The document is a review on bacterial virulence factors, detailing their roles in infection and disease causation. It outlines various mechanisms through which bacteria adhere, invade, produce toxins, and evade host defenses, including adhesins, invasins, exotoxins, and biofilm formation. The conclusion emphasizes the importance of understanding these factors for future vaccine development and the need for deeper research into bacterial pathogenesis.

1. AMBO UNIVERSITY
GUDER MAMO MEZEMIR CAMPUS
SCHOOL OF VETERINARY MEDICINE
DEPARTMENT OF VETERINARY LABORATORY TECHNOLOGY
ASSIGNMENT OF MICROBIAL GENETICS AND VIRULENCE
TITLE: REVIEW ON VIRULENCE FACTORS OF BACTERIA
BY
MOHAMMED BUSHURA

2. VIRULENCE FACTORS
OF BACTERIA

3. OUTLINE
 Introduction
 Bacterial Virulence Factors
 Conclusion
 Recommendation

4. INTRODUCTION
What Is Virulence Factors?
The definition of what constitutes a virulence factor is
varied and controversial.
Virulence is described as an ability of an organism to infect
the host and cause a disease.
Virulence factors are the molecules that assist the Bacterium
colonize the host at the cellular level.
Therefore, the objective of this review is to revise mainly
the bacterial virulence factors.

5. BACTERIAL VIRULENCE FACTORS
1. ADHESINS
 Bacterial components help the organism to adhere to the host
 Located on the surface of bacteria
 Bacteria can also adhere to and internalize into host cells by direct
interaction with integrin's.

6. Adhesins…

7. Adhesins….

8. 1.1. Chaperone-Usher Pili: P Pili and Type I Pili
CU pili are some of the most well-characterized bacterial adhesins.
 They form long proteinacious strands
 Extend from many gram negative and some gram positive bacterial
surfaces.
 pili can also be utilized for the transfer of DNA during conjugation

9. 1.2.Type IV Pili
Type IV pili are another group of polymeric surface organelles
Type IV pilus formation involves the translocation of pre-pilins
across the inner membrane
 pre-pilin peptidase recognizes and cleaves a conserved N-terminal
type III signal sequence

10. 1.3. Adhesive Amyloids
 Amyloids are insoluble polymeric protein fibril-like structures
 first recognized in human diseases such as Alzheimer’s,
 Huntington’s and prion encephalopathies but have since
been found in nature
 Curli are the best described class of functional amyloids
produced by enteric bacteria

11. Adhesive Amyloids…
The main role of amyloid fiber adhesion
 During biofilm formation, they help to increase biofilm stability
 Interactions with host ECM proteins such as fibronectin and laminin
 Enhance resistance to protease degradation

12. 1.4. Autotransporters
 Diverse family of outer membrane and secreted proteins
 found in Gram-negative bacteria and form a monomeric or trimeric
 they facilitate adhesion to host cell surfaces
 All autotransporters share conserved structural features,
Including: N-terminal signal sequence which enables secretion
C-terminal translocation domain which inserts into the
outer membrane,

13. 1.5. Multivalent Adhesion Molecules
 MAMs are a relatively recent class of bacterial adhesins
 participate in high affinity binding during the early stages of infection
 MAMs consist of an N-terminal hydrophobic region
MAM6 and MAM7 molecules are found exclusively in Gram-
negative bacteria

14. 2. INVASINS
 virulence factors that specifically promote internalization of a
bacterium by a host cell.
 assigned to general virulence strategies required for host
colonization.
 A typical pathogen must use one or a combination of
mechanisms to colonize the host.

15. 3. EXOTOXINS
 Bacterial toxins contribute to virulence by interfering with cellular homeostasis
 Produced by several toxigenic bacteria, including Corynebacterium diphtheria,
Vibrio cholera and Clostridium tetani,
the causes of diphtheria, cholera and tetanus, respectively.
 Genes carried in phages, plasmids or p. islands usually encode these toxins
 abolition of toxin production is usually accompanied by abrogation of virulence.

16. 4. MODULINS
A large group of microbial compounds can damage a host by eliciting
inflammatory responses.
Microbial products that elicit detrimental cytokine responses, such as
lipopolysaccharide, have been called modulins
 lipopolysaccharide is a well-known example of a microbial compound that can
cause massive host damage
 by interacting with Toll-like receptors and triggering an inflammatory cascade.

17. 5. ENZYMES
Numerous enzymes have been implicated in bacterial virulence.
Enzymes that are considered virulence factors are generally
active against host components.
Tissue damage makes the host permissive for microbial
infection.

18. ENZYMES…
Enzyme virulence factors that damage tissue include proteases,
neurominidases and phospholipases.
These enzymes damage cells and provide nutrients by digesting
substrates into smaller components

19. ENZYMES…
they also alter host cellular receptors in a manner that can
subvert the binding of their usual ligands,
such as complement, and alter microbial behavior to promote
invasiveness, serum resistance and evasion of host immune
mechanisms.

20. 6. Motility
 Motility is a complex trait that has been associated with virulence in
bacteria
 Motility is manifested by approximately 80% of known bacterial
species
 Bacterial cells can move by the action of specialized organelles called
flagella.

21. Motility…
Actin-based motility is used by several intracellular pathogens
including Shigella spp., Listeria monocytogenes and
Rickettsiae for cell-to-cell spread.
the ability to move is intimately linked with other traits that are
associated with virulence.

22. 7. CAPSULES
Many pathogenic bacteria possess polysaccharide capsules,
which are required for virulence in mammalian hosts.
Encapsulated bacteria with polysaccharide capsules include:-
 Streptococcus pneumoniae,
 Neisseria meningiitidis
 Haemophilus influenzae.

23. CAPSULES…
Most capsules function in microbial pathogenesis:-
 protecting the microbe against host immune mechanisms,
 the capsular structures can serve as adhesins.
protect microbes from phagocytosis and intracellular killing.

24. 8. Complement evasion
The complement system is a central component of innate immunity
and host defense against microbial agents.
Complement proteins serve diverse host functions, including:-
 having direct antimicrobial activity,
 mediating opsonization,
 promoting the release of inflammatory mediators

25. 9. Pigments
Pigment production, and specifically melanin-like pigments,
have been associated with virulence
Melanin in melanotic organisms can protect against a variety
of host defense mechanisms, includes:-
 free radical fluxes,
 Defensins
 phagocytosis

26. 10. Pro-apoptotic mechanisms
Apoptosis is a non-inflammatory form of cell death
Microbial inhibition of apoptosis has the potential to enhance virulence
by preventing downregulation of the inflammatory response,

27. Pro-apoptotic mechanisms…
Pro-apoptotic effects have been demonstrated for toxins, such as-
 alpha toxin of S. aureus,
 L. monocytogenes listerolysin O,
 E. coli alpha hemolysin,
 diphtheria toxin,
 P. aeruginosa exotoxin A,

28. 11. Biofilm formation
Biofilms are dense aggregates of microorganisms embedded in an
exopolysaccharide matrix
The phenomenon of biofilm formation is closely linked to other
processes involved in bacterial pathogenesis, including;
 quorum sensing,
 attachment and
 signaling

29. Biofilm formation…
For some diseases, such as bacterial endocarditis, biofilm
formation is an essential component of the pathogenic
process.
In these diseases, biofilm are composed of both bacterial and
host components, which serve to isolate the microbes from
host defense mechanisms and antimicrobial therapy.

30. 12. Two-component systems, histidine kinases and
quorum sensing
Bicterias sense the environment and respond to environmental stimuli
by the initiation of signal transduction events.
Prokaryotes have various types of two-component systems,
which achieve signaling by transferring a phosphoryl group from a
phosphohistidine moiety in the sensor kinase component to an
aspartate in the response regulator.

31. Two-component systems, histidine kinases and
quorum sensing…
Quorum sensing is a cell-to-cell communication mechanism by which
bacteria can sense their population density by the production of small molecules.
Quorum sensing regulation has three distinct phases:
 production of the signaling small molecules by bacteria,
 accumulation of signaling molecules as a function of bacterial density
 the response by bacteria when a threshold concentration is reached

32. 13. Secretion systems
Bacterial secretion systems export microbial effector proteins
that are essential for virulence
Type I secretion system is a protein-mediated secretion system,
used in the export of certain toxins and in drug efflux

33. Secretion systems.…
The Type II secretion system, also known as the general secretion
system,
 responsible for the export of certain toxins and enzymes
 The Type II secretion system is composed of a multi-subunit protein
it functions to export proteins to the extracellular compartment

34. Secretion systems.…
TIISS specialized systems for secreting proteins into host
cells.
consist of a syringe-like structure that functions to inject
microbial effector proteins directly into the host cell cytoplasm

35. Secretion systems.…
Type IV secretion systems constitute another type of protein
delivery system to eukaryotic cells
evolutionarily related to bacterial conjugation systems
Many of the bacterial effector molecules delivered by Type IV
secretion pathways interfere host cellular pathways

36. 14. IRON ACQUISITION
Iron is essential for microbial growth and metabolism.
The close relationship between iron acquisition and
virulence is illustrated by associations between iron
overload states and infectious diseases.

37. IRON ACQUISITION….
There are several mechanisms by which bacteria
obtain iron from human or animal tissues
the expression of siderophores,
 low molecular weight chelators of iron
 surface receptor proteins that bind transferrin,
lactoferrin,ferritin, hemoglobin, ferrous iron transporters,
heme or haptoglobin–hemoglobin complexes.

38. IRON ACQUISITION….
In general, bacteria that can survive either within or
outside of a host use siderophores to obtain iron,
whereas species-specific organisms that do not
survive in the environment acquire iron from the
host through surface receptors.

39. 15. Intracellular survival
 the capacity for surviving inside phagocytic cells or
 mechanisms that ensure intracellular survival.
 Each intracellular pathogen has a unique approach for
ensuring intracellular survival
E.g. Listeria monocytogenes avoids phagosomal killing by
producing a toxin known as Lysteriolysin

40. Intracellular survival….
 Other microbes interfere with phagosome maturation
and function
E.g. Legionella pneumophila, a Gram-negative bacterium
that interferes with phagosome maturation,

41. CONCLUSION
 The virulence factor concept has been a powerful engine in driving
research
 At a practical level the finding that effective immune responses often
target virulence factors provides a roadmap for future vaccine design.
However, there are significant limitations to this concept, which are
rooted in the inability to define virulence and virulence factors in the
absence of host factors and the host response.
This concept appears to work best for bacterial pathogens and
commensal organisms with pathogenic potential.

42. RECOMMENDATION
In the future, further and deep study should
be needed to know more about bacterial virulence
and their pathogenesis mechanism.