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Kathleen Ross S. Caligagan, MD, FPSNM
PATHOGENESIS OF BACTERIALINFECTIONNORMAL HUMAN MICROBIOTA
PROPHYLAXIS
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PATHOGENESIS OFBACTERIALINFECTION
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PATHOGEN is a microorganism that isable to cause disease in a plant, animalor insect.
PATHOGENECITY is the ability toproduce 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 adisease. It is determined by the genetic orbiochemical or structural features of the microbe.
BACTERIAL PATHOGENESISTERMINOLOGIES
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KOCH’S POSTULATES • Bacillus anthracis is the first
microorganism to satisfy Koch’s postulatesin 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 PATHOGENESISID BACTERIA THAT CAUSE DISEASE
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Evidence for a potential pathogenbeing 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 topathogen
- Fits with clinical picture
BACTERIAL PATHOGENESISID BACTERIA THAT CAUSE DISEASE
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- Adherence factors- Invasins- Toxins
- Enzymes- Antiphagocytic factors- Intracellular pathogenecity
- Antigenic heterogeneity- Iron requirement- Bacterial biofilms
BACTERIAL PATHOGENESISVIRULENCE FACTORS
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ADHERENCE FACTORS
• Bacterial adherence to mucosal surfacesrequires the participation of two factors:
1. RECEPTOR - a complementary macromolecular
binding site on a (eucaryotic) surfacethat binds specific adhesins or ligands
2. LIGAND, called ADHESIN- macromolecular component of the
bacterial cell surface which interactswith the host cell receptor.
BACTERIAL PATHOGENESISVIRULENCE FACTORS
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BACTERIAL PATHOGENESISVIRULENCE FACTORS
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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 bacterialcapsule
2. SPECIFIC ADHERENCE:- reversible permanent attachment of the microorganism to the surface
- sometimes called "anchoring"- specific adherence involves permanent formation of many specific
BACTERIAL PATHOGENESISVIRULENCE FACTORS
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BACTERIAL PATHOGENESISVIRULENCE FACTORS
COMPONENTS DESCRIPTION
FimbriaeFilamentous proteins on the surface of bacterial cells that maybehave as adhesins for specific adherence
Common pili Same as fimbriae
Sex pilus A specialized pilus that binds mating procaryotes together for thepurpose of DNA transfer
Type 1 fimbriae Fimbriae in Enterobacteriaceae which bind specifically to mannoseterminated glycoproteins on eucaryotic cell surfaces
Type 4 piliPili in certain Gram-positive and Gram-negative bacteria.In Pseudomonas, thought to play a role in adherence and biofilmformation
S-layerProteins that form the outermost cell envelope component of a broadspectrum of bacteria, enabling them to adhere to host cellmembranes and environmental surfaces in order to colonize.
Capsule A detectable layer of polysaccharide (rarely polypeptide) on thesurface of a bacterial cell which may mediate specific or nonspecificattachment
M protein A major virulence factor that acts as an antiphagocytic molecule
Lipopolysaccharide(LPS)
A distinct cell wall component of the outer membrane of Gram-negative bacteria with the potential structural diversity to mediate
specific adherence. Probably functions as an adhesinTeichoic acids Cell wall components of Gram-positive bacteria that may be involved
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BACTERIAL PATHOGENESISVIRULENCE FACTORS
Bacterium Adhesin ReceptorAttachmentsite Disease
Streptococcus pyogenes
Protein FAminoterminus offibronectin
Pharyngealepithelium Sore throat
Streptococcus
mutans
Glycosyltransferase
Salivaryglycoprotein Pellicle of tooth Dental
caries
Streptococcus salivarius
Lipoteichoicacid Unknown
Buccalepithelium oftongue
None
Streptococcus
pneumoniae
Cell-bound
protein
N-acetylhexos-amine-
galactosedisaccharide
Mucosal
epitheliumpneumonia
Staphylococcus aureus
Cell-boundprotein
Aminoterminus offibronectin
Mucosalepithelium Various
Neisseria gonorrhoeae
Type IV pili (N-
methylphenyl-alanine pili)
Glucosamine-
galactosecarbohydrate
Urethral/
cervicalepithelium
Gonorrhea
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BACTERIAL PATHOGENESISVIRULENCE FACTORS
Bacterium Adhesin ReceptorAttachmentsite Disease
UropathogenicE. coli
Type I fimbriae Complexcarbohydrate
Urethralepithelium Urethritis
UropathogenicE. coli
P-pili (pap)Globobioselinked to
ceramide lipid
Upper urinarytract
Pyelonephritis
Bordetella pertussis
Fimbriae("filamentoushemagglutinin")
Galactose onsulfatedglycolipids
Respiratoryepithelium
Whoopingcough
Vibrio cholerae N-methylphenyl-alanine pili
Fucose andmannose
carbohydrate
Intestinalepithelium Cholera
Treponema pallidum
Peptide in outermembrane (P1,P2, P3)
Surface protein(fibronectin)
Mucosalepithelium Syphilis
Mycoplasma Membraneprotein Sialic acid Respiratory
epithelium Pneumonia
Conjunctival or
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INVASINS
• bacterial extracellular substances which act againstthe host by breaking down primary or secondarydefenses of the body.
• most are proteins (enzymes) that act locally todamage host cells and/or have the immediateeffect of facilitating the growth and spread of thepathogen.
• usually act at a short range and may not actually
kill cells as part of their range of activity (unlikeexotoxins which are cytotoxic, act at remote sites, and are
BACTERIAL PATHOGENESISVIRULENCE FACTORS
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BACTERIAL PATHOGENESISVIRULENCE FACTORS
Invasin Bacteria Involved Activity
HyaluronidaseStreptococci,staphylococci andclostridia
Degrades hyaluronic acid ofconnective tissue
Collagenase Clostridium species Dissolves collagen framework ofmuscles
NeuraminidaseVibrio cholerae andShigella dysenteriae
Degrades neuraminic acid ofintestinal mucosa
Coagulase Staphylococcus aureus Converts fibrinogen to fibrinwhich causes clotting
KinasesStaphylococci andstreptococci
Converts plasminogen to plasminwhich digests fibrin
Leukocidin Staphylococcus aureusDisrupts neutrophil membranesand causes discharge oflysosomal granules
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BACTERIAL PATHOGENESISVIRULENCE FACTORS
Invasin Bacteria Involved Activity
Streptolysin Streptococcuspyogenes
Repels phagocytes and disruptsphagocyte membrane andcauses discharge of lysosomalgranules
HemolysinsStreptococci,staphylococci andclostridia
Phospholipases or lecithinasesthat destroy red blood cells (andother cells) by lysis
Lecithinases Clostridium perfringens Destroy lecithin in cellmembranes
Phospholipases Clostridium perfringens
Destroy phospholipids in cellmembrane
Anthrax EF Bacillus anthracis
One component (EF) is anadenylate cyclase which causesincreased levels of intracellularcyclic AMP
One toxin component is anadenylate cyclase that acts
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TOXINS• TWO TYPES OF TOXINS
1. EXOTOXIN- Proteins
- may be released into the extracellular environmentof pathogenic gram (-) and gram (+) bacteria- bears the name exotoxins, since they are
"released" from the bacteria and act on host cellsat a distance
2. ENDOTOXIN- Lipopolysaccharides- associated with the cell walls of Gram-negative
bacteria-
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BACTERIAL PATHOGENESISVIRULENCE FACTORS
ENDOTOXIN Lipopolysaccharide
(mw = 10kDa)
Part of outer membrane
No (heat stable)Yes (weakly)
No
Relatively low (>100ug)
Low degree
No
Yes
CHEMICALNATURE
RELATIONSHIP TOCELL
DENATURED BY
BOILING ANTIGENIC
FORM TOXOID
POTENCY
SPECIFICITY
ENZYMATICACTIVITY
PYROGENICITY
EXOTOXIN Protein
(mw = 50-1000kDa)
Extracellular, diffusible
Usually (heat-labile)Yes (highly)
Yes
Relatively high (1 ug)
High degree
Usually
Occasionally
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EXOTOXINS- are soluble proteins produced by both Gram-positive and Gram-negative bacteria duringexponential growth
- are the most potent poisons known and may showactivity 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 diphtheriaeproduces the diphtheria toxin) or (terms such as
BACTERIAL PATHOGENESISVIRULENCE FACTORS
BACTERIAL PATHOGENESIS
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EXOTOXINS- can be converted to toxoid since they are
inherently unstable, in time they lose their toxicproperties 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 bacterialvirulence is toxin production
- are the immunizing agents against diphtheria and tetanus
that are part of the DPT vaccine.
BACTERIAL PATHOGENESISVIRULENCE FACTORS
BACTERIAL PATHOGENESIS
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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 theenzyme across the membrane
- are nontoxic
BACTERIAL PATHOGENESISVIRULENCE FACTORS
BACTERIAL PATHOGENESIS
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EXOTOXINS- ARRANGEMENTS:
1. A-B or A-5B- indicates that subunits synthesized separately and
associated by noncovalent bonds2. A/B
- denotes subunit domains of a single protein thatmay be separated by proteolytic cleavage
3. A+B
- indicates separate protein subunits that interact atthe target cell surface4. 5B
- indicates that the binding domain is composed of 5identical subunits.
BACTERIAL PATHOGENESISVIRULENCE FACTORS
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BACTERIAL PATHOGENESIS
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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 apore in the membrane through which the A subunit istransferred 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 internalizedin the cell in a membrane-enclosed vesicle called anendosome. H+ ions enter the endosome lowering the internalpH which causes the A+B subunits to separate. Somehow,the B subunit affects the release of the A subunit from theendosome so that it will reach its target in the cell cytoplasm.The B subunit remains in the endosome and is recycled tothe cell surface.
BACTERIAL PATHOGENESISVIRULENCE FACTORS
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the native toxin bindsto the target cell andthe A+B structure istaken into the cell by
endocytosis. The toxinis internalized in thecell in a membrane-enclosed vesiclecalled an endosome.H+ ions enter the
endosome loweringthe internal pH whichcauses the A+Bsubunits to separate.Somehow, the Bsubunit affects therelease of the Asubunit from theendosome so that itwill reach its target inthe cell cytoplasm.The B subunit remainsin the endosome and
BACTERIAL PATHOGENESIS
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BACTERIAL PATHOGENESISVIRULENCE FACTORS
NAME OF
TOXIN
BACTERIUM
INVOLVEDACTIVITY
Anthraxtoxin (EF)
Bacillusanthracis
Edema Factor (EF) is an adenylate cyclase that causesincreased levels in intracellular cyclic AMP in phagocytesand formation of ion-permeable pores in membranes(hemolysis)
Adenylate
cyclasetoxin
Bordetellapertussis
Acts locally to increase levels of cyclic AMP in
phagocytes and formation of ion-permeable pores inmembranes (hemolysis)
Choleraenterotoxin
Vibrio choleraeADP ribosylation of G proteins stimulates adenylatecyclase and increases cAMP in cells of the GI tract,causing secretion of water and electrolytes
E. coli LT
toxinEscherichia coli Similar to cholera toxin
Shiga toxinShigelladysenteriae
Enzymatically cleaves rRNA resulting in inhibition ofprotein synthesis in susceptible cells
Tetanustoxin
Clostridiumtetani
Zn++ dependent protease that inhibitsneurotransmission at inhibitory synapses resulting inspastic paralysis
Diphtheria Corynebacteriu ADP ribosylation of elongation factor 2 leads to inhibition
BACTERIAL PATHOGENESIS
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BACTERIAL PATHOGENESISVIRULENCE FACTORS
NAME OF TOXIN BACTERIUM
INVOLVEDACTIVITY
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 withthese toxins .
Staphylococcusenterotoxins Staphylococcus aureus
Massive activation of the immune system,including lymphocytes and macrophages,leads to emesis (vomiting)
Toxic shock syndrometoxin (TSST-1)
Staphylococcus aureus
Acts on the vascular system causinginflammation, fever and shock
Pyrogenic exotoxins(SPE) e.g.Erythrogenic toxin
Streptococcuspyogenes Causes localized erythematous reactions
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BACTERIAL PATHOGENESIS
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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 bythe 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 theproperty of "smoothness" of bacterial cells, which may
BACTERIAL PATHOGENESISVIRULENCE FACTORS
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BACTERIAL PATHOGENESIS
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teps in successful infection:
BACTERIAL PATHOGENESISSTEPS OF BACTERIAL PATHOGENICITY
S ex• comes beforedisease• acquire virulencegenes
S ense environment
S witch virulencegenes on and off
S wim to site ofinfection
S tick to site ofinfection
S cavenge fornutrients (Iron)
S urvive stress
S tealth• avoid immunesystem
S trike-back• damage hosttissues
S ubvert• host cellcytoskeletal andsignalling pathways
S pread throughcells and organs
S catter in theenvironment
BACTERIAL PATHOGENESIS
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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
STEPS OF BACTERIAL PATHOGENICITY
BACTERIAL PATHOGENESIS
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1. Bacterial SEX• MOBILE GENETIC ELEMENTS
- transfer of these elements result in transfer of virulencefactor
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 inSalmonella
3. Transposons
STEPS OF BACTERIAL PATHOGENICITY
BACTERIAL PATHOGENESIS
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1. Bacterial SEX• MOBILE GENETIC ELEMENTS
- transfer of these elements result in transfer of virulencefactor
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 inSalmonella
3. Transposons
STEPS OF BACTERIAL PATHOGENICITY
VIRULENCE FACTOR & DISEASE
PLASMID ENCODEDEscherichia coli Heat-labile and heat stable enterotoxins that cause diarrhea
Escherichia coliHemolysin (cyotoxin) of invasive disease and urinary tractinfection
E. Coli, Shigella sp.Adherence factors and gene products involved in mucosalinvasion
Bacillus anthracis Capsule, edema factor, lethal factor, protective antigen
PHAGE ENCODEDClostridium botulinum Botulinum toxin that causes paralysis
Corynebactriumdiphtheria
Diphtheria toxin that inhibits human protein synthesis
Vibrio cholerae Cholera toxin that can cause a severe watery diarrhea
BACTERIAL PATHOGENESIS
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1. Bacterial SEX• PATHOGENICITY ISLANDS
- large organized group of genes located on the bacterialchromosomes
- 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 ofthe bacterial genome
- commonly associated with tRNA genes- found with parts of the genome associated with MGE
- have genetic instability (prone to deletion)- re resent mosaic structures with com onent ac uired at
STEPS OF BACTERIAL PATHOGENICITY
BACTERIAL PATHOGENESIS
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1. Bacterial SEX• PATHOGENICITY ISLANDS
- large organized group of genes located on the bacterialchromosomes
- 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 ofthe bacterial genome
- commonly associated with tRNA genes- found with parts of the genome associated with MGE
- have genetic instability (prone to deletion)- re resent mosaic structures with com onent ac uired at
STEPS OF BACTERIAL PATHOGENICITY
PAINAME VIRULENCE CHARACTERISTICS
Escherichia coli PAI I536
Alpha hemolysin, fimbriae, adhesions in UTIEscherichia coli PAI I J96 Alpha hemolysin, P-pilus in UTI
Escherichia coli(EHEC) O1#7
Macrophage toxin of enterohemorrhagic E. coli(EHEC)
Salmonellatyphimurium PAI-I Invasion and damage of host cell; diarrhea
Yersinia pestis HPI/pgm Genes that enhance iron uptake
Vibrio cholerae El TorO1 VPI-1 Neuraminidase, utilization of amino sugars
Staphylococcus aureus SCCmec
Methicillin and other antiobiotic resistance
Staphylococcus aureus SaPI1 Toxic shock syndrome toxin-1, enterotoxin
BACTERIAL PATHOGENESIS
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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
STEPS OF BACTERIAL PATHOGENICITY
BACTERIAL PATHOGENESIS
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3. SWITCH virulence factors on andoff
- Changes in DNA sequence- Gene amplification- Genetic rearrangements
- Transcriptional Regulation
- Translational Regulation- Post-translational Regulation
STEPS OF BACTERIAL PATHOGENICITY
BACTERIAL PATHOGENESIS
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4. SWIM
- many bacterial pathogensare motile
- eg) Enterics,Campylobacter,Helicobacter,spirochaetes
- motility is crucial for
virulence in some cases- usual organelle of motility isthe flagellum
- Variants:- Twitching motility- Swarmin
STEPS OF BACTERIAL PATHOGENICITY
Flagellum of Gram-negativeBacteria
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BACTERIAL PATHOGENESIS
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5. STICK
- Colonization/Invasion,adherence and initialmultiplication
- to avoidphysical/immunologicalremoval, bacteria mustadhere to:
- cell surfaces andextracellular matrix (inrespiratory tract , GIT, GUT)
- solid surfaces (in teeth,heart valves, prostheticmaterial)
- Adherence factors and
STEPS OF BACTERIAL PATHOGENICITY
BACTERIAL PATHOGENESIS
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6. SCAVENGE nutrients
- Iron is needed for bacterial growth making itsbioavailability an important factor in controlling infectionespecially those with aggressive virulence factors (suchas Diphtheria toxin, Shiga-like toxin, Pseudomonasaeruginosa 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
STEPS OF BACTERIAL PATHOGENICITY
BACTERIAL PATHOGENESIS
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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 ironby:
- using iron from hemin in the gut of the biting flea (Y.perstis)
- obtain iron from the host’s intracellular iron pools(Legionella, listeria, salmonella)
STEPS OF BACTERIAL PATHOGENICITY
BACTERIAL PATHOGENESISS S O AC A A OG C
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7. SURVIVE stress
- Nutrient-limitation stress- Acid stress within stomach
- Heat shock during fever- Oxidative stress within phagocytes
STEPS OF BACTERIAL PATHOGENICITY
BACTERIAL PATHOGENESISSTEPS OF BACTERIAL PATHOGENICITY
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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
STEPS OF BACTERIAL PATHOGENICITY
BACTERIAL PATHOGENESISSTEPS OF BACTERIAL PATHOGENICITY
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8. STEALTH c. Avoiding host immunological responses
- production of IgA proteases (metalloproteases active againstIgA)
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 toa 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-
STEPS OF BACTERIAL PATHOGENICITY
BACTERIAL PATHOGENESISSTEPS OF BACTERIAL PATHOGENICITY
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9. STRIKE-BACK - Toxigenesis- Damage host tissue thru production of endotoxin and
exotoxins
10. SUBVERT - inject proteins into host cells to subvert or weakens the
cytoskeleton and signal-transduction pathways
STEPS OF BACTERIAL PATHOGENICITY
BACTERIAL PATHOGENESISSTEPS OF BACTERIAL PATHOGENICITY
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11. SPREAD- through cells and organs:
- within macrophages (eg: typhoid); through blood(need to be complement-resistant); within cells (eg:actin-based motility of Listeria monocyogenes,
depends on ActA protein)
12. SCATTER - Transmission, virulence and evolution- through biting arthopods, shedding into water, airborne,
etc.
STEPS OF BACTERIAL PATHOGENICITY
BACTERIAL PATHOGENESISSTEPS OF BACTERIAL PATHOGENICITY
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CORRESPONDING INFECTION-DISEASE STAGES
STEPS OF BACTERIAL PATHOGENICITY
INCUBATION STAGE• No signs and
symptoms
PRODROMAL STAGE• First signs and
symptoms• Pathogens
may be highlycommunicable
CLINICALSTAGE• Peak of
characteristic signs andsymptomsof infection
STAGE OFDECLINE• Condition of
hostdeterioratespossibly todeath; or
• Signs andsymptomsbegin to
subside ashostconditionimproves
CONVALENSCENT STAGE• Full recovery of
surviving host; or• Chronic infection
develops
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NORMAL HUMANMICROBIOTA
NORMAL FLORADEFINITION
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NORMAL/INDIGENEOUSFLORA
• is the mixture of microorganisms(bacteria and fungi) that are regularly foundat any anatomical site of human body like:- Skin- Conjunctiva- Respiratory tract- Oral Cavity- External ears- Urogenital tract- Gastrointestinal tract
DEFINITION
STERILE AREAS:BrainCSF
Amniotic fluidBonesHeartLiver
LungsMuscleBlood
Urinary bladder
Middle and innerear
NORMAL FLORANORMAL FLORA
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Associations Between Humans and theNormal Flora:
1. MUTUALISTIC/SYMBIOTIC- both host and organism are thought to derive benefit
from each other2. 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
host’s defense mechanism breaks down
NORMAL FLORA
NORMAL FLORANORMAL FLORA
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COMPONENTS: • Mainly bacteria• Eukaryotic fungi
• Protists• Methanogenic Archaea
NORMAL FLORA
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NORMAL FLORANORMAL FLORA
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TWO GROUPS: 1. RESIDENT flora
- fixed types of microorganisms regularly found in agiven area at a given age
- if disturbed, it promptly reestablishes itself/ transientmicroorganisms may colonize, proliferate andproduce disease
- more important2. TRANSIENT flora
- non-pathogenic or potentially pathogenicmicroorganisms that inhabit the skin or mucousmembranes for hours, days, or weeks
- derived from the environment, does not producedisease
- does not establish itself permanently on the surface- little significance
NORMAL FLORA
NORMAL FLORANORMAL FLORA
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RESIDENT FLORA - acquired rapidly during & after birth and changes
continuously through out life- Factors influencing composition of normal flora:
- genetics - nutrition- age - geographic location- stress - drug therapy- diet - hormonal changes- climate
- 90% is S. epidermidis; S. aureus, may be inmoist areas
NORMAL FLORA
NORMAL FLORANORMAL FLORA
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BENEFICIAL EFFECTS - prevent colonization by pathogens by competing for
attachment sites or for essential nutrients. This isthought to be their most important beneficial effect
- synthesize and excrete vitamins in excess of their ownneeds, which can be absorbed as nutrients by their host- eg) enteric bacteria secrete Vitamin K and Vitamin
B12, and lactic acid bacteria produce certain B-vitamins
- may antagonize other bacteria through the production ofsubstances which inhibit or kill nonindigenous species.
- stimulate the development of certain tissues like thecaecum and Peyer's patches in the GI tract
- stimulate the production of natural antibodies. Low levelsof antibodies produced against components of the normalflora are known to cross react with certain relatedpathogens, and thereby prevent infection or invasion
NORMAL FLORA
NORMAL FLORANORMAL FLORA
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HARMFUL EFFECTS- Bacterial synergism (cross-feeding) between a member
of the normal flora and a potential pathogen. This meansthat one organism is helping another to grow or survive
- Competition for nutrients. Normal flora in thegastrointestinal tract must absorb some of the host'snutrients for their own needs
- Induction of a low grade toxemia. Minute amounts ofbacterial toxins (e.g. endotoxin) may be found in thecirculation and these small amounts of bacterial antigenstimulate the formation of natural antibodies.
- May be agents of disease. Members of the normal floramay cause endogenous disease if they reach a site ortissue where they cannot be restricted or tolerated by thehost defenses
- Transfer to susceptible hosts. Some pathogens of
humans that are members of the normal flora may also
NORMAL FLORA
NORMAL FLORANORMAL FLORA
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SKIN- majority of skin microorganisms
are found in the most superficiallayers 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 FLORANORMAL FLORA
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CONJUCTIVA
- Important bacteria:• Staphylococcus epidermidis
• Neisseria sp.• Corynebacterium sp.• Propoinibacterium acnes• Staphylococcus aureus• Viridans streptococci• Haemophilus influenza
NORMAL FLORANORMAL FLORA
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EXTERNAL EAR
- Important bacteria:• Staphylococcus epidermidis
• Staphylococcus aureus• Corynebacterium sp
NORMAL FLORANORMAL FLORA
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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 FLORANORMAL FLORA
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RESPIRATORY TRACT:NARES (nostrils)
- Important bacteria:• Staphylococcus epidermidis• Staphylococcus aureus• Neisseria sp.
• Haemophilus sp• Corynebacteria• Streptococcus pneumoniae
NORMAL FLORANORMAL FLORA
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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 FLORANORMAL FLORA
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RESPIRATORYTRACT: LRT (trachea, bronchi,
and pulmonary tissues): - usually sterile- individual may become
susceptible to infection by
pathogens descending fromthe nasopharynx like:• H. influenzae• S. pneumoniae
NORMAL FLORANORMAL FLORA
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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 FLORANORMAL FLORA
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UROGENITAL TRACT:VAGINA
- Important bacteria:• Lactobacillus acidophilus• Staphylococci• Corynebacterium sp.• Nonpyogenic streptococci• Escherichia coli• Flavobacterium sp.• Clostridium sp.• Viridans streptococci• Other Enterobacteria
NORMAL FLORANORMAL FLORA
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GASTROINTESTINAL TRACT:SMALL INTESTINE
- Important bacteria:• Lactobacilli• Enterococcus faecalis• Coliforms• Bacteroides
- At birth, the entire intestinal tract is sterile, but bacteriaenter with the first feed. The initial colonizing bacteriavary with the food source of the infant.
NORMAL FLORANORMAL FLORA
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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 &
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STAPHYLOCOCCI &CORYNEBACTERIA
occur at almost every site,skin, conjunctiva, nose,
pharynx, mouth, lower GIT,anterior urethra, vagina
STAPHYLOCOCCUSEPIDERMIDIS
is highly adapted to thediverse environments of itshuman host
STAPHYLOCOCCUS AUREUSis a potential pathogenit is a leading cause ofbacterial disease in humansit can be transmitted from thenasal membranes of anasymptomatic carrier to asusceptible host
Staphylococcus aureus
Staphylococcus epidermidis
Many of the normal flora are
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Many of the normal flora areeither pathogens oropportunistic pathogens. Thefollowing indicate members of
the normal flora that may beconsidered major pathogensof humans:STAPHYLOCOCCUSAUREUS
STREPTOCOCCUSMUTANSENTEROCOCCUSFAECALISSTREPTOCOCCUSPNEUMONIAESTREPTOCOCCUSPYOGENESNEISSERIA MENINGITIDISESCHERICHIA COLIPSEUDOMONASAERUGINOSA
STREPTOCOCCUS MUTANS
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STREPTOCOCCUS MUTANSis the primary bacteriuminvolved in plaque formationand initiation of dental caries
viewed as an opportunisticinfection
ENTEROCOCCUS FAECALISwas formerly classified asStreptococcus faecalishas emerged as a significant,antibiotic-resistant,nosocomial pathogen.
Streptococcus mutans
Enterococcus faecalis
STREPTOCOCCUS
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STREPTOCOCCUSPNEUMONIAE
is present in the upperrespiratory tract of about half
the populationif it invades the lowerrespiratory tract, it can causepneumoniacauses 95%of all bacterial
pneumonia
STREPTOCOCCUSPYOGENESrefers to the Group A, Beta-hemolytic streptococcicause tonsillitis (strep throat),pneumonia, endocarditissome can lead to rheumaticfever or nephritis which can
Streptococcus pneumoniae
Streptococcus pyogenes
NEISSERIA AND OTHER
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GRAM-NEGATIVE COCCIare frequent inhabitants of theupper respiratory tract, mainly
the pharynxNeisseria meningitidis is animportant cause of bacterialmeningitis
PSEUDOMONASAERUGINOSAis the quintessentialopportunistic pathogen ofhumans that can invadevirtually any tissueit is a leading cause ofhospital-acquired(nosocomial) Gram-negativeinfections, but its source is
Neisseria sp
Pseudomonas aeroginosa
ESCHERICHIA COLI
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is a consistent resident of thesmall intestineother enteric bacteria that may
reside in SI includesKlebsiella, Enterobacter andCitrobactersome strains of E. coli arepathogens that cause
intestinal infections, urinarytract infections and neonatalmeningitis.
HAEMOPHILUS INFLUENZAEis a frequent secondaryinvader to viral influenzathe leading cause ofmeningitis in infants andchildren until the recentdevelopment of the Hflu type
Escherichia coli
Haemophilus influenzae
BACTEROIDES
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in the lower intestinal tractarethe Bacteroides, a group ofGram-negative, anaerobic,
non-sporeforming bacteriaThey have been implicated inthe initiation colitis and coloncancer
LACTOBACILLIcontribute to acid formation inthe oral cavity that leads todental caries
LACTOBACILLUSACIDOPHILUScolonizes the vaginal
epithelium during child-bearing years and establishesthe low pH that inhibits the
Bacteroides fragilis
Lactobacillus acidophilus
BIFIDOBACTERIA
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are Gram (+), non-sporeforming, lactic acidbacteria. They have been
described as "friendly"bacteria in the intestine ofhumans
BIFIDOBACTERIUM BIFIDUM
is the predominant bacterialspecies in the intestine ofbreast-fed infants, where itpresumably preventscolonization by potentialpathogens. These bacteria aresometimes used in themanufacture of yogurts andare frequently incorporatedinto probiotics.
Bifidobacterium bifidum
CLOSTRIDIUM
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PERFRINGENScolonize the bowelcommonly isolated from feces
CLOSTRIDIUM DIFFICILEmay colonize the bowel andcause "antibiotic-induceddiarrhea" or
pseudomembranous colitis
CLOSTRIDIUM TETANI"transiently associated" withhumans as a component ofthe normal floracan be isolated from feces in0 - 25 percent of thepopulationthe endospores are probablyingested with food and water,and the bacterium does not
Clostridium perfringens
Clostridium tetani
CORYNEBACTERIA, AND
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CERTAIN RELATEDPROPIONIC ACID BACTERIA
are consistent skin flora
some have been implicated asa cause of acne
CORYNEBACTERIUMDIPHTHERIAEcausative agent of diphtheriaconsidered a member of thenormal flora before thewidespread use of thediphtheria toxoid, which isused to immunize against thedisease.
Propionibacterium acneCorynecbacterium
diphtheriae
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PROPHYLAXIS
PROPHYLAXISDEFINITION
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IMMUNIZATION• administration of an individual with
antibodies possessing power to destroy orinactivate the disease producing agent orneutralize its toxin
• ULTIMATE GOAL: eradication of the disease• IMMEDIATE GOAL: prevention of the
disease in an individual
PROPHYLAXISIMMUNIZATION
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TWO TYPES OF IMMUNIZATION
1. ACTIVE IMMUNIZATION2.
PASSIVE IMMUNIZATION
PROPHYLAXISIMMUNIZATION
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ACTIVE IMMUNIZATION• involves the administration of all or part of a
microorganism (Ag) or a modified product ofthat microorganism to evoke an immunologicresponse that mimics the natural infection,but this infection usually presents with littleor no risk to the recipient.
• some immunizing agent may producelifelong protection and some only providepartial protection, thus, must be re-administered at regular intervals to maintainprotection.
PROPHYLAXISIMMUNIZATION
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PASSIVE IMMUNIZATION• administration of exogenously produced or
preformed antibody (Ig)
• provides temporary protection• Artificial Ig: tetanus, measles, chicken pox,
rabies, rubella• Natural Ig: through transplacentaltransmission of antibody to a fetus providing
protection against many infectious diseasesfor the first 3-6 months of the infant's life.
PROPHYLAXISIMMUNIZATION
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TYPES OF VACCINES
1. Inactivated or killed vaccines2. Attenuated or live vaccines3. Subunit vaccines4. Toxoids
5. Conjugate vaccines6. Recombinant vaccines7. DNA vaccines
PROPHYLAXISIMMUNIZATION
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1. INACTIVATED/KILLEDVACCINES
• these are usually inactivated or purified components
of virus and bacteria or those that are conjugatedchemically 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 boosterdoses for maintenance of long lasting immunity
• immune response is mostly humoral or antibody-mediated
PROPHYLAXISIMMUNIZATION
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2. ATTENUATED/LIVEVACCINES
• this are attenuated or weakened form of the wild
virus or bacteria that induce an immunologicresponse simulating the response to naturalinfection.
• produces the active infection by viral replicationhowever, these produces little or no adversereaction to the host.
• these organisms multiply in the recipient until thedesired immune response occurs conferringlifelong protection with a single immunizing dose.
PROPHYLAXISIMMUNIZATION
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3. SUBUNIT VACCINE
• are fragment of inactivated or attenuatedmicroorganism to create an immune response
• eg) meningococcal, pneumococcal
PROPHYLAXISIMMUNIZATION
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4. CONJUGATE VACCINE
• combining or linking of the polysaccharide outercoats (which are poorly immunogenic) ofmicroorganism with proteins (like toxins) tobecome highly immunogenic.
• eg) Hib , pneumococcal (Prevnar)
PROPHYLAXISIMMUNIZATION
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5. RECOMBINANT VACCINE
• combining the physiology of one microorganismand the DNA of other microorganism
• eg) Hepatitis B, Human Papilloma (Gardasil,Cervarix)
PROPHYLAXISIMMUNIZATION
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6. TOXOID
• are chemically or thermally modified toxins torender them non-toxic but still immunogenic
• eg) diphtheria, tetanus
PROPHYLAXISIMMUNIZATION
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7. DNA VACCINE
• created from an infectious agents DNA• it works by insertion (and expressiom, triggering
immune system recognition) into human or animalcells, of viral or bacterial DNA
• still experimental
PROPHYLAXISSITE & ROUTE OF ADMINISTRATION
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1. ORAL2. INTRAMUSCULAR
3. SUBCUTANEOUS4. INTRADERMAL
5. INTRANASAL
PROPHYLAXISSITE & ROUTE OF ADMINISTRATION
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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
PROPHYLAXISSITE & ROUTE OF ADMINISTRATION
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3. SUBCUTANEOUS• 45˚ angle into the anterolateral aspect of thethigh 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 othernostril.
• e Live attenuated influenza vaccine
PROPHYLAXISCONTRAINDICATIONS
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ABSOLUTE RELATIVE NOT • Severe anaphylactic
reaction or allergicreaction to previousvaccine
• Encephalopathywithin 7 days ofadministration(Pertussis)
• Immunosuppressivetherapy
• Egg allergy
• Seizure within 3 daysof last dose (Pertussis)
• Shock within 48 hrs oflast dose
• Fever >/+ 40.5 Cwithin 48 hours of lastdose
• Mild illness with or withoutlow grade fever
• Current antibiotic therapy
• Recent infectious disease
• Positive PPD
• Prematurity, except in infantsstill hospitalized at 2 mos,
OPV should be delayed untildischarge. OR, if mother isHBsAg (-), Hep B vaccinedelayed until child >2000gm
PROPHYLAXISSCHEDULE
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PROPHYLAXISIMMUNIZATION
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EXPANDED IMMUNIZATIONPROGRAM (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 byproviding pregnant women with tetanus toxoidimmunization
PROPHYLAXISEXPANDED IMMUNIZATION PROGRAM
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VACCINE AGE INTERVAL AMOUNT SITE/ROUTE BOOSTER
BCG1 dose
At birth If >2 months-do PPD 1 st before givingBCG
NB: 0.05 ml>1mo: 0.1 ml
ID at deltoidarea
DPT3 doses
6 weeks 4 weeks 0.5ml IM atanterolateral
thigh
1 st- 1 yr after thelast dose
2nd
- 4-6 y/o OPV3 doses
6 weeks 4 weeks 0.5 ml mouth 1 st- 1 yr after thelast dose2nd- 4-6 y/o
HEPA B3 doses
At birth 1-2 monthsand 6-8 mos
0.5ml IM atanterolateralthigh
HEPA B3 doses
MEASLES1 dose
6 months / 9 months
0.5 ml SQ, thigh MMR 1 st-6 moafter measles2nd-4- 6 y/o or11-14 y/o
PROPHYLAXIS VACCINE
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BACILLE CALMETTE GUERIN (BCG)
BCG vaccines are live vaccine from attenuated strains ofMycobacterium bovis
the WHO recommends that all children in countries with highincidence of TB infection should be immunized with a singledose of BCG at or soon after birth.does not prevent infection with pulmonary TB but preventsextra-pulmonary manifestations of tuberculosis (Military TB,TB meningitis)protection from PTB: 65%protection from Extra-pulmonary TB: 85%
PROPHYLAXIS VACCINE
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BACILLE CALMETTE GUERIN (BCG)AGE/
INTERVAL AMOUNT SITE/ROUTE BOOSTER ADVERSE REACTION
single dose givenat birth:
<1month: 0.05cc
> 1 month:0.1cc
at 2nd month ofage: do PPD 1 st
newborn:0.05 ml
>1month:0.1 ml
intradermal at deltoidarea
none Koch’s phenomenon:accelerated BCGreaction
Indolent ulcers:ulceration of morethan 3 weekssubcutaneousabscess &lymphadenopathyosteomyelitis &muscle necrosisuncommonly (1-2%)result in local adversereactions
PROPHYLAXIS VACCINE
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BACILLE CALMETTE GUERIN (BCG)NATURAL COURSE:
Wheal formation: disappears after 30 minutes of
injectionInduration: occurs after 2-3 weeks of injectionPustule formation: after 2-3 weeks of indurationUlceration: after 2-3 weeks of pustule formationScar formation: after 8-12 weeks after injection
PROPHYLAXIS VACCINE
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DIPHTHERIA, PERTUSSIS &TETANUS (DPT)
is a combination vaccine composed of a diphtheria,
pertussis and tetanus components.
Inactivated vaccine
PROPHYLAXIS VACCINE
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DIPHTHERIA, PERTUSSIS &TETANUS (DPT)
AGE/ INTERVAL
AMOUNT SITE/ROUTE
BOOSTER ADVERSE REACTION
3 doses given asearly as 6 weeksold at 4 weeksapart
0.5 cc IM 2 doses:1st:1 year afterthe last dose
2nd:4-6 yearsold
Local & febrile reactionsBacterial or sterileabscesses at the site ofinjectionAllergic reactionsSeizuresHypotonichyporesponsiveepisodes (HHE)“collapse” or “ shocklikestate”
Fever of 40.5°CIncessant crying
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POLIO VACCINE (OPV/IPV)
The Live Oral Polio Vaccine (OPV)composed of an attenuated poliovirus types 1, 2 and 3derived 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 3derived from monkey kidney or human diploid cellsinactivated with formaldehydehas trace amounts of streptomycin, neomycin & polymyxin B.lifelong immunity.inhibits pharyngeal acquisition of poliovirus & has a lesser extent ofintestinal acquisition of the virus.
PROPHYLAXIS VACCINE
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POLIO VACCINE (OPV/IPV)
AGE/ INTERVAL
AMOUNT SITE/ROUTE
BOOSTER ADVERSE REACTION
3 doses given asearly as 6 weeksold at 4 weeksapart
IPV:0.5 cc
OPV:2 drops
IPV:IM
OPV:PO
2 doses:1st:1 year afterthe last dose
2nd:4-6 yearsold
IPV:hypersensitivityreaction
OPV:vaccine-associatedparalytic polio(VAPP)
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MEASLESAGE/
INTERVAL AMOUNT SITE/ROUT
E BOOSTER ADVERSE REACTION
3 doses:1st:6-12 months old
2nd:6 months afterthe first dose3rd:4-6 years old
0.5 cc SC none Fever after 5-7 daysfrom the time of injectionLocal swelling or pain
from site of injectionRashes
PASSIVE IMMUNIZATION with measles immunoglobulin ispreferred in susceptible and immuno-compromised patients
Give immunoglobulin within 6 days after exposureDose: 0.25cc/kg , IM or IVIG at a dose of 100-400 mg/kg
PROPHYLAXIS VACCINE
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HEPATITIS B VACCINE
Killed/ inactivated vaccine
WHO recommendation that in any country whosecarrier rate is >2% should immunize their infantsagainst 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 ageOlder persons in certain high-risk groups
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HEPATITIS B VACCINE
AGE/ INTERVAL
AMOUNT SITE/ROUTE
BOOSTER ADVERSE REACTION
3 doses: (0-1-6
mo)1st:at birth2nd:1 month after 1 st dose
3rd:6 months after1st dose
0.5 cc IM none Pain at the injection site
Fever (>37.7°C)Allergic reactions
PROPHYLAXIS VACCINE
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HAEMOPHILUS INFLUENZAE TYPEB (Hib)Inactivated vaccine
The WHO now recommends that Hib vaccine shouldbe included as appropriate to national capacities andpriorities in routine infant immunization because
Haemophilus influenzae remains to be the mostcommon cause of meningitis in the first year of life.
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HAEMOPHILUS INFLUENZAE TYPEB (Hib)AGE/
INTERVAL AMOUNT SITE/ROUT
E BOOSTER ADVERSE REACTION
3 doses given asearly as 2months old, at 2months apart:
If first given at 6months old, 2doses is enough
If first given at 1year old, singledose is enough>5 years old, nolonger advisable
0.5 cc IM Singledose at 1year ofage
Pain at the injection site
PROPHYLAXIS VACCINE
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VARICELLA VACCINE
The AAP and PPS recommends the universalimmunization for all healthy infants 12 months oldand susceptible older children and adolescents of
varicella vaccine
The recommendation for the post-exposureprophylaxis administration of varicella vaccine tosusceptible children is within 72 hours to 120 hoursafter exposure to prevent or significantly modify thedisease.
PROPHYLAXIS VACCINE
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VARICELLA VACCINEAGE/
INTERVAL AMOUNT SITE/ROUT
E BOOSTER ADVERSE REACTION
3 doses:1st:1 year old2nd:4-6 years old3rd:13 years old
If first given at>13 years old, 2doses is givenat 1 monthinterval
0.5 cc SC or IM none Pain at the injection site
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TYPHOID VACCINE
The WHO recommends the administration of typhoidvaccine to those people living in endemic areas. Inthe Philippines the recommended age of
administration is 2 years old given intramuscularly.
AGE/ INTERVAL
AMOUNT SITE/ROUTE
BOOSTER ADVERSE REACTION
single dose givenat 2 years ofage
0.5 cc IM single doseat 2-3 yearsof age
Pain at the injectionsite
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PNEUMOCOCCAL VACCINE
Types:1. 23-Valent Polysaccharide vaccine which is given
in children 2 years and older2. 7- valent conjugate polysaccharide vaccine
which could be given in infants as early as 2months old.
These vaccines are associated with the reduction innasopharyngeal carriage with vaccine-typeorganisms but does not however, prevent theoccurrence of Otitis Media.
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THANK YOUGOOD DAY