CONTROL AND

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)
FUNCTIONS OF INNATE IMMUNE
SYSTEM
1. RECRUIT IMMUNE CELLS TO SITES OF INFECTION (CYTOKINES)
2. ACTIVATION OF COMPLEMENT CASCADE FOR IDENTIFICATION AND
CLEARANCE
3. IDENTIFICATION AND REMOVAL OF FOREIGN SUBSTANCES (WBC)
4. ACTIVATES ADAPTIVE IMMUNE SYSTEM (AG-AB)
5. PHYSICAL AND CHEMICAL BARRIERS
REACTION OF BODY TO PATHOGEN

1. INFLAMMATION
4 CLASSIC SIGNS:
- RUBOR (REDNESS)
- CALOR ( TEMPERATURE)
- DOLOR (PAIN)
- TUMOR (SWELLING)
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
ADAPTIVE IMMUNE SYSTEM

-HIGHLY SPECIFIC
-LONG TERM
E.G IMMUNIZATION
ADAPTIVE IMMUNE SYSTEM

• RECOGNITION AND ANTIBODY PRODUCTION TO

ANTIGENS
• GENERATION OF RESPONSES FOR MAXIMAL
ELIMINATION OF PATHOGENS
• DEVELOPMENT OF IMMUNOLOGICAL MEMORY (B-
CELLS)
T-LYMPHOCYTES
• T HELPER CELL (CD4+ T CELLS)
– SECRETES CYTOKINES
– ASSIST B CELLS MATURATION
– ACTIVATES CYTOTOXIC T-CELLS & MACROPHAGE

• CYTOTOXIC T CELL (CD8+ T CELLS)

– DESTROYS VIRUS INFECTED CELLS

• MEMORY T CELL (EITHER CD8+ OR CD8+)

– GETS REACTIVATED UPON EXPOSURE

• SUPPRESOR T CELL
– SHUTS DOWN T CELL-MEDIATED IMMUNITY

• NATURAL KILLER T CELL

– PRODUCE SYTOKINES AND CYTOLYTIC MOLECULES
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
HOW THEY “SEES” AND ANTIGEN

T cells
• MHC - Processed form of antigen (peptide)
B cells
• Needs helper T cells
• Differentiates into an effector cell (plasma cell)
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
IMPLICATION OF PUBLIC HEALTH

• ACUTE vs CHRONIC
• TRANSMISSION: direct, indirect, airborne, blood-borne,
droplet, sexual contact
• Infectivity: DISEASE
• (Host, Pathogen, Environment)
• Add: TIME
CHAIN OF INFECTION

• Insert chart here

THE GOALS OF EPIDEMIOLOGY

•Eradicate
•Prevention
•Intervention
•Control
PREVENTIVE MEASURES

• Primary – forestall onset

• Secondary (self-diagnosis & Self Treatment);
isolation & quarantine
• Tertiary – Control and Prevention
COMMUNICABLE
DISEASES
TUBERCULOSIS
• 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.

CASE FINDING THROUGH (PASSIVE,
ACTIVE, INTENSIFIED)
Diagnosis
1. DSSM
2. TB Culture & Drug Susceptibility
3. Tuberculin Skin Testing (PPD)
4. Rapid Molecular Diagnostic Test (GenEXpert)
Lowenstein Jensen media
PPD test/ Mantoux Test
-delayed hypersensitivity
TB CLASSIFICATION

1. Bacteriological Status
a. Bacteriologically-confirmed
b. Clinically diagnosed
2. Anatomical location
a. Pulmonary TB
b. Extra-pulmonary TB
3. History
a. New Case
b. Retreatment Case
 CASE HOLDING

• Set of procedures which ensures that patients complete

their treatment

 Method developed to ensure treatment compliance by

providing constant and motivational supervision to TB
patients.
TB DISEASE REGISTRATION GROUPS

• New
• Relapse
• Treatment after Failure
• Treatment After Lost to Follow-up
• Previous Treatment Outcome Unknown
• Others
 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”
• Leishman’s stain (thin smear)
• Wright’s stain (rapid)
MALARIA RAPID DIAGNOSTIC TEST
TREATMENT FOR P. FALCIFARUM
MALARIA

•Uncomplicated Malaria
•Antipyretics
•Anti-emetics
•Convulsions
TREATMENT FOR NON- P. FALCIFARUM
MALARIA

•Oral chloroquinoline
•Primaquine (contraindicated with
G6PD)
PROPHYLAXIS

• NO prophylaxis regimen offers complete protection

• Chloroquine
• Chloroquine plus proguanil
• Mefloquine
• doxycyline
INSECTICIDE TREATED BED NETS

• Pyrethoid insecticides
• Piperonyl butoxide
• Long lasting insecticide-treated nets
DENGUE
DENGUE FEVER/ DENGUE
HEMORRHAGIC FEVER
ADMINISTRATIVE ORDER NO. 2012-
0006
• Revised Dengue Clinical Case Management Guidelines
2011
• Classification of levels of severity & Appropriate Clinical
Management (Dengue w/o warning signs, Dengue w/
warning signs, Severe Dengue)
TREATMENT AND PREVENTION
RABIES
INCUBATION PERIOD (TIME OF EXPOSURE
TO SIGNS AND SYMPTOMS APPEARANCE)
• FACTORS
- amount of virus inoculated
- severity of exposure
- Location of Exposure
PRODROMAL Acute Neurologic
STAGE Stage
• Initial viral ■ Virus reach brain (Gray
matter)
multiplication in muscle ■ 2 types
cells - encephalitic/ furious
• Paresthesia – pain at the - paralytic/ dumb
site of bite - hypersalivation
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)
TREATMENT AND PREVENTION

•Chemical and Physical Means

•Pets Vaccination
•Pre-exposure immunization
SCHISTOSOMIASI
S
MOT:
CONTAMINA
TED WATER
PATHOPHYSIOLOGY
• It’s not the egg, but the cellular infiltration from the immune response
• Katayama Fever.

Treatment: Praziquantel (annual)

FIL ARIASIS
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”
MASS ANNUAL TREATMENT

•Diethylcarbamazine Citrate & Albendazole

•“ November as Filiriasis Mass Treatment
Month”