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Dr. N. Al-Mously
R
 

s the ability to cause disease and it is a multi-factorial

process which depends on:
1. The immune status of the host
2. The nature of the species or strain (virulence factors)
3. The number of organisms in the initial exposure
(inoculum size).

c


t describes the aggressiveness (is quantitative; more or

less virulent). Virulence factors of bacteria are factors that
enhance bacterial ability to cause disease.
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‡ Shedding and spread from original host

‡ Survival during spread
‡ Entry in new host
‡ Growth, adhesion
‡ Colonisation
‡ Survival in the host
‡ Survival of the host response
‡ Damage to the host

3
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Exposure

Organisms become Colonization

Organisms   




 
by host defenses








(no symptoms
but organisms
are shed) R
 



   v
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Specific bacterial species (or strains within a species) initiate
infection after being transmitted by different routes to
specific sites in the human body.

For example, bacteria are transmitted in airborne droplets

to the respiratory tract, by ingestion of food or water or by
sexual contact.
Site of entry of organisms:
 Ö 

 
     
One of several pathogenic mechanisms
and it is a virulence factor that results in colonisation
‡ Bacterial infections are usually initiated by adherence
of the microbe to a specific epithelial surface of the
host.

‡ Otherwise the organism is removed e.g. by peristalsis

and defecation (from the gut) ciliary action, coughing
and sneezing (from the respiratory tract) or urination
(from the urogenital tract).
‡ Adhesion is not non-specific "stickiness".

‡ Specific interactions between external constituents on

the bacterial cell (adhesins) and on the host cell
(receptors) occur i.e. an adhesin-receptor interaction.

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Ò Common adherence mechanisms
Ò Capsules and slime
Ò Biofilm formation
Ò Gram-positive adhesins
Ò MSCRAMMs (microbial surface components
recognizing adhesive matrix molecules), e.g.
protein A
Ò Fimbriae
Ò Gram-negative adhesins (CHO and protein
receptors)
Ò Fimbriae, Afimbrial adhesins (FHA, Pertactin
etc.)
Ò Outer Membrane Proteins
Ò Types

-
V secretion
 Ä   
h
 has surface fimbriae which contain two major
components the M protein and lipoteichoic acid.

The protein fibronectin binds to epithelial cells and fatty

acid moieties of lipoteichoic acid in turn interact with fibronectin.

Among the most thoroughly studied pili are those of uropathogenic

. Certain adhesins present on the tips of fimbriae of E. coli
facilitate binding to epithelial cells.
Type 1 fimbriae bind to mannose containing receptors.

While P fimbriae allow binding to galactose containing glycolipids

(e.g. cerebrosides) and glycoproteins present on epithelial cells.
They are referred to as "P" fimbriae since they were originally shown to
bind to P blood group antigens on human erythrocytes.
Ä
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 Bacterial Adhesion
Tropism

‡ O 
 ‡ Nasopharyngeal epithelium

‡ O 
  ‡ Uretral epithelium
‡  

  ‡
ntestinal epithelium
‡  
  ‡ Respiratory epithelium
‡ h
  ‡
ntestinal epithelium
‡ 


  ‡ Gastric mucosa
‡ h 



 ‡ Pharyngeal epithelium

‡ 

 ‡
ntestinal epithelium
‡ 

 ‡ Respiratory epithelium
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‡Some bacterial pathogens reside on epithelial surfaces

e.g.  

 .

‡Other species are able to penetrate these barriers but remain locally.

‡Others pass into the bloodstream or from there onto other systemic
sites.

‡This often occurs in the intestine, urinary tract and respiratory

tract, and much less commonly through the skin.
‡ For example, h

 penetrates by activating
epithelial cells of the intestine to become endocytic; the
h
do not usually spread into the bloodstream.

‡
n other cases, bacteria (e.g. h
) pass through
epithelial cells into the bloodstream.

‡
nvasion can refer to the ability of an organism to enter
a cell, although in some instances it can mean further
passage into the systemic vasculature.

‡Certain degradative exotoxins secreted by some bacteria

(e.g. hyaluronidase or collagenase) can loosen the
connective tissue matrix increasing the ease of passage of
bacteria through these sites.
Invasion of cells

15
@ovement of bacterium
from cell to cell

16
  



  




‡ Local toxins and enzymes
‡ Peripheral toxins (toxin diseases)

‡ Activation of immune response

‡ Cell invasion

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19
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Many bacteria produce proteins (exotoxins) that modify, by
enzymatic action, or by other means destroy cellular
structures.

Effects of exotoxins are usually seen acutely

acutely, since they
are sufficiently potent that serious effects (e.g. death) often
result.

Examples of exotoxin produced diseases are

botulism, anthrax
botulism anthrax, cholera and diphtheria
diphtheria.

f the host survives the acute infection, neutralizing

antibodies (anti-
(anti-toxins) are often elicited that neutralize the
affect of the exotoxin.

Exotoxins which act on extracellular matrix of connective

tissue. e.g.  
   (collagenase) .
tissue
h



  (hyaluronidase)

Toxin diseases:
When the toxin is responsible completely for causing
the characteristic symptoms of the disease. E.g.:

‡ Food poisoning ‡ h




 
‡ Botulism ‡  


‡ Tetanus ‡  


‡ Diphteria ‡  
 
 

‡ Cholera ‡  

 

‡ Pertussis ‡  
 

‡ Gas gangrene ‡  
  

‡ Anthrax ‡ 

 

21

   
 
A) Proteases

B) Phospholipases

C) Detergent -like action

These toxins enzymatically digest the phospholipid

(or protein) components of membranes or behave as
detergents.
detergents

n each case holes are punched in the cell membrane

and the cytoplasmic contents can leach out.
The    
 _
_
 



 

 is an
example of a membrane damaging toxin.

t destroys blood vessels stopping the influx of inflammatory

cells.

This also helps create an anaerobic environment which is

important in the growth of this strict anaerobe.

The 

  of h
  is an 


 


  that 

 

 and is believed to
have a detergent-like action.
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Ä

Ä
 
Damage to the connective tissue matrix (by
hyaluronidase and collagenase) can "loosen up" the
tissue fibers allowing the organism to spread through the
tissues more readily.

Also included in this group is the exfoliatin of

h



  which causes separation of the

layers within the epidermis and is the causative agent of
scalded skin syndrome in the newborn.
newborn
‡   - one benefits, other is unaffected
(microbes on your skin)
‡ 
  - both benefit (E. coli makes vitamin K
for humans)
‡ R

- one benefits at the others expense (if
a flora gets into an area of the body other
than that from which he lives)