Seroprevalence of measles IgG antibody

SEROPREVALENCE OF MEASLES IgG ANTIBODY IN
CHILDREN IN DISTRICT BANNU
by
Sahib Ullah
Department of Zoology
Kohat University of Science & Technology, Kohat-26000
Khyber Pakhtunkhwa, Pakistan
July, 2018

SEROPREVALENCE OF MEASLES IgG ANTIBODY IN
CHILDREN IN DISTRICT BANNU
Submitted in partial fulfillment of the requirement for the Degree of
Master of Science in Zoology
by
SAHIB ULLAH
(ZO220162065)
Department of Zoology
Kohat University of Science & Technology, Kohat-26000
Khyber Pakhtunkhwa, Pakistan
July, 2018

ii
″O MY LORD˝! ADVANCE ME IN KNOWLEDGE″
(AL-QURAN)

ii
CERTIFICATION FROM THE SUPERVISOR
This is to certify that the thesis entitled “Seroprevalence of measles IgG antibody in
children in district Bannu” submitted by Sahib Ullah to the Kohat University of Science &
Technology for the award of Master of Science in Zoology represents bonafide research
work carried out under my supervision. This work (in full or in part) has not been submitted
to any other Institution for award of any degree/ diploma.
Supervisor: __________________________
Dr. Kalim Ullah
Chairman: __________________________
Dr. Shahid Niaz Khan

iii
CERTIFICATION FROM THE EXAMINERS
This is to certify that this thesis presents a bonafide record of original research work carried
out by Sahib Ullah in partial fulfillment of the degree of Master of Science in Zoology
Kohat University of Science & Technology, Kohat. We find the work satisfactory for the
award of the degree if other requirements are met. The Viva Voce held
on__________________________
Undergraduate Research Evaluation Committee
__________________________ __________________________
Member Member
Dr. IshtiaqAnjum Dr. Kalim Ullah
(Assistant Professor) (Assistant Professor)
__________________________ __________________________
Member Member
Miss Sumbal Haleeem Mr. Faiz-Ur-Rehman
(Lecturer) (Lecturer)
__________________________ __________________________
Member Convener
Mr. Abdul Majid Dr. Shahid Niaz Khan
(Lecturer) (Associate Professor)
(2018)

iv
ACKNOWLEDGEMENT
First praise is to Allah, the Almighty, whom ultimately we depend for sustenance and
guidance, granting me much more than I deserve and desire. Peace and blessings of Allah be
upon Prophet Muhammad (SallallahoAaleh-e-Wa-Aaleh-e Wassalam) a mercy to all creation.
I wish to express my sincere and cordial thanks to my supervisor, Dr.Kalimllah khan,
Assistant Professor, ‘Department of Zoology’ Kohat University of Science &Technology
Kohat, for his inspiring guidance and dedicated supervision. His generous help, good
manners and thought provoking discussions enabled me to complete my research work within
the stipulated time.
I would also express my sincere gratitude especially to Dr. Shahid naiz for his inspiring
guidance, most affectionate behavior and moral support throughout my research carrier.
I am also thankful to Mr. Abdul Majid sb, Mr. Faiz ur Rehman sb, Mr. Shehzad Zareen sb,
Miss. Irum Gul, Miss. Nalila Gul for their ongoing support me during my research work.
I pay special thanks to Mr. Aamir Khan PhD scholars Department of Zoology KUST, Kohat
for encouraging and help me to complete my research work, data analysis and thesis writting.
I am also thankful to my colleagues and friends Hafiz Naeed Ullah, Muhammad Jalal,
Waseem Khan, Shahid Nawaz dawar, Nasir, Malik Shuhab, Noor Zada and Shafi Ullah
Marwat for their help and support during my research work and thesis writing.
I would also express my sincere gratitude to my Parents and brothers for their prayers, love,
encouragement and support throughout, which always inspired me.
I would also express my sincere thanks to chairman, all Faculty members for their guidance
and office & laboratory staff of Department of Zoology Kohat University of Science &
Technology, Kohat, Khyber Pakhtunkhwa, Pakistan.
Sahib Ullah

v
Dedicated to
My dearest and loving parents for their great
support, encouragement
and prayers.

vi
LIST OF CONTENTS
Certification ii, iii
Acknowledgement iv
Dedication v
List of Contents vi
List of Table vii
List of figure viii
Abbreviations ix
Abstract x
Chapter No. 1 INTRODUCTION
1.1 Measles 1
1.2 History 1
1.3 Morphology of measles virus 2
1.4 Pathogenicity 2
1.5 Symptoms of measles diseases 2
1.6 Epidemiology 3
1.6.1 Occurrence 3
1.6.2 Reservoirs 3
1.7 Transmissions 3
1.8 Control measure 4
1.9 Complications 5
1.10 Treatments 6
1.11 Measles vaccine 6
`1.11.1 Characteristics 6
1.11.2 Immunogenicity and vaccine efficacy 7
1.11.3 Vaccination schedule and use 8
1.11.4 Vaccination of adults 9
1.11.5 Re-vaccination 10
1.11.6 Post exposure prophylaxis 10
1.11.7 Contraindications and precautions to vaccination 12
1.11.8 Adverse events following vaccination 13
1.11.9 Adverse reactions of the following vaccination 14
1.11.10 Vaccine storage and handling 15

vii
1.10 Objectives 15
Chapter No. 2 MATERIALS AND METHODS
2.1 Study area 16
2.2 Data collections 16
2.3 Ethical approval 17
2.4 Data analysis 17
Chapter No. 3 RESULTS 18
3.1 Prevalence of measles IgG antibodies in the children based on
there gender 19
the age 20
the residence 21
Months 22
Chapter No. 4 DISCUSSION 24
Conclusion 25
Study limitation 27
Feature recommendation 28
References 29

viii
LIST OF TABLES
Table
no.
Title Page
no.
3.1 Demographic features of study population 18
3.2 Over all prevalence of measles infection in the children in district
Bannu
18
their gender
19
3.4 Prevalence of measles IgG antibodies in the children based on the
Age
20
residence
21
Months
22
LIST OF FIGURE
Fig no. Title Page no.
2.1 Map of KP showing the study area 16
their gender
19
age
20
residence
21
Months
23

ix
LISTS OF ABBREVIATIONS
WHO World health organization
SEAR South east Asian region
MMRV Measles mumps rubella vaccine
ICT Immunochromatography Test
MV Measles virus
MMR Measles, mumps, rubella
FGR Fetal growth restriction
KMV Killed measles vaccine
KGNH Khalifa Gul Nawaz Hospital

x
ABSTRACT
Introduction:
Measles is a highly contagious infection caused by the measles virus. Initial signs and
symptoms typically include fever often greater than 40 °C (104.0 °F), cough, runny nose
and inflamed eyes.
Material and methods:
Data were collected from different hospital and health care center of district Bannu. The
population survey in this was composed resident in district Bannu of different aged children.
Clinical record and vaccination status of all the children was recorded on a pre-set Performa.
The sera samples of these patients were already analyzed in hospital through ICT test using
IgG antibodies
Results:
650 blood Sample were studied out of which 123 were positive for IgG antibodies. Our result
showed that IgG antibodies were high female population as compare to male. Children of the
rural area showed high IgG antibodies (12.42%) than urban area (6.42%).
Conclusion:
Measles is common in unvaccinated children. It is recommended that all the children should
be vaccinated against measles. Majority of deaths occurred in the neonatal period, which
enhances the importance of antenatal care in the first month after birth.
Key words: Bannu, IgG, ICT, KP, Children

1
Chapter 1 INTRODUCTION
1.1 Measles
Measles is a highly contagious infection caused by the measles virus [1]. Initial signs and
symptoms typically include fever often greater than 40 °C (104.0 °F) cough runny nose
and inflamed eyes [2]. Two or three days after the start of symptoms small white spots may
form inside the mouth known as Koplik's spots. A red flat rash which usually starts on the
face and then spreads to the rest of the body typically begins three to five days after the start
of symptoms [3]. In developing countries with a high level of infection infants below the age
of 12 months are at high risk for measles virus (MV) infection. Despite the widespread
availability of measles vaccine for nearly 40 years’ measles remains a major cause of
childhood mortality. There were an estimated 30-40 million cases of measles in 2000 causing
some 777 000 deaths [4]. Measles infection has been controlled by vaccination in developed
countries like United States and Europe [5]. However, measles is still affecting the
developing countries due to insufficient coverage and improper handling of vaccines [6].
1.2 History
Measles is an acute viral infectious disease. References to measles can be found from as early
as the 7th century. The disease was described by the Persian physician Rhazes in the 10th
century as more to be dreaded than smallpox. In 1846 Peter Panum described the incubation
period of measles and lifelong immunity after recovery from the disease. Enders and Peebles
isolated the virus in human and monkey kidney tissue culture in 1954. The first live
attenuated vaccine was licensed for use in the United States in 1963 (Edmonston B strain).
Before a vaccine was available infection with measles virus was nearly universal during
childhood and more than 90% of persons were immune by age 15 years. Measles is still a
common and often fatal disease in developing countries. The World Health Organization
estimates there were 145,700 deaths globally from measles in 2013 [7].
1.3 Morphology of measles virus
The measles virus is a paramyxovirus genus Morbillivirus. It is 120–250 nm in diameter with
a core of single-stranded RNA and is closely related to the rinderpest and canine distemper
viruses. Two membrane envelope proteins are important in pathogenesis. They are the F
(fusion) protein, which is responsible for fusion of virus and host cell membranes, viral
penetration and hemolysis and the H (hem agglutinin) protein, which is responsible for
adsorption of virus to cells. There is only one antigenic type of measles virus. Although

2
studies have documented changes in the H glycoprotein, these changes do not appear to be
epidemiologically important (i.e., no change in vaccine efficacy has been observed). Measles
virus is rapidly inactivated by heat, sunlight, acidic pH, ether, and try sin. It has a short
survival time (less than 2 hours) in the air or on objects and surfaces [8].
1.4 Pathogenicity
Measles is a systemic infection. The primary site of infection is the respiratory epithelium of
the nosalpharynx. Two to three days after invasion and replication in the respiratory
epithelium and regional lymph nodes, a primary vermeil occurs with subsequent infection of
the reticuloendothelial system. Following further viral replication in regional and distal
reticuloendothelial sites, a second vermeil occurs 5–7 days after initial infection. During this
vermeil, there may be infection of the respiratory tract and other organs. Measles virus is
shed from the nosalpharynx beginning with the proteome until 3–4 days after rash onset [9].
1.5 Symptoms of measles diseases
The incubation period of measles, from exposure to proteome, averages 10–12 days. From
exposure to rash onset averages 14 days (range, 7–21 days). The proteome lasts 2–4 days
(range 1–7 days). It is characterized by fever, which increases in stepwise fashion, often
peaking as high as 103°F –105°F. This is followed by the onset of cough, crazy (runny nose),
or conjunctivitis. Kopi spots, a rash present on mucous membranes, are considered to be path
gnomonic for measles. It occurs 1–2 days before the rash to 1–2 days after the rash and
appears as punctuate blue-white spots on the bright red background of the buckle mucosa
[10]. The measles rash is a maculopapular eruption that usually lasts 5–6 days. It begins at the
hairline, and then involves the face and upper neck. During the next 3 days, the rash
gradually proceeds downward and outward, reaching the hands and feet. The maculopapular
lesions are generally discrete but may become confluent, particularly on the upper body.
Initially lesions blanch with fingertip pressure. By 3–4 days, most do not blanch with
pressure. Fine desquamation occurs over more severely involved areas. The rash fades in the
same order that it appears, from head to extremities. Other symptoms of measles include
anorexia diarrhea, especially in infants and generalized lymphadenopathy [11].
• Incubation period 10-12 days
• Prodrome 2-4 days’ stepwise increase in fever to 103°F–105°F
• cough, coryza, conjunctivitis
• Kop like spots (rash on mucous membranes)
• Rash 2-4 days after prodrome, 14 days after exposure
• persists 5-6 days

3
• begins on face and upper neck
• maculopapular, becomes confluent
• Fades in order of appearance [12].
1.6 Epidemiology
1.6.1 Occurrence
Measles occurs throughout the world. However, interruption of indigenous transmission of
measles has been achieved in the United States and other parts of the Western Hemisphere
[13]. However, measles occurs outside of the region of the Americas and remains a serious
and common disease in developing countries. According to the World Health Organization, it
is a leading cause of vaccine preventable deaths in children worldwide and especially impacts
malnourished children [14].
1.6.2 Reservoirs
Measles is a human disease. There is no known animal reservoir, and an asymptomatic carrier
state has not been documented [15].
1.6.3 Transmissions
Measles transmission is primarily person to person via large respiratory droplets. Airborne
transmission via aerosolized droplet nuclei has been documented in closed areas (e.g., office
examination room) for up to 2 hours after a person with measles occupied the area [16].
Likelihood of Secondary Transmission Clinical attack rates are approximately 90% among
susceptible exposed persons. If immunization rates are maintained at or above 95%, sustained
community outbreaks are largely prevented by herd immunity. [17]. Temporal Pattern in
temperate areas measles disease occurs primarily in late winter and spring. Communicability
Measles is highly communicable with greater than 90% secondary attack rates among
susceptible persons. Measles may be transmitted from 4 days before to 4 days after rash
onset. Maximum communicability occurs from onset of prodrome through the first 3–4 days
of rash [18].
1.6.4 Control measure
Investigate reports of possible measles immediately. If Clinical Case Definition is met, regard
as true measles case implement control actions unless measles is ruled out by lab testing or
other information. Cases should be excluded and isolated from group activity settings e.g.
schools, day-care centers, work place, camps, etc. immediately and through the 4th day after
the onset of rash to limit further exposures. In health care settings, use of Airborne
Precautions is recommended. Identify exposed contacts. Measles is highly communicable.
Measles cases are communicable (contagious) starting 3-5 days before rash onset through the

4
4th day after rash onset exposure includes household contact and same-room contact [19].
Measles vaccine is universally recommended as part of the routine childhood immunization
schedule, thus persons 4 years of age and born after 1956 should have a history of 2 doses of
MMR vaccine, and persons 1 year and <4 years of age should have a history of at least 1 dose
of MMR vaccine. Susceptible contacts should be recommended to receive post-exposure
prophylaxis with either Measles (MMR) vaccine, if given within 72 hours of exposure
Immune globulin (IG), if given within 6 days of exposure in most settings, post-exposure
vaccination is preferable to use of immune globulin, provided vaccine can be given within 72
hours. IG, rather than vaccine, should be used for infants under 6 months of age, pregnant
women, and severely immune compromised person [20]. Infants aged <12 months who have
been exposed to measles should receive 0.5 mL/kg [0.11ml/lb] of body weight of IG given
intramuscularly (IGIM) (maximum dose = 15 mol). Alternatively, MMR vaccine can be
given instead of IGIM, to infant’s age 6–11 months, if it can
• Be given within 72 hours of exposure.
• Pregnant women without evidence of measles immunity who are exposed to measles should
receive 400 mg/kg of IG given intravenously (IGIV) [21].
• Severely immune compromise persons, irrespective of evidence of measles immunity, who
have been exposed to measles, should receive 400 mg/kg of IG given intravenously (IGIV).
• Other people who do not have evidence of measles immunity can receive an IG Dose of 0.5
mol/kg of body weight. Give priority to people who were exposed to Measles in settings
where they have intense, prolonged close contact (e.g., Household, child care, classroom,
etc.). Give IG intramuscularly; the maximum Dose is 15 ml [22]. Exclusion of exposed,
susceptible contacts Exposed persons attending group-activity settings (e.g. schools, day-care
centers, work place, camps) who cannot readily provide documentation of Measles immunity
(including those with medical, religious and philosophical exemptions) should be vaccinated
or excluded from the setting. Exclusion should continue until 21 days after the onset of rash
of the final case of measles in the group activity setting. In general, persons who Are
vaccinated (for the 1st time or receiving a required 2nd dose) may be re-admitted
immediately to the activity setting; however, such a re-admittance policy may be modified
depending upon the circumstances involved. While routinely the 2nd dose of measles,
mumps, rubella vaccines is not given until 4– 6 years of age, in outbreak situations involving
day care, pre-school, and other settings with children less than 4 years of age consideration
should be given to requiring the 2nd dose as a control measure, following appropriately
minimum intervals between doses [23].

5
1.6.5 Complications
Approximately 30% of reported measles cases have one or more complications.
Complications of measles are most common among children younger than 5 years of age and
adults 20 years of age and older. Death from measles was reported in approximately 0.2% of
the cases in the United States from 1985 through 1992. As with other complications of
measles, the risk of death is highest among young children and adults Sub acute sclerosing
pan encephalitis (SSPE) is a rare degenerative central nervous system disease believed to be
due to persistent measles virus infection of the brain [24]. Onset occurs an average of 7 years
after measles (range 1 month–27 years), and occurs in five to ten cases per million reported
measles cases. The onset is insidious, with progressive deterioration of behavior and intellect,
followed by ataxia (awkwardness), cyclonic seizures, and eventually death. SSPE has been
extremely rare since the early 1980s. Measles illness during pregnancy results in a higher risk
of premature labor, spontaneous abortion, and low-birth weight infants. Birth defects (with no
definable pattern of malformation) have been reported rarely, without confirmation that
measles was the cause. Atypical measles occurs only in persons who received inactivated
(killed) measles vaccine (KMV) and are subsequently exposed to wild-type measles virus
[25]. An estimated 600,000 to 900,000 persons received KMV in the United States from 1963
to 1967. KMV sensitizes the recipient to measles virus antigens without providing protection.
Subsequent infection with measles virus leads to signs of hypersensitivity polyserositis. The
illness is characterized by fever, pneumonia, pleural effusions, and edema. The rash is usually
maculopapular or petechial, but may have urticarial purpuric or vesicular components. It
appears first on the wrists or ankles. Atypical measles may be prevented by revaccinating
with live measles vaccine. Moderate to severe local reactions with or without fever may
follow vaccination these reactions are less severe than with wild measles virus infection.
Modified measles occurs primarily in patients who received immune globulin (IG) as post
exposure prophylaxis and in young infants who have some residual maternal antibody. It is
usually characterized by a prolonged incubation period, mild prodrome, and sparse, discrete
rash of short duration. Similar mild illness has been reported among previously vaccinated
persons. Rarely reported in the United States, hemorrhagic measles is characterized by high
fever (105°F–106°F), seizures, delirium, respiratory distress, and hemorrhage into the skin
and mucous membranes. Measles in an immune compromised person can be severe with a
prolonged course [26]. It is reported almost exclusively in persons with T-cell deficiencies
(certain leukemia, lymphomas, and acquired immunodeficiency syndrome [AIDS]). It may
occur without the typical rash, and a patient may shed virus for several weeks after the acute

6
illness. Measles in developing countries has resulted in high attack rates among children
younger than 12 months of age. Measles is more severe in malnourished children, particularly
those with vitamin A deficiency. Complications include diarrhea, dehydration, steatites,
inability to feed, and bacterial infections (skin and elsewhere). The case-fatality rate may be
as high as 25%. Measles is also a leading cause of blindness in African children [27].
1.6.6 Treatments
Vitamin A treatment for children with measles in developing countries has been Associated
with a marked reduction in morbidity and mortality. The WHO recommends Vitamin A
administration to all children with measles in communities where vitamin A Deficiency is a
recognized problem and where the MV-related mortality rate exceeds 1%. Of note, low
serum concentrations of vitamin A are found in children with severe measles In USA. Thus,
supplemental vitamin A in patients aged 6 months to 2 years who are Hospitalized with
measles and its complications [28]. Reported cases of measles declined rapidly after the
1989–1991 resurgence. This decline was due primarily to intensive efforts to vaccinate
preschool-aged children [29].
1.7 Measles vaccine
1.7.1 First measles vaccine
Measles virus was first isolated by John Enders in 1954. The first measles vaccines were
licensed in 1963. In that year, both an inactivated (“killed”) and a live attenuated vaccine
(Edmonston B strain) was licensed for use in the United States. The inactivated vaccine was
withdrawn in 1967 because it did not protect against measles virus infection [30].
Furthermore, recipients of inactivated measles vaccine frequently developed a unique
syndrome, atypical measles, if they were infected with wild-type measles virus. The original
Edmonston B vaccine was withdrawn in 1975 because of a relatively high frequency of fever
and rash in recipients. A live, further attenuated vaccine (Schwarz strain) was first introduced
in 1965 but also is no longer used in the United States. Another live, further attenuated strain
vaccine (Edmonston-Enders strain) was licensed in 1968. These further attenuated vaccines
caused fewer reactions than the original Edmonston B vaccine [31].
1.7.2 Characteristics
The only measles virus vaccine now available in the United States is a live, more attenuated
Edmonston-Enders strain (formerly called “Mora ten”). The vaccine is available combined
with mumps and rubella vaccines as MMR, or combined with mumps, rubella, and varicella
vaccine as MMRV (Proud). The Advisory Committee on Immunization Practices (ACIP)
recommends that MMR be used when any of the individual components is indicated. Single-

7
antigen measles vaccine is not available in the United States. Measles vaccine is prepared in
chick embryo fibroblast tissue culture. MMR and MMRV are supplied as a lyophilized
(freeze-dried) powder and are reconstituted with sterile, preservative-free water. The vaccines
contain small amounts of human albumin, neomycin, orbital, and gelatin [32].
1.7.3 Immunogenicity and vaccine efficacy
Measles vaccine produces an in apparent or mild, no communicable infection. Measles
antibodies develop in approximately 95% of children vaccinated at 12 months of age and
98% of children vaccinated at 15 months of age. Seroconversion rates are similar for single-
antigen measles vaccine, MMR, and MMRV. Approximately 2%–5% of children who
receive only one dose of MMR vaccine fail to respond to it (i.e., primary vaccine failure)
[33]. MMR vaccine failure may occur because of passive antibody in the vaccine recipient,
damaged vaccine, incorrect records, or possibly other reasons. Most persons who fail to
respond to the first dose will respond to a second dose. Studies indicate that more than 99%
of persons who receive two doses of measles vaccine (with the first dose administered no
earlier than the first birthday) develop serologic evidence of measles immunity [34].
Although the titer of vaccine-induced antibodies is lower than that following natural disease,
both serologic and epidemiologic evidence indicate that vaccine-induced immunity appears to
be long-term and probably lifelong in most persons. Most vaccinated persons who appear to
lose antibody show an anamnesis immune response upon revaccination, indicating that they
are probably still immune. Although revaccination can increase antibody titer in some
persons, available data indicate that the increased titer may not be sustained. Some studies
indicate that secondary vaccine failure waning immunity may occur after successful
vaccination, but this appears to occur rarely and to play only a minor role in measles
transmission and outbreaks [35].
1.7.4 Vaccination schedule and use
Two doses of measles-containing vaccine, as combination MMR, separated by at least 4
weeks, are routinely recommended for all children 12 months of age or older. All persons
born during or after 1957 should have documentation of at least one dose of MMR or other
evidence of measles immunity. Certain adolescents and adults should receive two doses of
MMR. The first dose of MMR should be given on or after the first birthday. Any dose of
measles-containing vaccine given before 12 months of age should not be counted as part of
the series [36]. Children vaccinated with measles-containing vaccine before 12 months of age
should be contaminated with two doses of MMR vaccine, the first of which should be
administered when the child is at least 12 months of age. A second dose of MMR is

8
recommended to produce immunity in those who failed to respond to the first dose. The
second dose of MMR vaccine should routinely be given at age 4–6 years, before a child
enters kindergarten or first grade. The recommended visit at age 11 or 12 years can serve as a
catch-up opportunity to verify vaccination status and administer MMR vaccine to those
children who have not yet received two doses of MMR. The second dose of MMR may be
administered as soon as 4 weeks (28 days) after the first dose [37]. Children who have
already received two doses of MMR vaccine at least 4 weeks apart, with the first dose
administered no earlier than the first birthday, do not need an additional dose when they enter
school. Children without documentation of adequate vaccination against measles, mumps,
and rubella or other acceptable evidence of immunity to these diseases when they enter
school should be admitted after receipt of the first dose of MMR. A second dose should be
administered as soon as possible, but no less than 4 weeks after the first dose. Only doses of
vaccine with written documentation of the date of receipt should be accepted as valid. Self-
reported doses or a parental report of vaccination is not considered adequate documentation
[38]. A health care provider should not provide an immunization record for a patient unless
that health care provider has administered the vaccine or has seen a record that documents
vaccination. Persons who lack adequate documentation of vaccination or other acceptable
evidence of immunity should be vaccinated. Vaccination status and receipt of all vaccinations
should be documented in the patient’s permanent medical record and in a vaccination record
held by the individual. MMRV is approved by the Food and Drug Administration for children
12 months through 12 years of age (that is, until the 13th birthday). MMRV should not be
administered to persons 13 years of age or older. For the first dose of MMR and varicella
vaccine at age 12 through 47 months either MMR vaccine and varicella vaccine or MMRV
vaccine may be used. Providers who are considering administering MMRV vaccine should
discuss the benefits and risks of both vaccination options with the parents or caregivers.
Unless the parent or caregiver expresses a preference for MMRV vaccine CDC recommends
that MMR vaccine and varicella vaccine should be administered at separate sites for the first
dose in this age group. For the second dose of MMR and varicella vaccine at any age (15
months through 12 years) and for the first dose at 48 months of age or older use of MMRV
vaccine generally is preferred over separate injections of its equivalent component vaccines
i.e. MMR vaccine and vermicelli vaccine[39].
1.7.5 Vaccination of adults
Adults born in 1957 or later who do not have a medical contraindication should receive at
least one dose of MMR vaccine unless they have documentation of vaccination with at least

9
one dose of measles- mumps- and rubella-containing vaccine or other acceptable evidence of
immunity to these three diseases. With the exception of women who might become pregnant
and persons who work in medical facilities, birth before 1957 generally can be considered
acceptable evidence of immunity to measles, mumps, and rubella [40]. Certain groups of
adults may be at increased risk for exposure to measles and should receive special
consideration for vaccination. These include persons attending colleges and other post-high
school educational institutions, persons working in medical facilities, and international
travelers. Colleges and other post-high school educational institutions are potential high-risk
areas for measles, mumps, and rubella transmission because of large concentrations of
susceptible persons. Prematriculation vaccination requirements for measles immunity have
been shown to significantly decrease the risk of measles outbreaks on college campuses
where they are implemented and enforced [41]. Colleges, universities, technical and
vocational schools, and other institutions for post-high school education should require
documentation of two doses of MMR vaccine or other acceptable evidence of measles,
mumps, and rubella immunity before entry. Students who have no documentation of live
measles, mumps, or rubella vaccination or other acceptable evidence of measles, mumps, and
rubella immunity at the time of enrollment should be admitted to classes only after receiving
the first dose of MMR. A second dose of MMR should be administered no less than 4 weeks
(28 days) later. Students with evidence of prior receipt of only one dose of MMR or other
measles-containing vaccine on or after their first birthday should receive a second dose of
MMR provided at least 4 weeks have elapsed since their previous dose. Persons who work in
medical facilities are at higher risk for exposure to measles than the general population. All
persons who work within medical facilities should have evidence of immunity to measles
mumps and rubella. Because any healthcare personnel (i.e., medical or nonmedical, paid or
volunteer full time or part time student or non-student with or without patient-care
responsibilities) who lack evidence of immunity to measles or rubella can contract and
transmit these diseases all medical facilities i.e. inpatient and outpatient private and public
should ensure measles and rubella immunity among those who work within their facilities
[42]. Adequate vaccination for measles mumps and rubella for health care personnel born
during or after 1957 consists of two doses of a live measles- and mumps-containing vaccine
and at least one dose of a live rubella-containing vaccine. Health care personnel needing a
second dose of measles-containing vaccine should be re vaccinated at least 4 weeks after their
first dose. For unvaccinated personnel born before 1957 who lack laboratory evidence of
measles mumps and/or rubella immunity or laboratory confirmation of disease health care

10
facilities should consider vaccinating personnel with two doses of MMR vaccine at the
appropriate interval (for measles and mumps) and one dose of MMR vaccine (for rubella)
respectively. For unvaccinated personnel born before 1957 who lack laboratory evidence of
measles mumps and/or rubella immunity or laboratory confirmation of disease health care
facilities should recommend two doses of MMR vaccine during an outbreak of measles or
mumps and one dose during an outbreak of rubella [43]. Serologic testing does not need to be
done before vaccinating for measles and rubella unless the health care facility considers it
cost-effective. Serologic testing is appropriate only if tracking systems are used to ensure that
tested persons who are identified as susceptible are subsequently vaccinated in a timely
manner. Serologic testing for immunity to measles and rubella is not necessary for persons
documented to be appropriately vaccinated or who have other acceptable evidence of
immunity. If the return and timely vaccination of those screened cannot be assured serologic
testing before vaccination should not be done. Persons who travel outside the United States
are at increased risk of exposure to measles. Measles is endemic or epidemic in many
countries throughout the world. Although proof of immunization is not required for entry into
the United States or any other country, persons traveling or living abroad should have
evidence of measles immunity. Adequate vaccination of persons who travel outside the
United States is two doses of MMR [44].
1.7.6 Re-vaccination
Revaccination is recommended for certain persons. The following groups should be
considered unvaccinated and should receive at least one dose of measles vaccine persons 1)
vaccinated before the first birthday, 2) vaccinated with killed measles vaccine (KMV), 3)
vaccinated from 1963 through 1967 with an unknown type of vaccine or 4) vaccinated with
immune globulin (IG) in addition to a further attenuated strain or vaccine of unknown type.
(Revaccination is not necessary if IG was given with Edmonston B vaccine) [45].
1.7.7 Post exposure prophylaxis
Live measles vaccine provides permanent protection and may prevent disease if given within
72 hours of exposure. IG may prevent or modify disease and provide temporary protection if
given within 6 days of exposure. The dose is 0.5 mol/kg body weight with a maximum of 15
mol intramuscularly and the recommended dose of IG given intravenously is 400mg/ kg. IG
may be especially indicated for susceptible household contacts of measles patients
particularly contacts younger than 1 year of age (for whom the risk of complications is
highest). If the child is 12 months of age or older live measles vaccine should be given about

11
5 months later when the passive measles antibodies have waned. IG should not be used to
control measles outbreaks [46].
1.7.8 Contraindications and precautions to vaccination
Contraindications for MMR and MMRV vaccines include history of anaphylactic reactions to
neomycin, history of severe allergic reaction to any component of the vaccine, pregnancy,
and immunosuppressant. In the past, persons with a history of anaphylactic reactions
following egg ingestion were considered to be at increased risk for serious reactions after
receipt of measles-or mumps-containing vaccines, which are produced in chick embryo
fibroblasts [47]. However, data suggest that anaphylactic reactions to measles- and mumps-
containing vaccines are not associated with hypersensitivity to egg antigens but to other
components of the vaccines (such as gelatin). The risk for serious allergic reactions following
receipt of these vaccines by egg-allergic persons is extremely low, and skin-testing with
vaccine is not predictive of allergic reaction to vaccination. Therefore, MMR may be
administered to egg-allergic children without prior routine skin testing or the use of special
protocols. MMR vaccine does not contain penicillin. A history of penicillin allergy is not a
contraindication to vaccination with MMR or any other U.S. vaccine [48]. Women known to
be pregnant should not receive measles vaccine. Pregnancy should be avoided for 4 weeks
following MMR vaccine. Close contact with a pregnant woman is not a contraindication to
MMR vaccination of the contact. Breastfeeding is not a contraindication to vaccination of
either the woman or the breastfeeding child. Replication of vaccine viruses can be prolonged
in persons who are immune suppressed or immune deficient. Severe immunosuppressant can
be due to a variety of conditions, including congenital immunodeficiency, HIV infection,
leukemia, lymphoma, generalized malignancy, or therapy with alkylation agents, ant
metabolites, radiation, or large doses of corticosteroids. Evidence based on case reports has
linked measles vaccine virus infection to subsequent death in at least six severely immune
compromised persons. For this reason, patients who are severely immune compromised for
any reason should not be given MMR vaccine [49]. Healthy susceptible close contacts of
severely immune compromised persons should be vaccinated. In general, persons receiving
large daily doses of corticosteroids (2 mg/kg or more per day, or 20 mg or more per day of
prednisone) for 14 days or more should not receive MMR vaccine because of concern about
vaccine safety. MMR and its component vaccines should be avoided for at least 1 month after
cessation of high-dose therapy. Persons receiving low-dose or short-course (less than 14
days) therapy, alternate-day treatment, maintenance physiologic doses, or topical, aerosol,
intra-articular, bursal, or tendon injections may be vaccinated. Although persons receiving

12
high doses of systemic corticosteroids daily or on alternate days for less than 14 days
generally can receive MMR or its component vaccines immediately after cessation of
treatment, some experts prefer waiting until 2 weeks after completion of therapy [50].
Patients with leukemia in remission who have not received chemotherapy for at least 3
months may receive MMR or its component vaccines. Measles disease can be severe in
persons with HIV infection. Available data indicate that vaccination with MMR has not been
associated with severe or unusual adverse reactions in HIV-infected persons without evidence
of severe immunosuppressant, although antibody responses have been variable. MMR
vaccine is recommended for all persons 12 months of age or older with HIV infection who do
not have evidence of current severe immunosuppressant absence of severe
immunosuppressant is defined as CD4 percentages greater than or equal to 15% for 6 months
or longer for persons five years of age or younger and CD4 percentages greater than or equal
to 15% and CD4 count greater than or equal to 200 cells/mm3 for 6 months or longer for
persons older than five years or other current evidence of measles, rubella, and mumps
immunity [51]. Asymptomatic children do not need to be evaluated and tested for HIV
infection before MMR or other measles-containing vaccines are administered. A theoretical
risk of an increase (probably transient) in HIV viral load following MMR vaccination exists
because such an effect has been observed with other vaccines. The clinical significance of
such an increase is not known. MMR and other measles-containing vaccines are not
recommended for HIV-infected persons with evidence of severe immunosuppressant. MMRV
is not approved for and should not be administered to a person known to be infected with
HIV. Persons with moderate or severe acute illness should not be vaccinated until the patient
has improved. This precaution is intended to prevent complicating the management of an ill
patient with a potential vaccine adverse reaction, such as fever. Minor illness (e.g., obits
media, mild upper respiratory infections) concurrent antibiotic therapy, and exposure to or
recovery from other illness are not contraindications to measles vaccination. Receipt of
antibody-containing blood products (e.g., immune globulin, whole blood or packed red blood
cells, intravenous immune globulin) may interfere with Seroconversion after measles vaccine
[52]. The length of time that such passively acquired antibody persists depends on the
concentration and quantity of blood product received. Persons who have a history of
thrombocytopenic purport or thrombocytopenia (low platelet count) may be at increased risk
for developing clinically significant thrombocytopenia after MMR vaccination. No deaths
have been reported as a direct consequence of vaccine-induced thrombocytopenia. The
decision to vaccinate with MMR depends on the benefits of immunity to measles, mumps,

13
and rubella and the risks for recurrence or exacerbation of thrombocytopenia after
vaccination or during natural infection with measles or rubella. The benefits of immunization
are usually greater than the potential risks, and administration of MMR vaccine is justified
because of the even greater risk for thrombocytopenia after measles or rubella disease.
However, deferring a subsequent dose of MMR vaccine may be prudent if the previous
episode of thrombocytopenia occurred within 6 weeks after the previous dose of the vaccine.
Serologic evidence of measles immunity in such persons may be sought in lieu of MMR
vaccination [53]. A personal or family (i.e., sibling or parent) history of seizures of any
etiology is a precaution for MMRV vaccination. Studies suggest that children who have a
personal or family history of febrile seizures or family history of epilepsy are at increased
risk for febrile seizures compared with children without such histories. Children with a
personal or family history of seizures of any etiology generally should be vaccinated with
MMR vaccine and varicella vaccine at separate sites because the risks for using MMRV
vaccine in these children generally outweigh the benefits. Tuberculin skin testing (TST) is not
a prerequisite for vaccination with MMR or other measles-containing vaccine [54]. TST has
no effect on the response to MMR vaccination. However, measles vaccine (and possibly
mumps, rubella, and varicella vaccines) may transiently suppress the response to TST in a
person infected with Mycobacterium tuberculosis. If tuberculin skin testing is needed at the
same time as administration of measles-containing vaccine, TST and vaccine can be
administered at the same visit. Simultaneously administering TST and measles-containing
vaccine does not interfere with reading the TST result at 48–72 hours and ensures that the
person has received measles vaccine. If the measles-containing vaccine has been
administered recently, TST screening should be delayed at least 4 weeks after vaccination. A
delay in administering TST will remove the concern of any theoretical suppression of TST
reactivity from the vaccine. TST screening can be performed and read before administering
the measles-containing vaccine. This option is the least favored because it will delay receipt
of the vaccine [55].
1.7.9 Adverse events following vaccination
Arthralgias and other joint symptoms are reported in up to 25% of susceptible adult women,
given MMR vaccine. This adverse event is associated with the rubella component. Allergic
reactions including rash, prorates, and purport have been temporally associated with mumps
vaccination, but these are not common and usually mild and of brief duration. To date there is
no convincing evidence that any vaccine causes autism or autism spectrum disorder. Concern
has been raised about a possible relation between MMR vaccine and autism by some parents

14
of children with autism. Symptoms of autism are often noticed by parents during the second
year of life, and may follow administration of MMR by weeks or months. Two independent
nongovernmental groups, the Institute of Medicine (IOM) and the American Academy of
Pediatrics (AAP), have reviewed the evidence regarding a potential link between autism and
MMR vaccine. Both groups independently concluded that available evidence does not
support an association, and that the United States should continue its current MMR
vaccination policy. Additional research on the causes of autism is needed [56].
1.7.10 Adverse reactions of the following vaccination
Of increased risk of adverse reactions following MMR vaccination in persons who are
already immune to the diseases, Fever Adverse reactions following measles vaccine (except
allergic reactions) may be caused by replication of measles vaccine virus with subsequent
mild illness. These events occur 5 to 12 days post vaccination and only in persons who are
susceptible to infection. There is no evidence is the most common adverse reaction following
MMR vaccination. Although measles, mumps, and rubella vaccines may cause fever after
vaccination, the measles component of MMR vaccine is most often associated with fever
[57]. After MMR vaccination, 5% to 15% of susceptible persons develop a temperature of
103°F (39.4°C) or higher, usually occurring 7 to 12 days after vaccination and generally
lasting 1 or 2 days. Most persons with fever are otherwise asymptomatic. In MMRV vaccine
prelicensure studies conducted among children 12–23 months of age, fever (reported as
abnormal or elevated 102°F or higher moral equivalent) was observed 5-12 days after
vaccination in 21.5% of MMRV vaccine recipients compared with 14.9% of MMR vaccine
and varicella vaccine recipients. Two post licensure studies indicated that among children
12–23 months of age, one additional febrile seizure occurred 5–12 days after vaccination per
2,300–2,600 children who had received the first dose of MMRV vaccine, compared with
children who had received the first dose of MMR vaccine and varicella vaccine administered
as separate injections at the same visit. Data from post licensure studies do not suggest that
children 4–6 years of age who received the second dose of MMRV vaccine had an increased
risk for febrile seizures after vaccination compared with children the same age who received
MMR vaccine and varicella vaccine administered as separate injections at the same visit [58].
Rarely, MMR vaccine may cause thrombocytopenia within 2 months after vaccination.
Estimates of the frequency of clinically apparent thrombocytopenia from Europe are one case
per 30,000–40,000 vaccinated susceptible persons, with a temporal clustering of cases
occurring 2 to 3 weeks after vaccination. The clinical course of these cases was usually
transient and benign, although hemorrhage occurred rarely. The risk for thrombocytopenia

15
during rubella or measles infection is much greater than the risk after vaccination. Based on
case reports, the risk for MMR-associated thrombocytopenia may be higher for persons who
have previously had immune thrombocytopenic purport, particularly for those who had
thrombocytopenic purport after an earlier dose of MMR vaccine. Transient lymphadenopathy
sometimes occurs following receipt of MMR or other rubella-containing vaccine, and partitas
has been reported rarely following receipt of MMR or other mumps-containing vaccine [59].
Allergic reactions following the administration of MMR or any of its component vaccines are
rare. Most of these reactions are minor and consist of a wheal and flare or urticaria at the
injection site. Immediate, anaphylactic reactions to MMR or its component vaccines are
extremely rare. Measles- and rubella-containing vaccines, including MMR, may cause a
transient rash. Rashes, usually appearing 7 to 10 days after MMR or measles vaccination,
have been reported in approximately 5% of vaccines [60].
1.7.11 Vaccine storage and handling
MMR vaccine can be stored either in the freezer or the refrigerator and should be protected
from light at all times. MMRV vaccine should be stored frozen between -58°F and +5°F (-
50°C and -15°C). When MMR vaccine is stored in the freezer, the temperature should be the
same as that required for MMRV, between -58°F and +5°F (-50°C and -15°C). Storing MMR
in the freezer with MMRV may help prevent inadvertent storage of MMRV in the refrigerator
[61].
1.8 Objectives
 To assess the prevalence of measles infection visiting major hospitals of District
Bannu
 To determine the effect of various factors on measles infection in children of the study
area

16
Chapter 2 MATERIALS AND METHODS
2.2 Study area
The study area is district Bannu which is located in province Khyber Pakhtunkhwa. There are
26 districts in KPK. It is situated at a distance of 190 Km, in the south of Peshawar. It is
population is more than half a million. Majority of the population live in villages. Still the
urban area is overcrowded with peoples.
2.1 Data collections
Data were collected from different hospital and health care center of district Bannu. The
population survey in this was composed resident in district Bannu of different aged children.
Clinical record and vaccination status of all the children was recorded on a pre-set proforma.
The sera samples of these patients were already analyzed in hospital through ICT test using
IgG antibodies. All data of these patients were grouped using different parameter. 123
children were affected by this diseases during December 2017 to May 2018 in which males
and female are included which belong from different areas.
Fig 2.1: Map showing the study area

17
2.2 Ethical approval
Ethical clearance was obtained from the institutional review board of the Kohat University of
Science and Technology Kohat. After explaining the objective of the study to the MS of the
hospitals they issued us written orders to their lab assistance to cooperate with us and give the
available data.
2.3 Data analysis
SPSS statistical software version 18 was utilized for data entry and analysis. The chi-square
test was used to determine the significant association between two variables. P value was
calculated, where 0.05 was considered significant at the 95% CI (Confidence Interval) level.

18
Chapter 3 RESULTS
This study was conducted to investigate the prevalence of measles IgG antibodies among
children. For this purpose, 650 were studied out of which 123 were positive as shown in table
2.
Table 3.1: Demographic features of study population
Demographics feature
Sample size (n=650)
Characteristic Total number
Gender
Male 259
Female 391
Age Groups (Year)
10 months to 1 year 191
1- 3 (y) 179
3-5 ( y) 153
5 -7 ( y) 127
Residence
Urban 253
Rural 397
Table 3.2: Over all prevalence of measles infection in the children in district Bannu
No. of samples Measles Positive (ICT) Percentage %
650 123 18.92

19
3.1 Prevalence of measles IgG antibodies in the children based on their gender
We also find out relationship of measles IgG antibodies to the gender of the study
participants. Based on their sex children were divided into male and female as shown in
table3. Table3 revealed that there are 259 male children out of which. 8% were positive and
391 were female out of which 10.92% were positive. Chi-square test was used for data
analysis.
Table 3.3: Prevalence of measles IgG antibodies in the children based on their gender
Gender Total number Measles positive Percentage % P Value
Male 259 52 8
0.0585
Female 391 71 10.92
Male Female
0
100
200
300
400
500
Prevalance%
Total Positive
Fig 3.1: Prevalence of measles IgG antibodies in the children based on their gender

20
3.2 Prevalence of measles IgG antibodies in the children based on the age
To know the relation of prevalence of measles IgG antibodies with age, participants were
divided into four age groups (10 months to 1 year, 1 year to 3 years, 3 years to 5 years, 5
years 7 year) as shown in table 4. Children having age 1 year were 191 in number out
ofWhich.7.84 were positive. In age group 2(1year to 3years) there were 179 children out of
which 6 were positive. In 3rd age group 153 children were present out of which 3.23% were
positive. Similarly, in age group 4 (5 years 7 years) there 127 children were present out of
which 1.8% were positive. Chi-square test was used for data analysis.
Table 3.4: Prevalence of measles IgG antibodies in the children based on the age
10 months 1 year 1 y - 3 y 3 y - 5 y 5 y - 7 y
0
50
100
150
200
250
Age groups
Prevalance%
Total Positive
Fig 3.2: Prevalence of measles IgG antibodies in the children based on the age
Age groups (year) Total number Measles positive Percentage % P value
10 months to 1 year 191 51 7.84
0.0002
1 y - 3 y 179 39 6
3 y – 5 y 153 21 3.23
5 y – 7 y 127 12 1.84

21
3.3 Prevalence of measles IgG antibodies in the children based on the residence
In table 5, prevalence of measles IgG antibodies among children based on their localities
were identified. On the basis of area children were divided into two i.e. rural and urban area
children. Table 5 showed that 397 children belong from rural area out of which 12.15% were
positive and 253 from urban area out of which 6.76% were positive. Chi square test was used
for data analysis and was statistically non-significant.
Table 3.5: Prevalence of measles IgG antibodies in the children based on the residence
Area Total number Measles positive Percentage % P Value
Rural 397 79 12.15
0.0708
Urban 253 44 6.76
Fig 3.3: Prevalence of measles IgG antibodies in the children based on the residence

22
3.4 Prevalence of measles IgG antibodies in the children based on the Months
There are four different seasons in year and we co-relate the prevalence of measles virus
infection among children on the basis of different season. We found that 1.69% children were
positive in December followed by January 2.92%, February 4.15% in March5.05% in April
3.23% and in May 1.84% Chi squar-test was used for data analysis. P value was calculated
and was significant (0.0001).
Table 3.6 Prevalence of measles IgG antibodies in the children based on the Months
Season Total Number Measles positive Percentage % P value
December 76 11 1.69
0.0001
January 97 19 2.92
February 121 27 4.15
March 131 33 5.07
April
120 21 3.23
May
105 12 1.84

23
Fig 3.4 Prevalence of measles IgG antibodies in the children based on the Months

24
Chapter 4 DISCUSSIONS
Measles is a highly contagious infection caused by the measles virus. Initial signs and
symptoms typically include fever often greater than 40 °C (104.0 °F) cough runny nose
and inflamed eyes. A red flat rash which usually starts on the face and then spreads to the rest
of the body typically begins three to five days after the start of symptoms. In developing
countries with a high level of infection infants below the age of 12 months are at high risk for
measles virus (MV) infection. Despite the widespread availability of measles vaccine for
nearly 40 years measles remains a major cause of childhood mortality. There were an
estimated 30-40 million cases of measles in 2000 causing some 777 000 deaths. Measles
infection has been controlled by vaccination in developed countries like United State and
Europe. However, measles is still affecting the developing countries due to insufficient
coverage and improper handling of vaccines [62]. Before the measles vaccine era, there were
∼500,000 cases of measles and 500 deaths due to measles reported annually in the United
States [63]. Since the introduction of measles virus vaccines in 1963, the endemicity of
measles has been dramatically reduced in many countries and eliminated in some [64]. The
current study was carried out to provide up to date information about the prevalence of
Measles in district Bannu children.
In the present study we found that prevalence of measles IgG antibodies is 18.92%. A less
dissimilar study, of Measles reported in children from several countries. In 2006, a large
measles outbreak (number = 614) occurred in Duisburg city, Germany, with 54% of cases
aged > 9 years [65]. Variation of the present study from the previous studies may be due to
vaccination, different sample population, geographic conditions and climate.
We also analyzed the sero-positivity of measles IgG antibodies with different parameters like
age, area of residency, economic position and sex. When categorized by age then it was
found that age has a indirect impact on positivity of measles IgG antibodies among children.
The reported prevalence of the current study indicates that prevalence of measles IgG
antibodies decreased gradually along the age and were high among the children of age >1
years old. This is an agreement with the study conducted by Girdler J et al., [7].
In this study, though it was not properly investigated but in a general view it was well
understood that urban children are at risk of contracting measles virus infection as compared
to children of rural areas. This may be due to overcrowding in urban area which facilitates the
transmission of measles virus due to close contact. But the current study conflict the above
rules that is rural area children showed high positivity (12.15%) as compared to urban area

25
children (6.76%). The confliction among the present report and general rules may be due to
improper management, less of education, poor vaccination and hygienic condition in rural
areas.
The result obtained in the study and also in a general view it was understood that majority of
measles positive cases were reported between March and Febrary. Measles spread mainly
concerned with climatic changes such as temperature and humidity that is why it is common
in late winter and early spring.
Conclusions
Measles is common in unvaccinated children. It is recommended that all the children should
be vaccinated against measles. Majority of deaths occurred in the neonatal period, which
enhances the importance of antenatal care in the first month after birth. Infant/ Child
mortality in this region can be reduced by improvement in the health care system at
peripheral level. Immunization of measles should be provided to children at their door step by
concerned health authorities with enthusiasm and passion. Cold chain should be properly
managed, checked and vigilantly observed by third party about actual efficacy of measles
vaccine by alternate sources of temperature maintenance of measles vaccine during such 18
hours of electricity power interruptions in urban, rural and semi urban areas of our country.
All the donor agencies can also play a significant role by improving its disease early warning
system more vigilant and bilateral cooperation between them and current decentralized
provincial health authorities with concerned quarters to avoid maximum measles epidemics.
A number of children are underprivileged of receiving immunization of measles vaccine by
sense of parents, irresponsibility, carelessness and tiredness to reach that place where the
vaccination is provided. So such task force should identify these communities and with
special attention to be focused on them. The majority of the rural and semi urban is
uneducated and live in the backward areas. They have no any basic awareness about the
health and immunization of their child. The best way to mobilize the community about the
child immunization is community. Local organizations should conduct seminars, workshops
and health programmers held with the participation of non government organizations and
government health officials as well as local social activists, political leaders, school teachers,
religious leaders especially imam massaged in their localities and villages accompanied by
their zeal and zest with strong political commitment and full participation of existing district
health system with honesty, punctuality, regularity, hard work and utmost contribution with
strong devotion and dedication. To encourage and sensitize the parents about the child
immunization during door to door visit because of the rural and semi urban communities have

26
no access to print media and electronic media due to poverty and illiteracy. Salaries should be
increased with hard area and risk allowances and bonuses to be awarded to those health
concerns with certificates of appreciation and gold medals with due honor, distinction,
respect and self-esteem. The health authorities should provide basic information to rural and
semi urban people about their health via truly trained and competent lady health workers,
lady health visitors and vaccinators visiting in their dwelling regularly and providing essential
information about positive perspective of immunization of measles vaccinations.

27
Study limitations
 The currently conducted study may not show the actual figure of measles infection in
the study area as was not conducted on whole population but was limited for small
size sample population.
 A much clear picture of the disease will be given by a study in depth which will
include large number of children.

28
Future recommendations…..
 Massive awareness campaign should be started about measles infection for small
children
 A basic dignostic laboratory should be made at each health care center both at rural
and urban areas for virus and bacteria detection.
 Key step should be taken by Govt. to decrease this viral infection

29
REFERENCES
1. A.L. Cohen, A. Salam, A. Bosan, R. Perry, S. Iqbal and S.N. Qureshi et al, (2009),
“Etiology of a suspected measles outbreak: preceding measles reduction activities in
Pakistan”, Journal of the College of Physician and Surgeons Pakistan, 19, 591-4.
2. I .F. Zaman and A. Rauf (2011) “Working toward decreasing infant mortality in developing
countries through change in the medical curriculum”, Asia Pacific Family Medicine, 10, 11.
3. K.M. Thompson, C.L. Odahowski, J.L. Goodson, S.E. Reef and R.T. Perry (2000-2001).
“World Health Organization. Global measles mortality reduction and regional elimination”,
Weekly epidemiological record, 77,49-56
4. A.M. Bhatti (2013) “Measles Outbreak in Pakistan”, Medical Forum Monthly.
5. T. Hashiguchi, K. Manama, Y. Yang (2011) “Structural insights into cell entry and measles
vaccine", Front Microbial, 2:247.
6. J. Girdler,S. Tinker , L. Markowitz, W. Atkinson, L. Dales, MJ. Paranoia (2009) “Acute
measles mortality in the measles”, American Academy of Pediatrics, 4,44–55.
7. WL. Atkinson, WA. Orenstein, S. Kurgan (1989–1990) “The resurgence of measles in the
United States”, Emerge Infect Disease, 4,29–35.
8. A. Leremy, J. Sean and G. Christopher (2007) “Structure of the measles virus hem
agglutinin”, Nature Structural and Molecular Biology, 14 (12), 1227-1228.
9. Y. Yanagi, M. Takeda and S. Ohno (2006) “Measles virus: cellular receptors, tropism and
pathogenesis”, Journal of General Virology, 87, 2767-2779.
10. WJ. Bellini, PA. Rota (1998) “Genetic diversity of wild-type measles virus implications for
global measles elimination programs”, Emerge Infect Disease 4,29–35.

30
11. B.K. Rima, J.A. Earle, R.P Yeo, L. Herlihy, K. Baczko, V. terMeulen et al (1995) “Temporal
and geographical distribution of measles virus genotypes”, The Journal of General Virology,
76(5), 1173–80.
12. DL. Heymann (2012) “Public Health Agency of Canada. Guidelines for the prevention and
control of measles outbreaks in Canada”. Journal of virology 21, 30-32
13. K.M. Thompson, C.L. Odahowski, J.L. Goodson, S.E. Reef and R.T. Perry (2016) “Synthesis
of evidence to characterize national historical measles and rubella exposure and
immunization histories”, Risk Anal, 36, 1427-1458.
14. M. Shah, S. Shams and Z. Rahman (2012) “Molecular relationship between field and vaccine
strain of measles virus and its persistence in Pakistan”, Genetic Vaccines and Therapy,
30(10), 1.
15. SY. Chen, S. Anderson, PK. Kutty, F. Lugo, M. McDonald (2011) “Health care–associated
measles outbreak in the United States after an importation challenges and economic impact”,
Infect Disease 203,1517-25.
16. E. Simons, M. Ferrari, J. Fricks, K. Wannemuehler, A. Anand, A. Burton et al (2012)
“Assessment of the global measles mortality reduction goal: results from a model of
surveillance data”, Lancet, 379, 2173-2178.
17. J. Dossetor, H. C whittle and B. M.G Greenwood (1977) “Measles virus and associated
central nervous system squeal”, Seminar in pediatric neurology 19.107-114
18. H. Holzmann, H. Hengel, H.Tenbusch (2016) “Eradication of measles remaining challenge”,
Medical microbiology and immunology 205, 201-208
19. Use of combination measles, mumps, rubella, and varicella vaccine: recommendations of the
Advisory Committee on Immunization Practices (2010), Journal of virology 59,1–12.

31
20. P. Plattet, L. Alves (2011) “Immunization of health-care personnel Recommendations of the
Advisory Committee on Immunization Practices”, virus 60, 1-45.
21. JS. Gerber, PA. Offit (2000–2008) “Measles — United States Global measles mortality”.
Frontiers in microbiology 5,1321–6.
22. NA. Halsey, SL. Hyman (2000) “Conference Writing Panel Measles-mumps-rubella vaccine
and autistic spectrum disorder report from the New Challenges in Childhood Immunizations
Conference”, Pediatrics 107, 8,112
23. CDC, “Prevention of measles, rubella, congenital rubella syndrome, and mumps” 2013,
summary recommendations of the Advisory Committee on Immunization Practices. Journal
of virology 62, 1-34.
24. UNICEF (2011) “UNICEF information by country Pakistan assessed”, Morbidity Mortality
Weekly Report 54, 1100-1104.
25. WHO (2006) “Progress in reducing global measles deaths”, Weekly Epidemiological Record
10, 89-96.
26. DE. Sugerman, AE. Barskey, MG. Delea et al (2010). “Increase protection during a measles
outbreak of children previously vaccinated with a second dose of measles-mumps-rubella
vaccine”. Pediatric Infect Disease 18,620–3.
27. R.L. de Swart, S. Yuksel and A.D. Osterhaus (2005), “Relative contributions of measles virus
hem agglutinin and fusion protein-specific serum antibodies to virus neutralization”, Journal
of Virology, 79, 11547–115451.
28. P. Plattet, L. Alves, M. Herren and H.C. Aguilar (2016), Measles virus fusion protein:
Structure, function and inhibition”, Viruses, 8, 112.

32
29. R.D. De Vries, S. McQuaid, G. van Amerongen, S. Yuksel, R.J. Verburgh, A.D. Osterhaus et
al (2012), “Measles immune suppression: Lessons from the macaque model”, PLOS
Pathogens, 8, 1002885.
30. D. Naniche, G. Varior-Krishnan, F. Cervoni, T.F. Wild, B. Rossi, C. RabourdinCombe and
D. Gerlier (1993), “Human membrane cofactor protein (CD46) acts as a cellular receptor for
measles virus”, Journal of Virology, 67, 6025–6032.
31. I. Gutsche, A. Desfosses, G. Effantin, W.L. Ling, M. Haupt, R.W.H. Ruigrok et al (2015),
“Near-atomic cryo-EM structure of the helical measles virus nucleocapsid”, Science, 348,
704.
32. WJ. Bellini, JS. Rota, and LE. Lowe, et al (2005), “Sub acute sclerosing panencephalitis:
more cases of this fatal disease are prevented by measles immunization than was previously
recognized”, J Infect Disease; 192:1686
33. C. Pohl, W.P. Duprex, G. Krohne, B.K. Rima and S. Schneider-Schaulies (2007), “Measles
virus M and F proteins associate with detergent-resistant membrane fractions and promote
formation of virus-like particles”, Journal of General Virology, 88(4), 1243–1250.
34. C.E. Patterson, J.K. Daley, L.A. Echols, T.E. Lane and G.F. Rall (2003), “Measles virus
infection induces chemokine synthesis by neurons”, Journal of Immunology, 171, 3102–3109
35. R.S. Fujinami and M.B. Oldstone (1985), “Amino acid homology between the
encephalitogenic site of myelin basic protein and virus: mechanism for autoimmunity”,
Science, 230, 1043–1045
36. M. Amir, I. Mohammad and K. Behram (2011), “A comparative study of measles
complications n vaccinated versus non vaccinated children”, Journal of postgraduate
Medical Institute, 25 (1), 4-8.

33
37. M.A. Riddell, W.J. Moss, D. Hauer, M. Monze and D.E. Griffin (2007), “Slow clearance of
measles virus RNA after acute infection”, Journal of Clinical Virology, 39, 31-37.
38. W.A. Orenstein, M.J. Papania and M.E. Wharton (2004), “Measles elimination in the United
States”, Journal of Infectious Diseases, 189, 1–3.
39. K.L. Berggren, M. Tharp and K.M. Boyer (2005), “Vaccine- measles among vaccinated
school going associated ―wild-type measles”, Pediatric Dermatology, 22, 130-132.
40. J. Stowe et al (2009), “No evidence of an increase of bacterial and viral infections following
Measles, Mumps and Rubella vaccine”, Vaccine, 271422–271425.
41. Y. Huiming, W. Chaomin and M. Meng (2005), “Vitamin A for treating measles in children”,
Cochrane Database of Systematic Reviews, 4, CD001479.
42. P. Jeffery, C. Kenneth and E. John et al (1993),”The risk of measles, mumps and varicella
among young adults: A sero survey of US Navy and Marine Corps recruits”, American
Journal of public health, 83 (12), 1717-1720.
43. P. Godoy, A. Dominguez and L. Salleras (1999), “Measles: effect of a two does vaccination
programme in Catalonia, Spain”, Bull World Health Organ, 77(2), 132-137.
44. M.A. Saleemi, M.A. Akhter and F. Zahoor (2013), “Measles prevention in historic
perspective and can it be controlled in Pakistan”? , Journal of Fatima Jinnah Medical
College, 7.
45. M.G. Alkuwari, Z.A. Nazzal and A.A. Alkhenji (2011), “Epidemiology of measles outbreaks
in Qatar in 2007”, Eastern Mediterranian Health Journal, 17(3).
46. M. Younas, I. Iqbal and N. Noreen (2003), “Complications of measles and risk factor
factors for mortality”, Pakistan Pediatric Association Journal, 27,13-17.

34
47. M. Rasmsory, R. Burgha and D. Brown (1997), “Surveillance of measles in England and
Wales: Implications of a national slim testing programme”, Bull world health organization,
75, 515-521.
48. E.A. Khan (2003), “Targeting zero measles in Pakistan: time to change the EPI schedule”,
Journal of Infectious Diseases, 12, 87-90.
49. J.J Rainey, M. Watkins, T.K. Ryman, P. Sandhu, A. Bo and K. Banerjee (2011), “Reasons
related to non-vaccination and under-vaccination of children in low and middle income
countries: findings from a systematic review of the published literature, 1999–2009”,
Vaccine, 29(46), 8215–8221.
50. C. Ariyasriwatana and S. Kalayanarooj (2004), “Severity of measles: a study at the Queen
Sirikit National Institute of Child Health”, Journal of Medical Association Thailand, 87, 581–
88.7
51. D. Robin and E. Leuridan et al (2010), “How Long Does Passive Immunity to Measles Last
in Infants”? , British Medical Journal, 1.
52. V. M. Caceres, P.M. Strebel and R.W. Sutter (2000), “Factors determining prevalence of
maternal antibody to MV throughout infancy: a review”, Clinical Infectious Diseases, 31,
110–119.
53. A.K. Niazi and R. Sadaf (2014), “Measles Epidemic in Pakistan: In Search of Solutions”,
Annals of Medical & Health Sciences Research, 4(1), 1-2.
54. N.K. Mangrio, M.M. Alam and B.T. Shaikh (2008), “Is expanded programme on
immunization doing enough? View point of health workers and managers in Sindh,
Pakistan”, Journal of Pakistan Medical Association, 58(2), 64.

35
55. K. Jamil, A. Bhuiya, K. Streatfield and N. Chakrabarty (1999), “The immunization
programme in Bangladesh: impressive gains in coverage, but gaps remain”, Health Policy
Plan, 14(1), 49–58.
56. M. Rasmsory, R. Burgha and D. Brown (1997), “Surveillance of measles in England and
Wales: Implications of a national slim testing programme”, Bull world health organization,
75, 515-521.
57. S. D. Torun, M. Aslam and G. G. Kingdom (2012), “Parental education and child health-
understanding the pathways of impact in Pakistan”, World Development (Oxford), 40(10),
2014-2032.
58. CA. De Quadros, JM. Olive, BS. Hersh, et al (1996), “Measles elimination Americas:
evolving strategies”, JAMA; 275:224–9.
59. B. Pourabbas, M. Ziyaeyan, A. Alborzi, J. Mardaneh (2008), “Efficacy of measles and
rubella vaccination one year after the nationwide campaign in Shiraz, Iran”, Journal of
virology .; 12(1):43–6.
60. MA. Spaendonck (1999), “Prevalence of antibodies against rubella virus in The Netherlands
9 years after changing from selective to mass vaccination”, Epidemiological Infect.
123(2):263–70.
61. Y. Akkoyunlu, G. Arvas, T. Ozsari, IN. Hakyemez, B. Kaya, T. Aslan (2013),
“Seroprevalence of rubella in northeastern Turkey”, Wien Klin Wochenschr. 125(13-14):368–
70.12.
62. S. Calimeri, A. Capua, V. La Fauci, R. Squeri, OC. Grillo, D. Lo Giudice (2012),
“Prevalence of serum anti-rubella virus antibodies among pregnant women in southern Italy”,
Journal of virology. 116(3):211–3.

36
63. CA. De Quadros, JM. Olive, BS. Hersh, et al (1996), “Measles elimination in the Americas:
evolving strategies”, JAMA, 275:224–9.
64. S. D. Torun, M. Aslam and G. G. Kingdom (2012), “Parental education and child health-
understanding the pathways of impact in Pakistan”, World Development (Oxford), 40(10),
2014-2032.
65. K. Lemon, R.D.de Vries, A.W. Mesman, S. McQuaid, S. Yuksel et al (2011), “Early target
cells of measles virus after aerosol infection of non-human primates”, PLOS Pathogens, 7,
1001263.
66. C.E. Patterson, J.K. Daley, L.A. Echols, T.E. Lane and G.F. Rall (2003), “Measles virus
infection induces chemokine synthesis by neurons”, Journal of Immunology, 171, 3102–
3109.
67. R. Son Neville, I.F. Klein and M. Wolff (2010), “Update on investigation and management of
post infectious encephalitis‖, Current Opinion in Neurology”, 23, 300–304.
68. V. Dietz, J. Rota, H. Izurieta, P. Carrasco and W. Bellini (2004), “The laboratory
confirmation of suspected measles cases in settings of low measles transmission: conclusions
from the experience in the Americas”, Bull World Health Organ, 82, 852 -857.

Seroprevalence of measles IgG antibody

Recommended

Recommended

More Related Content

What's hot

What's hot (18)

Similar to Seroprevalence of measles IgG antibody

Similar to Seroprevalence of measles IgG antibody (20)

More from Noor Zada

More from Noor Zada (20)

Recently uploaded

Recently uploaded (20)

Seroprevalence of measles IgG antibody