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Infectios

Diseases
Infectios diseases

-An illness due to an infectious agent or toxic products which is transmitted


directly or indirectly to a person or animal or through an agency of an
intermediate animal host, vector of the inanimate environment
ESSENTIAL ELEMENTS OF CD
I. AGENTS:
-Microorganisms that is living and capable of invading and multiplying the
body of the host
a. Viruses-smallest obligate intracellular pathogens that incapable of replicating
outside the cell
b. Bacteriae-prokaryotic cells
c. Fungi-free living, eukaryotic saphrophytes
d. Parasites-any organisms that derives benefits from its biologic relationship with
another organism .
2. HOST
-Livingbody,manoranimal
-Anyorganismthatcapableofsupportingphysicalgrowthandnutritionofanother
-Oncemicroorganismisalreadypresentonthebodyandbeginstomultiplythebodyisnowinfected
-Notallorganismthrivingthebodyaredetrimental
-Someorganismharmlesslyinhabitedthehumanbodybymultitudeofbacteriaecollectivelyknownas
normalflora
-Degreeofseverityofdiseaserangesfrommildtoseveredependsonthehealthstatusofthehost
andthevirulenceoftheorganism
Types:
1. Infectedbody-agentsenteredandmultiply
2. Susceptiblehost
ENVIRONMENT

- Encompassesthewaysandmeansoftransmissionofinfectiousagenttothe
susceptiblehost arteries
- Optimumenvironment
TERMS
1. Contagious-disease that are spread directly transmitted from one person to
another. E.g. SARS
2. Infectious-are those disease not transmitted by ordinary contact but
require direct inoculation through a break in the continuity of the mucous
membrane. All contagious disease are infectious
3. Infection-an invasion of the body by pathogenic organism
Types of Infections
1.Local-limitedtospecificsite.
2.Focal-localinfectionthatorganismcanspreadto otherparts(Toothabscess).
3.Systemic-involvesthewholebody(typhoidfever)
a.recurrent-aninfectionthatrecurperiodically
b.Reinfection-secondaryinfectionwithsameorganism
c.superinfection-usuallyoccursduringantimicrobialtx foranotherinfection
d.autoinfection-infectionthatisalreadypresentand developingtoanotherpartofthebody
e.Acuteinfection-developsrapidly
f.Chronicinfection-slowly,mildlybutlonger
g.Bacteremia
h.Septicemia
i.Toxemia
j.viremia
4.Carrier-apersonwhoisharboringtheinfectiousagentbutdoesnotpresentclinicalsignsandsymptoms
5.Contact-personwhohavebeenexposedtodisease
6.Contamination-aprocessbywhichsomethingrendereduncleanorunsterile.
7.Isolation-separationofpatientwithCDfromotherpersonssothattransmissionoftosusceptible
personsisprevented
8.Reverseisolation-separationofsusceptiblepersonfromcontacttopatientswithCD
9.Quarantine-limitationofmovementofpersonwhichhavebeenexposedtoCD,foraperiodoftime
longerthanthelongestusualincubationperiodoftheCDtowhichtheyareexposed.
TypesofQuarantine
a.complete-acompletelimitationorfreedomof movementofthepersonhasbeenexposedto
CDtohaveeffectivepreventionofcontactto thosewhoarenotexposed.
b.Modified-selectivepartiallimitationoffreedom ofmovement.Ex.Exclusionofchildrenin
school.
c.surveillance-closesupervisionofcontactswithout restrictionsofmovement.
d.segregation-separationforspecialconsideration, controlorobservationofsomepartofthe
groupofpersonsfromtheothertofacilitate thecontrolofsomeCD.
10.Pathogenicity-abilitytoproducedisease
11.Virulence-therelativedamagebypathogens
Course of Infectious Process

1. Incubation period-from the entry of organism into the body until the onset of
signs and symptoms. Pathogens begins active replication.
-salmonella-6-24hrs
-Hepatitis B 50-180 days
-HIV months to years
2. Prodromal-period from non-specific signs and symptoms to the appearance
specific signs and symptoms
3. Illness/invasion/acute stage-the period from which a patient experience
maximum impact of illness. Specific signs and symptoms develop and become
evident.
4. Convalescent/defervescent-characterized by containment of infection,
progressive elimination of pathogen, repair of damage tissue and resolution of
symptoms
5. Resolution-is the total elimination of a pathogen from the body without residual
signs and symptoms.
ETIOLOGIC/INFECTIOUSAGENT:
Bacteria,virus,fungi

SUSCEPTIBLEHOST:elderly,children, RESERVOIR
chronicallyill,trauma (SOURCE):humans,animals,objects,
plants,environment

PORTALOFENTRY:mucous PORTALOFEXIT:respiratory
membrane,nonintactskin,GI, secretions,blood,stool,
GUT,respiratorytract

MODEOFSPREAD:contact,
vehicle,respiratory,vectorborne
1. ETIOLOGIC/INFECTIOUS AGENTS
-Invading microorganism capable of producing the disease
-Can be bacteria, virus, fungi, parasites
-The ability of the infectious agent to produce a disease depends on its
pathogenicity, virulence, invasiveness and specificity.
a. Bacteria-canselfreproduceandproducetoxinsthatareharmful
b. Virus-obligateintracellularparasite
c. Fungus-plantlikeorganismthatgrowsassinglecells
d. Protozoans-simplestorganismofplantkingdom
e. Rickettsiae-parasitesthatdependonlivingorganismforgrowth.
2. RESERVOIR:

-Environment in which the invading organism lives and multiplies


-can be inanimate objects, humans, and other animals that can serve as
reservoir

3. PORTAL OF EXIT FROM RESERVOIR:

-Mode of escape from reservoir


-E.g. GIT, respiratory, GUT,
4. MODE OF TRANSMISSION
-Methodinwhichtheorganismistransportedtonewhost.
1. Contacttransmission-maybedirect,indirectordroplet
-droplet-occurswhenthemucousmembraneofthehostareexposedtosecretionsofaninfested
personwhoiscoughing,sneezing,laughingortalkingusuallywithin 3feetdistance
2.Vehicle-contaminateditemslikefood,water,bodilysecretionsandfluids,inanimateobjects
3.Airborne-fineparticlesordustharboringpathogenicorganismsaresuspendedintheairforprolong
periodoftime
4.Vectorborne-biologicormechanical(carriesmicroorganismontheirbodysurface)likerats,mosquitoes,
flies,lice.Mechanicallikeinanimateobjects
5.PORTALOFENTRY
-Thispermitstheorganismstogainentranceintothehumanhost.
-Throughthehostorificeslikemouth,nose,anus,urethra.
-Usuallythisistheportalofexit.
6.SUSCEPTIBLEHOST
-Apersonwhoareatriskofinfection
-Whoseownbodydefenseonceexposedareunabletowithstandtheinvasionofpathogen
-Canbeassociatedwithnumberofpathogensenteringthebody,durationofexposure,age,sex,stateof
health,nutritionalstatus
- humanbodyhasanormaldefenseagainstinvadingagents
DEFENSE MECHANISM
First Line of defense( non specific)
- External and mechanical barriers
- Skin, mucus membrane, chemical substances(acid in the stomach),
specialized structures cilia.
- Gag and cough reflex, peristaltic contraction of GIT
- Normal flora
- Fever
- Perspiration
- Interferon, IgA
SECOND LINE DEFENSE
-If the organism gets past the first line of defense, like entering the break skin-
WBC and inflammatory response come into play
- the main function of inflammatory response is to bring phagocyticand
inflammatory cells(monocytesand neutrophils) into the site of inflammation to
destroy the invading organisms and get rid of dead tissues and dying cells
-The pathogens the can past the body’s non specific immune defenses confronts
the specific immune responses in the form of cell mediated and humoralimmunity
Cell mediated immunity
-Involves T cell (T lymphocytes)
-T cells when activated secrete
and synthesize lymphokines,
other become cytotoxicT cell,
helper T cell or suppressor T cell
HUMORAL IMMUNITY

-Antibody mediated
immunity
-Involves B lymphocyte (B
cells)
Figure14.9
CONDITION THAT WEAKENS THE PERSON’S DEFENSE

1. Poorhygiene
2. Malnutrition
3. Extremeages
4. Climate
5. Inadequatephysicalbarriers
6. Inheritedandacquiredimmunedeficiencies
7. Emotionalandphysicalstressors
8. Chronicdisease
9. Medicalandsurgicaltreatments
10. Inadequateimmunizations
HERD IMMUNITY

-Is a group of people immune to a specific disease. Measles vaccine


TERMS:
1. Incidence-number of cases of disease or infection or other events during
prescribed time period in relation to the unit population in which they occur.
2. Prevalence-number of cases of disease of infected person
3. Sporadic-occurring occasionally and irregularly with no specific pattern. Ex:
tetanus
4. Endemic-a disease that is continuously present in a community. Ex: goiter,
malaria
5. Epidemic-a condition in which the disease attack a large number of
population in a community at the same time and disease tends to spread to
other rapidly.
6. Pandemic-widespread or a worldwide epidemic
7. Morbidity rate-sick rate, the proportion of health in a community
8. Mortality rate-relates to a number of deaths to the total number of
population
9. Morbidity-condition of being diseased
10. Mortality-condition of being subject to death.
SIGNS AND SYMPTOMS OF INFECTION
FEVER:
1.intermittent-tempfluctuatesbetweenperiodsoffeverandperiodsofnormal/subnormaltemp.Ex:malaria
2.remittent-tempfluctuateswithinawiderangeoverthe24hrperiodbutremainabovenormalrange.
3.hectic-feverthatoccurseachdaywithprofoundsweatingchillsandfacialflushing.
4.relapsing-temp.iselevatedforfewdays,alternatedwith1-2daysofnormaltemp.
5.factitious-selfinducedfever
6.Drugfever-inducedbydrugsormedicine.Theonsetoffeveroccursbetween7-10daysaftermedsis
begunandtemp.returntonormal2-3daysafterthemed.Isstopped.
7.Hyperpyrexia
8.Constant-bodytempthatisconsistentlyhigh.
1. RESPIRATORY
2. GIT
3. GUT
4. Blood picture
Immunity

-Refers to the body’s specific protective response to an invading organism


TYPES OF IMMUNITY:
1. Natural-non specific, present at birth,
Does not become efficient upon the second exposure to same
organism
-skin, mucous membrane, phagocytes, natural killer cell, inflammatory
response, interferon, complement, fever
-The body’s ability to distinguish between self and non self.
PHYSICAL BARRIES

-Intactskinandmucousmembrane
-Ciliaofrespiratorytract.
CHEMICALBARRIERS:
-Gastricjuice,bodyfluids
-Interferons
WBC-bothnaturalandacquiredimmuneresponse
-Releaseschemicalmediatorshistamine,bradykininandprostaglandins
GRANULOCYTES:
-Neutrophil-phagocytic,basophilandeosinophil
AGRANULOCYTES:
-monocyte-phagocyticmacrophages
-Lymphocyte-TcellsandBcells-inhumoralandcellmediatedimmunity.
Figure14.16
II. Acquired immunity

-specific, develops upon exposure to immunization or contracting a


disease
Figure14.18
ROLES OF LYMPHOCYTES IN ACQUIRED IMMUNITY

- immunoglobulinfunctionsasantibodies,
antigenbindingproteinsthatare
presentonthesurfaceofBcelland
secretedbyplasmacells.
1.Bcells–transformedintoplasmacells.
Plasmacellsaretheoneresponsiblefor
theproductionofantibodies.
IMMUNOGLOBULIN ISOTYPES
a. IgG-most abundant, 80% of total serumIg, major roles in blood borne and
tissue infections, activates complement, crosses the placenta.
b. IgA-10-15%, found in bodily secretion like breast milk, saliva, tears, GIT and
respiratory and GUT, passes to neonate in breast milk for protection.
c.IgM-5-10%oftotalserumIg,firstimmunoglobulinproducedinprimaryimmuneresponse.ThefirstIg
synthesizedbyneonate
-Mostlyintravascularserum
-FirstIgproducedinresponsetobacterialandviralinfections
-Goodactivatorofcomplementbecauseofitssize
d. IgE-mediates hypersensitivity response like hay, wheal and flare, fever ,
asthma and anaphylactic shock
-Appears inserum
-Combats parasitic infestations

e. IgD-unknown function
-Appears inserum insmall amounts
-Possibly influences B lymphocytes function becauseit is the firstIgpresent in the
surface of Bcell
Figure14.12
T LYMPHOCYTE
-For cellular immunity
a. Helper T cells-are activated upon recognition of antigens and stimulate the rest of
the immune system
-secretes cytokine that attracts and activates B cells,cytotoxicT cells, natural killer
cells, macrophages, and other cells of the immune system.
b. CytotoxicT cells-attacks the antigens directly by altering the cell membrane and
causing cell lysisand releasing cytolyticenzymes and cytokines.
C Suppressor T cell-terminate the normal immune response
d. Memory T cells-responsible for recognizing the antigens
Figure14.10
4 MAIN TYPES OF ANTIGEN PREPARARTION
1. Toxoids-soluble exotoxinsof bacteria, such as diphtheria and tetanus, which
have been modified and rendered less toxicbyaddition of formalin or gentle
heating
2. Killed-cultured organism that are killed by heat. Usually at 60°C for 1 hr, UV,
chemicals like phenol, alcohol or formalin. Whooping cough, polio, cholera
3. Antigens isolated from infectious agents( subunits vaccines)
4. Attenuated live vaccine-these are made from strains that have lost their
virulence by growth culture. BCG, cowpox, OPV
UNIVERSAL PRECAUTION( UNIVERSAL BLOOD AND BODY FLUIDS
PRECAUTIONS)
-Are apply to those body fluids associated with blood borne pathogens namely:
HepB, HepC, HIV
- this includes blood and body fluids containing visible blood
-Blood, vaginal secretion, seminal fluid, CSF, synovial fluid, pleural fluid, pericardial
fluid, peritoneal fluid, amniotic fluid, saliva in dental procedures, body fluids
contaminated with blood, body fluids in situations where it is difficult to
differentiate among body fluids
UNIVERSAL PRECAUTIONS
1. Wear mask and protective eyewear in situations where droplets of blood or
body fluids may spray onto the membranes of the eye, mouth or nose
2. Wear gloves when in contact with blood or other body fluids containing blood
and when handling supplies and equipment or surfaces soiled with blood or
other body fluid. Change gloves after client contact.
3. Wear gowns in situations where it is likely that droplets of blood or fluids will be
sprayed.
4. Immediately and thoroughly wash hands or other skin surfaces that come in
contact with blood or other body fluids
5. To prevent needle stick injuries, deposit it into puncture resistant container
that has secure lids. Do not recap, break or bend needles after use
6. Use mouthpieces, resuscitation bags, or other ventilatory equipment when
providing resuscitation
7. Do not provide direct client care when you have open or exudativeskin lesions
STANDARD PRECAUTIONS:
- All patients regardless of diagnosis or presumed infection
- Are the primary strategy for reducing the risk of and controlling nosocomial
infections

TRANSMISSION BASED PRECAUTIONS:


- These are the precautions are instituted for patients who are known to be
suspected of being infected with a highly transmissible infection
TYPES OF TRANSMISSION BASED PRECAUTIONS
1. AIRBORNEPrecautions:
- Aredesignedtoreducetheriskofairbornetransmissionofinfectiousagents.Includesspecialairhandling
andproperventilationprocedurestopreventspreadofinfection.Measles,varicella,TB
2.Droplet-aredesignedtoreducetheriskoftransmittinginfectiousagentsthroughlargeparticlesdroplets.
Largeparticlesdonotremainintheairandgenerallytravelshortdistance3feetorless.Theyrequireuse
ofmask,inadditiontostandardprecautions.Pneumonia,diphtheria,pertussis,rubella
3.Contact-arelessenedtoreducetransmission.Requirestheuseofmask,gloves,gowns,dedicatedpatient
careequipment(BP,thermometer).GITrespiinfections,skinandwoundinfectiins,entericinfections,skin
infections-highlycontagious-diphtheria,HSV,cellulitis,pediculosis,scabies
VIRUS
-Are the smallest infectious agent (20-300 mm) containing either DNA or RNA
as the genome. The entire unit is called the virion.
-They are inert in extracellular environment
-Replicate only in a living cell
-Invade host cell that also participate in formation of additional virus particles
-Lack genes for energy production
-Depends on ribosomesand nutrients of infected cells
-Ex: AIDS
STRUCTURE:
-Entire infectious unit is known as virioncontaining nucleic acid core
surrounded by protein coat called capsid
-Capsidis composed of repeating subunits of capsomeresarranged in helical
pattern or icosahedral
-Nucleic acid together with capsidis known as nucleocapsidor naked viruslope
that surrounds the nucleocapsidwhich becomes part of virion
-Encapsulated viruses are less susceptible to drying , gastric juices and bile.
GENERAL STEPS IN VIRAL REPLICATION CYCLES
A.Attachment,PenetrationandUncoating
-Attachment-isthefirststepinviralinfectionisinteractionofaviriontoaspecificreceptorsiteonthe
surfaceofcelle.g.polioinCNS,HIVtoCD4
-Penetration,Viropexisorengulfment:virusisbeingtakenupinsidethecell
-Uncoating,ViralShedding-physicalseparationofviralnucleicacidfromtheouterstructuralcomponents
-Syntheticphase-hostcellreplicatenewviralstructuralandenzymaticproteinsandviralnucleicacids
-Assemblytoformnewvirus-newlysynthesizeviralgenomesandcapsidsassembletoformprogenyvirus
-Release-infectedcellslyseandreleasenakedviruses.
STEPS IN VIRAL PATHOGENICITY:
1. Entry and primary replication-virus must first attach to enter host cell. Virus
usually replicates at the primary site of entry
2. Viral spread and cell trophism-after primary replication the virus spread within
the host via bloodstream(viremia) or lymphatics.
3. Cell injury and clinical illness-destruction of virus infected cells in the target
tissues and physiologic alterations.
4. Recovery from infection-development of immune response.
5. Virus shedding-necessary step to maintain a viral infection into population of host.
TRANSMISSION OF VIRUSES:
1. Direct person to person contact
-droplet (chickenpox, measles, small pox
-oral-fecal route-HepA
-sexual contact-HepB, HSV type 2, AIDS
-hand to eye, hand to mouth, mouth to mouth contact (HSV type I, rhinovirus,
EBV
2. Exchange of contaminated blood HepB AIDS
3.Animaltomantransmission
-animalbites-rabies
-dropletinfectionfromrodentinfected quarters–lassafever(arenavirus,leptospirosis
-arthropodvector(arbovirus)
DIAGNOSIS OF VIRAL INFECTIONS:
1. Clinical manifestation like incubation period, rash, fever and etc
2. Viral serology-detects antibody titers in the blood, method employed includes:
complement fixation, neutralization,hemagglutination, usually a 4 fold rise in
titer is diagnostic.
3. Examination for inclusion bodies ( viral remnants in to the cell). Negribodies,
guerneribodies.
4. Detection of viral antigens, viral genetic materials
5. Tissue culture
MANAGEMENT
1.Viralinfectionsareselflimitingandrequirenospecifictreatment(symptomatictreatment)
2.Useofagentsthatinterfereswithviralreplication.
Amatadine:preventsviralpenetrationandshedding
Idoxuribicin:vidarabine,Zidovudine:inhibitsDNAorRNAsynthesis
Interferon:inhibitsviralproteinsynthesis
3.Prevention
a. Passiveimmunization:givingantibodiestohaveimmediateprotection
b. Activeimmunization:givingvaccine
1. Killed:rabies,polio,influenza
2. Attenuated:measles,chickenpox,mumps
3. Subunit:hepatitisBvaccine
TERMS:

1. Macule: flat, or flush skin lesion


2. Papule: elevated skin lesions
3. Vesicle: a tear drop on a pink base a
-fluid filled papule
4. Crust: a scab, secondary lesion caused by secretion of vesicle drying on teskin
5. Discrete lesion: lesion that are separated into the area of the skin
6. Pruritus: itchy skin lesion
7. Pustular: a vesicle that is infected or filled with pus.
Measles( hard measles rubeola,
Etiology:
1. Morbilivirus
2. Filterable virus of measles
3. paramyxovirus
Sorcesof infection:
-respiratory secretion
(nose and throat) , blood and urine
of infected person
Description :
• Itisoneofthemostcommonandmostseriousofallcommunicablechildhooddiseases.
• Useofvaccinehasreducedtheoccurrenceofmeaslesduringchildhood,asaresultmeaslesis
becomingmoreprevalentinadolescentsandadults.
MOT:
Dropletordirectcontactwithinfectedpersonsorindirectlythroughsoiledarticles.Somesaysits
airborne
PeriodofCommunicability:
• Duringtheperiodofcoryzaorcatarrhalsymptoms—9days(from4daysbeforeand5daysafter
rashappears)Prodromalstage•
Incubation Period:
• 10 days from exposure to appearance of fever about 14 days until rash appears.
(8 —20 days)

Susceptibility, resistance and Occurrence :


•All persons are susceptible. Babies born of mothers who had disease before the
baby is born are immune for one month of life. Permanent acquired immunity is
usually after attack of measles.
Clinical manifestations:
Prodromalstagelastsfor4—5dayssymptomsincludes:feverphotophobiamalaiseanorexia,
conjunctivitis,coryza,hoarseness,hackingcough
-Attheendoftheprodromalstage,KOPLIK'sSpotsappearwhichisthehallmarksignofthedisease.
•Koplik'sspotsareliketiny,bluishgrayspeckssurroundedbyaredhalo.Theyappearontheoralmucosa
oppositethemolarandoccasionallybleed.
•About5daysalterKopliksspotappears,temperaturerisessharply,spotssloughoffandslightlypruritic
rashappears.
•Thisrashstartsasfaintmaculesbehindtheearsandontheneckandcheeks.
•Thismaculesbecomespopularanderythematous
•Rapidlyspreadingovertheentireface,neck,eyelids,arms,chest,back,abdomenandthighs.
-When the rash reaches the feet ( 2- 3 days later) it begins to fade
in the same sequenced It appeared.
-leaving a brownish discoloration that disappears in 7 —10 days.

-The disease climax occurs 2 3 days after the rash appears and is
marked by a temperature (39.4 to 40.6°C severe cough,
rhinorrhea, and puffy red
-About 5 days after the rash other symptoms disappear and
communicability ends.
S/Sx:•Complications:severeinfectionmayleadtosecondarybacterialinfectionandtoautoimmune
reactionororganinvasionbythevirus,resultinginotitismedia,pneumonia,andencephalitis.
a.preeruptive-feverhighgrade(3-4day)highlycommunicable,3C'sCoryza,conjunctivitis,coughand
photophobia,Koplik'sspot
Koplik'sspotsareliketiny,bluishgrayspeckssurroundedbyaredhalo.Theyappearontheoralmucosa
Oppositethemolarandoccasionallybleed.
Samsonline--transverselineoftheinflammation alongthemarginoftheeyelid.
b.eruptive—rashes,maculopapularrashes,reddish andblotchy(painful)"morbiliformrash"
firstappearonthehairlinebehinddieears— cephalocaudaldistributionentire
bodyis completelycoveredwithrashes
Whentherashreachesthefeet(2-3days later)itbeginstofadeinthesamesequenced
Itappeared.
c.posteruptive--eventuallyrushesbecomesbrown•brannydesquamation"-Asevereformknown
as"blackmeasles"—withhemorrhagicrashes,epistaxis,melenaandmarkedtoxicitymayoccur.

Diagnosis:
•koplik—distinctclinicalfeatures
•labtestfordifferential,causesomemildmeaslesmayresemblerubella,roseolainfantum,
toxoplasmosisandetc.

•Ifnecessary,measlesvirusmaybeisolatedfromtheblood,nasopharyngealsecretionsduringthe
febrileperiod.Serumantibodieswillappearwithindaysafteronsetoftherashandreachpeak
titers2—4weekslater.
Management:
I.Bedrest
2.Reliefofsymptoms
3.Immediateisolationthroughoutcommunicableperiod
4.Vaporizersandwarmenvironmenthelpreducerespiratoryirritation.
5.Observeforcomplicationslikepneumonia
6.Explainproceedingsonproperdisposalofdischarges.
7.Teachconcurrentandterminaldisinfection
NursingCare:
I.ProtecteyesofpatientfromglareofstronglightastheyapttoBeinflamed2.properventilation
3.Spongebath
4.Increasefluidintake
5.Sunglasses
6.Outofschoolforatleast4daysaltertherashappears,
Prevention:vaccine
Complications:
severe infection may lead to secondary bacterial infection and to autoimmune
reaction or organ invasion by the virus, resulting in otitismedia, pneumonia,
encephalitis (SSPE)
GERMANMEASLES(Rubella.Rotheln,Roseola,3daymeasles)Isanacute,mildlycontagiousviral
diseasesthatproducesadistinctive3-dayrashandlymphadenopathy

Commonamongchildrenages5—9,adolescentsandyoungadult.Thediseaseisself-limitingthe
prognosisisexcellent.

Etiology:Rubellavirus—atogavirus
SourceofInfection:Contactwithblood.urine,stools.nasopharyngealsecretionsandarticlesofinfected
persons,Transplacentaltransmission,especiallyinthefirsttrimesterofpregnancy,cancauseserious
birthdefect

-Humansaretheonlyknownhost
PeriodofCommunicability:10daysbeforetherashappearsuntil5later.IncubationPeriod:14—21days
S/SX
Prognosis:deathishighestinthefirsttwoyearsoflife.Inchildren,aftertheincubationperiod,rash
appearsabruptly.Inadolescentsandadults,prodromalsymptomssuchusheadache,anorexia,malaise,
lowgradefever,coryza.lymphadenopathyandsometimesconjunctivitisappearsfirst.Suboccipilal,
postauricular,andpostcervicallymhnodeenlargementisthehallmarksign.
-Rubellarashstartsattheface
-Thismaculopapulareruptionsspreadsrapidlyoftencoveringthetrunkandextremitieswithinhours
-Forscheimer'sspotmayprecedeoraccompanytherash.Forscheimerspotsaresmall,red,petechial
maculesonthesoftpalate.
Bytheendofthesecondday,thefacialrashesbegintofade,buttherashonthetrunkmaybeconfluent
andbemistakenforscarletfever.
-Therashcontinueslo,fadedownwardorderinwhichitappeared.
-Rashgenerallydisappearsonthe3rdday(sometimes4-5)sometimeswithcoryzaandconjunctivitis.
-Therapidappearanceandrapiddisappearanceoftherubellarashdistinguishesitfromrubeola
-Rubellacanoccurwithoutarashbutthisisrare
-Others:Lowgradefever,malaise,headache,mildconjunctivitis,sorethroat,stiffnessoftheneckand
anorexia.Splenomegaly,Testicularpain
-Complicationsarerarebutwhentheydo,theyoftenappearashemorrhagicproblemsuchas
thrombocytopenia.encephalitis,sinusitisorotitismedia.Youngwomensometimesexperiencesarthritis
Clinical Mnifestation:
a. Rash
b. fever less than 100°F
c. lymphadenopathy
d. Cold like symptoms usually accompanies the disease in the form of Cough.
congestion and coryza
e. forscheimersspot
Diagnosis:
-Therubellarash,lymphadenopathyandhistoryofexposurepermitsclinicaldiagnosisvidiomlabtest.
Cellculture,blood,urine.andc/f—confirmatory
- Convalescentserumthatshowsafourfoldriseinantibodytiters,confirmsthediagnosis.
Prevention:
a.immunizationbylive—virusinjection
Management:
-Rubella rash is self-limiting and only mildly pruritic, it doesn't require topical
or systemic medications.
-Purely symptomatic, treatment consists of aspirin for fever and joint pain.
-Bed rest isn't necessary but the patient should be isolated until the rash
disappears.
Congenital Rubella
-Growth retardation and congenital heart disease. (microcephaly, congenital
cataract, deaf and mute)
Measles German Measles

Incubation period 10-21 days 14-21 days

Evolution 3-5 Days 24hrs

Fever before lesion High grade with skin Low grade before skin
rashes rashes

prodromal Long and severe Mild and short

incidence Common in children Late childhood

pathognomonic koplik,’s spot none


VARICELLA —ZOSTER (chicken pox)
Etiology:
• varicellazostervirus(airborne),samevirusthatinhislatentstage,causesherpeszoster(shingles)
common2--8yearsofageor5to9nyearsold
SourceofInfection:
-Secretionofrespiratorytract.Lesionsofskin(little).Scabsthemselvesarenotinfectious.
MOT:
• DirectcontactandindirectorairbornethroughtheairPeriodofCommunicability:
• 1daybeforelesioneruptsto6daysaftervesicleform(contagiousonthefirsteruptions).
Signsandsymptoms:
• Pruriticrash(takeabathdaily)
• Prodromal:slightfever,malaise.anorexia
.

-Within24hourstherashtypicallybeginsassmallcropsofsmall,erythematousmaculesonthe
TRUNKorscalpthatprogressestopapulesandthenclearvesiclesonanerythematousbase."dewdrop
onarosepetal"
-Thevesiclesbecomecloudyandbreakseasilythenscabsform.therashspreadstothefaceandto
theextremities.
-Newvesiclescontinuetoappearfor3-4dayssotherashcontainsacombinationofredpapules,
vesicles,andscabsinvariousstages.
-Allstagesarepresentsimultaneouslybeforeallcoveredwithscabs."celestialmap“
-Congenitalvaricellacauseshypoplasticdeformity.scarringofthelimb,retardedgrowthandCNSand
eyemanifestation.Severeprurituswiththisrashmayprovokepersistentscratching,whichcanleadto
infection.cellulitis,furuncles,impetigo.
- Rarecomplications:pneumonia,reye'ssyndrome(fulminatingencephalitis)
Incubationperiod:
-2-3weeks.commonly13to17days.
PeriodofCommunicability:
• notmorethanonedaybeforeandmorethan6daysafterappearanceofthefirstcropofvesicles.
SusceptibilityandResistanceandOccurrence:
a.Universalamongthosenotpreviouslyattacked.Conferslongimmunity.
b.Secondattacksarerare.
c.Notcommoninearlyinfancy
Prevention:
a.Caseover15yearsoldshouldbeinvestigatedtoeliminatepossibilityofsmallpox.
b.Reportingtolocalauthority
c.Isolation
d.Concurrentdisinfectionofthroatandnosedischarges
e.Exclusionfromschoolfor1weekaftereruptionfirstappearsandavoidcontactwithsusceptible.
Treatment:
• Symptomatic
• Strictisolation
• Localorsystemicantipruritic
• Coolbicarbonateofsodabaths
• Calaminelotion
• Antihistamine
• Antibioticsifbacterialinfectiondevelops
• SalicylatesarecontraindicatedbecauseoftheirlinkwithReye's
• Acycloviritmayslowvesicleformation,andcontrolsystemicspreadofinfection
• VZIgmayprovidepassiveimmunity,lessensseverityifexposed
• Liveattenuated
Diagnosis:
Clinicalsigns
Doesnotrequirelaboratory,tests
Prevention:
-Good hygiene
-Don't scratch the lesions
-Trim the linger nails or tic mittens on his hands
-Report signs of complications , severe skin burning or secondary infection

Prognosis: Excellent
SMALL POX (variola) eradicated 1981
Etiology : Poxyvirusvariola
Three major forms
1. variolamajor (classic small pox) -contagious from onset until after the last scab was
shed.
2. variolaminor -a mild form that occurred in non vaccinated people and resulted
from a less virulent strain
3. varioloid-mild variant of small pox that occurred in previously vaccinated people
who had only partial immunity.
MOT:
• directly by respiratory droplets or dried scales of virus containing lesions a
Indirectly through contaminated linens or other objects. Period of
Communicability:
Incubation Period: 10 -14 days
ClinicalManifestation:
• aftertheincubationperiod;
• abruptonsetofchills(possibleseizuresinchildren)
• highfever40C
• headache
• backache
• severemalaise
• vomiting
• prostration(severeexhaustion)
Occasionallyviolentdelirium,stupororcoma.
• 2daysafteronsetsymptomsbecomessevere
• Onthethirddaypatientbegantofeelbetter.
• Howeverthepatientsoondevelopedasorethroatandcoughaswellasirritation/LESIONSonthe
mucusmembraneofthemouth,throat,andrespiratorytract.
• Withindaysskinrushesappears
• Progressingfrommaculartopopular,vesicularandpustular
• Beginstoappearontheface,wristsandankles,spreadstotheextremitiesandofteninareasofpressure
andtightskin.
• Pustulesaslargeas1/3"(8inmindiameter)
• Duringthepustularstagepatient'stemperatureagainroseandearlysymptomsreturned.
- Byday10thepustulesbegantoruptureandeventuallydriedandformedscabs.
- Symptomssubsidedabout14daysafteronset
-Desquamationcommonlyofthescab
took1-2weekscausedintense
pruritusandcommonlypresentpermanentlydisfiguringscars
• Deathresultedfromencephaliticmanifestation,extensivebleedingfrom
:anyorallorificesorsecondary,bacterialinfections.
Diagnosis
1.Cultureofvariolavirus,fromanaspirateofvesiclesandpustules.
2.Microscopicexaminationofsmearsfromlesionscrapingsorvesicle(Guarneribodies)
3.Paul'stestkeratoconjunctivitis
Treatment:
• Hospitalizationwithstrictisolation
• Antimicrobialtherapyforcomplications
• Supportivemeasures
• Symptomatictreatmentoflesionswithantipruritic,startingduringthe pustularstage
• Painreliever
• IV, NGT feeding because pharyngeal lesions made swallowing difficult.
Complications:
• Secondaryskininfections
• Laryngitis,pleurisyandemphysema
• Keratitis.laryngealulcerationswithedema
• Encephalitisandbronchopneumonia
Prevention:Smallpoxvaccination
Chicken Pox Small pox

Evolution Centrifugal- trunk Centripetal- face down

fever Low grade High grade

Characteristic lesion Unilocular- over the body Multilocular- tight areas of the
Non communicate yellow body
scar

Paul’s test Keratoconjuctivitis fluid


dropped or instilled on the
rebbit’s eye
INFLUENZA(GRIPE, LA GRIPPE, FLU)

Etiology: virus A, B, C, myxovirus


Source of infection: discharges from mouth and nose of infected persons
Period of Communicability:
- day before their symptoms begin and remain infectious 5 days after illness
onset/ until 5th day of disease
MOT:
• directcontact,throughdropletinfectionorbyarticlesfreshlysoiledwithdischargeofnoseand
throatoinfectedperson,airborne
IncubationPeriod:
• 1-4daysor24-72hours
Clinical Manifestation:
• After the incubation period, there is a sudden onset of chills
• Temperature ranging from 38°C
• With headache, myalgiaat the back and limbs, non productive cough
• and occasionally, laryngitis. hoarseness, conjunctivitis. rhinitis and rhinorrhea.
• Usually those symptoms .subside in 3 -5 day's but cough and weakness may
persist
• Fever that persists longer than 3-5 days signals the onset of complications.
• Most common complication: pneumonia (viral / bacterial)
• It may also cause exacerbation COPD.
San Lazaro: 3 distinct type of Flu
a. Respiratory -most common
-Feverchills.coryza,cough,billertaste,anorexia,musclepain,sorethroat.painbehindtheeyeballs.
b.Intestinal-vomiting,fever,severediarrhea,abdominalpain,constipation
c.Nervous-headache,musclepainandJointpain,fever
Diagnosis:
-mistakenforotherrespiratorydisorders
• Becausesignsandsymptomsarenotpathognomonic
• IsolationoftheVirusisdone
• Noseandthroatculturesandincreaseserumantibodytitershelpconfirmthedisease
• Aftertheseobservationofclinicalsignandsymptomsisdone
• UncomplicatedcaseshowsadecreaseinWBCwithincreaseinlymphocytes.
Treatment:
• Uncomplicatedcasesistreatedwithbedrest,adequatefluidintake,aspirinoracetaminophento
relievefeverandmusclepaininchildren
• Guaifenesinorotherexpectoranttorelievenonproductivecough
• Amantadine,zanamivirreducethedurationofsignsandsymptoms.
• Incomplicatedcasesusuallypatientwithpneumonia,supportivecaresuchasfluidandelectrolyte
supplements,oxygen,assistedventilationandtreatmentofbacterialsuperinfection
SpecialConsiderations:
• Usemouthwash.increasefluidintake
• Warmbathsoruseofheatingpadtorelievemyalgia
-screen visitors to protect the patient from bacterial infection and the
visitor from influenza.
-Proper disposal of tissue
-Hand washing to prevent spreading of virus
-Watch for signs and symptoms of developing Pneumonia: crackles, fever,
coughing accompanied by purulent or bloody sputum
A -usually present in large variants. it develops into several variants.
B -found in similar epidemics
C -found in sporadic case
Common Colds (coryza)
-acute, usually afebrileinfection cause inflammation of the upper respiratory
tract.
-benign and self limiting, it can lead to secondary bacterial infection.
Etiology:
• Over a hundred virus can cause common colds
• Rhinoviruses, adenoviruses, coxsackieviruses and echoviruses
• Parainfluenzavirus, RSV, corona viruses
Source of Infection:
• Contact with contaminated objects and hand to hand transmission
MOT:
• Direct or indirect, Airborne respiratory droplets.
Period Of Communicability:
• 2 -3 days after the onset of symptoms Incubation Period:
• 1-4 days
Clinical Manifestation:
-phayrngitis, nasal congestion, rhinitis, headache, and, burning, watery eyes
• In children there maybe fever,
• chills, myalgia, arthralgia, malaise, lethargy. and hacking non-productive or
nocturnal cough.
As the cold progresses clinical features develop more fully
• After a day, symptom includes fullness with copious nasal discharges that
irritates the nose adding to discomfort.
• About 3 days after onset, major signs diminish, but the "stuffed up" feeling
often persist.
• Reinfectionwith productive cough is common
• Complications: otitismedia. pharyngitis, lower respiratory tract infection
are rare. Adult-sinusitis
Herpes zoster(shingles)
Herpes virus
Varicellazoster
• Reactivation of varicellavirus that has lain dormant in the ganglia.
MOT:
• Direct contact -droplet, airborne
• Indirect -articles soiled by discharges from vesicle and membrane of
infected persons.
Incubation Period:
• From the time of infection to the onset of illness, between 1-2 weeks.
ClinicalManifestation:
-Neuralgicpain,Malaise,Burning,Pruritus,Fever
-Clusterofskinvesiclesalongcoursesofperipheralsensorynerves(unilateralandfoundonthetrunk;thorax,
orface)appears3-4days.
• Beginswithfeverandmalaise
• Ifwithin2-4daysseveredeeppain,pruritus,andparesthesiaorhyperesthesiadevelopusuallyonthe
trunkandocassionallyonthearms,legsinadermatomaldistribution.
• Painmaybecontinuousorintermittentandusuallylastsfrom1-4weeks.
• AndUsuallyAfter2weeks,small,red,nodularskinlesionsstartseruptonthepainfulareas.
• Theselesionscommonlyspreadunilaterallyaroundthethoraxorverticallyoverthearmsorlegs.
Sometimes nodules don't appear but when they do they quickly becomes
vesicle filled with clear fluid or pus cluster of skin vesicle along the course
of peripheral sensory nerves. Appear 3-4 days.
• After 10 days, the vesicles dry and form scabs, when they rupture such
lesions often become infected and in severe cases may lead to the
enlargement of regional lymph nodes; they may even become gangrenous
-Intense pain may occur before the rush appears and after the scabs form.
-Occasionally it involves the cranial nerves especially cranial nerves 3 and 5.
• Geniculatezoster(Ramsayhuntsyndrome)/oculomotor-vesicleformationintheexternalauditory
canal,ipsilateralfacialpalsy,hearingloss,dizzinessandlostoftaste.
• Trigeminal(GasserianGanglionitis)-eyepain,andpossibly,cornealandsclera!damageandimpaired
vision.
• Rarely,oculomotorinvolvementcausesconjunctivitis,E0weakness,ptosis,andparalyticmydriasis.
Diagnosis:clinicalmanifestations,examinationofthevesiclefluidinfectedtissue,lumbarpuncture-î
ICP,îCHON
Management:
• No specific treatment
• The primary goal of supportive treatment is to relieve itching and
neuralgic pain.
• ANALGESIC -TO CONTROL PAIN
• Calamine lotion and aspirin possibly with codeine.
• Tincture of benzointo unerruptedlesion
• Antibiotics
• ldoxuridineointment cornea
Steroid -FOR PATIENT OLDER than 50 TO REDUCE THE INCIDENCE OF
POSTHERPETIC NEURALGIA (PERSISTENT PAIN ON TI1E NERVE
AFTER HEALING Triamcinolonesubcutaneous
• Acyclovir(zovirax), -prevents the spread of rashes and prevents visceral
complications. administered within 24 hours of the initial eruption of rashes
• Keep patient comfortable, maintain meticulous hygiene and prevent infection
• Avoid scratching the lesions, apply wet dressing
• If vesicle rupture apply cold compress
• Diversionalactivities.
MUMPS (infectious or epidemic parotitis)

-acute viral infection of the salivary glands particularly the parotids


-Characterized by swelling of one or both the parotid gland usually occurring
in an epidemic form.
Common among ages 5 -9
Etiology:
• filterable virus of mumps
• paramyxovirus
Source of Infection:
• secretion of the mouth and nose
MOT:
Direct contact with a person who has the disease or by contact with articles in his
immediate environment which have become freshly soiled with secretion from
the nasopharynx.
Period of Communicability:
- Theperiodofcommunicabilitybeginsbeforetheglandsareswollenandremainsforanunknown
lengthoftime,butitispresumedtolastaslongasanylocalizedglandularswellingremains
Incubation Period:
• 12-26daysusually18days.
Clinical Manifestation:
a. slightmalaisewithlowgradefever
b.headacheandlassitude
c.painbelowtheearparticularlyonmovingthejaws
d. parotid gland 70% are swollen. painful enlarged and tender in varying degrees
e. Submaxillaryand Sublingual may also he affected -which may lead to anorexia
and dysphagia
f. Complications, Meningoencephalitis, orchitis,oophoritis, pancreatitis, nephritis,
thyroiditis, myocarditis. mastitis, deafness.
Diagnosis:
• Blood examination
• Viral culture
• Viral serology
Management:
• Symptomatic
• Aspirin for fever, for pain (analgesics)
• Bed rest to prevent complications
• Advise the male to wear well-fitting support to relieve the pull of gravity on
the testes and blood vessel.
• Ice pack collar application
3 Isolation
• Diet soft bland diet.
Complication:
• Orchitis(sterility),
• Encephalitis
• Oophoritis
Prevention: MMR
SARS
Etiology :
• Corona virus can survive up to 24 hours
Source of Infection:
• Nasopharyngeal secretions
MOT :
• Respiratory droplet and direct contact with body fluid of person with
SARS.
-Oro-fecal, fomites.
Incubation Period:
• 2-7 days
Clinical Manifestation:
a. Prodromalsymptoms: sudden onset of fever, respiratory infections such as
cough, myalgia, chills, headache and body malaise.
b. Lower respiratory phase: sere do cough. shortness of breath progressing to
hypoxemia. 10-20% may require ventilation. Highly infectious stage.
c. High grade fever
d. Headache
e. Dry cough
f. Body aches
Diagnosis.
-CXR normal during the prodromalstage
-CXR may show early infiltrates progressing to a more generalized, patchy,
interstitial infiltrates. Some have areas with consolidation.
-In severe cases may show RDS
-Low white cell and platelet
-Abnormal liver function
Management:
• Quarantine, broad spectrum
• Supportive
Precautions:
a. standard precautions (hand hygiene)
b. airborne use N95 mask
c. contact (gown and gloves)

Prevention: isolation
MENINGITIS (epidemic Cerebrospinal Meningitis, cerebrospinal fever)

-acute contagious disease as a result of inflammation of meningesof the


spinal cord.
Etiology :
Haemophilusinfluenzae, EB virus, coxsackievirus
MOT
• Droplet contact or indirect Source of Infection:
• Secretions
Incubation Period:
• 2-10 days
Clinical Manifestation:

• headache
• photophobia cause is unclear
• malaise
• irritability
• chills and fever
• vomiting seizures–cortical irritability
• increase ICP –widening pulse pressure, irregular RR, headache, vomiting
and decreased LOC
• Childish pitch cry, bulging fontanels
Sign's of meningealirritation
1. nuchalrigidity –stiff neck, an early sign
a. Kernig'ssign pain in the hamstring muscle when attempting to extend the leg
when the hip is flexed.
- Theclientisplacedinsupineposition.Flextheknee,attempttoextendtheleg.Painisexperienced.
b. Brudzinski'ssign –flexionatthehipandkneeinresponsetoforwardflexionoftheneck.
- passiveflexedtheneck,spontaneousflexionofthehipsoccur.
- Diagnosis:
• Lumbar puncture increased ICP elevated WBC, CHON and decreased
glucose. Inc. lymphocytes
-Blood culture
Management:
• Drugs and antibiotics
• Provide nursing care for patient with increase ICP seizures and
hyperthermia -to9 decrease workload of the brain
• Bed rest, keep room quiet and dark
• Monitor fluid and electrolytes imbalance
• Neurologic test
• High protein, calorie, with small frequent feeding.
• Respiratory isolation
Prevention:

• Proper disposal of secretions.

Complication
• Pneumonia
• Otitismedia
• Hydrocephalus
ENCEPHALITIS (brain fever)
-acute inflammatory condition of the brain as a complication of various infectious
disease causing manifestations of cerebral dysfunction.
Classification:
a. Primary -virus attacks the brain directly e.g. japanese, stlouis.
MOT: mosquito bites (Culextarsalis, aedessollicitas), infected goat's milk
b. Secondary -occurs as a complication of communicable disease of viral origin
such as measles, mumps, chicken pox
c. Toxic as a result of the of metal poisoning such as lead and mercury.
Clinical Manifestation:
• Lethargy and alteration on the LOC
• Fever, nuchalrigidity
• Headache, convulsions
• Fever chills and vomiting
• Decorticate rigidity: extremities towards cortex
• Decerebraterigidity: hands extension
• Signs of meningealirritation Diagnosis:
• Lumbar puncture -CSF studies
• EEG
• Blood culture -positive for specific microorganism
Management:
• Similar to Meningitis
POLIOMYELITIS (infantile paralysis, (H) Geine-medinDisease)

Etiology :
• Filterable virus
• Legiodebilitans

Type I-Brunhilde
Type II-Lansing
Type III-Leon
Port of entry: Nasopharynx, feces
Incubation Period:
-7-12 days
MOT: direct contact from one person to another
Clinical Manifestation:
• Usually enters in the alimentary tract, multiplies in theoropharynxand
lower intestinal tract.
• Then spreads in the regional lymph node and blood
Manifestation follow three basic forms:
1. Inapparent(subclinical) —95%
2. Abortive( minor illness) (4 —8%) --causes slight fever, malaise, headache, sore
throat, inflamed oropharynx, and vomiting. Recovers usually after 72 hours.
3. Major polio —involves the CNS and takes two form:
a. non —paralytic —produces moderate fever, headache, vomiting, lethargy,
irritability and pain in the neck, back, arms, legs and abdomen.
b. Paralytic —usually develops within 5 —7 days up to onset of fever. Extent of
paralysis depends on the level of the spinal cord lesions.
Types of Paralysis
1. Spinal paralysis -anterior horn cells of the cord are affected; paralysis of
the upper and lower extremities andintercostalmuscle.
2. Bulbar paralysis cranial nerve nuclei affected; respiratory paralysis.
3. Bulbo-spinal paralysis -combination of spinal and bulbar paralysis. a.
Landry’s paralysis -rapid progressive flaccid paralysis starting in the legs,
abdominal and back muscles, arms and neck and the respiratory.
Diagnosis:
• Muscle testing, Lumbar puncture
• Electromyelography—determines the extent of muscle involvement.
• Stool exam
• Pandy'stest —increased CHON in the CSF
Management:
• Maintaincompletebedrestduringacuteperiod.
• Providerespiratoryventilationifrespiratoryparalysisoccurs
• Assistwithphysiotherapy
• Preventpotentialcomplication
Prevention:
• OPV
• Properdisposalofwaste
HEPATITIS
• Widespread inflammation of the liver tissue with liver cell damage due to
hepatic cell degeneration and necrosis

• Proliferation and enlargement of theKufferCells and inflammation of


the peel portal are does may cause interruption of the bile flow.
Type A Type B Type C

Infectious Serum hepa, Post transfusion,


transfusion, HCV, non A and
non B hepa

Can produce fulminant Chronic hepa, chronic


hepatitis to liver failure cirrhosis, liver
ca
Age Older children, young Young adult All age group
group adult
IP 15-45 days 50-180 days 7-50 days

MOT Fecal oral route, poor Parenteral, parenteral


hygiene contaminated sexual IV drug
PC 3 week prior and 1
Delta same with hepaB
Clinical Manifestation:
1. Pre –icteriestage
Anorexia
nausea and vomiting fever
weight loss
body malaise
RUQpain
Hepatomegaly
Splenomegaly
Lymphadenopathy
Anemia.
Decrease lifespan of RBC
2. Icteric stage
fatigue
clay colored stool
lymphadenopathy
jaundice
continued hepatomegalywith tenderness
weight loss
dark urine/ tea colored
pruritus
3. Post icteric stage
-fatigue but increased sense of well being, hepatomegaly: gradually decreasing.
-Jaundice subside and sign and symptoms subside also.
Diagnosis:
All three types
a. SGPT, SCOT, alkaline phosphatase, bilirubinall increased in preicteric
b. Leukocytes, lymphocytes, neutrophilsall decreased in preicteric
c. Prolonged PT
HepaA
a. hepaa in stool before onset
b. anti HAV (1gG) appears soon after onset of jaundice, peaks in 1 -2
months and persist indefinitely
c. anti HAV (1g M) positive in acute infection lasts 4 -8 weeks
• HepaB
a. HbsAG(surface antigen: (+)develops 4-12 weeks after infection
b. Anti HbsAg—negative 80% cases
c. Anti HBC associated with infectivity; develops 2 -26 weeks after
infection
e. HbeAg-highly infectious
f. Anti Hbe-
Prevention
A. type A •
1. handwashing
2. good personal hygiene
3. Control and screening of food handlers
4. Passive immunization
B. type B
1. screen blood donors
2. use disposable needles and syringes
3. registration of all carriers
4. passive immunization
5. active immunization
Management:
1. promote adequate nutrition -small frequent meals of high CHON,
moderate CHON, high vitamin, high calorie diet, avoid very hot very cold
foods
2. Insure rest
3. Monitor/ relieve pruritus-use moist compress, emolientlotion
4. Administer steroids as ordered
5. Isolation procedure are required
6. Provide client teaching and discharge planning with regard to:
a. importance of avoiding alcohol
b. importance of donating blood
c. recognition/reporting of signs of inadequate convalescence
d. avoidance of persons with known infection
7. drugs -liver protector (Essentiale-adult, jectofer, interferon drugs)
8. anti viral agent lamivudineonce a day for 1 year 180 pesos per tab
RABIES (hydrophobia, lyssa)
-transmitted by dog bites
-acute CNS infection caused by RNA virus Etiology :
• Rhabdovirus
Incubation Period:
• 3 -8 weeks for rabid animals
• 10 days to 10 years for man
MOT:
• saliva of infected animal, bite of dog
Clinical Manifestation:

• for rabid animals


a. Dumb form complete change in disposition animal becomes withdrawn
very affectionate and walking, to and from paralysis and copious flow of
saliva
b. furious form -vicious, agitated. then become paralyzed, emits excessive
saliva and dies.
For man,
a. invasive stage -numbness on site of bite
-malaise, headache, restlessness, fever,
Photosensitivity, apprehension
b. excitement stage -hydrophobia
spasm of laryngeal and pharyngeal muscle, which expels liquid from the mouth
then eventually even the sight, sound or thought of water will cause spasm of
muscle.
Maniacal-climbingthewallandexcessivesalivation
c.paralyticstage-laryngospasmstopped
- lastforhowmanysecondsorhours.
- Gradualflaccidparalysisthatleadstoperipheralvascularcollapse,comaanddeath.
Diagnosis:
• Fluorescent rabies antibody -examination of blood
• Specimen: blood of individual
• Brain biopsy of animal -viral inclusion "negribodies"
• 10 days observation of the animal
Management:
-provide dim and quiet non stimulating room for the patient wear gown, mask
and goggles always
-restraint me patient when needed
-stimulation of any senses by fluid must be avoided
-anti rabies vaccine
Prevention:
• immunization of animals
• keep away from stray. animals
First aid
• immediately wash with soap and water at least for 10 minutes to remove
saliva
• don't suture the wound allow blood flow
• apply sterile dressing
ACQUIRED IMMUNE DEFICIENCY SYNDROME

- In 1981 clinicians from LA, NY and SF recognized new


Immunodeficiency syndrome in homosexual men.
Initially the syndrome was called GRIDS Gay related
IDS.
- Is a retrovirus that affects the CD4 t cells and
macrophages.
CD4 cells or the helper T cells
-Serves as the master switch for the immune system

-Influence the function of nearly all other cells of the immune


system.

-Helper T cells -are activated upon recognition of antigens and


stimulate the rest of the immune system.
Etiology :
- Retrovirus
- Human Immunodeficiency virus previously
referred to as Human T lymphotropic virus type
III
- Common among homosexuals and bisexuals
Mode of transmission
-It can be transmitted from one person to another through
sexual contact, blood, perinatally.
-HIV is not transmitted through casual contact.
-HIV is not transmitted by insects or vectors.
-Sexual contact is the most frequent way that HIV is transmitted. through
unprotected sex, bloodstream or mucous membrane.
-Fellatio and Cunnulingus
-Blood, sexual contact, contaminated needles, perinatal
transmission.
-HIV is infectious even without clinical features.

Incubation Period:
-6 months to 9 years
Clinical Manifestation:
PRIMARY INFECTION
• acute mononucleosis like syndrome (fever, fatigue, sore throat
night sweats, GI problems lymphadenopathy. maculopapular
rash and headache)
-anorexia
-Dyspnea
-Fever
-enlarged lymph nodes
- chronically swollen for 3 months
LATENT STAGE
- no signs and symptoms

- drop in CD4 count

- Lympadenopathy (for 3 months)


OVERT
• CD4 count is less than 200 if without antiretroviral therapy this will lead to
death after 2 -3 years)
• HIV encephalopathy: memory loss, lack of coordination, partial paralysis,
mental deterioration
• HIV wasting syndrome, emaciation -involuntary weight loss; two stools per
day with chronic weakness and fever.
• Opportunistic infection: -once the CD4 count drops below 200 cells/ulthe
risk of developing Opportunistic infection is 33% after 1 year and 58% after
2 years.
Opportunistic infection
-involve common organism that normally do not produce infection unless
there is impaired immune function.
a. pneumocystiisCarinii-cough, fever sob. infiltrates in the xray, (tx.
Trimethoprimsulfamethoxazole)
b. cytomegalovirus
c. kaposi'ssarcoma -is a malignancy of endothelial cells that line the small
blood vessels.Maculepapules, violet skin lesions and becomes darker.
d. tuberculosis -leading cause of death for people with HIV
e. candidiasis
Diagnosis:
1. ELISA test (enzyme linked immunosorbent assay) -
screening test, inexpensive
2. Western Blot - confirmatory test, more sensitive
3. Blood exam - CD4 and T cell are decrease
Management:
• Provide frequent rest periods
• Provide skin care.
• Provide high caloric, high protein to prevent weight loss
• Provide good oral hygiene
• Provide oxygen and maintain pulmonary function
• Provide measures to reduce pain
• Protect the client from secondary infection; carefully assess for early
signs
• Encourage verbalization of feelings
Teach client the importance of:
a. informing sexual contacts of diagnosis
b. not sharing needles with other individuals
c. continuing medical supervision
• zidovudine. Ritonavir-delays the HIV natural progression
• Nucleoside transcriptase Inhibitorszidovudine, Abacavir
NON NRTI ( Nevirapine) Protease inhibitors ( Saquinavir)
• Combination
• AlDSVAXPrevention
• Condoms
• Abstinence
Dengue Hemorrhagic Fever (breakbone or dandy)

-acute infectious disease characterized by severe pain behind the eyes,


joints and bones, accompanied by initialerythemaand terminal rash of
varying morphology.
Etiology :
• Dengue virus type 1,2,3,4
• Chikungunya
• Onyongyang virus
West vile
• flavivirus
Mode of Transmission

• Mosquito bites of the following:


a. AedesAegypti-biological transmitter
b. Aedesalbopticus-
c. Culexfatigans-mechanical transmitter
Clinical Manifestation:

-Grade I -last for 3 to 5 days


1. anorexia
2. abdominal pain
3. bone and joint pain
4. petechiae
5. Herman's Sign (generalized flushing of the skin) pain behind the eyes
6. Nausea and vomiting
7. Headache
Grade II
-grade I plus spontaneous bleeding melena
hematochezia
epistaxis
hematemesis
Grade III
-grade II plus circulatory failure hypotension
cold clammy perspiration
restlessness
rapid, weak pulse

Grade IV -gradeplus hypovolemicshock


Complications
Dengue Fever
a. Epistaxis, menorrhagia
b. Gastrointestinal bleeding
c. Concomitant gastrointestinal disorder (peptic ulcer)
2. D F
a Metabolic acidosis
b. Hyperkalemia
c. Tissue anoxia
D. Hemorrhage into the CNS or adrenal glands
e. Uterine bleeding may occur
f. Myocarditis
Severe manifestations

-Dengue encephalopathy is manifested by increasing restlessness,


apprehension or anxiety, disturbedsensorium, convulsions, spasticity, and
hyporeflexia.,
Diagnostic Tests
1. Tourniquet test –screening test, done by occluding the arm veins for about
five minutes to detect capillary fragility
2. Platelet count (decreased) –confirmatory test
3. Hemoconcentration
4. Occult blood
Hemoglobin determination
Management: There is no effective antiviral therapy for dengue fever.
Treatment is entirely symptomatic.
1. Analgesic drugs other than aspirin maybe required for relief of headache,
ocular pain; and myalgia. '
2. Initial phase may require intravenous infusion to prevent dehydration and
replacement of plasma.
3. Blood transfusion is indicated in patient with severe bleeding.
4. Oxygen therapy is indicated to all patients in shock.
5. Sedatives maybe needed to allay anxiety and apprehension.
Nursing Management
1. Patient should be kept in mosquito-free
environment to avoid further transmission of infection.
2. Keep patient at rest during bleeding episodes.
3.Vital signs must be promptly monitored.
4.For nose bleeding, maintain patients position in elevated trunk, apply ice bag to
the bridge of nose arid to the forehead.
5.Observesignsofshock,suchasslowpulse,coldclammyskin,prostration,andfallofbloodpressure.
6.RestorebloodvolumebyputtingthepatientinTrendelenbergpositiontoprovidegreaterbloodvolume
totheheadpart.
Prevention and Control
1. Early detection and treatment of case will not worse the victim's condition.
2.Treat mosquito nets with insecticides.
3.House spraying is advised.
4.Eliminate vector by:
a. changing water and scrubbing sides of lower vases once a week,
b. destroying the breeding places of mosquitoes cleaning the surroundings, and
c. keeping the water containers covered.
5. Avoid too many hanging clothes inside the house.
BIRD’S FLU
- Caused by bird’s flu virus
- Avian influenza( in influenza virus)
- Exist worldwide

ETIOLOGIC agent
-Avian influenza virus
Mode of Transmission
- Spreads through air and in humans
- Contaminated feeds, water, equipment, and clothing
- Cats are also thought to be possible infection vectors for H5N1 strains
of Avian virus
- Avian influenza spreads rapidly among birds and no confirmed evidence
of human to human transmission
- There are 15 subtypes known, subtypes. H5 and H7 are known to be
capable of crossing the species barriers
Incubation period
-3-5 days
Signs and symptoms
1. In animals may vary, but for virulent strains can
cause death within few days
2. In humans
- fever, sore throat, cough, and in severe cases
pneumonia
Prevention and Treatment

- Can be detected reliably through standard influenza test


- Antiviral drugs are effective for both preventing and
treating the disease
- Vaccines will take at least 4 months to produce and must be
prepared for each subtype
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