PATHOGENESIS OF

INFECTIOUS DISEASES

CHAPTER 14
PATHOGENESIS
 is the steps or mechanisms involved in the development
of the disease

PATHOGENICITY
 is the ability to cause disease

PATHOGEN
 a microorganism capable of causing disease

PATHOLOGY
 is the study of the structural and functional
manifestations of the disease
Infection Versus Infectious
Disease
• Infectious Disease
-is a disease caused by a microbe and the microbes
that cause infectious disease are collectively referred to
as pathogens.

• Infection
-according to many microbiologists, infection means
colonization by a pathogen.
WHY INFECTIONS DOES NOT ALWAYS
OCCCUR
• The microbe may land at an anatomical site where it is unable
to multiply
• Many pathogens must attach to specific receptor site before
they are able to multiply and cause damage
• Antibacterial factors that destroy or inhibit the growth of
microbes maybe present at the site where the pathogen lands
• The indigenous microflora at the site may inhibit growth of the
foreign microbe by occupying space and using up the
available nutrients
• The indigenous microflora at the site may produce
antibacterial factors (bacteriocins) that destroy the newly
arrived pathogen.
• The individuals nutritional and overall health status often
influences the outcome of the pathogen/host encounter
• The person maybe immune to that particular pathogen as a
result of prior infection or vaccination
• Phagocytic white blood cells may engulf and destroy before it
has an opportunity to multiply, invade and cause disease
FOUR PERIODS IN THE COURSE OF AN
INFECTIOUS DISEASE

• INCUBATION PERIOD- is the time that elapses between

the arrival of the pathogen and the onset of symptoms.

FACTORS INFLUENCING THE INCUBATION

PERIOD:
• Overall health and nutritional status of the host
• Virulence of the pathogen
• Numbers of the pathogens that enters the body
• PRODROMAL PERIOD- time during which the patient starts to feel
something wrong but does not yet experience the actual symptoms of
the disease

• PERIOD OF ILLNESS- time when the person experience the typical

symptoms of the disease. Communicable diseases are most easily
transmitted during this stage.

• CONVALESCENT PERIOD- time when the person recovers.

Person may recover from the illness but there may be permanent
damage of tissues of the affected area
The course of an infectious
disease
Exposure to pathogen


Incubation Period


Prodromal Period


Period of Illness

Convalescence  Death

Disability
Localized Versus Systemic
Infections

• LOCALIZED INFECTIONS
-an infection that remains localized at one site or it may
spread.

• SYSTEMIC/GENERALIZED INFECTIONS
-an infection that has spread throughout the body.
Acute, Subacute, and
Chronic Diseases

• ACUTE DISEASE
-has rapid onset usually by a relatively rapid recovery

• CHRONIC DISEASE
-has an insidious (slow) onset and lasts a long time

• SUBACUTE DISEASE
- diseases that come on more suddenly than chronic
diseases but less suddenly than acute diseases
Symptoms of a Disease Versus Signs
of a Disease

• SYMPTOM OF A DISEASE
- some evidence of a disease that is
experienced or perceived by the patient.
 Asymptomatic disease (clinical disease)
-a disease in which the patient is experiencing
symptoms
 Symptomatic disease (subclinical disease)
-a disease that the patient is unaware of because she/he

is not experiencing any symptoms.

• SIGN OF A DISEASE
- some type of objective evidence of a disease
Latent Infections

• LATENT INFECTIONS
- a disease that may go from being symptomatic to asymptomatic,
and then some time later, go back to being symptomatic.
Stages of syphilis
Syphilis infection (3 weeks)

Primary: Chancre (2-6 months)

Secondary: Rash, lesions, fever, hair loss (2-6 months)

Latent Stage: No symptoms (5-10 years)

Tertiary: Destruction of brain, heart, spinal cord, and/or other
organs
Primary Versus Secondary
Infections

• One infectious disease may commonly follow another:

• PRIMARY INFECTION- the first disease

• SECONDARY INFECTION- the second disease
STEPS IN THE PATHOGENESIS OF
INFECTIOUS DISEASES
• ENTRY of the pathogen into the body.
- Portals of entry include penetration of skin or
mucous membranes by the pathogen, inoculation of the
pathogen into bodily tissues by an arthropod, inhalation,
ingestion, introduction of the pathogen into the
genitourinary tract or introduction of the pathogen directly
into the blood.

• ATTACHMENT of the pathogen to some tissues within the

body.

• MULTIPLICATION of the pathogen.

• INVASION/SPREAD OF THE PATHOGEN

• EVASION OF HOST DEFENSES

Virulence

• VIRULENT STRAINS
- are capable of causing disease.

• AVIRULENT STRAINS
-not capable of causing disease.
VIRULENCE FACTORS
ATTACHMENT
• RECEPTORS
- receptors and integrin are molecule on the
surface of the host cell that a particular pathogen is
able to recognize and attach to which are often
glycoprotein molecules
Adhesins and ligand are used to describe the
molecule on the surface of the pathogen that is able to
recognize and bind to a particular receptor

• BACTERIAL FIMBRIAE (PILI)

- long thin hair like, flexible projections
composed primarily of an array of proteins called pilin
which enable the bacteria to attach to surfaces and
cause infection in that part of the body
OBLIGATE INTRACELLULAR PATHOGENS

• Rickettsia, Chlamydia as well as Ehrlichia must live within the

host cells in order to survive and multiply.
FACULTATIVE INTRACELLULAR
PATHOGENS

These are pathogens that are able to survive intracellularly and

extracellularly. These microorganisms are able to survive within
phagocytes.

Once bacteria are ingested by white blood cells like

macrophages, the phagosome fuses with the lysosome. Lysosomes
contain hydrolytic enzymes, hydrogen peroxide, superoxide anions
which will cause the destruction of bacteria.

But some organisms like the Mycobacterium tuberculosis contain

wax on their cell wall which prevent the digestion of the organism from
the enzymes of the macrophages.

Rickettsia produce phospholipases that destroy the phagosome

membrane thus preventing the fusion of the lysosome and phagosome
sparing the bacteria from digestion of hydrolytic enzymes.
CAPSULES

The presence of capsules that surround the bacteria protects the

bacteria from phagocytes because phagocytes lack receptors for
polysaccharide material of which the capsule is made. Because they
are not phagocytosed, they are able to multiply and cause disease.

Encapsulated bacteria include Klebsiella, Haemophilus and

Neisseria meningitides as well as S. pneumoniae.
FLAGELLA

Bacterial flagella are considered virulence factor because they

enable the bacteria to invade aqueous areas of the body that
nonflagellated bacteria are unable to reach.

Flagella also enable bacteria to evade phagocytosis because of its

movement which enable it to move at a faster pace thus making it
difficult for the phagocytes to catch a motile organism.
EXOENZYMES
• NECROTIZING
ENZYMES
- bacteria produce
proteases and lipases which
cause destruction of tissues
like necrotizing fasciitis by
Strep pyogenes and gas
gangrene or myonecrosis with
Clostridium species
• COAGULASE
-Staph aureus produce
coagulase which enable it to
clot plasma and thereby form a
sticky coat of fibrin around
themselves for protection from
phagocytes, antibodies and
other host defenses
• KINASES
-or fibrinolysins. This
substance will dissolve the
fibrin clot that the host will
attempt to form in order to wall
and prevent the organism to
invade deeper into body
tissues in order for the
organism to escape from the
clots. Streptococcus produce
streptokinase which is able to
dissolve blood clots.
Streptokinases are also able to
dissolve blood clots in cases of
thrombotic stroke or
myocardial infarction.
• HYALURONIDASE
- called spreading factor
because it enables the
pathogen to spread through
connective tissue by breaking
down hyaluronic acid, which is a
polysaccharide cement that
holds tissues together. It is
secreted by staph, strep and
clostridium species
• COLLAGENASE
-breaks down collagen which
is the supportive protein found
in tendons, cartilage and
bones, enabling the pathogen
to invade tissues. Clostridium
perfringens are able to invade
tissues by secreting
collagenase and hyaluronidase
• HEMOLYSINS
-enzymes that cause the
destruction of red blood cells
producing lysis as well as
providing iron to the pathogen.
Alpha hemolytic strep causes a
green color around the colony
whereas beta hemolytic strep
produces a clear zone around
the colony
• LECITHINASE
-enzyme produced by Clostridium
perfringens which breaks down phospholipids
collectively referred to as lecithin. This
enzyme is destructive to cell membrane of rbc
and other tissues
TOXINS
• ENDOTOXINS
-toxins that are integral part of the cell walls of Gram negative
bacteria that can cause adverse physiologic reactions like septicemia
which produces chills, fever, prostration and the presence of bacteria
and their toxins in the bloodstream.
The cell wall contain lipopolysaccharide called Lipid A or
endotoxin, causing fever and shock. There is reduced mental
alertness,, confusion, rapid breathing, chills, fever and there is low
perfusion of organs due to shock leading to organ failure.
Blood clots may form within blood vessels. There is 30-35%
mortality rate associated with Gram negative sepsis
•EXOTOXINS
- poisonous proteins produced by pathogens often named for the
target organs they affect

1. NEUROTOXIN
- most potent exotoxin produced by Clostridium tetani and
Clostridium botulinum.
Tetanospasmin affects control of nerve transmission where
there is blockade of the inhibitory impulses producing continuous
contraction producing spasm. This is called a spastic paralysis.
Botulinal toxin on the other hand blocks nerve impulses
producing flaccid paralysis in which the patient’s muscles are relaxed
2. ENTEROTOXINS
-cause diarrhea and sometimes vomiting (toxin A).
Toxin B produced by Clostridium difficile damages the lining
of the colon, leading to pseudomembranous colitis

3. TOXIC SHOCK SYNDROME TOXIN l

-produced by strains of Staph aureus and Strep pyogenes
which primarily affects the integrity of capillary walls
4. EXFOLIATIVE TOXIN
EPIDERMOLYTIC TOXIN
-cause sloughing of the epidermal layers of the skin leading to
SCALDED SKIN SYNDROME

5. LEUKOCIDINS
-toxin that destroys leukocytes produced by staph and strep
6. DIPHTHERIA TOXIN
-toxin produced by Corynebacterium diphtheria, which inhibits
protein synthesis killing mucosal epithelial cells and PMN’s as well as
adversely affecting the heart and nervous system. The toxin is coded
for by a bacteriophage gene
MECHANISMS BY WHICH PATHOGENS
ESCAPE IMMUNE RESPONSES
• ANTIGENIC VARIATION
-pathogens able to periodically change their surface antigens.
Ex are influenza viruses, HIV, Neisseria gonorrhea, trypanosomes

• CAMOUFLAGE AND MOLECULAR MIMICRY

-adult shistosomes are able to conceal their foreign nature by
coating themselves with host proteins. In molecular mimicry, the
pathogen’s surface closely resemble host antigens and are therefore
not recognized as foreign

• DESTRUCTION OF ANTIBODIES
- H. influenza. Neisseria gonorrhea and streptococci produce
an enzyme IgA protease that destroys IgA antibody
 Thank you!

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