SlideShare une entreprise Scribd logo
1  sur  136
INFECTIONS
Chain of Infection
Susceptible host
Portal of Entry
Etiologic Agent (microorganism)
Reservoir
Method of transmission from reservoir to
  (Source) susceptible host
Portal of exit
Pathogens
• Bacteria
    – Aerobic
    – Anaerobic
• Viruses
    - intracellular parasite capable of reproducing outside of a living cell.
• Mycoplasma
    – similar to bacteria and have no cell wall
    – resistant to antibiotics that inhibit cell wall synthesis
• Rickettsiae & Chlamydia
    - rigid cell wall; with some feature of both bacteria and viruses.
     – Chlamydia- transmitted by direct contact
    – Rickettsiae- infect cells of arthropods and are transmitted by these vectors.
• Fungi
    - self-limited, affecting the skin and subcutaneous tissue.
• Parasites
Reservoir

  -where the pathogen lives and multiplies
      – Endogenous
      – Exogenous
• Mode of Transmission
      – Direct contact
      – Indirect contact
• Vector
      – Droplet or airborne transmission
Host Factors
• Factors that enable a host to resist infections:
  • Physical barriers
  • Hostile environment created by stomach acid
  secretions, urine & vaginal secretions.
  • Antimicrobial factors e.g. saliva, tears
  • Respiratory defenses
  • Specific and nonspecific immune responses to
  pathogenic invasion.
  • Age
  • Nutrition
Portal of Entry
• Respiratory Tract
• GI Tract
• Genitourinary Tract
• Skin and mucous membrane
• Bloodstream
Stages of Infectious Process
• Incubation period
       – period begins with active replication but with no symptoms
• Prodromal stage
      – Symptoms first appear
• Acute phase
      – proliferation and dissemination of pathogens
• Convalescent stage
      - containment of infection and pathogens are eliminated
• Resolution
      – total elimination of pathogens without residual manifestation

Nosocomial infection
– Infection acquired in a health care setting.
– Typically manifest after 48 hrs.
– UTI most common type
FACTORS AFFECTING RISK
              OF INFECTION
•   AGE
•   HEREDITY
•   LEVEL OF STRESS
•   NUTRITIONAL STATUS
•   CURRENT MEDICAL THERAPY
•   PRE-EXISTING DISEASE
•   IMMUNIZATION STATUS
Standard precautions
•   Blood
•   All body fluids, secretions, excretions,
•   Non-intact skin
•   Mucous membranes

• Essential elements:
  • Use barrier protection
  • Prevent inadvertent percutaneous exposure,
  dispose of needles
  • Immediate and thorough hand washing
Infection Control and Prevention
Infection Control in In-Patient Health
               Care Agencies
•   Hand Hygiene
•   Patient Placement
•   Protective Equipment
•   Proper disposal of Soiled Equipment
Infection Control In Community –
               Based Setting
•   Sanitation
•   Proper Disposal of Waste
•   Food Preparation
•   Report CD Occurrence
Pharmacology
• Check for:
      – History of hypersensitivity.
      – Age and childbearing status of the client.
      – Renal function
      – Hepatic function
      – Site of infection
• Classification of antimicrobial preparations:
      – Bacteriostatic
      – Bactericidal
COMMUNICABLE DISEASE

 – Is any disease that can be transmitted directly or
   indirectly from one person to another
INFECTION
 – Is a condition caused by the entry and
   multiplication of pathogenic microorganisms
   within the host body.
 – It is also an invasion of an organisms
   (bacteria, helminths, fungi, parasite, ricketsia and
   prion)
ISOLATION

– It is necessary when a person is known or
  suspected to be infected with pathogens that can
  be transmitted by direct or indirect contact.
– The principle behind isolation technique is to
  create a physical barrier that prevents the transfer
  of infectious agents. To do this you have to know
  how the organisms are transmitted.
Transmission-Based Precautions

  –Airborne
  –Droplets
  –Contact
AIRBORNE

– PRIVATE ROOM
– NEGATIVE AIR PRESSURE
– VENTILATION SAFEGUARDS air from room is not
  recirculated to other areas
– DOOR SHOULD BE KEPT CLOSED
– BARRIER TO SMALL PARTICLES masks HEPA high
  efficiency particulate air
– COVER MOUTH OF PATIENT WITH MASK DURING
  TRANSPORT
DROPLET
•
    – PRIVATE ROOM
    – WEAR MASK IF WORKING WITHIN 3 FEET
    – WEAR MASKS UPON ENTRY INTO THE ROOM
    – COVER MOUTH OF PATIENT WITH MASK DURING
      TRANSPORT
CONTACT
– PRIVATE ROOM
– WEAR GLOVES
– GLOVES ARE REMOVED BEFORE EXITING FROM
  THE ROOM
– HANDS ARE WASHED THOROUGHLY
– NOTHING IS TOUCHED BEFORE EXITING THE
  ROOM
– GOWN IS WORN WHEN ENTERING THE ROOM
– REMOVE GOWN CAUTIOUSLY BEFORE LEAVING
  THE ROOM
– PATIENT CARE ITEMS SHOULD BE RESTRICTED TO
  SINGLE PATIENT
AFB ISOLATION
 – VISITORS REPORT TO NURSES’ STATION BEFORE
   ENTERING ROOM
   • MASKS ARE TO BE WORN IN THE PATIENT’S ROOM
   • GOWNS ARE INDICATED TO PREVENT CLOTHING
     CONTAMINATION
   • GLOVES ARE INDICATED FOR BODY FLUIDS AND NON-
     INTACTSKIN
   • HANDWASHING-after touching the patient or
     potentially contaminated articles and after removing
     gloves
   • articles should be discarded, cleaned or sent for
     decontamination and reprocessing
   • room is to remain closed
   • patient is to wear mask during transport
STRICT ISOLATION
– VISITORS-REPORT TO NURSES’ STATION BEFORE
  ENTERING ROOM
– PRIVATE ROOM-necessary, door must be kept closed
– GOWNS-must be worn by all persons entering the
  room
– MASKS- must be worn by all persons entering the
  room
– HANDS-must be washed on entering and leaving room
– GLOVES-must be worn by all persons entering the
  room
– ARTICLES-must be discarded, or wrapped before being
  sent to CENTRAL SUPPLY for disinfection or
  sterilization
RESPIRATORY ISOLATION
 – VISITORS-REPORT TO NURSES’ STATION BEFORE
   ENTERING ROOM
 – PRIVATE ROOM-necessary, door must be kept closed
 – GOWNS-gowns not necessary
 – MASKS- must be worn by all persons entering the
   room if susceptible disease
 – HANDS-must be washed on entering and leaving room
 – GLOVES-not necessary
 – ARTICLES-those contaminated with secretions must be
   disinfected
 – CAUTION-all persons susceptible to the specific
   disease should be excluded from the
   area, susceptibles must wear masks
WOUND AND SKIN PRECAUTIONS
– VISITORS-REPORT TO NURSES’ STATION BEFORE
  ENTERING ROOM
– PRIVATE ROOM-desirable
– GOWNS-must be worn by all persons having direct
  contact with the patient
– MASKS- during dressing changes
– HANDS-must be washed on entering and leaving
  room
– GLOVES-must be worn by all persons having direct
  contact with infected area
– ARTICLES-instruments, dressing, linens
ENTERIC PRECAUTIONS
– VISITORS-REPORT TO NURSES’ STATION BEFORE
  ENTERING ROOM
– PRIVATE ROOM-necessary FOR CHILDREN ONLY
– GOWNS- must be worn by all persons having direct
  contact with the patient
– MASKS- not necessary
– HANDS-must be washed on entering and leaving room
– GLOVES-must be worn by all persons having direct
  contact with patient or articles contaminated with
  fecal material
– ARTICLES-special precautions necessary for articles
  contaminated with urine and feces, must be
  disinfected or discarded
PROTECTIVE ISOLATION
– VISITORS-REPORT TO NURSES’ STATION BEFORE
  ENTERING ROOM
– PRIVATE ROOM-necessary, door must be kept
  closed
– GOWNS- must be worn by all persons entering
  room
– MASKS- - must be worn by all persons entering
  room
– HANDS-must be washed on entering and leaving
  room
– GLOVES-must be worn by all persons having direct
  contact with patient
Airborne Diseases
Diphtheria

– Corynebacterium diphtheriae
– Klebsloeffler’s bacillus (bacteria)
– MOT = droplets and airborne
   • HIGHLY CONTAGIOUS
– IP 2-5 days
– IMMUNITY
   • Active = DPT
   • Passive = DAT
   • Natural = xxx
– Dx = throat swab, MOLONEY, SCHICK
– Pseudomembrane, Bullneck
– Penicillin or erythromycin
– Resp Acidosis with hypoxemia
– Cx: myocarditis, septicemia
Nursing Considerations:

– OBSERVE CNS, CARDIAC AND KIDNEY COMPLICATIONS
– PSEUDOMEMBRANOUS MAY LEAD TO RESP.
  OBSTRUCTION
– ISOLATION UNTIL 2 NEGATIVE CULTURE AT 24 HOUR
  INTERVAL
– F&E RESUSCITATION
– PARENTS OR SIBLINGS WHO HAVE NEVER IMMUNIZED
  SHOULD RECEIVE A DOSE OF DIPH. ANTI-TOXIN
– ATTENTION TO NASOPHARYNGEAL DISCHARGE
– ANTIBIOTICS-PENICILLIN, ERYTHROMYCIN IF ALLERGIC
  TO PENICILLIN
Diphtheria KEY POINTS!

– Highly contagious
– Pseudomembrane and bullneck
– Immunization best intervention PREVENTION
– Obstruction and myocarditis
– Isolation technique
Measles, Rubeola, 7 Day Fever, Hard
           Red Measle

– Paramyxo virus
– MOT = droplets and airborne
   • PC 4 days before and 5 days after rash
   • HIGHLY CONTAGIOUS
– IP 7-14 days
– IMMUNITY
   • Active = measles vaccine, MMR
   • Passive = measles Ig
   • Natural = lifetime
– Rashes:
– Maculopapular
– Cephalocaudal
– With desquamation
– Pruritus
• Rashes: maculopapaular, cephalocaudal (hairline and
  behind the ears to trunk and
  limbs), confluent, desquamation, pruritus
– PS koplik’s spot
– Characteristic: stimsons, photophobia (typical
  complaint)
– Fever: high fever
– CX pneumonia, meningitis
German Measles, Rubella, Rotheln
    Disease, 3 Day Measles
– RNA rubella virus
– MOT = droplets and airborne
   • PC 5 days before and 5 days after rash
   • HIGHLY CONTAGIOUS
– IP = 10-21 days
– IMMUNITY
   • Active = MMR
   • Passive = rubella Ig
   • Natural = lifetime
– Rashes:
– Maculopapular
– Diffuse
– No desquamation
– Rashes: Maculopapular, Diffuse/not confluent, No
      desquamation, spreads from the face downwards
•
Chicken Pox, Varicella

– Herpes Zoster Virus
– Varicella Zoster Virus
– MOT = droplets and airborne
   • PC one day before rash and 6 days after first crop of vesicles
   • HIGHLY CONTAGIOUS
– IP 14-21 days
– IMMUNITY
   • Active = varicella vaccine
   • Passive = xxx
   • Natural = lifetime
– Rashes: Maculopapulovesicular (covered areas),
  Centrifugal, starts on face and trunk and spreads
  to entire body
– Leaves a pitted scar (pockmark)
– Dx = Tzanck smear (scraping of ulcer for staining)
– Rashes:
   • Maculopapulovesicular (covered areas)
   • Centrifugal
   • Leaves a pitted scar (pockmark)
– CX furunculosis, erysipelas, meningoencephalitis
– Dormant: remain at the dorsal root ganglion and
  may recur as shingles
Meningitis Menigococcemia

– Neisseria meningitides (bacteria)
– MOT = droplets
– IP = 1-2 days
– IMMUNITY = xxx
– Immunocompetent are susceptible
– Petechiae (volar/palm of hands) EARLY
– Opisthotonus MENIGEAL IRRITATION
– Brudzinski MENINGEAL IRRITATION
– Kernigs MENINGEAL IRRITATION
– Increased ICP BRAIN
– Seizure BRAIN
– S/sx:
  – Meningococcemia – spiking fever, chills, arthralgia,
    petechial rash
  – Fulminant Meningococcemia (Waterhouse
    Friderichsen) – septic shock; hypotension,
    tachycardia, enlarging petecchial rash, adrenal
    insufficiency
• Meningitis – most common; nuchal rigidity,
  brudzinski, kernigs, Photophobia, confusion
– Dx: CT/ MRI, CSF analysis, CSF gram stain, CSF and
  blood culture
– Mgmt: antibiotics (Pen G, ceftriaxone), steroids,
  anticonvulsants, Rifampin for close contacts of
  meningococcemia
Amoebiasis

– Entamoeba Hystolitica –protozoan (parasite)
– MOT = 5 F’s, fecal oral route
– IP = 2-4 weeks
– IMMUNITY = xxx
– Dx microscopic stool exam or rectal secretions
– (tetra nucleated cyst and trophozoites)
– Diarrhea and constipation (non dysenteric)
– Blood streaked, diarrhea and watery mucoid, abd’l
  cramps (dysenteric)
– Extra amoebiasis-
  penile, vagina, spleen, liver, anal, lungs and
  meninges
– Metronidazole (Flagyl)
Typhoid Fever
– Salmonella typhosa (bacteria)
– MOT = same with amoebiasis (5 F’s)
– IP = 1-3 weeks
– IMMUNITY
   • Active = vaccine
   • Passive = xxx
   • Natural = lifetime immunity
Pathophysiology

– Oral ingestion
– Bloodstream
– Reticuloendothelial system (lymph node, spleen,
  liver)
– Bloodstream
– Gallbladder
– Peyer’s patches of SI
– necrosis and ulceration
– 1st week step ladder (BLOOD)
– 2nd week rose spot and fastidial
   • typhoid pyschosis (URINE & STOOL)
– 3rd week (complications) intestinal bleeding,
   • perforation, peritonitis, encephalitis,
– 4th week (lysis) decreasing S?SX
– 5th week (convalescent)
– Blood (typhi dot) 1st week after
– Stool and urine 2nd week after
– Chloramphenicol
– Rose spot (abdominal rashes)
– Step ladder fever to fastidial (peak of fever)
  typhoid psychosis
– Peyer’s patches of small intestine
– May stay in the gallbladder (hiding area)
BLOOD BORNE DISEASES
RABIES
CONTENTS:
What is rabies? (DEFINITION & ETIOLOGY)
•   Is an acute infectious disease of warm-blooded animals and
    humans characterized by an involvement of the nervous system
    resulting in death.
•   It is caused by the RABIES VIRUS, a rhabdovirus of the genus
    lyssavirus.
Rabies is a serious disease. Each year, it kills more than
50,000 people and millions of animals around the world.
Rabies is a big problem in Asia, Africa, and Central and South
America. In the United States, rabies has been reported in
every state except Hawaii. Any mammal can get rabies.
Raccoons, skunks, foxes, bats, dogs, and cats can get rabies.
Cattle and humans can also get rabies. Only mammals can get
rabies. Animals that are not mammals -- such as
birds, snakes, and fish -- do not get rabies. Rabies is caused
by a virus. An animal gets rabies from saliva, usually from a
bite of an animal that has the disease.
The Rabies Virus
RV – a neurotropic filterable virus present in the
saliva of rabid animals. It has a preferrence for          Rod-shaped
nerve tissues.                                             rabies viruses
                                                           colored for
                                          Virus – minute organism not visible
                                                           effect
                                         with ordinary light microscopy. It
                                         is parasitic in that it is entirely
                                         dependent on nutrients inside
                                         cells for its metabolic and
                                         reproductive needs. Can only be
                                         seen by use of eclectron
                                         microscopy. Consists of DNA or
                                         RNA covered with a protein
          Parts of the rabies            covering called capsid.
 A rhabdovirus
          virus of the genus lyssavirus. Neurotropic – viruses that
                                         reproduce in nerve tissue
                                         Filterable virus – virus causing
    RHABDOVIRUS: any group of rod-shaped
                                         infectious disease, the essential
                                                                     This is a
    RNA viruses with 1 important member,
                                         elements of which are so photograph of
                                                                      tiny that
    rabies virus, pathogenic to man. The
                                         they retain infectivity aftervirus under
                                                                     the
    virus has a predilection for tissue of
      RHABDO: from Greek                 passing through a filter of the
                                                                     electron
    mucus-secreting glands and the Central
      rhabdos, "rod"                     Berkefeld type.             microscope
    Nervous System. All warm-blooded
How do you get rabies? (MODE & MEDIA OF TRANSMISSION, IMMUNITY)

•All warm-blooded mammals are susceptible. Natural immunity in man is
unknown.
•You get rabies through the saliva of an infected animal by an exposure to
an open break in the skin such as bites, open wound or scratch and
inhalation of infectious aerosols such as from bats.
•In some cases, it is transmitted through organ transplants (corneal
transplant), from an infected person.
•The virus gets transmitted through saliva, tears, semen, some liquor
(amniotic fluid, CST) but not blood, urine or stool.

                          You get rabies from the saliva of a rabid animal, usually
                          from a bite. The rabies virus is spread through saliva.
                          You cannot get rabies by petting an animal. You may get
                          rabies from a scratch if the animal, such as a cat, was
                          licking its paw before it scratched you. (Remember that
                          the rabies virus is found in the saliva of an animal).
How do you know if an animal has rabies?

• Animals with rabies may act differently from
  healthy animals.
• Some signs of rabies in animals are:
       changes in an animal’s behavior
       general sickness (fever, restlessness)
       problems swallowing
       increased drooling
       aggression (biting at inanimate objects, aimless running)
•   Wild animals may move slowly or may act as if they are tame. Some wild animals
    (foxes, raccoons, skunks) that normally avoid porcupines, may even try to bite
    these prickly rodents.
•   A pet that is usually friendly may snap at you or may try to bite.
How do you know if one has rabies?
                         (DIAGNOSIS)
•There is yet no way of immediately knowing who had acquired
rabies virus. No tests are available to diagnose rabies in humans
before the onset of clinical disease.

•The most reliable test for rabies in patients who have clinical signs
of the disease is a DIRECT IMMUNOFLUORESCENT STUDY of a
full thickness biopsy of the skin taken from the back of the neck
above the hair line.

•The RAPID FLUORESCENT FOCUS INHIBITION TEST
is used to measure rabies-neutralizing antibodies in
serum. This test has the advantage of providing results
within 24 hours. Other tests of antibodies may take as
long as 14
•days.
EPIDEMIOLOGY
RABIES INCIDENCE:

WORLDWIDE:35, 000-
50, 000 cases/ year
(WHO)
EPIDEMIOLOGY
PHILIPPINES: 350-450 cases/ year
             5-7 per million population
DOG BITE INCIDENCE: 140, 000- 560, 000/ year
200-800 per 100, 000 population/ year

AGE MOST AFFECTED: 5-14 year age group
              (53% of cases)

BITING ANIMALS: (SLH STUDY 1982- 2002)

        DOGS:     98%
           PET:     88%
           STRAY:      10%
        CATS:     2%
• Based on the report from NCDPC (2004), the
  six regions with the most number of rabies
  cases are Western Visayas, Central Luzon,
  Bicol, Central Visayas, Ilocos and Cagayan
  Valley

• Data shows that 53.7 percent of animal bite
  patients are children

• Dogs remain the principal animal source of
  rabies
STAGES OF RABIES INFECTION
Rabies virus   Entry into the body
                                     INCUBATI0N PERIOD
                                     (20 – 90 days)




                                     INVASION
                                     (0 – 10 days)




                                     EXCITEMENT
                                     (2 – 7 days)



                                     PARALYTIC           COMA
                                                         (5 – 14 days)
                                                                         DEATH
RABIES CLASSIFICATION
ANIMAL RABIES
• There are two common types of rabies. One type is "furious" rabies.
  Animals with this type are hostile, may bite at objects, and have an
  increase in saliva. In the movies and in books, rabid animals foam at the
  mouth. In real life, rabid animals look like they have foam in their mouth
  because they have more saliva.
  The second and more common form is known as paralytic or "dumb" rabies.
  The dog pictured below has this type. An animal with "dumb" rabies is timid
  and shy. It often rejects food and has paralysis of the lower jaw and
  muscles.
• Another two types of rabies. One type is “urban” rabies. The type of
  rabies in domestic dogs and cats.
  The other type is called “ sylvatic” rabies. These type came from wild
  animals such as bats, weasels, skunks and moles & voles.
HUMAN RABIES
• Humans also have a “furious” type, the
  classic foaming of the mouth,
  aggression, apprehension & hydrophobia,
  and the “dumb” type, progressive
  paralysis of the body until they couldn’t
  breathe anymore.
DIFFERENT STAGES OF RABIES
                INFECTION
                      C                                         B
                      A                                         A
                      T                                         T
D                     S                                         S
O
G
S
                               VIRUS IN SALIVA           INHALED AEROSOLS



    VIRUS IN SALIVA
                                             INVASION PHASE



    INVASION PHASE


                                                     PARALY
                                                     SIS
       EXCITEMENT



                      PARALY
                      SIS

          DEATH                                     DEATH
INVASION STAGE
•   Also called PRODOME PERIOD; Prodrome – symptom indicative of an
    approaching disease
•    2-10 DAYS
•   Sensory changes on the site of entry.
    Pain: dull, constant pain referable to the nervous pathways proximal to
    the location of the wound or itching, intermittent, stabbing pains
    radiating distally to the region of inoculation. In general, sensitivity is
    the early symptom which may be ascribed to the stimulative action of
    the virus affecting groups of neurons, esp. sensory system. Though
    there is apt to be decreased sensitivity to local pain e.g. needle
    introduction, patient may complain bitterly of drafts & bed clothes
    which produce a general stimulation



                                                                              Tick me!
• Fever,headache malaise sore throat
  anorexia increased sensitivity (bright
  lights, loud noises) increased muscle
  reflex irritability, tics and muscle tone
• Overactive facial expression
EXCITATION STAGE
•   Also called ACUTE NEUROLOGICAL PHASE;
    hyperactivity
•   2 – 10 DAYS
•   Imminent thoraco-lumbar involvement (SNS):
    pupillary dilation, lacrimation increased thick
    saliva production / foaming of mouth, excessive
    perspiration, increased HR
•   Anxiety: increased
    nervousness, insomnia, apprehension; a strong
    desire to be up, wandering aimlessly about, and
    Fear: a sense of impending doom
•   Hydrophobia (perhaps, SNS stimulation:
    depresses GI activity > inhibits
    esophageal, gastric & intestinal function) >
    violent expulsion of fluids, drooling (in attempt
    not to swallow) > dehydration and parched mouth
    & tongue
•   Pronounced muscular stimulation & general
    tremor
•   Mania (tearing of clothes & bedding, cases of
    biting & fighting rare but may occur) and
    Hallucinations with lucid intervals (normal mental
    function in which patient is well-oriented &
    answers questions intelligently)
•   Convulsions( besides r/t pronounced muscular
    stimulation, further precipitated by sensory
    stimuli – sight, sound, name of water > throat
    spasms > choking > apnea, cyanois, gasping
                                                             Sympathetic nervous system
•   > death, but if patient survive excitement phase…
                                                   Tick me   Parasympathetic nervous system
                             Tick me 1st!          next!
Tick me!
PARALYTIC STAGE
-also called DEPRESSION PHASE
• Gradual weakness of muscle groups
    – muscle spasms cease
    – OCULAR PALSY – strabismus, ocular
      incoordination, nystagmus, diplopia, central
      type partial blindness > responds poorly to
      light, @ times pupil is constricted or unequal
      (parasympathetic involvement)
    – Oro-facial: FACIAL & MASSETER PALSY >
      difficulty closing eyes & mouth, face
      expressionless
    – Oral: Weakness of muscles of phonation >
      hoarsness & loss of voice
• Loss of tendon reflexes, always precedes
   weakness of extremity
• Corneal reflex decreased or absent, dry
• Ears: VERTIGO . Middle ear disease . Early
  symptom, but may develop @ any period
• Neck stiffness
• (+) Babinski [lesions of pyramidal tract], ( - )
  Kernig’s ( - ) Brudzinski’s
• Cardiac: shifts from tachycardia (100 –
  120bpm) @ bed rest to bradycardia (40 -60
  bpm)
• Respi: Cheyne-Stokes > breathing pattern
  characterized by a periodic 10 – 6- sec of apnea
  followed by gradual increasing depth and
  frequency of respiration
• Local sensation (pin prick, heat, cold)
  diminished
• Incoordination
• Hydrophobia and aerophobia gone, but still has
  some difficulty swallowing
• General arousal (PNS stimulation)
• Bladder & intestinal retention and obstipation
  (damage to to innervation of the musculature of
  intestine & bladder)(SNS damage)
  in some cases, patient shows period of recovery, this
  apparent remission is followed by progressive
• Ascending, flaccid paralysis of extremities until
  it reaches the respiratory muscle
• Apathy, stupor
• Complications: Pneumothorax, thrombosis,
  secondary infections
MANAGEMENT
NURSING INTERVENTIONS
• HIGH RISK FOR INFECTION TRANSMISSION
          » provide patient isolation
          » handwashing. Wash hands before and
            after each patient contact and following
            procedures that offer contamination risk
            while caring for an individual patient.
            Handwashing technique is important in
            reducing transient flora on outer
            epidermal layers of skin.
          » Wear gloves when handling fluids and
            other potential contaminated articles.
            Dispose of every after patient care.
            Gloves provide effective barrier
            protection. Contaminated gloves becomes
            a potential vehicle for the transfer of
            organisms.
• KNOWLEDGE DEFICIT (about the disease,
  cause of infection and preventive measures)
           »assess patient’s and family’s level
             of knowledge on the disease
             including concepts, beliefs and
             known treatment.
           »Provide pertinent data about the
             disease:
           »organism and route of transmission
           »treatment goals and process
           »community resources if necessary
           »allow opportunities for questions
             and discussions
• ALTERED BODY TEMPERATURE:
  FEVER RELATED TO THE PRESENCE
  OF INFECTION. Since fever is
  continuous, provide other modes to
  reduce discomfort.
          »If patient is still well oriented,
           Inform the relation of fever to
           the disease process. The
           presence of virus in the body …
          »Monitor temperature at
           regular intervals
          »Provide a well ventilated
           environment free from drafts
           and wind.
• DEHYDRATION related to refusal to take in
  fluids secondary to throat spasms and fear of
  spasmodic attacks.
           »Assess level of dehydration of
             patient.
           »Maintain other routes of fluid
             introduction as prescribed by the
             physician e.g. parenteral routes
           »Moisten parched mouth with cotton
             or gauze dipped in water but not
             dripping.
IMMUNIZATION
 ACTIVE IMMUNIZATION
- induce antibody and T-cell production in order
  to neutralize the rabies virus in the body. It
  induces an active immune response in 7-10
  days after vaccination, which may persist for
  one year or more provided primary
  immunization is completed.
TYPES:
 a. PVRV (Purified Vero Cell Rabies Vaccine)
 b. PCEVC (Purified Chick Embryo Cell Vaccine)
PASSIVE IMMUNIZATION
- RIG (Rabies Immune Globulins)
- provide the immediate availability of antibodies
   at the site of exposure before it is physiologically
   possible for the pt.to begin producing his own
   antibodies after vaccination.
- Important for pts. w/ Cat III exposures
Types:
 a. HRIG (Human Rabies Immune Globulins)
 b. Highly Purified Antibody Antigen Binding
     fragments
 c. ERIG (Equine Rabies Immune Globulins)
VACCINATION
        (Intradermal Schedule)
   Day of      PVRV/PCECV             Site
Immunization
   DAY 0          0.1 ml    L & R deltoids/
                            anterolateral thighs of
                            infants
   DAY 3          0.1 ml    L & R deltoids/
                            anterolateral thighs of
                            infants
   DAY 7          0.1 ml    L & R deltoids /
                            anterolateral thighs of
                            infants
  DAY 28/30       0.1 ml    L & R deltoids/
                            anterolateral thighs of
                            infants
Intramuscular Schedule

Day of         PVRV     PCECV    Site
Immunization

Day 0          0.5 ml   1.0 ml   One deltoid/
                                 anterolateral
                                 thigh of infants
Day 3          0.5 ml   1.0 ml   Same

Day 7          0.5 ml   1.0 ml   Same

Day 14         0.5 ml   1.0 ml   Same

Day 28         0.5 ml   1.0 ml   same
MANAGEMENT OF RABIES PATIENT
• Once symptoms start, treatment should center
  on comfort care, using sedation & avoidance of
  intubation & life support measures once
  diagnosis is certain

1.   MEDICATIONS
a.   Diazepam
b.   Midazolam
c.   Haloperidol + Dipenhydramine
2. SUPPORTIVE CARE
- Pts w/ confirmed rabies should receive adequate
   sedation & comfort care in an appropriate
   medical facility.
 a. Once rabies diagnosis has been confirmed,
     invasive procedures must be avoided
 b. Provide suitable emotional and physical
     support
 c. Discuss & provide important info. to relatives
     concerning transmission of dse. & indication for
     PET of contacts
 d. Honest gentle communication concerning
     prognosis should be provided to relatives of pt
3. INFECTION CONTROL
 a. Patient should be admitted in a quiet, draft-
     free, isolation room
 b. HLCR workers & relatives in contact w/ pt
     should wear proper personal protective
     equipment (gown, gloves, mask, goggles)

4. DISPOSAL OF DEAD BODIES
Tetanus
• Tetanus
  – Clostridium tetani
  – MOT = wound setting
  – IP = 3 -21 days
  – IMMUNITY
     • Active = TT
     • Passive = TAT and TIG
     • Natural = active none, passive (+)
– Wound Infection
– FATAL INFECTION OF THE CNS
– TOXIN-NEUROTOXIN
• PATHOPHYSIOLOGY:
  – SETTING OF WOUND ---- ENTRANCE OF C.T. ----
    RELEASES TETANUS TOXIN ---- TETANOSPASMIN
    (CNS), TETANOLYSIN (BLOOD) ---- ABSORBED BY
    MOTOR NERVE ENDINGS ---- SYNAPSE
    (CONNECTION BETWEEN NEURONS) ----
    MYONEURAL JUNCTION ---- ACETYLCHOLINE
    DISTURBANCE IN THE TRANSMISSION OF NERVE
    IMPULSE
– Trismus – lock jaw
– Risus sardonicus - maskface
– Risorius - grinsmile
– Dx wound and blood extraction (non specific)
• Immunization
  – DPT (0.5 ml IM) 1 – 1 ½ months old 2 - after 4
    weeks 3 – after 4 weeks
  – 1 st booster – 18 mos
  – 2 nd booster – 4-6 yo
  – subsequent booster – every 10 yrs thereafter
  – TT (0.5 ml IM) TT1 - 6 months within preg TT2 -
    one month after TT1 TT3 to TT5 - every
    succeeding preg or every year
  – TAT (horse) and TIG (human)
• Management
  – 1. Anticonvulsant, muscle relaxants,
  – antibiotics, wound cleansing and debridement,
    hyperbaric chamber
  – 2. Active-DPT and tetanus toxoid
  – 3. Passive-TIG and TAT, placental immunity
VECTOR-BORNE
  DISEASES
DENGUE HEMORRHAGIC FEVER
IINTRODUCTION:

    Philippine Hemorrhagic Fever was first reported in 1953. In
    1958, hemorrhagic became a notifiable disease in the
    country and was later reclassified as Dengue Hemorrhagic
    Fever.


What is Dengue
Hemorrhagic Fever?

         • A severe mosquito transmitted viral illness endemic
         in the tropics.

          • It is characterized by increased vascular
          permeability, hypovolemia and abnormal blood
          clotting mechanisms.
WHO case definition for DHF:
• fever or history of recent fever
• thrombocytopenia (platelet count equal to or less than 100 x 10 /
cu mm)
• hemorrhagic manifestations such as petechiae or overt bleeding
phenomena, and
• evidence of plasma leakage due to increase vascular permeability



Infectious Agent / Etiologic Agent:


                      Flaviviruses; Dengue Virus Types 1, 2, 3, and 4
Occurrence:


     Dengue occurrence is sporadic throughout the year.
     Epidemic usually occurs during the rainy seasons June
     – November.
     Peak months are September and October.
     DHF are observed most exclusively among children of
     the indigenous population under 15 years of age.
     Occurrence is greatest in the areas of high Aedis
     Aegypti prevalence.
Notifiable Diseases and Deaths by Cause in
             the Philippines (2001 – 2004)


                     2001               2002                   2003                 2004
Notifiable
 Diseases       Reported           Reported               Reported             Reported

             Cases     Deaths   Cases      Deaths      Cases      Deaths   Cases       Deaths

 Dengue
  Fever      23,235             13,187                18,039               15,838




                                                    Source: National Statistics Office
INCIDENCE OF DENGUE HEMORRHAGIC FEVER IN
           CEBU CITY (YEAR 2007)


  Selected     Number of New Cases           Number of Deaths         Year
Communicable

  Disease:      total    male   female     total   male   female




Dengue / DHF   43, 350    …          …     416      …        …        2007




                                     Source: Department of Health Region VII
• The DOH reported 70,204 dengue cases for
  week ending September 10, 2011. This was
  over 24,000 cases less or 25.87% lower than
  for the same period last year. In addition, the
  number of cases in July and August (the peak
  months for dengue) was 52% lower than last
  year. A total of 396 deaths were reported for
  this year, which is lower than last year’s
  number of 620.
Reservoir / Source of Infection:

           • Some source is a vector mosquito, the Aedes
           Aegypti or the common household mosquito
           • The infected person
Mode of Transmission: Mosquito bite (Aedis Aegypti)

Incubation Period:        Probably 6 days to one week


Period of                 Presumed to be on the 1st week
                          of illness – when virus is still
Communicability:
                          present in the blood

Susceptibility and         All persons are susceptible. Both
                           sexes are equally affected. The age
resistance:                groups predominantly affected are
                           the preschool age and school age.
                           Adults and infants are not
                           exempted. Peak age affected 5-9
                           years. Susceptibility is universal.
                           Acquired immunity may be
                           temporary but usually permanent.
Diagnostic Test:
   1.) Tourniquet Test (Rumpel Leads Tests)
   • Inflate the blood pressure cuff on the upper arm to
      a point midway between the systolic and diastolic
      pressure for 5 minutes
   • Release cuff and make an imaginary 2.5 cm
      square or 1 inch just below the cuff, at the
      antecubital fossa
   • Count the number of petechiae inside the box
   • A test is (+) when 2 or more petechiae per 2.5 cm
      square or 1 inch square are observed


   2.) A con firmed diagnosis is established by
      culture of the virus, polymerase-chain-reaction
      (PCR) tests, or serologic assays.
Clinical Manifestations (Public Health Nursing in
the Philippines, 2007):
An acute febrile infection of sudden onset with 3 stages:

• 1st-4th day (febrile or invasive stage)

-high fever, abdominal pain and headache; later flushing which
may be accompanied by vomiting, conjunctiva infection and
epistaxis.

• 4th-7th day (toxic or hemorrhagic stage)

-lowering of temperature, severe abdominal pain, vomiting and
frequent bleeding from gastrointestinal tract in the form of
hematemesis or melena. Unstable blood pressure, narrow pulse
pressure and shock. Death may occur. Tourniquet test which may be
positive may become negative due to low or vasomotor collapse.
• 7th-10th day (convalescent or recovery
   stage)

   -generalized flushing with intervening areas of
   blanching, appetite regained and blood
   pressure already stable.



• Dengue shock syndrome is defined as dengue
hemorrhagic fever plus:

*Weak rapid pulse,
*Narrow pulse pressure (less than 20 mm Hg) or,
*Cold, clammy skin and restlessness
Grading of Dengue Fever:

The severity of DHF is categorized into four grades:

• grade I, without overt bleeding but positive for tourniquet test

• grade II, with clinical bleeding diathesis such as petechiae, epistaxis and
hematemesis

• grade III, circulatory failure manifested by a rapid and weak pulse with
narrowing pulse pressure (20 mmHg) or hypotension, with the presence of
cold clammy skin and restlessness; and

• Grade IV, profound shock in which pulse and blood pressure are not
detectable. It is note-worthy that patients who are in threatened shock or
shock stage, also known as dengue shock syndrome, usually remain
conscious.

* Grade III and IV are considered to be Dengue Shock Syndrome
MANAGEMENT
• Promote rest
• Medication
  –Paracetamol – for
    fever and muscle
    pains.
  –Analgesic – for
    headache
  –DON’T GIVE ASPIRIN
• Rapid replacement of body
  fluids is the most important
  treatment
   – Give ORESOL to replace
     fluid as in moderate
     dehydration at 75ml/kg in
     4-6 hours or up to 2-3L in
     adults. Continue ORS
     intake until paient’s
     condition improves.
   – Intravenous fluid
• For hemorrhage
  – Keep patient at rest during
    bleeding periods
  – For epistaxis – maintain an
    elevated position of trunk
    and promote
    vasoconstriction in nasal
    mucosa membrane through
    an ice bag over the
    forehead.
  – For melena – ice bag over
    the abdomen.
• Provide support during the
  transfusion therapy
• Diet
   – Low fat, low fiber, non-
     irritating, non-carbonated
   – Noodle soup may be given
• Observe signs of
  deterioration (shock) such as
  low pulse, cold clammy
  perspiration, prostration.
PREVENTION
• Eliminate vector by:
   –Changing water and scrubbing sides
     of lower vases once a week
   –Destroy breeding places of mosquito
     by cleaning surroundings
   –Proper disposal of rubber tires,
     empty bottles and cans
   –Keep water containers covered
OTHER PRECAUTIONS:

• When outdoors in an area where
  dengue fever has been found
  –Use a mosquito repellant
  –Dress in protective clothing-long-
    sleeved shirts, long pants, socks, and
    shoes
• Keeping unscreened windows and
  doors closed
• Keeping window and door screens
  repaired
• Use of mosquito nets
MALARIA
• Malaria, King of Tropical       – P. VIVAX AND OVALE
  Disease                           MAY HAVE RECCURENCE
                                    OF SYMPTOMS
   – Protozoan plasmodium
                                    • tertian-febrile paroxysm
      • plasmodium ovale -            q24H-48H
        dormant (liver)
                                    • quartan-febrile paroxysm
      • plasmodium vivax -            q48H-72H
        benign
      • plasmodium malariae -
        mild but resistant
      • plasmodium falciparum -
        malignant (cerebral
        malaria)
– MOT
   • Bite from infected anopheles mosquito or minimus
     flavire (night biting)
   • Blood Transfusion
   • Sexual cycle
      – sporogony (mosquito)
      – gametes is the infective stage
   • Asexual cycle
      – schizogony (human)
– IP (Incubation Period) 5-6 days
– Nursing Considerations
– Dx:
   • blood extraction (extract blood at the height of fever)
– Fever, chills, profuse sweating-convulsion
– Anemia and fluid and electrolytes imbalance,
  hepatomegaly, splenomegaly, rigor, headache and
  diarrhea.
– Chloroquine and Primaquine drug of choice
– Chloroquine for pregnant women
– For resistant plasmodium-use chemo drug
– RBC is being attack
– Nursing Considerations
– IV FLUIDS AND ELECTROLYTES
– Blackwater Fever – hemolysis and hemoglobinuria
– Sickle Cell Trait – provides natural resistance
– DECREASE FLUIDS IN CEREBRAL EDEMA
– ASSISTED VENTILATION IN PULMONARY EDEMA
– DIALYSIS IN RENAL FAILURE
– BT IN ANEMIA
– TRAVELERS TO MALARIA ENDEMIC area SHOULD FOLLOW
  PREVENTIVE MEASURES- (CHEMOPROPHYLAXIS CHLOROQUINE
  MAY BE TAKEN 1 WEEK BEFORE ENTERING ENDEMIC AREA)
– SOAKING OF MOSQUITO NET IN AN INSECTICIDE SOLUTION
– BIO PONDS FOR FISH
– ON STREAM CLEARING (TO EXPOSE THE BREEDING STREAM TO
  SUNLIGHT)
– VECTORS PEAK BITING AT NIGHT 9PM-3AM
– PLANTING OF NEEM TREE (REPELLENT EFFECT)
– ZOOPROPHYLAXIS (DEVIATE MOSQUITO BITES FROM MAN TO
  ANIMALS)
– INFECTED MOTHER CAN STILL CONTINUE BREAST FEEDING
Filariasis, Elephantiasis, Human
         Lymphatic Filariasis
– CAUSATIVE AGENT-NEMATODE PARASITE
  •   MICROFILARIAE OR FILARIAL WORMS
  •   WUCHERERIA BRONCOFTI
  •   BRUGIA MALAYI
  •   BRUGIA TIMORI
– MOT
  • Bite from aedes poecilius (night biting)
  • Invade the lymph vessel, obstructing the lymphatic
    channel-leads to edema and may infiltrate the
    reproductive organs.
– IP 8-16 months
CLINICAL MANIFESTATIONS:



– ASYMPTOMATIC STAGE
   • (+) MICROFILARIAE IN THE BLOOD
– NO CLINICAL S/SX
– ACUTE STAGE
   • LYMPHADENITIS (LYMPH NODES)
   • LYMPHANGITIS (LYMPH VESSELS)
   • GENETALIA-FUNICULITIS, EPIDYDIMITIS, ORCHITIS
– CHRONIC STAGE
   • HYDROCOELE
   • LYMPHEDEMA (UPPER AND LOWER EXTREMITIES)
   • ELEPHANTIASIS
– INCIDENCE-REGION 5,8,11 AND CARAGA,
  MARINDUQUE, SARANGGANI
– Drug: Diethyl Carbamazine Citrate or Hetrazan
  6mg/KgBW one dose every year
– Dx:
   • NBE nocturnal blood exam (night)
   • ICT immunochromatographic test (day)
Nursing Considerations

– MASS TREATMENT-DOSE IS 6mg/KBW, SINGLE
  DOSE PER YEAR.
– ENVIRONMENTAL SANITATION
– PERSONAL HYGIENE
– MOSQUITO NETS
– LONG SLEEVES, LONG PANTS AND SOCKS
– INSECT REPELLENT
– SCREENING OF HOUSES
– HEALTH EDUCATION
Schistosomias, Snail Fever, Takayama


 – Blood fluke
 – Schistosoma japonicum
 – S. hematobium
 – S. mansoni
 – MOT skin entry (cercaria) travel in to the blood
   stream where they will infiltrate the liver, from
   liver to intestines
– Cycle: Egg-larvae (miracidium)-intermediary host
  (oncomelania quadrasi-tiny snail)-cercaria
– Itchiness at the site
– RUQ pain (hepatomegaly)
– Intestine infiltration-abd’l cramps, diarrhea with
  blood
– Praziquantel
– Dx COPT (stool exam)
– Egg– miracidium– snail– cercaria- human
– Itchiness – liver – intestines
– Praziquantel
– COPT
– PREVENTION
– Samar and Leyte
HIV and AIDS

– Retrovirus (HIV1 & HIV2)
– Attacks and kills CD4+ lymphocytes (T-helper)
– Capable of replicating the lymphocytes
  undetected by the immune system
– Immunity declines and opportunistic microbes
  sets in
HIGH RISK GROUP

– Homosexual or bisexual
– Intravenous drug users
– BT recipients before 1985
– Sexual contact with HIV+
– Babies of mothers who are HIV+
MOT

– Sexual intercourse (oral, vaginal and anal)
– Exposure to contaminated blood, semen, breast
  milk and other body fluids
– placenta
HIV TEST

– Elisa
– Western Blot
– Rapid hiv test
   •   Suds hiv-1
   •   Results are obtained in less than 10 minutes
   •   Color indicator similar to pregnancy test
   •   Positive result needs a confirmatory test
How to Diagnose

– HIV+ 2 consecutive positive ELISA and 1 positive
  Western Blot Test
– AIDS+ HIV+ CD4+ count below 500/ml Exhibits
  one or more of the ff: (next slide)
– Full blown AIDS CD4 is less than 200/ml
– Exhibits one or more of   –   Weight loss
  the ff:                   –   Severe diarrhea
– Extreme fatigue           –   Apathy and depression
– Intermittent fever        –   PTB
– Night sweats              –   Kaposis sarcoma
– Chills                    –   Pneumocystis carinii
– Lymphadenopathy           –   AIDS dementia
– Enlarged spleen
– Anorexia
• HIV CLASSIFICATION
  – CATEGORY 1 – CD4+ 500 OR MORE
  – CATEGORY 2 – CD4+ 200-499
  – CATEGORY 3 – CD4+ LESS THAN 200
• Management
  – Prevention of spread (safe sex)
  – Universal precautions
  – Health Education
  – Symptomatic intervention
  – No known cure
  – Prevent CD4 reduction
Communicable diseases immunologic

Contenu connexe

Tendances (20)

Isolation
Isolation  Isolation
Isolation
 
Isolation practices
Isolation practicesIsolation practices
Isolation practices
 
Infection control,
Infection control, Infection control,
Infection control,
 
Concepts of infection control
Concepts of infection controlConcepts of infection control
Concepts of infection control
 
Infection control
Infection controlInfection control
Infection control
 
New precaution manual new version june 2010
New precaution manual   new version june 2010New precaution manual   new version june 2010
New precaution manual new version june 2010
 
Infection control
Infection controlInfection control
Infection control
 
Isolation 2014
Isolation 2014Isolation 2014
Isolation 2014
 
Infection control and standard safety precautions
Infection control and standard safety precautionsInfection control and standard safety precautions
Infection control and standard safety precautions
 
Isolation precautions in clinical practice
Isolation precautions in clinical practiceIsolation precautions in clinical practice
Isolation precautions in clinical practice
 
Transmission based precaution techniques
Transmission based precaution techniquesTransmission based precaution techniques
Transmission based precaution techniques
 
Infection control sandra
Infection control sandraInfection control sandra
Infection control sandra
 
Isolation Precaution
Isolation PrecautionIsolation Precaution
Isolation Precaution
 
infestion control
infestion controlinfestion control
infestion control
 
ANES 1501 - M8 PPT: Infection Control - Asepsis
ANES 1501 - M8 PPT: Infection Control - AsepsisANES 1501 - M8 PPT: Infection Control - Asepsis
ANES 1501 - M8 PPT: Infection Control - Asepsis
 
Isolation and standard precautions
Isolation and standard precautionsIsolation and standard precautions
Isolation and standard precautions
 
Hospital infection
Hospital infectionHospital infection
Hospital infection
 
Infection control
Infection controlInfection control
Infection control
 
04 infection prevention and control
04 infection prevention and control04 infection prevention and control
04 infection prevention and control
 
Isolation guidelines
Isolation guidelinesIsolation guidelines
Isolation guidelines
 

Similaire à Communicable diseases immunologic

Infection control presentation
Infection control presentationInfection control presentation
Infection control presentationjewapinder
 
sterilization in dentistry/Infection control
sterilization in dentistry/Infection controlsterilization in dentistry/Infection control
sterilization in dentistry/Infection controlDandu Prasad Reddy
 
Infection control in pediatric care unit
Infection control in pediatric care unitInfection control in pediatric care unit
Infection control in pediatric care unitArnab Nandy
 
95-infection-control-in-dentistry.pptx
95-infection-control-in-dentistry.pptx95-infection-control-in-dentistry.pptx
95-infection-control-in-dentistry.pptxAlaaAlharak1
 
Surgical site infection (2)
Surgical site infection (2)Surgical site infection (2)
Surgical site infection (2)orthoprince
 
4a. Basic Infection Control.pptx
4a. Basic Infection Control.pptx4a. Basic Infection Control.pptx
4a. Basic Infection Control.pptxroszansapon
 
ebola-prevention and challenges
ebola-prevention and challengesebola-prevention and challenges
ebola-prevention and challengesChitra Pai
 
Hospital acquired infections
Hospital acquired infections Hospital acquired infections
Hospital acquired infections Ashna Ajimsha
 
Share_smallpoxchickenpoxrizwan-160925004343.pdf
Share_smallpoxchickenpoxrizwan-160925004343.pdfShare_smallpoxchickenpoxrizwan-160925004343.pdf
Share_smallpoxchickenpoxrizwan-160925004343.pdfEkranthkumar
 
Small pox and chicken pox
Small pox and chicken poxSmall pox and chicken pox
Small pox and chicken poxRizwan S A
 
The Role of Microorganism in Hospital Acquired Infection.pptx
The Role of Microorganism in Hospital Acquired Infection.pptxThe Role of Microorganism in Hospital Acquired Infection.pptx
The Role of Microorganism in Hospital Acquired Infection.pptxManitaPaneri
 
Hospital aquired infections
Hospital aquired infectionsHospital aquired infections
Hospital aquired infectionsDr Smita Padhi
 
Infection Control. Bsc nursing ppt for students for nursing foundation
Infection Control. Bsc nursing ppt for students   for nursing foundationInfection Control. Bsc nursing ppt for students   for nursing foundation
Infection Control. Bsc nursing ppt for students for nursing foundationrayanraifa7
 
COVID 19- How to prevent HCWs from getting infected & protect family
COVID 19- How to prevent HCWs from getting infected & protect familyCOVID 19- How to prevent HCWs from getting infected & protect family
COVID 19- How to prevent HCWs from getting infected & protect familyDr.Ashwin Menon
 

Similaire à Communicable diseases immunologic (20)

Infection control presentation
Infection control presentationInfection control presentation
Infection control presentation
 
Hospital infections
Hospital infectionsHospital infections
Hospital infections
 
Communicable diseases
Communicable diseasesCommunicable diseases
Communicable diseases
 
sterilization in dentistry/Infection control
sterilization in dentistry/Infection controlsterilization in dentistry/Infection control
sterilization in dentistry/Infection control
 
Infection control in pediatric care unit
Infection control in pediatric care unitInfection control in pediatric care unit
Infection control in pediatric care unit
 
Hospital Acquired Infection
Hospital Acquired InfectionHospital Acquired Infection
Hospital Acquired Infection
 
95-infection-control-in-dentistry.pptx
95-infection-control-in-dentistry.pptx95-infection-control-in-dentistry.pptx
95-infection-control-in-dentistry.pptx
 
Epidemiology 5th Year.pdf
Epidemiology 5th Year.pdfEpidemiology 5th Year.pdf
Epidemiology 5th Year.pdf
 
Surgical site infection (2)
Surgical site infection (2)Surgical site infection (2)
Surgical site infection (2)
 
4a. Basic Infection Control.pptx
4a. Basic Infection Control.pptx4a. Basic Infection Control.pptx
4a. Basic Infection Control.pptx
 
ebola-prevention and challenges
ebola-prevention and challengesebola-prevention and challenges
ebola-prevention and challenges
 
Hospital acquired infections
Hospital acquired infections Hospital acquired infections
Hospital acquired infections
 
Share_smallpoxchickenpoxrizwan-160925004343.pdf
Share_smallpoxchickenpoxrizwan-160925004343.pdfShare_smallpoxchickenpoxrizwan-160925004343.pdf
Share_smallpoxchickenpoxrizwan-160925004343.pdf
 
Monkey Pox IPC.pptx
Monkey Pox IPC.pptxMonkey Pox IPC.pptx
Monkey Pox IPC.pptx
 
Small pox and chicken pox
Small pox and chicken poxSmall pox and chicken pox
Small pox and chicken pox
 
The Role of Microorganism in Hospital Acquired Infection.pptx
The Role of Microorganism in Hospital Acquired Infection.pptxThe Role of Microorganism in Hospital Acquired Infection.pptx
The Role of Microorganism in Hospital Acquired Infection.pptx
 
Hospital aquired infections
Hospital aquired infectionsHospital aquired infections
Hospital aquired infections
 
H1N1 outbreak in Pune
H1N1 outbreak in PuneH1N1 outbreak in Pune
H1N1 outbreak in Pune
 
Infection Control. Bsc nursing ppt for students for nursing foundation
Infection Control. Bsc nursing ppt for students   for nursing foundationInfection Control. Bsc nursing ppt for students   for nursing foundation
Infection Control. Bsc nursing ppt for students for nursing foundation
 
COVID 19- How to prevent HCWs from getting infected & protect family
COVID 19- How to prevent HCWs from getting infected & protect familyCOVID 19- How to prevent HCWs from getting infected & protect family
COVID 19- How to prevent HCWs from getting infected & protect family
 

Plus de Nhelia Santos Perez

Nursing Research IntroDuction SOP Hypothesis.ppt
Nursing Research IntroDuction SOP Hypothesis.pptNursing Research IntroDuction SOP Hypothesis.ppt
Nursing Research IntroDuction SOP Hypothesis.pptNhelia Santos Perez
 
Nrusing Research 1 Scope and limitation Significance of the study.pptx
Nrusing Research 1 Scope and limitation Significance of the study.pptxNrusing Research 1 Scope and limitation Significance of the study.pptx
Nrusing Research 1 Scope and limitation Significance of the study.pptxNhelia Santos Perez
 
The Introduction, Statement of the Problems, Hypothesis
The Introduction, Statement of the Problems, HypothesisThe Introduction, Statement of the Problems, Hypothesis
The Introduction, Statement of the Problems, HypothesisNhelia Santos Perez
 
Advancement Patterns and Careeer Development PPT.pptx
Advancement Patterns and Careeer Development PPT.pptxAdvancement Patterns and Careeer Development PPT.pptx
Advancement Patterns and Careeer Development PPT.pptxNhelia Santos Perez
 
THEORETICAL_AND_CONCEPTUAL_FRAMEWORKS.pptx
THEORETICAL_AND_CONCEPTUAL_FRAMEWORKS.pptxTHEORETICAL_AND_CONCEPTUAL_FRAMEWORKS.pptx
THEORETICAL_AND_CONCEPTUAL_FRAMEWORKS.pptxNhelia Santos Perez
 
The Research Problem and Statement.pptx
The Research Problem and Statement.pptxThe Research Problem and Statement.pptx
The Research Problem and Statement.pptxNhelia Santos Perez
 

Plus de Nhelia Santos Perez (20)

Nursing Research IntroDuction SOP Hypothesis.ppt
Nursing Research IntroDuction SOP Hypothesis.pptNursing Research IntroDuction SOP Hypothesis.ppt
Nursing Research IntroDuction SOP Hypothesis.ppt
 
Nursing Research 1 Day 1.pptx
Nursing Research 1 Day 1.pptxNursing Research 1 Day 1.pptx
Nursing Research 1 Day 1.pptx
 
Nrusing Research 1 Scope and limitation Significance of the study.pptx
Nrusing Research 1 Scope and limitation Significance of the study.pptxNrusing Research 1 Scope and limitation Significance of the study.pptx
Nrusing Research 1 Scope and limitation Significance of the study.pptx
 
Nursing Research 1 - Ethics
Nursing Research 1 - Ethics Nursing Research 1 - Ethics
Nursing Research 1 - Ethics
 
The Introduction, Statement of the Problems, Hypothesis
The Introduction, Statement of the Problems, HypothesisThe Introduction, Statement of the Problems, Hypothesis
The Introduction, Statement of the Problems, Hypothesis
 
Advancement Patterns and Careeer Development PPT.pptx
Advancement Patterns and Careeer Development PPT.pptxAdvancement Patterns and Careeer Development PPT.pptx
Advancement Patterns and Careeer Development PPT.pptx
 
Liniment Group 8.pptx
Liniment Group 8.pptxLiniment Group 8.pptx
Liniment Group 8.pptx
 
Repellant PPT.pptx
Repellant PPT.pptxRepellant PPT.pptx
Repellant PPT.pptx
 
BREAST-CANCER_PPT.pptx
BREAST-CANCER_PPT.pptxBREAST-CANCER_PPT.pptx
BREAST-CANCER_PPT.pptx
 
NCM111 Day 2.pptx
NCM111 Day 2.pptxNCM111 Day 2.pptx
NCM111 Day 2.pptx
 
tHEORETICAL FRAMEWORK.pptx
tHEORETICAL FRAMEWORK.pptxtHEORETICAL FRAMEWORK.pptx
tHEORETICAL FRAMEWORK.pptx
 
Corn COffee.pptx
Corn COffee.pptxCorn COffee.pptx
Corn COffee.pptx
 
Isolation-Centers.pptx
Isolation-Centers.pptxIsolation-Centers.pptx
Isolation-Centers.pptx
 
THEORETICAL_AND_CONCEPTUAL_FRAMEWORKS.pptx
THEORETICAL_AND_CONCEPTUAL_FRAMEWORKS.pptxTHEORETICAL_AND_CONCEPTUAL_FRAMEWORKS.pptx
THEORETICAL_AND_CONCEPTUAL_FRAMEWORKS.pptx
 
The Research Problem and Statement.pptx
The Research Problem and Statement.pptxThe Research Problem and Statement.pptx
The Research Problem and Statement.pptx
 
Sampling.ppt
Sampling.pptSampling.ppt
Sampling.ppt
 
Nervous System Day 1.pptx
Nervous System Day 1.pptxNervous System Day 1.pptx
Nervous System Day 1.pptx
 
Pharma Nervous Day 2.pptx
Pharma Nervous Day 2.pptxPharma Nervous Day 2.pptx
Pharma Nervous Day 2.pptx
 
Pharma Day1.pptx
Pharma Day1.pptxPharma Day1.pptx
Pharma Day1.pptx
 
Lear · SlidesCarnival.pptx
Lear · SlidesCarnival.pptxLear · SlidesCarnival.pptx
Lear · SlidesCarnival.pptx
 

Communicable diseases immunologic

  • 2. Chain of Infection Susceptible host Portal of Entry Etiologic Agent (microorganism) Reservoir Method of transmission from reservoir to (Source) susceptible host Portal of exit
  • 3. Pathogens • Bacteria – Aerobic – Anaerobic • Viruses - intracellular parasite capable of reproducing outside of a living cell. • Mycoplasma – similar to bacteria and have no cell wall – resistant to antibiotics that inhibit cell wall synthesis • Rickettsiae & Chlamydia - rigid cell wall; with some feature of both bacteria and viruses. – Chlamydia- transmitted by direct contact – Rickettsiae- infect cells of arthropods and are transmitted by these vectors. • Fungi - self-limited, affecting the skin and subcutaneous tissue. • Parasites
  • 4. Reservoir -where the pathogen lives and multiplies – Endogenous – Exogenous • Mode of Transmission – Direct contact – Indirect contact • Vector – Droplet or airborne transmission
  • 5. Host Factors • Factors that enable a host to resist infections: • Physical barriers • Hostile environment created by stomach acid secretions, urine & vaginal secretions. • Antimicrobial factors e.g. saliva, tears • Respiratory defenses • Specific and nonspecific immune responses to pathogenic invasion. • Age • Nutrition
  • 6. Portal of Entry • Respiratory Tract • GI Tract • Genitourinary Tract • Skin and mucous membrane • Bloodstream
  • 7. Stages of Infectious Process • Incubation period – period begins with active replication but with no symptoms • Prodromal stage – Symptoms first appear • Acute phase – proliferation and dissemination of pathogens • Convalescent stage - containment of infection and pathogens are eliminated • Resolution – total elimination of pathogens without residual manifestation Nosocomial infection – Infection acquired in a health care setting. – Typically manifest after 48 hrs. – UTI most common type
  • 8. FACTORS AFFECTING RISK OF INFECTION • AGE • HEREDITY • LEVEL OF STRESS • NUTRITIONAL STATUS • CURRENT MEDICAL THERAPY • PRE-EXISTING DISEASE • IMMUNIZATION STATUS
  • 9. Standard precautions • Blood • All body fluids, secretions, excretions, • Non-intact skin • Mucous membranes • Essential elements: • Use barrier protection • Prevent inadvertent percutaneous exposure, dispose of needles • Immediate and thorough hand washing
  • 10. Infection Control and Prevention
  • 11. Infection Control in In-Patient Health Care Agencies • Hand Hygiene • Patient Placement • Protective Equipment • Proper disposal of Soiled Equipment
  • 12. Infection Control In Community – Based Setting • Sanitation • Proper Disposal of Waste • Food Preparation • Report CD Occurrence
  • 13. Pharmacology • Check for: – History of hypersensitivity. – Age and childbearing status of the client. – Renal function – Hepatic function – Site of infection • Classification of antimicrobial preparations: – Bacteriostatic – Bactericidal
  • 14. COMMUNICABLE DISEASE – Is any disease that can be transmitted directly or indirectly from one person to another
  • 15. INFECTION – Is a condition caused by the entry and multiplication of pathogenic microorganisms within the host body. – It is also an invasion of an organisms (bacteria, helminths, fungi, parasite, ricketsia and prion)
  • 16. ISOLATION – It is necessary when a person is known or suspected to be infected with pathogens that can be transmitted by direct or indirect contact. – The principle behind isolation technique is to create a physical barrier that prevents the transfer of infectious agents. To do this you have to know how the organisms are transmitted.
  • 17. Transmission-Based Precautions –Airborne –Droplets –Contact
  • 18. AIRBORNE – PRIVATE ROOM – NEGATIVE AIR PRESSURE – VENTILATION SAFEGUARDS air from room is not recirculated to other areas – DOOR SHOULD BE KEPT CLOSED – BARRIER TO SMALL PARTICLES masks HEPA high efficiency particulate air – COVER MOUTH OF PATIENT WITH MASK DURING TRANSPORT
  • 19. DROPLET • – PRIVATE ROOM – WEAR MASK IF WORKING WITHIN 3 FEET – WEAR MASKS UPON ENTRY INTO THE ROOM – COVER MOUTH OF PATIENT WITH MASK DURING TRANSPORT
  • 20. CONTACT – PRIVATE ROOM – WEAR GLOVES – GLOVES ARE REMOVED BEFORE EXITING FROM THE ROOM – HANDS ARE WASHED THOROUGHLY – NOTHING IS TOUCHED BEFORE EXITING THE ROOM – GOWN IS WORN WHEN ENTERING THE ROOM – REMOVE GOWN CAUTIOUSLY BEFORE LEAVING THE ROOM – PATIENT CARE ITEMS SHOULD BE RESTRICTED TO SINGLE PATIENT
  • 21. AFB ISOLATION – VISITORS REPORT TO NURSES’ STATION BEFORE ENTERING ROOM • MASKS ARE TO BE WORN IN THE PATIENT’S ROOM • GOWNS ARE INDICATED TO PREVENT CLOTHING CONTAMINATION • GLOVES ARE INDICATED FOR BODY FLUIDS AND NON- INTACTSKIN • HANDWASHING-after touching the patient or potentially contaminated articles and after removing gloves • articles should be discarded, cleaned or sent for decontamination and reprocessing • room is to remain closed • patient is to wear mask during transport
  • 22. STRICT ISOLATION – VISITORS-REPORT TO NURSES’ STATION BEFORE ENTERING ROOM – PRIVATE ROOM-necessary, door must be kept closed – GOWNS-must be worn by all persons entering the room – MASKS- must be worn by all persons entering the room – HANDS-must be washed on entering and leaving room – GLOVES-must be worn by all persons entering the room – ARTICLES-must be discarded, or wrapped before being sent to CENTRAL SUPPLY for disinfection or sterilization
  • 23. RESPIRATORY ISOLATION – VISITORS-REPORT TO NURSES’ STATION BEFORE ENTERING ROOM – PRIVATE ROOM-necessary, door must be kept closed – GOWNS-gowns not necessary – MASKS- must be worn by all persons entering the room if susceptible disease – HANDS-must be washed on entering and leaving room – GLOVES-not necessary – ARTICLES-those contaminated with secretions must be disinfected – CAUTION-all persons susceptible to the specific disease should be excluded from the area, susceptibles must wear masks
  • 24. WOUND AND SKIN PRECAUTIONS – VISITORS-REPORT TO NURSES’ STATION BEFORE ENTERING ROOM – PRIVATE ROOM-desirable – GOWNS-must be worn by all persons having direct contact with the patient – MASKS- during dressing changes – HANDS-must be washed on entering and leaving room – GLOVES-must be worn by all persons having direct contact with infected area – ARTICLES-instruments, dressing, linens
  • 25. ENTERIC PRECAUTIONS – VISITORS-REPORT TO NURSES’ STATION BEFORE ENTERING ROOM – PRIVATE ROOM-necessary FOR CHILDREN ONLY – GOWNS- must be worn by all persons having direct contact with the patient – MASKS- not necessary – HANDS-must be washed on entering and leaving room – GLOVES-must be worn by all persons having direct contact with patient or articles contaminated with fecal material – ARTICLES-special precautions necessary for articles contaminated with urine and feces, must be disinfected or discarded
  • 26. PROTECTIVE ISOLATION – VISITORS-REPORT TO NURSES’ STATION BEFORE ENTERING ROOM – PRIVATE ROOM-necessary, door must be kept closed – GOWNS- must be worn by all persons entering room – MASKS- - must be worn by all persons entering room – HANDS-must be washed on entering and leaving room – GLOVES-must be worn by all persons having direct contact with patient
  • 28. Diphtheria – Corynebacterium diphtheriae – Klebsloeffler’s bacillus (bacteria) – MOT = droplets and airborne • HIGHLY CONTAGIOUS – IP 2-5 days – IMMUNITY • Active = DPT • Passive = DAT • Natural = xxx
  • 29. – Dx = throat swab, MOLONEY, SCHICK – Pseudomembrane, Bullneck – Penicillin or erythromycin – Resp Acidosis with hypoxemia – Cx: myocarditis, septicemia
  • 30. Nursing Considerations: – OBSERVE CNS, CARDIAC AND KIDNEY COMPLICATIONS – PSEUDOMEMBRANOUS MAY LEAD TO RESP. OBSTRUCTION – ISOLATION UNTIL 2 NEGATIVE CULTURE AT 24 HOUR INTERVAL – F&E RESUSCITATION – PARENTS OR SIBLINGS WHO HAVE NEVER IMMUNIZED SHOULD RECEIVE A DOSE OF DIPH. ANTI-TOXIN – ATTENTION TO NASOPHARYNGEAL DISCHARGE – ANTIBIOTICS-PENICILLIN, ERYTHROMYCIN IF ALLERGIC TO PENICILLIN
  • 31. Diphtheria KEY POINTS! – Highly contagious – Pseudomembrane and bullneck – Immunization best intervention PREVENTION – Obstruction and myocarditis – Isolation technique
  • 32. Measles, Rubeola, 7 Day Fever, Hard Red Measle – Paramyxo virus – MOT = droplets and airborne • PC 4 days before and 5 days after rash • HIGHLY CONTAGIOUS – IP 7-14 days – IMMUNITY • Active = measles vaccine, MMR • Passive = measles Ig • Natural = lifetime
  • 33. – Rashes: – Maculopapular – Cephalocaudal – With desquamation – Pruritus
  • 34. • Rashes: maculopapaular, cephalocaudal (hairline and behind the ears to trunk and limbs), confluent, desquamation, pruritus
  • 35. – PS koplik’s spot – Characteristic: stimsons, photophobia (typical complaint) – Fever: high fever – CX pneumonia, meningitis
  • 36. German Measles, Rubella, Rotheln Disease, 3 Day Measles – RNA rubella virus – MOT = droplets and airborne • PC 5 days before and 5 days after rash • HIGHLY CONTAGIOUS – IP = 10-21 days – IMMUNITY • Active = MMR • Passive = rubella Ig • Natural = lifetime
  • 37. – Rashes: – Maculopapular – Diffuse – No desquamation
  • 38. – Rashes: Maculopapular, Diffuse/not confluent, No desquamation, spreads from the face downwards •
  • 39. Chicken Pox, Varicella – Herpes Zoster Virus – Varicella Zoster Virus – MOT = droplets and airborne • PC one day before rash and 6 days after first crop of vesicles • HIGHLY CONTAGIOUS – IP 14-21 days – IMMUNITY • Active = varicella vaccine • Passive = xxx • Natural = lifetime
  • 40. – Rashes: Maculopapulovesicular (covered areas), Centrifugal, starts on face and trunk and spreads to entire body – Leaves a pitted scar (pockmark)
  • 41. – Dx = Tzanck smear (scraping of ulcer for staining) – Rashes: • Maculopapulovesicular (covered areas) • Centrifugal • Leaves a pitted scar (pockmark) – CX furunculosis, erysipelas, meningoencephalitis – Dormant: remain at the dorsal root ganglion and may recur as shingles
  • 42. Meningitis Menigococcemia – Neisseria meningitides (bacteria) – MOT = droplets – IP = 1-2 days – IMMUNITY = xxx
  • 43. – Immunocompetent are susceptible – Petechiae (volar/palm of hands) EARLY – Opisthotonus MENIGEAL IRRITATION – Brudzinski MENINGEAL IRRITATION – Kernigs MENINGEAL IRRITATION – Increased ICP BRAIN – Seizure BRAIN
  • 44. – S/sx: – Meningococcemia – spiking fever, chills, arthralgia, petechial rash – Fulminant Meningococcemia (Waterhouse Friderichsen) – septic shock; hypotension, tachycardia, enlarging petecchial rash, adrenal insufficiency • Meningitis – most common; nuchal rigidity, brudzinski, kernigs, Photophobia, confusion
  • 45. – Dx: CT/ MRI, CSF analysis, CSF gram stain, CSF and blood culture – Mgmt: antibiotics (Pen G, ceftriaxone), steroids, anticonvulsants, Rifampin for close contacts of meningococcemia
  • 46. Amoebiasis – Entamoeba Hystolitica –protozoan (parasite) – MOT = 5 F’s, fecal oral route – IP = 2-4 weeks – IMMUNITY = xxx
  • 47. – Dx microscopic stool exam or rectal secretions – (tetra nucleated cyst and trophozoites) – Diarrhea and constipation (non dysenteric) – Blood streaked, diarrhea and watery mucoid, abd’l cramps (dysenteric) – Extra amoebiasis- penile, vagina, spleen, liver, anal, lungs and meninges – Metronidazole (Flagyl)
  • 48. Typhoid Fever – Salmonella typhosa (bacteria) – MOT = same with amoebiasis (5 F’s) – IP = 1-3 weeks – IMMUNITY • Active = vaccine • Passive = xxx • Natural = lifetime immunity
  • 49. Pathophysiology – Oral ingestion – Bloodstream – Reticuloendothelial system (lymph node, spleen, liver) – Bloodstream – Gallbladder – Peyer’s patches of SI – necrosis and ulceration
  • 50. – 1st week step ladder (BLOOD) – 2nd week rose spot and fastidial • typhoid pyschosis (URINE & STOOL) – 3rd week (complications) intestinal bleeding, • perforation, peritonitis, encephalitis, – 4th week (lysis) decreasing S?SX – 5th week (convalescent)
  • 51. – Blood (typhi dot) 1st week after – Stool and urine 2nd week after – Chloramphenicol
  • 52. – Rose spot (abdominal rashes) – Step ladder fever to fastidial (peak of fever) typhoid psychosis – Peyer’s patches of small intestine – May stay in the gallbladder (hiding area)
  • 56. What is rabies? (DEFINITION & ETIOLOGY) • Is an acute infectious disease of warm-blooded animals and humans characterized by an involvement of the nervous system resulting in death. • It is caused by the RABIES VIRUS, a rhabdovirus of the genus lyssavirus. Rabies is a serious disease. Each year, it kills more than 50,000 people and millions of animals around the world. Rabies is a big problem in Asia, Africa, and Central and South America. In the United States, rabies has been reported in every state except Hawaii. Any mammal can get rabies. Raccoons, skunks, foxes, bats, dogs, and cats can get rabies. Cattle and humans can also get rabies. Only mammals can get rabies. Animals that are not mammals -- such as birds, snakes, and fish -- do not get rabies. Rabies is caused by a virus. An animal gets rabies from saliva, usually from a bite of an animal that has the disease.
  • 57. The Rabies Virus RV – a neurotropic filterable virus present in the saliva of rabid animals. It has a preferrence for Rod-shaped nerve tissues. rabies viruses colored for Virus – minute organism not visible effect with ordinary light microscopy. It is parasitic in that it is entirely dependent on nutrients inside cells for its metabolic and reproductive needs. Can only be seen by use of eclectron microscopy. Consists of DNA or RNA covered with a protein Parts of the rabies covering called capsid. A rhabdovirus virus of the genus lyssavirus. Neurotropic – viruses that reproduce in nerve tissue Filterable virus – virus causing RHABDOVIRUS: any group of rod-shaped infectious disease, the essential This is a RNA viruses with 1 important member, elements of which are so photograph of tiny that rabies virus, pathogenic to man. The they retain infectivity aftervirus under the virus has a predilection for tissue of RHABDO: from Greek passing through a filter of the electron mucus-secreting glands and the Central rhabdos, "rod" Berkefeld type. microscope Nervous System. All warm-blooded
  • 58. How do you get rabies? (MODE & MEDIA OF TRANSMISSION, IMMUNITY) •All warm-blooded mammals are susceptible. Natural immunity in man is unknown. •You get rabies through the saliva of an infected animal by an exposure to an open break in the skin such as bites, open wound or scratch and inhalation of infectious aerosols such as from bats. •In some cases, it is transmitted through organ transplants (corneal transplant), from an infected person. •The virus gets transmitted through saliva, tears, semen, some liquor (amniotic fluid, CST) but not blood, urine or stool. You get rabies from the saliva of a rabid animal, usually from a bite. The rabies virus is spread through saliva. You cannot get rabies by petting an animal. You may get rabies from a scratch if the animal, such as a cat, was licking its paw before it scratched you. (Remember that the rabies virus is found in the saliva of an animal).
  • 59. How do you know if an animal has rabies? • Animals with rabies may act differently from healthy animals. • Some signs of rabies in animals are:  changes in an animal’s behavior  general sickness (fever, restlessness)  problems swallowing  increased drooling  aggression (biting at inanimate objects, aimless running) • Wild animals may move slowly or may act as if they are tame. Some wild animals (foxes, raccoons, skunks) that normally avoid porcupines, may even try to bite these prickly rodents. • A pet that is usually friendly may snap at you or may try to bite.
  • 60. How do you know if one has rabies? (DIAGNOSIS) •There is yet no way of immediately knowing who had acquired rabies virus. No tests are available to diagnose rabies in humans before the onset of clinical disease. •The most reliable test for rabies in patients who have clinical signs of the disease is a DIRECT IMMUNOFLUORESCENT STUDY of a full thickness biopsy of the skin taken from the back of the neck above the hair line. •The RAPID FLUORESCENT FOCUS INHIBITION TEST is used to measure rabies-neutralizing antibodies in serum. This test has the advantage of providing results within 24 hours. Other tests of antibodies may take as long as 14 •days.
  • 62. EPIDEMIOLOGY PHILIPPINES: 350-450 cases/ year 5-7 per million population DOG BITE INCIDENCE: 140, 000- 560, 000/ year 200-800 per 100, 000 population/ year AGE MOST AFFECTED: 5-14 year age group (53% of cases) BITING ANIMALS: (SLH STUDY 1982- 2002) DOGS: 98% PET: 88% STRAY: 10% CATS: 2%
  • 63. • Based on the report from NCDPC (2004), the six regions with the most number of rabies cases are Western Visayas, Central Luzon, Bicol, Central Visayas, Ilocos and Cagayan Valley • Data shows that 53.7 percent of animal bite patients are children • Dogs remain the principal animal source of rabies
  • 64. STAGES OF RABIES INFECTION Rabies virus Entry into the body INCUBATI0N PERIOD (20 – 90 days) INVASION (0 – 10 days) EXCITEMENT (2 – 7 days) PARALYTIC COMA (5 – 14 days) DEATH
  • 65. RABIES CLASSIFICATION ANIMAL RABIES • There are two common types of rabies. One type is "furious" rabies. Animals with this type are hostile, may bite at objects, and have an increase in saliva. In the movies and in books, rabid animals foam at the mouth. In real life, rabid animals look like they have foam in their mouth because they have more saliva. The second and more common form is known as paralytic or "dumb" rabies. The dog pictured below has this type. An animal with "dumb" rabies is timid and shy. It often rejects food and has paralysis of the lower jaw and muscles. • Another two types of rabies. One type is “urban” rabies. The type of rabies in domestic dogs and cats. The other type is called “ sylvatic” rabies. These type came from wild animals such as bats, weasels, skunks and moles & voles.
  • 66. HUMAN RABIES • Humans also have a “furious” type, the classic foaming of the mouth, aggression, apprehension & hydrophobia, and the “dumb” type, progressive paralysis of the body until they couldn’t breathe anymore.
  • 67. DIFFERENT STAGES OF RABIES INFECTION C B A A T T D S S O G S VIRUS IN SALIVA INHALED AEROSOLS VIRUS IN SALIVA INVASION PHASE INVASION PHASE PARALY SIS EXCITEMENT PARALY SIS DEATH DEATH
  • 68. INVASION STAGE • Also called PRODOME PERIOD; Prodrome – symptom indicative of an approaching disease • 2-10 DAYS • Sensory changes on the site of entry. Pain: dull, constant pain referable to the nervous pathways proximal to the location of the wound or itching, intermittent, stabbing pains radiating distally to the region of inoculation. In general, sensitivity is the early symptom which may be ascribed to the stimulative action of the virus affecting groups of neurons, esp. sensory system. Though there is apt to be decreased sensitivity to local pain e.g. needle introduction, patient may complain bitterly of drafts & bed clothes which produce a general stimulation Tick me!
  • 69. • Fever,headache malaise sore throat anorexia increased sensitivity (bright lights, loud noises) increased muscle reflex irritability, tics and muscle tone • Overactive facial expression
  • 70. EXCITATION STAGE • Also called ACUTE NEUROLOGICAL PHASE; hyperactivity • 2 – 10 DAYS • Imminent thoraco-lumbar involvement (SNS): pupillary dilation, lacrimation increased thick saliva production / foaming of mouth, excessive perspiration, increased HR • Anxiety: increased nervousness, insomnia, apprehension; a strong desire to be up, wandering aimlessly about, and Fear: a sense of impending doom • Hydrophobia (perhaps, SNS stimulation: depresses GI activity > inhibits esophageal, gastric & intestinal function) > violent expulsion of fluids, drooling (in attempt not to swallow) > dehydration and parched mouth & tongue • Pronounced muscular stimulation & general tremor • Mania (tearing of clothes & bedding, cases of biting & fighting rare but may occur) and Hallucinations with lucid intervals (normal mental function in which patient is well-oriented & answers questions intelligently) • Convulsions( besides r/t pronounced muscular stimulation, further precipitated by sensory stimuli – sight, sound, name of water > throat spasms > choking > apnea, cyanois, gasping Sympathetic nervous system • > death, but if patient survive excitement phase… Tick me Parasympathetic nervous system Tick me 1st! next!
  • 72. PARALYTIC STAGE -also called DEPRESSION PHASE • Gradual weakness of muscle groups – muscle spasms cease – OCULAR PALSY – strabismus, ocular incoordination, nystagmus, diplopia, central type partial blindness > responds poorly to light, @ times pupil is constricted or unequal (parasympathetic involvement) – Oro-facial: FACIAL & MASSETER PALSY > difficulty closing eyes & mouth, face expressionless – Oral: Weakness of muscles of phonation > hoarsness & loss of voice • Loss of tendon reflexes, always precedes weakness of extremity • Corneal reflex decreased or absent, dry
  • 73. • Ears: VERTIGO . Middle ear disease . Early symptom, but may develop @ any period • Neck stiffness • (+) Babinski [lesions of pyramidal tract], ( - ) Kernig’s ( - ) Brudzinski’s • Cardiac: shifts from tachycardia (100 – 120bpm) @ bed rest to bradycardia (40 -60 bpm) • Respi: Cheyne-Stokes > breathing pattern characterized by a periodic 10 – 6- sec of apnea followed by gradual increasing depth and frequency of respiration • Local sensation (pin prick, heat, cold) diminished • Incoordination
  • 74. • Hydrophobia and aerophobia gone, but still has some difficulty swallowing • General arousal (PNS stimulation) • Bladder & intestinal retention and obstipation (damage to to innervation of the musculature of intestine & bladder)(SNS damage) in some cases, patient shows period of recovery, this apparent remission is followed by progressive • Ascending, flaccid paralysis of extremities until it reaches the respiratory muscle • Apathy, stupor • Complications: Pneumothorax, thrombosis, secondary infections
  • 75. MANAGEMENT NURSING INTERVENTIONS • HIGH RISK FOR INFECTION TRANSMISSION » provide patient isolation » handwashing. Wash hands before and after each patient contact and following procedures that offer contamination risk while caring for an individual patient. Handwashing technique is important in reducing transient flora on outer epidermal layers of skin. » Wear gloves when handling fluids and other potential contaminated articles. Dispose of every after patient care. Gloves provide effective barrier protection. Contaminated gloves becomes a potential vehicle for the transfer of organisms.
  • 76. • KNOWLEDGE DEFICIT (about the disease, cause of infection and preventive measures) »assess patient’s and family’s level of knowledge on the disease including concepts, beliefs and known treatment. »Provide pertinent data about the disease: »organism and route of transmission »treatment goals and process »community resources if necessary »allow opportunities for questions and discussions
  • 77. • ALTERED BODY TEMPERATURE: FEVER RELATED TO THE PRESENCE OF INFECTION. Since fever is continuous, provide other modes to reduce discomfort. »If patient is still well oriented, Inform the relation of fever to the disease process. The presence of virus in the body … »Monitor temperature at regular intervals »Provide a well ventilated environment free from drafts and wind.
  • 78. • DEHYDRATION related to refusal to take in fluids secondary to throat spasms and fear of spasmodic attacks. »Assess level of dehydration of patient. »Maintain other routes of fluid introduction as prescribed by the physician e.g. parenteral routes »Moisten parched mouth with cotton or gauze dipped in water but not dripping.
  • 79. IMMUNIZATION ACTIVE IMMUNIZATION - induce antibody and T-cell production in order to neutralize the rabies virus in the body. It induces an active immune response in 7-10 days after vaccination, which may persist for one year or more provided primary immunization is completed. TYPES: a. PVRV (Purified Vero Cell Rabies Vaccine) b. PCEVC (Purified Chick Embryo Cell Vaccine)
  • 80. PASSIVE IMMUNIZATION - RIG (Rabies Immune Globulins) - provide the immediate availability of antibodies at the site of exposure before it is physiologically possible for the pt.to begin producing his own antibodies after vaccination. - Important for pts. w/ Cat III exposures Types: a. HRIG (Human Rabies Immune Globulins) b. Highly Purified Antibody Antigen Binding fragments c. ERIG (Equine Rabies Immune Globulins)
  • 81. VACCINATION (Intradermal Schedule) Day of PVRV/PCECV Site Immunization DAY 0 0.1 ml L & R deltoids/ anterolateral thighs of infants DAY 3 0.1 ml L & R deltoids/ anterolateral thighs of infants DAY 7 0.1 ml L & R deltoids / anterolateral thighs of infants DAY 28/30 0.1 ml L & R deltoids/ anterolateral thighs of infants
  • 82. Intramuscular Schedule Day of PVRV PCECV Site Immunization Day 0 0.5 ml 1.0 ml One deltoid/ anterolateral thigh of infants Day 3 0.5 ml 1.0 ml Same Day 7 0.5 ml 1.0 ml Same Day 14 0.5 ml 1.0 ml Same Day 28 0.5 ml 1.0 ml same
  • 83. MANAGEMENT OF RABIES PATIENT • Once symptoms start, treatment should center on comfort care, using sedation & avoidance of intubation & life support measures once diagnosis is certain 1. MEDICATIONS a. Diazepam b. Midazolam c. Haloperidol + Dipenhydramine
  • 84. 2. SUPPORTIVE CARE - Pts w/ confirmed rabies should receive adequate sedation & comfort care in an appropriate medical facility. a. Once rabies diagnosis has been confirmed, invasive procedures must be avoided b. Provide suitable emotional and physical support c. Discuss & provide important info. to relatives concerning transmission of dse. & indication for PET of contacts d. Honest gentle communication concerning prognosis should be provided to relatives of pt
  • 85. 3. INFECTION CONTROL a. Patient should be admitted in a quiet, draft- free, isolation room b. HLCR workers & relatives in contact w/ pt should wear proper personal protective equipment (gown, gloves, mask, goggles) 4. DISPOSAL OF DEAD BODIES
  • 87. • Tetanus – Clostridium tetani – MOT = wound setting – IP = 3 -21 days – IMMUNITY • Active = TT • Passive = TAT and TIG • Natural = active none, passive (+)
  • 88. – Wound Infection – FATAL INFECTION OF THE CNS – TOXIN-NEUROTOXIN
  • 89. • PATHOPHYSIOLOGY: – SETTING OF WOUND ---- ENTRANCE OF C.T. ---- RELEASES TETANUS TOXIN ---- TETANOSPASMIN (CNS), TETANOLYSIN (BLOOD) ---- ABSORBED BY MOTOR NERVE ENDINGS ---- SYNAPSE (CONNECTION BETWEEN NEURONS) ---- MYONEURAL JUNCTION ---- ACETYLCHOLINE DISTURBANCE IN THE TRANSMISSION OF NERVE IMPULSE
  • 90. – Trismus – lock jaw – Risus sardonicus - maskface – Risorius - grinsmile – Dx wound and blood extraction (non specific)
  • 91. • Immunization – DPT (0.5 ml IM) 1 – 1 ½ months old 2 - after 4 weeks 3 – after 4 weeks – 1 st booster – 18 mos – 2 nd booster – 4-6 yo – subsequent booster – every 10 yrs thereafter – TT (0.5 ml IM) TT1 - 6 months within preg TT2 - one month after TT1 TT3 to TT5 - every succeeding preg or every year – TAT (horse) and TIG (human)
  • 92. • Management – 1. Anticonvulsant, muscle relaxants, – antibiotics, wound cleansing and debridement, hyperbaric chamber – 2. Active-DPT and tetanus toxoid – 3. Passive-TIG and TAT, placental immunity
  • 95. IINTRODUCTION: Philippine Hemorrhagic Fever was first reported in 1953. In 1958, hemorrhagic became a notifiable disease in the country and was later reclassified as Dengue Hemorrhagic Fever. What is Dengue Hemorrhagic Fever? • A severe mosquito transmitted viral illness endemic in the tropics. • It is characterized by increased vascular permeability, hypovolemia and abnormal blood clotting mechanisms.
  • 96. WHO case definition for DHF: • fever or history of recent fever • thrombocytopenia (platelet count equal to or less than 100 x 10 / cu mm) • hemorrhagic manifestations such as petechiae or overt bleeding phenomena, and • evidence of plasma leakage due to increase vascular permeability Infectious Agent / Etiologic Agent: Flaviviruses; Dengue Virus Types 1, 2, 3, and 4
  • 97. Occurrence: Dengue occurrence is sporadic throughout the year. Epidemic usually occurs during the rainy seasons June – November. Peak months are September and October. DHF are observed most exclusively among children of the indigenous population under 15 years of age. Occurrence is greatest in the areas of high Aedis Aegypti prevalence.
  • 98. Notifiable Diseases and Deaths by Cause in the Philippines (2001 – 2004) 2001 2002 2003 2004 Notifiable Diseases Reported Reported Reported Reported Cases Deaths Cases Deaths Cases Deaths Cases Deaths Dengue Fever 23,235 13,187 18,039 15,838 Source: National Statistics Office
  • 99. INCIDENCE OF DENGUE HEMORRHAGIC FEVER IN CEBU CITY (YEAR 2007) Selected Number of New Cases Number of Deaths Year Communicable Disease: total male female total male female Dengue / DHF 43, 350 … … 416 … … 2007 Source: Department of Health Region VII
  • 100. • The DOH reported 70,204 dengue cases for week ending September 10, 2011. This was over 24,000 cases less or 25.87% lower than for the same period last year. In addition, the number of cases in July and August (the peak months for dengue) was 52% lower than last year. A total of 396 deaths were reported for this year, which is lower than last year’s number of 620.
  • 101. Reservoir / Source of Infection: • Some source is a vector mosquito, the Aedes Aegypti or the common household mosquito • The infected person
  • 102. Mode of Transmission: Mosquito bite (Aedis Aegypti) Incubation Period: Probably 6 days to one week Period of Presumed to be on the 1st week of illness – when virus is still Communicability: present in the blood Susceptibility and All persons are susceptible. Both sexes are equally affected. The age resistance: groups predominantly affected are the preschool age and school age. Adults and infants are not exempted. Peak age affected 5-9 years. Susceptibility is universal. Acquired immunity may be temporary but usually permanent.
  • 103. Diagnostic Test: 1.) Tourniquet Test (Rumpel Leads Tests) • Inflate the blood pressure cuff on the upper arm to a point midway between the systolic and diastolic pressure for 5 minutes • Release cuff and make an imaginary 2.5 cm square or 1 inch just below the cuff, at the antecubital fossa • Count the number of petechiae inside the box • A test is (+) when 2 or more petechiae per 2.5 cm square or 1 inch square are observed 2.) A con firmed diagnosis is established by culture of the virus, polymerase-chain-reaction (PCR) tests, or serologic assays.
  • 104. Clinical Manifestations (Public Health Nursing in the Philippines, 2007): An acute febrile infection of sudden onset with 3 stages: • 1st-4th day (febrile or invasive stage) -high fever, abdominal pain and headache; later flushing which may be accompanied by vomiting, conjunctiva infection and epistaxis. • 4th-7th day (toxic or hemorrhagic stage) -lowering of temperature, severe abdominal pain, vomiting and frequent bleeding from gastrointestinal tract in the form of hematemesis or melena. Unstable blood pressure, narrow pulse pressure and shock. Death may occur. Tourniquet test which may be positive may become negative due to low or vasomotor collapse.
  • 105. • 7th-10th day (convalescent or recovery stage) -generalized flushing with intervening areas of blanching, appetite regained and blood pressure already stable. • Dengue shock syndrome is defined as dengue hemorrhagic fever plus: *Weak rapid pulse, *Narrow pulse pressure (less than 20 mm Hg) or, *Cold, clammy skin and restlessness
  • 106. Grading of Dengue Fever: The severity of DHF is categorized into four grades: • grade I, without overt bleeding but positive for tourniquet test • grade II, with clinical bleeding diathesis such as petechiae, epistaxis and hematemesis • grade III, circulatory failure manifested by a rapid and weak pulse with narrowing pulse pressure (20 mmHg) or hypotension, with the presence of cold clammy skin and restlessness; and • Grade IV, profound shock in which pulse and blood pressure are not detectable. It is note-worthy that patients who are in threatened shock or shock stage, also known as dengue shock syndrome, usually remain conscious. * Grade III and IV are considered to be Dengue Shock Syndrome
  • 108. • Promote rest • Medication –Paracetamol – for fever and muscle pains. –Analgesic – for headache –DON’T GIVE ASPIRIN
  • 109. • Rapid replacement of body fluids is the most important treatment – Give ORESOL to replace fluid as in moderate dehydration at 75ml/kg in 4-6 hours or up to 2-3L in adults. Continue ORS intake until paient’s condition improves. – Intravenous fluid
  • 110. • For hemorrhage – Keep patient at rest during bleeding periods – For epistaxis – maintain an elevated position of trunk and promote vasoconstriction in nasal mucosa membrane through an ice bag over the forehead. – For melena – ice bag over the abdomen.
  • 111. • Provide support during the transfusion therapy • Diet – Low fat, low fiber, non- irritating, non-carbonated – Noodle soup may be given • Observe signs of deterioration (shock) such as low pulse, cold clammy perspiration, prostration.
  • 113. • Eliminate vector by: –Changing water and scrubbing sides of lower vases once a week –Destroy breeding places of mosquito by cleaning surroundings –Proper disposal of rubber tires, empty bottles and cans –Keep water containers covered
  • 114. OTHER PRECAUTIONS: • When outdoors in an area where dengue fever has been found –Use a mosquito repellant –Dress in protective clothing-long- sleeved shirts, long pants, socks, and shoes
  • 115. • Keeping unscreened windows and doors closed • Keeping window and door screens repaired • Use of mosquito nets
  • 116. MALARIA • Malaria, King of Tropical – P. VIVAX AND OVALE Disease MAY HAVE RECCURENCE OF SYMPTOMS – Protozoan plasmodium • tertian-febrile paroxysm • plasmodium ovale - q24H-48H dormant (liver) • quartan-febrile paroxysm • plasmodium vivax - q48H-72H benign • plasmodium malariae - mild but resistant • plasmodium falciparum - malignant (cerebral malaria)
  • 117. – MOT • Bite from infected anopheles mosquito or minimus flavire (night biting) • Blood Transfusion • Sexual cycle – sporogony (mosquito) – gametes is the infective stage • Asexual cycle – schizogony (human) – IP (Incubation Period) 5-6 days
  • 118. – Nursing Considerations – Dx: • blood extraction (extract blood at the height of fever) – Fever, chills, profuse sweating-convulsion – Anemia and fluid and electrolytes imbalance, hepatomegaly, splenomegaly, rigor, headache and diarrhea. – Chloroquine and Primaquine drug of choice – Chloroquine for pregnant women – For resistant plasmodium-use chemo drug – RBC is being attack
  • 119. – Nursing Considerations – IV FLUIDS AND ELECTROLYTES – Blackwater Fever – hemolysis and hemoglobinuria – Sickle Cell Trait – provides natural resistance – DECREASE FLUIDS IN CEREBRAL EDEMA – ASSISTED VENTILATION IN PULMONARY EDEMA – DIALYSIS IN RENAL FAILURE – BT IN ANEMIA
  • 120. – TRAVELERS TO MALARIA ENDEMIC area SHOULD FOLLOW PREVENTIVE MEASURES- (CHEMOPROPHYLAXIS CHLOROQUINE MAY BE TAKEN 1 WEEK BEFORE ENTERING ENDEMIC AREA) – SOAKING OF MOSQUITO NET IN AN INSECTICIDE SOLUTION – BIO PONDS FOR FISH – ON STREAM CLEARING (TO EXPOSE THE BREEDING STREAM TO SUNLIGHT) – VECTORS PEAK BITING AT NIGHT 9PM-3AM – PLANTING OF NEEM TREE (REPELLENT EFFECT) – ZOOPROPHYLAXIS (DEVIATE MOSQUITO BITES FROM MAN TO ANIMALS) – INFECTED MOTHER CAN STILL CONTINUE BREAST FEEDING
  • 121. Filariasis, Elephantiasis, Human Lymphatic Filariasis – CAUSATIVE AGENT-NEMATODE PARASITE • MICROFILARIAE OR FILARIAL WORMS • WUCHERERIA BRONCOFTI • BRUGIA MALAYI • BRUGIA TIMORI – MOT • Bite from aedes poecilius (night biting) • Invade the lymph vessel, obstructing the lymphatic channel-leads to edema and may infiltrate the reproductive organs. – IP 8-16 months
  • 122. CLINICAL MANIFESTATIONS: – ASYMPTOMATIC STAGE • (+) MICROFILARIAE IN THE BLOOD – NO CLINICAL S/SX – ACUTE STAGE • LYMPHADENITIS (LYMPH NODES) • LYMPHANGITIS (LYMPH VESSELS) • GENETALIA-FUNICULITIS, EPIDYDIMITIS, ORCHITIS – CHRONIC STAGE • HYDROCOELE • LYMPHEDEMA (UPPER AND LOWER EXTREMITIES) • ELEPHANTIASIS
  • 123. – INCIDENCE-REGION 5,8,11 AND CARAGA, MARINDUQUE, SARANGGANI – Drug: Diethyl Carbamazine Citrate or Hetrazan 6mg/KgBW one dose every year – Dx: • NBE nocturnal blood exam (night) • ICT immunochromatographic test (day)
  • 124. Nursing Considerations – MASS TREATMENT-DOSE IS 6mg/KBW, SINGLE DOSE PER YEAR. – ENVIRONMENTAL SANITATION – PERSONAL HYGIENE – MOSQUITO NETS – LONG SLEEVES, LONG PANTS AND SOCKS – INSECT REPELLENT – SCREENING OF HOUSES – HEALTH EDUCATION
  • 125. Schistosomias, Snail Fever, Takayama – Blood fluke – Schistosoma japonicum – S. hematobium – S. mansoni – MOT skin entry (cercaria) travel in to the blood stream where they will infiltrate the liver, from liver to intestines
  • 126. – Cycle: Egg-larvae (miracidium)-intermediary host (oncomelania quadrasi-tiny snail)-cercaria – Itchiness at the site – RUQ pain (hepatomegaly) – Intestine infiltration-abd’l cramps, diarrhea with blood – Praziquantel – Dx COPT (stool exam)
  • 127. – Egg– miracidium– snail– cercaria- human – Itchiness – liver – intestines – Praziquantel – COPT – PREVENTION – Samar and Leyte
  • 128. HIV and AIDS – Retrovirus (HIV1 & HIV2) – Attacks and kills CD4+ lymphocytes (T-helper) – Capable of replicating the lymphocytes undetected by the immune system – Immunity declines and opportunistic microbes sets in
  • 129. HIGH RISK GROUP – Homosexual or bisexual – Intravenous drug users – BT recipients before 1985 – Sexual contact with HIV+ – Babies of mothers who are HIV+
  • 130. MOT – Sexual intercourse (oral, vaginal and anal) – Exposure to contaminated blood, semen, breast milk and other body fluids – placenta
  • 131. HIV TEST – Elisa – Western Blot – Rapid hiv test • Suds hiv-1 • Results are obtained in less than 10 minutes • Color indicator similar to pregnancy test • Positive result needs a confirmatory test
  • 132. How to Diagnose – HIV+ 2 consecutive positive ELISA and 1 positive Western Blot Test – AIDS+ HIV+ CD4+ count below 500/ml Exhibits one or more of the ff: (next slide) – Full blown AIDS CD4 is less than 200/ml
  • 133. – Exhibits one or more of – Weight loss the ff: – Severe diarrhea – Extreme fatigue – Apathy and depression – Intermittent fever – PTB – Night sweats – Kaposis sarcoma – Chills – Pneumocystis carinii – Lymphadenopathy – AIDS dementia – Enlarged spleen – Anorexia
  • 134. • HIV CLASSIFICATION – CATEGORY 1 – CD4+ 500 OR MORE – CATEGORY 2 – CD4+ 200-499 – CATEGORY 3 – CD4+ LESS THAN 200
  • 135. • Management – Prevention of spread (safe sex) – Universal precautions – Health Education – Symptomatic intervention – No known cure – Prevent CD4 reduction