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- Kalpesh Zunjarrao
Definition
Resistance exhibited by the host towards injury
caused by microorganism & their products
Immunity is concerned with reaction of body
against any foreign antigen
Types
Immunity against infectious diseases is of different types
Innate (native) immunity
Non-specific
Species
Racial
Individual
Specific
Species
Racial
Individual
Acquired (adaptive) immunity
Active
Natural
Artificial
Passive
Natural
Artificial
Innate immunity
Resistance to infections that an individual
possesses by virtue of his genetic constitutional
make-up
Immunity present since birth (inborn)
It is not affected by prior contact with
microorganisms or immunisation
Non-specific: degree of resistance to infections in
general
Specific: resistance to particular pathogen
Species immunity:
Total or relative resistance to pathogen, shown by all
members of species
Eg: All human beings are resistant to plant pathogens
& many animal pathogens
Mechanism is not clearly understood but may be due
to physiological & bichemical differences between
tissues of different species
3 levels of innate immunity: species, racial, individual
Racial immunity:
Different races within same species may show
differences in susceptibility to infection
Eg: high resistance of Algerian sheep to anthrax
Another example: genetic resistance to Plasmodium
falciparum in some parts of Africa
Racial differences are genetic in origin, by selection
& inbreeding
Individual immunity:
Difference in immunity exhibited by different
individuals in race
It is well documented that homozygous twins show
similar degrees of susceptibility to leprosy & TB
This immunity is due to genetic constitution of
individual
Factors affecting individual innate immunity
1. Age:
Very young & very old: more susceptible to
infectious disease
Fetus in uterus is protected from maternal infection
by placental barrier. But some pathogens cross the
barrier causing overwhelming infection resulting in
fetal death
Some infections are more severe in adults than in
young children due to hypersensitivity
Old persons are highly susceptible to infections due
to declined immune responses
2. Hormonal influence:
Endocrine disorders (diabetes, hypothyroidism,
adrenal dysfunction) are associated with enhanced
sensitivity to infections
High incidence of staphylococcal sepsis in diabetes:
due to increased level of carbohydrates in tissues
Corticosteroid hormones have anti-inflammatory &
anti-phagocytic effect: depress host’s resistance
Elevated steroid level during pregnancy: hightened
susceptibility to many infections
3. Nutrition:
Malnutrition: reduced cell mediated & humoral
immunity
Cell mediated immune responses decrease in severe
protein deficiency
Mechanisms of innate immunity
1. Epithelial surface:
Skin & mucus membrane covering body protect it
against invasion by microorganisms
Skin:
Mechanical barrier
Possesses bactericidal activity due to high salt
concentration in drying sweat, sebaceous secretions &
long chain fatty acids
Normal flora on skin: prevents colonisation by
pathogens
Respiratory tract:
Inhaled particles are arrested in nasal passages on
moist mucus membrane surface
Pathogens are trapped by mucus lining epithelium &
given to pharynx where they are swallowed or
coughed out
Cough reflex: important defense mechanism
Nasal & respiratory secretions contain
mucopolysaccharides that combine with influenza &
other viruses
Particles that reach alveoli are ingested by phagocytic
cells
Digestive tract:
Mouth saliva: inhibitory effect on many microbes
Swallowed pathogens: destroyed by acidic pH of
gastric juice
Normal flora of ileum inhibits growth of pathogens
Conjunctiva:
Tear secretion flush away bacteria & other foreign
particles
Tear contains antibacterial lysozyme: break down
polysaccharide of bacterial cells
Genitourinary tract:
Flushing action of urine: eliminates bacteria from
urethra
Spermine & zinc in semen: antibacterial activity
Acidic pH of vaginal secretions in females, due to
fermentation of glycogen by lactobacilli, inhibit
pathogens
2. Antibacterial substances in blood & tissues:
Complement system: bactericidal activity & result in
destruction of pathogenic bacteria
Antibacterial substances:
beta lysin, leukins, plakins, lactic acid,
lactoperoxidase, lysozyme
Interferons produced by cells: antiviral activity
3. Cellular factors:
Pathogens invading blood & tissue: destroyed by
phagocytic cells
Phagocytes: microphages & macrophages
Microphages are polymorphonuclear leucocytes
Macrophages are wandering amoeboid cells in
tissues, reticuloendothelial cells & monocytes in
blood
Phagocytic action of phagocytes is divided in 4
stages:
Chemotaxis:
Phagocytic cells attracted by chemotactic substances
→ reach site of inflammation
Attachment:
Infective agent gets attached to phagocytic membrane
Ingestion:
Bacteria are engulfed by phagocytes
Membrane of phagosome fuses with lysosome to
form phagolysosome
Intracellular killing:
Lytic enzymes in phagolysosome destroy bacteria
Some bacteria (mycobacteria) resist such killing &
can multiply within phagolysosome
A class of lymphocyts called Natural killer (NK) cells
play important role in non-specific defence against
viral infections & tumor
Immunity
4. Inflammation:
Entry of pathogens → tissue injury & irritation →
leads to inflammation
Inflammation leads to vasodilation, increased
vascular permiability & cellular infiltration
Arterioles at the site of infection constrict initially &
then dilate leading to increased blood flow →
leucocytes escape into tissues by diapedesis →
accumulate in large numbers → attracted by
chemotactic substances at site of injury →
phagocytose microbes
Inflammation is characterised by: Pain (Dolor),
Redness (Rubor), Heat (Calor), Swelling (Tumor)
Plasma helps in diluting toxic products
Fibrin barrier forms wall around site of infection
5. Fever:
Rise in temperature after infection: helps to accelerate
physiological processes
Fever stimulates production of interferons & helps in
recovery from viral infections
6. Acute phase proteins:
Infection or injury leads to sudden increase in
concentration of certain proteins: called Acute phase
proteins
Eg: C ractive protein (CRP), alpha-1-acid
glycoprotein, mannose binding protein
Acquired immunity
Resistance that an individual acquires during life
Two types:
o Active immunity
o Passive immunity
Active immunity:
Resistance developed by individual as a result of
antigenic stimulus
Involves active functioning of host’s immune
apparatus to produce antibodies & immunologically
active cells
Active immunity sets in after a latent period
During its development, there is often a negative
phase (immunity lower than it was before antigenic
stimulus): because Ag combines with pre-existing Ab
in circulation
Once developed, it is long-lasting
When actively immunised individual encounters
subsequent attack of same Ag, immune response
occurs more quickly (called as secondary response)
Besides cell mediated & humoral immune response, it
is also associated with immunological memory
Active immunisation is more effective & confers
better protection than passive immunisation
Passive immunity:
Resistance transmitted passively to recipient in a
readymade form
Recipient’s immune system plays no active role
There is no antigenic stimulus; instead, preformed Ab
are administered
No latent period
No negative phase
Immunity is transient lasting for days or weeks
No secondary type response occurs in this immunity.
When Ab is administered 2nd time, they are
eliminated more rapidly
Passive immunisation is less effective
Employed when instant immunity is desired
Both Active & Passive immunities are further
classified as Natural & artificial
Natural active immunity:
Results from either clinical or inapparent infection by
a microbe
Eg: person recovered from attack of measles develops
natural active immunity
Such immunity is usually long-lasting but duration
varies with types of pathogen
Immunity is lifelong following many viral diseases
Immunity following bacterial infection is generally
less permanent
Artificial active immunity:
Resistance induced by vaccine
Examples of vaccines:
Bacterial vaccines:
o Live (BCG for tuberculosis)
o Killed (Cholera vaccine)
o Subunit (Typhoid Vi antigen)
o Bacterial products (Tetanus toxoid)
Viral vaccines:
o Live (Oral polio vaccine- Sabin)
o Killed (Injectable polio vaccine- Salk)
o Subunit (Hepatitis B vaccine)
Live vaccines initiate an infection without causing
any injury or disease
Immunity following live vaccine administration
resembles that following natural infection
Immunity lasts for several years but booster doses
may be required
Live vaccines can be administered orally or
parenterally
Killed vaccines are less immunogenic than live
vaccines, & protection lasts for short period.
Thus, administered repeatedly
Natural passive immunity:
Resistance passively transferred from mother to baby
In human infants, maternal Ab are transmitted
predominantly through placenta
In animals such as pigs, Ab are transmitted through
colostrum
Human fetus acquires ability to produce antibodies
from 20th week of life. Till then, maternal Ab give
passive protection against infectious diseases
Artificial passive immunity:
Resistance passively transferred to recipient by
administration of Ab
Agents used for this purpose:
- Hyperimmune sera of animal or human origin
- Convalescent sera
- Pooled human gammaglobulin
These are used for prophylaxis & therapy
Hyperimmune sera:
Antitetanus serum prepared form hyperimmune
horses
Give temporary protection
Disadvantage: hypersensitivity & immune
elimination
Human hyperimmune globulin: more lasting
protection
Convalescent sera:
Sera of patients recovering from disease
Contains high levels of specific Ab
Pooled human gammaglobulin:
Gammaglobulin from pooled sera of healthy
individuals
Contains Ab against all common pathogens prevalent
in the region
Active immunity Passive immunity
Produced actively by host’s immune
system
Received passively. No active host
participation
Induced by infection or by
immunogens
Readymade Antibody transferred
Durable effective protection Transient, less effective
Immunity effective only after lag
period
Immediate immunity
Immunological memory present No memory
Booster effect on subsequent dose Subsequent dose less effective
Negative phase may occur No negative phase
Not applicable in immunodeficient Applicable in immunodeficient
Immunity

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Immunity

  • 2. Definition Resistance exhibited by the host towards injury caused by microorganism & their products Immunity is concerned with reaction of body against any foreign antigen
  • 3. Types Immunity against infectious diseases is of different types Innate (native) immunity Non-specific Species Racial Individual Specific Species Racial Individual
  • 5. Innate immunity Resistance to infections that an individual possesses by virtue of his genetic constitutional make-up Immunity present since birth (inborn) It is not affected by prior contact with microorganisms or immunisation Non-specific: degree of resistance to infections in general Specific: resistance to particular pathogen
  • 6. Species immunity: Total or relative resistance to pathogen, shown by all members of species Eg: All human beings are resistant to plant pathogens & many animal pathogens Mechanism is not clearly understood but may be due to physiological & bichemical differences between tissues of different species 3 levels of innate immunity: species, racial, individual
  • 7. Racial immunity: Different races within same species may show differences in susceptibility to infection Eg: high resistance of Algerian sheep to anthrax Another example: genetic resistance to Plasmodium falciparum in some parts of Africa Racial differences are genetic in origin, by selection & inbreeding
  • 8. Individual immunity: Difference in immunity exhibited by different individuals in race It is well documented that homozygous twins show similar degrees of susceptibility to leprosy & TB This immunity is due to genetic constitution of individual
  • 9. Factors affecting individual innate immunity 1. Age: Very young & very old: more susceptible to infectious disease Fetus in uterus is protected from maternal infection by placental barrier. But some pathogens cross the barrier causing overwhelming infection resulting in fetal death Some infections are more severe in adults than in young children due to hypersensitivity Old persons are highly susceptible to infections due to declined immune responses
  • 10. 2. Hormonal influence: Endocrine disorders (diabetes, hypothyroidism, adrenal dysfunction) are associated with enhanced sensitivity to infections High incidence of staphylococcal sepsis in diabetes: due to increased level of carbohydrates in tissues Corticosteroid hormones have anti-inflammatory & anti-phagocytic effect: depress host’s resistance Elevated steroid level during pregnancy: hightened susceptibility to many infections
  • 11. 3. Nutrition: Malnutrition: reduced cell mediated & humoral immunity Cell mediated immune responses decrease in severe protein deficiency
  • 12. Mechanisms of innate immunity 1. Epithelial surface: Skin & mucus membrane covering body protect it against invasion by microorganisms Skin: Mechanical barrier Possesses bactericidal activity due to high salt concentration in drying sweat, sebaceous secretions & long chain fatty acids Normal flora on skin: prevents colonisation by pathogens
  • 13. Respiratory tract: Inhaled particles are arrested in nasal passages on moist mucus membrane surface Pathogens are trapped by mucus lining epithelium & given to pharynx where they are swallowed or coughed out Cough reflex: important defense mechanism Nasal & respiratory secretions contain mucopolysaccharides that combine with influenza & other viruses Particles that reach alveoli are ingested by phagocytic cells
  • 14. Digestive tract: Mouth saliva: inhibitory effect on many microbes Swallowed pathogens: destroyed by acidic pH of gastric juice Normal flora of ileum inhibits growth of pathogens Conjunctiva: Tear secretion flush away bacteria & other foreign particles Tear contains antibacterial lysozyme: break down polysaccharide of bacterial cells
  • 15. Genitourinary tract: Flushing action of urine: eliminates bacteria from urethra Spermine & zinc in semen: antibacterial activity Acidic pH of vaginal secretions in females, due to fermentation of glycogen by lactobacilli, inhibit pathogens
  • 16. 2. Antibacterial substances in blood & tissues: Complement system: bactericidal activity & result in destruction of pathogenic bacteria Antibacterial substances: beta lysin, leukins, plakins, lactic acid, lactoperoxidase, lysozyme Interferons produced by cells: antiviral activity
  • 17. 3. Cellular factors: Pathogens invading blood & tissue: destroyed by phagocytic cells Phagocytes: microphages & macrophages Microphages are polymorphonuclear leucocytes Macrophages are wandering amoeboid cells in tissues, reticuloendothelial cells & monocytes in blood
  • 18. Phagocytic action of phagocytes is divided in 4 stages: Chemotaxis: Phagocytic cells attracted by chemotactic substances → reach site of inflammation Attachment: Infective agent gets attached to phagocytic membrane Ingestion: Bacteria are engulfed by phagocytes Membrane of phagosome fuses with lysosome to form phagolysosome
  • 19. Intracellular killing: Lytic enzymes in phagolysosome destroy bacteria Some bacteria (mycobacteria) resist such killing & can multiply within phagolysosome A class of lymphocyts called Natural killer (NK) cells play important role in non-specific defence against viral infections & tumor
  • 21. 4. Inflammation: Entry of pathogens → tissue injury & irritation → leads to inflammation Inflammation leads to vasodilation, increased vascular permiability & cellular infiltration Arterioles at the site of infection constrict initially & then dilate leading to increased blood flow → leucocytes escape into tissues by diapedesis → accumulate in large numbers → attracted by chemotactic substances at site of injury → phagocytose microbes
  • 22. Inflammation is characterised by: Pain (Dolor), Redness (Rubor), Heat (Calor), Swelling (Tumor) Plasma helps in diluting toxic products Fibrin barrier forms wall around site of infection
  • 23. 5. Fever: Rise in temperature after infection: helps to accelerate physiological processes Fever stimulates production of interferons & helps in recovery from viral infections 6. Acute phase proteins: Infection or injury leads to sudden increase in concentration of certain proteins: called Acute phase proteins Eg: C ractive protein (CRP), alpha-1-acid glycoprotein, mannose binding protein
  • 24. Acquired immunity Resistance that an individual acquires during life Two types: o Active immunity o Passive immunity Active immunity: Resistance developed by individual as a result of antigenic stimulus Involves active functioning of host’s immune apparatus to produce antibodies & immunologically active cells
  • 25. Active immunity sets in after a latent period During its development, there is often a negative phase (immunity lower than it was before antigenic stimulus): because Ag combines with pre-existing Ab in circulation Once developed, it is long-lasting When actively immunised individual encounters subsequent attack of same Ag, immune response occurs more quickly (called as secondary response) Besides cell mediated & humoral immune response, it is also associated with immunological memory Active immunisation is more effective & confers better protection than passive immunisation
  • 26. Passive immunity: Resistance transmitted passively to recipient in a readymade form Recipient’s immune system plays no active role There is no antigenic stimulus; instead, preformed Ab are administered No latent period No negative phase Immunity is transient lasting for days or weeks
  • 27. No secondary type response occurs in this immunity. When Ab is administered 2nd time, they are eliminated more rapidly Passive immunisation is less effective Employed when instant immunity is desired
  • 28. Both Active & Passive immunities are further classified as Natural & artificial Natural active immunity: Results from either clinical or inapparent infection by a microbe Eg: person recovered from attack of measles develops natural active immunity Such immunity is usually long-lasting but duration varies with types of pathogen Immunity is lifelong following many viral diseases Immunity following bacterial infection is generally less permanent
  • 29. Artificial active immunity: Resistance induced by vaccine Examples of vaccines: Bacterial vaccines: o Live (BCG for tuberculosis) o Killed (Cholera vaccine) o Subunit (Typhoid Vi antigen) o Bacterial products (Tetanus toxoid) Viral vaccines: o Live (Oral polio vaccine- Sabin) o Killed (Injectable polio vaccine- Salk) o Subunit (Hepatitis B vaccine)
  • 30. Live vaccines initiate an infection without causing any injury or disease Immunity following live vaccine administration resembles that following natural infection Immunity lasts for several years but booster doses may be required Live vaccines can be administered orally or parenterally Killed vaccines are less immunogenic than live vaccines, & protection lasts for short period. Thus, administered repeatedly
  • 31. Natural passive immunity: Resistance passively transferred from mother to baby In human infants, maternal Ab are transmitted predominantly through placenta In animals such as pigs, Ab are transmitted through colostrum Human fetus acquires ability to produce antibodies from 20th week of life. Till then, maternal Ab give passive protection against infectious diseases
  • 32. Artificial passive immunity: Resistance passively transferred to recipient by administration of Ab Agents used for this purpose: - Hyperimmune sera of animal or human origin - Convalescent sera - Pooled human gammaglobulin These are used for prophylaxis & therapy
  • 33. Hyperimmune sera: Antitetanus serum prepared form hyperimmune horses Give temporary protection Disadvantage: hypersensitivity & immune elimination Human hyperimmune globulin: more lasting protection Convalescent sera: Sera of patients recovering from disease Contains high levels of specific Ab
  • 34. Pooled human gammaglobulin: Gammaglobulin from pooled sera of healthy individuals Contains Ab against all common pathogens prevalent in the region
  • 35. Active immunity Passive immunity Produced actively by host’s immune system Received passively. No active host participation Induced by infection or by immunogens Readymade Antibody transferred Durable effective protection Transient, less effective Immunity effective only after lag period Immediate immunity Immunological memory present No memory Booster effect on subsequent dose Subsequent dose less effective Negative phase may occur No negative phase Not applicable in immunodeficient Applicable in immunodeficient