Antimicrobial agents and there classifications

1. Chemotherapy
Presented by,
Holkar Sujata Sahebrao,
(M.pharm Pharmacology)
1

2. Definition chemotherapy
◼ Aminoglycosides
◼ Antimicrobial agent
◼ Classification of
Antimicrobial agent
◼ Cellular mediators
of inflammation
◼ Biomediators of
immune responces
◼ Allergy and
hypersensitivity 2
Contents:

3. Chemotherapy is a drug treatment
that uses powerful chemicals to kill
fast-growing cells in your body.
chemotherapy is most often used to
treat cancer, since cancer cells grow
and multiply much more quickly than
most cells in the body. many different
chemotherapy drugs are available.
◆ Chemotherapy
◆ Definition
3

4. Definition: An antimicrobial therapy kills or inhibits
the growth of microorganisms such as bacteria,
fungi, or protozoans. Therapies that kill
microorganisms are called microbiocidal therapies
and therapies that only inhibit the growth of
microorganisms are called microbiostatic therapies.
◆ Antimicrobial agents
The use of antimicrobial medicines to treat
infection is known as antimicrobial chemotherapy,
while the use of antimicrobial medicines to prevent
infection is known as antimicrobial prophylaxis.
4

5. ◆ Classification of antimicribial agents
• Cell wall synthesis inhibitors
-Beta lactams(penicillin ,
cephalosporin,azetriona)
-poly-peptides(bacitracin,vancomycin)
• Protein synthesis inhibitor
• -Aminoglycosides
• -tetracyclin
• -macrolides
• -chloramphenicol
• Inhibitors of essential metabolites
• -Sulphonamides
• -Trimethaprim
• Injury to plasma membrane
• -PolymaxinB
• -Mystatin
• -AmphoterecinB
• -Miconazole
• Inhibitor of nucleic acid
replication and transcription
• -Quinolones
• -rRefampicin
5

6. ◆ Aminoglycosides
Aminoglycosides are called bactericidal
antibiotics because they kill bacteria directly.
They accomplish this by stopping bacteria
from producing proteins needed for their
survival.
• Examples of aminoglycosides include:
Gentamicin
Amikacin
Tobramycin
Gentak and Genoptic
Kanamycin
Streptomycin
Neo-Fradin
Neomycin
6

7. Mechanism of action
 Aminoglycosides binds to 30s ribosomal units
of bacteria.
 Prevents the formation of initiation complex
which is the prerequisite for peptide
synthesis.
 Lack of the formation of initiation complex
causes the 30s sub unit to misread the genetic
code on mRNA
 Incorrect aminoacides are thus incorporated
into the growing peptide chain, which are of
no use for bacterial growth.
 Leads to bacterial growth.
7

8. 8

9. CONTD…
 Aminoglycosides also act by;
 Formed improper initiation complex blocks
the movement of ribosomes
 Resulting in a mRNA chain attached with
single ribosomes (monosomesThus amino
glycosides also interfer in the assemble of
polysomes
 Results in the accumulation of non functional
ribosomes.
9

10. ◆ Common Side Effects
Aminoglycosides are very powerful
antibiotics, and their side effects can be
severe —
-Damage to the hearing structures in the ear,
resulting in hearing loss
-Damage to the inner ear, resulting in trouble
maintaining balance
-Kidney damage (noted by protein in the
urine, dehydration, and low levels of
magnesium)
-Paralysis of skeletal muscles
10

11. 11

12. ◆ Cellular mediators of Inflammation
-Also called as permeability factors or endogenous
mediators of increased vascular permeability.
-Large and increasing number of endogenous compound
which can enhance vascular permeability.
-Chemical mediators are released from cells,plasma or
damaged tissue.
12

13. ◆ Inflammatory mediators classification
a)Vasoactive amines (serotonin, histamine)
b)Arachidonic acid metabolites
-Cycloxygenase pathway
-Lipoxygenase pathway
c) Lysosomal components
b) Platelet activating factor
e) Cytokines
f) Nitric oxide and oxygen metabolites
1)cell derived mediators
13

14. a) The kinin system
b) clotting system
c) The fibrinolytic system
d) The complement system
2)plasma derived mediators
14

15. 1)cell derived mediators
A)vasoactive Amines
◼ Histamine
• Stored in the granules of mast
cells,basophiles and platelets
• Main action
• Vasodilation,itching,pain,increased vascular
permeability.
• Present in tissue like chromaffin cells of
GIT,spleen,nervous tissue, mast cell and
platelets.
5-hydroxytriptamine
15

16. 2)Arachidinic acid metabolites
-Arachidonic acid (fatty acid)is released from the cell
membrane by phospholipases.
-It is then activated to form arachidonic acid
metabolites or eicosanoids by one of the following two
pathways cyclo-oxygenase and lipo-oxygenase
pathways.
16

17. The inflammatory cells neutrophiles and monocytes
contain lysosomal granules which on release
elaborate a variety of mediators.
i)Granules of monocytes and tissue
macrophages.
On degranulation these cells release acid
protease, collagenase, elastase and
plasmonogen activator
3)Lysosomal components
17

18. ii)Granules of neutrophils
18

19. 4)platelet activating factor(PAF)
Release from IgE sensitised basophiles or
mast cells, leucocytes, endothelium and
platelets
• Actions:
• -Increased vascular permiability
• -Vasodilation and vasoconstriction
• -Bronchoconstriction
• -Adhesion of leucocytes to endothelium
• -Chemotaxis.
19

20. 5)Cytokines
These are polypeptide substances produced by
activated lymphocytes (lymphokines)and activated
monocytes (monokines)
-Major cytokines interleukin-1(IL-1)tumor necrosis
factor (TNF) AND alpha and beta ,chemokines.
Actions
•IL-1 AND TNF-ALPHA ,TNF-BETA
-Induced endothelial effects
-Increased leucocytes adherence
-Thrombogenicity
-Fibroblastic proliferation.
20

21. •INF-Y
-Activation of macrophages and neutrophiles
•Synthesis of nitric acid synthase.
•Chemokines
-IL-8 chemotactic for eosinophil
21

22. • Bradikinin
Actions.
-Smooth muscle contraction
-Vasodilation
-Increased vascular permeability
-Pain
-Increased vascular permeability
-Chemotaxis
-Anticoagulant activity
• Fibrinipeptides
Actions.
22

23. • The complement system
I)The activation of complement system
occur by:
i)Classic pathway via non immunological agents
ii)Alternate pathway via non immunological
agent
Complement system on activation yields
activated products-anaphylotoxins
(C3a,C4a,C5a) and membrane attack complex
(MAC)-C5b,C6,C7...
23

24. The immune response is how your body
recognizes and defends itself against bacteria,
viruses, and substances that appear foreign
and harmful.
• Examples of innate immunity include:
• Cough reflex.
• Enzymes in tears and skin oils.
• Mucus, which traps bacteria and small
particles.
• Skin.
• Stomach acid.
◆ Allergy and Hypersensitivity
24

25. The immune system protects the body from
possibly harmful substances by recognizing
and responding to antigens. Antigens are
substances (usually proteins) on the surface
of cells, viruses, fungi, or bacteria. Nonliving
substances such as toxins, chemicals, drugs,
and foreign particles (such as a splinter) can
also be antigens. The immune system
recognizes and destroys, or tries to destroy,
substances that contain antigens.
◼ Information
25

26. • Your body's cells have proteins that are
antigens. Your immune system learns to see
these antigens as normal and usually does
not react against them.
26

27. Innate, or nonspecific, immunity is the defense
system with which you were born. It protects
you against all antigens. Innate immunity
involves barriers that keep harmful materials
from entering your body.These barriers form
the first line of defense in the immune
response.
•Examples of innate immunity include:
-Cough reflex
-Enzymes in tears and skin oils
-Mucus, which traps bacteria and small p-
articles
-Stomach acid
• INNATE IMMUNITY
27

28. Innate immunity also comes in a protein
chemical form, called innate humoral
immunity. Examples include the body's
complement system and substances called
interferon and interleukin-1 (which causes
fever).
If an antigen gets past these barriers, it is
attacked and destroyed by other parts of the
immune system.
28

29. ACQUIRED IMMUNITY
Acquired immunity is immunity that develops with
exposure to various antigens.Your immune system
builds a defense against that specific antigen.
PASSIVE IMMUNITY
Passive immunity is due to antibodies that are
produced in a body other than your own. Infants
have passive immunity because they are born
with antibodies that are transferred through the
placenta from their mother.These antibodies
disappear between ages 6 and 12 months.
29

30. The immune system includes certain types of
white blood cells. It also includes chemicals and
proteins in the blood, such as antibodies,
complement proteins, and interferon. Some of
these directly attack foreign substances in the
body, and others work together to help the
immune system cells.
BLOOD
COMPONENTS
30

31. The term allergy was originally defined by
ClemensVon Pirquet as “an altered capacity
of the body to react to a foreign substance,”
which was an extremely broad definition that
included all immunological reactions.Allergy is
now defined in a much more restricted
manner as “disease following a response by
the immune system to an otherwise
innocuous antigen.”
31

32. Allergic reactions occur when an individual
who has produced IgE antibody in response
to an innocuous antigen, or allergen,
subsequently encounters the same allergen.
The allergen triggers the activation of IgE-
binding mast cells in the exposed tissue,
leading to a series of responses that are
characteristic of allergy.
◆ Allergy and Hypersensitivity
32

33. there are circumstances in which IgE is
involved in protective immunity, especially in
response to parasitic worms, which are
prevalent in less developed countries. In the
industrialized countries, however, IgE
responses to innocuous antigens predominate
and allergy is an important cause of disease
33

34. Fig. IgE-mediated reactions to extrinsic
34

35. All IgE-mediated responses involve mast-cell
degranulation, but the symptoms experienced
by the patient can be very different depending
on whether the allergen is injected, inhaled, or
eaten, and depending also on the dose of the
allergen.
35

36. Immune responses to innocuous antigens that
lead to symptomatic reactions upon
reexposure are called hypersensitivity
reactions. These can cause hypersensitivity
diseases if they occur repetitively. This state of
heightened reactivity to antigen is called
hypersensitivity.
◆ Hypersensitivity reactions
36

37. Hypersensitivity reactions are classified by
mechanism: type I hypersensitivity reactions
involve IgE antibody triggering of mast cells;
type II hypersensitivity reactions involve IgG
antibodies against cellsurface or matrix
antigens; type III hypersensitivity reactions
involve antigen:antibody complexes; and type
IV hypersensitivity reactions are T cell-
mediated.
37

38. Fig.There are four types of hypersensitivity reaction
mediated by immunological mechanisms that cause
tissue damage. 38

39. Types I–III are antibody-mediated and are
distinguished by the different types of antigens
recognized and the different classes of
antibody involved. Type I responses are
mediated by IgE, which induces mast-cell
activation, whereas types II and III are
mediated by IgG, which can engage Fc-
receptor and complement-mediated effector
mechanisms to varying degrees, depending on
the subclass of IgG and the nature of the
antigen involved.
39

40. Type II responses are directed against cell-
surface or matrix antigens, whereas type III
responses are directed against soluble
antigens, and the tissue damage involved is
caused by responses triggered by immune
complexes.
40

41. Type IV hypersensitivity reactions are T cell-
mediated and can be subdivided into three
groups. In the first group, tissue damage is
caused by the activation of macro-phages by
TH1 cells, which results in an inflammatory
response. In the second, damage is caused by
the activation byTH2 cells of inflammatory
responses in which eosinophils predominate;
in the third, damage is caused directly by
cytotoxic T cells (CTL).
41

42. References
1. The Pharmacological basis of therapeutics-
Goodman and Gill man‘s pp.1505-1520
2.https://www.google.com/url?sa=t&source=web&rct=j
&url=https://www.ncbi.nlm.nih.gov/books/NBK10756/
&ved=2ahUKEwiC85LomZLnAhVsILcAHbHRAy4QFj
AKegQIBRAC&usg=AOvVaw2EndS8c0voA5rKtqIZW-
CM&cshid=1579530366147
3)https://www.slideshare.net/mobile/aiswarya1995/c
hemical-mediators-of-inflammation
4)https://www.google.com/url?sa=t&source=web&rct=j&
url=https://www.everydayhealth.com/aminoglycosides/g
uide/&ved=2ahUKEwiBxvfT2ZLnAhUbU30KHRRxCUU
QFjAZegQIAhAB&usg=AOvVaw02OQQiHy6QrzDJMd
MkR0-Q&cshid=1579541255035
42

43. THANKYOU
43