This document discusses bacterial virulence and pathogenicity. It defines Koch's postulates for identifying disease-causing pathogens. Virulence factors like capsules, pili, toxins and enzymes allow bacteria to cause disease by adhering to and damaging host cells. Routes of entry into the body and host defenses that bacteria must overcome are described. The document outlines different types of bacterial-host interactions and factors that facilitate pathogenesis.

1. BACTERIAL VIRULENCE
Dr Shireen Rafiq
MBBS, M.Phil, Ph.D

2. Koch’s PostulateKoch’s Postulate
isolatedisolated
diseased not healthy peoplediseased not healthy people
growthgrowth
pure culturepure culture
induce diseaseinduce disease
susceptible animalssusceptible animals
re-isolatedre-isolated
susceptible animalssusceptible animals

3. Normal flora
Resident ------commensals
Transient
Carrier state
Colonization

4. A pathogen is a microorganism that is able to
cause disease in a plant, animal or insect.
Pathogenicity is the ability to produce disease
in a host organism.
Microbes express their pathogenicity by means
of their virulence=the degree of
pathogenicity.
Infectious dose depends on virulence factors

5. ROUTES OF
ENTRY

6. Host defensesHost defenses
GutGut
peristalsisperistalsis
 defecationdefecation
respiratory tractrespiratory tract
ciliary actionciliary action
coughingcoughing
sneezingsneezing
urogenital tracturogenital tract
urinationurination

7. MICROBES
Pathogens
Opportunistic Pathogens
Obligate Pathogens
Symbiosis: Mutualism
Parasitism
Commensalism

9. PEPTIDOGLYCAN
CAPSULE/BIOFILMS
PILI
FIMBRIA
LIPOTECHOIC ACID
PLASMIDS
VACUOLE FORMATION (in
Host)
HYDROPHOBIC MOLECULES
TOXINS (Exotoxin and
Endotoxin)
ENZYMES
SIDEROPHORES (ferric ions)
STRUCTURAL NON
STRUCTURAL

11. ADHERENCE FACTORS
Adhesin/Ligand: A surface structure
or macromolecule that binds a
bacterium to a specific surface.
 Receptor: A complementary
macromolecular binding site on a
(eucaryotic) surface that binds
specific adhesins or ligands
Biofilms: protect bacteria from
antibiotics and host defense resulting
in chronic wound infections

14. E. coli with fimbriae

15. Factors Facilitating Pathogenesis
ADHESINS
ANTIPHAGOCYTIC FACTORS
-CAPSULE -M PROTEIN -CYTOTOXIN
SURVIVAL WITHIN PHAGOCYTES (PREVENTION OF)
-OXID. BURST -FUSION AND DEGRANULATION
-LYSOZYMES -ESCAPE FROM PHAGOSOMES
 SIDEROPHORES
TOXINS AND ENZYMES
PLASMIDS

17. Toxigenesis is the ability to produce
toxins.
Exotoxins (gram positive and gram
negative) secreted by bacteria,
polypeptide
Endotoxins (gram negative ) part of cell
wall, lipopolysaccharide.

19. A-B toxinsA-B toxins
ActiveActive
BindingBinding
AA
Cell surfaceCell surface
BB

20. • ProteasesProteases
• PhospholipasesPhospholipases
• Detergent-like actionDetergent-like action
Membrane damaging exotoxins

22. EXOTOXIN ENDOTOXIN
1. EXCRETED INTEGRAL
2.GRAM POSITIVE AND NEGATIVE GRAM NEGATIVE
3. POLYPEPTIDE LIPOPOLYSACCHARIDE
4. UNSTABLE/DESTROYED ABOVE
60C
STABLE ABOVE 60C
5. HIGHLY ANTIGENIC
Toxoid formation
WEAKLY ANTIGENIC
6. HIGHLY TOXIC (ug) MODERATELY TOXIC (mgs)
7. BIND TO RECEPTORS RECEPTORS NOT INVOLVED
8. NOT PYROGENS PYROGENIC
9. PLASMID OFTEN INVOLVED CHROMOSOMAL

23. EFFECTS OF ENDOTOXIN Lipid A
Fever
Shock
Stimulation of immune system
Greater susceptibility to stress
Lethality

24. Stages of infectious disease
Incubation period
Prodromal period
Specific illness period
Recovery period

25. MUTATIONS
Change in the base sequence of DNA resulting in altered
phenotype. Mutations result from three type of
molecular changes
1 Base substitutions
2 Frameshift mutation
3 Transposons or insertion sequence
Chemicals , radiations and viruses

28. TRANSDUCTION

33. RECOMBINATION
Homologous
Non homologous
different endonucleases and
ligases are involved