Sheen Ann John

1st year PG
Dept of pedodontics
 1.Introduction
 2. Immunity
 3. Vaccines
 4.Immunisation schedules
 5.Caries Vaccine
 6. Conclusion
 7. References.
 Definition
Immunity can be defined as the
ability of the body to neutralise and
eliminate the pathogenic microorganisms
and their toxic products thus affording
protection.
IMMUNITY
1.Innate immunity
2.Acquired immunity.
 INNATE IMMUNITY
1. SPECIFIC
2. NONSPECIFIC
 ACQUIRED IMMUNITY
1.ACTIVE
NATURAL
ARTIFICAL

2.PASSIVE
NATURAL
ARTIFICAL
 Resistance that is transmitted passively to a
recipient in a “readymade” form.
 Recipient ‘s immune system has no active
role.
 No antigenic stimulus .
 No secondary response.
 Preformed antibodies are administered.
 Immunity is transient.
 Resistance passively transferred from mother
to baby.
 In humans maternal antibodies are
transmitted predominantly through the
placenta .
 The human colostrum also rich in IgA gives
protection.
 Only by the age of 3 months infant acquires
some measure of immunological
independence.
 Until then maternal antibodies.
 Resistance transferred to a recipient by the
administration of antibodies.
 Indicated for immediate and temporary
protection in a nonimmune host faced with
the threat of an infection.
 Passive immunisation may also be employed
for the suppression of active immunity when
the latter may be injurious.eg:use of Rh
immune globulin during delivery to prevent
immune response to the Rhesus factor in Rh
negative mothers with Rh positive babies.
 Agents used are :
 1.Hyperimmune sera of animal
 2.Human hyperimmune globulin
 3. Convalescent sera :passive immunisation
against some viral diseases
 4. Pooled human gammaglobulin : used in the
treatment of patients with some
immunodeficiencies.
 Resistance developed by an individual as a
result of antigenic stimulus.
 Also known as adaptive immunity.
 Involves active functioning of the individual
‘s immune response leading to synthesis of
antibodies and production of immunologically
active cells.
 Secondary response.
 Immunological memory.
 More effective and long lasting.
 Results from either a clinical or an
inapparent infection.
 A person recovering from measles develops
natural active immunity.
 This type of immunity is lifelong.
 But in diseases like common cold the lack of
immunity is due to the large number of
viruses that can cause the same clinical
picture.
 Resistance induced by vaccines.
VACCINES ARE DEFINED AS
IMMUNOBIOLOGICAL SUBSTANCES DESIGNED
TO PRODUCE SPECIFIC PROTECTION AGAINST
A DISEASE.
 1798 – smallpox  1954 –Salks polio
 1885 – rabies  1957 – Sabin oral
 1892 – cholera polio
 1913- toxin against
 1960 – measles
diptheria .
 1962 – rubella
 1923 – diptheria
 1923 – pertussis  1976 – hepatitis B

 1927 – influenza vaccines.

 1949 – mumps
 Vaccines stimulate the production of
protective antibody and other immune
mechanism from reticuloendothelial
system.
 B cell fights the infection and retains
memory.
 1.Live vaccines

Development of live vaccines:

Pathogen is grown in animals or tissue

culture under conditions that make it less
virulent.
 Prepared from live organisms.
 More potent than killed vaccines.
 Immunisation is achieved with a single dose.
 Rarely reverts to its virulent form .
 Not to be administered to patients whose
immune response is suppressed.
 Bacterial – BCG , Typhoid oral ,Plague.
 Viral –Oral polio ,Yellow fever ,Measles
,Rubella , Mumps ,Influenza.
 Rickettsial – Typhus.
 Development of killed vaccines:

Viruses are grown in tissue culture and then

treated with chemicals like formalin,
formaldehyde and betapropiolactone so that
it cannot reproduce in the person who
receives the vaccine.
 Usually safe .
 Risk of infection is very low.
 In immune compromised patients.
 Periodic booster doses.
 Less effective than live vaccines.
 Bacterial : Pertussis ,Cholera, Typhoid,
Meningitis, .
 Viral: Rabies, Polio, Influenza, Hepatitis B,
Encephalitis.
 Develoment of toxoid vaccines:
 Exotoxins produced by diptheria and tetanus
bacilli.
 Toxins are detoxified .
 Highly efficacious
 Safe immunising agents.

Toxoids:
Bacterial :Tetanus,Diphtheria.
 Development of vaccines:

Part of the protein of the organism is used

as an immunising agent.
 Safeand efficient.
 Duration is limited .

Egs :Meningococcal vaccine from the

polysaccharide antigen of the cell wall.
Pnemococcal vaccine from the
polysaccharide contained in the capsule of
the organism.
Hepatitis B polypeptide vaccines.
BENEFICIARY AGE VACCINE
INFANTS BIRTH BCG & OPV
6 WEEKS DPT & OPV

10 WEEKS DPT & OPV

14 WEEKS DPT & OPV

9 MONTHS MEASLES VACCINE

18 MONTHS DPT & OPV (BOOSTER

DOSE)
CHILDREN 5 YEARS DT VACCINE

10 YEARS TETANUS TOXOID

16 YEARS TETANUS TOXOID

 Age Disease Vaccination

Birth to 2 weeks TUBERCULOSIS BCG

POLIOMYELITIS OPV(1)

HEPATITIS B HB(1)

6 WEEKS OPV(2)

DIPTHERIA,PERTUSSIS, DPT(1)
TETANUS
HB(1) OR(2)

HIB(1)

10 WEEKS OPV(3)

DPT(2)

HIB(2)

HB(2)
14 WEEKS OPV(4)
DPT(3)
HB(3)
HIB(3)
9 MONTHS MEASLES

15 MONTHS MMR

16-18 MONTHS OPV(5)

DPT(BI)
HIB(4)
2 YEARS TYPHOID VACCINE

4 – 5 YEARS OPV(6)
DPT(B2)

10 YEARS TT/Td

16 YEARS TT/Td
 Above 1 year : VARICELLA
 Above 2 years : HEPATITIS A
 Less than 24 months old and 24 -59 months –
pneumococcal conjugate vaccine(PCV)
 Older children & adults – pnuemococcal
polysaccharide vaccine (PPV)
ANTIGEN OR DESCRIPTION SCHEDULE
SUPPLEMENTATION

BCG BACILLE CALMETTE GUERRIN BIRTH

DT DIPTHERIA,TETANUS TOXOID 5 YEARS

DTwP WITH WHOLE VACCINE PERTUSSIS 6,10,14 WEEKS,16-

24 MONTHS
HEP B HEPATITIS B 6,10,14 WEEKS.

MEASLES MEASLES VACCINE 9 -12 MONTHS

OPV ORAL VACCINE BIRTH,6,10 ,14

WEEKS,16 – 24
MONTHS
TT TETANUS TOXOID 10 -16 YEARS

VITAMIN A VITAMIN A SUPPLEMENTATION 9,18,24,30,36

MONTHS.
 1.Reaction inherent to inoculation.
 2.Reaction due to faulty technique.
 3. Reaction due to hypersensitivity.
 4.Neurological symptoms.
 5. Others .
Indications Route of Instructions Reactions Complication
administrati s
on

Primary intradermal Raised wheal Nonhealing Risk of

immunization will disappear ulcer and tuberculous
for TB within 1 hr . regional disease in
Caused by Local lymphadeniti immuno-
Mycobacterium reaction s compromised
tuberculosis. occurs after patients.
3-6 wk with a
nodule
formation
which
ulcerates and
heals by
scarring.
Indications route of Instructions Adverse complication
admn reactions s

Primary IM (Deep) Freezing and Fever and Convulsions,

immunization thawing local pain screaming
destroys episodes,
vaccine . shock and
encephalitis
indications Route of Instructions Adverse Complications
admn reactions

Primary IM -------------- Pain at the Anaphylactoid

immunization site of reaction
injection
Instructions Route of Instructions Adverse Complication
admn reactions s

Used for pre IM Do not give IV Swelling, Allergic

and post or warmth, reactions .
exposure intradermally Erythema,
prophylaxis . Low grade
against HBV fever rare.
infection.
Indication Route of Instructio Adverse Complicat
s admn ns reactions ions

Primary SC ------------- Fever and May cause

immunisat rash allergic
ion reaction in
patients
with
history of
severe
anaphylac
tic
reactions
to
egg,chicke
n.
Indicati Route Instruct Advers complic
ons of ions e ations
admn reactio
ns
Primary SC Protecti Mild ----------
immuni ve fever -
sation. efficacy and
is 90- rash.
95 %
Indicati Route Instruc Advers Compli
ons of tions e cations
admn reactio
ns
Primary IM --------- Pain at ---------
immuni (deep) -------- the site -------
sation and
occasio
nal
febrile
reactio
ns.
Indications Route of Instructions Adverse Complication
admn reactions s

Primary PO Not to given -------------- Vaccine

immunisation in immuno- induced
compromised poliomyelitis.
patients or in
patients with
persistent
diarrhoea or
vommiting.
indicatio Route of Instructi Adverse Complic
ns admn ons reaction ations
s
Primary IM ----------- ----------- -----------
immunis (upper - -
ation arm)
with
DPT.
Indicati Route Instruct Adverse Complic
ons of admn ions reactio ations
ns
Primary SC Not in Fever,lo ----------
immunis children cal ----
ation below 2 pain,ma
years. laise,he
adache
and
chills.
 Dentaldecay (caries) is the most common
disease of mankind.It has increased in
modern times due to the rich refined sugar
diet which has been consumed.

 Asearly as 1924 J.K.CLARKE concluded that a

specific organism was associated with carious
lesions for which he proposed the name
“streptococcus mutans”
 Sincedental decay fulfills the criteria for
infectious disease the possibilities of
vaccination have been considered.
 1910- Goadby first to advocate caries control
by innoculation of the mouth with organisms
which would produce alkaline reaction.
 Bowen (1974)and cole et al (1977) showed
that lactoferrin,lactoperoxidase and
lysozyme possess antibacterial effects.
 1985 – Lehner et al found that local
immunisation with topical application of
monoclonal antibodies to a surface protein of
S.mutans has found to be protective in
rhesus monkey.
 - When animals are injected with whole S.
mutans bacteria, they form antibodies which
reacts not only with the bacteria but also with
heart tissue. So there is a chance that antibodies
induced by heart cross-reactive antigen (HCRA)
will cause damage to heart.
 - Therefore current approaches are directed
towards defining individual molecular
components of the bacteria which may have
been responsible for inducing the protection.
 1) the surface fibrillar adhesins known as
AgI/II
 (synonyms: antigen B, P1, PAc,
SpaA,PAg)

 2) the glucosyltransferases (GTF)

 3) the glucan-binding proteins

It may be desirable that a salivary antibody
response should be induced and sustained
throughout the ‘window of infectivity’,the
period from approximately 18 to 32 months of
age when infants are most likely to become
infected with mutans streptococci [Caufield et
al., 1993].
 - It may also be desirable that responses should
be recallable either by booster immunization or
by natural exposure to mutans streptococci, if
further opportunities for infection arise at later
times, such as when children enter school or
their permanent teeth erupt.
 An alternative approach lies in the development
of antibodies suitable for passive oral
application against dental caries.
- This has considerable potential advantage in
that it completely avoids any risks that might
arise from active immunization.
 - Conversely, in the absence of any active
response on the part of the recipient, there is no
induction of immunological memory, and the
administered antibodies can persist in the mouth
for only a few hours at most or up to 3 days in
plaque.
 Strategies include:-
 - the development of antibodies to mutans
 - streptococcal antigens in cow’s milk and
hen’s eggs
- the genetic engineering of human-like S-IgA
antibodies in plants (‘plantibodies’)
(i) To immunize infants or young children in
order to provide immune protection
prior to initial colonization with mutans
streptococci
(ii) To provide booster immunization to
recall responses as it might be desirable
to forestall colonization at later time
points.
 As the transmission of mutans streptococci
appears to be primarily from mother to infant
[Liand Caufield, 1995], a third possibility is that
young mothers might be immunized actively or
passively with the objective of reducing their
oral load of mutans streptococci (possibly in
combination with conventional prophylaxis or
other interventions), thereby diminishing the
probability and extent of transmission to their
infants.
 1. Textbook of Microbiology – Ananthanarayan
and Paniker.
 2.Immunology – David Male,David B Roth
 3.Pharmacology and Pharmacotherapeutics –
R.S.Sathoshkar.
 4.Manual of Pediatric drug therapy – Sohrab
.N.Tomaraei.
 5.Essentials of preventive and community
dentistry – Soben Peter.
A Caries Vaccine? Michael .W. Russell et al
.Caries Res 2004:38:230-235.