CPH Prefinal CHAPTER 5 Control and Prevention of Communicable Diseases
CPH Prefinal CHAPTER 5 Control and Prevention of Communicable Diseases
CPH Prefinal CHAPTER 5 Control and Prevention of Communicable Diseases
PREVENTION OF
COMMUNICABLE
DISEASES
PRECIOUS DIANNE E. BARDON, RMT
- COMMUNICABLE VS
NONCOMMUNICABLE
- GERM THEORY
- PATHOGEN
- SUSCEPTIBILITY
- PATHOGENICITY
IMMUNE SYSTEM
INNATE IMMUNITY
- PHYSICAL (ANATOMICAL BARRIERS)
- CELLULAR
- CHEMICAL
ACQUIRED IMMUNITY
-HUMORAL (B-CELLS & AB)
- CELLULAR (T-CELLS & LYMPHOKINES)
LEUKOCYTES (WBC)
NEUTROPHIL MOST ABUNDANT, 1ST TO ARRIVE
DENDRITIC CELL PRESENT IN TISSUES, LINK BETWEEN INNATE AND
ADAPTIVE
BASOPHIL RELEASE HISTAMINE
EOSINOPHIL RELEASE TOXIC MOLECULES, MAY DAMAGE TISSUES
MAST CELL RELEASE HEPARIN, HISTAMINES, CHEMOKINES, CHEMOTAXIC
CYTOKINES. INVOLVED IN ALLERGIC/ANAPHYLAXIS AND WOUND HEALING.
MACROPHAGE - PHAGOCYTIC CELL
NATURAL KILLER CELL - AUTOLYTIC ACTION
T-LYMPHOCYTES
T HELPER CELL (CD4+ T CELLS)
SECRETES CYTOKINES
ASSIST B CELLS MATURATION
ACTIVATES CYTOTOXIC T-CELLS & MACROPHAGE
SUPPRESOR T CELL
SHUTS DOWN T CELL-MEDIATED IMMUNITY
IMMUNOGLOBULINS
IgG - majority, trans placental
IgA mucosal areas, prevents colonization of
pathogens
IgM eliminates pathogen in the early stage
IgE binds allergens and triggers histamine
release from mast cells and basophils, protects
from parasite
IgD antigen receptor
IMMUNOLOGICAL MEMORY
Passive (short term)
Active (long term)
Immunization process where person is made immune
or resistant to an infectious disease, typically by
administration of a vaccine.
- Live attenuated (modification)
- Inactivated (wholes or fractions)
Live attenuated
- VIRUS
Measles, mumps, rubella, varicella, rotavirus,
influenza (intranasal)
oral polio vaccine
- BACTERIA
Bacile Calmette- Guerin (BCG)
Oral typhoid vaccine
INACTIVATED VACCINES
Needs booster
INACTIVATED WHOLE VIRAL VACCINES
- polio, hepatitis, rabies, influenza
INACTIVATED WHOLE BACTERIAL VACCINES
- pertussis, typhoid, cholera, plague
FRACTIONAL VACCINES
- Subunits: hepatitis B, influenza, acellular pertussis, human
papillomavirus ,anthrax
- Toxoids: diphtheria, tetanus
POLYSACCHARIDE VACCINES
- Pneumococcal disease, meningococcal
disease and salmonella typhi
- Haemophilus influenza
RECOMBINANT VACCINES
- genetic engineering
- Hep B & HPV
- Look at pp. 66 table
BACTERIA
Prokaryotic
Biofilms (bacterial mats)
Do not usually have membrane bound
organelles within cytoplasm
Taxis influenced behaviors (chemo,
photo,energy,magneto)
Gram Staining + (blue) (pink)
ANTIBIOTICS
- Bacteriocidal (KILL)
- Bacteriostatic (prevent
growth
VIRUS
3 major components
- Genetic material
- Protein coat
- Envelope of lipids
Virion (complete virus particle)
Capsid (protein protective coat) (formed by capsomeres)
- Bacteriophage, mutation, Antigenic Shift
VIRUS REPRODUCTION
1.Attachment
2.Penetration
3.Replication
4.Release
PARASITES
PROTOZOA
HELMINTHS (Egg-Larvae-Adult): Flatworms,
Acanthocephalans, Roundworms
ECTOPARASITES
ARTHROPODS
CHAIN OF INFECTION
Insert chart here
PREVENTIVE MEASURES
Primary forestall onset
Secondary (self-diagnosis & Self
Treatment); isolation & quarantine
Tertiary Control and Prevention
COMMUNICABLE
DISEASES
TUBERCULOSIS
TUBERCULOSIS OR TB
an infectious disease caused by the bacteria called
Mycobacterium tuberculosis.
Transmitted from a TB patient to another person through
coughing, sneezing and spitting. Thus, close contacts,
especially household members, could be infected with TB.
Lungs are commonly affected but it could also affect other
organs such as the kidney, bones, liver and others.
Curable and preventable. However, incomplete or irregular
treatment may lead to drug-resistant TB or even death.
Lowenstein Jensen
media
TB CLASSIFICATION
1. Bacteriological Status
a. Bacteriologically-confirmed
b. Clinically diagnosed
2. Anatomical location
c. Pulmonary TB
d. Extra-pulmonary TB
3. History
e. New Case
f.
Retreatment Case
CASE HOLDING
Set of procedures which ensures that patients
complete their treatment
DRUG TREATMENT
Fixed Dose combination
Single drug formulation
Type of treatment regimen given depends on
category
Treatment discontinued either by disappearance
of symptoms or by adverse reactions (Minor &
Major)
STAGES OF TB PATHOGENESIS
Exposure to infection
Progression to disease
Late or inappropriate diagnosis and
treatment
Poor treatment adherence and
success.
PLASMODIUM
P. falcifarum
P. vivax (hypnozoites)
P. ovale
P.malariae
P. knowlesi
ENDEMICITY
a.Stable Malaria Areas
b.Unstable Malaria Areas
.Uncomplicated Malaria
.Complicated Malaria
* Signs and symptoms are nonspecific
PARASITOLOGICAL DIAGNOSIS
Improved
Identification
Prevention
Confirmation
Improved
TYPE OF STAINS
Romanowsky (Nucleus(RED);
Cytoplasm (BLUE)
Giemsa Stain Gold Standard
Leishmans stain (thin smear)
Wrights stain (rapid)
PROPHYLAXIS
NO prophylaxis regimen offers complete
protection
Chloroquine
Chloroquine plus proguanil
Mefloquine
doxycyline
DENGUE
RABIES
PRODROMAL
STAGE
Acute Neurologic
Stage
Initial viral
multiplication in
muscle cells
Paresthesia pain
at the site of bite
DIAGNOSIS
Clinical Manifestations (hydrophobia/
aerophobia)
History of Exposure
If paralytic: lab diagnosis on fresh tissue
specimen with glycerine preservative
Post-Exposure Prophylaxis (PEP)
RABIES
Vaccine- preventable disease (active and
passive immunization)
Intradermal (ID) 0.1 ml (PVRV & PCECV);
One dose per deltoid (0,3,7,28 days)
Passive: Rabies Immunoglobulin (RIG)
Human RIG (HRIG): 21 days hf
Equine RIG (ERIG) : 14 days hf
SKIN TEST
Performed prior to ERIG
Positive (>6 mm)
SCHISTOSOMIASI
S
MOT:
CONTAMINATED
WATER
PATHOPHYSIOLOGY
Its not the egg, but the cellular infiltration from the immune
response
Katayama Fever.
FILARIASIS
Elephantiasis
PARASITES
Wuchereria bancrofti
Brugia malayi & timori
Microfilaraemic Direct
observation on Peripheral
Blood
Amicrofilaraemic Clinical
Observations or Antigen
Detection
DIAGNOSIS
Microfilariae in blood smear
Giemsa Stained
Finger prick test gold
standard