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Origin of Microbial Flora

1.Introduction (Host Microbe Relationship)

Symbiosis (Mutualism)
Biological relationship between two or more
organisms where both benefit from one another.
Commensalism
Organism benefits but there is no beneficial or
harmful effects to the host.
Parasitism
The microbe benefit at the expense of the other
(host).
 Origin of Microbial Flora

2.Characteristics of Indigenous Microbial Flora

Commonly found in body sites of healthy persons.
a. Resident microbial flora
Microorganisms that colonize an area for months or
years.
b. Transient microbial flora
Present at a site temporarily, eliminated by host
immune defense / competition with resident flora.
Carrier state may be acute (like S. aureus) or
chronic (like S. typhi)
 Origin of Microbial Flora

3.Factors for Composition of the Usual Flora

Nutritional and Environmental factors
E.g: Diptheroids in moist areas,armpits,groin
Resistance to bile, lysozymes or fatty acids
E.g: P. acnes in hair follicles
pH
E.g: Lactobacillus in Female genital tract
Oxidation-reduction potential
E.g: Obligate anaerobes in the colon
 Role of the Usual Microbial Flora
I. Origin of Microbial Flora
II. Composition of the Microbial Flora at
Different Body Sites
III. Role of the Microbial Flora in the Host
Defense Against Infectious Disease
IV. Role of the Microbial Flora in the
Pathogenesis of Infectious Disease
 Usual Flora at Body Sites
Composition of the Microbial Flora at Different
Body Sites
A. Skin
B. Mouth
C. Respiratory Tract
D. Gastrointestinal Tract
 Usual Flora at Body Sites

A. Skin
Armpit, groin, perineum,
axillae and between toes
(Aerobic Diptheroids)
Hair follicles, sweat and
sebaceous glands
(S. epidermidis and
Propionibacterium)
 Usual Flora at Body Sites

B. Respiratory Tract
Upper Respiratory Tract
Mouth, nasopharnyx,
oropharnyx and larynx
Example:
Mouth Viridans Strep.
and Gram (-) anaerobes
Nose and Nasopharnyx
Diplococci and Diptheroids
Orophaynx Gram (-)
anaerobes and Diptheroids
 Usual Flora at Body Sites

C. Gastrointestinal Tract
Anaerobes makes up 90% of
the microbial flora
Esophagus, stomach, small
intestine, and colon
Example:
G(+) staph and Enterococcus
Anaerobic G(+) cocci and
sporeforming bacilli
Enterobacteriaceae
 Usual Flora at Body Sites

D. Genitourinary Tract
Sites urethra and vagina
Sterile Kidneys, bladder
and fallopian tubes
Example:
Lactobacillus
Anaerobic
Sporeformers
G(+) cocci / Diptheroids
 Role of the Usual Microbial Flora
Role of the Microbial Flora in the Host Defense
Against Infectious Disease
Activates or primes the immune system (e.g. cell
mediated immunity)
Blocks the colonization of extraneous pathogens.
 Role of the Usual Microbial Flora
Role of the Microbial Flora in the Pathogenesis
Infectious Disease
Opportunists:
Cause disease when their habitat is damaged,
disturbed or changed by trauma or;
When the hosts immune system is weakened or
compromised
Pathogenesis of Infection
 Pathogenesis of Infection
I. Microbial Factors Contributing to
Pathogenesis and Virulence
II. Host Resistance Factors
III. Mechanisms by Which Microbes May
Overcome the Host Defenses
IV. Routes of Transmission
 Pathogenesis of Infection

Microbial Factors Contributing to Pathogenesis

and Virulence
A. Pathogenesis
B. Virulence
C. Ability to Resist Phagocytosis
D. Surface Structures for Adhesion
E. Ability to Survive Intracellular
F. Production of Toxins and Enzymes
 I. Microbial Factors
A. Pathogenesis
Pathogenicity
Is the ability of a microbe to produce disease in a
susceptible individual.
i. True Pathogen
Organisms recognize to cause disease in healthy
immune-compenent inidividuals.
B. anthracis and Y. pestis
ii. Opportunistic Pathogen
Organisms that cause opportunistic or iatrogenic
infections (medical treatment or procedures)
H. influenzae and S. epidermidis
 I. Microbial Factors
B. Virulence
Is the relative ability of a microorganism to cause disease or
the degree of pathogenecity
Microbial Virulence Factors
Allows pathogens to evade or overcome host defenses
and cause disease
E.g. Fimbriae, Capsules and Toxins
 I. Microbial Factors

C. Ability to Resist Phagocytosis

Type of
Microorganisms Mechanism
Interference
Staphylococcus Leucocidin induces lysosomal
Kill phagocyte
Streptococcus Streptolysin discharge
H. influenzae Polysaccharide capsule
P. aeruginosa Resist Surface slime (polysaccharide)
E. coli Phagocytosis O and K antigen
S. typhi Vi antigen
 Microbial Factors

D. Surface Structures that Promotes Adhesion

to Host Cells and Tissues
Adhesins
Cell surface structures that mediate attachment
E.g. fimbriae and surface polysaccharides

Hyaluronidase
Nuclease
Collagenase
 Microbial Factors

E. Ability to Survive Intracellularly and

Proliferate
Prevent fusion of phagosomes and lysosomes
Resistance to effects of lysosomal contents
Ability to escape from the phagosome
Ability to avoid or overcome local factors
e.g. lactoferrin meningcocci; IgA protease H. influenzae
and Niesseria)
Ability to Survive Intracellularly
e.g. Chlamydia, Mycobacterium, Brucella and Listeria
Ability to Proliferate (Dissemination)
e.g. Salmonella
 I. Microbial Factors

E. Ability to Survive Intracellularly and

Proliferate
i. Prevent fusion of phagosomes and lysosomes
ii. Resistance to effects of lysosomal contents
iii. Ability to escape from the phagosome
iv. Ability to avoid or overcome local factors
e.g. lactoferrin meningcocci; IgA protease H. influenzae
and Niesseria)
v. Ability to Survive Intracellularly
e.g. Chlamydia, Mycobacterium, Brucella and Listeria
vi. Ability to Proliferate (Dissemination)
e.g. Salmonella
 Microbial Factors

F. Ability to Produce Toxins and Enzymes

Toxins
Poisonous substances produced by organisms that
interact with host cells, disrupting normal
metabolism and causing harm.
Two types of Toxins
i. Exotoxins
ii. Endotoxins
 Microbial Factors

F. Ability to Produce Toxins and Enzymes

Two types of Enterotoxins
i. Exotoxins
Secreted by the organism into the extracellular
environment
Toxin gene is commonly encoded by phages,
plasmids or transposons.
ii. Endotoxins
A constituent Lipid A of the outer membrane of
gram (-) bacteria
Released upon lysis of the organism.
 Microbial Factors

F. Ability to Produce Toxins and Enzymes

Two types of Enterotoxins

Characteristic Exotoxins Endotoxins

Organism Type Gram (+) / Gram (-) Gram (-)
Chemical Nature Simple protein Lipid A
Stability at 100C Labile Stable
Ab neutralization Detoxified Not Detoxified
Biologic Activity Individual to toxin Same for all toxins
Toxicity (strychnine as
100 to 106 0.1
1)
 Pathogenesis of Infection

Host Resistance Factors

1.Physical Barriers
2.Cleansing Mechanisms
3.Antimicrobial Substances
4.Indigenous Microbial Flora
5.Phagocytosis
6.Inflammation
7.Immune Responses
 II.Host Resistance Factors

1.Physical Barriers
Skin epithelium presents as
mechanical barrier.
Except Leptospira spp.,
F. tularensis, Treponema spp. and
bite from arthropods
Microbial flora compete for nutrients
and produce bactericidal substances.
Microbial flora and Sebaceous gland
contribute to low pH.
 Host Resistance Factors

2.Cleansing Mechanisms
Desquamation of skin surfaces.
Flushing of tears and urine
Mucus production of membrane
lining the nasopharynx.
Sweeping of particles by Ciliary
epithelium (trachea)
Low pH of the stomach
 Host Resistance Factors
3.Antimicrobial Substances
i. HCl in the stomach
ii. Secretory IgA of the
mucosa
iii. Complement, Lysozyme
(hydrolyzes peptidoglycan
layer of bacterial cell walls)
and -lysin in serum
and/or body fluids
iv. Interferons-cellular proteins
that inhibit proliferation of
viruses
 Host Resistance Factors
4.Indigenous Microbial Flora
Compete with pathogens for
nutrients and space
Produce bacteriocins (inhibit
the growth of closely related
bacteria)
Production of metabolic by-
products that inhibits pathogens
Synthesis of vitamins and other
essential nutrients
 Host Resistance Factors

5.Phagocytosis
i. Chemotaxis
ii. Attachment
iii. Ingestion
iv. Killing

Diapedesis
Opsonization
Chemotaxis
Diapedesis
 Host Resistance Factors
6.Phagocytosis
Tissue Distribution of
Monocyte or
Macrophages
* Opsonization- enhanced
phagocytosis by PMNs due to
coating of bacterium with
antibody or complement
(opsonins)
* Chemotaxis- migration of PMNs
into area of infection
* Diapedesis- movement of PMNs
from blood vessel into tissues
(surveillance)
 Host Resistance Factors

7.Inflammation
i. Bodys response to injury or
foreign body
ii. Hallmark is accumulation of
phagocytic cells
iii. Leucoytes and other cells
release mediators to cause
erythema, edema and pus
iv. Enzymes digest foreign
particles, injured cell and
cell debris
 Host Resistance Factors

7.Inflammation
 Responses to Microbial Invasion

Nonspecific Responses
Cardinal Signs of Inflammation
1. Swelling vasodilation of blood vessels (T)
2. Redness increase blood flow (R)
3. Heat increase temperature of affected tissue (C)
4. Pain tissue damage and pressure from increased (D)
flow of fluid and cells
 Host Resistance Factors

Immune Responses
a.Innate or Natural Immunity
b.Adaptive or Specific Immunity
c.Humoral Immune Response
d.Cell Mediated Immune Response
 Host Resistance Factors

Immune Responses
a.Innate or Natural Immunity (nonspecific)
Physical & Chemical barriers- skin and mucous
membranes
Blood Proteins-acts as mediator of infection
Cellular Mechanisms- phagocytosis
(neutrophils,macrophages,natural killer cells)
 Host Resistance Factors

Immune Responses
b.Adaptive or Specific Immunity
Cellular (B Cells, T Cells) Humoral (Antibodies)
Mechanisms
 Host Resistance Factors
Specific Acquired Immunity
o Natural
1. Active-after infection
2. Passive-Abs from mother to child
o Artificial
1. Active- Vaccination-Abs devt.
2. Passive- Anti-toxin/ Immune globulin
ex. Anti-tetanus
 Host Resistance Factors

Immune Responses
c.Humoral Immune responses (Latin:humor- body fluid)

Antigen
(Virus)
 Host Resistance Factors
Immune Responses
Humoral Immune responses
Antibody
Specific protein
produced by B cells in response
to presence of foreign molecules
(antigen)
 Host Resistance Factors

Immune Responses *Immunologic

memory-able to
Humoral Immune responses *
remember each time
it encounters a
particular antigen

*Anamnestic immune
response(rapid
increase in IgG Abs)
 II. Host Resistance Factors

Immune Responses
d.Cell Mediated Immune Response
 II. Host Resistance Factors

Immune Responses
Cell Mediated Immune Response
Cytotoxic T Cell
Natural Killer T Cell
Humoral vs Cellular Immunity
II. Host Resistance Factors
III.Mechanisms by Which Microbes
May Overcome the Host Defenses
Tolerance (feeble antigen)
Immune Suppression (HIV virus)
Change in the appropriate target for the immune
system
Antigenic Variation
III Mechanisms by Which Microbes
May Overcome the Host Defenses

Host Defense Mechanism of Evasion Example

Hydrodynamic flow Attachment Fimbriae

Surface Igs Masking of Antigen Capsules

Destruction IgA Protease
Fibrin trapping Fibrinolysis Fibrinolysin
Phagocytosis Inhibition of Attachment Capsules
and Ingestion
Resistance to oxidative Catalase
attack
 IV Routes of Transmission

A. Airborne Transmission
B. Food and Water
C. Close Contact
D. Cuts and Bites
E. Arthropods
F. Zoonoses
 Routes of Transmission

Route of Exit Route of Transmission Example

Respiratory Aerosol droplet Inhalation M. tuberculosis

Salivary Animal Bite Rabies, P. multocida

Gastrointestinal Stool water or food Salmonella /
mouth Shigella
Blood Transfusion or needle prick HIV, Hepatitis B
Skin Skin to skin S. aureus
Genital Urethral or cervical Gonorrhea,
secretions secretions Chlamydia
Urine Urine hand Catheter Hospital-acquired
UTI
Zoonotic Arthropod, animal bite Plague, RMSF, Lyme
 Pathogenesis of Infection
IV. Routes of Transmission
Zoonotic Infections

Disease Organism
Anthrax Bacillus anthracis
Brucellosis Brucella spp.
Tuberculosis Mycobacterium bovis
Gastroenteritis Camphylobacter spp., Salmonella spp.
Leptospirosis Leptospira interogans
Plague Yersinia pestis