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PATHOGENESIS OF BACTERIAL INFECTION NORMAL HUMAN MICROBIOTA PROPHYLAXIS

Kathleen Ross S. Caligagan, MD, FPSNM

PATHOGENESIS OF BACTERIAL INFECTION

BACTERIAL PATHOGENESIS

TERMINOLOGIES

PATHOGEN is a microorganism that is able to cause disease in a plant, animal or insect. PATHOGENECITY is the ability to produce disease in a host organism.
- Microbes express their pathogenicity by means

of their VIRULENCE, a term which refers to the quantitative ability of a microbe to cause a disease. It is determined by the genetic or biochemical or structural features of the microbe.

BACTERIAL PATHOGENESIS

ID BACTERIA THAT CAUSE DISEASE

KOCHS POSTULATES
1. The organism must always be found in

humans with the infectious disease but not found in healthy ones.
2. The organism must be isolated from humans

with the infectious disease and grown in pure culture.


3. The organism isolated in pure culture must

initiate disease when re-inoculated into susceptible animals.

BACTERIAL PATHOGENESIS

ID BACTERIA THAT CAUSE DISEASE

KOCHS POSTULATES
Bacillus anthracis is the first

microorganism to satisfy Kochs postulates in the late 19th century

Exemptions: - cannot be grown in vitro but can infect animals Treponema pallidum (syphilis) Mycobacterium leprae (leprosy) - can be grown in vitro but cannot infect animals

BACTERIAL PATHOGENESIS

ID BACTERIA THAT CAUSE DISEASE

Evidence for a potential pathogen being clinically significant


Isolated in abundance Isolated in pure culture Isolated on more than one occasion Isolated from deep tissues Evidence of local inflammation Evidence of immune response to pathogen - Fits with clinical picture
-

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS

Adherence factors Invasins Toxins Enzymes Antiphagocytic factors Intracellular pathogenecity Antigenic heterogeneity Iron requirement Bacterial biofilms

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS

ADHERENCE FACTORS
Bacterial adherence to mucosal surfaces

requires the participation of two factors: 1. RECEPTOR - a complementary macromolecular binding site on a (eucaryotic) surface that binds specific adhesins or ligands 2. LIGAND, called ADHESIN - macromolecular component of the bacterial cell surface which interacts with the host cell receptor.

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS

Mechanisms of adherence to cell surfaces may involve two steps:


1. NONSPECIFIC ADHERENCE: - reversible attachment of the bacterium to the eucaryotic surface - sometimes called "docking" - involves nonspecific attractive forces which allow approach of the bacterium to the eucaryotic cell surface.
hydrophobic interactions

electrostatic attractions
atomic and molecular vibrations resulting from fluctuating dipoles of

similar frequencies Brownian movement recruitment and trapping by biofilm polymers interacting with the bacterial capsule

2. SPECIFIC ADHERENCE: - reversible permanent attachment of the microorganism to the surface - sometimes called "anchoring" - specific adherence involves permanent formation of many specific

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS

COMPONENTS

Fimbriae
Common pili Sex pilus Type 1 fimbriae Type 4 pili

S-layer

Capsule M protein Lipopolysaccharide (LPS) Teichoic acids

DESCRIPTION Filamentous proteins on the surface of bacterial cells that may behave as adhesins for specific adherence Same as fimbriae A specialized pilus that binds mating procaryotes together for the purpose of DNA transfer Fimbriae in Enterobacteriaceae which bind specifically to mannose terminated glycoproteins on eucaryotic cell surfaces Pili in certain Gram-positive and Gram-negative bacteria. In Pseudomonas, thought to play a role in adherence and biofilm formation Proteins that form the outermost cell envelope component of a broad spectrum of bacteria, enabling them to adhere to host cell membranes and environmental surfaces in order to colonize. A detectable layer of polysaccharide (rarely polypeptide) on the surface of a bacterial cell which may mediate specific or nonspecific attachment A major virulence factor that acts as an antiphagocytic molecule A distinct cell wall component of the outer membrane of Gramnegative bacteria with the potential structural diversity to mediate specific adherence. Probably functions as an adhesin Cell wall components of Gram-positive bacteria that may be involved

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS
Attachment site
Pharyngeal epithelium
Pellicle of tooth Buccal epithelium of tongue Mucosal epithelium

Bacterium

Adhesin
Protein F Glycosyl transferase

Receptor
Amino terminus of fibronectin Salivary glycoprotein Unknown N-acetylhexosaminegalactose disaccharide Amino terminus of fibronectin Glucosaminegalactose carbohydrate

Disease
Sore throat Dental caries None

Streptococcus pyogenes
Streptococcus mutans

Streptococcus salivarius
Streptococcus pneumoniae Staphylococcus aureus Neisseria gonorrhoeae

Lipoteichoic acid

Cell-bound protein

pneumonia

Cell-bound protein Type IV pili (Nmethylphenylalanine pili)

Mucosal epithelium Urethral/ cervical epithelium

Various

Gonorrhea

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS
Attachment site
Urethral epithelium Upper urinary tract

Bacterium Uropathogenic E. coli Uropathogenic E. coli

Adhesin
Type I fimbriae

Receptor
Complex carbohydrate Globobiose linked to ceramide lipid Galactose on sulfated glycolipids Fucose and mannose carbohydrate Surface protein (fibronectin) Sialic acid

Disease
Urethritis
Pyelonephriti s

P-pili (pap) Fimbriae ("filamentous hemagglutinin") N-methylphenylalanine pili

Bordetella pertussis
Vibrio cholerae Treponema pallidum Mycoplasma

Respiratory epithelium
Intestinal epithelium Mucosal epithelium Respiratory epithelium Conjunctival or

Whooping cough

Cholera

Peptide in outer membrane (P1, P2, P3)


Membrane protein

Syphilis

Pneumonia

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS

INVASINS
bacterial extracellular substances which act against

the host by breaking down primary or secondary defenses of the body.


most are proteins (enzymes) that act locally to

damage host cells and/or have the immediate effect of facilitating the growth and spread of the pathogen.
usually act at a short range and may not actually kill cells as part of their range of activity (unlike exotoxins which are cytotoxic, act at remote sites, and are

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS

Invasin

Bacteria Involved Streptococci, staphylococci and clostridia Clostridium species Vibrio cholerae and Shigella dysenteriae Staphylococcus aureus Staphylococci and streptococci Staphylococcus aureus

Activity Degrades hyaluronic acid of connective tissue Dissolves collagen framework of muscles Degrades neuraminic acid of intestinal mucosa Converts fibrinogen to fibrin which causes clotting Converts plasminogen to plasmin which digests fibrin Disrupts neutrophil membranes and causes discharge of lysosomal granules

Hyaluronidase
Collagenase

Neuraminidase
Coagulase Kinases Leukocidin

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS

Invasin Streptolysin

Bacteria Involved

Activity Repels phagocytes and disrupts phagocyte membrane and causes discharge of lysosomal granules Phospholipases or lecithinases that destroy red blood cells (and other cells) by lysis Destroy lecithin in cell membranes Destroy phospholipids in cell membrane One component (EF) is an adenylate cyclase which causes increased levels of intracellular cyclic AMP One toxin component is an adenylate cyclase that acts

Streptococcus pyogenes
Streptococci, staphylococci and clostridia Clostridium perfringens Clostridium perfringens

Hemolysins Lecithinases Phospholipases

Anthrax EF

Bacillus anthracis

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS

TOXINS
TWO TYPES OF TOXINS
1. EXOTOXIN - Proteins - may be released into the extracellular environment

of pathogenic gram (-) and gram (+) bacteria - bears the name exotoxins, since they are "released" from the bacteria and act on host cells at a distance
2. ENDOTOXIN - Lipopolysaccharides - associated with the cell walls of Gram-negative

bacteria

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS ENDOTOXIN EXOTOXIN


Protein (mw = 50-1000kDa) Extracellular, diffusible Usually (heat-labile)

CHEMICAL NATURE RELATIONSHIP TO CELL DENATURED BY BOILING ANTIGENIC FORM TOXOID POTENCY SPECIFICITY ENZYMATIC ACTIVITY PYROGENICITY

Lipopolysaccharide (mw = 10kDa) Part of outer membrane No (heat stable)

Yes (weakly)
No Relatively low (>100ug) Low degree No Yes

Yes (highly)
Yes Relatively high (1 ug) High degree Usually Occasionally

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS

EXOTOXINS
- are soluble proteins produced by both Gram-

positive and Gram-negative bacteria during exponential growth - are the most potent poisons known and may show activity at very high dilutions - resemble enzymes in a number of ways:
- are soluble proteins - are denatured by heat, acid, proteolytic enzymes - have a high biological activity (most act catalytically) - exhibit specificity of action (e.g. only Clostridium tetani

produces tetanus toxin; Corynebacterium diphtheriae produces the diphtheria toxin) or (terms such as

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS

EXOTOXINS
- can be converted to toxoid since they are

inherently unstable, in time they lose their toxic properties but retain their antigenic ones.
- TOXOIDS
- are detoxified toxins which retain their antigenicity and their

immunizing capacity - use for artificial immunization against diseases caused by pathogens where the primary determinant of bacterial virulence is toxin production - are the immunizing agents against diphtheria and tetanus that are part of the DPT vaccine.

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS

EXOTOXINS
- COMPONENTS: 1. Subunit A - is responsible for the enzymatic activity of the

toxin - enzymatically active and but lack binding and cell entry capability 2. Subunit B - is concerned with binding to a specific receptor on the host cell membrane and transferring the enzyme across the membrane - are nontoxic

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS

EXOTOXINS
- ARRANGEMENTS:
1. A-B or A-5B - indicates that subunits synthesized separately and

associated by noncovalent bonds 2. A/B - denotes subunit domains of a single protein that may be separated by proteolytic cleavage 3. A+B - indicates separate protein subunits that interact at the target cell surface 4. 5B - indicates that the binding domain is composed of 5 identical subunits.

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS

EXOTOXINS
- ATTACHMENT AND MECHANISM OF ENTRY: 1. DIRECT ENTRY
- the B subunit of the native toxin (A+B) binds to a specific

receptor on the target cell and induces the formation of a pore in the membrane through which the A subunit is transferred into the cell cytoplasm.

2. RECEPTOR-MEDIATED ENDOCYTOSIS (RME)


- the native toxin binds to the target cell and the A+B structure

is taken into the cell by endocytosis. The toxin is internalized in the cell in a membrane-enclosed vesicle called an endosome. H+ ions enter the endosome lowering the internal pH which causes the A+B subunits to separate. Somehow, the B subunit affects the release of the A subunit from the endosome so that it will reach its target in the cell cytoplasm. The B subunit remains in the endosome and is recycled to the cell surface.

the native toxin binds to the target cell and the A+B structure is taken into the cell by endocytosis. The toxin is internalized in the cell in a membraneenclosed vesicle called an endosome. H+ ions enter the endosome lowering the internal pH which causes the A+B subunits to separate. Somehow, the B subunit affects the release of the A subunit from the endosome so that it will reach its target in the cell cytoplasm. The B subunit remains in the endosome and

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS

NAME OF TOXIN

BACTERIUM INVOLVED

ACTIVITY Edema Factor (EF) is an adenylate cyclase that causes increased levels in intracellular cyclic AMP in phagocytes and formation of ion-permeable pores in membranes (hemolysis) Acts locally to increase levels of cyclic AMP in phagocytes and formation of ion-permeable pores in membranes (hemolysis) ADP ribosylation of G proteins stimulates adenylate cyclase and increases cAMP in cells of the GI tract, causing secretion of water and electrolytes Similar to cholera toxin Enzymatically cleaves rRNA resulting in inhibition of protein synthesis in susceptible cells Zn++ dependent protease that inhibits neurotransmission at inhibitory synapses resulting in spastic paralysis

Anthrax toxin (EF)


Adenylate cyclase toxin Cholera enterotoxin E. coli LT toxin Shiga toxin Tetanus toxin

Bacillus anthracis

Bordetella pertussis

Vibrio cholerae

Escherichia coli Shigella dysenteriae Clostridium tetani

Diphtheria

Corynebacteriu

ADP ribosylation of elongation factor 2 leads to inhibition

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS
BACTERIUM INVOLVED

NAME OF TOXIN

ACTIVITY

PYROGENIC EXOTOXINS or SUPERANTIGENS - represent a family of molecules with the ability to elicit massive activation of the immune system. - hyperstimulate the immune system leading to shock - cause of toxic shock syndrome (TSST) by Staphylococcus aureus and Streptococcus pyogenes - share the ability to stimulate T cell proliferation by interaction with Class II MHC molecules on APCs and specific V beta chains of the T cell receptor. - the important feature of this interaction is the resultant production of IL-1, TNF, and other lymphokines which are the principal mediators of disease processes associated with these toxins. Staphylococcus enterotoxins Toxic shock syndrome toxin (TSST-1) Pyrogenic exotoxins (SPE) e.g. Erythrogenic toxin Staphylococcu s aureus Staphylococcu s aureus Streptococcus pyogenes Massive activation of the immune system, including lymphocytes and macrophages, leads to emesis (vomiting) Acts on the vascular system causing inflammation, fever and shock

Causes localized erythematous reactions

BACTERIAL PATHOGENESIS

VIRULENCE FACTORS

ENDOTOXINS
- always associated with Gram-negative bacteria as

part of the outer membrane of the cell wall (e.g. E.


coli, Salmonella, Shigella, Pseudomonas, Neisseria, Haemophilus)
- Biological activity is associated with the

lipopolysaccharide. LPS activates complement by the alternative (properdin) pathway:


Lipid component (Lipid A) responsible for toxicity Core (R) polysaccharide components responsible for

immunogenicity (antigenicity) O polysaccharide (O antigens) act as a determinant of virulence in Gram-negative bacteria and responsible for the property of "smoothness" of bacterial cells, which may

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

teps in successful infection:


Sex
comes before disease acquire virulence genes

Stealth
avoid immune system

Strike-back
damage host tissues

Sense environment Switch virulence genes on and off Swim to site of infection

Survive stress

Subvert
host cell cytoskeletal and signalling pathways

Scavenge for nutrients (Iron) Stick to site of infection

Spread through cells and organs Scatter in the environment

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

1.

Bacterial SEX

Acquiring virulence genes


Bacteria have three ways of exchanging DNA
1. Transformation
-

cells directly take up naked DNA

2. Transduction
-

injection of foreign DNA by a bacteriophage into the host bacterium (phages carry DNA)

2. Conjugation
-

transfer of genetic material between two bacterial cells in direct contact through specialised appendages

What are being transferred?


1. Extrachromosomal Mobile Genetic Elements (MGE)

2. Pathogenicity Islands

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

1.

Bacterial SEX
- transfer of these elements result in transfer of virulence

MOBILE GENETIC ELEMENTS

factor 1. Plasmids - eg) TTSSs in Shigella, Yersinia; toxins in Salmonella, E. coli, anthrax
2. Bacteriophage
- eg) botulinum toxins, diphtheria toxin, shiga-like

toxin, staphylococcal toxins, TTSS substrates in Salmonella


3. Transposons

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

1.

Bacterial SEX
- transfer of these elements result in transfer of virulence

MOBILE GENETIC ELEMENTS


VIRULENCE FACTOR & DISEASE factor PLASMID ENCODED 1. Plasmids Heat-labile and heat stable enterotoxins that cause diarrhea Escherichia coli - eg) TTSSs Hemolysin (cyotoxin) of invasivetoxins and urinary tract in Shigella, Yersinia; disease in Escherichia coli infection Salmonella, E. coli, anthrax E. Coli, Shigella sp. 2. Adherence factors and gene products involved in mucosal Bacteriophage invasion

Capsule, edema factor, lethal factor, protective antigen Bacillus anthracisbotulinum toxins, diphtheria toxin, shiga-like - eg)

toxin, staphylococcal toxins, TTSS substrates in PHAGE ENCODED


Clostridium SalmonellaBotulinum toxin that causes paralysis botulinum Corynebactrium diphtheria Vibrio cholerae Diphtheria toxin that inhibits human protein synthesis Cholera toxin that can cause a severe watery diarrhea

3. Transposons

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

1.

Bacterial SEX
- large organized group of genes located on the bacterial

PATHOGENICITY ISLANDS
chromosomes - concept originated from study of uropathogenic E. coli strains - Can encode for secretion system, adhesins, siderophores, toxins - MAJOR PROPERTIES: - have one or more virulence genes - present in the genome of pathogenic members of a specie but absent in the nonpathogenic members - large, usually 10-200 kb - have different guanine plus cytosine content than the rest of the bacterial genome - commonly associated with tRNA genes - found with parts of the genome associated with MGE - have genetic instability (prone to deletion) - represent mosaic structures with component acquired at

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

1.

Bacterial SEX
- large organized group of genes located on the bacterial

PATHOGENICITY ISLANDS
chromosomes PAI VIRULENCE CHARACTERISTICS - concept originated from study of uropathogenic E. coli strains NAME - Can encode for secretion Alpha hemolysin, fimbriae, adhesions in UTI toxins system, adhesins, siderophores, Escherichia coli PAI I536 - MAJOR Escherichia coli PROPERTIES: Alpha hemolysin, P-pilus in UTI PAI IJ96 - have Escherichia coli one or more virulence genes of enterohemorrhagic E. coli Macrophage toxin O1#7 (EHEC) present in the genome of pathogenic members of a specie (EHEC) but Salmonella absent in the nonpathogenic members Invasion and damage of host cell; diarrhea PAI-I typhimurium - large, usually 10-200 kb Yersinia pestis different guanineGenes that enhancecontent than the rest of HPI/pgm - have plus cytosine iron uptake the bacterial genome Vibrio cholerae El Tor Neuraminidase, utilization of amino sugars VPI-1 O1 - commonly associated with tRNA genes SCC - found with genome associated with MGE Staphylococcus aureus parts of theMethicillin and other antiobiotic resistance mec - have genetic instability (prone to deletion) Staphylococcus aureus Toxic shock syndrome toxin-1, enterotoxin SaPI1 - represent mosaic structures with component acquired at

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

2.

SENSE environment
- bacteria can sense changes in environment - Environmental signals often control the expression of the

virulence genes - Temperature - Iron availability - Osmolality - Growth phase - pH - Specific ions (eg Ca2+) - In simplest cases, change in intracellular concentration of ion is linked directly to gene expression - eg) fall in intra-cellular iron levels triggers de-repression of diphtheria toxin gene

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

3.

SWITCH virulence factors on and off


- Changes in DNA sequence - Gene amplification

- Genetic rearrangements
- Transcriptional Regulation - Translational Regulation

- Post-translational Regulation

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

4.

SWIM
- many bacterial pathogens

are motile - eg) Enterics, Campylobacter, Helicobacter, spirochaetes - motility is crucial for virulence in some cases - usual organelle of motility is the flagellum - Variants: - Twitching motility - Swarming

Flagellum of Gram-negative Bacteria

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

5.

STICK
- Colonization/Invasion,

adherence and initial multiplication - to avoid physical/immunological removal, bacteria must adhere to: - cell surfaces and extracellular matrix (in
respiratory tract , GIT, GUT)

- solid surfaces (in teeth, heart valves, prosthetic material)

- Adherence factors and

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

6.

SCAVENGE nutrients
- Iron is needed for bacterial growth making its

bioavailability an important factor in controlling infection especially those with aggressive virulence factors (such as Diphtheria toxin, Shiga-like toxin, Pseudomonas aeruginosa exotoxin A)
- Bacteria require 0.4 4 umol of iron in order to grow

- Free iron levels very low in body fluids


- Acute phase response causes further drop - Iron overload increases susceptibility to infection

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

6.

SCAVENGE nutrients
- Siderophores (MW 500-1000):
- small ligands secreted by some microorganism that

are specific for ferric iron - function to capture iron


- some bacteria without siderophores obtain and utilize iron

by:
- using iron from hemin in the gut of the biting flea (Y.

perstis) - obtain iron from the hosts intracellular iron pools (Legionella, listeria, salmonella)

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

7.

SURVIVE stress
- Nutrient-limitation stress
- Acid stress within stomach - Heat shock during fever - Oxidative stress within phagocytes

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

8.

STEALTH
- ability of the bacteria to bypass or overcome host defense

mechanism by: a. Avoiding contact with phagocytes thru production of antiphagocytic substances on the bacterial surface
- Polysaccharide capsules of S. pneumoniae, H. influenzae, T. -

pallidum & K. pneumoniae M protein and fimbriae of Group A streptococci Surface slime (polysaccharide) produced by P. aeruginosa O antigen associated with LPS of E. coli K antigen of E. coli or the analogous Vi antigen of S. typhi Cell-bound or soluble Protein A produced by S. aureus

b. Evading complement
- elastase enzyme inactivates components of complement by

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

8.

STEALTH
c. Avoiding host immunological responses
- production of IgA proteases (metalloproteases active against

IgA)

d. Immunological tolerance to a bacterial antigen


- Tolerance is a property of the host in which there is an

immunologically-specific reduction in the immune response to a given Ag, which can arise in a number of ways such as: - 1. Fetal exposure to Ag - 2. High persistent doses of circulating Ag - 3. Molecular mimicry.

e. Antigenic mimicry
- e.g. sialic acid capsule of group B meningococcus

f.

Immunosuppression

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

9.

STRIKE-BACK
- Toxigenesis

- Damage host tissue thru production of endotoxin and

exotoxins

10.

SUBVERT
cytoskeleton and signal-transduction pathways

- inject proteins into host cells to subvert or weakens the

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

11.

SPREAD
- within macrophages (eg: typhoid); through blood

- through cells and organs:

(need to be complement-resistant); within cells (eg: actin-based motility of Listeria monocyogenes, depends on ActA protein)

12.

SCATTER
etc.

- Transmission, virulence and evolution - through biting arthopods, shedding into water, airborne,

BACTERIAL PATHOGENESIS

STEPS OF BACTERIAL PATHOGENICITY

CORRESPONDING INFECTIONDISEASE STAGES


INCUBATI ON STAGE
No signs and symptoms

PRODROM AL STAGE
First signs and symptoms Pathogens may be highly communicable

CLINICAL STAGE
Peak of characteristi c signs and symptoms of infection

STAGE OF DECLINE
Condition of host deteriorates possibly to death; or Signs and symptoms begin to subside as host condition improves

CONVALENSCE NT STAGE
Full recovery of surviving host; or Chronic infection develops

NORMAL HUMAN MICROBIOTA

NORMAL FLORA

DEFINITION

NORMAL/INDIGENEOUS FLORA
is the mixture

of microorganisms (bacteria and fungi) that are regularly found STERILE AREAS: Brain at any anatomical site of human body like: CSF
-

Skin Conjunctiva Respiratory tract Oral Cavity External ears Urogenital tract Gastrointestinal tract

Amniotic fluid Bones Heart Liver Lungs Muscle Blood Urinary bladder Middle and inner ear

NORMAL FLORA

NORMAL FLORA

Associations Between Humans and the Normal Flora:


1. MUTUALISTIC/SYMBIOTIC
- both host and organism are thought to derive benefit

from each other

2. PARASITIC
- the organism live at the expense of their host

3. COMMENSAL
- no apparent benefit or harm to either organism or host

4. PATHOGENIC/OPPORTUNISTS
- the organism is capable of producing disease when

hosts defense mechanism breaks down

NORMAL FLORA

NORMAL FLORA

COMPONENTS:

Mainly bacteria Eukaryotic fungi Protists Methanogenic Archaea

NORMAL FLORA

NORMAL FLORA

TWO GROUPS:
1. RESIDENT flora
- fixed types of microorganisms regularly found in a

given area at a given age - if disturbed, it promptly reestablishes itself/ transient microorganisms may colonize, proliferate and produce disease - more important

2. TRANSIENT flora
- non-pathogenic or potentially pathogenic

microorganisms that inhabit the skin or mucous membranes for hours, days, or weeks - derived from the environment, does not produce disease - does not establish itself permanently on the surface - little significance

NORMAL FLORA

NORMAL FLORA

RESIDENT FLORA
- acquired rapidly during & after birth and changes

continuously through out life - Factors influencing composition of normal flora:


- genetics - age - stress - diet - climate - nutrition - geographic location - drug therapy - hormonal changes

- 90% is S. epidermidis; S. aureus, may be in

moist areas

NORMAL FLORA

NORMAL FLORA

BENEFICIAL EFFECTS
- prevent colonization by pathogens by competing for -

attachment sites or for essential nutrients. This is thought to be their most important beneficial effect synthesize and excrete vitamins in excess of their own needs, which can be absorbed as nutrients by their host - eg) enteric bacteria secrete Vitamin K and Vitamin B12, and lactic acid bacteria produce certain Bvitamins may antagonize other bacteria through the production of substances which inhibit or kill nonindigenous species. stimulate the development of certain tissues like the caecum and Peyer's patches in the GI tract stimulate the production of natural antibodies. Low levels of antibodies produced against components of the normal flora are known to cross react with certain related pathogens, and thereby prevent infection or invasion

NORMAL FLORA

NORMAL FLORA

HARMFUL EFFECTS
- Bacterial synergism (cross-feeding) between a member -

of the normal flora and a potential pathogen. This means that one organism is helping another to grow or survive Competition for nutrients. Normal flora in the gastrointestinal tract must absorb some of the host's nutrients for their own needs Induction of a low grade toxemia. Minute amounts of bacterial toxins (e.g. endotoxin) may be found in the circulation and these small amounts of bacterial antigen stimulate the formation of natural antibodies. May be agents of disease. Members of the normal flora may cause endogenous disease if they reach a site or tissue where they cannot be restricted or tolerated by the host defenses Transfer to susceptible hosts. Some pathogens of humans that are members of the normal flora may also

NORMAL FLORA

NORMAL FLORA

SKIN
- majority of skin microorganisms

are found in the most superficial layers of the epidermis and the upper parts of the hair follicles. - Important bacteria: Staphylococcus epidermidis Staphylococcus aureus Micrococcus sp. Propionibacterium acne Mycobacterium smegmatis - Non-bacteria: Pityrosporum (yeast), Demodex spp. (mites)

NORMAL FLORA

NORMAL FLORA

CONJUCTIVA
- Important bacteria:
Staphylococcus epidermidis Neisseria sp.

Corynebacterium sp.
Propoinibacterium acnes Staphylococcus aureus Viridans streptococci Haemophilus influenza

NORMAL FLORA

NORMAL FLORA

EXTERNAL EAR
- Important bacteria:
Staphylococcus epidermidis Staphylococcus aureus

Corynebacterium sp

NORMAL FLORA

NORMAL FLORA

ORAL CAVITY
- Important bacteria: Staphylococci epidermidis Streptococcus sanguis (dental plaque) Streptococcus mutans (dental plaque) Streptococcus salivarius Staphylococci aureus Viridans streptococci Lactobacilli Corynebacterium sp. Bacteroides sp. Actinomyces sp.

NORMAL FLORA

NORMAL FLORA

RESPIRATORY TRACT:
NARES (nostrils)
- Important bacteria: Staphylococcus epidermidis Staphylococcus aureus Neisseria sp. Haemophilus sp Corynebacteria Streptococcus pneumoniae

NORMAL FLORA

NORMAL FLORA

RESPIRATORY TRACT:
URT (nasopharynx)
- Important bacteria: Staphylococcus epidermidis Non-hemolytic streptococci Alpha-hemolytic streptococci Neisseria sp. Streptococcus pneumoniae Streptococcus pyogenes Haemophilus influenzae Neisseria meningitidis

NORMAL FLORA

NORMAL FLORA

RESPIRATORY TRACT:
LRT (trachea, bronchi, and pulmonary tissues):
- usually sterile
- individual may become

susceptible to infection by pathogens descending from the nasopharynx like: H. influenzae S. pneumoniae

NORMAL FLORA

NORMAL FLORA

UROGENITAL TRACT:
ANTERIOR URETHRA
- Important bacteria: Staphylococcus epidermidis Enterococcus faecalis Apha-hemolytic streptococci. Some enteric bacteria (e.g. E. coli, Proteus sp.) Corynebacteria sp. Acinetobacter sp. Mycoplasma sp. Candida sp. Mycobacterium smegmatis

NORMAL FLORA

NORMAL FLORA

UROGENITAL TRACT:
VAGINA
- Important bacteria: Lactobacillus acidophilus Staphylococci Corynebacterium sp. Nonpyogenic streptococci Escherichia coli Flavobacterium sp. Clostridium sp. Viridans streptococci Other Enterobacteria

NORMAL FLORA

NORMAL FLORA

GASTROINTESTINAL TRACT:
SMALL INTESTINE
- Important bacteria: Lactobacilli Enterococcus faecalis Coliforms Bacteroides - At birth, the entire intestinal tract is sterile, but bacteria

enter with the first feed. The initial colonizing bacteria vary with the food source of the infant.

NORMAL FLORA

NORMAL FLORA

GASTROINTESTINAL TRACT:
COLON
- Important bacteria: Enterococci Clostridia Lactobacilli Bacteroides Bifidobacterium (account for >90% in breast-fed infants) Escherichia coli Methanogenic bacteria Viridans streptococci Staphylococcus sp. Proteus sp. Candida albicans (Yeast) Mycoplama sp.

STAPHYLOCOCCI & CORYNEBACTERIA occur at almost every site, skin, conjunctiva, nose, pharynx, mouth, lower GIT, anterior urethra, vagina STAPHYLOCOCCUS EPIDERMIDIS is highly adapted to the diverse environments of its human host STAPHYLOCOCCUS AUREUS is a potential pathogen it is a leading cause of bacterial disease in humans it can be transmitted from the nasal membranes of an asymptomatic carrier to a susceptible host

Staphylococcus aureus

Staphylococcus epidermidis

Many of the normal flora are either pathogens or opportunistic pathogens. The following indicate members of the normal flora that may be considered major pathogens of humans: STAPHYLOCOCCUS AUREUS STREPTOCOCCUS MUTANS ENTEROCOCCUS FAECALIS STREPTOCOCCUS PNEUMONIAE STREPTOCOCCUS PYOGENES NEISSERIA MENINGITIDIS ESCHERICHIA COLI PSEUDOMONAS AERUGINOSA

STREPTOCOCCUS MUTANS is the primary bacterium involved in plaque formation and initiation of dental caries viewed as an opportunistic infection

Streptococcus mutans

Enterococcus faecalis
ENTEROCOCCUS FAECALIS was formerly classified as Streptococcus faecalis has emerged as a significant, antibiotic-resistant, nosocomial pathogen.

STREPTOCOCCUS PNEUMONIAE is present in the upper respiratory tract of about half the population if it invades the lower respiratory tract, it can cause pneumonia causes 95%of all bacterial pneumonia

Streptococcus pneumoniae

Streptococcus pyogenes
STREPTOCOCCUS PYOGENES refers to the Group A, Betahemolytic streptococci cause tonsillitis (strep throat), pneumonia, endocarditis some can lead to rheumatic fever or nephritis which can

NEISSERIA AND OTHER GRAM-NEGATIVE COCCI are frequent inhabitants of the upper respiratory tract, mainly the pharynx Neisseria meningitidis is an important cause of bacterial meningitis Neisseria sp

Pseudomonas aeroginosa
PSEUDOMONAS AERUGINOSA is the quintessential opportunistic pathogen of humans that can invade virtually any tissue it is a leading cause of hospital-acquired (nosocomial) Gram-negative infections, but its source is

ESCHERICHIA COLI is a consistent resident of the small intestine other enteric bacteria that may reside in SI includes Klebsiella, Enterobacter and Citrobacter some strains of E. coli are pathogens that cause intestinal infections, urinary tract infections and neonatal meningitis.

Escherichia coli

Haemophilus influenzae

HAEMOPHILUS INFLUENZAE is a frequent secondary invader to viral influenza the leading cause of meningitis in infants and children until the recent development of the Hflu type

BACTEROIDES in the lower intestinal tractare the Bacteroides, a group of Gram-negative, anaerobic, non-sporeforming bacteria They have been implicated in the initiation colitis and colon cancer Bacteroides fragilis

Lactobacillus acidophilus
LACTOBACILLI contribute to acid formation in the oral cavity that leads to dental caries LACTOBACILLUS ACIDOPHILUS colonizes the vaginal epithelium during childbearing years and establishes the low pH that inhibits the

BIFIDOBACTERIA are Gram (+), nonsporeforming, lactic acid bacteria. They have been described as "friendly" bacteria in the intestine of humans BIFIDOBACTERIUM BIFIDUM is the predominant bacterial species in the intestine of breast-fed infants, where it presumably prevents colonization by potential pathogens. These bacteria are sometimes used in the manufacture of yogurts and are frequently incorporated into probiotics. Bifidobacterium bifidum

CLOSTRIDIUM PERFRINGENS colonize the bowel commonly isolated from feces CLOSTRIDIUM DIFFICILE may colonize the bowel and cause "antibiotic-induced diarrhea" or pseudomembranous colitis CLOSTRIDIUM TETANI "transiently associated" with humans as a component of the normal flora can be isolated from feces in 0 - 25 percent of the population the endospores are probably ingested with food and water, and the bacterium does not

Clostridium perfringens

Clostridium tetani

CORYNEBACTERIA, AND CERTAIN RELATED PROPIONIC ACID BACTERIA are consistent skin flora some have been implicated as a cause of acne

CORYNEBACTERIUM DIPHTHERIAE causative agent of diphtheria considered a member of the normal flora before the widespread use of the diphtheria toxoid, which is used to immunize against the disease.

Propionibacterium acne Corynecbacterium diphtheriae

PROPHYLAXIS

PROPHYLAXIS

DEFINITION

IMMUNIZATION
administration of an individual with

antibodies possessing power to destroy or inactivate the disease producing agent or neutralize its toxin
ULTIMATE GOAL: eradication of the disease IMMEDIATE GOAL: prevention of the

disease in an individual

PROPHYLAXIS

IMMUNIZATION

TWO TYPES OF IMMUNIZATION


1. ACTIVE IMMUNIZATION 2. PASSIVE IMMUNIZATION

PROPHYLAXIS

IMMUNIZATION

ACTIVE IMMUNIZATION
involves the administration of all or part of a

microorganism (Ag) or a modified product of that microorganism to evoke an immunologic response that mimics the natural infection, but this infection usually presents with little or no risk to the recipient.
some immunizing agent may produce

lifelong protection and some only provide partial protection, thus, must be readministered at regular intervals to maintain protection.

PROPHYLAXIS

IMMUNIZATION

PASSIVE IMMUNIZATION
administration of exogenously produced or

preformed antibody (Ig)


provides temporary protection Artificial Ig: tetanus, measles, chicken pox,

rabies, rubella Natural Ig: through transplacental transmission of antibody to a fetus providing protection against many infectious diseases for the first 3-6 months of the infant's life.

PROPHYLAXIS

IMMUNIZATION

TYPES OF VACCINES
1. 2. 3. 4. 5. 6. 7.

Inactivated or killed vaccines Attenuated or live vaccines Subunit vaccines Toxoids Conjugate vaccines Recombinant vaccines DNA vaccines

PROPHYLAXIS

IMMUNIZATION

1.

INACTIVATED/KILLED VACCINES
of virus and bacteria or those that are conjugated chemically to be immunobiologically active proteins. not capable of replicating in the host must contain a sufficient antigenic mass to stimulate a desired response may require periodic administration of booster doses for maintenance of long lasting immunity immune response is mostly humoral or antibodymediated

these are usually inactivated or purified components

PROPHYLAXIS

IMMUNIZATION

2.

ATTENUATED/LIVE VACCINES

this are attenuated or weakened form of the wild

virus or bacteria that induce an immunologic response simulating the response to natural infection. produces the active infection by viral replication however, these produces little or no adverse reaction to the host. these organisms multiply in the recipient until the desired immune response occurs conferring lifelong protection with a single immunizing dose.

PROPHYLAXIS

IMMUNIZATION

3.

SUBUNIT VACCINE
microorganism to create an immune response

are fragment of inactivated or attenuated

eg) meningococcal, pneumococcal

PROPHYLAXIS

IMMUNIZATION

4.

CONJUGATE VACCINE
coats (which are poorly immunogenic) of microorganism with proteins (like toxins) to become highly immunogenic.

combining or linking of the polysaccharide outer

eg) Hib , pneumococcal (Prevnar)

PROPHYLAXIS

IMMUNIZATION

5.

RECOMBINANT VACCINE
and the DNA of other microorganism

combining the physiology of one microorganism

eg) Hepatitis B, Human Papilloma (Gardasil,

Cervarix)

PROPHYLAXIS

IMMUNIZATION

6.

TOXOID
render them non-toxic but still immunogenic

are chemically or thermally modified toxins to

eg) diphtheria, tetanus

PROPHYLAXIS

IMMUNIZATION

7.

DNA VACCINE

created from an infectious agents DNA it works by insertion (and expressiom, triggering

immune system recognition) into human or animal cells, of viral or bacterial DNA still experimental

PROPHYLAXIS

SITE & ROUTE OF ADMINISTRATION

1.

2.
3. 4. 5.

ORAL INTRAMUSCULAR SUBCUTANEOUS INTRADERMAL INTRANASAL

PROPHYLAXIS

SITE & ROUTE OF ADMINISTRATION

1.

PER OREM
most common eg) OPV, rotavirus

2.

INTRAMUSCULAR
based on volume and size of the muscle ANTEROLATERAL ASPECT of the THIGH: < 1

year of age DELTOID AREA: older children and adults BUTTOCKS: rarely used eg) DTP, Hepatitis B vaccines

PROPHYLAXIS

SITE & ROUTE OF ADMINISTRATION

3.

SUBCUTANEOUS
45 angle into the anterolateral aspect of the

thigh or upper outer triceps eg) Measles, MMR

4.

INTRADERMAL
Volar aspect of the forearm eg) Rabies (pre-exposure) and BCG

5.

INTRANASAL
Upright position, 0.25 mL is sprayed into one

nostril, the 2nd half is administered to the other nostril. eg) Live attenuated influenza vaccine

PROPHYLAXIS

CONTRAINDICATIONS

ABSOLUTE

RELATIVE

NOT

Severe anaphylactic reaction or allergic reaction to previous vaccine Encephalopathy within 7 days of administration (Pertussis)

Immunosuppressive therapy Egg allergy Seizure within 3 days of last dose (Pertussis) Shock within 48 hrs of last dose Fever >/+ 40.5 C within 48 hours of last dose

Mild illness with or without low grade fever Current antibiotic therapy Recent infectious disease Positive PPD Prematurity, except in infants still hospitalized at 2 mos, OPV should be delayed until discharge. OR, if mother is HBsAg (-), Hep B vaccine delayed until child >2000gm

PROPHYLAXIS

SCHEDULE

PROPHYLAXIS

IMMUNIZATION

EXPANDED IMMUNIZATION PROGRAM (EPI)


Main Objectives: To reduce the morbidity and mortality rates of

the seven EPI diseases which are: Poliomyelitis, Measles, Diphtheria, Pertussis, Tetanus, Tuberculosis, Hepatitis B
To reduce the incidence of neonatal tetanus by

providing pregnant women with tetanus toxoid immunization

PROPHYLAXIS

EXPANDED IMMUNIZATION PROGRAM

VACCINE

AGE

INTERVAL

AMOUNT

SITE/ROUTE

BOOSTER

BCG 1 dose

At birth

If >2 monthsdo PPD 1st before giving BCG 4 weeks

NB: 0.05 ml >1mo: 0.1 ml

ID at deltoid area

DPT 3 doses

6 weeks

0.5ml

IM at anterolateral thigh

1st- 1 yr after the last dose 2nd- 4-6 y/o

OPV 3 doses
HEPA B 3 doses MEASLES 1 dose

6 weeks

4 weeks

0.5 ml

mouth

1st- 1 yr after the last dose 2nd- 4-6 y/o


HEPA B 3 doses MMR 1st-6 mo after measles 2nd-4- 6 y/o or 11-14 y/o

At birth

1-2 months and 6-8 mos

0.5ml

IM at anterolateral thigh SQ, thigh

6 months / 9 months

0.5 ml

PROPHYLAXIS

VACCINE

BACILLE CALMETTE GUERIN (BCG)


BCG vaccines are live vaccine from attenuated strains of

Mycobacterium bovis
the WHO recommends that all children in countries with high

incidence of TB infection should be immunized with a single dose of BCG at or soon after birth. does not prevent infection with pulmonary TB but prevents extra-pulmonary manifestations of tuberculosis (Military TB, TB meningitis) protection from PTB: 65% protection from Extra-pulmonary TB: 85%

PROPHYLAXIS

VACCINE

BACILLE CALMETTE GUERIN (BCG)


AGE/ INTERVAL AMOUNT SITE/ROUTE BOOSTER ADVERSE REACTION

single dose given at birth:


<1month:

newborn:

0.05 ml
>1month:

intraderma none l at deltoid area

Kochs

0.05

cc
>

0.1 ml

1 month: 0.1cc

at

2nd month of age: do PPD 1st

phenomenon: accelerated BCG reaction Indolent ulcers: ulceration of more than 3 weeks subcutaneous abscess & lymphadenopathy osteomyelitis & muscle necrosis uncommonly (1-2%) result in local adverse reactions

PROPHYLAXIS

VACCINE

BACILLE CALMETTE GUERIN (BCG)


NATURAL COURSE:
Wheal formation: disappears after 30 minutes of

injection Induration: occurs after 2-3 weeks of injection Pustule formation: after 2-3 weeks of induration Ulceration: after 2-3 weeks of pustule formation Scar formation: after 8-12 weeks after injection

PROPHYLAXIS

VACCINE

DIPHTHERIA, PERTUSSIS & TETANUS (DPT)


is a combination vaccine composed of a diphtheria,

pertussis and tetanus components.


Inactivated vaccine

PROPHYLAXIS

VACCINE

DIPHTHERIA, PERTUSSIS & TETANUS (DPT)


AGE/ INTERVAL AMOUNT SITE/ROUT E BOOSTER ADVERSE REACTION

3 doses given as early as 6 weeks old at 4 weeks apart

0.5

cc

IM

2 doses: 1st: 1 year after the last dose


2nd:

Local

4-6 years old

& febrile reactions Bacterial or sterile abscesses at the site of injection Allergic reactions Seizures Hypotonic hyporesponsive episodes (HHE) collapse or shocklike state Fever of 40.5C Incessant crying

PROPHYLAXIS

VACCINE

POLIO VACCINE (OPV/IPV)


The Live Oral Polio Vaccine (OPV) composed of an attenuated poliovirus types 1, 2 and 3 derived from monkey kidney cell cultures contains trace quantities of streptomycin & neomycin. 3 doses confers a sustained, probably lifelong immunity.
The Inactivated Polio Vaccine (IPV) contains 3 types of poliovirus types 1, 2 and 3 derived from monkey kidney or human diploid cells inactivated with formaldehyde has trace amounts of streptomycin, neomycin & polymyxin B. lifelong immunity. inhibits pharyngeal acquisition of poliovirus & has a lesser extent of intestinal acquisition of the virus.

PROPHYLAXIS

VACCINE

POLIO VACCINE (OPV/IPV)


AGE/ INTERVAL AMOUNT SITE/ROU TE
IPV:

BOOSTER

ADVERSE REACTION

3 doses given as early as 6 weeks old at 4 weeks apart

IPV:

0.5 cc
OPV:

IM
OPV:

2 doses: 1st: 1 year after the last dose


2nd:

IPV: hypersensitivity reaction OPV: vaccine-associated paralytic polio (VAPP)

2 drops

PO 4-6 years old

PROPHYLAXIS

VACCINE

MEASLES
Measles vaccine is a live attenuated vaccine from

strains prepared in chick embryo cell culture

PROPHYLAXIS

VACCINE

MEASLES
AGE/ INTERVAL AMOUNT SITE/ROUT E BOOSTER ADVERSE REACTION

3 doses: 1st: 6-12 months old 2nd: 6 months after the first dose 3rd: 4-6 years old

0.5 cc

SC

none

Fever after 5-7 days from the time of injection Local swelling or pain from site of injection Rashes

PASSIVE IMMUNIZATION with measles immunoglobulin is

preferred in susceptible and immuno-compromised patients Give immunoglobulin within 6 days after exposure Dose: 0.25cc/kg, IM or IVIG at a dose of 100-400 mg/kg

PROPHYLAXIS

VACCINE

HEPATITIS B VACCINE
Killed/ inactivated vaccine
WHO recommendation that in any country whose

carrier rate is >2% should immunize their infants against Hepa B at birth Routine Pre-Exposure Immunization All infants at or soon after birth (0-2 months) All children by 11-12 years of age Older persons in certain high-risk groups

PROPHYLAXIS

VACCINE

HEPATITIS B VACCINE
AGE/ INTERVAL AMOUNT SITE/ROUT E BOOSTER ADVERSE REACTION

3 doses: (0-1-6 0.5 cc mo) 1st: at birth 2nd: 1 month after 1st dose 3rd: 6 months after 1st dose

IM

none

Pain

at the injection site Fever (>37.7C) Allergic reactions

PROPHYLAXIS

VACCINE

HAEMOPHILUS INFLUENZAE TYPE B (Hib)


Inactivated vaccine

The WHO now recommends that Hib vaccine should

be included as appropriate to national capacities and priorities in routine infant immunization because Haemophilus influenzae remains to be the most common cause of meningitis in the first year of life.

PROPHYLAXIS

VACCINE

HAEMOPHILUS INFLUENZAE TYPE B (Hib)


AGE/ INTERVAL AMOUNT SITE/ROUT E BOOSTER ADVERSE REACTION

3 doses given as early as 2 months old, at 2 months apart:


If

0.5 cc

IM

Single dose at 1 year of age

Pain

at the injection site

first given at 6 months old, 2 doses is enough If first given at 1 year old, single dose is enough >5 years old, no longer advisable

PROPHYLAXIS

VACCINE

VARICELLA VACCINE
The AAP and PPS recommends the universal

immunization for all healthy infants 12 months old and susceptible older children and adolescents of varicella vaccine

The recommendation for the post-exposure

prophylaxis administration of varicella vaccine to susceptible children is within 72 hours to 120 hours after exposure to prevent or significantly modify the disease.

PROPHYLAXIS

VACCINE

VARICELLA VACCINE
AGE/ INTERVAL AMOUNT SITE/ROUT E BOOSTER ADVERSE REACTION

3 doses: 1st: 1 year old 2nd: 4-6 years old 3rd: 13 years old
If

0.5 cc

SC or IM

none

Pain

at the injection site

first given at >13 years old, 2 doses is given at 1 month interval

PROPHYLAXIS

VACCINE

TYPHOID VACCINE
The WHO recommends the administration of typhoid

vaccine to those people living in endemic areas. In the Philippines the recommended age of administration is 2 years old given intramuscularly.
AGE/ INTERVAL AMOUNT SITE/ROUT E BOOSTER ADVERSE REACTION
Pain

single dose given 0.5 cc at 2 years of age

IM

single dose at 2-3 years of age

at the injection

site

PROPHYLAXIS

VACCINE

PNEUMOCOCCAL VACCINE
Types:
1. 23-Valent Polysaccharide vaccine which is given

in children 2 years and older 2. 7- valent conjugate polysaccharide vaccine which could be given in infants as early as 2 months old.
These vaccines are associated with the reduction in

nasopharyngeal carriage with vaccine-type organisms but does not however, prevent the occurrence of Otitis Media.

PROPHYLAXIS

VACCINE

PNEUMOCOCCAL VACCINE
AGE/ INTERVAL AMOUNT SITE/ROUT E BOOSTER ADVERSE REACTION

3 doses given as early as 2 months old, at 2 months apart:

0.5 cc

SC or IM

Single dose at 1 year after the 3rd dose

Mild

erythema Pain at injection site Fever

PROPHYLAXIS

VACCINE

MENINGOCOCCAL VACCINE
Routine immunization is NOT recommended:
Indicated for children >2 year old in high-risk groups: Functional or anatomic asplenia

Terminal component or properdin deficiency


Beneficial for travelers to hyperendemic countries
AGE/ INTERVAL AMOUNT SITE/ROUT E BOOSTER ADVERSE REACTION
Pain

single dose given 0.5 cc at 2 years of age

IM

single dose at 2-3 years of age

at the injection

site

THANK YOU GOOD DAY

Kathleen Ross S. Caligagan, MD, FPSNM