Principles of microbial

pathogenicity and
epidemiology
Johnmartin M. De Los Reyes, RMT MSc

Introduction
Microorganisms are free living and require nutrients to survive
Normal flora
Opportunistic
Pathogenic

Viruses obligate intracellular parasite

Introduction
Some organisms may cause disease through ingestion of substances
(toxins) produced during microbial growth on foods
Number of bacterial cells is associated in the ability of the bacteria to
cause disease
Minimum infective number

Introduction
Organism must arrive at the portal of entry
Viruses must rapidly gain entry to the host cell
Organisms can be asymptomatic (carrier) or symptomatic

The human microbiome

The human body harbours millions of mutualistic and commensal
symbionts
Mutualistic relationship both the microbial and host cell benefit
from the interaction
Commensalism one member of the relationship benefits without
affecting the other

Portal of entry (SKIN)

The major part of the body that is widely exposed to microorganisms
Intact skin is a protective barrier, acid pH
Survivor must compete with the commensal microflora for nutrients
in order to grow
Hospital acquired infection (bacteremia)

Portal of entry (SKIN)

Mucous membrane present a much more favorable environment for
microbial growth (warm, moist and rich in nutrients)
Colonization resistance
Infection start from direct and indirect contact
Direct infected to non-infected individual
Indirect inanimate vectors like soil, food, drink, air and airborne
particles

Portal of entry (RESPIRATORY TRACT)

Airborne particles (suspended)
Blanket of mucus (protection)
A pathogen must avoid being trapped in the mucus and avoid
phagocytosis in the alveolar region
Attachment to epithelial surface and increase mucin production that
decreases ciliated epithelial cells (smoking)

Portal of entry (INTESTINAL TRACT)

Extreme acidity and digestive enzymes (protection)
Small intestine is colonized by lower number of organisms than the
colon
Pathogen must resist the acidity of the stomach or able to attach or
penetrate the gut wall

Portal of entry (UROGENITAL TRACT)

The bladder, ureters and urethra are sterile
Organisms must avoid being detached from the epithelial surface and
washed out during urination
Female are more prone to infection than male
Catheter (mode of infection)

Lactic acid in female

Portal of entry (CONJUCTIVA)

It is usually free of microoragnisms
Protected by continuous flow of secretions
Infection is thus promoted by the use of soft and hard contact lens,
physical damage, exposure to chemicals

Consolidation
A pathogen must be able to survive at its initial portal of entry
Competition with the normal flora, evading the macrophages and
WBC, establish attachment (fimbriae, pili)
Factors:
Organisms growth rate
Initial number at the site
Ability to resist immune response

Consolidation
Virulence: The ability of an agent of infection to produce disease
Associated with MIN
Nutrient acquisition
Biofilms
Resistance to host defense

Nutrient acquisition
Pathogens must acquire sufficient nutrients to multiply and increase
in number
Must compete with the normal flora organism
Example: in consumption of iron, organism produces siderophores
which have greater affinity with iron than the host iron binding
proteins

Biofilms
It is a means by which pathogens can remain in a favorable
environment
Surface (soft tissue, bone, medical implants)
May contain only one or more species
Extremely difficult to remove because of their size and morphology
that can help protect the underlying cells, resist removal, resist
phagocytosis and antibiotics

Resistance to host defense

Most bacterial infections confine themselves to the surface of
epithelial tissue
Firm attachment and production of toxins (disease)
Some gain entry to susceptible cells that enables them to evade body
defense (macrophages)

Modulation of the inflammatory response

Some organisms cause nonspecific inflammation
This increase capillary flow and increased lymphatic flow from the
inflamed tissues carries the organisms to lymph nodes
White blood cell accumulation
Many bacteria have adapted mechanisms that allow them to
overcome this initial defense
Example: mucopeptide suppress early inflammation

Avoidance of phagocytosis
Resistance to phagocytosis is associated with specific components of
the cell wall or the presence of capsule surrounding the cell wall
M-capsule of streptococci
Polysaccharide capsule of pneumococci
Avoidance of opsonization will enhance the chance of the bacteria to
survive s

Survival following phagocytosis

Microorganism can survive following phagocytosis when it avoids the
killing and digestion process within the phagocyte
Prevention of fusion between the lysosomes with phagocytic vacuole

Killing of phagocyte
Microorganism can kill phagocyte through the production of
leucocidins
This promote the discharge of lysosomal substances into the
cytoplasm of the phagocyte, thus directing the phagocytic lethal
activity towards itself

Manifestation of disease
The course of bacterial infection can proceed in a number of ways
Can be related to the ability of the organism to penetrate and invade
surrounding tissues and organs
Small group of pathogens are fully invasive (circulated around the
body to initiate secondary site of infection)

Fully invasive pathogens (active spread)

Haemolysin have lytic effect on red blood cells, releasing iron
containing nutrients
Fibrinolysin activate plasminogen to dissolve fibrin clots
Collagenases and hyaluronidases dissolves collagen ibres and
hyaluronic acids that function as intracellular cements. Thus causing
tissue damage
Phospholipases damage tissue cells
Amylases, peptidases and deoxyribonucleases mobilize many
nutrients that are released from lysed cells

Fully invasive pathogen (passive spread)

When invading organisms crossed the epithelial barrier and carried in
the lymphatic ducts
This sometimes spread the infection (blood stream)
Bacteremia

Damage to tissues (Direct damage)

Specific effects the damage caused by the organism to the tissue or
organ has specific effect
Example: Clostridium tetani causes tissue necrosis and lockjaw
Non-specific effects if the infective agent damages an organ and
affects its functioning
Example: Vibrio cholerae causes diarrhea that would result to water
loss and electrolytes. That might follow kidney malfunction

Damage to tissues (Indirect damage)

Inflammatory materials (endotoxins)
The most notable effect is pyrogenecity (high body temperature)
Antibiotics are co-administered with steroid to counter pyrogenecity

Recovery from infection (exit of

microorganism)
Primary requirement control the multiplication of the infective
agent
Accompanied by complete destruction of the organism and
restoration of a sterile tissue
Exit of microorganism to infect other individual is co-related to the
portal of entry