Standard case
definition:
Any childsuffering from the following
symptoms
•Fever (38.5 and lasting for >=3 days).
•MacuIopapuIar rash
•Cough, Coryza (i.e. running nose) or
•Conjunctivitis .
A confirmed case is one in which
suspected case is confirmed by
laboratory( virus isolation or antibody
8.
Place :
Countries inwhich measles vaccine is
widely used are already experiencing a
marked decrease in the incidence of the
disease.
9.
Time:
The seasonal trendthat is observed in
winter months.
era was 2-3 years according to
accumulation of susceptibles.
10.
Person
:Age and sex:
Measlesis mainly a disease of
children. The incidence is equal in
both sex.
Following the widespread use of measles
vaccine, the disease is now seen in older age-
groups and the incidence increases in adults
Nutrition:
Measles tends to be very severe in the
malnourished child
13.
dgenr:
Measles virus.
Reservoir:
Man inthe form of :
•Cases: Mild cases are more frequent
than before vaccination era .
•Carriers are not known to occur .
The source of infection:
is the secretion of nose , throat, respiratory
discharge
Exit:
Upper respiratory tract.
15.
Mode of transmission:
Measlesis highly communicable
diseases.
It can be transmitted by:
- Droplet spread
- Direct contact with nasal or
throat
secretions of infected persons.
- Less commoniy it is spread by air
born mode or indirect contact
Inlet:
Nose and mouth.
16.
Susceptibility :
Practically allpersons who have not had the disease or
been immunized are susceptible.
•Acquired natural immunity: is permanent.
•Acquired passive immunity: Infants born to
mothers
who have had the disease are immune for the first
6-9 month or more depending on the amount of
residual maternal antibody at the time of
pregnancy.
• Artificial passive immunization
(Immunoglobulin)
19.
Period of communicability:
Theperiod of communicability is four days before and
four
days after the appearance of the rash.
The vaccine virus has not been shown to be
communicable
22.
Measles like smallpox, has several favorable
factors
that make it a suitable candidate for
eradication.
0 The virus exists in a single serotype
that is of antigenicaly stable
0 Absence of nonhuman reservoir
0 The disease provides durable immunity.,
0 Available elective live vaccine stable
and produces durable immunity.
24.
The strategies recommendedfor achieving
measles elimination and mortality reduction
include:
1-Maintain high vaccination coverage
rate for measles vaccine
2 Enhancing measles surveillance
systems.
3 Improve management of
complicated
cases of measles.
4 Provide Vit. A supplementation
25.
Standard case
definition:
Any patientwith the following :
1.Fever (>37.2O
C)
2.Generalized maculopapular
rash. 3.Lymphadenopathy.
A confirmed case is one in which the
suspected case is confirmed by laboratory
(virus isolation or antibody elevation or
epidemiological.
26.
• In rareinstances, encephalitis,
thrombocytopenic purpura and
neuritis may occur.
• Joint involvement (arthralgia and
arthritis) is a common complication in
young adults, particularly women.
• Congenital rubella syndrome:
27.
Manifestations of congenitalrubella
Ear :Deafness
Eyes : cataracts, glaucoma, retinopathy and microophthalmia
Heart : patent ductus a%eriosus, ventricular septal defect,
pulmonary stenosis
Neurologic : microcephaly and mental retardation
Others:
bone lesions, splenomegaly, hepatitis, and thrombocytopenia
with purpura may occur.
These congenital malformations and even fetal death may
occur
following either clinically manifest or inapparent rubella
infection during
Place :
Worldwide, universally
endemicTime:
The disease is prevalent
in winter and spring.
Person:
Aqe and sex:
•ln unvaccinated population, rubella is
primarily a disease of childhood and young
adults.
•ln communities where children are well
immunized, adolescent infection become more
32.
Agent:
Rubella
virus.
Reservoir:
Man in theform of clinical and subclinical
cases.
Source of infection:
Nasopharyngeal secretions of infected
persons
Exit:
Nose , mouth and placenta.
33.
Mode of
transmission:
•Droplet
spread.
•Direct contactwith patients.
-Indirect contact with articles freshly soiled
with discharges from nose and throat,
-Air borne transmission
-Transplacental.
Inlet:
Nose and mouth.
34.
Susceptibility
:
1. Infants borneto immune mothers are protected
for 6-9 months.
2. Active immunity acquired by natural infection is
permanent
3. Immunity after vaccination:
A single dose of live attenuated rubella virus
vaccine elicits a significant antibody response.
According to the Schedule in KSA ,MMR is given in
Two
doses ( at 12th months & at 4-6th Years)
Duration of immunity: Rubella antibody persists
for a long period after vaccination.
35.
Vaccine and pregnancy:
Becausevaccine virus theoretically might infect the
fetus and cause congenital defects if given to
susceptible women early in pregnancy,
immunization of women known to be pregnant is
contraindicated.
vaccination.
4 - Immunoglobulin: is given to women
exposed during early pregnancy
36.
For about oneweek before and four days
after onset of rash.
Infants with congenital rubella may shed
virus for months after birth.
37.
Prevention
:
1 Apply basicmeasures for prevention of
respiratory tract infection
2 Immunization: In KSA, 2 doses of rubella
vaccine is given in
combination with measles and mumps
vaccines (MMR) in the 12th & at 4-6 years of age
The single rubella live attenuated vaccine is
recommended for susceptible women in the post
partum period for teachers, nurses, doctors are
exposed to rubella patients.
38.
Control:
Measures for cases:
•Reporting to local health authority:
•IsoIation: to protect non-immune women during
pregnancy.
¥'Specific treatment: None.
/Ideasnres for confacf :
1. Pregnant contact :
3* Put under observation for the incubation period .
3'Laboratory investigation :Rising IgM or a IgG ,
indicates recent infection. Given either immunoglobulin or
abortion is done .
2. Children contacts :
•Put under observation
The complications occurmore in teenage
children and adults than in infants and
young children.
These
include:
• Orchitis: sterility is rare because the condition
is unilateral
• Oophoritis , mastitis and myocarditis,
Pancreatitis
• Neurological : meningitis and
meningoencephalitis.
• Congenital anomalies involving the heart if
the infection occurs during pregnancy.
43.
• Place :
Mumpsis rarely an endemic disease .
Outbreaks are associated with overcrowding .
• Time:
Winter is the season of greatest incidence.
• Person:
Age: It añects any age if there is no
previous immunity. The disease tends to be
more severe in adults than in children, with
more frequent complications.
45.
• Agent:
Mumps virus.
•Reservoir:
Man in the form of clinical and sub clinical
infection.
The source of infection is the saliva of infected
person.
• Exit:
Mout
h.
• Mode
of
trans
missi
on:
• Dropl
et
47.
• Susceptibility :
•Susceptibility is general .
• Post infection immunity is generally
life long and develops after subclinical
as well as clinical attacks..
• Vaccination: Live attenuated
vaccine in combination with Measles
& german measles vaccine (MMR)
48.
• The virushas been isolated from
saliva from six days before the
appearance of the swelling of the
parotid up to nine
days after.
49.
1 Apply basicmeasures for prevention
of respiratory tract infection
2 Vaccination: live attenuated
vaccine
The vaccine is available as
combined vaccine (combined measles
— mumps —
In KSA, 2 doses of MMR are given in
the 12th & at 4-6 years of age.
50.
• Report tolocal health authority
.
• Isolation: Invalidbecause the
maximum infectiousness occurs
before onset of illness,
articles soiled with patient's
secretions.
• Contacts: Put under surveillance .
• No specific treatment,
51.
Standard Case
definition:
Suspected case:
Aperson with a cough at least 2 weeks with one
of the
following:
-Paroxysms of coughing or.
-Inspiratory whoop or.
-Post-tussive vomiting (ie vomiting immediately
after coughing) and without other
apparent cause.
Confirmed case:
A confirmed case is a suspected case that is
laboratory confirmed.
-By isolation of Bordetella pertussis.
- Serologically
52.
Complications of whoopingcough
include
- Hernia,
—Prolapsed rectum,
—Sub-conjunctival
haemorrhage,
—Encephalopathy,
—Pneumonia and
bronchiectasis.
53.
eDmesci i ee
iolo
• Person:
Age and sex: Whooping cough is a disease of
infants and pre-school children.
• Place
Whooping cough occurs in all countries. During
the past four decades, a marked decline
has occurred in incidence and mortality rates,
chiefly in countries with active immunization
programs.
• Time
It occurs more ie winter
.
55.
• Causative agent
Bordetellapertussis bacilli.
• Reservoir
Man in the form of cases.
There is no evidence that the infection is subclinical.
There is no carriers in whooping cough ( bacteriologically
free
before the clinical cure)
Sources of infection: Nasopharyngeal and
bronchial secretions.
• Exit
Nose and mouth.
• Mode of transmission
Direct contact
and Droplet
contact .
The role of
56.
Susceptibility
:
• Susceptibility tothe disease is general.
• There is no passive maternal immunity even
if
the mother is immune.
• Post-infection immunity is long lasting.
• There is no evidence of the efficacy of
hyper-
immune globulin in pertussis
prophylaxis.
• The efficacy of the vaccine in children
57.
Vaccination:
•lt is akilled vaccine given in combination with
diphtheria and tetanus toxoids (DPT) in three intra-
muscular injections at 2, 4, 6 months old. Two booster
dose at 18th months & 4-6 years of age.
Side eñects of Whole cell pertussis vaccine is
local adverse events (eg. Erythema, swelling & pain at
the injection site.), fever, drowsiness & anorexia.
Systemic events ( Convulsions, encephalopathy,
shock.) occur less frequently. This calls for the
development of
58.
2.AceIlular pertussis vaccine(DTaP):
• It contains purified, components inactivated
toxin and filamentous haemaqqlutinin ol
bordetella pertussis cells.
• Certain types of DTaP have been licensed
only for administration of the fourth and fifth
doses in the series to children aged 15 months
to 6 years who previously had received 3 doses
of DPT vaccine.
• In general, pertussis vaccine is not given to
person 7 years of age or older
since the disease is usually milder and the
reaction to the vaccine may be
59.
‹ .
. iftùe following exerits ocau,r’ager
ädmțnistratio'n
”-... of DPT or DTaP; subæque,nt vaccination .is
conłra-
i
/
/
ą
ț
c
a
ş
e
ą
;
60.
• It extendsfrom the early catarrhal
stage to 3 weeks after onset of typical
paroxysms in patients not treated with
antibiotics.
• When treated with erythromycin, the
period of communicability is usually 5
days or less after onset of therapy
61.
• Apply basicmeasures for
prevention of
respiratory diseases.
• Immunization
62.
Contro
l
Cases:
•Reporting to localhealth authority.
•IsoIation :IsoIation of cases , until receiving at
least 5 days of antibiotic. Cases who do not
receive antibiotics should be isolated for 3
weeks.
•Concurrent and terminal disinfection of
the respiratory discharges
•Treatment: Erythromycin is the drug of
choice.
63.
Contacts:
4•CIose observation forhousehold contacts for
the incubation period.
1•Chemoprophylaxis (Erythromycin) should be
administered to all contacts regardless of
immunization status and age.
•!•Household contact less than 7 years of age
•If not vaccinated or not receiving four doses of
pertussis vaccine should receive a dose of DPT
vaccine soon after exposure.
• Previously immunized :No vaccination.
64.
Standard Case
definition:
A) Suspectedcase :
A patient is suffering from an
illness characterized by
adherent membrane on the
tonsils, pharynx and or nose
and any one of the following:
Pharyngitis, laryngitis or
tonsillitis.
B) Confirmed case:
Is a suspected case, laboratory
confirmed by one of the
following:
65.
1 Cardiovascular complications:
—Peripheral circulatory failure due
to diñuse toxic changes in all organs
including the adrenals and the vascular
endothelium.
— Myocarditis and congestive heart
failure.
2 Paralysis .
Case fatality rate ranges from 5-10O
›9.
66.
emesc i i
e
e
iolo
•Person:
• Age :
Diphtheria primarily involves non-
immunized children under 15 years of
age. It is found among unimmunized
adults
• Place:
The incidence has declined in many
countries, but in some developing
countries (especially those without
compulsory vaccines ) it remains a
serious problem.
• Time:
68.
• Causative agent:
•Corynebacterium diphtheriae , it produces a
powerful exotoxin.
• Reservoir:
• Man in the form of cases (clinical and sub-
clinical) and carriers.
• Carriers may be temporary or chronic,
contact or incubatory, nasal or throat
carriers.
• Source of infection:
• Discharges from the nose and throat.
• Exit
69.
• Mode oftransmission:
• Contact transmission : direct, indirect
and droplet.
• Air-borne transmission by droplet
nuclei.
• A common vehicle (raw milk).
Inlet
• Upper respiratory tract.
70.
• Susceptibility :
•Infants born to immune mothers are
relatively immune for the first six months.
Post-infection immunity is specific and
long-lasting.
• Active artificial immunity can be induced
by
toxoid vaccine (DPT).
• Short passive artificial immunity (2-3
weeks) can be gained by administration of
antitoxin.
71.
• Period ofcommunicability:
• Variable, until virulent bacilli have
disappeared from discharges and
lesions, usually 2 weeks or less and
rarely more than 4 weeks.
• Effective antibiotic therapy
promptly terminates shedding.
• Chronic carriers may shed
organisms for 6
months or more.
Control
:
For Cases
1-Reporting tolocal health
authority. 2-Isolation:
Strict isolation for all cases until proved free of
infection, at least 2 consecutive nose and throat
cultures taken not less than 24hours apart should
be negative before terminating isolation. When
culture is impractical
isolation is ended after 14 days of antibiotic
treatment.
3-Concurrent& Terminal disinfection of all patients
articles
4-Treatment:
i)antitoxin should be given immediately
after bacteriologic
specimens are taken
77.
Poliomyelitis
• Any childunder 15 years of age with
acute, flaccid paralysis (AFP).
• Any person- at any age- with paralytic
illness
when polio is suspected.
B) Confirmed case
• A suspected case is confirmed with
isolation of wild poliovirus from the stools of
either the case or its contacts.
81.
• Place
As aresult of Global Polio Eradication
strategy, many regions have been
certified polio free . These are America,
Western Pacific, and Europe
82.
Country 2002 20032004 2005
Date of
last
case
Somalia 3 0 0 0 10/2002
0
1
(importe
d
) 0 0 01/2003
Lebanon
Saudi
Arabia
0 0
2
(imported) 0 12/2004
Egypt 7 1 1 0 05/2004
Afghanista
n 10 4 0 11/2004
Pakistan
Sudan
90
0
103 54
127
(imported)
4
22
01/2005
03/2005
Yemen 0 0 0 4 03/2005
Total 110 113 187 30
Number of confirmed cases of polio 2002-2005 in diNerent
countries
Source: WHO Eastern Mediterranean Region Office
83.
Conditions that mustbe fulfilled
before a country is certified as polio
• Reporting Zero Polio cases tor at
least
Three past years.
• Adequate strategy to detect, report
and respond to any discovered case
of polio.
• Adequate surveillance system for AFP.
84.
Person
• Age andsex:
• In developing countries Poliomyelitis
is a disease of young children and
adolescents
• In developed countries adults were
añected more commonly than children with
increased both the disease severity and
deaths.
• Sex diXerence have been noticed in the
ratio of three male to one female
Agent
OPoliovirus : threeserotypes (P1, P2, P3) with diñerent
antigenicity
OThe virus can live in water for three months and in the
faeces for
six months.
OThe poliovirus is rapidly inactivated by heat,
formaldehyde, chlorine and ultraviolet light.
Reservoir
Cases : clinical & subclinical plays a role in the spread
of infection
Carriers: faecal temporary. There is no chronic carrier.
Source of infection:
Mode of transmission
1Feaces(feco-oral): in areas with lack of personal hygiene
especially in young children in developinq countries. It results
in infection not paralysis.
2 Droplet : in develo ed countries with high standard of
sanitation, droplet is common mode of transmission during
the
acute phase of the disease when the virus is in the throat.
3 Direct contact with respiratory discharge
4 Common vehicle: ingestion of food or drink
contaminated with faeces
5 Indirect contact with articles contaminated with
pharyngeal
discharge of infected person.
89.
Susceptibility
• Susceptibility toinfection is general,
95O
â of cases are of subclinical type
and in the remaining 1% of cases
paralysis occurs
• Most paralyticpatients recover and
residual paralysis occurs in 0.1% to
1%.
• The rate of paralysis among infected,
non immune adults is higher than that
among non immunized infants and
90.
• Natural immunityfollowing infection is solid
although reinfection can occur , since infection
with one strain does not protect against the
other two strains of virus.
• Infants born of immune mothers have
maternal antibodies which gradually disappear
during the first 6 months of life.
• Risk factors that precipitate paralytic polio are
stress,
• fatigue,
• trauma,
• intramuscular injection,
91.
• Poliovirus ishighly infectious;
cases are most infectious from 7-
10 days before and after the onset
of symptoms.
• The virus is excreted in the faeces
for 3-6 weeks
93.
IPV (Salk) OPV(Sabin)
Type
of
vaccine
Killed formalin
inactivated contains the
3 strains .
Live attenuated
contains the 3 strains
Mode of
administratio
n & number
of doses
Subcutaneous or IM, 2-
3 doses in first year of
life and 1 booster
commonly given in 4-6
years.
Oral ,5 doses 2nd ,
4th, 6th, 18th
months& 4- 6th
years
Differences between IPV and OPV vaccines
94.
IPV (Salk) OPV(Sabin)
Effect -Induces
circulatory
antibodies but
not intestinal
immunity.
-Induces both circulatory and intestinal
antibodies
-Prevent both paralysis and
intestinal reinfection
-Prevent
paralysis but not
reinfection by
wild poliovirus
-Due to the interference between the
three strains of the vaccine, booster
doses are required to ensure protective
immunity. In the first dose, one strain
will grow most effectively inducing
immunity to this strain. With the second
dose, immunity will be inhibited to the
first strain allowing the second strain to
induce its immunity.
Similarly, immunity is induced to the
strain
with the third booster.
95.
IPV (Salk) OPV(Sabin)
Advantages -Does not require
precautions during storage
and transportation
-Useful to control
epidemics even with single
dose
-No evidence of vaccine
associated polio
paralysis (VAPP)
-Easy
manufacture &
administration
-cheap
-Could be given to
immunocompromis
ed ( such as HIV
patients)
-The vaccinees excrete the
virus and so infect
contacts
thereby they become
immune (Herd
immunity)
96.
Disadvantage
s
!PV (Salk)
-Not usefulto
control epidemics
because:
•Immunity is not
rapidly achieved as
more than one doses is
required
•No intestinal immunity
•lnjections are avoided
during epidemic as they
increase the risk of
paralysis
-Difficult to
manufacture
-Expensive
-No herd immunity after
administration of the
vaccine
OPV (Sabin)
-Requires adequate cold
chain
-Rarely post vaccinal
paralysis
occur in:
•Immunosupressed
persons
•After first dose of vaccine
•Adult >18 years
-Not given to HIV patients
or even to their
household contacts
-Other GIT viruses
interfere with the
replication of the
vaccine viruses in
the intestine of the
vaccinees
In countries undertakingpolio eradication, a
single case of poliomyelitis is considered a
pu6lis health emergency.
103.
1 Disease notification,collection of information (clinical
and epidemiological including vaccine history and
contact with OPV vaccine) of any suspected cases of
paralytic polio.
Collection of appropriate specimens for viral isolation
and
serology.
2 Mass vaccination should be carried out but not needed
if
the disease is confirmed to be vaccine associated.
3 Postpone elective nose and throat surgery; avoid IM
injections including immunizations (iPV) until after
epidemic. 4-Start control measures immediately while
waiting for laboratory confirmation of the case
5 Identify the route of introduction of poliovirus
into the community
6Active surveillance for AFP cases should continue
104.
• In 1988the WHO adopted the goal of
global eradication of polio virus by the
year 2000.
• Although substantial progress has
been made the goal was not
achieved .
106.
Strategies of polioeradication
There are four core strategies to
stop
transmission of the wild poliovirus
A-Routine immunization of
infants B-SuppIementary
immunization
National immunization days
( EPI) Mopping up immunization
( EPI)
107.
• Case definition
•Chickenpox is an acute highly
infectious disease, characterized by
vesicular rash, mild fever and mild
constitutional symptoms.
• Herpes zoster is a local manifestation
of reactivation of latent varicella
infection in the dorsal root ganglia. It
occurs in 15O›9 of normal immune
adults.
• Person:
• Ageand sex
• Chickenpox occurs primarily among
children under 10 years of age.
• Few persons escape infection until
adulthood.
• The disease can be severe in normal
adults.
• No sex diñerence has been reported.
• Place:
• Chickenpox has a worldwide
114.
• Causative agent
•Varicella zoster virus, which is a
member of
herpes virus group.
• Reservoir
• Man in the form of cases.
Source of infection
Discharges of respiratory tract of
infected persons and fluid of vesicles
115.
• Upper respiratorytract and lesions of the
skin and mucosa.
• Mode if transmission
• Contact, direct, indirect and droplet.
• Air borne transmission by droplet nuclei.
• TranspIacentaI.The virus can cross the
placenta and may result in a condition
known as congenital varicella.
• Inlet
• Upper respiratory tract and skin.
116.
• Susceptibility
• Susceptibilityto chickenpox is general
among
non-immune individuals.
• Infection usually confers Long lasting
immunity.
• The viral infection may remain latent, and
disease may recur years later as herpes
zoster in about 15% of older adults.
• Varicella zoster immune-globulin is
effective in modifying or preventing disease
i
f given within 96 hours after exposure.
• Infants born to immune mothers have
passive immunity for the first 6 months of
117.
Varicella vaccine
• Itis a live-attenuated vaccine.
• It was licensed for use since 1995.
A single 0.5 ml subcutaneous dose is recommended for routine
immunization of children aged 18 months and for immunization of
children up to 12 years of age who have not had varicella.
• The vaccine effectiveness ranged from 85-90% for prevention of all
disease
• If vaccine given within 3 days of exposure, it prevents the disease.
• Varicella vaccine is recommended for susceptible persons more
than 13 years old e.g. health workers. They require 2 doses of
vaccine 4-8 weeks apart.
118.
Some may notrecommend varicella
vaccination because:
• Chicken pox is a mild illness there is no
need for the vaccine .
• It may be risk if chicken pox is
postponed for childhood (where it is
mild) to adulthood where it is more
severe with more complications.
• Live vaccine may establish latent
infection this may produce zoster in
later years or in a more severe form
than natural disease.
119.
• Usually 1-2days before onset of rash,
and continuing until all lesions are
crusted (usually about 5 days).
123.
An acute diseaseinduced by the
tetanus bacillus which grows
anaerobically at the site of an injury
and produces a neurotoxin. There
are two types of tetanus:
• Adult
Tetanus
tetanus
124.
A-Adult
Tetanus
It is characterizedby:
0 Painful muscular contractions of the masseter
muscles (lock jaw or trismus) and neck muscles, then
the trunk muscles and the muscles of the face causing
risus sardonicus.
OThe first sign of tetanus is abnormal rigidity at
the region of injury.
OGeneralized spasms induced by sensory
stimuli.
OThe adult tetanus usually follows an injury or
surgical operation, delivery or abortion. However,
history of an injury or apparent portal of entry is
often lacking.
126.
B-Neonatal tetanus:
(NT)
Case definition(NT):
A) Suspected case:
Any death of unknown cause between 3 to 28
days of life.
B) Confirmed cases:
NT is diagnosed on clinical findings and does
not depend on laboratory confirmation
A confirmed case is
— An infant is able to suck and cry normally
during the first 2 days of life ,he becomes unable to
feed or suck between the ages of 3 and 28 days
— He has episodes of convulsions
129.
Case fatality:-
• Neonataltetanus (NT) is always
fatal (>90%).
depending on age, severity of injury,
immune status and time of intervention
(diagnosis and treatment).
130.
• Place:
It isworld wide disease, occurs sporadically, it
is more common in agricultural regions and
in underdeveloped areas, where contact with
animal excreta is more likely and
immunization is inadequate.
Neonatal tetanus is common in areas where
birth is traditional particularly in the rural
areas.
Parenteral use of drugs by addicts results in
individual cases or occasional
circumscribed outbreaks.
131.
• Person:
Age andsex:
Tetanus affects all ages especially under
15
years. In the agricultural It areas
añects adult males.
Neonatal tetanus affects the
newborn.
Time:
In Summer especially when
133.
• Agent:
Clostridium tetani,(the tetanus bacillus). The
vegetative form of the organism is fragile,
but under unfavorable conditions changes
to spores which are highly resistant,
• Reservoir :
• The soil and intestinal tract of animals
specially horses and cattle ie which the
organism is harmless normal inhabitant.
• Source of infection:
is the soil or street dust containing the
spores.
• Exit :
• The stools of animals specially horses.
Cycle of
infection
134.
•Mode of transmission:
•Tetanus spores introduced into the body
during
• injury, contaminated with soil, street dust
or animal faeces,
• laceration, burns and unnoticed wounds.
• Neonatal tetanus occurs through infection
of the unheated umbilicus, during cutting,
ligature or dressing of the umbilical cord
under septic technique.
• Inlet :
Wounds, puncture, burns or umbilical cord
stump.
135.
•Susceatibilitv
Susceptibility is general.
•The presence of necrotic tissue or foreign
bodies favors the growth of
anaerobic pathogens.
• Second attack may occur because
protective post infection immunity is
absent.
• Vaccination with Tetanus toxoid (TT)
produces a long active immunity.
• Tetanus antitoxin or tetanus
immunoglobulin produces passive
137.
Prevention:
1.Active immunization withtetanus
toxoid gives solid protection:
a. In infancy: it is given with diphtheria
and whooping cough vaccine (DPT) at
the end of second, fourth, and sixth
month of age and a booster dose at 18
months & 4-6 years of age.
• Booster dose is needed every 10
years (Td).
138.
b. Tetanus toxoidcan be given at any age,
for workers in contact with soil, sewage
or domestic animals, members of
military forces, policemen and others
with greater than usual risk of
traumatic injury.
The schedule for previously non
immunized individuals (>7years) a
primary series of 3 doses of (TD) is given.
The first 2 doses are given at 4-8 weeks
interval and a third dose 6-12 months
after the 2nd dose.
139.
Prevention of neonatal
tetanus:
Immunizationschedule for women in the
reproductive period has been
recommended. It consists of five doses of
tetanus toxoid (TT), respecting the
minimum interval between doses will
provide immunity through a woman's
childbearing years.
140.
- TT1: Atfirst contact or as early as
possible
" .
.
””-during
pregnancy.
TT2: 4 weeks aher
7T1.
"
”
.,
“*
:'
TT3: 6 months after TT2 or dur.
ing the
second
I pregnancy.
TT4: 1 year aher TT3 or during next
pregnancy.
’
"
:
'”- TT5: 1 year aKer TT4 or during next
pregnancy.
:.’’
141.
Health education
Reqardin¿;:
a- Thevalue of routine immunization
with tetanus toxoid, the kinds of injury
particularly liable to be complicated by
tetanus and the need after injury for
either a booster dose or passive
protection by tetanus immunoglobulin
(TIG) or tetanus antitoxin if not
previously immunized
142.
3.In case ofinjury:
Proper wound management with
removal of foreign matter from
wounds by through cleaning of any
necrotic tissue.
The following table is a summary
guide
for tetanus prophylaxis:
4.Training of midwivesand traditional
birth attendants with provision of
professional supervision, education
and training to methods, equipment
and techniques of aseptic technique
in child birth
145.
Control
:
1 Reporting tolocal health authority.
2 Isolation of the patient in a hospital for the benefit of the
patient
3 Treatment:
• Tetanus immunoglobulin (TIG) IM, if not available,
intravenous
tetanus antitoxin
• Penicillin in large doses intravenous.
• The wound should be excised if possible, if not it should
be
infiltrated with TIG.
• Maintain an adequate airways; and sedation if indicated;
• muscle relaxants together with tracheostomy
4 Active immunization should be initiated concurrently with
therapy.