• Types of Infection
COMMUNICABLE DISEASE
 is an illness caused by an infectious agent or its toxic products
that are transmitted directly or indirectly to a well person
through an agency, and a vector or an inanimate object.
 Is one that is spread from one person to another through a
variety of ways that include: contact with blood and bodily
fluids; breathing in an airborne virus; or by being bitten by an
insect.
TERMINOLOGIES
Communicable Disease Nursing –a branch of nursing that
deals with the treatment and care of the patient with CD.
Communicable Disease –transmitted directly or indirectly
• Infectious Disease
o can’t easily be transmitted; inoculation of
organisms
o are disorders caused by organisms-such as
bacteria, viruses, fungi or parasites.
o Many organisms live in and on our bodies. They’re
normally harmless or even helpful. But under
certain conditions, some organisms may cause
disease.
o Can easily be contaminated unless the organism is
included upon your body (rabies, malaria, tetanus)
• Contagious Disease
o easily transmitted.
o Such as the flu, colds or strep throat
o Spread from person to person in several days.
o One way is through direct physical contact, like
touching or kissing a person who has the infection.
Another way is when an infectious microbe travels
through the air after someone already nearby
sneezes or coughs
o Discusses spread by contact either direct or
indirect with other individuals who either care the
specific causative organisms in their person or
they actually suffering from the disease/easily be
contaminated (measles, colds)
Carrier
o capable of transmission but not manifest the disease.
o A person who is without apparent symptoms of a
communicable disease, harbors the specific infectious
agent and may serve as a source of infection
Contact –in close association with infected host
• Direct–actual association or contact to an infected
patient & by harboring the organisms from the
contaminated secretions.
• Indirect-a contact that may be transmitted through
touching of things of an infected person.
Contamination-mere presence of pathogenic agents
Disinfection –destruction of pathogens
• Concurrent –indicates the application of disinfection as
rapidly as possible after discharge of infection.
• Terminal–process of rendering personal clothing &
immediate physical environment of the patient free from
the possibility of conveying the infection.
Fumigation –killing of microorganism by means of gaseous
agents.
Isolation –separation from other person
Immunization –induction or introduction of specific
protective antibodies in a susceptible person.
Infection –implantation and replication of an organism
• Sources of Infection:
o Convalescent-microorganism is acquired during
recovery.
o Active Carrier –Microorganism long after, recovered
from a disease.
o Passive Carrier –Without having disease.
o Vectors–any biting insects that transmit disease to
man.
Virulent –power of organism to produce disease.
o Localized Infection –microorganism remains
confine to a particular anatomical spot (FOCAL)
o General –spread generally all over the body via the
blood stream (measles)
o Mixed–caused by 2 or more microorganisms.
o Inapparent or Subclinical –an infection that does
not cause any detectable manifestations . (Pre-
infection , asymptomatic).
o Latent –an infection that is inactive or dormant; held
in check by defensive forces of the body activated
only when the body resistance is low.
o Inoculation –caused by accidental /surgical
penetration of skin or mucous membrane.
o Self –Limiting –under secondary condition of both
resistance and microbial virulence the disease will
last a certain rather definite length of time and
recovery will take place.
o Cross –faulty medical asepsis.
• Kinds of General Infection:
o Viremia–presence of virus n the blood stream.
o Bacteremia–presence of bacteria in the blood
stream.
o Septicemia –bacteria enter the blood stream the
multiply.
o Pyremia–presence of pus in the blood stream.
o Toxemia –presence of toxin in the blood stream.
WHY INFECTION OCCURS
1. Some bacteria develop resistance to antibiotics.
2. Some microbes such as influenza viruses have so many
different trains that a single vaccine cannot protect against all
of them.
3. Most viruses resist antiviral drugs.
4. New infectious agents occasionally arise. (e.g. HIV &
coronaviruses).
5. Somemicrobeslocalizeinareasofthebody(e.g.bones,CNS)whic
hmakestreatmentdifficult.
6. Opportunistic organisms can cause infection in immune
compromised patients.
7. Most people have not received immunization.
8. Increased air travel can cause the spread of the virulent
organism to a heavily populated area in hours.
9. Biological welfare & bioterrorism using organisms such as
anthrax & plaque is an increasing threat.
10. The expanded use of immunosuppressive drugs and invasive
procedures increases the risk of infection.
❑ Pathogenic-any organism that is capable of causing disease.
❑ Pathognomonic-typical S/Sxonly associated with that certain
disease.
❑ Toxins-poisonous substance produced by bacterial action.
▪ Exotoxin–released by the organism while it is alive.
▪ Endotoxin-released when an organism dies or
disintegrates.
❑ Quarantine–limitation of freedom.
❑ Antigen-stimulates the production of antibodies.
❑ Antibodies-immune substance in the blood.
❑ Habitat–place organisms lives
❑ Host–where organisms depends for survival
❑ Reservoir–infectious agents lives
❑ Surveillance–act of watching
LEVELS OF PREVENTIVE CARE • The most recent methods and concepts of prophylaxis for
1. Primary Prevention communicable disease.
 is true prevention. It precedes the onset of disease or • The rationale and control measures, including isolation
dysfunction and is applied to clients considered techniques.
physically and emotionally healthy.
 It aims at health promotion and includes health Nursing care of patients to patient with communicable diseases
education, immunization, and physical and nutritional • Self-protection
fitness. • Prevention of the spread of the infectious agent through
2. Secondary Prevention medical asepsis and concurrent disinfection
 focuses on individuals who are experiencing health • Physical care of the patient
problems or illnesses and who are at risk of developing • Emotional support of the patient
complications or worsening conditions. • The provision of spiritual aspect of care
 Activities are directed at diagnosis and prompt
intervention, thereby reducing severity and enabling the
client to return to a normal level of health as early as WE MUST REMEMBER THE 5F’S
possible. o F -ingers
3. Tertiary Prevention o F -ood
 occurs when a defect or disability becomes permanent and o F -lies
irreversible. This involves minimizing the effects of long-term o F -eces
disease or disability through interventions directed at o F -omites
preventing complications and deterioration.

IT IS A MUST TO KNOW
A. Keep things other than food away from the mouth.
B. Wash hands often and always before eating.
C. Keep hands from cuts, scratches, chapping, hangnails &
abrasions
D. Wash hands before putting them into the pockets
E. Keep hands away from the face
PATTERNS OF OCCURRENCE AND DISTRIBUTION OF DISEASES
1. Sporadic Disease
o are diseases that occur occasionally and irregularly.
2. Epidemic Disease
o are diseases that occur in a greater number than what is
expected in a specific area over a specific time.
3. Endemic Disease
o are those that are present in a population or community at
times. They usually involve few people during specific
periods.
4. Pandemic Disease
o is an epidemic that affects several countries or continents.

Responsibilities Of The Nurse On Communicable Disease

• The nature of the specific microorganism and its capacity for
survival both within and outside the body.
• The most effective method of destruction of the specific
organism.
• How the organism invades the host and its route of escape
from the body.
• The incubation period, prodromata, and the length of
communicability.
• How a specific drug alters the clinical signs and the infectious
course of the disease.
CHAIN OF DISEASE MODE OF TRANSMISSION
 A microorganism may be spread by a single or multiple
routes.
 Contact, direct or indirect
 Droplet
 Airborne
 Vector-borne (usually arthropod) and
 Common environmental sources or vehicles -includes food-
borne and waterborne, medications e.g., contaminated IV
fluids

1. COMMON TRANSMISSION
a. Direct-contact
Direct body surface-to-body
▪
surface contact and
▪ Physical transfer of
microorganisms between a
susceptible host and an
infected or colonized
person.
b. Indirect-contact ------
▪ Contact of a susceptible host
with a contaminated
intermediate object, usually
inanimate, such as
contaminated instruments,
needles, or dressings, or
contaminated hands or
gloves

Mononucleosis is an infectious illness that’s sometimes

CHAIN OF INFECTION
 Is a process of infection that begins when an agent leaves its
reservoir through portal of exit and is conveyed by mode of
transmission then enters through an appropriate portal of
entry to infect a susceptible host or
 A process in which a favorable condition is required for
microorganism to spread or transfer from reservoir to a
susceptible host
 This process can only occur when all six links in the chain are
intact.
Caustive Agent (Pathogen)- the microorganism (for example
bacteria, virus or fungi, parasites)
Reservoir (Source)- a host which allows the microorganism to
live, and possible grow and multiply. Humans, animals and the
environment can all be reservoirs for microorganism. (people,
animals, pets (dogs, cats, reptiles), wild animals, food, soil,
water)
Portal of exit- a path for the microorganism to escape from the
host; the blood, respiratory tract, skin and mucous
membranes, genitourinary tract, gastrointestinal tract, and
transplacental route from mother to her unborn infant are
some examples
Mode of transmission- since microorganism cannot travel on
their own, they require a vehicle to carry them to other people
and places. (direct, indirect, droplet, airborne, vector)
Portal of entry-a path for the microorganism to get into a new
host, similar to the portal of exit. (mouth, cuts in the skin, eyes)
Susceptible host- a person susceptible to the microorganism
(babies, children, elderly, people with weakened immune
system/ immune suppressed, unimmunized people, anyone
called mono or “the kissing disease”. While you can get the
virus that causes it through kissing, you can also get it in
other ways like sharing drinks and utensils. It is contagious,
but you’re less likely to catch mono than other ill ness like
common cold Transplacental Transmission Vertically
Transmitted infection.
A vertically transmitted infection is an infection caused by
pathogens (such as bacteria and viruses) that uses mother-
to -child transmission, that is, transmission directly from the
mother to an embryo, fetus, or baby during pregnancy or
childbirth e.g. ZIKA VIRUS
Maternal infections caused by most organisms which can
cross the placenta (including rubella, mumps, poliomyelitis,
smallpox, rubeola, syphilis, malaria, toxoplasmosis, and
infection caused by s typhosa , V fetus, L monocytogenes,
cytomegalovirus, and herpes simplex virus) may result in
abortion or stillbirth
In horizontal transmission, viruses are transmitted among
individuals of the same generation. While vertical
transmission occurs from mother to their offspring
Indirect contact- occurs when there is no direct human-
human contact. Contact occurs from a reservoir to
contaminated surfaces or objects or to vector such as
mosquitoes, flies, mites, fleas, tick, rodents or dogs
2. DROPLET TRANSMISSION
• Droplet generation
o coughing,
o sneezing,
o talking,
• procedures such as suctioning and bronchoscopy
• Droplet transmission
• Droplet deposited on the host’s conjunctivae, nasal
mucosa, or mouth.
 3. AIRBORNE TRANSMISSION ISOLATION PRECAUTIONS
• Small-particle residue {5µm or smaller} of evaporated
droplets containing microorganisms
• Suspended in the air for long periods of time
• Dispersed by air currents
• Inhaled by a susceptible host within the same room or over
a longer distance

Types of Isolation Precautions

The micrometre or micrometer, also commonly known by the 1. Standard precautions
previous name micron, is an SI derived unit of length equaling 2. Transmission-based precautions
1x10¯⁶ metre; that is, one millionth of a metre. Wikipedia 3. Contact precautions
4. Airborne precautions
5. Droplet precautions

DEFINITION OF STANDARD PRECAUTIONS

DEFINITION OF ISOLATION PRECAUTIONS
Source: Mosby's Medical Dictionary, 8th edition. © 2009, Elsevier.
o Special precautionary measures, practices, and procedures
used in the care of patients with contagious or communicable
diseases
7 CATEGORIES RECOMMENDED IN ISOLATION
1. Strict Isolation –to prevent highly contagious or virulent
infections.
2. Contact Isolation –to prevent the spread of infection primarily
by close or direct contact.
3. Respiratory Isolation-to prevent transmission of infectious
diseases over short distances through the air.
4. TB Isolation-for TB patients with positive smear or with chest-
xray which strongly suggests active tuberculosis.
5. Enteric Isolation –is for infectious with direct contact with
feces.
6. Drainage/ Secretion precaution-to prevent infections that
are transmitted by direct or indirect contact with purulent
materials or drainage from an infected body site.
7. Universal Precaution –which is applied when handling blood
and body fluids.
1996 CDC Guidelines for Isolation Precautions in Hospitals
Hospital infection control practices advisory committee (HICPAC)
• HICPAC is a federal advisory committee appointed to provide
advice and guidance to DHHS and CDC regarding the practice
of infection control and strategies for surveillance, prevention,
and control of healthcare-associated infection, antimicrobial
resistance and related events in United States healthcare.
• Apply to all patients receiving care in hospitals regardless
of their diagnosis or presumed infection status.
• Apply to (1) blood; (2) all body fluids, secretions, and
excretions except sweat, regardless of whether or not they
contain blood; (3) nonintact skin; and (4) mucous
membranes.
Standard Precaution -Hand hygiene
a. Handwashing with either plain or antiseptic
b. containing soap and water, and use of alcohol-based
c. products (gels, rinses, foams) that do not require the
d. use of water
e. Perform hand hygiene:
f. Before and after patient contact
g. After removing gloves or any other PPE item
h. After touching blood, body fluids, secretions, excretions, and
contaminated items, whether or not gloves are worn
Standard precautions Personal protective equipment (PPE)
a. The selection of PPE based on
b. The nature of patient interaction and/or
c. The likely mode(s) of transmission
d. Designated containers for used disposable or reusable PPE
should be placed in a convenient to the site of removal
e. Hand hygiene is always the final step after removing and
disposing of PPE

FUNDAMENTALS OF ISOLATION PRECAUTIONS

1. Handwashing and gloving
2. Personal protective equipment :
3. Masks, respiratory protection, eye protection, face shields,
gowns and protective apparel
4. Patient-care equipment and articles
5. Linen and laundry
6. Routine and terminal cleaning
7. Patient placement
8. Transport of infected patients
(PPE) Personal Protective Equipment is
equipment that will protect the user
against health or safety risks at work. It
can include items such as safety helmets,
gloves, eye protection, high-visibility
clothing, safety footwear and safety
harnesses

Standard precautions -prevent HCWS Exposure to Bloodborne
Pathogens
a. Prevent needles and other sharps instrument injuries
b. Prevent mucous membrane exposures
c. Safe work practices and PPE to protect mucous membranes
and non-intact skin
Health care workers (HCWs) are at high risk for occupational
blood exposures (OBEs) and transmission of bloodborne
pathogens
Standard precautions: Environmental measures
a. Clean and disinfect non-critical surfaces in patient-care areas
are part of SP.
b. Clean and disinfect all frequently touched surfaces in patient-
care areas
c. EPA-registered disinfectants or detergents
Protecting our health is an integral part of the U.S.
environmental Protection Agency’s mission. If a product claims
to disinfect or sanitize microbes on a surface or object, for
example, a spray that claims to sanitize pedicure foot trays, it
must have an EPA Registration Number and Establishment
Number
Standard precautions: Patient Care equipment and
instruments/devices
a. Clean and maintain medical equipment and
instruments/devices according to the manufacturers’
instructions
Standard Precautions: Textile and Laundry
a. Key principles for handling of soiled laundry:
b. Don’t shaking items or handle them in any way that may
aerosolize infectious agents
c. Avoid contact with one’s body and personal clothing
d. Contain soiled items in a laundry bag or designated bin
Standard Precautions –2007 guidelines for isolation precautions
a. Three new elements added to standard precautions:
b. Respiratory hygiene/cough etiquette
c. Safe injection practices
d. Use of masks for insertion of catheters or injection into spinal
or epidural areas
Respiratory hygiene and cough etiquette
a. Three elements include:
b. Educate healthcare workers, patients, and visitors
c. Post signs in appropriate language(s)
d. Source control measures:
e. Cover the nose/mouth when coughing or sneezing
f. Use tissue paper respiratory secretions and dispose in the
waste receptacle
g. Perform hand hygiene after contact with respiratory secretions
and contaminated objects
h. Place a surgical mask on the coughing person when tolerated
and appropriate
i. Spatial separation, ideally >3 feet
Safe injection practices
a. Large outbreaks of HBV and HCV among patients in the United
States
b. The primary breaches
c. Reinsertion of used needles into a multiple-dose vial or solution
container (e.g., saline bag)
d. Use of a single needle/syringe to administer intravenous
medication to multiple patients.
Health advisory #46
Use of fingerstick
devices on more than
one person poses risk for
transmitting bloodborne
pathogens (public health
clinical reminder
Masks for special lumbar puncture procedures or central line
placement
a. Face masks limit dispersal of oro-pharyngeal droplets during:
b. central venous catheters placement
c. Placement of catheter or injection to epidural space
d. HICPAC recommends the use of a face mask when placing a
catheter or injection to epidural space.
CVP- Central Venous Pressure
• Venous Pressure= is a term that represents the average
blood pressure within the venous compartment
• Central Venous Pressure= considered a direct measurement
of blood pressure in the right atrium and vena cava
Injection to Epidural space
• An epidural corticosteroid (steroid) injection is a way to
deliver pain medicine quickly into the body with a syringe.
The medicine is injected into the epidural area. This is a fat-
filled area that covers the spinal cord to protect it and the
surrounding nerves from damage
HICPAC Hospital Infection Control Practices Advisory
Committee
• HICPAC is a federal advisory committee appointed to
provide advice and guidance to DHHS and CDC regarding
the practice of infection control and strategies for
surveillance, prevention, and control of healthcare-
associated infection, antimicrobial resistance and related
events in United States healthcare
TRANSMISSION-BASED PRECAUTIONS
TRANSMISSION-BASED PRECAUTIONS -Patient Placement
• Single patient rooms -always indicated for patients placed on
airborne precautions and preferable for those who require
contact of droplet precautions
• Cohort patients with same organism or expecting similar
symptoms
Transmission-Based Precautions -Management Of Visitors
a. Visitors as sources of healthcare associated infections –e.g.,
pertussis, influenza, tuberculosis
b. Cough etiquette
c. Use of barrier precautions by visitors
d. Educate patients and family members
e. Follow signs for isolation precautions

Transmission-Based Precautions -Contact Precautions
a. Infections spread by direct or indirect contact with patients or
patient-care environment –shigellosis, C. difficile, MRSA
b. Limit patient movement
c. Private/SINGLE room or cohort with patients with same
infection
d. Wear disposable gown and gloves when entering the patient
room
e. Remove and discard used disposable gown and gloves inside
the patient room
f. Wash hands immediately after leaving the patient room
g. Clean patient room daily using a hospital disinfectant, with
attention to frequently touched surfaces (bed rails, bedside
tables, lavatory surfaces, blood pressure cuff, equipment
surfaces)
h. Use dedicated equipment if possible (e.g., stethoscope)
CONTACT PRECAUTIONS
GLOVES
• Use gloves when entering the room.
• Change gloves after contact with infective material.
• Remove gloves before leaving the room.
• Wash hands or use appropriate gel after glove removal.
• Do not touch infective material or surfaces with hands.
• Clean, non-sterile gloves are usually adequate.
GOWN
• Use protective gown when entering the room if
• direct contact with patient or
• potentially contaminated surfaces or
• equipment near patient is anticipated or
• if the patient has diarrhea or
• colostomy or wound drainage that is not covered by a
dressing.
DROPLET PRECAUTIONS
• Reduce the risk of transmission by large particle droplets
(larger than 5 m in size).
• Requires close contact between the source person and the
recipient
• Droplets usually travel 3 feet or less
• E.g., influenza, rubella, parvovirus B19, mumps, H. influenzae,
and Neisseria meningitidis
• A private/single room or
• Cohort with patient with active infection with same
microorganism
• Use a mask when entering the room and definitely if within 3
feet of patient
• Limit movement and transport of the patient. Use a mask on
the patient if they need to be moved and follow respiratory
hygiene/cough etiquette
• Keep at least 3 feet between infected patient and visitors
AIRBORNE PRECAUTIONS
• Tuberculosis, measles, varicella
• Place the patient in an airborne infection isolation room (AIIR)
• Pressure should be monitored with visible indicator
• Use of respiratory protection (e.g., fit tested N95 respirator) or
powered air-purifying respirator (PAPR) when entering the room
• Limit movement and transport of the patient. Use a mask on the
patient if they need to be moved
• Keep patient room door closed.
INFECTION DISEASE
 Aka Communicable Diseases
o Caused by micro-organisms
o Parasite –lives in/on and feeds on host
PATHOGENS
• Micro-organisms
• Enter the body
• Multiply
• Cause disease
BACTERIA
• Single-cell micro-organisms
• Release toxins
• Examples
o Food poisoning –bacteria in food
o Tetanus –bacteria on objects/soil
E.Coli, Streptococcal, Staphylococcus, Escherichia,
Staphylococcus Aureus, Clostridium, Salmonella,
Vibrio, Mycobacterium, Pseudomonas, Streptococcal
pneumoniae, Lactobacillus, Cyanobacteria, Spirillum,
Shigella, Neisseria, Mycobacterium Tuberculosis, Spiro
chaetae, Asiatic cholera, Pseudomonas Aeruginosa,
Clostridium botulinum, Anthrax bacterium, Neisseria
Gonorrhoeae, Mycoplasma, Bacillus, Treponema,
MRSA, Corynebacterium, Treponema Pallidum,
Enterococcus, Clostridium Tetani, Meningococcus,
Hemophilus Influenzae, Chlamydia, Trachomatis,
Rickettsia, Mold
VIRUS
• Smallest parasite
• Enter cells and take over
• Multiply
• Cause colds/ flu
Epstein- Barr Virus, Mega virus, Norwalk Virus,
Coxsackievirus, Nipah Virus, Middle East
Respiratory Syndrome-Related Corona Virus
(MERS-COV), Severe Acute Respiratory
Syndrome- related coronavirus (SARS),
Hepatitis A,B,C Virus. Influenza A Virus (Bird’s
Flu) Canine Parvovirus, Varicella Zoster Virus,
Dengue Virus, Rabies Virus, Human Papilloma
Virus, Measles Morbillivirus, Variola Virus,
Kaposi’s Sarcoma associated herpes virus,
Ebola Virus, HIV,
Ex: Varicella, HIV, Rubella, Variola
 Recovery Stage
FUNGI • Signs/ symptoms begin to decrease
• Not all are harmful • Temperature is reduced
o Mushroom/ yeast/ mold/ fungi • Feeling better
• Some cause rashes Convalescence
o Ringworm & athlete’s foot • Infection is gone
• Still not quite 100%
Candidiasis. Candida infection of the mouth, • Can relapse
throat, and esophagus. Vaginal candidiasis, • Need rest, sleep, healthy diet, antibiotics
Candida auris, C.albicans Immunity
C.tropicalis, C.guilliermondii, C.krusei, • Feel 100%
C.kefyr, C.glabrata, C.parapsilosis, • Body has antibodies
C.lusitaniae, C.zeylanoides, C.glabrata • Cannot catch same infection

Tinea pedis, Tinea unguium, Tinea manus,

Tinea cruris, Tinea corporis, Tinea faciei, Tinea
capitis, Tinea incognito

Tinea incognito, Tinea barbae, Trichophytic

granuloma

Spreading Infectious Disease

a. Physical contact w/ infected person
b. Contact w/ contaminated object
c. Environmental sources
d. Contact w/ contaminated animals

Contaminated Animals
• Animal bites
• *Eating bad food*
• Rabies/ Malaria/ Bird flu
• HIV/ AIDS
Contaminated Object
• Most infections die quickly when exposed to air
• Some can live on objects
• Lice
Contact w/ Contaminated Person
• Skin to skin contact
• Sneeze/ cough
• Cold/ STI/ flu/ chicken pox
Environmental Sources
• Food/ water/ soil
• Lead poisoning/ food poisoning
• Fungi/ mold/ pathogens in water
• Old food left out
• Contaminated animals

Stages of Disease
1. Exposure
2. Incubation Period
3. Prodromal Period
4. Acute Stage
5. Recovery Stage
6. Convalescence
7. Immunity

Exposure & Incubation

• Exposure = contact
Incubation = growth/ maturation
• No signs/ symptoms
• Pathogen/ parasite grows and multiplies
Prodromal Stage
• Slight signs & symptoms
• Ex: ache/ sore/ tired
• Contagious!
Acute Stage
• Severe symptoms
• Most contagious
• Most affected
 BACTERIA IN ORIGIN
Oral-Fecal Disease Transmission
FECES IN WATER
1. TYPHOID FEVER or Salmonellosis
o Typhoid and paratyphoid fever are diseases of the
intestinal tract caused by the Salmonella Typhi and
Salmonella paratyphi – Salmonella Enterica bacteria.
Paratyphoid fever is very similar to typhoid fever, but is
a lot milder not fatal
Synonym: Enteric Fever
Causative Agent: Salmonella typhosa /typhi
Incubation Period: Usually 7-14 days, but this depends
on infective dose & can vary from between 5-40 days with
a mean of 10 to 20 days
Period of Communicability: for as long as the bacteria
are in the stools.
Mode of Transmission - By food and water contaminated
by stools and urine of patient or carriers.
Fecal –Oral route = direct
Vehicles 5 F’s: Feces, Food, Flies, Fomites, Fingers
PHATOPHYSIOLOGY
 During the 1st week, these lymph nodes are swollen.
Necrosis of the lymph nodes follows, caused by
progressive edema and eventual vascular obstruction from
the center to the periphery of the node, resulting in an oval
ulcer along the long axis of the small intestine.
 During the 2nd week, they form sloughs which are often bile
– colored.
 During the 3rd week, the sloughs separate and leave an
ulcerated surface. Hemorrhage and perforation may occur
due to growth of the lesion and continuous erosion of the
epithelial lining of the small intestine---melena
 The organism gains access to the bloodstream through the
bowels, principally through infected Peyer’s patches in the
lymphoid tissue. P Peyer’s Patches detect antigen such as
bacteria or toxins in small intestine and mobilize highly
WBC termed B-cell to produce antibody
 Since the toxin is absorbed in the bloodstream almost all
the organs of the body are affected, but most commonly
the heart, liver and spleen.
Signs and Symptoms
a. Prodromal Stage –3-4 days
• dull headache, body malaise
• Chills, high fever 39-40C, -body aches
• nausea & vomiting or diarrhea
b. Fastigeal/pyrexial Stage-during the second week
• Exanthem:
• Rose Spots
o 7th-9th days
o Ladder like fever
o Enlarged Spleen
o Tachypnea
o Tongue furred
c. Defervescence Stage –3rd week
• Intestinal hemorrhage
• Intestinal perforation
• Cough due to hypostatic congestion of the lungs;
pneumonia
• PR-weak heart
• Leukopenia
d. Lysis/Convalescence stage-4th week
• Although signs and symptoms subsides, patient
should still be observed for relapses which could
be fatal.
e. Coma vigil look
• pupils dilate and patient appears to have blank
stares or staring without seeing
• pt. staring blankly
• headache, chilly, sensation and body aches
f. Difficulty putting out the tongue
g. Carphologia
• involuntary and aimless picking of linen Diagnostic/Laboratory Exams
• pt. mutters deliriously and picks up aimlessly at a. Blood culture
bedclothes with his finger in continuous fashion • Widal’s Test
• 4th-5th days (all symptoms are worst) • Typhidot
h. Subsultus tandinum b. Urine Culture
• involuntary twitching of the tendon of the wrists c. Stool Culture
• Twitching of the tendons set in, esp wrist
• Nausea, vomiting and diarrhea Widal agglutination
i. Constant tendency  was introduced as a serologic technique to aid in
diagnosis of typhoid fever. The test was based on
• to slip down toward the foot of the bed.
demonstrating the presence og agglutinin (antibody) in
• Fever is higher in the morning than in the
the serum of an infected patient against the H (flagellar)
afternoon (step-ladder pattern fever continuous)
and O (somatic) antigens of Salmonella typhi
 it should be done after 5-7 days of fever by tube method
s/s Typhoid State and level of 1 in 160 for both H and O antibodies are
• symptoms decline in severity usually taken as diagnostic Slide Widal test should be false
• tongue protrudes, dry & brown positive result.
• teeth & lips accumulate a dity-brown collection  The widal test is positive if TO antigen titer is more than
of dried mucus & bacteria (sordes- preventable 1:160 in an active infection, or if TH antigen titer is more
by good nursing care ONSET) that 1:160 in past infection or in immunized persons
• Coma Vigil
• Subsultus Tendinum Typhidot
• Carphologia  Is a medical test consisting of a dot ELISA kit that
• Delirium detects IgM and IgG antibodies against the outer
membrane protein (OMP) of the Salmonella typhi. The
typhidot test becomes positive within 2-3 days of
infection and separately identifies IgM and IgG
antibodies.
 Modalities of Treatment
a. Chloramphenicol
b. Ampicillin
c. Co-trimoxazole
d. Ciprofloxacin or Ceftriaxone
Site: Epithelial Tissue / cells of
e. F/E balance-IVF
f. Supportive methods (BT, Surgery) (perforation) intestinal mucosa

Nursing Management Function of Epithelial Tissue:

a. Isolation , medical aseptic technique • Protect of underlying
b. Maintain/restore fluid and electrolyte balance tissues
c. Monitor patient’s vital signs • Absorption
d. Prevent further injury • Secretion
e. Maintain good personal hygiene & mouth care • Reception of sensory
f. Cooling measures stimuli
g. Watch out for signs of intestinal bleeding
h. Terminal & concurrent disinfection.
i. *Two vaccines have been used for many years to
prevent typhoid.
j. A new typhoid conjugate vaccine with longer lasting Signs and Symptoms
immunity was prequalified by WHO in December a. 1stPhase 1-3 days
2017.(6 months) • Fever, Chills
k. *If the patient does not respond to chloramphenicol, • Nausea, Vomiting and headache
3rd & 4th generation drugs are administered. • anorexia and body malaise
• Tenesmus – a continual or recurrent inclination to
Health Teachings /Control evacuate the bowels, caused by disorder of the
a. Proper hand washing, clean environment rectum or illness/painful straining during BM
b. Proper food handling • Colicky/cramping abdominal pain
c. Boil drinking water • Diarrhea with bloody mucoid stool
d. Avoid street foods and improperly washed or • Rapid dehydration and weight loss.
improperly cooked food b. 2ndPhase
e. Pasteuration of public milk supply • char. of stool changes-no. of BM & quantity
f. Proper disposal of excreta • Stool bright red blood , mucoid w/ foul odor
g. Reporting of cases to health authorities • anorexia
h. Detection and monitoring of typhoid carriers/areas
i. Education of the general public on MOT Complications:
j. Protection & Purification of public H20 supply a. Rectal prolapse
b. Pneumonia
PARATYPHOID FEVER c. Non-suppurativearthritis and peripheral neuropathy
Causative Agent:
Salmonella Paratyphoid A Diagnostic Procedure
Salmonella Paratyphi Schott muelleri a. Fecalysis
Salmonella Paratyphi hirschfeldii b. Rectal swab
IP1-10 days c. Blood exam / culture
MOT same as Typhoid (only large intestines are involve d. Sheets of polymorphonuclear leukocytes seen in
Signs and Symptoms same as Typhoid although less staining with methylene blue
severity & shorter duration
Complication-less frequent Modalities of Treatment
a. Antibiotics –Ampicillin
2. Bacillary Dysentery b. Tetracycline-Cotrimoxazole
Shigellosis / bloody flux c. IV Therapy
• Acute bacterial infection of the intestines d. Low Residue Diet
characterized fever and diarrhea with bloody mucoid
accompanied by tenesmus. Nursing Management:
• Causative Agent a. Maintain fluid & electrolytes
o Shigella Flexneri b. Keep pt. warm and comfortable
o Shigella Boydii c. Restrict food until N/V subsides
o Shigella Connei d. Isolation /Medical asepsis
o Shigella Dysenteriae e. Hygiene and disinfection
 Considered as the most infectious f. Proper excreta disposal
 Their habitat is exclusively the GIT of man g. Gradual return to activities
 Like other Gram-Negative bacilli, they h. Monitor I & O
develop resistance against antibiotics
 They rarely invade the blood stream
Incubation period
• 7 hours to seven days ( ave.3-5 days)
Period of communicability
• During acute infection
• Some patient remain carrier until 2 years.
Mode of transmission: (Indirect Contact)
• Ingestion of contaminated food or water or milk
• Flies or other fomites
• Fecal oral transmission
3. Amoebiasis (Amoebic Dysentery)
 Protozoal infection of human beings initially involves the
colon and may spread to soft tissues.
Etiologic agent
a. Entamoeba histolytica
• Prevalent in unsanitary areas
• Cysts survives a few days outside the body
• Common in warm climates
• Cysts passes to the large intestine and hatches into a
trophozite. It passes into the mesenteric veins
• Acquired swallowing the portal vein, and finally to
the liver, where it causes amoebic liver abscess
b. Entamoeba Histolytica has two Developmental stages:
AREAS:
• Trophozoites /vegetative form- are facultative
o SECAL- ileum, cecum, appendix, ascending colon
parasites that may invade the tissues or may be
o RECTAL- sigmoid colon, rectum
found in parasitized tissues and liquid colonic
contents
• Cysts – is passed out with formed or semi-formed
Period of Communicability
stools and is resistant to environment conditions. It
a. Entire duration of an illness, as long as the cysts are
is considered as the ineffective stage in the life cycle
present in the feces, may continue for years.
of E. histolytica
o Mode of Transmission
Source
b. Fecal-oral transmission – can be passed from one
a. Human excreta
person to another through fecal -oral-transmission
Incubation Period
c. Direct contact – sexual contact- oro-genital, oro-anal,
• Severe Infection : 3 days procto-genital activity
• Sub Acute / Chronic lasts for several mos. d. Sexual contact
• Average Cases (3-4 wks) e. Indirect contact- ingestion of uncooked vegetables or
foods contaminated with fecal material containing E.
histolytica cysts ; food and drinks contaminated by cysts
through pollution of water supply exposure to flies, use
of night soil for fertilizing vegetables, and through
unhygienic practices of food handlers.

o Clinical manifestations:
a. Acute amoebic dysentery
b. Chronic amoebic dysentery
c. Extraintestinal forms

o Diagnostic Exam
a. Stool exam – (cysts, white and yellow pus with plenty of
amoeba)
b. Blood exam (leukocytosis) increase WBC
c. Proctoscopy – Rectum and bottom part of the colon
d. Sigmoidoscopy- examination in the lower large bowel/
far into the colon

Acute Amoebic Chronic Amoebic Extraintestinal

Dysentery Dysentery Forms
• Slight diarrhea, • Constipation • Pain in upper right
altered • Tenesmus, desire to defecate quadrant with liver
constipation- • Anorexia, weight loss, weakness tenderness
tenesmus • Liver may be enlarged • Jaundice
• Diarrhea, watery, • Stool semi-fluid –watery, bloody • Intermittent fever
foul smelling, blood & mucoid • Loss of weight or
streaked mucus • Vague abdominal distress, anorexia
• Colic, gaseous flatulence, constipation or • Lung abscess–coughs-
distension of the irregularity of bowel mov’t anchovy-sauce
lower abdomen • Mild toxemia, fatigue, lassitude sputum
• Nausea • Signs of dehydration
• Flatulence • Sigmoid-ulceration, yellowish,
• Abdominal erythematous borders
distention • Gangrenous type-hemorrhage
• Tenderness right
iliac region over the
colon

*Lassitude - a state of Physical or mental weariness; lack of energy

*Anchovy – sauce like ous or sputum may be found. Presence of bile
in sputum indicates that the pus is of liver origin
*Amebic antigen can be detected from serum and pus by ELISA
 4. Cholera
 Synonym: eltor
 An acute bacterial enteric disease of the GIT characterized
by profuse diarrhea, vomiting, massive loss of fluid and
electrolytes that could result to hypovolemic shock,
acidosis, and death
o Etiologic Agent
• Vibrio cholerae/Vibrio coma
o survive well to ordinary temperature
can survive longer in refrigerated foods
o Incubation period
• few hours to five days usually one to three days
o Treatment Modalities
o Mode of Transmission
a. Metronidazole
• INDIRECT CONTACT
b. Tetracycline
o Fecal transmission
c. Ampicillin, quinolone, sulfadiazine
o Ingestion of food
d. Streptomycin SO4, chloramphenicol
o Flies, soiled hands, and utensils
e. IV Therapy
• Period of Communicability
o During acute infection & until the infectious
o Nursing Management
agent is no longer present in feces, usually
a. Observe Isolation & Enteric Precaution
within 4 weeks after illness.
b. Provide Health Education
c. V/S monitoring
o Clinical Manifestations
d. Proper collection of stool specimen
• Acute profuse watery diarrhea
e. Skin Care
f. Oral/Anal Care • Brown stool to pale gray stool –(rice water), bloody
g. Provide Optimum comfort mucoid
h. Diet –easily digested food • Vomiting
i. Prevent complication & S/E of the drug • Poor skin turgor
• Cold skin
Enteric Precaution are a way of preventing this spread. Direct • Cyanosis
contact means physical contact between people, often the hands. • RR-rapid and deep
Indirect contact means contact with a contaminated object, such as • Oliguria and anuria
toys, clothing or surfaces

Health Education:
• Boil water for drinking or use purified water
• Avoid washing food with water from open drums or pails
• Cover left over foods
• Wash hands after defecation and before eating
• Avoid eating ground vegetables (lettuce, carrots, etc.)

Stool Collection
• Never give paraffin or any oil preparation for at least 48 hours
prior to the collection of specimen
• Instruct pt. to avoid mixing urine with stools
• If whole stools cannot be sent to laboratory, select as large
portion containing blood and mucus as possible
• Send specimen immediately to lab; stool not fresh are useless
• Label specimen properly
*Release toxins = (CHOLERAGEN) ->increases capillary
Skin care
Cleanliness and freedom from wrinkles on the sheet will be helpful permeability >fluid will enter the intestine > get out in the form of
with all the usual precautionary measures against pressure sores. stool
*Loss of Bicarb (HCO3) stores through diarrhea or renal tubular
Provide Optimum Comfort wasting leads to metabolic acidosis state characterized by increased
The pt. should be kept warm. Dysenteric pt. should never be allowed plasma chloride concentration and decreased plasma bicarbonate
to feel cold even for a moment concentration (hyperchloremic metabolic acidosis)

Diet o Principal Deficits

• During the acute stage fluid should be forced a. Extracellular volume
• Cereals and strained meat broths without fat should be given • severe dehydration
• Chicken and fish may be added when convalescence is • circulatory collapse
established b. Metabolic Acidosis- loss of large volume of
• Bland diet without cellulose or bulk-producing foods should be
bicarbonate-rich stool
maintained for a long time
c. Hypokalemia- Massive loss of potassium
o Methods of prevention d. Renal Failure-consequence of untreated shock or
a. Health Education hypokalemia
b. Sanitary disposal e. Convulsions & Tetany-due to loss of Mg
c. Protect, chlorinate, & purify drinking water f. Hypoglycemia untreated children –stupor for days
d. Observe scrupulous cleanliness in food preparation g. Corneal scarring –stuporous pt. lost wink reflex
e. Detection & Treatment of carriers h. Acute pulmonary edema-follow hydration in cases of
f. Fly control (they can serve as vectors) uncorrected metabolic acidosis
o Diagnostic Exams  It is also known as infectious hepatitis because it spreads
a. Rectal swab relatively easy to individuals who have close contact with
b. 2.Stool exam the infected.
c. Darkfield or phase microscopy- (stool-presence of pus Synonyms: Infectious hepatitis; Catarrhal jaundice;
cells) Epidemic Hepatitis; Botkin’s dse
Causative agent–RNA-containing virus
o Modalities of Treatment Mode of transmission –food and water
a. intravenous treatment contaminated with feces and saliva of patient with
b. ORT – oral rehydration therapy Hepatitis A. MOT =Direct contact = person to
c. Antibiotics person ; the virus is transmitted through the fecal-
• tetracycline oral pathway
• furazolidone • Ingestion of contaminated drinking water or
• chloramphenicol ice, uncooked fruits and vegetables, and
• cotrimoxazole fruits and vegetable grown in washed with
contaminated water; and contaminated food
o Nursing Management / drinks by infected food handlers.
a. Medical aseptic Predisposing factor
b. Enteric Isolation • Food handlers
c. V/S accurate recording • Unsanitary living conditions
d. I & O , wt . accurately measured • Oral-anal sex
e. Provide good Personal hygiene Incubation period
f. Proper excreta disposal • 3 –5 weeks or 15-60 days; mean of 30 days
g. Disinfection Period of Communicability
h. Food properly prepared • 2 weeks before illness to 1 week after onset of
i. Environmental Sanitation jaundice
• The infected patient is capable of transmitting
the organism from a week before until a week
o Prevention: after the appearance of symptoms
a. Food & water supply must be protected from fecal Groups at Risk for HAV
contamination. a. Children in day care center can transmit
b. Water should be boiled or chlorinated. the infection through diapers and toys
c. Milk should be pasteurized. b. Troops living in crowded conditions at
d. Sanitary disposal of human excreta. military camps or in the field area at great
e. Sanitary supervision is important. risk
c. Homosexual men are at an increased at
risk of HAV infection from oral-anal sexual
contact
5. Hepatitis d. People who live in areas with a breakdown
Hepatitis is define as an inflammation of the liver, of sanitary conditions, such as after flood
and is classified as either viral or non viral or other natural disasters.
The condition can be self limiting or can progress
to fibrosis (Scarring), cirrhosis or liver cancer.
Hepatitis viruses are the most common cause of
hepatitis in the world but other infection, toxic
substances (e.g. alcohol, certain drug), and
autoimmune disease can also cure hepatitis

o Causative agents
• Microorganisms –bacteria, viruses,
protozoa, spirochetes
• Too much alcohol
• Drug intoxication
o Chemical intoxication
o TYPES:
• Hepatitis A
• Hepatitis B
• Hepatitis C
• Hepatitis D
• Hepatitis E

HEPATITIS A

Following ingestion, HAV enters the bloodstream through the

 It is a liver disease caused by the hepatitis A virus. This is an
inflammation of the liver that is not really very severe and
runs an acute course. This generally starts within two to six
weeks after contact with the virus, and lasts no longer than
two months
epithelium of the oropharynx or intestines.
The blood carries the virus to its target, the liver, where it lives and
multiplies within the hepatocytes and Kupffer cell (i.e., liver
macrophages)
Virions are secreted into the bile and released in stools. HAV is
excreted in large quantities approximately 11 days prior appearance
of symptoms or anti-HAV lgM antibodies in the blood.

Clinical manifestation
a. Flu-like illness with chills and high fever
b. Diarrhea, fatigue and abdominal pain
c. Loss of appetite
d. Nausea, diarrhea and fever
e. Jaundice and dark-colored urine
f. The infection in young children is often mild and
asymptomatic
g. Hepatitis A does not have a chronic stage and
does not cause permanent liver damage
h. Following infection, the immune system makes
antibodies against the Hep A virus that confer
immunity against future infection. The disease
can be prevented by hepatitis A Vaccine.
Complications:
a. Progressive encephalopathy characterized by
drowsiness and cerebral edema
b. GIT bleeding progressing to stupor and later
coma. Bleeding is not responsive to parental
vitamin K administration
c. Clonus and hyperreflexia are later replaced by
loss of deep tendon reflexes
d. Edema and ascites
e. Aplastic anemia
f. In the late course of the disease, loss of corneal
and papillary reflexes, elevated arterial blood,
respiratory failure, cerebrovascular collapse may
be present.
Diagnostic procedures
a. HAV and HBV complementation fixation rate
b. Liver Function test (SGOT, SGPT, ALT)
c. Bile examination of stool and urine samples
d. lgM level
Treatment modalities
a. There is no specific treatment, although bed rest is
essential
b. Diet must be high in carbohydrates and protein,
low in fat
c. Patient must have to take vitamin supplements,
especially the B complex group
d. IV therapy is occasionally necessary
e. Isoprinosine (methisoprenol) may enhance the
cell-mediated immunity of the cell T-lymphocytes
f. Alkaline, belladonna and anti-emetics should be
administered to control dyspepsia and malaise
Diagnostic procedure
1. HAV and HBV- complementation fixation rate= As an
alternative approach, detection of antibodies which the
patients had produced against the antigens of the disease-
causing agents. However, this approach was problematic as
it depended upon detection of the reaction of the patient’s
antibodies with the viral antigen. This method is most often
used was the quite difficult
2. Liver Function Test- to determine the presence and
extent of liver damage & check the progress of the liver.
3. Bile examination of stool and urine samples-
Hyperbilirubinemia results from increased bilirubin
production, Decreased liver uptake or conjugation,
Decreased biliary excretion (Jaundice).
• Bilirubinuria reflects the presence of conjugated
bilirubin in urine; bilirubin spills into urine because
blood levels are markedly elevated, indicating severe
disease. Such increases in unconjugated bilirubin
are usually <5 times normal (to <6 mg/dL [ < 100
micromol/L]) unless there is concurrent liver injury.
1.
4. AST= SGOT and ALT= SGPT;
• they are enzymes produced by the liver and other types of
cells.
• Blood tests pertaining to the liver are measurements of
some of the other enzymes found in the liver. In addition to
AST and ALT, alkaline phosphatase, 5’ nucleosidase, and
gamma-glutamyl transpeptidase (GGT) are a few of the
other enzymes located in the liver. Another name for
aminotransferase is transaminase.
• The enzyme aspartate aminotransferase (AST) is also known
as serum glutamic oxaloacetic transaminase (SGOT).
• Alanine aminotransferase (ALT) is also known as serum
glutamic pyruvic transaminase (SGPT).
✓ ALT- serum alanine transaminase- Elevated ALT is somewhat
specific for liver injury.
✓ Because AST is present in the heart, skeletal muscle, kidneys,
red blood cells, and pancreas, elevated AST may reflect
rhabdomyolysis or injury to one of these organs.
(Rhabdomyolysis is a potentially life- threatening syndrome
resulting from the breakdown of skeletal muscle fibers with
leakage of muscle contents into the circulation. The most
common causes are crush injury, overexertion, alcohol abuse
and certain medicines and toxic substances).
✓ Aminotransferase enzymes Normal range
AST (SGOT) 5 to 40 units per liter of serum (the liquid part of
the blood) ALT (SGPT) 7 to 56 units per liter of serum)
✓ HBsAg (Hepatitis B surface antigen)- a “positive” or “reactive”
HBsAG test result means that the person is infected with
Hepatitis B. this test can detect the actual presence of the
hepatitis B virus (called the “surface antigen”)
✓ Normal result are negative or non reactive, meaning that no
hepatitis B surface antigen was found.
5. IgM level- The IgM antibody to hepatitis A virus (anti-HAV)
for acute hepatitis A.
• The liver is constantly engaged in a balancing act to
ensure that the right nutrients get to the right parts of
the body in the right amount.
• If the right balance of food is consumed, the already
burdened liver won’t have to work hard. Nutrition is
one aspect of disease where a person has some
degree of control and can actively participate in
speeding recovery and minimizing the likelihood of
additional injury.
• Some people suffering from hepatitis may need extra
nutrition to prevent unplanned weight loss and may
benefit from a high calorie and protein diet. In
hepatitis, diet and exercise are important.
• A good balanced diet which is low in fat, high in fibre
with plenty of fresh fruit and vegetable plus regular
exercise will be beneficial and can help our body deal
effectively with the viral infection.
• All foods, beverages and even medications that we
ingest pass through the liver to be metabolized.
• Therefore, diet plays an important role in maintaining
a healthy liver. People with hepatitis often need a
high-calorie diet to help rejuvenate the damaged liver
and maintain adequate nutrition.
Objectives
▪ To provide adequate nutrition.
▪ To relieve symptoms. Avoid dehydration. Drink
plenty of water.
▪ To aid in the regeneration of liver tissues.
▪ To prevent further liver damage.
✓ Rigorous bed rest in acute viral hepatitis is
necessary only for short period of time; it is
necessary in chronic liver disease only in rare cases
and during terminal stage
✓ Proteins normally help the body repair tissue. They
also prevent fatty buildup and damage to the liver
cells. But in Hepatitis it must be Low Protein,
Cutting down the amount of animal protein you
eat. This will help limit the buildup of toxic waste
products.
✓ Protein intake needs to be increased to promote
regeneration of the liver. However, a very high
protein load may not be tolerable and needs are to
be adjusted depending on the extent of liver
damage. Adequate protein intake is important to
build and maintain muscle mass and to assist in
healing and repair of tissues. Therefore, protein
intake should be between about 60- 120 grams a
day in patients with hepatitis, unless a complication
of cirrhosis known as encephalopathy is present.
✓ Increasing your intake of carbohydrates to be in
proportion with the amount of protein they eat. A
high carbohydrate diet is recommended to meet
the increased energy needs. If too much protein is
consumed and not enough carbohydrates, the liver
will be forced to use protein as an energy source.
This is an unwise and inefficient use of protein, as
protein will be diverted from its protein will be
diverted from its primary job of building cells and
tissues. Therefore, this will put undo stress on the
liver, as it is more taxing for the liver to convert
protein into energy than it is to convert
carbohydrates into energy.
✓ In case of hepatitis, the digestion and absorption of
fat is impaired. Therefore, it is advisable to
decrease fat intake, though not severely. Emulsified
fats such as fat from milk, butter, cream, eggs
should be given as they are easily digested.
✓ Eat fruits and vegetables and lean protein such as
legumes, poultry, and fish. Avoid uncooked
shellfish.
✓ Taking vitamins and medicines prescribed by your
health care provider for low blood count, nerve
problems, or nutritional problems from liver
disease.
✓ Minerals- The diet should provide all minerals,
particularly calcium in adequate amounts.
✓ Vitamins- The requirement of vitamin A, B, C and K
are to be adjusted. Vitamins if taken in excess have
the potential to cause serious health problems.
Depending upon the severity of liver damage the
intake of vitamins has to be judged.
✓ Limiting your salt intake. Salt in the diet may
worsen fluid buildup and swelling in the liver.
Belladonna alkaloids used to treat ulcers in the
intestine.
Nursing management
• The patient must be isolated (enteric
isolation
• The patient should be encouraged to rest
during the acute or symptomatic phase
• The patient’s nutrition status must be
improved
• Appropriate measures to minimize spread
of the disease must be taken
• Observe the patient for melena and check
stools for the presence of blood
• Provide optimum skin and oral care
• Increase the ability to carry out activities
Increase the ability to carry out activities
• Encourage the patient to limit activity
when fatigued.
• Assist the client in planning periods of rest
& activity.
• Encourage gradual resumption of
activities & mild exercise during recovery.
Prevention and control
• Hands should be washed thoroughly after
using the toilet
• Travelers should avoid water and ice if
unsure of their purity
• Food handlers should be carefully
screened
• Safe preparation and serving food must
be practiced
• The public should be educated on the
mode of transmission of the disease
Hepatitis B
• most fatal
Synonym: Serum hepatitis; Homologous hepatitis; Viral
hepatitis
Causative agent –DNA-containing virus or HBV
Mode of transmission
• blood and other body fluids; percutaneous/inoculation
• Use of contaminated needles
• Blood transfusion
• Sexual transmission
• Vertical/transplacental transmission
• Perinatal transmission /mother to child @ birth
• Horizontal/exposure to infected blood
Predisposing factors
• Health workers
• Blood recipients
• Drug addicts
• Promiscuous individual/multiple sex partners
Incubation period–2 to 5 months 50-189 days; M=90 days
✓ Hepatitis B virus was originally recognized as the agent responsible
for “serum Hepatitis B virus hepatitis”, the most common form of
parenterally transmitted viral hepatitis, and an important cause of
acute and chronic infection of liver.
✓ Hepatitis B is the inflammation of the liver caused by hepatitis B
Virus. This is considered to be more serious than hepatitis A due to
the possibility of severe complications such as massive damage and
hepatocarcinoma of the liver.
✓ It was once thought to be transmitted only through direct exchange
of contaminated blood.
✓ Hepa B is now known to be transmitted also by contact with human
secretion & stools. Recipients of Plasma-derived products &
hemodialysis clients are particularly at risk.
 Etiologic Agent
✓ This virus has very limited tissue tropism
✓ HBV infects the liver & possibly the pancreas.
✓ HBsAg appears in the blood 30 to 60 days after
exposure & persists for variable periods of time.
a. HBV primarily interferes with the functions of the liver
by replicating in liver cells, known as hepatocytes.
b. During HBV infection, the host immune response
causes both hepatocellular damage and viral
clearance.
c. The virus replicates and large amounts of HBsAg are
released into the blood, in addition to Virions.
d. Initiation of virus replication, maybe as soon as 3 days
from acquisition, but symptoms may not be observed
until after 45 days or much longer.
e. Replication of the virus is not cytopathic proceeds for
relatively long periods without causing liver damage
f. During the acute phase of infection, the liver
Hepatitis D
parenchyma shows degenerative changes consisting of
cellular swelling & necrosis especially in hepatocytes.
Period of Communicability
• During the latter part of the IP & during acute phase.
• Virus persist in the blood for many years.
The acute illness damages & destroys so many liver
cells that the liver can no longer function, This is
called Fulminant liver failure and may cause death.
Clinical Manifestation
a. Prodromal Period
• Fever , malaise, anorexia
• N/V, abdominal discomfort, fever, chills
• Jaundice, dark urine, & pale stools
• Rec0very =decline fever & improved appetite
b. Fulminant Hepatitis
• fatal, severe symptoms like ascites & bleeding
Hepatitis C (Non A Non B Hepatitis)
Synonym: Post-transfusion hepatitis
(blood-borne virus)
Causative agent –Hepatitis C virus
Mode of transmission
• percutaneous (sharing of needles), particularly blood
transfusion
• Reuse or inadequate sterilization of medical equipment
• unscreened blood & blood products
• sexual activity
• transplacental
• hemodialysis
• perinatal
Predisposing factors
• Paramedical team
• Blood recipients
Incubation Period –2 weeks to 6 months
Clinical Manifestations: Often asymptomatic
Hepatitis C
• Is a blood borne infectious disease caused by
hepatitis C virus (HCV) originally known as “non-A,
non-B hepatitis”
• The infection is often asymptomatic, but once
established, can cause scarring of the liver (fibrosis)
and eventually, cirrhosis (advance scarring).
• The heap C virus is associated with a high rate of
chronic liver disease (chronic hepatitis, cirrhosis, and
an increased risk for hepatocellular carcinoma).
• Clients with chronic hepatitis C are considered
infectious,
• No vaccine is available for hepatitis C.
Hepatitis D(Delta Virus)
• Dormant type of hepatitis
• Co-Infection-can be acquired only if with Hepatitis B
• Super Infection-there is established infection after HDV is
acquired can transform mild infection to persistent
infection.
mode of transmission
• person to person in household situation in endemic
areas
• IV drug abuse and incubation period as Hepatitis B
Incubation period
• Co-infection-90 days
• Super infection-2-8 weeks
• Hepatitis D virus (also called delta virus) is a small, circular
RNA Virus.
• Hepatitis D virus is replication-defective & therefore
cannot propagate in the absence of another virus. In
humans, hepatitis D virus infection occurs only in the
presence of hepatitis B infection.
• Hepatitis D Virus infection is transmitted by blood & blood
products. The risk factors for infection are similar to those
in hepatitis B virus infection.
• A patient can acquire hepatitis D virus infection at the
same time that he/she is infected with the hepatitis B
virus. This is called Co-infection.
• A patient can also be infected with hepatitis D virus at
anytime during acute hepatitis B virus infection. This is
called Super infection.
• Found only in patients with an acute episode of or chronic
hepatitis B & requires the presence of HBsAG (Hepatitis B
surface antigen).
MANIFESTATION/ SIGNS AND SYMPTOMS
a. Pre-icteric stage /Prodromal
• flu –like illness
• chills & high Fever
• Diarrhea
• Fatigue
• body malaise
• Loss of appetite
• Weight loss
• Anorexia
• Nausea & vomiting
• Abdominal pain /Right upper quadrant pain
• Anemia
 b. Icteric stage
• Jaundice
• Pruritus
• Tea-colored urine
• gray-colored
• Hepatomegaly

c. Post-icteric stage
• Signs and symptoms subside
• Takes 3-4 months for the liver to regenerate

Diagnostic/laboratory exam
• Complement fixation rate (detect the presence of
spec. antibody or spec. antigen in the pt’s serum.
• Radio-Immunoassay-hemagglutinin test
• Liver Functions Test
o PT, a PTT, albumin, bilirubin, AST or SGOT, ALT or
SGPT ( biomarkers of liver injury)
o Serum Antigen Antibody Test-Liver biopsy
,Urinalysis Ultrasound
o HBs Ag-surface antigen, 1stmarker to appear
(active)

Management
SIGNS AND SYMPTOMS
• Prevention –Immunization for Hepatitis A and B a. Prodromal Stage
• Control –avoid mode of transmission; handwashing • Easy fatigue, anorexia, body malaise, headache,
• NO vaccine available for HCV arthralgia, myalgia, photophobia, & N/V.
• Changes in senses of smell & taste
Nursing care
• mod. grade fever 37.8-38.9 C
• Complete bed rest
• Urine dark colored
• Diet-dec fat, inc carbo, inc protein if with simple
• Stools are clay colored
hepatitis
• dec fat, dec carbo, inc protein if with severe hepatitis b. Clinical Jaundice stage
• Pruritus, abdominal pain or tenderness & indigestion
Protein intake needs to be increased to promote • Yellowish discoloration of sclerae, mucous membrane &
regeneration of the liver. However, a very high protein load skin lasts for 1-2 wks
may not be tolerable and needs are to be adjusted • Pain , tenderness RUQ ( hepatomegaly,
depending on the extent of liver damage. Adequate protein splenomegaly & cervical adenopathy are present)
intake is important to build and maintain muscle mass and to
assist in healing and repair of tissues. Therefore, protein c. Recovery Stage: Lasts for 2-12 weeks
intake should be between about 60 - 120 grams a day in
patients with hepatitis
HAV : Detection of Antibodies to HAV confirms the diagnosis. (IgM-=
antibodies in the blood.
Hepatitis E
HBV: The presence of HbsAg & Hepa B antibodies (HBsAb)
Synonym: Enteric hepatitis
HCV: depends on serologic testing for specific antibody one or more
Causative agent : Hepatitis E virus
months after the onset of acute hepatitis.
Mode of transmission
HDV: detection of intrahepatic delta or Immunoglobulin M (IgM)
• fecal-oral
establishes the diagnosis.
• water borne routes
HEV: detection of Hep E antigen supports the diagnosis
Predisposing factors and incubation :same as Hepatitis A
GENERAL NURSING MANAGEMENT
Hepatitis E
a. Suggest that a large meal be eaten in the morning because
• Transmitted enterically (fecal-oral and waterbone
nausea tends to intensify as the day progresses.
routes), like hepatitis A.
b. Provide diversional activities to relieve boredom and
• Hepatitis E Virus is inconsistently shed in stools; anxiety.
therefore detection is difficult. c. encourage anorexic pt. to take juices with occasional ice
• Hepatitis E Virus is a common cause of hepatitis that is chips to maintain hydration without inducing vomiting.
transmitted via the intestinal tract. Spread most often d. Monitor the pt’s wt. daily. Record I&O.
by drinking contaminated water. e. Observe stools for color, consistency & amount. Record the
• Hepatitis E Virus never becomes a chronic (long- frequency of bowel movement.
lasting) illness but on rare occasion the acute illness f. Before the pt. is discharge, discuss restrictions & how to
damages & destroys so many liver cells that the liver prevent recurrence of hepatitis.
can no longer function, This is called Fulminant liver
failure and may cause death.
• Pregnant women are at a much higher risk of dying
from fulminant liver failure.
• The great majority who recover from acute infection do
not continue to carry HEV and cannot pass the
infection to others.
Non –Viral Hepatitis Mode of Transmission
• Non Viral Hepatitis –toxic or drug induced • Ingestion
• Contact with the skin
✓ Relieving your symptoms- get plenty of rest - • Mucous membrane (nose, mouth, break in the skin)
especially during the initial stages of the infection,
as the pt. probably feel very tired. Clinical Manifestations
✓ Is a zoonotic infectious bacterial disease carried by a. Septic stage
animals, both domestic and wild. Infected urine • Fever, chills, headache, anorexia, abdominal pain and
contaminates water or food which causes disease severe prostration
when ingested or inoculated through the skin b. Immune or toxic Stage
• Iritis, meningeal manifestation, oliguria, anuria, shock,
coma, CHF
Causes • Convalescence-relapse may occur.
a. Alcohol overuse
b. Direct hepatotoxicity C.M.
c. Idiosyncratic hepatotoxicity • The symptoms range in severity from
d. Cholestatic reaction asymptomatic to fatal.
e. Metabolic and autoimmune disorders
• Clinical course is generally biphasic (2 phases)
Nursing care & the majority of the cases are unicteric
• Complete bed rest (protein precipitation reaction in blood serum).
• Diet-decrease fat, inc carbo, inc protein if with simple • 3 stages
hepatitis o Septic stage
• decrease fat, decrease carbo, inc protein if with severe ✓ This stage is marked by febrile lasting
hepatitis for four to seven days.
✓ There is an abrupt onset of remittent
6. Leptospirosis
fever, chills, headache, anorexia,
Is a zoonotic infectious bacterial disease carried by
animals, both domestic and wild, whose urine
abdominal pain, & severe prostration.
contaminates water or food which is ingested or inoculated ✓ There is also respiratory distress. Fever
through the skin. subsides with lysis.
Synonym o Immune or Toxic Stage
• Mud fever ✓ This stage can be with or without
• Canicola fever jaundice & lasts for 4 to 30 days.
• Weil’s disease ✓ Convalescence- At this stage, relapse
• Swine herds disease may occur during the 4th to 5th.
• Hemorrhagic jaundice
Etiologic Agent: Leptospira interrogans

E.A.
A spirochete of the genus Leptospira (Leptospira
interorgans).
a. These are chiefly saprophytic aquatic organisms which
are found in the liver and lake waters, sewage and in
the sea.
b. These are 150 serotypes divided among 18
serogroups; some species are pathogenic to man &
animals.
c. Weil’s disease is specifically caused by the serovar
icterohaemorrhagiae.

Characteristics
• Chiefly saprophytic aquatic organism
• Found in river and lake water and in the sea ORGANS OF THE BODY INVADED BY ORGANISM
Incubation period : 6 to 15 days a. After the organism gains entrance into the body, it multiplies
Period of communicability –leptospira is found in the urine in the bloodstream & invades the liver, resulting in jaundice.
between 10 to 20 days after the onset b. In the kidneys, the presence of the organism causes
Sources of Infection inflammation of the nephrons & tubular necrosis, resulting in
• Rats renal failure.
• Dogs c. Leptospira may affect the muscles, resulting in pain &
• Mice sometimes edema.
Source: Infection comes from contaminated food & water & d. The organism also invades the eyes, resulting in conjunctivitis.
infected wildlife & domestic animals, especially rodents. In addition, due to liver involvement, the patient becomes
a. Rats (L.ictherohaemorrhagiae) are the source of Weil’s disease icteric, thereby giving an orange-colored sclera.
frequently observed among mine, sewer, and abattoir workers
(a-ba-twar)(slaughter house workers e.g. butcher).
▪ Rats (L. bataviae) are also the source of infection
that attacks ricefield workers.
b. Dogs (L. canicola) can also be the source of infection among
veterinarians, breeders & owner of dogs.
c. Mice (L. grippotyposa) may also be a source of infection that
affects farmers & flax workers.
Lab Dx 7. Red Tide
a. BUN, Creatinine Is caused by “population explosion” of toxic, naturally
b. Enzyme-linked immunosorbent assay (ELISA) occurring microscopic phytoplankton specifically a
c. Liver Function Test subgroup known as dinoflagellates
• AST (aspartate aminotransferase)
• ALT (alanine aminotransferase)
• GGT(gamma-glutamyl transferace)
d. LAAT (Leptospira antigen –antibody test)
e. LAT (Leptospira antibody test)

Management
What Causes a red tide?
• Pen G, Doxycycline,
• The over proliferation of dinoflagellates
• ampicillin, amoxicillin
• Brought upon by:
• Tetracycline
o Warmer water temperature and minimal wind,
• Peritoneal dialysis
causing nutrients to settle on the bottom of the bay
• Fluid and electrolyte, BT o Favorable wing and water currents
o Overfeeding: when nutrients such as phosphorous,
Complications nitrogen, and carbon from lawns and farmlands
• Meningitis (e.g.) flow
• Respiratory Distress Into the ocean and build up at a rate that overfeeds
• Renal Interstitial tubular necrosis-renal failure (Weil’s the algae in the environment
dse) Natural phenomena such as sluggish water
• Cardiovascular problems circulation, unusually high water temperatures, and
extreme weather events such as hurricanes, floods,
Nursing Care and drought.
• Isolation, proper disposal of urine
• I & O monitoring What is Dinoflagellates?
• V/S monitoring • Dinoflagellates
• Darken the pt’s room o Temperature, salinity, depth
• Keep pt.under close surveillance o Photosynthetic or mixotrophic
• Prevent water stagnation o Produce neurotoxin
• Eradicate rats & rodents • Dinoflagellate movement:
• H.E on MOT https://www.youtube.com/watch?v=6iM63hIUiuU
• Encourage fluid intake • This is what gives red tides their distinct color

Prevention and control The name red tide was coined due to the sea water
• Sanitation in homes, workplaces & farms is a must discoloration which ranges from amber, red, brown,
• There is a need for proper drainage system and yellow orange to purple caused by the highly-dense
population of dinoflagellates.
control of rodents.
• Animals must be vaccinated. Etiologic Agent
• Infected humans & pets should be treated. The marine red tide organisms used to be referred to as
• Information dissemination campaign must be Gonyaulax, Protogonyaulax, Alexandriumand Gessnerium.
conducted effectively. Presently, they are known by the accepted name
Alexandriums pecies.
▪ Alexandrium tamarenseare found along the Atlantic
MEDICAL Ocean.
• Treatment of leptospirosis is geared toward: ▪ Alexandrium catanellaare found in the Pacific West
A. Suppressing the causative agent Coast.
B. Fighting possible complications ▪ Ptychodiscus brevis is present in the gulf of Mexico
o Aetiotropic drugs- penicillin, doxycycline, along the West Florida Coast.
ampicillin, amoxicillin
o For prophylaxis, doxycycline 100mg p.o. every 12
hours for 1 week
o Peritoneal Dialysis
o Administration of fluid & electrolytes & blood as
indicated

NURSING
o Isolate the patient; urine must properly disposed of.
o Darken the patient’s room because light is irritating to the
pt’s eyes.
o Observe meticulous skin care to ease pruritus
o Keep clients under close surveillance
o Keep homes clean. Regularly replace water in pools,
vases, aquaria, etc. to prevent stagnation.
o Eradicate rats & rodents
o Provide health education on the modes of transmission of
the disease.
o Encourage oral fluid intake
 • A red tide occurs when the population of certain kinds of
algae known as dinoflagellates explodes, creating what’s
called an “algal bloom.”
• Explosions caused by environmental conditions which
promote explosive growth of microorganism.
Factors which are favorable for growth are:
• Warm surface temperature
• High nutrient content
• Low salinity and calm seas
• Rainy days followed by sunny weather
Water in the costal areas can be colored red by the algae, thus
the term RED TIDE:
• Shellfish are particularly prone to contamination as the
feed by filtering microscopic food out of the water.
• Planktonic organisms are filtered from water along with
their non toxic food
• Toxic plankton maybe numerous enough to toxify
shellfish
Explosions or “blooms” are coastal phenomena caused by
environmental conditions which promote explosive growth of
microorganism.
Shellfish include:
Quahogs Soft shell clam oysters
Mussels Scallops Moon snail
Lobster, crabs, shrimps and fish do not accumulate toxin and are
safe to eat even if they are from affected water.
• Eating toxic shellfish can cause Paralytic Shellfish Poisoning
(PSP) in humans. PSP is caused by SAXITOXIN which is
produced by A. Catenella and is one of the most potent
toxins known.
• After ingestion, the toxin affects immediately the nervous
system with symptoms usually occurring within 30 minutes.
Severity depends on the toxin consumed.
• Toxic shellfish and cooking does not destroy the organism
Clinical manifestation:
a. Initial sign is tingling of the lips and tongue which
spreads to the face, neck, fingertips and toes.
b. Headache, dizziness and nausea follow which maybe
mistaken for a drunken condition.
c. Such symptoms are aggravated by alcohol
consumption.
d. In severe cases, muscular paralysis and breathing
difficulty may occur in five to twelve hours due to
paralysis of the diaphragm and the victim can survive
only with the aid of a respirator.
e. Fatalities from respiratory arrest have been reported.
Modalities of Treatment
a. The patient is induced to vomit.
b. Charcoal hemoperfusion is a process done by pumping
the arterial blood through an activated charcoal filter to
remove the poison.
c. Alkaline fluids, such as sodium bicarbonate are thought
to be helpful because toxin is unstable in alkaline
condition.
d. Artificial respiration is required if patient exhibits
respiratory stress.
Prevention and control
a. All shellfish-producing areas should have a monitoring
program to test water, sediments and shellfish for
contamination.
b. Department of Environmental Quality Engineering
(DEQE) is responsible for year round testing of shellfish
and shellfish growing area.
c. When blooms subside, shellfish purify themselves of the
toxin, and when testing indicates a return to safe levels,
the areas are reopened.
d. If accidental ingestion of toxic shellfish is suspected,
seek medical attention immediately.
e. Recreational shellfish gatherers should look for posted
warnings and pay close attention to local media
announcements.
FECES IN SOIL
8. Ascariasis
 An infection caused by a parasitic roundworm
 A chronic condition often producing no symptoms.
Causative agent : Ascaris lumbricoides
Ascariasis is an infection caused by a parasitic roundworm,
Ascaris lumbricoides.
Ascaris lumbricoides
a. They are elongated, cylindrical worms that are tapered at
the oral portion & pointed at the anal end.
b. They appear creamy & pinkish yello when fresh
c. They can grow as thick as a pencil & live for 1-2 years.
d. A female worm can produce up to 240,000 eggs per day,
which are then discharged Into the feces & incubated in
the soil for weeks.
Mode of Transmission
a. Ascaris lumbricoides is transmitted through contaminated
fingers put into the mouth.
b. Ingestion of food and drinks contaminated with
embryonated eggs can transmit ascariasis.
Transmission
• Infection may start with the ingestion of contaminated water
or with eating raw vegetables, especially if “night soil” is
used as fertilizer.
• After ingestion, Ascaris lumbricoides hatches & releases
larvae, which penetrate the intestinal wall & reach the lungs
through the bloodstream.
• After ten days in the pulmonary capillaries & alveoli, the
larvae migrate to the bronchioles, the bronchi, trachea &
epiglottis.
• They are then swallowed & returned to the intestine where
they mature & mate
Larval Stage
Symptoms
• The larvae penetrate the walls of the
intestine (duodenum) *nausea &
vomiting
• The larvae are picked up by lymphatics
or bloodstream. *Periumbilical pain
• They are carried to the liver *Right upper
quadrant pain
• Some larvae may reach the heart
• Sometimes they are carried to the biliary
tract.
Intestinal obstruction may be
caused by a bolus of entangled
worms which may be palpable.
 Incubation period –2 months after ingestion 9. Pinworm-infestation (Enterobiasis)

Period of communicability–as long as mature gravid worms

are in the intestines.

Signs and symptoms –seen only when with heavy

infestation
• Abdominal pain; marked disturbances of digestion
• Insomnia; restlessness
• Sequela–destruction of the bowel when there is a bolus
of worms
Treatment
• Albendazole or mebendazole–15cc as a single dose
• Piperazine Citrate –75mg.kg, daily x 2 doses orally
• Pyrantel Pamoate–1 mg./kg as a single dose, orally
DIAGNOSTIC TESTS
• Stool for ova-(Kato-Katz technique)
• Abdominal X-ray
• Routine blood counts
COMPLICATIONS
• Biliary tract obstruction; patient develops cholestatic
jaundice.
• Hepatic abscess & cholangitis
• Intestinal obstruction, perforation, peritonitis
• Malnutrition due to damage of the intestinal mucosa,
w/c impairs the absorption of nutrients.
Stool for ova-(Kato-Katz technique)- demonstration of
fertilized or unfertilized egg in the stools.
Abdominal X-ray-densed shadow of adult ascaris which
look like strands of spaghetti (‘dot” sign)
Routine blood counts-significant eosinophelia
Nursing Interventions
• Handwashing
• Health education
• washing of fruits and vegetables
• Personal hygiene
• Sanitation
• Availability of toilet facilities
• Proper disposal of diapers
✓ Isolation is NOT needed.
✓ Preventive measured in each home and in the community
should be enforced.
✓ All members of the family must be taught on sanitary
practices such as washing of hands before handling food,
washing of all fruits and vegetables that are eaten raw, and
effective sewage disposal.
✓ Availability of toilet facilities must be ensured.
✓ Importance of personal hygiene should be explained.
✓ Proper disposal of diapers should be emphasized to
mothers.
Parasitic in origin (via ingestion)
PINWORM-INFESTATION
Important Information
• An intestinal roundworm which infects only man.
• If found in one family member, the are most probably
infected also
Synonym: Nocturnal Ani; Entorobiasis, Oxyurasis
Causative agent Enterobiusvermicularis, a nematode,
Synonym: seatwormor threadworm
• Lives and breads in the small intestine.
• Not destroyed by ordinary laundering.
Incubation period : 2-6 weeks
Period of communicability : as long as gravid females are
discharging eggs on the perianal skin.
Mode of transmission : direct transfer indirectly through
contaminated clothing, linen, food, etc. Dust borne
infection is also possible.
MOT
✓ Accidentally swallowing or breathing in pinworm eggs
causes a pinworm infection.
✓ The tiny (microscopic) eggs can be carried to your
mouth by contaminated food, drink or your fingers.
✓ Female pinworms move to the anal area to lay their
eggs, While the infected person sleeps, female
pinworms lay thousands of eggs in the folds of skin
surrounding the anus
Diagnostic exam
• Test tape- Best done upon waking up in the morning
before bathing or bowel movement.
Management
• Handwashing
• Wear well-fitting underwear
• all members of the household should be treated with
Piperazine hexahydrate (500 mg/tsp) for 1 week
o ½ tsp OD for children
o 2 tsps BID for adults
Clinical manifestation
• Itching of anal or vaginal area
• Insomnia
• Irritability
• Restlessness
• Intermittent abdominal pain & nausea

PREVENTION
a. Improved Sanitation
b. Improved Nutrition
c. Deworming may be advised.
d. Avoid water or food that may be contaminated.

Complications
✓ Thypical pinworm infections don’t cause serious problems. In rare circumstances, heavy infestations
can cause infection of female genitals.
✓ The parasite can travel from the anal area up the vagina to the uterus, fallopian tubes and around the
pelvic organs. This can cause problems such as inflammation of the vagina (vaginitis) and inflammation
of the inner lining of the uterus (endometritis
 10. Hookworm Disease
 Is an intestinal parasite of humans that usually causes
diarrhea or cramps.
 Occurs mostly in tropical & suptropical countries.
ANCYLOSTOMIASIS /MINER’S DSE/EGYPTIAN
CHLOROSIS
• Intestinal parasites causes diarrhea or cramps
Etiologic Agent
• Ancylostoma Duodenale - is the agent which is most
prevalent in Europe & Asia
• Necator Americanus - is distributed in Central & South
America & West Africa
Incubation Period: 2-8 weeks
• Hookworm ova appear in the stools about four to six
weeks after the larvae penetrate the skin.
• 40 to 100 days or two to 8 wks
Period of communicability
Persons remain spreaders of infection ad long as they are
infected.
• Host Blood may consume as much as 50 ml/day.
• Infected children tend to be malnourished &
undersized.
• Infected children are lazy, have no energy & lack of
ambition.
• Infected children have strong desire for food
Mode of Transmission
• Skin of foot
• Ingestion of contaminated H2O & food
Signs and Symptoms
• Gradual loss of blood in iron deficiency anemia
• Abdominal pain
• Diarrhea
• Urticaria
• Malnourishment
• Pupils become dilated
• Perverted appetites
• Pedal edema
SYMPTOMS
a. The type & severity of the symptoms of hookworm disease
depend on the number of worms present in the intestine.
b. The worms engulf small bits of tissue from the intestinal mucosa,
causing the development of small lesions.
c. They feed on the host’s blood & may consume as much as 50ml
daily. The gradual loss of blood results in iron
d. Other symptoms include abdominal pain, diarrhea & allergic
reactions like urticaria.
e. Children infected with worms are often mentally & physically
underdeveloped. They have protruding abdomens & are
lethargic.
f. Infected children tend to be malnourished & undersized.
g. Infected children are lazy, have no energy & lack of ambition.
h. The pupils of the patient’s eyes are more or less dilated.
i. Many of the infected children have perverted appetites.
j. Pedal edema & edema in other portions of the body may be
present.
PATHOLOGY
Female Hookworm may produce as many as 10,000 to 20,000 eggs per
day.
Eggs deposited in moist & O2-rich soil will develop into embryos w/in 24
to 72 hrs (1-3 days)
RHABDITIFORM (young) larvae takes 6 wks to develop into
FILARIFORM (mature) larvae w/c cause human infection.
a. The larvae penetrate the unbroken skin of the feet & legs of the host,
entering through the sudoriferous glands & hair
b. The larvae penetrate the blood & lymph vessels, damaging them in
the process, after which they enter the inferior vena cava & right
atrium, then proceed to the lungs where they pierce the capillary
walls & pass into the alveoli.
c. Some may be coughed out & expectorated, while some are
swallowed & reach the small intestine where maturation occurs &
egg production takes place.
d. The adult worm survives by attaching itself to the duodenal & jejunal
mucosa from where it continuously sucks blood.
e. Hemorrhagic spots in the intestinal mucus membrane mark the site
of previous worm attachments.
f. Death may result from severe anemia & cachexia. (extreme weight
loss and muscle wasting, and can include loss of body fat.)
Diagnostic Procedures
• Microscopic examination of feces for the eggs
• Blood exam reveals eosinophilia
Modalities of Treatment
• Pyrantel embonate (Quantrel)
• Tetrachloroethylene
• Carbon tetrachloride
Nursing Management
• Diet should be high in calories, vitamins & minerals.
• Personal hygiene should be maintained.
Prevention
• Proper disposal of excreta
• Regulations to prevent pollutions of streams & lake with
human excreta
• Avoid walking barefoot
• Good Hygiene
• Proper disposal of animal waste
• Purified or boiled water must be used for drinking
• Vegetables should not be eaten raw.
• Night soil & sewage effluent & dangerous to use as
fertilizer.
Normal levels of eosinophils vary between 0% and
4%, which is under 350 cells per micro-liter of blood.
Night soil- a historically used euphemism for human
excreta.
Sewage Effluent- septic tank
BACTERIA IN ORIGIN Pathophysiology
11. TETANUS Stimulates contraction of the muscles supplied by the neurons
Synonym : Lockjaw
Causative Agent: Clostridium Tetani
• spore forming
• vegetative form
• releases toxins
Characteristics
• A common inhabitant of the soil specially if fertilized
with manure.
• Extremely resistant to heat and ordinary antiseptic
• Extremely anaerobic
✓ Tetanus is an infectious disease caused by Clostridium
Tetani, which produces a potent exotoxin with prominent
systemic neuromuscular effects such as generalized
spasmodic contractions of the skeletal musculator.
✓ Tetanus is fatal in up to 60% of unimmunized persons, with
death occurring usually within 10 days of onset. When The toxin (TETANOSPASMIN) has a high affinity for CNS & Spinal
symptoms develop within 3 days, the prognosis is poor. motor ganglia. It induces hyperexcitability of the motor neurons by
interfering with the release of an inhibitory transmitter.
The organism releases two types of toxin: Other tissue exhibit effects of toxic degeneration, inanition & non-
o Tetanospasmin- which is responsible for muscle specific complications.
spams
o Tetanolysin- which is responsible for the destruction a. When CI.tetani enters the body, it causes local infection &
of RBCs. extensive tissue destruction.
b. Local multiplication of microorganisms occurs more
Predisposing Factors frequently when the wound has healed. While reproducing,
• Newborns whose method of delivery and umbilical CI.tetani also releases toxins that are absorbed by the
cord care are not aseptic bloodstream and lymphatics or directly by the peripheral
• Following surgeries, infected wound. motor nerves. These eventually spread into the central
nervous system.
Sources of infection c. The toxin (tetanospasmin) has a high affinity for CNS tissues
• Animal and human feces & spinal motor ganglia. It induces hyperexcitability of the
motor neurons by interfering with the release of an
• Soil and dust
inhibitory transmitter.
• Plaster of pairs, unsterile sutures, pins, rusty
d. Other tissue exhibit effects of toxic degeneration, inanition
materials, scissors
& non-specific complications.
Incubation Period
• Adult-3 days to 3 weeks Clinical Manifestation
• Neonates –3 to 30 days • Neonate
• (tetanus neonatorum) a. Newborn infants have feeding & sucking
• The longer the incubation the greater the probability difficulties
of recovery b. he infant may cry excessively; most of the time the
cry is short mild & voiceless
c. An attempt to suck results in spasm & cyanosis.
Mode of Transmission
d. There is fever due to infection & dehydration
• Break in skin integrity
e. The jaw becomes so stiff that the baby cannot suck
• rugged traumatic wounds and burns
or swallow
• umbilical stump
f. Tonic or rigid muscular contractions, spasms or
• unrecognized wounds
convulsions are provoked by stimuli.
• Dental extractions, circumcision, ear piercing
g. Cyanosis & pallor develop.
h. Severe cases may end in flaccidity, exhaustion &
Normally, the MOT is through punctured wounds contaminated by
finally death.
dust, soil or animal excreta containing Clostridium Tetani.
• Older Children and adult: OPISTHOTONOS
o S/S
o Rugged, traumatic wounds & burns;
a. (localized)Signs of onset are spasm & increase
o The umbilical stump of the newborn especially if delivered at
muscle tone near the wound.
home & thus have faulty cord dressings; (tetanus neonatorum)
b. (systemic) or generalized signs
o Babies delivered to mothers without tetanus toxoid
✓ Hypertonicity, hyperactive deep tendon
immunization;
reflexes, tachycardia, profuse
sweating/diaphoresis ,low grade fever,
painful involuntary muscle contractions.
✓ neck & facial muscle rigidity (trismus)
✓ Grinning expression (risus sardonicus) –
considered pathognomonic of the
disease.
✓ Board like abdomen / abdominal rigidity
✓ Opisthotonos-spasm of the muscles
causing backward arching of the head,
neck & spine as in severe tetanus.
 ✓ Intermittent tonic convulsions lasting for
several minutes w/c may result in cyanosis
& sudden death due to asphyxiation.
✓ In several cases, laryngospasm is followed
by the accumulation of secretions in the
lower airways, resulting in respiratory
distress due to the involvement of
respiratory muscles.
✓ Fracture of the vertebrae may occur
during severe spasms , yielding to coma &
death.
✓ In mild cases, after a period of weeks,
spasms gradually diminish in frequency &
severity, with trismus (lock jaw), being the
last symptom to disappear.
✓ In fatal cases, death usually occurs during
the first 10 days of the disease.
Types of Stimuli
• Exteroceptives –outside the patient, bright lights, loud
noise
• Interoceptives –from the patient himself e.g. flatus
• Proprioceptives –touching the patient, jamming the
bed, turning the patient
Complications
a. Resulting from laryngospasm and involvement of
respiratory muscle
• Hypostaticpneumonia –collection of fluid in the
dorsal region of the lungs & occurs especially those
( bedridden or elderly) confined to a supine position
for extended periods.
• Hypoxiadue to laryngospasm & decreased oxygen.
• Atelectasis(collapse or closure of the lung),alveoli is
deflated down to little or no vol as distinct from
pulmonary consolidation, w/c they are filled with
liquid. blocked airway. Obstructive or pressure
outside the lung, usually unilateral. Pneumothorax –
collapse lung when air leaks into the space between
your lung & chest wall.
• Traumatic glossitis & macroglossia-Inflammation of
the tongue/ abnormal smallness of the tongue
b. Changes R/T Sympathetic Nervous System
• Transitory Hallucinosis –temporary hallucinations
• Hyperalivation, diaphoresis, & unusual tachycardia,
esp. with the use of aerosolized bronchodilators
• Cardiac standstill & bradycardia (high mortality)—
cessation of cardiac output due to ventricular
fibrillation( cardiac arrest)
c. Due to trauma
• Laceration of the tongue & buccal mucosa their
toxins.
• Intramuscular hematoma –Internal bleeding
between muscle fascia & interstitial spaces
• Fracture of the spine & ribs
d. Septicemia
• Septicemia –blood poisoning caused by bacteria
ATS- Anti Tetanus Serum= purified antibodies prepared from
Equine Blood./ Enzyme Refined Equine Globulin Solution.
TT- (aluminum potassium sulfate)
= stimulates the body to create protective antibodies to the
tetanus toxin.5cc IM PEN G Na, to control infection
Muscle Relaxant to decrease muscle rigidity & spasm
Management
Prevention
• Active Immunization with tetanus toxoid
• Tetanus toxoid for non-pregnant women
• Antitoxin
• DPT for babies and children
Control : Medical aseptic technique
Treatment
a. Specific
• ATS, or TIG
• Tetanus toxiod (.5 cc IM)
• Pen G Na
• muscle relaxant to control
o Sedative-Valium (diazepam)
o Tranquilizer -Thorazine
b. Nonspecific
• Oxygen inhalation
• NGT Feeding
• Tracheostomy if needed
• Adequate fluid, electrolyte, and caloric intake
• Nursing Care
o Maintain adequate airway
o Provide cardiac monitoring
o Maintain IV line
o Wound care
o Avoid stimulation
o Avoid contractures and pressure sores
o Watch out for urinary retention
o Monitor V/S
o Provide optimal comfort measures
Prevention and Control
• Active Immunization with tetanus toxoid for adults &
pregnant women ( in the latter, to prevent the
occurrence of tetanus neonatorum)
• DPT for babies & children
Tetanus toxoid is what a tetanus vaccine contains. Your body will make
anti-bodies to tetanus once given the tetanus vaccine, offering your
protection for “up to” 10 years from the bacterial disease in case you
cut or burn yourself.
3000-5000 units of anti-tetanus serum is injected into and around the
site of a wound for people that haven’t completed a series of 3 tetanus
vaccine shots, or, even if so, it’s been more than
12. Poliomyelitis
 Disease of the lower motor neuron involving the
anterior horn cells, characterized by changes in the
CNS
 An acute paralytic condition which is very contagious
and infectious.
Synonym: Infantile paralysis, Heine medin disease
Causative Agents: Legio debilitans
Characteristics
• May exist in contaminated water supplies and sewage
or infected milk
• Can survive in body secretions at ordinary
temperature outside the body for long periods.
Predisposing Factors
• Age :children below 10 years old
• Sex: M vs F 3:2
• poor environmental and hygienic conditions –flies may
act as mechanical vectors
Incubation Period:7-21days,(paralytic cases) may vary from
3-35 days
Period of Communicability
• -first 3 days to 3 months of illness
• 3-4 days before the onset of symptoms
 Mode of Transmission Types of paralysis
• droplet infection –in early infection • bulbar –cranial nerve are affected
• Direct contact -body secretions –oropharyngeal • spinal –anterior horn cells are affected, causing paralysis
• fecal-oral –during late stage of the affected extremities
• indirectly, flies & contaminated water, food, utensils & • bulbospinal –involvement of the neurons both in the
other articles brainstem & spinal cord.

Direct Contact with feces Baby in tripod Position

The lesions are found mainly in the anterior horn cells at the
following sites:
• Spinal cord
• Vestibular nuclei of the medulla & the cranial nerves
• The roof & dermis of the cerebellum
• Gray matter of the midbrain
• The motor cortex

TYPES OF POLIOMYELITIS
a. Abortive Type
• Does not invade the CNS
• Headache and sore throat
• Slight or moderate fever
• Occasional vomiting Nursing Management
• Low lumbar pain • Enteric Isolation
• The patient usually recovers within 72 hours. • Perform Neurologic assessment
b. Non Paralytic Type • Check V/S regularly
• All of the above signs • Watch for signs of fecal impaction
• Spasm of the muscles of the hamstring • Prevent pressure sores
• Changes in deep and superficial reflexes • Dispose excreta and vomitus properly
• Pain in the neck, back, arms, legs, and abdomen • Handwashing
• Inability to place the head in between the knees • Apply hot packs to affected limbs to relieve pain &
• Positive Pandy’stest muscle shortening
• Transient paresis may occur • Emotional support
• Usually last for about a week, with meningeal • Good personal hygiene
irritation persisting for two weeks
c. Paralytic Type Diagnostic/ Laboratory Exam
• The signs and symptoms listed above are present. • Good personal hygiene
• Positive hoyne’s sign • Throat swab
• paralysis • Stool culture
• Urine retentions, constipation and abdominal • CSF culture
distention
• Less tendon reflexes
• Positive kernig’s and brudzinski’s test
• Weakness of the muscles
• Hypersensity to touch
 Complications: Liver cysts increase their diameter 2-3 Cm each year
• Respiratory Failure
• Circulatory collapse Mode of Transmission
• Electrolyte Imbalance • Humans can be exposed to these eggs by “hand-to-
• Bacterial Infection mouth” transfer or contamination.
• Urinary problems • By ingesting food, water or soil contaminated with stool
• Abdominal Distention from infected dogs.
• By petting or handling dogs infected with the
Modalities of Tx Echinococcus granulosus tapeworm. These dogs may
• Analgesics shed the tapeworm eggs in their stool, and their fur may
• Moist heat application be contaminated.
• Bed rest • Risk factors for human infection include uncontrolled
• Rehabilitation dogs living closely with people, uncontrolled slaughter
of livestock, and unsanitary living
Modalities of Tx
✓ Analgesics - headaches, back pain, leg spasms
Clinical Manifestation
(MORPHINE IS CONRAINDICATED- danger of
• Pain or discomfort in the upper abdominal region or
additional respiratory suppression.
chest, nausea, vomiting, or coughing may occur a
✓ Moist heat application-reduce muscle spasm & pain
resulting of the growing cysts.
✓ Bed rest
✓ Rehabilitation for paralytic polio using PT, braces, • Rupture of cysts fluid can lead to allergic reactions or
even death
corrective shoes, orthopedic surgery.
Complication
Prevention & Control • Cyst biliary complication
• Immunization: OPV • Intra biliary rupture
• Proper disposal of GIT secretions • Intra abdominal rupture
• Isolation • Intra thoracic rupture
• Implementation of standard precaution • Infection of hepatic hydatid
• Sanitation, proper food handling, avoid contamination • Death
of flies
Most common Manifestation
13. HYDATID DISEASE • s/s occur depend on the cyst location.
 is also known as HYDATIDOSIS • Painful or painless hepatomegaly or abdominal mass
 is a parasitic infestation by a tapeworm of the genus
Echinococcus granulosus.
Location Liver
Tape worm
Abdominal pain, Weight loss, Slightly yellow from jaundice
Location Lung
Pain in the chest, Shortness of breath , Coughing

Diagnostic Studies
• Imaging techniques
• Echinococus Alveolaris • Immunologic diagnosis
• Echinococus Vogeli
• Echinococus Granolosus Imaging techniques
• X-ray
• Sonography
• CT scan
• Radio-nuclide scaning

Immunologic diagnosis
• Immuno electro phoresis
• Indirect hemagglutination test
• Latex agglutination test
• Complement fixation test
• ELISA
• Casoni test

Medical treatment
Incubation Period : Months to years • Mebendazole
It can affect most of the body organs • Albendazole
• Lung • Praziquantel
• Spleen The most effective treatment for hydatid cyst is Surgery (Surgical
• Pancreas resection of the parasite in all organs).
• Ovary
• Bone
• Brain
• Breast
• Kidney
• Soft tissue
• Heart & Pericardium
 VIRAL IN ORIGIN

Airborne Diseases MEASLES

Synonyms:
Common Colds • Rubeola, morbilli, Little red disease, hard measles, 7-day
Acute Rhinitis or Coryza measle, 9-day measle
o Irritation and inflammation of the mucous membrane • Is a contagious exanthematous disease of acute onset most
inside the nose. often affects children.
o common kind is allergic rhinitis. Incubation Period: 10-12 days (longest is 20 days and the shortest is
eight days). * A single attack conveys lifelong immunity
Mode of Transmission: Droplet Infection Causative Agent Paramyxovirus, measles virus, rubeola
Causative Agent: Cold Virus or Rhino Virus Mode of Transmission :direct and indirect transmission.
I.P: 1-4 days Pathognomonic Sign: Koplik’s spots, stimson’s line
Period of Communicability: At early stage
Clinical Manifestations
Classified into three stages
1. Pre-eruptive stage
• Patient is highly communicable
• Fever
• Catarrhal symptoms
• Respiratory symptoms -appears first as a common cold,
sneezing, coughing
• Excessive lacrimation
4 Classic Signs: Coryza, Conjunctivitis, Photophobia, cough
Clinical Manifestations
• Enanthem sign
• Koplik’s Spot
• Stimson’s line
2. Eruptive Stage- Exanthem
• Maculopapular Rashes - cephalocaudal
With high fever
• Anorexia and irritability
• Pruritus and lethargy
Symptoms Stage of Convalescence
o rhinorrhea • Rashes fade in the same manner as they appeared.
o sneezing • Fever gradually subsides as the eruption disappear on the
o slight headache hands and feet
o nasal itching • Fine branny desquamation of the skin
o watery, reddened, itchy eyes & puffiness around eyes Diagnostic Test
o Itchiness of the throat • Nose and throat swab
o chills • Urinalysis
o lacrimation • Blood Chem
LATE STAGE
• Compliment fixation or hemagglutination inhibition
o stuffy nose & post nasal drip
Complications
o profuse mucoid secretions
• Common complication - Otitis media
o nasal congestion
• Serious complication - Bronchopneumonia
o cough
Management
o thick & purulent secretions
• Prevention
o smell & taste disrupted
o Passive immunization -gamma globulin if the child has
o sore throat (pharyngitis)
been expose; immunity last for 2-3 weeks
o ear itchiness
o *Active immunization -MMR or measles vaccine at 9
o Fatigue
months of age or as early as 6 months.
o malaise
• Control Proper disposal of nasopharyngeal secretions,
o cough
isolation
PREVENTION: Vaccination
MANAGEMENT: • Penicillin -Given only when secondary infection sets in
Symptomatic Nursing Care
o Depends on underlying cause • CBR
o Intranasal corticosteroids • Adequate nutrition,
o Intranasal antihistamines • increase fluids, vitamin C
NURSING CARE: • Prevent eye and ear infection
o Place in a well ventilated room
o Complete Bed Rest
o Vit C to increase body resistance
o Increase Fluid intake
GERMAN MEASLES SMALL POX (VARIOLA)
Synonyms: Rubella, 3 day measles  Acute highly contagious disease cause by a filtrable virus, char.
Causative Agent: By severe constitutional symptoms & a macular eruption &
• (Rubella virus (Family- Togaviridae: Genus - Rubivirus); appears about the 4th day of the disease & changes rapidly
pseodoparamyxo virus through distinct popular vesicular, pustular & crusting stages.
• Is an acute infection and is characterized by fever, and Leaving a pitted scar.
exanthem. Causative Agent: VARIOLA POX VIRUS
Pathognomonic Sign: Forchiemers spots (small red lesions) Incubation period: 7-16 days
Mode of Transmission`: Droplet infection Mode Of Transmission: DIRECT OR INDIRECT CONTACT
Incubation Period: From exposure to the appearance of the Period of Communicability: 1st s/s up to the last crust
rash, 14-21 days. PRODROMAL S/S
• sudden onset of fever, headache, erythematous eruption
Signs & Symptoms • headache, severe backache, enanthem
1. Pre-eruptive Stage
• Forcheimer’s Spots - consist of fine red spots in the ERUPTIVE (rash formation)
soft palate or uvula. A. Period of Maculopopular rashes (2nd day)
• With or without fever, sore throat, loss of appetite, B. Period of Vesiculation (3rd, 4th day), multilocular (more
runny nose division)
2. Eruptive Stage C. Period of Pustular, (fever appears with prominent
• Rash - Cardinal sign umbilication)
• *oval rose red papules about the size of a pinhead CONVALESCENT
• *begins in the face, covers the entire body within • Desquamation-leaving pitted scar (POCKMARK)
24 hours • Become confluent (merging)
• Enlargement of the lymph nodes TYPES VARIOLA MINOR
3. Post Eruptive Signs • (ALASTRIM)
• Rashes disappear on the 3rd day o Milder form
• Lymph nodes subsides o Fewer systemic symptoms, a less extensive rash, less
scarring, and fewer fatalities
MANAGEMENT o Mild prodromal s/s
• Similar to Rubeola TYPES VARIOLA MAJOR
• Symptomatic • (CLASSICAL)
o virus to move from cell to cell
o virus was found in the bloodstream in large numbers
(viremia)
o second wave of multiplication occurred in the spleen,
bone marrow, and lymph nodes.

Four types of Varicella Major

1. Ordinary-Ninety percent or more cases among unvaccinated
CHICKEN POX persons
Synonym: varicella 2. Modified-occurred mostly in previously vaccinated people. This
Causative Agent: form of variola major was more easily confused with chickenpox.
• Herpes virus varicellae, Varicella Zoster virus 3. Malignant (or flat) - prolonged high fever, and severe symptoms
• Is a highly contagious disease characterized by vesicular of toxemia; was nearly always fatal. vesicles are flat ; severe
eruptions on the skin and mucous membranes prodromal s/s.
Mode of Transmission: 4. Hemorrhagic (black pox)- a severe form accompanied by
• Direct/indirect/airborne extensive bleeding into the skin, mucous membranes, and
• Droplet-nasopharyngeal secretions/discharges from the gastrointestinal tract
vesicles RXN:
Incubation Period: 10-21 days or maybe prolonged after passive ERYTHEMA - SWELLING - VESICULAR -PUSTULLAR – CRUST - SCAR
immunization Dx
• Electron microscope using vesicle fluid
Signs & Symptoms • compliment fixation test (CFT)- presence of either specific
1. Pre-eruptive stage - with or without fever, malaise, antibody or specific antigen
muscle pains • CS
2. Eruptive stage – Exanthem appears one at a time and
disappears in the same manner (CENTRIFUGAL). Starts PREVENTION
in covered areas of the body as macules -papules Active immunization
successive crops of vesicles occasionally by pustules - VACCINATION (Edward Jenner)
spread throughout the body in 6 hours-end as granular (VACCINIA IMMUNE GLOBULIN)
crust/scabs A. Multiple pressure
3. Post eruptive - falling off of exanthem B. Multiple puncture
C. Bifurcated needle
Diagnostic Test D. Mono vac
1. Determination of V-Z antibody titers by any of the
following
• Compliment fixation test (Continuation...)
• Fluorescent antibody antigen
• Immune adherence hemagglutination antigen
• Passive hemaglutination
• Neutralization test
2. Demonstration of V-Z virus by electron microscopic
examination of vesicular fluid
Smallpox vaccine administration INFLUENZA; FLU; LA GRIPPE
• DO NOT apply alcohol to the skin prior to vaccination.  Highly contagious acute viral disease of man occurring
Alcohol will inactivate the vaccinia virus. Dip the bifurcated  sporadically & endemically with periodic severe pandemics
needle into the vaccine vial and withdraw it. that sweep around the world with unusual speed.
• The needle is designed to hold a tiny drop of vaccine of Causative Agent
sufficient size and strength to ensure a successful vaccination • INFLUENZA VIRUS (A,B,C)
(if administered correctly). • Easily killed by UV rays, formaldehyde & other solution
Tx • Contains RNA & classified as MYXO Viruses, types A,
SYMPTOMATIC Aprime, B,C.
• Supportive measures, MgSo4,KMNO4, IV, liquid or soft diet Incubation Period: 24-48 hours
Use of antiviral, antibiotic Period of Communicability: Until the 5th day of Illness (up to the
• Tecovirimat (TPOXX) In laboratory tests, cidofovir and 7th day in children)
brincidofovir have been shown to be effective Against the Mode Of Transmission
virus that causes smallpox. • Airborne
NURSING CARE • Droplet
• Isolation • Direct contact
• Medical Asepsis • Virus persist 4hrs in dried mucus
• CBR Clinical Manifestations:
• Oral/Nasal hygiene • Chilly sensation, hyperpyrexia, malaise, sore throat,
• Nutritional Diet coryza, rhinorrhea, myalgia, headache.
COMPLICATION • Severe aches & pain (back), severe sweating
• Dermatitis; pyoderma; gangrene; abscess; furuncles. • Joint pain (pathognomonic)
• Pharyngitis; bronchopneumonia; sinusitis; pleurisy; • GI symptoms, vomiting
empyema. • Worst symptoms 3-5 days
• Otitis media, eye lesion, conjunctivitis; blindness. Complications:
• Hepatitis, Nephritis • r/t primary viral infection
• Hemorrhagic pneumonia
• Encephalitis, Meningitis
MUMPS
• Reye’s syndrome-acute encephalopathy & fatty
 An acute viral disease manifested by the swelling of one or
degeneration of liver
both parotid glands.
• Myocarditis-cardiac failure
Synonym: Infectious Parotitis
• SIDS (Sudden Infant Death Syndrome)
Etiologic Agent: paramyxovirus
• Myoglobinuria
Incubation Period –14-25 days (the average is 18 days)
• Otitis Media
Period of communicability – six days before and nine days after the
• Sinusitis
onset of swelling
• Pneumonia
Mode of transmission droplet infection- Saliva is the most infectious
of all body secretions
INFLUENZA VIRUS
INVADES RESPIRATORY MUCOSA
Signs and symptoms
DAMAGES CILIATED EPITHELIUM
• sudden headache, earache, loss of appetite, fever and
OF THE TRACHEOBRONCHIAL TREE
swelling of the parotid glands
Pt. vulnerable to secondary infection
• Pain in the parotid gland
Other organisms give rise to severe reactions, producing
edema of the respiratory tract
Complications/sequela
Serosanguinous discharge
• Orchitis
• Oophoritis
Complications DIAGNOSTIC PROCEDURE
• Mastitis and edema of the vulva
• Leukopenia
• Central nervous system involvement may occur
• Oropharyngeal washings or swabs (Culture of virus)
• Viral Serology -complement fixation test
Management
• Prevention – immunization with MMR (measles mumps- • hemo-agglutination test
rubella) vaccine • neutralization test
• Control – proper disposal of secretions; lactation MANAGEMENT:
• Treatment • No specific Tx
• Stay at home
Medical care • Drink plenty of fluids
• Cortisone • Take the following to relieve fever & headache:
• Antiviral drugs o Paracetamol
• Analgesics for pain o aspirin (unless contraindicated, should not be given
to children below 16 y/o
Nursing care o ibuprofen or other anti-inflammatory drugs
• Application of hot or cold • TSB
• Oral care and personal hygiene
• Bedrest PREVENTIVE MEASURES
• Diversional activities 1. Immunization
• Soft and semisolid food 2. Avoidance of crowded places
3. Personal hygiene
4. Annual Vaccine
• elderly
• -people who have poor immunity
• -with diabetes, lung, kidney, heart, liver disease.
DIPHTHERIA PERTUSSIS
 An acute disease that can infect the body in two areas, the Synonym: Whooping cough
throat, and the skin. Causative agent
 Infants born of immune mothers remain immune for the first • Bordetella Pertussis- easily destroyed by light, heat and
6 months of life. drying.
 One attack does not necessarily confer lifelong immunity. Incubation period – 7 –14 days
Causative agent Period of communicability : the early catarrhal stage before the
• Corynebacterium diphtheria, also called Klebs-Loffler paroxysmal cough stage
bacillus. Mode of transmission
• Very resistant to ordinary conditions of environment and • direct contact – droplet
disinfectants. • Indirect- soiled linens other articles
• Readily killed by boiling and will die in 3 minutes. Signs symptoms
Incubation period : After being exposed to the bacterium it usually • Invasions or catarrhal stage
takes 2-5 days for symptoms to develop.
• Spasmodic or paroxysmal stage
Period of communicability
• Recovery/Convalescence
• 2 – 4 weeks in untreated
Diagnostic/ laboratory exams
• patients, 1-2 days in treated patients
• to isolate microorganism from nasopharyngeal
Mode of transmission
secretions
• Direct contact with contaminated secretions discharged from
• Nasopharyngeal swabs
the respiratory passages or the saliva of the diphtheria
• Sputum culture
carrier or patient.
• CBC
• Indirect transmission from drinking fountains, cups, toilet
seats, toys, and infected milk supplies
Complications/Sequelae
Diagnostic/laboratory exams
• Bronchopneumonia
a. Schick Test- To determine immunity or susceptibility to
• Abdominal hernia
diphtheria.
• Severe malnutrition
b. Moloney’s Test - to determine hypersensitivity to diphtheria.
c. Nose and throat swab - to determine presence of • Atelectasis
microorganism and if patient is still communicable. • Convulsions
• Malnutrition
Type of Diphtheria/Signs and Symptoms Management
• Nasal –serosanguinous and foul-smelling • Prevention – immunization (DPT)
• Cervical or submaxillary glands enlarged. • Control – isolation medical asepsis, concurrent and
• Tonsillar – has low fatality rate terminal disinfection.
Treatment
Nasopharyngeal- more sever type • Medical care
• Sore throat causing dysphagia (difficulty in swallowing) • Supportive Therapy
• Fever in which prostration is pronounced. o Fluid and electrolyte replacement
• Pseudo membrane in the soft palate, uvula and tonsils. o adequate nutrition
o oxygen therapy
• Bullneck appearance
• Antibiotics chloramphenicol (chloramycetin), terramycin,
• Wound or Cutaneous – affects mucous membranes and any
penicillin.
break in the skin.
o gamma globulins
Complications/Sequelae Nursing care
• Isolation and Medical Asepsis
• Myocarditis – the most common
• Maintain patent airway
• Polyneuritis – inflammation of the nerves
• CBR
• Airway obstruction
• Warm baths
• Control – isolation, concurrent and terminal disinfection
• Prevent aspiration
Treatment • I & O monitoring
• Medical care
• Anti-diphtheria (ADS) serum
• Epinephrine/corticosteroid
• Antibiotics Penicillin, erythromycin
• tracheostomy or endo tracheostomy.

Management
Prevention
• Active (DPT vaccine)
• Passive – 1500 units of diphtheria antitoxin.

Nursing care
• CBR
• Maintain patent airway
• Ice Collar
• Vitamin C
• Nose and throat care
• Soft diet
PNEUMONIA 2. LOBAR PNEUMONIA: A consolidation of the entire Lobe.
 An acute infectious disease caused by Clinical manifestations: (chills, chest pain on breathing & cough with
PNEUMOCOCCUS and is associated with general blood streaked sputum (“prune juice” or rusty appearance) may be
toxaemia and a consolidation of one or more lobes of replaced by “thinner” or yellowish color.
either or both lungs. Severe cases: heart failure, edema of the lungs, severe general
 It is an inflammation of the lungs in which the air sacs are exhaustion.
filled with pus or exudate so that air is excluded, and the
lungs become solid. 3. PRIMARY ATYPICAL PNEUMONIA
Viral pneumonia
Causative Agent • solidification of the lungs that comes in patches.
1. STREPTOCOCCUS PNEUMONIAE • cough often delayed
2. STAPHYLOCOCCUS AUREUS • greenish to whitish secretions often expelled by coughing on
3. HAEMOPHILUS INFLUENZAE the 3rd to the 5th days.
4. KLEBSIELLA PNEUMONIAE (Friedlander’s bacilli)
5 Main Causes GENERAL CLASSIFICATION OF PNEUMONIA
1. Bacteria 1. PRIMARY PNEUMONIA
2. Viruses • direct result of inhalation or aspiration of pathogens or
3. Mycoplasma noxious substance,
4. Other infectious agents, such as fungi • some cases of pneumococcal pneumonia, mycoplasma
5. Various chemicals pneumonia and pneumonia caused by TUBERCLE BACILLI.
Incubation Period: 1-3 days with sudden onset of shaking chills, 2. SECONDARY PNEUMONIA
rapidly rising fever and stabbing chest pains aggravated by • develops as a complication of the disease.
coughing and respiration.
Types:
Mode Of Transmission A. Primary Pulmonary
• Droplet Infection • Infection(viral)-predisposed to superinfection.
• Indirect Contact • e.g staphylococcal pneumonia
• superimposed upon viral
Classification according to Exposure • pneumonia caused by type A influenza virus.
1. COMMUNITY -ACQUIRED PNEUMONIA (CAP) B. Secondary Bacterial Infection
• Acquired in one’s daily life(work, school, gym) • damage caused by noxious chemical insult to the lungs
• Causes: Streptococcus pneumoniae(most common) (aspiration of gastric contents)
• Haemophilus influenzae and Legionella can also cause of C. Hematogenous Spread of Bacterial pathogens from a distant
the disease. focus may result in secondary pneumonia.
2. NOSOCOMIAL PNEUMONIA - (Hospital Acquired)
3. ASPIRATION PNEUMONIA PATHOGENESIS
• -foreign matter is inhaled (aspirated) o Pneumococcus, Staphylococcus Aureus, Klebsiella Pneumoniae, H.
• -most commonly when gastric contents enter the lungs Influenzae
after vomiting. o M.O. Passes Through The Tracheobronchial Tree To The
4. PNEUMOCYSTIS CARINII PNEUMONIA Parenchyma Of The Lungs
• opportunistic organisms that are not harmful for healthy o No. Of Bacteria In Thealveoli, Multiply & Spread To Adjacent Alveoli
people but can be extremely dangerous to people with o Via Pores Of Kohn/Enzymatic Destruction Of Tissues
compromised immune system. (HIV/AIDS, Sickle Cell o Inflammation May Spread In Pleural Space & Stimulate Effusion
Disease) o When Invaded By Bacteria Becomes Empyema
5. ACTINOMYCOSIS o M.O enters lymphatic system-bloodstream-establish Bacteremia
• bacterial species (Actinomyces Israeli) infections(meningitis, endocarditis & arthritis)
o FEVER & Other Systemic Signs of Infection
• The organisms cause pleural infection, resulting in a
thickened pleura, empyema, and a fistulous tract.
PATHOLOGY
• usually associated with poor dental hygiene
FOUR STAGES
6. NOCARDIA
1. Stage of Lung Engorgement
• caused by inhalation of soil particles where the
a. The lung is heavy.
microorganisms Nocardia asteroids, may be found
b. The lung is dark red in color.
• pulmonary infection can seed the bloodstream & form a
c. The lung pits upon pressure with the fingers.
brain abscess, which is often mistaken as a CNS
d. The lung exudes a bubbly, bloodtinged forth.
metastasis of lung cancer.
2. Red hepatization
a. The lung is still heavy
ANATOMICAL CLASSIFICATION b. It sinks in water
1. BRONCHOPNEUMONIA(Lobular or catarrhal a. it looks like a piece of red granite
pneumonia) most common type 3. Gray hepatization
Causative Agent: a. The red color changes to gray.
• pneumococcus, klebsiella b. It looks like ordinary granite
• pneumoniae, hemophilus c. It is softer and tears more easily.
• influenzae d. When pressed, it exudes a Purulent fluid.
4. Stage of Resolution
Mode of Transmission : Droplet • The inflammatory exudate is either absorbed in the bloodstream or
Period of Communicability: Unknown expectorated.
PATHOGENESIS • chills with rising fever
• pneumococcus, klebsiella pneumoniae, h. influenzae • stabbing chest pain aggravated by respirations & coughing
• infection starts at the bronchus & bronchioles • paroxysmal or choking cough
• spread to the alveoli in the periphery • rusty sputum or prune juice in color(pathognomonic)
• lobules inflamed & consolidated • pain in the abdomen mistaken as appendicitis
• (or)collapsed due to mucopurulent plugging of the • herpes may appear on the lips
bronchioles • body malaise
• fever • respiratory grunting with marked tachypnea & flaring of the nares.
• pulse is rapid & bounding
• Diaphoresis
• Convulsion & vomiting in children
DIAGNOSTIC PROCEDURES
• Chest X-ray
• Sputum analysis, smear, and culture MENINGITIS/CEREBROSPINAL FEVER
• Blood / Serologic exam MENINGES
 The meninges are the membranes covering the brain
I. Antimicrobial Therapy and spinal cord
A. Streptococcus (Macrolidesbest initial antibiotic) for 7-10
days, mostly for CAP. BACTERIAL MENINGES
• nafcillin or oxacillin for 14 days  inflammation of the meninges of the brain and spinal
• Klebsiella (Aminoglycosides and cephalosporins) cord as a result of viral or bacterial infection. (dura
• Pneumocystis carnii-(Cotrimoxazole or Pentamidine) matter, arachnoid and the pia matter)
• Pen G- drug of choice Synonym: Cerebrospinal fever
II. Supportive Measures Causative Agent: Meningococcus neisseria meningitides
• Humidified O2 therapy for hypoxia Incubation Period: Varies the extreme limits being set from 1-10
• Mechanical ventilation for respiratory failure days.
• High calorie diet & adequate fluid intake, unless Predisposing Factors
contraindicated • Ear Infection
• absolute bed rest • Head Trauma
• Bronchodilators-aminophylline • Invasive Procedure
• Expectorants • Respiratory Infection
• Pain Relievers for pleuritic pain
Pathophysiology
NURSING MANAGEMENT • Decrease Cerebral Perfusion
1. Maintain the patient’s airway and adequate oxygenation. • Decrease Loc, Seizure
2. Teach the patient how to cough and perform deep- • Vs Changes, Resp Pattern, Papilledema
breathing exercises to clear secretions. Advise him/her • Coma
to do this often. • Death
3. Obtain sputum specimens as needed. Teach the correct
collection of specimen. Predisposing Factor
4. Maintain adequate nutrition to offset high calorie Pathogens Enters The Cns
utilization. Meningeal Irritation
5. Provide a calm environment as the patient needs rest. Inflammation- Brain And Spinal Cord
6. Control the spread of infection by disposing secretions Increase Icp
properly
7. Control temperature by implementing cooling Mode of Transmission
measures. • droplet (nasopharynx), ear discharges, after a skull
8. Monitor Vital signs closely & watch for danger fracture penetrating the head wound, lumbar puncture
or ventricular shunting procedure
Signs like:
• -marked dyspnea Diagnostic/Laboratory Exams
• -thready, small, irregular pulse • Lumbar puncture
• -delirium, extreme restlessness • WBC of 20,000-50,000 (Normal is 5-10,000)
• -cold, moist skin, cyanosis, exhaustion • Smear and blood culture
• Smear from petechiae
PREVENTION & CONTROL • Urine culture
1. Preventing common colds, influenza, and other upper • Positive nose and throat, and spinal fluid culture
respiratory infections. • Lumbar Tap
2. Immunization with Pneumonia Vaccine • Cerebrospinal fluid drawn from between two vertebrae
3. addressing environmental factors that can contribute to
lowering one’s resistance to pneumonia (exposure to Signs and Symptoms
cold, pollution, & physical condition of fatigue or • Headache, chills, fever and vomiting.
alcoholism) • Photophobia
• Nuchal rigidity
• Opisthotonos
• Convulsions
• skin eruptions
• kernigs signs
• Brudzinski sign
• Irritability, stupor, coma
• vomiting, constipation, or diarrhea
• suppression or retention of urine
• paralysis or paresis may occur
• bulging fontanelle or hollow percussion noted from the
skull

Kernig’s Sign - Knee

Brudzinski’s Sign – neck

 COMPLICATIONS
1. Subdural effusion
PETECHIAL OR PURPURIC RASH 2. Hydrocephalus
3. Deaf mutism
Diagnosis – CSF Examination 4. Blindness of either one or both eyes
• Typical CSF in Patients with Bacterial Meningitis 5. Otitis Media and Mastoiditis
• Opening pressure – 200-500 mmH2O 6. Pneumonia or Bronchitis
• White blood cell count – 1000-5000/mm3
• Neutrophils - ≥ 80% PREVENTION
• Protein - >100 mg/dl 1. Vaccines against certain types of meningitis
• Glucose < 40 mg/dl 2. Teach clients with chronic sinusitis or other chronic
• CSF/serum glu ratio - ≤ 0.4 infections the importance of proper and prompt medical
• Gram Stain – Positive in 50-80% treatment.
• Culture – Positive in ~85% 3. Give Rifampicin as prophylaxis as ordered by the
• Bacterial antigen detection – positive in 50-100% physician
4. Implement the universal precaution
Modalities of Treatment
• Antibiotic therapy
o ampicillin
o cephalosporin (ceftriaxone)
o Aminoglycosides
• Digitalis glycosides (digoxin)
• Mannitol
• Anticonvulsants
• Acetaminophen

Nursing Management
• Assess neurologic signs
o LOC
o ICP
• Watch for deterioration of patient condition
• Monitor fluid balance
• Watch for A/R of antibiotics
• Turn patient from side to side
• Maintain adequate nutrition
• Ensure patient’s comfort
• Provide comfort to patient relatives
• Follow strict aseptic technique
• Isolation (Nasal culture +)

Classifications
1. Acute Meningococcemia
 meningococci invade the bloodstream involving the
meninges.
 onset (nasopharyngitis, high-grade fever with chills, N/V,
malaise & headache
 adrenal lesions start to bleed into the medulla,
extending to the cortex
 combination of meningococcemia & adrenal medullary
hemorrhage is known as WATERHOUSE-FRIDERICHSEN
SYNDROME (petechiae-purpuric & echymotic spot =
shock fatal)
2. Aseptic Meningitis
 benign syndrome-(headache, fever, vomiting,
 meningeal symptoms).
 fever up to 40 C (drowsiness, confusion, stupor), neck &
spine stiffness
Characteristics Of meningeal irritation:
(Stiff neck or nuchal rigidity, opisthotonos, (+)
• Brudzinski’s sign (+) Kernig’s sign, exaggerated &
symmetrical deep tendon reflexes
o Sinus arrythmia, irritability, photophobia,
diplopia & other visual problems
Delirium, deep stupor & coma
o bulging fontanels in infants, N/V (projectile)
o severe frontal headache, blurring vision, alt
sensorium
TUBERCULOSIS (KOCH’S DISEASE/ PHTHISIS/ CONSUMPTION LEPROSY
DISEASE Synonyms: Hansens disease, Hansenosis
 Is a chronic, sub-acute or acute respiratory disease  Is a chronic disease with an insidious onset, transmitted
commonly affecting the lungs from man to man, affecting the skin, mucous membranes
 characterized by the formation of tubercles in and nervous tissue, and eventually producing deformities.
 the tissues which tend to undergo caseation, necrosis, Causative agent: Mycobacterium Leprae, or Hansen’s bacilli
and calcification Mode of transmission
Etiologic Agent & Incubation Period • Prolonged intimate skin to skin contact with untreated
• Mycobacterium tuberculosis leprosy patient
• Two to ten weeks • Respiratory-Droplet infection (nasopharyngeal secretions)
Mode Of Transmission Incubation Period: Ranges from 5 ½ months to 8 years
• Inhalation of organism from contaminated air Clinical Manifestations
• Direct or indirect contact Early Signs
• Contact with contaminated eating or drinking utensils • Changes in the color of the skin
Sources of Infection • Loss of sensation
• Sputum • Loss of sweat and hair growth at the skin patch
• Blood from hemoptysis • Epistaxis
• Nasal discharge and saliva • Thickened and or painful nerves (neuralgia)
Diagnostic Procedures • Muscle weakness and paralysis
• Sputum analysis for AFB • Pain and redness in the eyes
• Chest X-Ray • Plantar ulcer that do not respond to treatment
• Tuberculin Testing Late signs
o Mantoux test (PPD) • Madarosis (loss of eyebrows)
o Tine test (OT) • Lagopthalmos (inability to close the eyelids)
o Heat test • Clawing of the fingers and toes
• Contractures
Modalities of Treatment • Saddle nose (Sinking of the nasal bridge)
SCC (6mos.) • Chronic ulcers
1. Isoniazid (INH) • Neuralgia (Thickened and/or painful nerves)
2. Rifampicin Cardinal Signs
3. Pyrazinamide (PZA) • L- Loss of sensation on skin patches
4. Etambutol • E – Enlargement of peripheral nerves
Drug Resistant patients • P- Presence of leprosy bacilli in the skin smear
1. Capreomycin
2. Streptomycin Types
3. Cycloserine Lepromatous or malignant
4. Amikacin • Many microorganisms are found
5. Quinolone drugs • Open or infectious cases
• DOT – Direct observed therapy • Negative reaction to lepromin test
• Relapsing -both • Tendency to from globi in the skin, mucous membranes,
peripheral nerves
Nursing Care • The most serious type, causes damage to the respiratory
• Maintain respiratory isolation tract, eyes and testes
• Administer medication Tuberculoid or Benign
• Rest • Only few organisms are found
• Importance of regular follow-up • Usually closed or noninfectious
• Teach & educate pt. about PTB • Positive reaction to lepromin test
• Encourage the pt. to stop smoking • Affects peripheral nerves and sometimes the surrounding
• Proper disposal of Secretions skin, especially on the face, arms, legs, and buttocks.
• Advise plenty of rest & eat balanced meal Borderline
• Be alert for signs of drug reaction • Signs and symptoms of lepromatous and tuberculoid
• If the patient is taking ethambutol, watch out for optic • Lesions are diffuse and poorly defined.
neuritis. If it develops, d/c the drug
• If the patient is receiving Rifampicin, watch out for Signs and Symptoms
hepatitis & purpura. Observe the patient for other • Attacks the peripheral nervous system, especially the
complications like hemoptysis ULNAR, RADIAL, POSTERIOR POPLITEAL, ANTERIOR –
• Instruct the pt. & his/her family about s/s of recurring TB TIBIAL, and FACIAL NERVES.
Elements of DOTS • CNS is highly resistant
1. Political commitment with increased & sustained • When skin is damage it causes anesthesia, anhidrosis, and
financing dryness
2. Case detection through quality- assured bacteriology • If they attack a large nerve trunk – motor nerve damage,
3. Standardize treatment with supervision & pa. support weakness and pain occur, followed by peripheral
4. An effective drug supply & management system anesthesia, muscle paralysis or atrophy.
5. Monitoring & evaluation system, & impact measurement
In later stages, clawhand, footdrop, and ocular complication such
PREVENTION & CONTROL as
1. Submit all babies for BCG Immunization 1. Corneal insensitivity and ulceration
2. Avoid overcrowding places 2. Conjunctivitis, photophobia, and blindness
3. Improve nutritional & health status 3. Injury, ulceration, infection, and induce of deformed parts
4. Advise persons who have been exposed to infected cause scarring and contractures
persons to receive the tuberculin test & if necessary,
chest X-ray & prophylactic isoniazid
 1. Neurologic complications occur in both lepromatous and HERPES ZOSTER
tuberculoid but are less extensive and develop more slowly Shingles / Acute
in the lepromatous form. Posterior Ganglionitis
2. Lepromatous leprosy can invade tissue in virtually every  is an acute viral infection of the sensory nerve caused by
organ of the body, but the organs generally remain a variety of chickenpox virus.
functional.
Etiologic Agent
Signs … 1. Varicella Zoster (V-Z) virus
The lepromatous and tuberculoid forms affect the skin in markedly • This disease has been found to cause two diseases,
different ways. varicella, and herpes zoster
1. In lepromatous early lesions are multiple, symmetrical, and • The virus still occurs in partially immune individuals due
erythematous, something appearing as macules or papules to previous varicella infection.
with smooth surfaces. Incubation Period: Unknown, believed to be 13-17 days
2. later they enlarge, and form plaques and nodules called Period of Communicability: A day before the appearance of the
lepromas in the earlobes, nose eyebrows, and forehead, first rash until five to six days after the last crust disappear
giving the patient a characteristic LEONINE APPEARANCE. Mode Of Transmission
• direct contact, spec. droplet & airborne spread
In advance Stages M leprae may infiltrate the entire skin surface. • indirect contact
• LL- may also case loss of eyebrows, eyelashes and Diagnostic Exam
sebaceous and sweat glands functions • char. Skin rash may be diagnostic
• Upper respiratory lesions may cause epistaxis, ulceration of • tissue culture technique
the uvula and tonsils, septal perforation, and nasal collapse • smear of vesicle fluid
• LL- can lead to hepatosplenomegaly and orchitis. • microscopy
• Fingertips and toes deteriorate as bone resorption follows Complications
trauma and infection in these insensitive areas. • Encephalitis
Signs… • Paralytic ileus, bladder paralysis
• When TL affects the skin, it produces raised, large • Ophthalmic herpes which may lead to blindness
erythematous plaques or macules with clearly defined Nursing Management
borders. • Keep the pt. comfortable. Maintain meticulous hygiene.
• As they grow they become rough, hairless, hypopigmented, • Keep the pt. in strict Isolation
and leave anesthetic scars. • Apply cool, wet dressings with NSS to pruritic lesions.
• In BL skin lesions are numerous, but smaller less anesthetic, • Efforts should be made to prevent secondary infection
and less sharply defined than TL. • Prevent entrance of microorganism into the lesions, especially if
• Untreated BL may deteriorate into LD. they are broken.
• Acute episodes intensify leprosy’s slowly progressing • Assess the degree of pain. To avoid neuralgic pain, do not
course. delay the administration of pain relievers as prescribed.
• Erythema Nodosum Leprosum (ENL), seen in LL produces • Encourage sufficient bed rest and provide supportive care to
fever, malaise, lymphadenopathy, and painful red skin promote proper healing of lesions.
nodules, usually during antimicrobial treatment, although it • Provide the patient with a diversionary activity to take his mind
off the pain and the pruritus.
may occur in untreated people.
• Lucios phenomenom which produces generalized punched
COMPARISON BETWEEN SHINGLES AND VARICELLA
out ulcers that may extend into muscle and facia.
Clinical Feature Chicken Pox Herpes Zoster: Varicella Virus VZ
• Leprosy may also lead to tuberculosis, malaria, secondary
Virus
bacterial infection of the skin ulcers, and amyloidosis.
Period of communicability
• a day before the eruption of the 1st rash up to 5 days
Laboratory Test
after the last crust
• Lepromin test
• Same as in chickenpox
• Skin smear test
Evolution of rashes
• Skin lesion biopsy Macule ->papule -> Vesicle -> pustule Same as chickenpox
• Wasserman Reaction Test Distribution of rashes
Management • Appear first on the unexposed part of the body
1.Prevention • Generalized
• Separation of infants from lepromatous parents at birth • Clustered
• BCG immunization • Unilateral
• Avoid contact • Does not cross the sagittal portion of the body
Treatment • Itchy
MDT -MULTI DRUG THERAPY MEDICAL CARE • Deep-seated burning pain that is usually worst at night
1. Paucibacillary (few organism) – given for 6-9 months or until • Lymphadenopathy
negative. • Corneal Anesthesia (Gasserian Ganglionitis)
• Rifampicin – once a month • Paralysis of the facial nerve and the external auditory canal
• Dapsone - once a day (Ramsay Hunt Syndrome)
2. Multibacillary (many organism)-given for 24-30 months/ 2 and • Acyclovir (Zovirax)
half years • Acyclovir
• Rifampicin – once a month • Immunization against chickenpox
• Dapsone – once a day • Avoid exposure to a patient suffering from either
• varicella or herpes zoster
• Lamprene – once a day
• Increase the patient’s immune resistance
• (causes blackish discoloration of the skin)
Prevention
Nursing Care
1. Emotional support • Immunization against chickenpox
2. Skin care • Avoid exposure to a patient suffering from either
3. Passive and active exercise to prevent contractures varicella or herpes zoster
4. Adequate information regarding drug therapy • Increase the patient’s immune resistance
SCABIES ANTHRAX
Causative Agent: Sarcopti Scabei
Mode of Transmission: direct contact with infected persons on Synonym: Malignant Pustule, Woolsorter’s Disease, Splenic Fever
their clothing  Anthrax is recognized as the most likely weaponized
biologic agent available and has been recognized as a
highly debilitating agent for centuries (G. Bare, 2018)
Signs and Symptoms  It occurs primarily in herbivores.
* Eruptive lesion caused by the burrowing of the female parasite
into the skin Causative Agent: Bacillus anthracis
1. slightly elevated Mode of Transmission
2. Grayish brown and dotted • Direct
3. intense itching
• Indirect
Incubation Period: The itch mite may burrow under the skin and
• Airborne
lay ova within 24 hours of the original contact.
Incubation Period: The incubation period is 2 to 7 days.
Management
TYPES:
Medical Care
• Cutaneous Anthrax
1. Benzyl Benzoate emulsion
2. Kwell ointment - drug of choice • Inhalation Anthrax
3. Lagundi • Gastrointestinal Anthrax
Nursing Care
• *Emphasis on hygiene 1. Cutaneous Anthrax
SIGNS AND SYMPTOMS
• A raised a small pimple or macule appears, itchy
PEDICULOSIS bump resembling an insect bite that quickly
• a ring vesicle develops around the papule develops
Synonyms: Head lice into a painless sore with a black center
• Swelling in the sore and nearby lymph glands
Causative Agent - Pediculosis capitis • there is no pus & the lesion is not painful, although
painful lymph adenitis may occur in the inguinal area.
Mode of Transmission: From person to person/personal 2. Gastrointestinal Anthrax
belongings SIGNS AND SYMPTOMS
• Nausea
Signs and Symptoms: itching, imitative dermatitis with • Vomiting
excoriations and crusting • Abdominal pain
• Headache
Management: Kwell shampoo • Loss of appetite
• Fever
• Severe, bloody diarrhea in the later stages of the
TINEA CORPORIS/ TINEA PEDIS disease
• Sore throat and difficulty swallowing
Synonyms: “Anan”/Athlete’s foot • Swollen neck
Causative Agent: Microsporum and Trichophyton Inhalation (Pulmonary) Anthrax
Mode of Transmission: SIGNS AND SYMPTOMS
• Direct or indirect contact with skin, contaminated • Flu-like symptoms, such as sore throat, mild fever,
clothing (towels, handkerchief, etc.) floors, shower stalls, fatigue and muscle aches, which may last a few hours
benches or days
Signs and Symptoms • - Mild chest discomfort
• Flat, spreading, ring shaped lesions • - Shortness of breath
• Reddish periphery, vesicular or pustular • - Nausea
• Maybe dry and scaly or moist crusted • - Coughing up blood
• - Painful swallowing
Management • *As the disease progresses, you may experience:
Prevention • - High fever
1. Wash towels and clothing with hot water • - Trouble breathing
2. General cleanliness in swimming pools, showers and • - Shock
dressing rooms • - Meningitis
Control DIAGNOSTIC EXAM
1. Use of fungicidal agents 1. Skin testing
2. Treatment Fungicides topical miconazide, ketoconazide, 2. Blood tests
clotrimoxazole 3. Chest X-ray or computerized tomography (CT) scan
4. Stool Exam
5. Spinal tap (lumbar puncture)
TREATMENT
The standard treatment for anthrax is a 60-day course of an antibiotic,
such as ciprofloxacin (Cipro) or doxycycline (Monodox, Vibramycin,
others).
o Parenteral penicillin G-2 million units every six hours, until
edema subsides, with subsequent administration of oral
penicillin for a seven-toten-day-course.
o Patients who are sensitive to penicillin can be treated with
erythromycin, tetracycline, or chloramphenicol.
COMPLICATIONS TREATMENT
1. Anthrax Meningitis • Antivirals (Oseltamivir)
• Is the intense inflammation of the meninges of the brain • Antibiotics
& spinal cord. • Low dose systemic corticosteroids
• Elevated CSF pressure with bloody CSF • NSAIDs, antipyretics (Nonsteroidal anti-inflammatory
• Loss of consciousness & death drugs)
2. Anthrax Sepsis
• develops after the lymphohematogenous spread of B. PREVENTION AND CONTROL
anthracis from the primary lesion. • Infection control
NURSING MANAGEMENT • Vaccines
1. Isolation
2. The patient should be kept in a well-ventilated room on NURSING MANAGEMENT
complete bed rest • Isolation
3. Daily cleansing baths should be given when the condition of • Appropriate instructions for household members on
the patient permits. personal hygiene and infection control measures are
4. Good oral hygiene must be practiced. important and should be provided
5. Daily elimination is desirable.
6. Liquid to soft diet as desired and tolerated.
7. Cooling measures like TSB and colonic irrigation. SEVERE ACUTE RESPIRATORY SYNDROME (SARS-COV)
 the first pandemic threat of a novel and deadly
coronavirus that emerged in late 2002 and caused an
outbreak of severe acute respiratory syndrome (SARS) is
BIRD’S FLU genetically closely related to the SARS-CoV2 virus.
(H5N1 Avian Influenza)  Severe Acute Respiratory Syndrome-2 (SARS-COV-2)
 Avian influenza (bird flu) is an infection caused by influenza o COVID-19
viruses that chiefly infect birds and poultry. The H5N1 strain o new (novel) strain of coronavirus
(named for the characteristics of the viral surface proteins o not previously identified in humans
hemagglutinin and neuraminidase) is of particular concern. o Severe Acute Respiratory Syndrome (SARS-CoV)
 It has caused a number of outbreaks in poultry since 2003, and = 2003 = both were also originally called “novel
the problem is ongoing; flocks of migratory birds have rapidly coronaviruses”
disseminated the virus throughout much of the world (Bare et o bats or pangolins transmitted to humans directly
al,2018). or through an intermediate host
CAUSATIVE AGENT: Avian Influenza (AI) virus- Influenza Virus A , a source location:
genus of the Orthomyxoviridae family o large live animal market in Wuhan, Hubei Province
MODE OF TRANSMISSION o human – to – human spread
• Direct Contact Clinical criteria: Asymptomatic or mild respiratory Illness
• Contaminated Surfaces Epidemiological Criteria
• Air (Droplets / Dust) o Travel
INCUBATION PERIOD: 3-5 days o Close contact to person with SARS
PERIOD OF COMMUNICABILITY Mode of Transmission
• The infectious period is 7 days after resolution of fever in o Direct contact
adults and 21 days after onset of illness in children. o Respiratory Droplets
• Communicability increases with the severity of disease and o Airborne
degree of direct exposure. Survive in water up to 4 days at o Indirect Contact
22 days Incubation Period
SIGNS & SYMPTOMS o The incubation period is usually 2 to 14 days.
• Symptoms in animals vary, but virulent strains can cause o symptoms usually begin around 5th day
death within a few days.
• The symptoms of avian influenza in humans are similar to
those of human influenza.
• Cough
• Fever (over100.4°F~ 38°C) Severe Acute Respiratory Syndrome-2 (SARS-COV-2)
• Sore throat
• Pneumonia VIRAL MUTATIONS
• Muscle aches • viruses naturally mutate over time
• Headache • severity of mutation depends on the change in virus’
• Dyspnea (shortness of breath) genetic material
COMPLICATIONS • some results in the production of a different protein
People with bird flu may develop life-threatening complications, during replication
including:
• Pneumonia Notable variants reported (as of January 15, 2021) WHO:
• Pink eye (conjunctivitis) • D614G (> infectivity & transmission)
• Respiratory failure • VOC 202012/01 (UK variant; > transmission)
• Kidney dysfunction • 501Y.V2 (South Africa variant; > viral load)
• Heart problems • B.1.1.28 (12 mutations; Brazil variant; travelers arrived in
DIAGNOSTIC EXAM Japan)
• LABORATORY TESTS
• IMAGING TESTS Variants of concern: UP Philippine Genome Center (PGC) March
• COMPLETE BLOOD COUNT 10, 2021
• LIVER FUNCTION TEST • B.1.1.7 (UK variant)
• B.1.351 (South Africa variant; > viral load)
• P.1 (17 mutations; Brazil variant *)
CYTOKINE
• small soluble molecules acting as messengers for
immune system CYTOKINE STORM in COVID-19
• produced by side variety of immune cells  Immune response is more than it should be!
• Neutrophils • Infection
• Basophils • Immune response to fight pathogen
• Eosinophils • Dysregulated immune response
• Mast cells • 2 weeks after infection
• Dendritic cells • Increase more
• Monocytes • Deadly uncontrolled local and systemic inflammatory
• Macrophages response
• B cells • Inc proinflammatory cytokine and many WBC
• T cells • Not sure of cause?
• Change activity of cell • PROGRESSION
o alter function of proteins o CORONAVIRUS
o change expression of certain genes o binds to ACE2 receptors
o enters the alveoli
CYTOKINE STORM o attacks the Type 2 alveolar cells
Structural groups of cytokines: Interleukins (IL) 1-35 o Inflammatory response
• key role in immune response o T cells, B cells, CYTOKINES storm
• Produced by leucocytes --> leucocytes o vasodilation, edema
• Proinflammatory o Inc extravascular pressure
o IL 1alpha, IL beta, IL 6 and IL-8 o Dec tissue perfusion
• Anti-inflammatory o Endothelial dysfunction
o IL-4, IL-10, IL-13 o Plasma proteins accumulate- TNFa & IL-6
Structural groups of cytokines: Tumor Necrosis Factor (TNF) o Major contributors to cytokine storm
• 19 known o acute lung injury
• mast cells, Macrophages, T cells o ARDS
• immune cell activation o May resolve
• differentiation, growth, death o FIBROSIS
TNFa o Long term dysfunction
• major proinflammatory cell
• potent activation of cytotoxic T cells Clinical Manifestations (Sars-Cov-2)
• viral disease and cytokine storm • Most common symptoms
• Blockage- autoimmune disease ✓ Fever ( 83% - 99 %% )
Structural groups of cytokines: Interferons (IFN) ✓ Cough ( 59% - 92 % )
• 20 known ✓ Shortness of breath ( 31% - 40 % )
• Type I: IFN alpha and beta ✓ Other symptoms
Produced by many cells to infection (Hep C) ✓ Anosmia
• Type II: ✓ Ageusia
o Role in immune responses ✓ Feeling tired
o Inc phagocytosis of macrophages ✓ Headache
• ANTIVIRAL ROLE ✓ Myalgias
✓ sore throat
Colony Stimulating Factors (CSF) ✓ nasal congestion
• act on stem cells in bone marrow to stimulate growth ✓ diarrhea
and differentiation
CLINICAL SPECTRUM of sars-cOv-2 INFECTION
Symptomatic or Pre symptomatic Infection:
• test positive for SARS-CoV-2 using a virologic test (i.e., a
nucleic acid amplification test [NAAT] or an
• antigen test but who have no symptoms that are consistent
with COVID19.
Mild Illness:
• fever
• * cough, sore throat, malaise,
• Headache.
• * muscle pain, nausea, vomiting, diarrhea,
• Ageusia
• * anosmia
• do not have shortness of breath, dyspnea, or abnormal chest
imaging.
• Managed at home or ambulatory care
Moderate Illness:
• evidence of lower respiratory disease during clinical
assessment
• imaging
• oxygen saturation (SpO2 ) ≥94% on room air at sea level
• If bacterial pneumonia or sepsis is suspected,
• Emperic antibitiotic treatment
• Close monitoring

Critical Illness:
For How long will SARS virus exist on surfaces?
• Respiratory failure
• The virus is stable in urine and feces at room temperature
• Septic shock
for at least one to two days and in stool from patients with
• MODS
diarrhea for up to four days
• Patients with comorbidities.
• It survives on paper, on a plastered wall after 36 hours, on
• higher risk of progressing to severe COVID-19
a plastic surface or stainless steel after 72 hours and on a
• 65 years or older
glass slide after 96 hours
• cardiovascular disease
• Hospital environment samples from a number of sites,
• chronic lung disease
including walls and ventilation systems, have tested
• sickle cell disease
positive for SARS virus
• Diabetes
• The virus loses its inefectivity after exposure to different
• cancer
commonly – used disinfectants and fixatives. Heat at 50 C
rapidly kills the virus
Patients with comorbidities;
THERAPEUTIC MANAGEMENT of OUTPATIENT ADULTS with
• Obesity
COVID-19
• chronic kidney disease
COVID-19 TREATMENT GUIDELINES US-NIH, UPDATED
• being pregnant
RECOMMENDATIONS APRIL 21, 2021
• being a cigarette smoker
• being a recipient of transplant or immunosuppressive
THERAPEUTIC MANAGEMENT of ADULTS with COVID-19
therapy
• No therapy has been proven to be beneficial in OP with mild to
❑Health care providers should monitor such patients closely until
moderate
clinical recovery is achieved
COVID-19 who are at high risk for disease progression
• Pathogenesis:
Diagnostics
o Early: replication of SARS-CoV-2.
• C-Xray
o Later: a dysregulated immune/inflammatory response to
• CT Scan- ground glass opacities, peripheral, asymmetrical
SARS-CoV-2 that leads to tissue damage.
and posterior distribution in early infection without pleural
• Therapeutics:
effusion
o Early: Antiviral therapies
• ECG
o Later: immunosuppressive/anti-inflammatory therapies
• Ferritin
o Male: 12-300, Female: 10-150
THERAPEUTIC MANAGEMENT of ADULTS with COVID-19
o inflammation: 1,000
• COVID-19 Treatment Guideline Panel
o inc in inflammation
➢ Supportive care
• early marker in CS in covid19 patients
✓ ✓ Reduce the risk of SARS-CoV-2 transmission
• Laboratory tests:
o CBC with differential ✓ ✓ Isolating patient
o Metabolic profile ✓ ✓ Advise when to contact a HCP or in-person
✓ SGPT/SGOT evaluation (AIII)
✓ BUN/Creatinine Symptomatic management to OP with COVID-19
o inflammatory markers ➢ Telehealth before receiving in-person care
✓ C-reactive protein (CRP) ➢ Triage
✓ D-dimer ferritin ➢ Patients with dyspnea : in-person evaluation by a HCP
• CRP and followed closely for worsening respiratory status
o produced by the liver in response to IL-6 (AIII)
o marker of inflammation
o rapid rise ->risk for CS
• D-dimer
o coagulation system is active during critical illness
o levels associated with proinflammatory cytokine
cascade
o Normal: < 500
o associated with inc risk for multi organ failure and
death
o Elevation -> 3-4x -> inc mortality