Disease Nursing
Florence V.Quintana RN
Host and Microbial Interaction
INTRODUCTION
1. Sporadic Disease
= disease that occurs only
occasionally & irregularly with no
specific pattern
i.e. botulism, tetanus
2. Endemic Disease
= constantly present in a
population, country or community
i.e. Pulmonary Tuberculosis;
malaria
3. Epidemic Disease
= patient acquire the disease
in a relatively short period of time
; greater than normal number of
cases in an area within a short
period of time
i.e, cholera; typhoid
4. Pandemic Disease
= epidemic disease that occurs
worldwide
i.e. HIV infection; SARS
Based on Severity or Duration of
Disease
1. Acute Disease
= develops rapidly (rapid
onset) but lasts only a short time
i.e. measles, mumps,
influenza
2. Chronic Disease
= develops more slowly (insidious onset)
disease likely to be continual or recurrent for
long periods
i.e. TB, Leprosy
3. Subacute Disease
= intermediate between acute and chronic
i.e. bacterial endocarditis
4. Latent Disease
= causative agent remains inactive for a time but
then becomes active to produce symptoms of
the disease
i.e. chickenpox → shingles (zoster); amoebiasis
Based on Extent of Affected Host’s
Body
1. Local Infection
= microbes invade a
relatively small area of the body
2. Generalized (Systemic)
Infection
= spread throughout the
body by blood or lymph
i.e. measles
3. Focal Infection
= local infection that spread
but are confined to specific areas
of the body
Based on State of Host Resistance:
1. Primary Infection
= acute infection that causes the initial
illness
2. Secondary Infection
= one caused by an opportunistic
pathogen after primary infection has
weakened the body’s defenses
3. Subclinical (Inapparent Infection)
= does not cause any noticeable illness
Stages of Disease
Incubation Period
- time interval between the initial infection and
the 1st appearance of any s/sx
- patient is not yet aware of the disease
Prodromal Period
- early, mild appearance of symptoms of the
disease
Period of Illness
Time of greatest symptomatic experience ( pt. is
sick)
- overt s/sx of disease
WBC may increase or decrease
can result to death if immune response or
medical intervention fails
Period of Decline
s/sx subside
pathogen replication is brought
under control
vulnerable to secondary infection
Period of Convalescence
Replication of pathogenic organisms is
stopped
regains strength and the body
returns to its
pre diseased state
= recovery has occurred
Nurse Alert!!!!
ANTIBODY
A. NATURAL :
1. Natural active – through
exposure or diseases; had
the disease & recovered
2. Natural Passive – maternal
antibodies; acquired through
placental transfer
B. ARTIFICIAL ( Laboratory )
1. Artificial active – introduction of antigen
Ex. Vaccines ; toxoids
( No exposure yet; preventive measure)
= gives long immunity – months to years
2. Artificial passive- introduction of antibodies Ex.
Antitoxins; immunoglobulin ( gammaglobulin),
antiserum, convalescent serum
Ex. TAT ( tetanus antitoxin)
( w/ exposure to the causative agent)
= gives short immunity – 3-4 weeks
Immunity
NATURAL ACQUIRED
- INHERENT BODY TISSUES Outside the
host
1. NATURAL 2.
ARTIFICIAL
( HUMAN)
( LABORATORY)
13% LRI
14% Bacteremia
22% Other (incldng skin Infxn)
Factors for Nosocomial Infection
Microorganism/Hospital Environment
Most common cause
Compromised Host
One whose resistance to infection is impaired
by
broken skin, mucous membranes and a
suppressed immune system
INFECTION
CONTROL
MEASURES
General Control Measures
Attained by:
Use strict aseptic precautions for invasive
procedures
Scrub hands and fingernails before entering O.R.
Use sterile gloves, masks, gowns and shoe covers
Use sterile solutions and dressings
Use sterile drapes and create an sterile field
Heat –sterilized surgical instruments
1. Universal Precaution ( Standard Precaution )
Defined by center for disease control (CDC) 1996
Primary strategy for reducing the risk of &
controlling Nosocomial infections
Used for care of all hospitalized patients, regardless
of diagnosis and are presumed infectious
Protect healthcare workers from contamination and
infection ( i.e. HIV, HBV)
Hand Washing
Routine: Plain (non microbial) soap
Linens
Handled, transported and processed to
prevent contamination and transfer of
microorganisms
Occupational Health and Blood –borne
Pathogens
Never recap used needles
Puncture – resistant containers
Revised C.D.C. Isolation
Precaution
( centers for disease control)
2. Transmission-Based Precautions
The second tier of precaution
Precaution are instituted for patients who
are known to be or suspected of being
infected with highly transmissible infection.
gloves
gown
shoe cover
goggles
Transmission based precautions
for Hospitalized
patient :
Category Single Masks Gowns Gloves
Precautio Room
n
3. Respiratory diseases
a. Pneumonia
b. Diphtheria
c. PTB
d. Mumps
5. CNS Infections 7. Emerging
a. Encephalitis
b. Meningitis
Diseases:
c.Meningococcemia SARS
d. Rabies
e. Tetanus
Birds FLU
f. Snake bite
6.Diarrheal diseases
a. E.coli
b. Staphyloccus aureus
c. Cholera
d. Rotavirus
e. Salmonella
f. Parasitism
VECTOR BORNE DISEASES
Dengue Fever, H-Fever,
Dandy Fever, Breakbone
Fever, Phil
Hemorrhagic fever
Acute Febrile Disease
Flavivirus, dengue virus 1,2,3,4
(petechiae,purpura,ecchymoses,pistaxis,
gum bleeding, hematemesis, melena)
Laboratory: thrombocytopenia </=
100,000mm3, hemoconcentration- an
increase of at least 20% in the
hematocrit or its steady rise
Assessment:
Tourniquet test (Rumpel Leedes test) -
screening test, done by occluding the arm
veins for about 5 minutes to detect
capillary fragility.
Keep cuff inflated for 6 – 10 minutes
( child); 10-15 minutes ( adults)
Count the petechiae formation 1 square
inch ( 20 petechiae/sq.in)(+)TT
Platelet count ( decreased) – confirmatory
test
Classification of Dengue
Fever according to severity
Grade I – Dengue fever, saddleback fever
plus constitutional signs and symptoms
plus positive torniquet test
Grade II – Stage I plus spontaneous
bleeding, epistaxis, GI, cutaneous bleeding
Grade III – Dengue Shock Syndrome, all of
the following signs and symptoms plus
evidence of circulatory failure
Grade IV – Grade III plus profound shock
and massive bleeding, undetectable BP and
pulse
Laboratory criteria DHF:
Platelet count Thrombocytopenia
<100,000
Hct – increased by 20 % or more
Circulatory failure
Dengue progress -hypotension death
-narrow pulse pressure
,20mm Hg (shock)
S/sx:
Mild dengue – abrupt onset of fever,
headache, muscle and joint pains,
anorexia, abdominal pain.
Petecchiae, Herman’s rash (5th-7th
day; purplish macules w/ blanched
areas on extremities)
Severe dengue – DHF/DSS
*TRIAD: fever, rashes and muscle pain
Bleeding leading to hypovolemic shock
Medical MX
There is no effective antiviral therapy for dengue
fever. Treatment is entirely SYMPTOMATIC
Paracetamol for headache ( never give ASPIRIN)
IVF for hydration & replacement of plasma
BT for severe bleeding
O2 therapy is indicated to all patients in shock
Sedatives for anxiety & apprehension
No IM injections
Nasal packing with epinephrine
Gastric lavage
Giving cytoprotectors
Nursing Mx
Symptomatic tx
Mosquito free environment to avoid further
transmission of infection
Keep patient at rest during bleeding episodes
VS must be promptly monitored
For nose bleeding, maintain pt’s position in
elevated trunk, apply ice bag to bridge of nose
Observe for signs of shock
Restore blood volume ( supine with legs
elevated)
Dengue hemorrhagic
Fever
PREVENTION : DOH 1995 Program
or minimus flavirustris
= infectious but not contagious
= thrives in clear, free flowing shaded streams
usually in the mountains
= bigger in size than the ordinary mosquito
= brown in color, usually does not bite a
person in motion
= assumes a 36 degree position when it alights
on walls, trees, curtains and the like
Incubation Period:
1. 12 days for P. falcifarum
Period of Communicability:
Untreated or insufficiently treated
patient may be the source of mosquito
infection for more than three years in
P. malariae; one to two years in P.
vivax; and not more than one year on
P. falcifarum
Pathogenesis
Anopheles mosquito >> gets parasites in the
blood of infected person >>parasites multiply in
mosquito >>parasites invade the salivary gland
of mosquito >> mosquito bites the individual &
thus, injects the parasites >> parasites invade
RBC where they grow & undergo asexual
propagation >> RBC ruptures or bursts releasing
tiny organisms ( MEROZOITES) >> merozoites
invade new batch Of RBC to start another
schizonic cycle
Pathology
the most characteristic pathology of
malaria is destruction of red blood
cells, hypertrophy of the spleen and
liver and pigmentation of organs.
The pigmentation is due to the
phagocytocis of malarial pigments
released into the blood stream upon
rupture of red cells
Plasmodium Life Cycle
Malaria
Transmission : sporozoites, injected travel
by anopheles mosquito to human liver
and vomiting
TSB , cold compress
Light clothing,
MALARIA (Ague)
Clinical manifestation :
I. Cold stage ( 10-15mins)
II. Hot stage (3-4Hrs)
Profuse sweating
Mosquito bites
Aedes poiculus , culex
faligans and Person infected – bitten by mosquito
anopheles flavirostris Transmitted to another person
Blood /vector-borne
Treatment :
Drugs Ivermectin , albendazole and
DIETHYLCARBAMAZINE (DEC)-
6mg/KBW in divided doses for 12
consecutive days
Eliminate the larvae
Supportive Therapy
Paracetamol
Antihistamine for allergic reaction due to DEC
Vitamin B complex
Elevation of infected limb, elastic stocking
PREVENTIVE MEASURE
Health teachings
Environmental Sanitation
Mgmt: Environmental sanitation
Personal Hygiene
Provide mosquito nets
Mosquito repellant
Jaundice, hepatomegally
Convalescent Period
Diagnosis
Specific
Penicillin 50000 units/kg/day
Tetracycline 20-40mg/kg/day
Non-specific
Supportive and symptomatic
Administration of fluids & electrolytes
Peritoneal dialysis for renal failure
LEPTOSPIROSIS
Blood /vector-borne
Prevention Control &
Nursing Considerations:
Avoidance of exposure to urine & tissues
from infected animals ( flood)
Rodent Control
Hygienic control in slaughterhouses,
farmyard buildings & bathing pools
Use of protective clothing & boots
Primarily a disease of domesticated & wild
animals transmitted via direct or indirect
contact. It enters the skin, mucus
membrane, conjunctiva, inhalation
Disease is usually short lived & mild but
severe infection can damage kidneys & liver
HEPATO-ENTERIC
DISEASES
GIT
Typhoid Fever
Salmonella typhosa, gram (-)
Carried only by humans
Bloodstream
Bloodstream
Gallbladder
3. Cotrimoxazole
Supportive therapy
Assessment of complications
(occuring on the 2nd to 3rd week
of infection )
- typhoid psychosis, typhoid
meningitis
- typhoid ileitis
Schistosomias/Snail
Fever/Bilharziasis/Katayama
Causative agent : Oriental Blood Fluke
Schistosoma japonicum (affects
intestinal tract)
S. hematobium ( affects urinary tract)
S. mansoni ( affects intestinal tract)
IP: 2 months
Source: feces of infected persons
Dogs, pigs, cows, carabaos, monkeys, wild rats
serve as HOSTS
Pathogenesis- Snail fever Ulceration in the mucosa
Eggs able to escape in the lumen
Larvae ( cercaria) Of intestine, excreted in the feces
Female cercaria lays egg in the blood vessels Blood flow interrupted
Large intestine or bladder Result to portal
hypertension
Schistosomias/Snail
Fever/Bilharziasis/Katayama
Causative agent : Oriental Blood Fluke
Schistosoma japonicum (affects
intestinal tract)
S. hematobium ( affects urinary tract)
S. mansoni ( affects intestinal tract)
IP: 2 months
intermediary
host
(oncomelania
quadrasi/tiny
amphibious
snail)
Schistosomias/Snail Fever
MOT: penetration of
cercaria to the skin
>parasites live in the
blood vessels of
intestines>cercaria
migrates to the liver for
maturation> gets out of
the liver & goes against
blood flow> obstruction
of hepatic portal vessels>
inc pressure>portal
hpn>leads to esophageal
& gastric varices, ascites
& hepatomegaly
Assessment :
Swimmer’s itch or cercarial dermattitis –
itching within 24hrs after penetration of the
skin by cercaria last 2-3 days
Migratory phase : sensitized individual
develop systemic reaction of FEVER, CHILLS ,
SWEATING , DIARRHEA , COUGH and
EOSINOPHILIA
Acute Phase : (+) fever , generalized
lympagenopathy, hepatomegaly and
splenomegaly ( KATAYAMA FEVER) 2-3
weeks after initial infection and last for 1-2
months
Diagnostics:
Fecalysis or direct stool exam
Kato katz technique
Immunosorbent Assay)
COPT ( circum-oval precipitin test)
confirmatory diagnostic test
Obstructed jaundice
s/sx: dark urine, pale feces, itchness
W – weight loss
M – malaise
Icteric
J – jaundice
A – acholic tool
Enteric fever
VIRAL HEPATITIS
Analysis
Knowledge deficit related to unfamiliarity with the
disease course and treatment
Activity intolerance related to decreased
metabolism of nutrient / increased basal metabolic
rate caused by viral infection
High risk for Diversional activity deficit secondary to
isolation / lack of energy
High risk for altered body nutrition : less than body
requirement secondary to anorexia
VIRAL HEPATITIS
Treatment
No specific treatment
Bed rest essential
Measles,
RNA, Paramyxoviridae
Measles virus is rapidly inactivated by heat, UV light, &
extreme degrees of acidity & alkalinity
Active immunity (MMR and Measles vaccine)
Lifetime Immunity
Diagnostics:
Nose & throat swab
Urinalysis
Urinalysis
Eruptive fever
MANAGEMENT
1. Supportive
2. Hydration
3. Proper nutrition
4. Vitamin A
5. Antibiotics – if w/
secondary
bacterial infection
6. Vaccine- measles
vaccine @ 9 mos
and MMR @ 15
mos
7. Anti viral drugs
( Isoprenosine)
Observe respiratory
Nursing Care
Isolation of the patient if necessary
TSB for fever
Skin care is of utmost importance. The pt.
should have a daily cleansing bed bath.
Oral & nasal hygiene is a very important
aspect of nursing care of patients with
measles
Restrict to quiet environment
Dim light if photophobia is present; care of
the eyes is necessary
Administer antipyretic
Use cool mist vaporizer for cough
German Measles, Rubella,
Rotheln Disease, 3 Day
Measles
= contagious viral disease characterized by fever, URTI,
arthralgia, DIFFUSED fine red maculopapular rash)
CA - RNA, rubella virus ( Togaviridae)
Immunity: Active natural ( permanent or lifetime)
Active immunity - rubella vaccine and MMR
Passive immunity - gammaglobulin
Period of communicability – contagious 7 days before & 7
days after appearance of rash & probably during the
catarrhal stage
German Measles, Rubella, Rotheln
Disease, 3 Day Measles
Given SC
S/sx:
Rashes:
Maculopapulovesiculopustular
Centripetal rash distribution
contagious until all crusts
disappeared
SMALL POX
Complications:
Scarring
Pneumonia
Blepharitis
Corneal ulceration
Adequate hydration
Mandatory reporting
PREVENTION
Pre-exposure vaccination
Strict isolation of identified cases
Respiratory Diseases
Meningococcemia
2. Active
Tuberculin test positive
CXR – progressive
(+) of symptoms
Sputum (+)
Hemoptysis – pathognomonic
Protein undernutrition
Destroy bacteria
bacteria dormant
4. Ethambutol = 15-20mg/day
SE = Optic neuritis ( dec visual acuity)
5. Streptomycin
SE = Ototoxicity, 8th cranial nerve
damage
( Tinnitus, dizziness, N&V)
MDT side effects
r-orange urine
i-neuritis and hepatitis
p-hyperuricemia
e-impairment of vision
s-8th cranial nerve damage
PTB- NURSING
MANAGEMENT
1. MAINTAIN REPIRATORY ISOLATION
2. Administer medicine as ordered
3. Always check sputum for blood or purulent
expectoration
4. Encourage questions and conversation so that the
patient can air his or her feelings
5. Teach or educate the patient all about PTB
6. Encourage patient to stop smoking
7. Teach how to dispose secretion properly
8. Advised to have plenty of rest and eat balanced
diet
9. Be alert of drug reaction
10. Emphasize the importance of follow-up
PULMONARY TUBERCULOSIS
( Koch’s Disease/Phthisis/
consumption Disease)
PREVENTION:
1. Submit all babies for BCG immunization
2. Avoid overcrowding
3. Improve nutritional and health status
4. Advise persons who have been
exposed to infected persons to receive
tuberculin test if necessary CXR and
prophylactic isoniazid.
Mumps ( Epidemic Parotitis);
Infectious Parotitis
-Acute contagious VIRAL disease. Characteristic
feature is swelling of one or both of the parotid glands
RNA, Mumps virus ; paromyxovirus of the Varicella
family( found in the saliva)
Mumps vaccine - > 1yo
MMR – 15 mos
Lifetime Immunity
Diseases
Cholera / El Tor
Causative agent: Vibrio coma (inaba,
ogawa, hikojima), vibrio cholerae,
vibrio el tor; gram (-)
Curved rod or coma shaped organism;
motile
Habitat: small intestine
Parasitism
INTESTINAL PARASITISM
are parasites that populate the
gastro-intestinal tract.
MOT : they are often spread by poor
hygiene related to feces
contact with animals, or poorly cooked
food containing parasites.
Two main types of intestinal
parasites:
A. Helminths
Tapeworms, pinworms, and roundworms are
among the most common helminths
B. Protozoa.
Cause of intestinal
Parasitism
high risk for getting intestinal parasites:
Living in or visiting an area known to have
parasites
Poor sanitation (for both food and water)
Poor hygiene
1. Trophozoites/vegetative form
Trophozoites are facultative parasites that may
invade the tissues or may be found in the
parasites tissues and liquid colonic contents.
2. Cyst
a. Cyst is passed out with formed or semi-
formed stools and are resistant to
environmental conditions.
b. This is considered as the infective stage in the
life cycle of E. histolytica
Pathology
When the cyst is swallowed, it passes through the
stomach unharmed and shows no activity while in
an acidic environment. When it reaches the
alkaline medium of the intestine, the metacyst
begins to move within the cyst wall, which rapidly
weakens and tears. The quadrinucleate amoeba
emerges and divides into amebulas that are
swept down into the cecum. This is the first
opportunity of the organism to colonize, and its
success depends on one or more metacystic
trophozoites making contact with the mucosa.
Mature cyst in the large intestines
leaves the host in great numbers (the
host remains asymptomatic). The cyst
can remain viable and infective in moist
and cool environment for at least 12
days, and in water for 30 days. The
cysts are resistant to levels of chlorine
normally used for water purification.
They are rapidly killed by desiccation,
and temperatures below 5 and above
40 degrees.
MOT: Ingestion of cysts from fecally
contaminated sources (Oral fecal
route)
oral and anal sexual practices
Extraintestinal amoebiasis- genitalia,
spleen, liver, anal, lungs and
meninges
lifecycle
s/sx: Blood streaked, watery mucoid diarrhea,
abdominal cramps
Dx: microscopic stool exam - trophozoites
Pd of Communicability: the microorganism
is communicable for the entire duration of
the illness
Mgmt:
Tetracycline 250 mg every 6 hours
Ampicillin, Quinolones, sulfadiazine
Metronidazole (Flagyl) 800 mg TID x 5 days
Strptomycin SO4, Chloramphenicol
F&E balance
Nsg. Mx
Observe isolation & enteric precaution
Provide health education & instruct patient to:
Boil water for drinking or use purified water
Avoid washing food from open drum or pail
Health education
Sanitary disposal of feces
Protect, chlorinate & purify drinking water
Observe scrupulous cleanliness in food
preparation & food handling
Detection & tx of carriers
Fly control ( they can serve as vectors)
CNS Infections
MENINGITIS
( Cerebrospinal fever)
Is the inflammation of the meninges of the
brain and spinal cord as a result of viral or
bacterial infection.
IP : varies from 1-10 days
MOT : respiratory droplet
direct invasion through otitis media
may result after skull fructure
Caused by bacterial pathogen,
N. menigitidis, H. Influenza,
Strep. Pneumoniae,
Mycobacterium Tuberculosis
Clinical manifestations
headache
irritability
fever
neck stiffness
pathologic reflexes: kernig’s,
Babinski, Brudzinski
Diagnostics:
Lumbar puncture
Gram staining
Urine culture
Supportive/Symptomatic:
a. Antipyretic
b. treat signs of increased ICP
c. Control of seizures
d. adequate nutrition
Poliomyelitis/Infantile Paralysis/
Heine Medin Disease
- acute infectious disease characterized by
changes in the CNS which may result in
pathologic reflexes, muscle spasm and paralysis
- it is a disease of the lower neurons, and there is
anterior horn involvement
CA: Filterable Virus ( Legio Debilitans)
3 Strains:
Legio Brumhilde
Legio Lansing
Legio Leon ( rare)
MOT: The virus is transmitted from person to person
by:
1. indirectly through contaminated articles and
flies, contaminated water, food & utensils
2. Intimate contact w/ infected person
3. Direct contact thru nasopharyngeal secretions
Dx: 1.Pandy’s test – culture of CSF (increased CHON)
2. Stool culture throughout the disease
Tetanic spasm
Clinical manifestations
Difficulty of opening the mouth
(trismus or lockjaw)
Risus sardonicus ( sneering grin) – “ngiting
aso”
Dysphagia
Generalized muscle rigidity
Opisthotonus ( severe arching of the back)
Localized or generalized muscle spasm
Respiratory paralysis to death
S/Sx:
Neonatal tetanus - Poor sucking,
irritability, excessive crying,
grimaces, intense rigidity, and
opisthotonus
Criteria Stage I Stage II Stage III
Mgmt:
Anticonvulsant, muscle relaxants,
antibiotics, wound cleansing and
debridement
Active-DPT and tetanus toxoid
Passive-TIG and TAT, placental immunity
Tetanus
Treatment:
1. Specific :
-within 72 hours after punctured wound
received ATS,TAT or TIG espicially if no
previous immunization
- Pen G to control infection
- muscle relaxant to decrease muscle rigidity.
2. Non-specific
- oxygen inhalation
Treatment:
anti-toxin
Tetanus Anti-Toxin (TAT)
chlorpromazine
Preventive Measures
Treatment of wounds
CA:Genus Lyssavirus,
Family Rhabdoviridae
( RNA virus)
Bite/wound setting
acute viral encephalomyelitis
incubation period is 4 days up to 19 years
risk of developing rabies, face bite 60%,
upper extremities 15-40%, lower
extremities 10%
100% fatal
Pathophysiology
Bite/wound
CNS encephalitis
ANS
4 STAGES
1. prodrome - fever, headache,
paresthesia,
2. encephalitic – excessive motor activity,
hypersensitivity to bright light, loud noise,
hypersalivation, dilated pupils
3. brainstem dysfunction – dysphagia,
hydrophobia, apnea
4. death
Dx: history
virus isolation from saliva and CSF
serial serum Ab sample
Staining of brain tissue (dog) -
Negri bodies
Postexposure
Category I prophylaxis
Observe the dog for 14 days
Licking of intact skin
Category III
Abrasion, laceration on upper 1.Active
extremities, head and neck 2.Passive
Dog is killed, lost, died
Category of bites
I – intact skin (lick or scratch)
II – mucosal, non bleeding wounds,
abrasions
III – bleeding bites and above neck,
stray dogs, laceration, multiple bites
Mgmt:
- wound cleansing
- tetanus prophylaxis
- Observe and quarantine dog for maniacal s/sx
- Active- antirabies vaccine (human diploid cell
vaccine)
- 7-10 days to induce an active immune response,
with immunity x 2 years
- Passive – human rabies immunoglobulin
Management
No treatment for clinical rabies
Prophylaxis
Active vaccine (PDEV,PCEC,PVRV)
Intradermal (0,3,7,30,90)
Intramuscular (0,3,7,14,28)
(0,7,21)
Post exposure prophylaxis
Antirabies vaccine
1 ml IM
day 0, 3, 7, 14, 28
OR
0.1 ml ID
day 0 (8 sites), 7 (4 sites), 28, 91 (1 site)
OR
0.1 ml ID
day 0, 3, 7 (2 sites), 30, 90 (1 site)
Preventive Measures
Education
China
Indonesia
Thailand
Vietnam.
BIRDS FLU
Incubation period : 3-5 days
S/sx :
Symptoms in animal vary - can cause death
within few days
In human – same as in human influenza
Fever/ sorethroat/ cough/ severe cases Pneumonia.
The highly pathogenic form spreads more
rapidly through flocks of poultry. This form
may cause disease that affects multiple
internal organs and has a mortality rate that
can reach 90-100% often within 48 hours.
BIRDSFLU
Prevention & treatment
Avian influenza in human can be detected with
: STANDARD INFLUENZA TEST
Antiviral drugs – clinically effective in both
preventing and treating the disease.
oseltamavir and zanamavir
Vaccines take at least 4 months to produce
and must be prepared for each sub-type
Nursing Intervention :
Health Teaching
Wash hands with soap and warm water for at least 20
seconds before and after handling raw poultry and eggs.
Clean cutting boards and other utensils with soap and hot
water to keep raw poultry from contaminating other foods.
Respiratory Tract
Gastrointestinal Tract
Genito-urinary tract
Open lesions
1. by contact transmission:
Direct contact – immediate direct transfer of
microorganism from person to person)
Touching, biting, kissing, sexual intercourse
Respiratory tract
Gastrointestinal tract
Genito-urinary tract