-acute Disease
Intermediate between acute and chronic
Develops rapidly and has long duration
Ex. Bacterial endocarditis

Latent Disease
Causative agent remains inactive for a time but then
becomes active to produce symptoms of the disease
an infection held in check by the defensive forces of
the body but activated when the body resistance is
reduced
Ex. Chicken pox- Shingles ZosteR
 TYPES OF INFECTION

RECURRENT REINFECTION SUPERINFECTION AUTOINFECTION

 Recurrent Infection
REAPPEARANCE OF SYMPTOMS
after infectious disease has

been treated or subsided

renewed presence of

same infectious agent

 Reinfection
after an initial infectious agent
has been eliminated, a NEW
infection occurs caused by
same organism or by another

strain of same species

 Superinfection

During the illness,additional

infection occurs by another
infectious agent
 Autoinfection
The infected person is
his own direct source of
 re-exposure
 Invasion
Incubation
Period/
Period
Period of
Illness/Acute

Convalescent
Period/
Period of
Prodromal
Decline
Period
 Incubation Period

extendsfrom entry of
microorganism to
body

to onset of nonspecific
s/s
 Prodromal Period
 Extends from the onset of
nonspecific signs and symptoms
to the appearance of specific
signs and symptoms
 Illness Period

host experiences
maximum impact of
infectious process
 Specific
signs and symptoms
develop and become
evident
 Convalescent Period

manifestations

subside
 Signs and symptoms start to abate
until the client returns to normal
state of health.
CHAIN OF INFECTION
 1. Causative Agent

Virus

Bacteria
Protozoa

Parasite Fungus
 2. Reservoir

Humans

Inanimate
objects Animals
 3. Portal of exit

Respiratory System

Genitourinary Tract (GUT)

Gastrointestinal Tract (GIT)

Skin and mucous membrane

 4. Mode of Transmission

1. Contact
2. Airborne

3. Vehicle-borne
4. Vector-borne

5. Transplacental
 5. Portal of Entry

Usually, this path

is THE SAME as
the portal of exit
 6. Susceptible Host

Final and most

important link in chain
of infection
CONTROL MEASURES
IN THE SPREAD
OF
INFECTION
 Refers to the practice of:

 Avoiding contact with the patient’s bodily

fluids by wearing gloves, goggles, face mask,
gown and shoe cover.
 Medical instruments should be handled
carefully and disposed properly in a sharps
container
 Proper handwashing
 Considering all patients are infectious
 Standard precautiongo beyond
universal precaution regardless of
 ISOLATION
infected
person

QUARANTINE
susceptible person
3. STERILIZATION

4. DISINFECTION
• a. Concurrent
Disinfection
• b. Terminal

Disinfection
 CONCEPT OF

IMMUNOLOGY
Definition of Terms

IMMUNOLOGY

IMMUNITY

SUSCEPTIBILITY
Immunology- a division of biology
concerned with the study of living
organisms’ exemption from harmful agents

Immunity- refers to the body’s specific

protective response to an invading foreign
agent or organism

Susceptibility- the reverse of immunity and

the result of the suppression of factors that
produces immunity
 TYPES OF IMMUNITY

NATURAL/IN ACQUIRED
NATE
IMMUNITY
(Nonspecific IMMUNITY
) (Specific)
 NATURAL IMMUNITY
Anatomic
and
Physiologic
Barrier

Inflammation WBC
•They provide non-specific response to any foreign
invader, regardless of the invader’s composition
ANATOMIC AND PHYSIOLOGIC DEFENSES
1.Intact skin and mucous membranes
>Body’s first line of defense against microorganism
> Has normal secretions (sweat) that make skin slightly acidic:
Acidity inhibits bacterial growth
2.Resident bacteria
>Prevent other bacteria from multiplying and use up available
nourishment
3.Nasal Passages
>Moist mucous membrane and cilia traps microorganism, dusts,
foreign materials
4.Lungs
>Have alveolar macrophages (large phagocytes) which are cells
that are responsible to ingest microorganisms and foreign
particles.
5.Oral Cavity >Sheds mucosal epithelium to rid the mouth of
colonizers
>The flow of saliva and it’s partially buffering action help
prevent infection
6.Eyes >Protected from infection by TEARS which continually
wash microorganisms away
7.Gastrointestinal Tract >High acidity of the stomach: Normally
prevents bacterial growth
>Resident flora of the large intestines: prevents the
establishment of disease producing
microorganism 8.Vagina
>When girl reaches puberty, LACTOBACILLI ferment sugars in
the vaginal secretions creating a vaginal pH of 3.5-4.5
>This low pH inhibits the growth of many disease-producing
microorganisms
9.Urethra >Urine: Flushing and bacteriostatic action keeps
bacteria from ascending
WBC (Leukocytes)
>Participates both on the natural and acquired
immune response

Two types of WBC:

1. Granulocytes (Granular leukocytes)

A.Neutrophiles
>Polymorphonuclear cells (PMN), are the first cells to
arrive at the site of inflammation
>Increased in ACUTE bacterial
infection B.Eosinophiles
>Increased during allergic and parasitic infections
C.Basophiles
>Not usually affected by infection
2. Agranulocytes

A. Monocytes (Macrophages)
>Are phagocytic cells engulfing, ingesting, and
destroying greater numbers and quantities of
foreign bodies or toxins

B. Lymphocytes
>Consisting of B-cells and T-cells that play major
role in Humoral and Cell-Mediated immune
response
>Increased in CHRONIC bacterial and viral
infections
 Acquired Immunity

Types
•1. Active
•2. Passive
ACQUIRED IMMUNITY (SPECIFIC)

•Specific immunity develops after

birth

•Acquired during life but not present

at birth

•Occurs after exposure to an antigen

like infectious agent
 Active Immunity

The host produces

its own antibodies in
response to natural
antigen.
 Passive Immunity

Antibodies are
produced by another
source, animal or
human.
 •a. Natural
Active
•b. Artificial
TYPES OF

IMMUNITY

•a. Natural
Passive
•b. Artificial
 ACTIVE NATURAL
Recovery from a disease
(mumps, measles, chicken pox)
Lifetime protection
Antibodies are formed
in the presence of active
infection (disease) in
the body
 ACTIVE ARTIFICIAL
Antigens (vaccines or toxoids)
are usually administered to the
person to stimulate antibody
production
All kinds of immunization
Many years but not
lifelong protection
 PASSIVE NATURAL
Transplacental transfer
of antibodies
Breastfeeding-colostrum
Transfer of IgA

6 mos- 1 year protection

 PASSIVE ARTIFICIAL

Immune serum
(antibody) from an
animal or another human
is injected
 Tetanus Ig, Gamma globulin
Antitoxin, Antiserum
Administration)
2-3 weeks protection
 ROLE OF LYMPHOCYTES IN
ACQUIRED
IMMUNITY
2 Types of Lymphocytes
• B-cells: Antibody-Mediated Immune Response

• T-cells: Cell-Mediated Response

COMPONENTS OF IMMUNE RESPONSE
Antibody-Mediated Defenses (B-Cells)
•Also known as Humoral (Circulating Immunity) because the
defenses reside ultimately in the B lymphocytes and are mediated
by antibodies produced by B cells
•Defend primarily against the extracellular phases of bacterial and
viral infections
Cell-Mediated Defenses (T-cells)
•Also known as Cellular Immunity, occurs through the T-cell
system
•On exposure to antigen, the lymphoid tissues release large
numbers of activated T-cells into the lymph system. These T-cells
pass into general circulation
•When Cell-Mediated Immunity is lost, as occurs with HIV
infection, an individual is “defenseless” against most viral,
bacterial and fungal infection
 Classes of Immunoglobulin
(Antibody-Mediated Immune
Response)

Ig G

Ig D Ig A

Ig E Ig M
•B-cells - ultimately responsible for the production of
antibodies (immunoglobulins) and for Humoral Immunity.

CLASSES OF IMMUNOGLOBULINS

Ig G
•The most abundant immunoglobulin in serum(about 80%
of the total serum immunoglobulins) and relatively
abundant extravascularly (interstitial fluid)
•Crosses placenta (hence responsible for natural
passive immunity of newborn because it crosses placental
barrier)
•Assumes major roles in blood-borne and tissue infections
•Enhances phagocytosis
Ig A

•It is the chief Ig in external secretions like

breastmilk, saliva, tears, and mucus of the
bronchial, genitourinary and digestive tracts

•Plays a major role in secretory immune response

•Has a protective function on mucosal surfaces

exposed to environment transported across
mucous membrane with secretions
Ig M

•The largest of the immunoglobulins and appears

mostly in the intravascular serum

•Provides a rapid protection because it is the first

antibody noted after antigen injection in an adult
(1stIg class produced in primary response to
bacterial and viral infections)

•First Ig to be synthesized by the neonate

Ig E

oMediates the immediate

hypersensitivity reactions that
responsible the symptoms of are
for asthma and anaphylactic shock
fever,
hay
oTakes part in allergic and
combats parasitic infections.
Ig D

•Appears in small amount in serum with

it biologic function UNKNOWN.

•It is located on the surface of

lymphocytes
B that serves as surface
receptors-reaction with
influences lymphocyte activity antigen
Francis Home (1757) a Scottish
physician, first discovered measles

Murice Hilleman – first discovered

measles vaccine – 1963 first available
1968 improved vaccine

21 strains
Other Names:

• Rubeola
• 7-day Measles
• Morbilli Disease
• Hard Measles
• Little Red
Disease
Etiologic Agent

• Morbilli Virus (paramyxovirus)

• Sensitive to heat, light, and
extreme acidity and alkalinity
Mode of Transmission

• Direct contact with respiratory

secretions coming from infected
patients
• Indirect contact with objects
contaminated with secretions
• Airborne transmission
Incubation Period

• 10-12 days (8-20 days)

Period of Communicability

• 4 days before and 5 days after the

appearance of rashes
Clinical Manifestations

Pre Eruptive

Eruptive/ Stage of Skin Rashes

Convalescent Stage
Pre Eruptive Stage - highly continuous stage

• High-grade fever
• 3 C’s and 1 P
• Coryza
• Cough
• Conjunctivitis
• Photophobia
Pre Eruptive Stage - highly contagious stage

• Enanthema
• Koplik’s spot- Pathognomonic sign
• a bluish-whitish spot with a red halo
margin usually located in the inner
cheek opposite the second molar
• Stimson’s line- line of inflammation
along the margin of lower eyelid
• Sore throat
Eruptive Stage / Stage of Skin Rashes

• Exanthema
• Maculopapular Rash
• Reddish in color; warm to
touch
• Cephalocaudal in
distribution
Eruptive Stage / Stage of Skin Rashes

• Pruritus
• Irritability
• Lethargy
• Anorexia
Convalescent Stage

• Rashes disappear in the same

manner as they appear in
the body
• LEAVES A BRANNY
DESQUAMATION
maculopapular

Reddish and warm

to touch
CEPHALOCAUDAL
distribution
Diagnostic Test

• Nose and Throat Swab

• Urinalysis
• Blood exam
• Viral serology
• -Complement Fixation
• -Hemagglutinin Inhibition Test
• -Neutralization Test
Complications

• Bronchopneumonia- most common

and dreaded complication
• Otitis media
• Nephritis
• Encephalitis
• Blindness
Medical Treatment

• Pen G – to prevent secondary

bacterial complication
• Antiviral: ISOPRENOSINE
• Vitamin A
• 6-12 months: 100,000 IU
• >12mos- 5 years: 200,00
IU
Nursing Interventions

• Isolation
• Antipyretic and TSB
• Increase oral fluid intake
• Bed rest
• Nasal and Oral Care
• Eye Care
• Skin Care
Preventive Measures

• Vaccine
• Live Attenuated Measles Vaccine: 9 months
• MMR
• 1st dose: 12- 15 months
• Booster dose:11-12 years
• Exposed: Measles Immune Serum Globulin
with 1 week after exposure
George de Malon (1814) first discovered
German measles

27 strains
Other Names:

• Rubella
• 3 Day Measles
 Rubivirus
(Rubella Virus)

Togavirus
• with an envelope
Mode of Transmission

• Direct contact with respiratory

secretions coming from infected
patients
• Indirect contact with objects
contaminated with secretions
• Transplacental Transmission
Incubation Period

• 2 – 3 weeks

Period of Communicability

• 7 days before and 5 days after the

appearance of rashes
Clinical Manifestations

• Pre Eruptive
• Eruptive
• Convalescent
Clinical Manifestations

• Pre-eruptive Stage
• Low grade fever
• Headache
• Malaise
• Anorexia
• Sorethroat
• Coryza
Pre Eruptive Stage

• Conjunctivitis
• Lympadenopathy
• Postcervical
• Postauricular
• Suboccipital
Eruptive Stage

• Exanthema
• Maculopapular rash
• Reddish in color; warm to touch
• Cephalocaudal in distribution
Eruptive Stage

• FORSCHEIMER SPOT
• a red, petecchial macule on the
surface of the soft palate
• Testicular pain especially in younger
adults
• Polyarthralgia and Polyarthritis
Convalescent Stage

• Rashes disappear in the same

manner as they appear on the body
• DOES NOT LEAVE A BRANNY
DESQUAMATION
Diagnostic Test

• Viral Isolation from Nasopharyngeal

secretions
• Viral Serology
• Complement Fixation
• Hemagglutinin Inhibition Test
• Neutralization Test
Complications

• Encephalitis- most common

• Otitis media
• Rubella Syndrome
• IUGR
• Mental retardation
• Cardiac defects
• Eye defects: glaucoma and cataract
• Ear defects: hearing loss
Medical Treatment

• Symptomatic and Supportive

• Antipyretic
• Analgesic
 Same with MEASLES
Preventive Measures

• Live Attenuated Rubella Vaccine

• MMR
• Exposed: Immune Serum Globulin,
IM within 1 week after exposure
(especially for pregnant women)
Giovanni Filippo (1500) – first discovered
chicken pox
 Other Name:
◦ Varicella
 Varicella-Zostervirus
 Herpesvirus varicellae

◦ Only pathogenic to humans

 Direct contact with respiratory
secretions coming from infected
patients
 Indirect Contact with objects

contaminated with secretions

 Airborne transmission
 Transplacental transmission
 10 – 21 days

2 days before the rashes

appear until all vesicles have
encrusted
Clinical Manifestations

• Pre Eruptive
• Eruptive
• Convalescent
 Fever
 Headache
 Sore throat
 Malaise
 Exanthema
oVESICULOPAPULAR RASHES
 Centrifugal in distribution
 Extremely pruritic

o5 Stages of Rashes
a. Macule- “flat”
b. Papule- “elevated”
c. Vesicle- “fluid-filled”
d. Pustule- “pus-filled”
e. Crust/Scab- dry
oCelestial Map: a condition wherein all
the stages of chicken pox rash are
simultaneously present

Rashes disappear
Determination of V-Z virus
through:
oViral Isolation
oMicroscopic Examination of
Vesicular Fluid
oViral Serology
Skin

Infections
oErysipelas
oCellulitis
oImpetigo
 Antivirals: to slow down vesicle formation
and speed up skin healing
o ACYCLOVIR
o ZOVERAX
 Antipyretic: No NSAID- strong link with
Reye’s Syndrome
 For pruritus
o Antihistamine
o Calamine lotion
o Soda bath
Nursing Interventions
 Symptomatic and Supportive

 PREVENTIVE MEASURES
 Vaccine

◦ Live Attenuated Varicella Vaccine

 2 doses at 1 month apart
◦ MMRV
Synonym: Hansen’s disease
Chronic disease of the skin, peripheral nerves
and nasal mucosa
“Living dead”, Was perceived to be caused by sin
Causative agent: Mycobacterium leprae
 MOT:

a.Intimate skin
to skin contact
b. Droplet
Types:
1. Multibacillary (MB) – infectious, malignant
- Numerous macules, papules
and nodules
1. Paucibacillary (PB)– hypopigmented
macule
 Late Manifestation
o Lagophthalmos – inability to

close eyelids
o Madarosis – loss of

eyebrows
o Sinking of the bridge of the

nose
o Leonine face
o Contractures (clawing of

fingers and toes)

o Gynecomastia
 Slit Skin smear – to demonstrate M. leprae
(-) in all site = Paucibacillary
(+) in all sites = Multibacillary
Number of lesions = 2-5 PB
> 5 MB
Treatment:
Multi drug therapy (MDT) RA
4073
A. Paucibacillary:Rifampicin(600mg)
/once a mo
Dapsone (100mg) OD
(6-9 mos)

B.Multibacillary: Rifampicin, dapsone, lamprine

Day 1: R-600 D-100 C-300 once month
Day 2-28: Dapsone 100
OD Clofazimine
Health education
o Dapsone: cutaneous eruptions, also
iritis, orchitis
o Lamprine: Brownish black skin
discoloration, dryness and flakiness
o Skin care: Prevent injury
o Nursing Diagnosis
o Altered body image
o Social stigma
Preventive: BCG @birth
Pediculosis
Types
: . Pediculosis capitis – head lice
a
b. Pediculosis corporis – body lice
c. Phthirus pubis – pubic or crabs lice
MOT: direct contact, beddings, towel,
clothes and hairbrush
Clinical manifestations:
1. Intense pruritus, leads to
secondary excoriation
2. Eggs (nits) attached to the
hair shaft
Scabies: an
infestation of the
skin by Sarcoptes
scabiei mites
a. Intense itching
b.Superficial
burrows,
especially between
fingers, the surface
of the wrist and in
axilla
c.Redness, swelling
may be noted
Treatment
A. Pediculosis
1. Permethrin 1% (Nix)
2. Pyrethrine compunds (Rid)
B. Scabies
1. Permethrin 5% cream (Elimite)
Home care:
1. All family members and close contacts need to be
treated
2. Concurrent Disinfection
a.Daily washing of recently worn clothes, towels
and bedding.
b.Areas such as shared toilet and shared commode
chair seats need to be thoroughly wiped after
each use
 Other Names:
 “La Grippe”
 Flu
 Influenza Virus
 A: epidemic and pandemic cases
 H (Hemagglutinin)- 16
 N (Neuraminidase) – 9

 B: epidemic cases
 C: sporadic cases
Direct Contact with
nasopharyngeal secretions
Indirect Contact with

objects contaminated with

secretions
Airborne
1-4 days average of 2 days
24-48 hours
 Adult:
◦ Until the 5th day of illness up
to 7 days

 Children:

◦ Up to 10 days
 Chills
 Hyperpyrexia
 Malaise
 Coryza
 Headache
 Myalgia
 Sorethroat
 GI manifestations: Nausea and vomiting
 Nose and Throat Swab
 Viral Culture
 Viral Serology
 RTPCR (Real Time Polymerase

Chain Reaction)- Confirmatory

Test
Atypical

Pneumonia
 Influenza A: Amantadine HCl
(Symmetrel)- prevention and
treatment of RTI caused by the virus
 Antibiotics: secondary infection
 AH1N1

◦ Oseltamivir (Tamiflu)
◦ Zanamivir (Relenza)
 Vaporizer- reduce irritation to
respiratory mucosa
 Symptomatic and
Supportive
 Respiratory

Isolations
 Bed Rest: Limit strenuous

activity
 Watch out for

complications
 Instruct patient to avoid

crowded areas and close

contact with infected
 LiveAttenuated
Influenza Vaccine
◦ Single dose
◦ Annual vaccination to
people at risk like elderly
and immunocompromised
persons
Robert Koch (1882) - a German physician
and scientist, discovered of Mycobacterium
tuberculosis, the bacterium that causes
tuberculosis (TB)
 Tuberculosis is considered as the
world’s deadliest disease and remains
as a major public health problem in
the Philippines

 Is
a chronic bacterial infection
characterized by granuloma
formation, necrosis and calcification
of involved tissues
Koch’s Disease
Consumption
Phthisis
 Class 0 – no exposure, no infection
 Class 1 – (+) exposure, (-) infection
 Class 2 – (+) infection, (-) disease
 Class 3 – (+) symptoms, PTB active
 Class 4 – disease, not clinically active
 Class 5 – diagnosis pending; suspect
 Mycobacterium tuberculosis-
most common
 Mycobacterium africanum
 Mycobacterium bovis
 2 – 10 weeks

 Airborne transmission through coughing and

sneezing
 Direct invasion through mucous membranes
or breaks in the skin may occur, but
extremely RARE
 Bovinetuberculosis results from
exposure to tuberculosis cattle:
Ingestion of unpasteurized
milk or dairy products
 Fever – low grade. Late afternoon or
early evening
 Chronic cough – more than 2 weeks
 Anorexia
 Weight loss
 Nocturnal sweating
 Fatigue
 Chest and back pains
 Dyspnea and hemoptysis
 Mantoux Test/ PPD/ Tuberculin Test
◦ Intradermal injection of PPD
◦ Results are read after 48-72 hours of
injection
◦ (+) for not immunocompromised is
10 mm or more induration
◦ (+) for immunocompromised is 5
mm or more induration
 DirectSputum Smear
Microscopy- primary diagnostic
tool
 Chest X-Ray
 Sputum Culture- Confirmatory

test
 Rifampicin (RIF)
 Isoniazid (INH)
 Pyrazinamidel (PZA)
 Ethambutol (EMB)
 Streptomycin
 Intensive Maintenance
Category Cases
phase phase
- New smear (+) PTB
- New smear (-) PTB
with extensive
parenchymal
RIPE
I RI (4months)
lesions on CXR (2months)
- Extrapulmonary
TB
- Severe
concomitant
HIV disease
- Treatment failure
- TB relapses RIPES
(2months)/ RIE
II - Return after default (5months)
 - New smear (-)
PTB with
minimal RI
RIPE
III (4month
parenchymal (2months) s)

damage on
CXR
- Chronic (still
smear positive Referral to
specialized
IV after facility or
supervised DOTS Plus
Center
 Provide patient with adequate rest
periods
 Promote adequate nutrition
 Advise to cover nose and mouth

when sneezing and coughing

 Provide frequent oral hygiene and

handwashing
 Monitor drug compliance
 AvoidMOT
 Immunization: BCG
 Modalities of Treatment
 Elements of DOTS
Edwin Klebs - first to observe bacteria in the
airways of persons having died of pneumonia
in 1875
 Inflammation of the lung
parenchyma with the production
of alveolar exudates resulting
to consolidation of the air sacs
 Streptococcus pneumoniae
 Haemophilus influenzae
 Staphylococcus aureus
 Klebsiella pneumoniae

(Friedlander’s bacilli)
 Mycoplasma

pneumonia
 Droplettransmission – mouth
& nose of an infected person
via nasopharynx, through
intimate contact w/ carriers

 Indirect contact contaminated

objects
 Systemic infection through inhalation
of caustic or toxic chemicals,
aspiration of food, fluid, and vomitus

 1- 3 days
1) Community-acquired PNM
◦ Acquired in the course of one’s daily life;
at work, at school or at the gym

◦ Hospitalized patient developed PNM in

<36 hours during his stay in hospital

◦ Streptococcus pneumoniae
(pneumococcus) – most common bacterial
cause of CAP;
2. Hospital-Acquired (Nosocomial
Pneumonia)
◦ Develops while client is in the
hospital; reflects the kind of nursing
care is given to the patient

◦ > 36 hours of hospital stay

3. Aspiration Pneumonia
◦ When a foreign matter is inhaled
(aspirated) into the lungs
◦ Most commonly when gastric
content enters lung after
vomiting
1. Bronchopneumonia (Lobular or
Catarrhal PNM) ; most common
type
◦ Infection usually start from bronchus
& bronchioles & spread to alveoli of
periphery
◦ Lobules inflamed & consolidated
◦ Caused by: Pneumococcus, Klebsiella
pneumoniae, H. influenzae
2. Lobar PNM (Croupous
Pneumonia)
◦ Consolidation of entire lobe

◦ As disease progresses, prune juice color

of sputum replaced by thinner or yellowish
color
3. Primary Atypical Pneumonia
(Virus Pneumonia)

◦ Solidification of lung that comes

in patches
1) Primary – direct result of
inhalation or aspiration of
pathogen or noxious substances

2) Secondary – develops as
complication to a disease
 Chillswith rising fever
 Chest pain (stabbing)
 Cough (paroxysmal and choking)
 Rusty or prune juice sputum-

pathognomonic sign
 Abdominal pain
 Malaise
 Labored respiration

 Respiratory grunting
 Tachycardia (rapid and bounding pulse

 Diaphoresis

 Convulsion and Vomiting in children

 SINGLE MOST IMPORTANT SYMPTOM IN

THE DIAGNOSIS OF PNEUMONIA: FAST
BREATHING
 Chest X-ray – confirmatory
diagnostic exam
 Sputum analysis, Smear and
Culture
 Antibiotics

◦ Pen G Na: Drug of Choice

◦ Alternative: Clotrimoxazole
◦ Tetracycline and Erythromycin
 Humidified 02 for hypoxia
 Mechanical ventilation – resp.

failure
 High calorie diet, adequate
fluid intake unless
contraindicated
 Absolute bed rest
 Bronchodilators –

Aminophylline, Salbutamol;
expectorants
 Pain relievers for pleuritic

pain
 Isolation
 Increase oral fluid intake may help liquefy

secretions in order to help expectorate

easily
 Chest Physiotherapy
 Deep Breathing Coughing and Turning

Exercise
 Elevate head & shoulders of patient by

means of pillow to relieve labored breathing

& lessen coughing
 Suction secretion
Increase resistance to
infection
Vaccination

◦Pneumococcal vaccine
◦Hib vaccine
Emil Adolf Behring - was a German
physiologist who first discovered a diphtheria
antitoxin
 An acute febrile infection of
the tonsil, throat, nose, larynx
or a wound marked by a
patch or patches of grayish
membrane from which
diphtheria bacillus is readily
cultured.
 Corynebacterium diptheriae
(Klebs-loeffler bacillus)
 Droplet transmission
 Indirect Contact with contaminated

objects

2 – 5 days, occasionally longer

Usually 2 weeks
and seldom more
than 4 weeks
Respiratory type of diptheria
1) Nasal – localized in the nares
◦ Excoriation of the upper lip and
alae nasi with serosanguinous
secretions which later becomes
bloody and foul smelling
2) Pharyngeal or faucial – pharynx
(tonsilar, uvular, palatar)
◦ Low grade fever
◦ Malaise
◦ Headache and sore throat
◦ Pseudomembrane very visible within 24 hrs.
 Pseudomembrane – false membrane, a grayish,
white color and leathery in consistency and
irregular in shape, usually inflamed which
decreases the opening of the nasopharynx.
◦ Bull neck appearance
3) Laryngotracheal
◦More common in infants
◦Laryngeal stridor
◦Hoarseness of voice
◦Signs of respiratory distress
 Nose and throat culture
 Schick’s test – determines

susceptibility and immunity to

diphtheria
 Moloney test – determines

hypersensitivity to diphtheria
toxoid
Antibiotics
Penicillin-
Drug of choice
Erythromycin- alternative
Diphtheria antitoxin
Tracheostomy – laryngeal
 Isolate the patient
 Provide liquid and soft diet
 Maintain good oral hygiene and

proper airway
 Complete bed rest
 Ice collar
 Monitor for respiratory distress
Immunization –
DPT
Proper disposal

of
nasopharyngeal
secretions
Jules Bordet (1906) – discovered pertusis

Octave Gengou - developed the first serology

and vaccine of pertusis
 An acute contagious disease
characterized by intermittent
episodes of paroxysmal cough
followed by an explosive
expiration ending in an
inspiratory “whoop” and ending in
vomiting (5-10x in succession
repeated 20-40x in a day)
 ”Whooping cough”

Entrance of air
in the epiglottis

 Bordetella pertussis: Gram (-)

coccobacilli
 Droplet transmission
 Indirect Contact with contaminated

objects

7 – 14 days
1) CATARRHAL STAGE– most
communicable stage
◦ Frequent sneezing
◦ Watery secretions
◦ Coryza
◦ Dry and hacking cough
increasing in intensity at night
2) PAROXYSMAL STAGE– most fatal
stage
◦ intermittent episodes of paroxysmal
cough followed by an explosive
expiration ending in an inspiratory
“whoop” and ending in vomiting (5-
10x in succession repeated 20-
40x in a day)
◦ Cough worsen
2) PAROXYSMAL STAGE
◦ Force of coughing may cause
involuntary micturation / defection,
intracerebral hemorrhage and
abdominal hernia
◦ Popping of eyeball
◦ Protrusion of tongue
◦ Vomiting signals end of attack
3) CONVALESCENT STAGE
◦frequency of attacks is
reduced

Incidence:
Infants is highly susceptible
Single attack usually
produces lifetime
immunity
Cough plate or agar
plate

Bordet – Gengou test

 Antibiotics– ampicillin,
erythromycin (DOC) – given for
5 to 7 days

 Antitussives:
sinecod – for
extremely dry cough
 Bed rest
 NPO in attacks (paroxysmal and catarrhal

stage – aspiration
 Positioning – prone for infants
 - upright for older persons
 Isolatethe pt.
 Provide a quiet, non-stimulating

environment
 Keep patient warm and out of

wind
 Small frequent feedings
Avoid MOT

Immunization:

DPT
Hepatitis
A Infectious hepatitis, Catarrhal-jaundice hepatitis

Mode of Transmission: fecal-oral, oral-anal sex
Hepatitis B
 Serum Hepatitis
 MOT: percutaneous, sexual contact, mother to
child.
Hepatitis C
 Post-transfusion hepatitis
 MOT: percutaneous, sexual intercourse

20
5
Clinical Manifestations:

Preicteric phase: anorexia, nausea, RUQ pain,

malaise, headache, low grade fever
Icteric phase: dark urine (increase bilirubin),
pruritus, clay colored stools, jaundice
Post icteric phase: malaise, fatigue, hepatomegaly
for several weeks

Diagnostic exams:
Hepatitis Profile
Liver function test
Liver UTZ

20
6
 Complications: chronic
hepatitis, cirrhosis
Meds for chronic hepatitis
B:
Antivirals: lamivudine, interferon
Nursing Interventions:
1. Bed rest
2. SFF, high CHO
3. Avoid alcohol and OTC
drugs
4. Implement Standard
precaution
Prevention:
Hepatitis B vaccination
@ 0, 6,
20
7
ViralParotitis
Epidemic Parotitis
Infectious Parotitis
 Paramyxovirus

◦ (Saliva- source of infection)

 Direct Contact with repiratory

secretions coming from infected
patients

Indirect Contact with
objects contaminated with
secretions
 14 – 25 days

7days before and 9days after the

onset of parotid swelling
 Low-grade fever
 Headache
 Earache
 Malaise
 Myalgia
 Anorexia
 Dysphagia
 Painand swelling in front and below
the ear
 Viral Isolation
 Blood Exam
 Viral Serology
 Serum Amylase Determination

Test
 Orchitis- most dreaded
complication in males;
Oophoritis-in females
 Mastitis
 Pancreatitis
 Myocarditis
Analgesic
Antipyretic
Moist heat and cold
application
MMR
Avoid

MOT
Waldemar Haffkine - Russian-Jewish
bacteriologist developed the first cholera
vaccine in July 1892.

Filippo Pacini (1854) - V. cholerae was first

isolated as the cause of cholera by Italian
anatomist
Kiyoshi Shiga (1897) - a Japanese Scientist
discovered Shigella bacteria causing dysentery
 Vibrio coma or vibrio cholera

 From a few hours to 5 days

(average of 3 days)
 As
long as microorganisms are
present in the bowel excreta
 Mild-diarrhea that becomes voluminous
 Rice-watery stool (pathognomonic sign)
 Washer woman’s hands
 Effortless vomiting
 Cramping of the extremities

(hypokalemia)
 Signs of severe dehydration
Severedehydration and ECF
volume deficit
Hypokalemia
Metabolic acidosis
Stoolor vomitus culture
Serum electrolytes
Dark field or

Phase Microscopy
 Correction of dehydration and
fluid imbalance
 Antibiotics- Tetracycline (drug

of choice)
Assess patient for signs of
dehydration and
complications
Observe enteric

precautions
Increase oral fluid intake
Violent Dysentery Bacillary Dysentery Amoebic Dysentery
Cholera Shigelosis Amoebiasis
Vibrio cholera Shigella dysenteriae Entamoeba
histolitica
Rice watery stool +/- fever +/- fever
Signs of severe +/- vomiting +/- vomiting
dehydration: Abdominal pain Abdominal pain
sunken eyeball, (colicky or Diarrhea with
Washer- woman’s tenesmus
hand, metabolic cramping)
acidosis, shock Muco-purulent
Diarrhea with blood
tenesmus streaked stool
Tx: Tetracycline Mucus and Blood Tx:
streaked stool Metronidazole
Tx:
Cotrimoxazole 22
7
 Salmonella Typhi

 Variable
 Usually 1 – 3 weeks, average: 2weeks
 Aslong as the bacilli appears in the
excreta

 Fecal – oral route

 Ingestion of contaminated food and

water 5 F’s – fingers, feces, flies, food,

fomites
 Gradual onset
 A-norexia and abdominal pain
 B-radycardia
 C-onstipation
 D-iarrhea, D-evelop skin
eruptions on the abdomen, back
and chest (ROSE SPOTS)
 E-nlarged spleen
 F-ever and chills
 G-eneralized body weakness
 H-eadache
 What are the three cardinal signs of Pyrexial
stage?
ROSE SPOT
CBC
Widal test
Typhidot exam
Blood culture
Urine and stool culture
 Antibiotics: chloramphenicol – drug of
choice
 IVF to correct dehydration or fluid

imbalance
 Paracetamol for the fever
 Oral therapy rehydration (oresol,

hydrites)
 Enteric isolation
 Vital signs must be

recorded accurately
 Intake and output must be

accurately measured
 Concurrent disinfection
 Isolation
 Increase oral fluid intake
 Is an endemic protozoan infection that affects
the liver and GIT
 Capable of producing obstructive jaundice
and liver cirrhosis
 Bilharziasis
 Schistosoma japonicum
 Schistosoma mansoni
 Schistosoma haematobium
 Adult female and male parasites
 Ova
 Miracidium – infective stage in snails
 Cercaria – infective stage in man and animals
 Snail (Oncomelania quadrasi)

 About 2-6 weeks from skin penetration

 Skin penetration by cercaria
 Abdominal pain
 Diarrhea with
bloody
stools
 Portal
hypertension and
signs of liver
cirrhosis
 Anemia
 Kato-katz – specimen is stool
 Circumoval precipitin test (COPT) – specimen
is blood
 HBT – UTZ
 Liver function tests
 Praziquantel (biltricide) – drug of choice
 Oxamniquine (vansil), metrifonate
 Travelers to endemic areas should avoid
exposure to fresh water that is likely to be
contaminated
 No accepted prophylactic regimens have been
developed and no vaccines are currently
available
 Eradication of snails
MOT: INGESTION
1. Pinworm- Enterobius,
Seatworm s/s: Nocturnal
itchiness of anus (female
pinworm lays eggs on the
2. Giant
analRoundworm
sphincter) (Ascariasis)
Potbelly
3. Whipworm (Trichuriasis)
4. Tapeworm
Taenia saginata- raw beef
Taenia solium- raw pork
Diphyllobotrium latum – raw fish
5. Lung fluke – Paragonimiasis
MOT: Raw mountain crab

24
9
II. MOT: Skin penetration
1. Hookworm (Ancyclostomiasis)
2. Threadworm (Strongyloidiasis)

25
0
Weil’sdisease
Canicola Fever
Mud Fever
Hemorrhagic

jaundice
Swineherd’s Disease
A spirochete of genus
Leptospira (Leptospira
interrogans)
 6-15 days

 Leptospira
is found in the urine
between 10 to 20 days after
the onset
1) Ingestion or contact with the skin
and mucous membrane of the
infected urine or carcasses of wild
and domestic animals.
2) Through the mucous membrane of
the eyes, nose, and mouth, and
through a break on the skin.
3) Direct human to human transmission
is rare.
a) Septic Stage
◦ This stage is marked with febrile lasting
for four to seven days.
◦ Abrupt onset of remittent fever
◦chills
◦headache
◦anorexia
◦abdominal pain
◦severe prostration
◦respiratory distress and fever
subsides by lysis
b) Immune or Toxic stage
◦ Iritis
◦ Headache
◦ Meningeal manifestations
 Disorientation
 Convulsions
 with CSF findings of aseptic meningitis.
 ◦ Oliguria and anuria with progressive renal
failure.
◦ Shock, coma, and congestive heart failure
are also seen in severe cases

c) Convalescent Stage
◦ At this stage, relapse may occur
during the 4th to 5th week
1) Blood urea-nitrogen and urea
2) Enzyme Link Immuno-sorbent
Assay (Elisa)
3) Leptospira Antigen-antibody test
(LAAT)
4) Leptospira Antibody Test (LAT)
5) Liver function test
 Meningitis
 Respiratory Distress
 Renal interstitial tubular

necrosis that result to renal

failure (Weil’s disease)
 Cardiovascular problems
1) Medical Treatment of
leptospirosis is geared toward:
◦ Suppressing the causative agent
◦ Fighting possible complications

 Penicillin G – drug of choice

 Ampicillin, Amoxicillin
 For prophylaxis, doxycycline
2) Peritoneal Dialysis
◦ Administration of fluid and
electrolyte and blood as
indicated.
 Isolate the patient, urine must be
properly disposed of.
 Darken patient’s room.
 Observe meticulous skin care
 Keep clients under close

surveillance.
 For home care, clean near dirty
places, pools, and stagnant water.
 Facilitate health education on the

modes of transmission of the

disease.
 Encourage oral fluid intake.
 Sanitation in homes, workplaces,
and farms is a must.
 There is a need for proper

drainage system and control of

rodents (40 to 60 percent
infected).
 Animals must be vaccinated

(cattle, dogs, cats, and pigs).

Legio
debilitans
 Type I – Brunhilde: permanent
immunity; most
paralytogenic
 Type II – Lansing: temporary

immunity
 Type III – Leon: temporary

immunity
 fecal-oral:through saliva,
vomitus and feces
 Direct contact from one

person to another
 Ingestion through of

contaminated food (fecal-oral

route)
7 – 3 5days
 Not accurately known
 Polio virus can be found in throat

secretions as early as 36 hours

and in the feces 72 hours after
exposure to infection.
 Risk of spreading the

microorganism is highest during

the prodromal period
1) Inapparent/ Subclinical Stage-
asymptomatic stage (90-95%)

2) Abortive (Minor Illness Stage)

◦ Fever
◦ Sore throat
◦ GI symptoms
◦ Low lumbar backache/ cervical stiffness
on ante-flexion of spine
3) Major Illness Stage
a) Non-paralytic/ pre-paralytic or
meningitic type
 Recurrence of fever
 Poker spine (stiffness of the
back)
 Tightness and spasm of
hamstring
 Hypersensitiveness of the skin
 Deep reflexes are exaggerated
 Paresis
b) Paralytic
◦With paralysis depending on
the part affected
◦Positive hoyne’s sign: head
drop
◦(+) kernig’s and brudzinki
signs
◦paralysis
Bulbar
◦ Respiratory paralysis

Spinal
◦ Paralysis of the upper and lower extremities
and intercostal muscles

Bulbospinal
Involvement of neurons both in brainstem
and the spinal cord
Blood and throat culture
Lumbar tap (pandy’s test)
EMG
Stool exam
 Strict
isolation, enteric precaution
 CBR / Firm and non-sagging bed

 ROM exercises
 Analgesics / Hot moist compress
 Protective devices
 Hand roll – claw hand
 Trochanter roll – outer

rotation of the femur

 Footboard
Lyssa
Hydrophobi

a
Rhabdo virus
◦a bullet-shaped virus with
strong affinity to CNS tissues
 Bite of an infected animal
 Licking of open wounds by a rabid

animal
 Scratch of a rabid animal
 Man to man transmission (10%)
 Saliva of infected animals
or human

 10-14 days (dogs)

 1 day – 5 yrs. (humans)
Rabid animal
Dumb stage – quiet, stays

in corner with copious

salivation
Furious stage – easily

agitated, hydrophobia
Rabid Man
1) Prodromal / Invasion stage
◦Mental depression, headache,
sore throat, low-grade fever
◦Copious salivation
◦Quiet
2) Excitement stage
◦ Restless, irritable
◦ Hydrophobic
◦ Aerophobic
◦ Drooling of saliva

3) Paralytic
◦ Flaccid ascending symmetric paralysis
◦ Coma, death
Fluorescent rabies anti body
(FRA)- Confirmatory test
Brain biopsy of the animal

(Negri bodies)
14 days observation of the

animal
No specific treatment
Prevention is the best

treatment
Anti – rabies vaccination of

animal and exposed

individual
 Provide a dim, quiet and non-
stimulating room for the patient
 Wear gown, mask and goggles
 All noises no matter how minor should

be avoided
 Restrain the patient when needed
 Stimulation of any senses by fluids

must be avoided
 Anti – rabies vaccine
Immunization
Keepaway from stray
animal
 Lockjaw
Clostridium tetani
Two types of toxin:
 > tetanospasmin
 > tetanolysin
3 days – 3 weeks in adult
 3 – 30 days in new born

 Through
breaks in the skin and
mucous membranes
Soil
Streetdust
Animal and human feces
Rusty materials
Neonates
Malaise, high fever
Difficulty in sucking
Excessive of crying
Stiffness of jaw
Adult
 Trismus – lock jaw
 Risus sardonicus (sardonic

smile) – pathognomonic sign

 Opisthotonus
 Muscular spasm
 Low grade fever, diaphoresis
Clinical

manifestations
History of wound
ATS, TAT, TIG
Pen

G,Metronidazole
Diazepam
Muscle relaxant
 Keep the room dim and
quiet. Avoid stimuli of spasm
 Avoid unnecessary handling
 Close monitoring of v/s and

muscle tone
 Provide adequate airway
 Ineffective
breathing pattern
related to muscles spasm and
neurologic impairment.

 Risk
for injury related to
muscle spasms.
Immunization with tetanus
toxoid for adults

DPT for babies and

children
Cerebrospinal

fever
 Neisseria meningitides
 Streptococcus pneumonia
 Haemophilus influenza
 Streptococcus agalactae and

Listeria monocytogenes
 Respiratory droplets through
nasopharyngeal mucosa
 Direct invasion through otitis

media
 May result after a skull

fracture, penetrating head

wound
3 – 6 days

 As
long as the microorganism is
present in the discharges
 Fever
 Petecchial/purpuric rashes
 Signs of increased ICP

◦ Severe frontal headache

◦ Altered level of consciousness
◦ Restlessness
◦ Projectile vomiting
◦ Blurring of vision; papilledema; diplopia
◦ Bulging fontanel in infants
 Signs of meningeal irritation
◦ Kernig’s sign
◦ Nuchal rigidity – pathognomonic sign
◦ Opisthotonus
◦ Brudzinski’s sign

 Late Signs
◦ Decerebration
◦ Decortication
 Blood Culture and Sensitivity

 CSFAnalysis/ Lumbar
Puncture/ Lumbar Tap
Bronchitis
Pneumonia
Otitismedia/ Mastoiditis
Blindness
Hydrocephalus
Antibiotic

◦ Penicillin G- drug of choice

◦ Alternative: Chloramphenicol
Mannitol
 Pyrentinol/Encephabol

CNS stimulant
Anticonvulsant
◦Diazepam
◦Phenytoin (Dilantin)

 Corticosteroid
◦Prednisone
◦Dexamethasone
 Respiratory Isolation: 24 hours
after onset of antibiotic therapy
 Provide non-stimulating

environment
 Initiate seizure

precaution
 Avoid factors that

increase ICP
Vaccination: Hib-
for children
Avoid MOT
Rifampicin- prophylactic

treatment
◦Alternative: Ciprofloxacin
Breakbone fever
Dandy fever
Infectious

Thrombocytopenic purpura
H-fever
Group B Arbovirus
(I,II,II,IV)
Flavivirus
 Bite
of infected female AEDES
AEGYPTI mosquito

6 – 7 days
 Grade I: Symptomatic and
Supportive
◦Fever
◦Headache
◦Malaise
◦Anorexia
◦Chills
◦ Pain (Abdominal, Bone and Joint, and
Ocular)
◦ Rashes
◦ + Herman’s Sign: Flushing of the skin
◦ + Tourniquet Test (Rumple Leeds
Test)
 Grade II: Manifestations of grade
I plus spontaneous bleeding –
BED REST
◦Epistaxis
◦Gingival Bleeding
◦Petechiae or ecchymosis
◦Gastro intestinal bleeding
 Ground coffee colored vomitus
 Hematemesis
 Melena
 Hematochezia
 Grade III:

◦ Manifestations of Grade II plus Beginning

symptoms of circulatory failure -Monitor
V/S and Watch out for complication of
shock
◦ Hypotension & narrowing of pulse
pressure

◦ Weak and thready pulse

◦ Cold, clammy skin

◦ Restlessness
GRADE IV: Manifestations of
Grade III plus Shock-
PROPER POSITIONING

◦Undetected BP and pulse

 Tourniquet Test- Presumptive
diagnosis; detects capillary fragility

 Platelet Count: Confirmatory test

Result: <100,000 cells/mm3

 Hemoconcentration- Increase in 20%

Hematocrit Count
 Dengue NS1 Ag

 Dengue Duo
Shock ----> DEATH
 Antipyretic/ Analgesic: Do not administer
NSAID for Fever

 Intravenous Fluid Therapy

a) Protocol for Fluid correction with NO SHOCK

 IVF Crystalloids- D5LR or D5 0.9 NaCl or PLR at
5-7
ml/kg/hr
b) Protocol for fluid correction with SHOCK
 IVF Crystalloids- PLR or P 0.9 NSS at 20ml/KBW
IV
bolus in <20 minutes
c. if no improvement
◦ Colloids- Dextran, Haemacel,
Haesteril at 10ml/kg bolus in <10
minutes

d) Still no improvement
◦ Fresh Frozen Plasma at 15cc/kg in 2
hours and start inotropes
Dopamine 7-15 ug/kg/m
 Search and destroy
 Self protection measures
 Seek early consultation
 Say no to indiscriminate fogging
 “AGUE”
 King of Tropical Diseases
 Plasmodium falciparum
 Plasmodium vivax
 Plasmodium malariae
 Plasmodium ovale
 Anopheles mosquito
 Bite
of infected female ANOPHELES
mosquito

 Through blood transfusion

 Contaminated needles and

syringes

 Congenital transmission (RARE)

 Coldstage: severe recurrent
chills

 Hot stage: fever 4-6 hrs.

 Wet
stage: profuse sweating
2-4 hrs.
 Early
signs of anemia: repeated
chronic symptoms: CBQ

a) Pallor

b) Easy fatigability

c) Dizziness
Malaise
Splenomegaly
Hepatomegaly
1) Malarial smear: Confirmatory test
o detects malaria parasite
o best done during the height of fever

2) Quantitative Buffy Coat (QBC)/ Rapid

Diagnostic Test (RDT)
o Detects malarial antigen
o taken anytime, the faster test
1) Cerebral Malaria:

2) Blackwater fever:
 First
line: Artemether-lumefantrine
combination tablet

 Second line: Chloroquine, Primaquine

Pyrimethamine and Sulfadoxine
 ForComplicated Malaria: Multi
drug resistant Falciparum:
*Artemether 20mg/ Lumefantrine
120mg (C0-Artem)

 Erythrocyte Exchange
Transfusion
 CHEMOPROPHYLAXIS

◦ Doxycycline: 1 day before going and

4 weeks after leaving malaria endemic
area

◦ Chloroquine: 1 week before going and 4

weeks after leaving malaria endemic area

◦ Mefloquine: 2-3 weeks before going and 4

weeks after leaving malaria endemic area
 ZOOPROPHYLAXIS

◦ Typing of domestic animals to divert

attention of mosquitoes
 No vaccine yet
 Chemically-treated mosquito nets
 Larvae-eating fish
 Environmental Sanitation
 Anti-mosquito soap
 Natural anti-mosquito plants
 Wuchereria bancrofti
 Brugia malayi
 Brugia timori
 Loa loa

MODE OF TRANSMISSION:
Bite of Aedes poecilius

INCUBATION PERIOD:
8-16 months
Acute Stage:
Lymphadenitis
Lmphangitis
Funiculitis,
orchitis,
epididymitis

Chronic Stage:
H-ydrocele
E-lephantiasis
L-
ymphedema
 Nocturnal blood exam
 Immunochromatographic test (ICT)

Management
Diethlycarbamazine citrate (Hetrazan)
 Acquired
Immunodeficiency
Syndrome (AIDS)
RED RIBBON
Is a symbol of solidarity with
HIV positive people and those
living with AIDS.
 Acquired immune deficiency syndrome or
acquired immunodeficiency syndrome (AIDS) is
a disease of the human immune system
caused by the human immunodeficiency virus
 Virus
classification

Group: Group VI
(ssRNA-RT)
Family: Retroviridae
Genus: Lentivirus
•HIV is thought to have originated in non-human
primates in sub-Saharan Africa and transferred to
humans early in the 20th century

•The first paper recognizing a pattern of

opportunistic infections was published on 4 June
1981.
•Helper T cells(specifically CD4+ T cells)

•macrophages

•Dendritic cells.
1. Persistent cough for one month
2. Generalized pruritic dermatitis
3. Recurrent herpes zoster
4. Oropharyngeal candidiasis
5. Chronic disseminated herpes simplex
6. Generalized lymphadenopathy
1. Loss of weight – 10 percent of
body weight
2. Chronic diarrhea for more than
one month
3. Prolonged fever for one month
Adult : 2 major & 1 minor
Child: 2 major & 2 minor
1. Pneumocystitis carinii pneumonia

2. Oral candidiasis

3. Toxoplasmosis of the CNS

4. Oropharyngeal candidiasis

5.Pulmonary / extra – pulmonary

tuberculosis
6. Cancer

a. Kaposi’s sarcoma

b. Cervical dysplasia and cancer.

c. Non – Hodgkin’s
lymphoma
BLOOD TRANSFUSION
BREASTFEEDING
PERINATAL TRANSMISSON
HOMOSEXUAL RELATIONSHIP
SEXUAL CONTACT
CONTAMINATED SYRINGES
•VARIABLE

•Time from infection to the development of

detectable antibodies is generally 1 -3
months, the time from HIV infection to
diagnosis of AIDS has been observed range
of less than 1 year to 15 years or longer
• Zedovudine (ZDV) – Retirvir
• Zalcitabine – Havid
• Stavudine – Zerit
•Lamivudine -Epivir
• Nevirapine – Viramune
• Didanosine - Videx
 .
• Saquinavir – Invarase
• Ritonavir – Norvir
• Indinavir – Crixivan
•Efavirenz
•Delavirdine
•Current HAART options are combinations (or
"cocktails") consisting of at least three drugs
belonging to at least two types, or "classes," of
antiretroviral agents.
1. Know the patient
2. Avoid Fear tactics
3. Avoid judgmental and moralistic
m e s sa g e s
4. B e c o n sistent and concise
5. Use positive statement
Safe SEX
CONDOMS
CIRCUMCISION
MONOGAMOUS RELATIONSHIP
Gram negative
diplococci
 Mode of Transmission
 Contact with exudates from the mucous
membrane of infected persons, usually as a
result of sexual activity

 May occur in the uterus upon rupture of the

membranes

 Direct contact with contaminated vaginal

secretions of the mother as the baby passes
comes out of the birth canal

 Also be transmitted through fomites

2-3 days with most
symptoms occurring
between 4-6 days
 30-60 % are asymptomatic

 Red swollen vulva

 Erythema of the cervix
 Abnormal menstrual bleeding
 Dysuria and dyspareunia
 Yellowish-green purulent discharges
Less advanced symptoms
 Infection can affect the:

◦ Uterus
◦ Fallopian tubes
◦ Ovary

 Development of Pelvic Inflammatory Disease

(PID)
◦ Cramps and pain
◦ Bleeding between menstrual period
◦ Vomiting
◦ Fever
 Yellowish discharge from the
penis
 Epididymitis
 Dysuria and discharges
 Urethritis

 Infection may affect the:

◦ Prostate
◦ Seminal vesicles
◦ Epididymis
◦ Testicles
 Diagnostic Exams
In Female
 THAYER MARTIN MEDIUM

In Male
 Gram Staining
For uncomplicated
gonorrhea in
nonpregnant patients
For pregnant women
with gonorrhea
In areas with
coinfection with
Chlamydia
 Sex education

 Case finding

 Contact tracing
 Lues Venereal
Morbus gallicus
 Treponema pallidum- a Gram (-),
motile spirochete

 10-90 days, average of 3-6 weeks

 Almost always through sexual contact

 Through indirect contact with articles freshly

soiled with discharges or blood containing
the organism

 Congenitally through the placenta of a

syphilitic mother

 Accidentally, from a syphilitic baby to a wet

nurse or to anyone carelessly handling
diapers
 PRIMARY SYPHILIS
 Typically via direct sexual contact with the
infectious lesions of a syphilitic person

 10-90 days after the initial exposure, a skin

lesion appears at the site of contact usually
the GENITALIA
 PRIMARY SYPHILIS
 CHANCRE
◦ A firm, painless skin ulceration localized
at the point of initial exposure to the
spirochete
◦ Often on the penis, vagina, or rectum
◦ May persist up to 4-6 weeks and usually
heals without treatment
 Chancre associated with
lymphadenopathy
 SECONDARY SYPHILIS

 Occurs approximately 1-6 months after the

primary infection

 Development of mucocutaneous lesions and

generalized lymphadenopathy
 SECONDARY SYPHILIS
 RASHES
◦ Symmetrical, reddish-pink, non-itchy
◦ Usually on the trunk and extremities and can
involve the palms of the hands and soles of the feet

 Mucous patches may also appear on the

genitals or in the mouth
 Flu-like symptoms
 SECONDARY SYPHILIS
 CONDYLOMA LATA
◦ Highly contaminated pink, or grayish-
white lesions

◦ Commonly seen on the moist areas of the

body, like the perineum, vulva, rolls of fats
in the scrotum.
 LATENT SYPHILIS

 Noclinical symptoms, but serologic

test proves to be reactive
LATE (TERTIARY) SYPHILIS

LATE
BENIGN

CARDIOSYPHILIS NEUROSYPHILIS
 Develops 1-10 years after infection

 May appear on the skin, bones, mucous

membranes, upper respiratory tract, liver, or
stomach

 GUMMA
◦ A chronic, superficial nodule, or deep
granulomatous lesion that is solitary, assymetric,
painless, and endurated
 Aorta is the most affected part

 Aortitis
and Aortic regurgitation
 Aneurysm
 DARK FIELD ILLUMINATION TEST

 VENEREAL DISEASE RESEARCH LABORATORY

(VDRL) TEST

 FLUORESCENT TREPONEMAL ANTIBODY

ABSORPTION (FTA-ABS)
First choice treatment
for all manifestations
of syphilis
Given to nonpregnant
patients who
develop allergy to
penicillin