INTRODUCTION
- As we know, bacteria enter our body through a number of routes or through breach in our skin or mucous membrane.
- But, it's ability to cause a disease and the immune response generated by the host depends very much on the inoculum size and it's virulence.
- If the inoculum size and the virulence both are low; then innate immunity comes in to play.
- On the other hand, if the inoculum and virulence both are high then adaptive response is generated.
- Immune response also depends on whether it's an extracellular or intracellular bacteria.
Immune response against extracellular bacteria :
Extracellular bacteria are pathogenic for 2 reasons:
1)They induce a localised inflammatory response.
2)They produce toxins.And, these toxins can be cytotoxic or cause pathogenesis in other ways.e.g. Diphtheria toxin blocks the protein synthesis.
In response to these bacteria, antibodies are secreted which can work in various ways to tackle the bacteria.
- Antibodies may bind to antigens on the bacterium and activate complement system.After this, the bacteria can be lysed or opsonized for phagocytosis.
- Antibody -activated complement can also lead to release of anaphylotoxins and chemotactic factors which further help in phagocytosis.
- Besides,antibody can bind to toxins to form antibody-toxin complex which is cleared by phagocytosis just as Ag-Ab complex.
Immune response against Intracellular bacteria :
- Innate immunity is not effective in this case ,although NK cells provide an early defense against these bacteria.
- CMI is the main response against Intracellular bacteria and among them too, more specifically DTH response acts. In this response, cytokines secreted by CD4+ T cells are important; notably IFN-gamma , which activates macrophages to kill ingested pathogens more effectively.
EVASION OF THE HOST RESPONSE BY BACTERIA
There are 4 steps in bacterial infection :
1) Attachment to host cell,
2) Proliferation,
3) Invasion of host tissue,
4) Toxin induced damage to host cells.
Host defense mechanisms act at each of these steps and many bacteria have evolved ways to circumvent some of them.
Attachment to the host cell:
Some bacteria have surface structures or molecules that enhance their ability to attach to host cells.e.g.
1) A number of gram negative bacteria have pili which enable them to attach to the membrane of the intestinal or genitourinary tract.
2) Others sub as bordetella secrete adhesion molecules which attach to both the bacterial and host cell .
Host defense mechanisms :
- secretory IgA molecules are the main host defense against bacterial attachment to the mucosal epithelial cells. But many bacteria have developed strategies to tackle this.
- E.g. Neisseria gonorrhoeae , hemophilus influenza, and neisseria meningitidis secrete protease which cleave IgA molecule at the hinge region and make it malfunctioning.
- Neisseria gonorrhoeae evade the immune response also by changing their surface antigens preferably pilin sequence ).
Proliferation :
Host defense mechanisms :
1) phagocytosis
2)complement mediated lysis and localised inflammatory response.
a) phagocytosis -
- host tries to handle the microbe through phagocytosis; but some bacteria possess surface structures to inhibit phagocytosis.
- Polysachharide capsule of S.pneumonia, M protein of S.pyogens and the ability of some staphylococcal bacteria to assemble a fibrin coat around them help to escape phagocytosis.
b)complement mediated lysis and localized inflammatory response :
- Mechanisms to interfere with the complement system help bacteria survive.
- E.g. long side chains on the lipid A moiety of the cell wall polysaccharide help to resist lysis in gram (-)ve bacteria.
- Some gram (+)ve bacteria show a generalized resistance to complement mediated lysis.
Invasion of host tissues:
- Host tackle this by Ab-mediated agglutination. e.g. pseudomonads secretes an enzyme elastase that inactivates both the C3a and C5a anaphylotoxins that diminish the localized inflammatory reaction.
Toxin induced damage to host cells:
- Host tackle this through neutralisation of toxin by antibody. But, bacteria secrete hyaluronidase that enhance bacterial infections .
NOTE:
- A lot of bacteria even has the Ability to survive within phagocytic cells:.e.g.Listeria monocytogens survive with in phagocytic cells by escaping from the phagolysosome in the cytoplasm which provides a favorable environment for growth.
- Mycobacterium avium block formation of phagolysosome and some mycobacteria are resistant to the oxidative attack that takes place within phagolysosome.
SOME COMMON BACTERIAL DISEASES:Diptheria and tuberculosis
