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3rd Discussion Group :
Melvy Purwanti


Tri Sandra


Muhammad Deni Kurniawan


Adinda Gupita


Vini Apriyanti


Teresa Asali


Mirantika Audina


Kristian Wilson


Maudy Nadya


Anton Lius



Seven- month old infant was brought to you because she didn’t respond to
sound, even loud sound like thunder. She can’t roll over and sit unsupported. Her
mother noticed the girl has white colour in the pupil since birth. The girl was
aterm and her birth weight was 2700 grams. You found microcephaly, cataracts,
and persistent ductus arteriosus in the infant. There rubella antibody is positive of
on laboratory finding. You planned to do further hearing testing for the infant.
1.2.Clarification and Definition
1. Microcephaly: A rare neurological condition in which an infant head is
significantly smaller than the head of other children of the same age and
2. Cataracts: A clouding or loss of transparency of the lens in the eye as a
result of tissue breakdown and protein clumping.
3. Persistent Ductus Arteriosus: One of the most frequently occurring
abnormalities of the great vessels (8/100000 births) especially in
premature infants, either maybe an isolated abnormality or may
accompany other heart defect.
4. Rubella: An acute, usually benign infectious disease caused by viruses of
genus Rubivirus, a togavirus, affecting, most often children and nonimmune young adult.
1. She didn’t respond to sound
2. 7 month old infant
3. She can’t roll over and sit
4. The girl has white colour in

5. Persistent ductus arteriosus
6. Positive Rubella antibody
7. Birth weight was 2700 grams
8. Microcephaly
9. Cataracts
10. Hearing testing

pupil since birth
12. 1.4. Problem’s Case



Seven month old infant didn’t respondto sound even like

thunder, can’t roll over, and sit unsupported, has white colour in the pupil
since birth also experience microcephaly, cataracts, persistent ductus
arteriosus with rubella antibody is positive.
15. 1.5. Problem’s Analyze

Seven-month old infant

Birth weight 2700 gr

Physical Examination






Lab Examination
Further Examination

Can’t roll over
Positive Rubella Antibody
Hearing test


Sit unsupported

25. 1.6. Hypotheses

Growth and development’s defect that occur in that seven-

month old infant is caused by rubella virus.
28. 1.7. Learning Issue

The basic needs for better growth and development
Eye development
Ear development
Infant’s Microcephaly
Infant’s cataract


7. Heart congenital
8. Milestone score of 0-2 years old infants
9. Measurement of child’s growth
10. Mechanism of intrauterine infection
11. Transitional circulation of neonate
12. What are the virus that can cause the congenital defect?
13. Rubella Disease
14. Congenital Rubella Syndrome
15. Hearing testing
16. Red flags
2.1.The Basic Needs for Better Growth and Development

The field of pediatrics is dedicated to optimizing the growth

and development of each child. Pediatricians require knowledge of normal
growth, development, and behavior in order to effectively monitor
children’s progress, identify delays or abnormalities in development,
obtain needed services, and counsel parents and caretakers.
1. Biological Needs
1.1. Nutrition (breastfeed exclusively)
The American Academy of Pediatrics (AAP) and World
Health Organization (WHO) have declared breastfeeding and the
administration of human milk to be the normative practice for infant
feeding and nutrition. Breastfeeding has documented short- and long-term
medical and neurodevelopmental advantages and rare thus the decision to
breastfeed should be considered a public health issue and not only a


lifestyle choice. The AAP and the WHO recommend that infants should be
exclusively breastfed or given breast milk for 6 months. Breastfeeding
should be continued with the introduction of complementary foods for 1
year or longer, as mutually desired by mother and infant. The success of
breastfeeding initiation and continuation depends on multiple factors, such
as education about breastfeeding, hospital breastfeeding practices and
policies, routine and timely follow-up care, and family and societal
40. 1.2 Immunization
Immunization is the process of inducing immunity against a
specific disease. Immunity can be induced either passively through
administration of antibody-containing preparations or actively by
administering a vaccine or toxoid to stimulate the immune system to
produce a prolonged humoral and/or cellular immune response. As of
2015, infants, children, and adolescents in the United States routinely are







poliomyelitis, H. influenzae type b (Hib) disease, hepatitis A, hepatitis B,
measles, mumps, rubella, rotavirus, varicella, pneumococcal disease,
meningococcal disease, influenza, and human papillomavirus (HPV)
42. 1.2.1 Passive Immunity
Passive immunity is achieved by administration of preformed
antibodies to induce transient protection against an infectious agent. Products
used include:1
a. Immunoglobulin (Ig) administered intramuscularly (IM)
b. Specific or hyper immune immunoglobulin preparations administered IM
c. Intravenous immunoglobulin (IVIG)
d. Specific or hyper immunoglobulin preparations administered IV
e. Subcutaneous (SC) human immunoglobulin, which has been
f. licensed to treat patients with primary immunodeficiency
g. Antibodies of animal origin
h. Monoclonal antibodies
44. 1.2.2 Active Immunization
Vaccines are defined as whole or parts of microorganisms
administered to prevent an infectious disease. Vaccines can consist of whole


polysaccharide capsules (e. pneumococcal and meningococcal polysaccharide vaccines). HPV..inactivated microorganisms (e. polysaccharide capsules conjugated to protein carriers (e. and hepatitis B).g.g. and toxoids (tetanus and diphtheria) . parts of the organism (e. polio and hepatitis A).g. live attenuated microorganisms (measles. Sources : IDAI. rubella. and live-attenuated influenza vaccines). mumps. and meningococcal conjugate vaccines).g. 6 . rotavirus. Hib..1 46.. a cellular pertussis. pneumococcal.

and compliance programs must pay special attention to this group of caregivers. these agents are the preferred agents for routine hand hygiene when hands are not visibly soiled. Although much attention is directed at the type of cleansing agent employed. 1. the most important aspect of hand washing is placing the hands under water and using friction with or without soap. water. Hands should be cleaned before and after every patient encounter. Meals.3. difficile outbreaks. These products are effective in killing most microbes but do not remove dirt or debris. However. sleep and wakefulness are evenly distributed throughout the 24 hr. Studies show that a 15 sec scrub removes the majority of transient flora but does not alter hand permanent flora.4 Sleep 51. Six behavioral states have been described. Initially. they are ineffective against C. snack are must be hygiene.2. The most important tool in any infection control program is good hand hygiene. vegetables. Waterless hand hygiene products increase hand hygiene compliance and save time. The danger environment agent must be avoid from baby in order to keep healthty. physicians are usually the least-compliant group studied. 1. difficile spores. requiring the use of other cleansing products during hospital C.2.2.47. Neurologic maturation 7 . In hospital hand washing compliance studies.3 Hygiene 48. A variety of hand gels and rubs can be used in place of hand washing.1 50. 1. fruit.1 Hand Hygiene 49.

Fathers play critical roles.1 52. 2. same-sex partners) becomes increasingly important. 8 . with brief awake. Psychosocial & Emotional Needs: 53. Contemporary models of child development recognize the critical importance of influences outside of the mother–child dyad. 2.1 Family Systems and the Ecologic Model 54. foster and adoptive parents. As traditional nuclear families become less dominant. both in their direct relationships with their children and in supporting mothers.accounts for the consolidation of sleep into blocks of 5 or 6 hour at night. the influence of other family members (grandparents. infants whose parents are consistently more interactive and stimulating during the day learn to concentrate their sleeping during the night. Children are increasingly raised by unrelated caregivers while parents work or while they are in foster care. Learning also occurs. feeding periods.

2. Within each of these categories are developmental lines or sequences of changes leading up to particular attainments. and society. language. children may be denied any decisionmaking. One child may be the troublemaker.2 Developmental Domains and Theories of Emotion and Cognition 61. culture. Family systems theory recognizes that individuals within systems adopt implicit roles. and the death of a grandparent are all changes that require renegotiation of roles within the family and have the potential for healthy adaptation or dysfunction. attainment of developmental milestones such as independent walking. and cognition. roles shift until a new equilibrium is found. with the parent–child dyad at the center (with associated risks and protective factors) and the larger society at the periphery. through its influence on family roles and patterns of interaction. roles. exacerbating rebelliousness. Child development can also be tracked by the child’s developmental progress in particular domains. emotional. and rules for interaction. The shift from an industrial economy to one based on service and information is an obvious example of societal change with profound effects on families and children.1 58. fine motor. Changes at any level are reflected in the levels above and below.55. social. In families with rigidly defined parental subsystems. Bronfenbrenner’s ecologic model depicts these relationships as concentric circles. Changes in one person’s behavior affect every other member of the system. subculture. with internal and external boundaries. the onset of nighttime fears. in turn. children may be required to take on responsibilities beyond their years. 60. Developmental lines in the gross motor domain. subsystems. such as gross motor. whereas another is the negotiator and another is quiet. or may be recruited to play a spousal role. Families are dynamic. Families function as systems. In families with poorly defined parent– child boundaries. Birth order may have profound effects on personality development. functions within the larger systems of extended family. leading from 9 . 57. The family system. 59. The birth of a new child. 56.

Erikson recognized that these stages arise in the context of Western European societal expectations. whereas a late adolescent may be more focused on establishing meaningful relationships and an occupational identity. “sexual”) drives. Others. Erikson recast Freud’s stages in terms of the emerging personality. are more subtle. Knowing that the salient issue for school-age 10 . In contrast. At the core of Freudian theory is the idea of bodycentered (or. are obvious. 1 62. The concept of a developmental line implies that a child passes through successive stages. different issues become salient. behavioral theories rely less on qualitative change and more on the gradual modification of behavior and accumulation of competence. they opened the door to subsequent theories of development. in other cultures.1 63. 66. such as the line leading to the development of conscience. Although Freudian ideas have been challenged. the salient issues may be quite different. 2. broadly. Several psychoanalytic theories are based on stages as qualitatively different epochs in the development of emotion and cognition.rolling to creeping to independent walking. 65.1 Psychoanalytic Theories 64. Erikson’s work calls attention to the intrapersonal challenges facing children at different ages in a way that facilitates professional intervention.2. As children progress through these psychosocial stages. the emotional health of both the child and the adult depends on adequate resolution of these conflicts. It is predictable that a toddler will be preoccupied with establishing a sense of autonomy. The child’s sense of basic trust develops through the successful negotiation of infantile needs.

Piaget described how children actively construct knowledge for themselves through the linked processes of assimilation (taking in new experiences according to existing schemata) and accommodation (creating new patterns of understanding to adapt to new information). Of undeniable importance is Piaget’s focus on cognition as a subject of empirical study. the universality of the progression of cognitive stages. (3) Open- 11 . pediatricians inquire about a child’s experiences of mastery and failure and (if necessary) suggest ways to ensure adequate successes. with little special equipment.2 Cognitive Theories 68. During the sensorimotor stage. Challenges have included questions about the timing of various stages and the extent to which context may affect conclusions about cognitive stage. and the image of a child as actively and creatively interpreting the world. The concept of “in” is embodied in a child’s act of putting a block into a cup. children are continually and actively reorganizing cognitive processes 69. Piaget’s basic concepts have held up well. In this way. With the arrival of language. In many children.2. Children’s understanding of cause and effect may be considerably more advanced in the context of sibling relationships than in the manipulation and perception of inanimate objects. (2) Piaget’s observations often lend themselves to quick replication in the office. Cognitive development is best understood through the work of Piaget.children is industry vs inferiority. 70. not just quantity. the nature of thinking changes dramatically. such as the common exacerbation of sleep problems at 9 and 18 months of age. logical thinking appears well before puberty. symbols increasingly take the place of objects and actions. Piaget’s work is of special importance to pediatricians for 3 reasons: (1) Piaget’s observations provide insight into many puzzling behaviors of infancy. the age postulated by Piaget. 2. A central tenet of Piaget’s work is that cognition changes in quality. an infant’s thinking is tied to immediate sensations and a child’s ability to manipulate objects. 67.

This theoretical perspective distinguishes itself by its lack of concern with a child’s inner experience. can provide insights into children’s understanding of illness and hospitalization. based on Piaget’s work. and. behavioral interventions using applied behavior 12 . justice. A behavioral approach lends itself to interventions for various common problems. children are guided by the basic precepts of moral behavior. and reciprocity in their understanding of interpersonal interactions through perspective-taking. such as temper tantrums. 71. behaviors that are negatively reinforced or ignored occur less frequently. motivated by externally applied controls.2. In its simplest form. adults. The basic theory has been modified to distinguish morality from social conventions. animals all respond in the same way. Kohlberg developed a theory of moral development in 6 stages.ended questioning. and dating expectations. the behaviorist orientation asserts that behaviors that are positively reinforced occur more frequently. The strengths of this position are its simplicity. children. fairness. Based on cognitive development. but also may take into account local standards. Whereas moral thinking considers interpersonal interactions. Preschoolers’ earliest sense of right and wrong is egocentric. wide applicability. and human welfare. Within each stage of development. social conventions are the agreed-on standards of behavior particular to a social or cultural group. 2.3 Behavioral Theory 73. and conduciveness to scientific verification. children perceive equality. aggressive preschool behavior. Its sole focus is on observable behaviors and measurable factors that either increase or decrease the frequency with which these behaviors occur. In cognitively limited children and children with autism spectrum disorders. Most youth will reach stage 4. by mid to late adolescence. conventional morality. such as dress code. and eating disorders in which behaviors are broken down into discrete units. Additional studies have even demonstrated some protomorality in infants.1 72. from early childhood through adulthood. No stages are implied. In later stages. classroom behavior. indeed.

or family problem. the hyaloids artery (later the central artery of the retina) enters the eye. Applied behavior analysis has been particularly useful in the treatment of early-diagnosed autism. draw. The repetitive experiences stimulates complicity connection (synapse) between brain cells.2 75. movement. the choroid fissure. 2.2. the lens placode invaginates to form the lens vesicle. and (c) an epithelial layer bordering the anterior chamber PAX6. which is continuous with the sclera. Through a groove at the inferior aspect of the optic vesicle. socio-emotional.Eye development 76. creativity. cooperation and leadership. speak. Behavioral approaches can be taught to parents to apply at home. restricting this gene’s expression to the optic cup and lens. an exclusive reliance on behavior therapy risks leaving the cause untreated. through repetitive experiences include parents sounds. perceptual. the master gene for eye development. The eyes begin to develop as a pair of outpocketings that will become the optic vesicles on each side of the forebrain at the end of the fourth week of development. spiritual etc. motoric. The optic vesicles contact the surface ectoderm and induce lens formation. is expressed in the single eye fi eld at the neural plate stage. write. The cornea is formed by (a) a layer of surface ectoderm. music. brain gym.analysis approaches have demonstrated their ability to teach new. Epithelial– mesenchymal interactions 13 . Stimulation Needs 74. When the optic vesicle begins to invaginate to form the pigment and neural layers of the retina. Stimulation needs consist of sensory. in cases in which misbehavior is symptomatic of an underlying emotional. play. (b) the stroma.1 3. act. singing. The eye field is separated into two optic primordia by SHH. cognitive. However. self-help. touch. which up regulates PAX2 expression in the optic stalks while down regulating PAX6. communication - language. complex behaviors. Nerve fibers of the eye also occupy this groove to reach the optic areas of the brain.

which converts sound waves into nerve impulses and registers changes in equilibrium. a sound conductor from the external to the internal ear. In the adult. optic vesicle.Ear development 78.3. In the embryo. and surrounding mesenchyme then regulate lens and optic cup differentiation. the ear forms one anatomic unit serving both hearing and equilibrium. Internal Ear 79. 2. 14 . the sound-collecting organ. a. however.3 77.between prospective lens ectoderm. and (3) the internal ear. (2) the middle ear. it develops from three distinctly different parts: (1) the external ear. The first indication of the developing ear can be found in embryos of approximately 22 days as a thickening of the surface ectoderm on each side of the rhombencephalon.

B.1 A. 24 days.2 A–C. the otic placodes. B. and endolymphatic duct. 4. Note the statoacoustic ganglia1 86.80.3. each vesicle divides into (1) a ventral component that gives rise to the saccule and cochlear duct and (2) a dorsal component that forms the utricle. These thickenings. 27 days. During later development. Region of the rhombencephalon showing the otic placodes in a 22-day embryo1 81. Figure 2. C. Transverse sections through the region of the rhombencephalon showing formation of the otic vesicles. 84. A. 85.3.5 weeks. invaginate rapidly and form the otic or auditory vesicles (otocysts). 82. 15 . semicircular canals. Figure 2. 83. An embryo at the end of the fourth week of development showing the otic and optic vesicles.

87.B. 88. Cochlear duct at 6. The cochlear duct (scala media) is separated from the scala tympani and the scala vestibuli by the basilar and vestibular membranes. During the 10th week. large vacuoles appear in the cartilaginous shell.3 A. On the development of the scala tympani and scala vestibuli the cochlear duct is surrounded by a cartilaginous shell. Note formation of the ductus reuniens and the utriculosaccular duct1 89. respectively. Figure 2. Note the auditory nerve fi bers and the spiral (cochlear) ganglion. and 8 weeks.3. C–E. 16 . respectively. Development of the otocyst showing a dorsal utricular portion with the endolymphatic duct and a ventral saccular portion. 7.

C. of the central portions of the walls of the semicircular outpocketings. Middle Ear 93. widens and gives rise to the primitive tympanic cavity. and the proximal part remains narrow and forms the auditory tube (eustachian tube.4 Development of the semicircular canals. The tympanic cavity.90. 91. these epithelial structures form the membranous labyrinth. D–F. through which the tympanic cavity communicates with the nasopharynx. which originates in the endoderm. 5 weeks. Apposition. b. A. Together. This pouch expands in a lateral direction and comes in contact with the floor of the first pharyngeal cleft. and disappearance. B. 8 weeks. 17 . is derived from the fi rst pharyngeal pouch. 6 weeks. The distal part of the pouch. fusion. 94. the tubotympanic recess. respectively. Note the ampullae in the semicircular canals1 92.3. Figure 2.

When the ossicles are entirely free of surrounding mesenchyme. and mesenchymal condensation. when the surrounding tissue dissolves. foreshadowing development of the ossicles.5 A. Transverse section of a 7-week embryo in the region of the rhombencephalon. they remain embedded in mesenchyme until the eighth month. The malleus and incus are derived from cartilage of the fi rst pharyngeal arch. Middle ear showing the cartilaginous precursors of the auditory ossicles.95. The supporting ligaments of the ossicles develop later within these mesenteries. B. the first pharyngeal cleft. Although the ossicles appear during the first half of fetal life. 18 . 96. Note the meatal plug extending from the primitive auditory meatus to the tympanic cavity1 97. showing the tubotympanic recess. Thin yellow line in mesenchyme indicates future expansion of the primitive tympanic cavity. and the stapes is derived from that of the second arch. Figure 2. The endodermal epithelial lining of the primitive tympanic cavity then extends along the wall of the newly developing space.3. The tympanic cavity is now at least twice as large as before. the endodermal epithelium connects them in a mesentery-like fashion to the wall of the cavity.

its muscle. the tensor tympani. the middle ear with its ossicles.98.6 Ear showing the external auditory meatus. 101. 19 . The stapedius muscle. is innervated by the facial nerve. the nerve to the second pharyngeal arch.3. and the inner ear1 100. which is attached to the stapes. is innervated by the mandibular branch of the trigeminal nerve. Figure 2. Because the malleus is derived from the first pharyngeal arch. 99.

The stapes will establish contact with the membrane in the oval window. c.3. the epithelium of the tympanic cavity invades the bone of the developing mastoid process. The eardrum is made up of (1) an ectodermal epithelial lining at the bottom of the auditory meatus. epithelial cells at the bottom of the meatus proliferate. 20 . In the seventh month. During late fetal life. the tympanic cavity expands dorsally by vacuolization of surrounding tissue to form the tympanic antrum. most of the mastoid air sacs come in contact with the antrum and tympanic cavity. Figure 2. B. The wall of the tympanic cavity is lined with endodermal epithelium 103. After birth. and the epithelial lining of the floor of the meatus participates in formation of the definitive eardrum.102. (2) an endodermal epithelial lining of the tympanic cavity. and (3) an intermediate layer of connective tissue that forms the fibrous stratum. resulting in congenital deafness. this plug dissolves. Expansion of infl ammations of the middle ear into the antrum and mastoid air cells is a common complication of middle ear infections. the meatal plug persists until birth. Occasionally. 105. Middle ear showing the handle of the malleus in contact with the eardrum. Note the malleus and incus at the dorsal tip of the first arch and the stapes at that of the second arch. and epithelium-lined air sacs are formed (pneumatization). Derivatives of the first three pharyngeal arches. The external auditory meatus develops from the dorsal portion of the first pharyngeal cleft. the meatal plug. External Ear 104. Later. forming a solid epithelial plate. At the beginning of the third month.7 A. and the remaining portion forms the separation between the external auditory meatus and the tympanic cavity. The major part of the eardrum is firmly attached to the handle of the malleus .

they ascend to the side of the head at the level of the eyes. The auricle develops from six mesenchymal proliferations at the dorsal ends of the first and second pharyngeal arches.3. developmental abnormalities of the auricle are common. Immunization of children have managed to reduce the impact of communicable diseases. Initially. which are located immediately posterior to the mandible. Figure 2. three on each side of the external meatus.4. the mandible is small. will be repositioned into their characteristic location at the side of the head. Active immunization induces immunity by vaccination 21 . As fusion of the auricular hillocks is complicated. later fuse and form the defi nitive auricle . B. 2. and 3 are part of the mandibular portion of the first pharyngeal arch and that the ear lies horizontally at the side of the neck. Six-week-old human embryo showing a stage of external ear development similar to that depicted in A. surrounding the first pharyngeal cleft. the ears. At this stage.8 A. As the mandible grows anteriorly and posteriorly. Note that hillocks 1. Fusion and progressive development of the hillocks into the adult auricle 107.3 108. Drawing of a 6-week-old embryo showing a lateral view of the head and six auricular hillocks surrounding the dorsal end of the first pharyngeal cleft. C–E. These swellings (auricular hillocks).Immunization 109.106. but with development of the mandible. 2. the external ears are in the lower neck region.

Many purified polysaccharides are T-independent antigens that stimulate proliferation of B cells without involving lymphocytes T CD4 but less immunoglobulin in children less than 2 years. 111.4 112.with either vaccine or toxoid (inactivated toxin). glubela. polio-2-3 can be administered polio 116. and the provision of antibodies. Babies born in RB / RS OPV vaccine is given when the baby is discharged in order to avoid transmission of the vaccine virus to infants others. The recommended location is part of the anterolateral thigh in infants and the deltoid in children and adults. and rubella) and varicella vaccine (chickenpox) can be administered simultaneously or separately at an interval of more than 30 days. needs to be 22 . If the BCG vaccine will be given after the age of 3 months. BCG Vaccine vaccine OPV or IPV 117. a virus that switched off or inactivated (polio vaccine injections. measles. Next to polio 1. Multiple vaccinations can be administered simultaneously at separate anatomical locations (extremity different or separate locations more than 1 inch). Hepatitis B vaccine 114. Given at the first visit. mump. Haemophilus influenza type B and streptococcus pneumoniae). While passive immunization include transplacental transfer of antibodies from mother to baby. mumps. this does not diminish the immune response. 115. tetanus). hepatitis A and influenza intramuscular). reassortant viruses (rotavirus) or immunogenic components of bacteria (pertussis. Given within 12 hours after birth. both in the form of immunoglobulin or monoclonal antibodies. Most vaccines are given by intramuscular or subcutaneous injection. Vaccines can be derived from a virus which is attenuated (polio vaccine. varicella and influenza nasal). Vaccines against measles. Optimal given at age 2-3 months. recombinant products (hepatitis B. Polio Vaccine 113. 110. and the group toxoid (diphtheria. human papillomavirus) . mumps and rubella (MMR measles.

the best in the age before entering elementary school. HPV 4 weeks. Influenza vaccine 132. the dose given on 126.done tuberculin test. the booster vaccine is given at age 5-7 years. if it has not received measles vaccine 9 months of age. Instead finished monovalent rotavirus vaccine administered before age 16 weeks and not beyond the age of 24 weeks. Pentavalent rotavirus vaccine: 1 dose given 6-12 weeks of age. 12-15 months. the 2nd dose given at intervals of at least 4 weeks. Given at age> 6 months.<9 years was given 2 times with a minimum interval of 4 weeks. For primary immunization children 6 months . need two doses with an interval of at least 128. if the pre-BCG tuberculin test is not possible. 127. pentavalent rotavirus vaccine (RotaTeq) given 3 times. Pneumoc occal vaccine 124. dosing interval of the 2nd and 3rd weeks 4-10. 125. Schedule 23 . DTwP or can be given in combination with DTaP or Hepatitis B or Hib. Measles vaccine given at the age of 9 months. Repeat DTP at the age of 18 months and 5 months. When given at age> 12 years. Measles vaccine 122. BCG can be given but must be observed within 7 days. 6. Rotaviru s vaccine (diagnostic TB) 119. At the age of 7-12 months are given two times at intervals of 2 months. 133. Given at age ≥ 6 weeks. 129. 121. Varisela vaccine the 3rd age <32 weeks (minimum interval of 4 weeks). I monovalent rotavirus vaccine doses given 6-14 weeks of age. If there is a local reaction quickly injected (accelerated local reaction) need further evaluation 118. 4. Monovalent (Rotarix) given 2 times. Can be given from the age of 10 years. Furthermore repeat MMR given at age 5-7 years. 131. 123. Can be administered after age 12 months. Can be administered after the age of 12 months. Can be given to the age of 2. every year. DTP vaccine 120. MMR vaccine 130.

later entrants pass through these layers. 2. Cerebrum will begin to be seen as a structure that can be recognized at 28 days gestation the embryo. 135.1 139. cycles and major gyrus has been demarcated. Brain term infants have the entire complement of adult neurons. 138.Infant’s Microcephaly a. These include genetic microcephaly due to familial and chromosome aberration. both dendrites and axons as well as an increase in glia cell. while the anterior end of the neural tube to experience a globular ekspensi. 134. 24 . accumulate and form the cerebral cortex. 6 months. Microcephaly due to the closure of the sutures (craniosynostosis). so that at term. The first entrants to form the bottom layer of the cortex. forming layers above. 1. A situation where the size of the circumference of the head is smaller than normal for age and gender. This type of microcephaly result in an abnormal head shape.vaccine vaccine HPV (Human Papilloma Virus) bivalent 0. Formed neuroblasts migrate from the ventricular wall to hemisferium primitive surface. the full development of neural processes. Postnatal weight gain is due to the subcortical white matter myelination. 2. presensefalon. In the next few ari. in the 5th. but weighs only about a third of the adult brain. b. HPV vaccine is tetravalent 0. but in most cases there is no obvious cerebral anomalies. Definition 136.5. Ventricular wall at this stage is formed by a layer of seed active neuroblasts divide. prosensefalon splitting into two lateral expansion which is the origin hemisfrum cerebral and lateral ventricles. Differentiation of neuroblasts forming neuron cell extensions that grew longer and eventually formed axons with ventricular lumen through cell extensions that grew longer and eventually formed axons alba subcortical substance. Pathogenesis 137. Axons crossing from 1 hemisferium to hemisferium other to form the corpus callosum. Benign primary microcephaly associated with genetic factors. At this time the surface was akorteks began to show progressive identity formed during the last trimester. fully formed. 8 months.

trauma. further decline in the rate of proliferation and neuronal levels can reduce cell production.17 Development of the nervous system begins with the formation of the neural tube 25 . progenitor cells that have the ability symmetrically cleavage is essential for cells to produce sufficient quantities and jointly serve as the core of an ongoing process of neurogenesis. Effect of pathological changes in the perinatal period tend to be mild. placental insufficiency.140. chronic heart defects. The end result is a brain smaller than usual and microcephaly. such as delays myelination and reduced the formation of dendrites. Severe brain malformations are usually not found in MCPH. and perinatal and postnatal disorders such as asphyxia. radiation. Several genes underlying primary microcephaly have been identified. maternal systemic diseases such as diabetes mellitus. toxoplasmosis. anoxia. The loss of the substance of the brain due to destructive lesions can occur at the end of fetal life and early infancy. This type of microcephaly associated with mental retardation in a range tingkat. In general the effect of abnormal before the 6th month of pregnancy tends to affect the growth of macroscopic structure of the brain and reduce the total number of neurons. and herpes simplex. Proliferation and differentiation processes is particularly the case in the ventricles and subventrikular zone lining the brain cavity. During the early stages of cortical development. infections. syphilis. rubella. previous studies have shown that there is interference with the process of mitotic division of cortical structures during embryonic development. Secondary microcephaly can be caused by intrauterine infections such as cytomegalic inclusion disease. phenylketonuria. Although the proteins encoded have diverse functions. 142. Primary autosomal recessive microcephaly (MCPH) or Autosomal Recessive Microcephaly Primer is a congenital disorder characterized by mental retardation and brain size small without additional severe brain malformations. Asymmetric neural progenitor cell portion produce stem cells and children with different results. 1 141. Disruption from the symmetrical division can cause the depletion of core neural progenitor cells. either separately or with other developmental disabilities. chronic renal disease. systemic hypotension maternal. Microcephaly secondary to cerebral atrophy. as well as disorders of the lungs and kidneys.

Any interruption during this period resulted in congenital abnormalities such as kranyosksis. Disturbances in this period can cause microcephaly. Herpes infects infants born vaginally (mother herpes) that infants be infected.6. The incidence of infantile cataracts is approximately 2-13/10.000 live births. Causing malformations of the eye. totalis. Meanwhile. An epidemiologic study of infantile cataracts published in 2003 suggests that approximately 60% of cataracts are an isolated defect.5 145. In some countries CMV infection is 1% obtained in ultra-infection and 10-15% in the prenatal period.Infant’s cataract 146. heart and teeth 144. Caused by the bacterium Treponema malibu through intact mucous membranes / skin lesions then enter the bloodstream and all organs in the body (one of the brain) to the fetus. The virus becomes latent and there are periodic reactivation with the release of the virus even though there are antibodies in the serum. It is estimated that the reduction in immune surveillance mediated by cells. causing the baby fetuses are in a high risk for the occurrence of squeal to this infection. A cataract is any opacity of the lens some are clinically unimportant. but the immunity in mediated by cells appears to be the primary mechanism for the recovery. The next phase of a proliferation of neurons that occurs during gestation.5 -2% of all newborns. 143. 10% of fetal infection causing symptomatic at birth and 5-25% leaving the induction of dorsal region that occurs in week 3 of gestation. 22% are part of a 26 . Humoral antibodies are produced. Rubeinstein-Taybi Syndrome occurs because absence of the gene that causes abnormalities in binding proteins CREB. Rubella infects the embryo to first 3 months of pregnancy. and the state of impaired immune either occurring naturally or as a result of drug use would increase the tendency of the incidence of serious cytomegalovirus infection. others significantly affect visual function. Syphilis infects its way through direct contact with lesions. After the primary infection is usually asymptomatic. Cytomegalovirus is an organism that is where and essentially infect most humans. evidence of fetal infection is found in between 0. 2. the inner ear. etc.

If the mother is infected after the seventh week of pregnancy. the lens escape damage. Startles to loud sounds 155. many children born to mothers who had Rubella (German measles) between the fourth and seventh weeks of pregnancy cataracts. Congenital cataract cause the lens to become opaque during intra uterine life. 2. gooing) 156.3 153.Heart congenital 150. 2. but also participate in formation of the membranous portion of the intervetricular septum and in closure of the ostium prinum.syndrome. Some cataracts are associated with other ocular or systemic diseases. Ebstein abnormaly is a condition where the sricuspid valve is displaced toward the apex of right ventricle. . and the remainder are associated with other unrelated major birth defects. Cries differently for different needs 27 . Atrial Septal Defect (ASD) is a congenital heart abnormality with an incidence of 6.Milestone score of 0-2 years old infants1 1.1 147.8.500 g have 3-4–fold increased odds of developing infantile cataracts. Although this anomaly is usually geneticallyy determined. characterized by a large opening between the left and right atria. Endocardial cushion of the atrioventricular canal not only divide this canal into a right and left orifice. Makes pleasure sounds (cooing. Because of the MMR vaccine.4/10. 151. 152. Infants who weigh at or below 2. but the child may have hearing loss as a result of cochlea abnormalities.3 149.7.000 births and with a 2:1 prevalence in female to male infants. 148. Quiets or smiles when spoken to 157. One of the most significant defects is the ostium secuncum defect. CRS has been nearly eradicated in USA. BIRTH–3 MO 154. Cataracts are more common in low birth weight infants.

Recognizes words for 179. sound 162. Uses speech or noncrying sounds to get and keep attention 176. Babbling has both long and short groups of sounds. Makes gurgling sounds when left alone and when playing with you 169. Moves eyes in direction of sounds 164. 7 MO–1 YR 172. with many different sounds. Dada. although shoe. Enjoys games such as peekaboo and pat-a-cake 170. Imitates different speech sounds 178. requests (Come here. such as tata upup bibibibi. Begins to respond to 181. including p. b. Listens when spoken to 177. Responds to changes in tone of your voice 167. Vocalizes excitement and displeasure 168. 173. Smiles when sees you voice and quiets if crying 160. and m 165. Pays attention to music 171.Want 28 . bye.158. 4–6 MO 163. Mama). Has 1 or 2 words (bye- common items. Seems to recognize your 159. and juice they may not be clear 180. Notices toys that make sounds 166. Increases or decreases sucking behavior in response to 161. 174. such as cup. Babbling sounds more speech-like. Turns and looks in direction of sounds 175.

188. Weight loss of ten percent in the first week of life is normal. 2. 194. 1.) 187. 3. 198. 205. 2. 201. include: Average birth weight for most full-term infants is between 2.9. 200. bye-bye? your shoe?) Kiss the baby. Points to a few body parts 184. 2. Child's age 0-3 months 3-6 months 6-12 months Between birth & 1 year 1-2 years 196. Normal growth of child. Birth weight is usually regained by 10-14 days. 204.9.6 Table 2. book when named Uses many different consonant sounds at the beginning of words 191. 192. songs. 203. Follows simple Says more words every month 186. Treponema pallidum. 199. Average weight gain 150-200 g / week 100-150 g / week 70-90 g / week Birth weight doubles (or more) 2-3 kg / year (40-50 g / week) 197. Mechanism of intrauterine infection 209.5 and 4. 207.10. 208. Uses some 1–2 word commands and understands questions (Where kitty? Go simple questions (Roll the ball.Measurement of child’s growth 193. 1–2 YR 183. 202.5 kg with a gestation of between 37 and 42 weeks duration. 206. when asked 185. Listens to simple stories. no juice. Points to pictures in a 190. mommy book) 189. 29 . and rhymes Puts 2 words together (more cookie. Intrauterine infection is a result of clinical or subclinical maternal infection with a variety of agents (cytomegalovirus [CMV]. Average weight gain from birth to five years of age 195.more?) 182.

syphilis). Functionally. in turn. To summarize. Third-trimester infection often results in active infection at the time of delivery (toxoplasmosis.1 212. acute or delayed disease in the neonatal period. Even without maternal antibody. The timing of infection during gestation affects the outcome. The septum primum is then opposed to the septum secundum. 211. This. or asymptomatic persistent infection with squeal later in life.11. the following changes occur in the vascular system after birth. Transplacental infection may occur at any time during gestation. is probably caused by thermal and mechanical stimuli and a change in oxygen tension.Toxoplasma gondii. Firsttrimester infection may alter embryogenesis. no apparent effects are seen in the newborn infant. varicella virus. 210. the amount of blood flowing through the lung vessels increases rapidly. parvovirus B19) and hematogenous transplacental transmission to the fetus. accomplished by contraction of the smooth musculature in their walls. intrauterine growth restriction. Since the ductus arteriosus loses by muscular contraction of its wall. rubella virus. Simultaneously. Infection may result in early spontaneous abortion. 214. Infections that occur late in gestation may lead to a delay in clinical manifestations until sometime after birth (syphilis). transplacental transmission of infection to a fetus is variable because the placenta may function as an effective barrier. In some cases. 2. maternal antibody may ameliorate the outcome of infection or may have no effect. maternal immunity is effective and antibody is protective for the fetus. the oval foramen closes. premature birth. still birth. and functionally. Closure of the umbilical arteries. For some etiologic agents (rubella). and signs and symptoms may be present at birth or may be delayed for months or years. Transitional circulation of neonate 213. pressure in the right atrium decreases as a result of interruption of placental blood flow. raises pressure in the left atrium. For other agents (CMV). congenital malformation. the arteries 30 . Maternal infection is a necessary prerequisite for transplacental infection. Changes in the vascular system at birth are caused by cessation of placental blood flow and the beginning of respiration. with resulting congenital malformations (congenital rubella).

and the proximal portions remain open as the superior vesical arteries. Closure of the umbilical vein and ductus venosus occurs shortly after that of the umbilical arteries. Crying by the baby creates a shunt from right to left. the obliterated ductus arteriosus forms the ligamentum arteriosum. blood from the placenta may after obliteration. 216. In the adult. which accounts for cyanotic periods in the newborn. Complete anatomical obliteration by proliferation of the intima is thought to take 1 to 3 months. perfect anatomical closure may never be obtained (probe patent foramen ovale). In 20% of individuals. this closure is reversible. The first breath presses the septum primum against the septum secundum. Constant apposition gradually leads to fusion of the two septa in about 1 year. Closure of the ductus arteriosus by contraction of its muscular wall occurs almost immediately after birth.a substance released from the lungs during initial infl ation. Hence. During the fi rst days of life. 215. The ductus venosus. it is mediated by bradykinin. however. combined with a decrease in pressure on the right side. although the actual obliteration of the lumen by fibrous proliferation may take 2 to 3 months. Closure of the oval foramen is caused by an increased pressure in the left atrium.close a few minutes after birth. the umbilical vein forms the ligamentum teres hepatis in the lower margin of the falciform ligament. 217.3 31 . however. Distal parts of the umbilical arteries form the medial umbilical ligaments. which courses from the ligamentum teres to the inferior vena cava. is also obliterated and forms the ligamentum venosum.

organisms may disseminate hematogenously to the placenta. When a mother acquires infection during gestation. The incidence of congenital infection in the United States ranges from 1 in 1. What are the virus that can cause the congenital defect? 2. Infection may be transmitted to the fetus transplacentally or during vaginal delivery. 219. usually with 32 .000 live births. usually with severe disease. 222.218. 2. approximately 65% of fetuses are infected.12. Congenital Toxoplasmosis 221.1 Toxoplasmosis (Toxoplasma gondii) a. The incidence of infection among pregnant women depends on the general risk for infection in the specific locale and the proportion of the population that has not been infected previously. Of untreated maternal infection acquired in the 3rd trimester. Congenital transmission from mothers infected before pregnancy is extremely rare except for immunocompromised women who are chronically infected.12. Transmission to the fetus usually follows acquisition of primary infection by an immunologically normal pregnant woman during gestation. Of untreated maternal infections acquired in the 1st trimester. 220. approximately 17% of fetuses are infected.000 to 1 in 8.

2 Cytomegalovirus a. Areas of calcification occur in the brain. Congenital Infection 224. liver. Severe multiorgan disease is infrequent and occurs in less than 5% of infants with congenital CMV infections. elevation of hepatic transaminases.1 2. Some severely involved infants with congenital infection appear to have Toxoplasma antigen–specific cell-mediated anergy. Congenital infection with CMV can present with symptomatic infections in approximately 10% of infected newborns.12. however. lungs. Almost all congenitally infected individuals who are not treated manifest signs or symptoms of infection.disease that is more mild or in apparent at birth. several authors have included intrauterine growth restriction as a finding of symptomatic congenital CMV infection. and spleen. gondii. such as chorioretinitis. These different rates of transmission and outcomes are most likely related to placental blood flow. and in some cases microcephaly. and abnormal findings on cranial ultrasonography. by adolescence. Examination of the placenta of infected newborns may reveal chronic inflammation and cysts. If cerebrospinal fluid is obtained. anemia. Tissue cysts stain well with periodic acid–Schiff and silver stains as well as with the immunoperoxidase technique. These findings were utilized for natural history studies to classify infants as having symptomatic or asymptomatic infections. skeletal muscle. petechial rashes. thrombocytopenia. there can be evidence of encephalitis with elevation of mononuclear cell number and in 33 . The clinical findings of infants with symptomatic congenital CMV infections can include hepatosplenomegaly. especially the CNS. Laboratory findings include direct hyperbilirubinemia. jaundice. Gross or microscopic areas of necrosis may be present in many tissues. 223. heart. Tachyzoites can be seen with Wright or Giemsa stains but are best demonstrated with immunoperoxidase technique. which may be important in the pathogenesis of disease. choroid and retina. virulence. whereas 90% of infected infants will have no clinical manifestations of infection in the newborn period. inoculum of T. and immunologic capacity of the mother and fetus to limit parasitemia.

elevation of cerebrospinal fluid protein. A small number of symptomatically infected infants (<10%) will be found to have chorioretinitis. the failure of an infant to pass a newborn hearing screening exam should raise the possibility of congenital CMV infection. because hearing loss is the most common long-term sequela associated with congenital CMV infection. long-term follow-up should include appropriate assessment of development and neuromuscular function in infected infants. Finally. These more severe infections are thought to develop in infants who lack transplacentally acquired 34 . perinatal infection can result in severe. Perinatal infections can be acquired during birth or following ingestion of CMV-containing breast milk. 225. with referral to specialized care if necessary.some cases. perhaps more importantly. In rare cases.1 b. Hearing loss in the older infant and young child should also alert the clinician to the possibility of congenital CMV infection. as approximately 50% of infants with hearing loss associated with congenital CMV infection will pass an initial hearing screening exam but develop hearing loss in later infancy and early childhood. but vision testing and comprehensive eye examinations should be included in the care plan. audiologic testing and follow-up are mandatory in these patients. disseminated infections associated with end-organ disease and death. An organized plan for follow-up is an important aspect in the clinical management of infants with congenital CMV infection. have not been associated with any long-term sequelae. perinatal infections are not associated with any clinical manifestations of infection and. Because permanent sequelae are limited to disorders of the nervous system. In almost all cases. Hearing loss will develop in approximately 11% of infected infants. Thus. Perinatal Infection 226. such as is seen in breast milk transmission of CMV to extremely premature infants or infants born to nonimmune women. Other sequelae such as vision loss are infrequent. and in some infants hearing loss will progress during infancy.

12. and extent of spread. (2) encephalitis with or without skin. eye findings including chorioretinitis and keratoconjunctivitis. eye. 228. Use of scalp electrodes may also increase risk. lungs. eye. Neonatal HSV infection is thought to never be asymptomatic. HSV infection may be acquired in utero. and (3) disseminated infection involving multiple organs. heart. Fewer than 30% of mothers of an infant with neonatal herpes have a history of genital herpes. or during the neonatal period. portal of entry. and skin. Infants with skin. Postpartum transmission may be from the mother or another adult with a nongenital (typically HSV-1) infection such as herpes labialis. and mouth disease generally present at 511 days of life and typically demonstrate a few small vesicles. Its clinical presentation reflects timing of infection. but only with ritual oral contact with the circumcision site.antiviral antibodies either secondary to extreme prematurity or being the product of a mother lacking anti-CMV antibodies. Infants infected during delivery or the postpartum period present with 1 of the following 3 patterns of disease: (1) disease localized to the skin. liver. or mouth. Intrauterine and postpartum infections are well described but occur infrequently. Infants with intrauterine infection typically have skin vesicles or scarring. usually during passage through an infected birth canal of a mother with asymptomatic genital herpes. during the birth process. eyes. including the brain. The risk for infection is higher in infants born to mothers with primary genital infection (>30%) than with recurrent genital infection (<2%). 229. adrenals. There also have been rare cases of neonatal herpes associated with Jewish ritual circumcisions. and mouth disease.3 Herpes Simplex Virus a.1 2. particularly on the presenting part or at sites of trauma such as sites of scalp electrode 35 . Perinatal Infections 227. and microcephaly or hydranencephaly that are present at delivery. and those who do generally have severe sequelae. Transmission is well documented in infants delivered by cesarean section. Few infants survive without therapy. Most cases of neonatal herpes result from maternal infection and transmission.

poor feeding. and most survivors have severe neurologic sequelae. Infants with disseminated HSV infections generally become ill at 5-11 days of life. jaundice. Infants with encephalitis typically present at 8-17 days of life with clinical findings suggestive of bacterial meningitis. poor tone. and vomiting. seizures are common. If untreated. 231. and skin vesicles occur in only approximately 60% of cases. eye. skin. 50% of infants with HSV encephalitis die and most survivors have severe neurologic sequelae. and mouth disease in infants may progress to encephalitis or disseminated disease.placement. 232. purpuric rash. 230. lethargy. apneic spells. whether the natural history of the infection in these infants is different is an unanswered question. Skin vesicles are seen in approximately 75% of cases. and seizures. Infants with neonatal herpes whose mothers received antiherpes antiviral drugs in the weeks prior to delivery may present later than their untreated counterparts. If untreated. They may also exhibit respiratory distress. cyanosis. approximately 90% of these infants die. including irritability. If untreated. poor feeding. irritability. Their clinical picture is similar to that of infants with bacterial sepsis.1 36 . Fever is relatively uncommon. consisting of hyperthermia or hypothermia. the infection causes shock and disseminated intravascular coagulation. and evidence of central nervous system infection.

E1 and E2 that are associated with the envelope. often exanthematous disease of infants and children that is typically more severe and associated with more complications in adults. Rubella (German measles or 3 day measles) is a mild.13.1 37 . It is a single-stranded RNA virus with a lipid envelope and 3 structural proteins. 235. Definition 236.233. Etiology 239. Rubella Disease a. Rubella virus is a member of the family Togaviridae and is the only species of the genus Rubivirus. and extremes of pH but is relatively stable at cold temperatures. including a nucleocapsid protein that is associated with the nucleus and 2 glycoproteins.1 237. The virus is sensitive to heat. Humans are the only known host. b. ultraviolet light. 2. Its major clinical significance is transplacental infection and fetal damage as part of the congenital rubella syndrome (CRS). 238. 234.

and 20. The endemic spread of rubella has been 38 . In the prevaccine era.45 per 100. Subsequently.000 in 1999 and a corresponding decrease of CRS.000 population in 1990 to 0. rubella appeared to occur in major epidemics every 6-9 yr. more than 13. During the rubella epidemic of 1964-1965 there were an estimated 12.c. the incidence of rubella fell 78% by 1976 and CRS cases fell 69%).000 cases of CRS. Mothers of these infants tended to be young. or foreign born.5 million cases of rubella associated with 2. a resurgence of rubella and CRS cases occurred during 1989-1991 in association with the epidemic of measles during that period. a 2 dose recommendation for rubella vaccine was implemented and resulted in a decrease in incidence of rubella from 0. with smaller peaks interspersed every 3-4 yr. and was most common in preschool-age and school-age children. After years of decline.000 abortions or perinatal deaths. Hispanic. with an average of 6 infants with CRS reported annually from 19922004. Epidemiology 240. including adolescents and college students. Further decline in rubella and CRS cases occurred when certain at-risk populations were added to those for whom rubella immunization is indicated.1 per 100. Following introduction of the rubella vaccine in 1969.000 cases of encephalitis. The number of reported cases of rubella continued to decline through the 1990s and first decade of this century.

even if fetal infection occurs. From 2004-2012 there were 79 cases of rubella and 6 cases of CRS. The pathologic findings for CRS are often severe and may involve nearly every organ system. 11% at 13-14 week. The viral mechanisms for cell injury and death in postnatal or congenital rubella are not well understood. Between January 1 and May 1. 2013.1 e. elimination of transmission of rubella in the Americas also may have been achieved. the virus replicates in the respiratory epithelium and then spreads to regional lymph nodes. Three of the CRS cases were acquired in Africa.eliminated in the United States. Pathology 241. Viremia ensues and is most intense from 10-17 days after infection. Pathogenesis 242.1 d. The period of highest communicability is from 5 days before to 6 days after the appearance of the rash. all of which were imported cases of unknown source. Maternal infection during the 1st 8 week of gestation results in the most severe and widespread defects. Defects occurring after 16 wek of gestation are uncommon. cases of rubella continue to be imported into the United States from countries where it remains endemic. Viral shedding from the nasopharynx begins approximately 10 days after infection and may be detected up to 2 week following onset of the rash. The risk for congenital defects has been estimated at 90% for maternal infection before 11 week of gestation.442 cases of rubella and 10 cases of CRS were reported. However. 5. 33% at 11-12 week. The most important risk factor for severe congenital defects is the stage of gestation at the time of infection. and 24% at 15-16 wk. Causes of cellular and 39 . The few reported studies of biopsy or autopsy material from cases of rubella revealed only nonspecific findings of lymphoreticular inflammation and mononuclear perivascular and meningeal infiltration. demonstrating that the elimination of rubella internationally has not been achieved and continued vigilance and maintenance of high levels of immunity in the United States are necessary. Little information is available on the pathologic findings in rubella occurring postnatally. Following infection.

Clinical Manifestation 243. and it spreads centrifugally to involve the torso and extremities. The rash fades from the face as it extends to the rest of the body so that the whole body may not be involved at any one time. examination of the oropharynx may reveal tiny. headache. and production of a protein inhibitor causing mitotic arrests in certain cell types. which is variable and not distinctive. In children. reduced cellular multiplication time. rose-colored lesions (Forchheimer spots) or petechial hemorrhages on the soft palate. The duration of the rash is generally 3 days. Subclinical infections are common. a prodrome consisting of low-grade fever. the first manifestation of rubella is usually the rash. It begins on the face and neck as small. Once the fetus is infected early in gestation. and anterior cervical lymph nodes are most prominent.1 h. Diagnoses 40 . About the time of onset of the rash. Suboccipital. Leukopenia. Laboratory Findings 244. and it usually resolves without desquamation.1 g. the virus persists in fetal tissue until well beyond delivery. postauricular. and mild thrombocytopenia have been described during postnatal rubella. and lymphadenopathy begins. where it tends to occur as discrete macules. sore throat. most notably in the brain. irregular pink macules that coalesce. Persistence suggests the possibility of ongoing tissue damage and reactivation. especially in children. anorexia. Following an incubation period of 14-21 days. red eyes with or without eye pain.tissue damage in the infected fetus may include tissue necrosis due to vascular insufficiency. malaise.1 f. neutropenia. The most distinctive feature of congenital rubella is chronicity. and 2540% of children may not have a rash. chromosomal breaks. Postnatal infection with rubella is a mild disease not easily discernible from other viral infections.

for epidemiologic diagnosis of infection in pregnant women. and demonstrates variability in the presence of typical findings. The absence of Koplik spots and a severe prodrome as well as a shorter course allow for differentiation from measles. A caveat for testing of congenitally infected infants early in infancy is that false-negative results may occur owing to competing IgG antibodies circulating in these patients. Rubella may manifest as distinctive features suggesting the diagnosis. Differential Diagnoses 246. rubella A specific diagnosis of is important for reasons. As with any serologic test. and for confirmation of the diagnosis rubella. or viral culture should be performed for confirmation. the positive predictive value of testing decreases in populations with low prevalence of disease. it may resemble measles.1 i. Other diseases frequently confused with rubella include infections caused by adenoviruses. reverse transcriptase polymerase chain reaction test. similar to other viral exanthematous diseases. and Mycoplasma pneumoniae.1 j. The relative sensitivity and specificity of commercialkits used in most laboratories range from 96-99% and 86-97%. Tests should be performed in the context of a supportive history of exposure or consistent clinical findings. In such patients. diagnostic The of congenital most test is common rubella immunoglobulin (Ig) M enzyme immunosorbent assay. Complications 41 . parvovirus B19 (erythema infectiosum). enteroviruses. an IgM capture assay. Epstein-Barr virus. It is frequently confused with other infections because it is uncommon. In severe cases.245. respectively.

however. 248. Arthritis following rubella occurs more commonly among adults. It occurs in 2 forms: a postinfectious syndrome following acute rubella and a rare progressive panencephalitis manifesting as a neurodegenerative disorder years following rubella. 250. Cerebrospinal fluid may be normal or have a mild mononuclear pleocytosis and/or elevated protein concentration. consisting of headache. and hematuria. epistaxis. There are anecdotal reports and some serologic evidence linking rubella with rheumatoid arthritis. coma. Progressive rubella panencephalitis (PRP) is an extremely rare complication of either acquired rubella or CRS. Most patients recover completely. 249. Postinfectious thrombocytopenia occurs in approximately 1 in 3. but mortality rates of 20% and long-term neurologic sequelae have been reported. It begins within 1 wk of onset of the exanthem and classically involves the small joints of the hands. focal neurologic signs. especially women. occurring in 1 in 5. seizures. It is usually self-limited. Virus is rarely. Postinfectious encephalitis is uncommon. Encephalitis is the most serious complication of postnatal rubella. infrequent Complications following postnatal infection with rubella are and generally not life-threatening. It appears within 7 days after onset of the rash. if ever. suggesting an infectious pathogenesis.000 cases of rubella and occurs more frequently among children and. confusion. and ataxia. albeit a “slow” one. It manifests about 2 wk following the onset of the rash as petechiae. but a true causal association remains speculative.000 cases of rubella. It also is self-limited and resolves within weeks without sequelae. in girls.247. suggesting a noninfectious pathogenesis. isolated from cerebrospinal fluid or brain. rubella virus may be isolated from brain tissue of the patient with PRP. Death occurs 42 . The clinical findings and course are undistinguishable from those of sub-acute sclerosing panencephalitis and transmissible spongiform encephalopathies. gastrointestinal bleeding. Unlike in the post infectious form of rubella encephalitis. It has an onset and course similar to those of the subacute sclerosing panencephalitis associated with measles. Fever may recrudesce with the onset of neurologic symptoms.

Congenital Rubella Syndrome 252. Other neurologic syndromes rarely reported with rubella include Guillain-Barré syndrome and peripheral neuritis. In 1964-1965 a pandemic of rubella occurred.100 neonatal deaths. an ophthalmologist first described a syndrome of cataracts and congenital heart disease that he correctly associated with rubella infections in the mothers during early pregnancy. Subsequent postnatal growth retardation and ultimate short stature have been reported 43 . In 1941.000 cases reported in the United States. followed by lesions of the pulmonary arteries and valvulardisease.2-5 yr after onset. Patent ductus arteriosus is the most frequently reported cardiac defect. 2. Interstitial pneumonitis leading to death in some cases has been reported. motor. Meningoencephalitis is present in 10-20% of infants with CRS and may persist for up to 12 mo. leading to more than 11. with 20. From this experience emerged the expanded definition of CRS that includes numerous other transient or permanent abnormalities. Unilateral or bilateral cataracts are the most serious eye finding. hearing loss was recognized as a common finding often associated with microcephaly. Neurologic abnormalities are common and may progress following birth. and behavioral abnormalities.1 251. Longitudinal follow-up through 9-12 yr of infants without initial retardation revealed progressive development of additional sensory. Most infants have some degree of intrauterine growth restriction. Nerve deafness is the single most common finding among infants with CRS. 253. including hearing loss and autism.000 spontaneous or therapeutic abortions and 2. occurring in about a third of infants.14. Myocarditis is a rare complication. Shortly after the first description. Retinal findings described as salt-and-pepper retinopathy are the most common ocular abnormality but have little early effect on vision. Cardiac abnormalities occur in half of the children infected during the 1st 8 week of gestation. PRP has also been recognized rarely after CRS.

Reinfection with wild virus occurs postnatal in both individuals who were previously infected with wild-virus rubella and in vaccinated individuals. Reinfection is defined serologically as a significant increase in Ig G antibody level and/or an Ig M response in an individual who has a documented preexisting rubella-specific Ig G above an accepted cutoff. Postnatal infection with rubella has an excellent prognosis. 259. Management of children with CRS is more complex and requires pediatric. 30% in dependent situations but functional. non-remitting thrombocytopenia. Prognosis 258. ophthalmologic. cardiac. A cohort from New York from the mid-1960s epidemic had less-favorable outcomes.1 a. In addition to PRP. and neurologic evaluation and follow-up because many manifestations may not be readily apparent initially or may worsen with time. Treatment 255. Longterm outcomes of CRS are less favorable and somewhat variable. Supportive Care 256. Postnatal rubella is generally a mild illness that requires no care beyond antipyretics and analgesics. 257. A variety of late-onset manifestations of CRS have been recognized. many had chronic conditions but most were married and had made good social adjustments. because early intervention may improve outcomes in children with hearing problems caused by CRS. and glaucoma and visual abnormalities associated with the retinopathy. There is no specific treatment available for either acquired rubella or CRS. with 30% leading normal lives. Hearing screening is of special importance. thyroid dysfunction (5%). b. In an Australian cohort evaluated 50 year-after infection. Reinfection may result in an anamnestic Ig G response. an Ig M and Ig G 44 . audiologic. a minority of cases. which had previously been considered benign. they include diabetes mellitus (20%).1 c. Intravenous immunoglobulin or corticosteroids can be considered for severe. Rare reports of immunologic deficiency syndromes have also been described. and 30% requiring institutionalization and continuous care.

If both of these test negative. There are 29 reports of CRS following maternal reinfection in the literature. suggesting recent infection. a frozen aliquot also should be saved for later testing. If both the 2nd and 3rd specimens test negative. 261. a 3rd specimen should be obtained 6 week after exposure and tested concurrently with the saved specimen. so contact precautions should be maintained for them until then. The routine use of immunoglobulin for susceptible pregnant women exposed to rubella is not recommended and is considered only if termination of pregnancy is not an option because of maternal preferences. A negative 1st specimen and a positive test result in either the 2nd and 3rd specimen indicate that second version has occurred in the mother. a 2nd specimen should be obtained 2-3 week later and tested concurrently with the saved specimen. Children with CRS may excrete the virus in respiratory secretions up to 1 yr of age. a blood specimen should be obtained as soon as possible for rubella Ig G-specific antibody testing.response. 262. the mother is likely immune. immunoglobulin 0. Exposure of susceptible pregnant women poses a potential risk to the fetus. unless repeated cultures of urine and pharyngeal secretions have negative results. Reinfection with serious adverse outcomes to adults or children is rare and of unknown significance. or clinical rubella. In such circumstances.55 mL/kg IM may be given with the understanding that prophylaxis may reduce the risk for clinically apparent infection but does not guarantee prevention of fetal infection. Standard plus droplet precautions are recommended for hospitalized patients. Patients with postnatal infection should be isolated from susceptible individuals for 7 days after onset of the rash. If the rubella antibody test result is positive. Counseling should be provided about the risks and benefits of termination of pregnancy. infection has not occurred. For pregnant women exposed to rubella. Similar precautions apply to patients with CRS with regard to attendance in school and out-of-home childcare. Prevention 260.1 d. If the rubella antibody test is negative.1 45 .

2) Use of the MMR vaccine rather than the monovalent measles vaccine as the immunizing agent in all immunization programs for measles worldwide to expedite the elimination of rubella. Thus. cataracts. 46 . Patients with illnesses that are compatible with rubella or measles should have a serum rubella and measles immunoglobulin (Ig) M serology requested.. hepatosplenomegaly. glaucoma. Ig M serology has a low positive predictive value for both measles and rubella. rubella Ig G avidity testing has been shown to be a very useful laboratory test for differentiating primary infection (with a high risk of CRS) from past infection (low risk of CRS). Standing orders on the postpartum ward should be implemented (similar to the RhoGam [Ortho-Clinical Diagnostics Inc. hearing impairment.263. In low-prevalence situations. Breastfeeding is not a contraindication to immunization. To prevent CRS: 1) Continued universal infant immunization to protect recipients and to decrease circulation of the virus. Infants with unexplained microcephaly. additional laboratory testing such as paired acute and convalescent Ig G serology (to look for a fourfold or greater rise in titre) and/or virus detection is necessary to confirm measles and rubella infections. in the absence of clear epidemiological links or travel history to endemic areas. thrombocytopenia or radiolucent bone densities should be evaluated for CRS with the appropriate investigations depending on the age of the child. This is not only important for surveillance purposes. patent ductus arteriosus. 3) Screening of all pregnant women to determine the need to confirm seropositivity and to enable postpartum immunization of all women found to be susceptible on prenatal screening. USA] standing order in the postpartum period) because they will expedite postpartum immunization. In this situation of suspected rubella in a pregnant woman. but is critical for the laboratory investigation of suspected rubella in pregnant women where important patient management decisions must be made. 264. Ongoing surveillance for all cases of rubella and of CRS is a vital component of a prevention program. pigmentary retinopathy.

the patient should be counseled on the theoretical risks to the fetus. 95% of persons 12 months of age and older develop serologic immunity. Although antibody levels may wane. Following a single dose of rubella RA 27/3 vaccine. Therefore. interruption of pregnancy is probably not warranted. of all health care personnel. Detectable antibodies remain for 15 year in most individuals vaccinated following 1 dose. Rubella RA 27/3 vaccine is highly protective as 97% of those vaccinated are protected from clinical disease after 1 dose. Patients with HIV infection who are not severely immunocompromised may benefit from vaccination. increased susceptibility to rubella disease does not occur. Immunoglobulin preparations may inhibit the serologic response to the vaccine. but if a more serious illness is suspected.4) Screening for immunity and vaccination. and 6) Fully investigating and reporting every case of possible rubella or CRS. It theoretically may be effective as post exposure prophylaxis if administered within 3 days of exposure. 5) Immunizing all non-pregnant immigrant and refugee women at their first encounter with the Canadian health care system unless they have documentation of effective vaccination or natural immunity. including students in training. Rubella vaccine in the United States consists of the attenuated Wistar RA 27/3 strain that is usually administered in combination with measles and mumps (MMR) or also with varicella (MMRV) in a 2 dose regimen at 12-15 months and 4-6 year of age. Vaccine should not be administered to severely immunocompromised patients (e. If pregnancy occurs within 28 days of immunization. especially after 1 dose of vaccine.. transplant recipients). Fever is not a contraindication. and 91% to 100% had antibodies after 12-15 yearafter 2 doses.8 e. Vaccine should not be administered during pregnancy. and after 2 doses 99% have detectable antibody. immunization should be delayed.g. 47 . Studies of more than 200 women who had been inadvertently immunized with rubella vaccine during pregnancy showed that none of their offspring developed CRS. if necessary. Vaccination 265.

Depending on the screening protocol. the screening test was developed in 1978 by David Kemp. Adverse reactions to rubella vaccination are uncommon in children. First described by a geophysicist in the middle 1940s. in response to received auditory input. As part of the worldwide effort to eliminate endemic rubella virus transmission and occurrence of CRS. These physiological. hearing screening in newborns is performed via otoacoustic emission (OAE) and automated auditory brainstem response (AABR) testing. a sound stimulus is sent to the newborn’s auditory system via ear-specific probes placed in the external ear canal. 270. they may be performed singly (OEA or AABR) or sequentially. noninvasive. Approximately 25% of post pubertal women experience arthralgia.1 268. Based on the natural phenomenon of ‘sound echoes’. automated screening tests can be performed at the bedside in term and pre-term infants. 2. generated by the outer hair cells of the human cochlea. maintaining high population immunity through vaccination coverage and high-quality integrated measles-rubella surveillance have been emphasized as being vital to its success. measured as sound. Hearing testing 269.15. The response is generally absent in ears with a hearing loss of 30 dB or greater. 271. Currently. MMR administration is associated with fever in 5-15% of vaccines and with rash in approximately 5% of vaccines. The probe simultaneously records emissions returning from the outer hair cells of the cochlea via the middle ear. and 10% experience arthritis. 267. Both the OAE and AABR tests are automated screening adaptations of more detailed diagnostic tests for hearing loss. In contrast to the OAE test. Arthralgia and arthritis are more common following rubella vaccination in adults. OAEs can be recorded in 99% of normally hearing ears. The AABR test records brainstem electrical activity in response to sounds presented to the infant via earphones. OAEs are forms of energy. the AABR evaluates the auditory pathway from the external ear 48 .266. Peripheral neuropathies and transient thrombocytopenia may also occur.

Red flags guidliness (6-24 months): 1) 6 month of age a. baby is unable to hold head in the middle to turn and look left and right and asymmetry (i. Gross motor: Does not pull up to sit or does not roll over. 274. and to be even more intentional in documenting observations and providing opportunities for the child to acquire the skill. Speech and language: Early babbling stops. persistence of grasp reflex. Red flag is an informal term that. and consistently ignores or has difficulty using one side of body.e. enabling diagnosis of auditory neuropathy. Social : Unresponsive to a familiar voice. which is a less common cause of hearing impairment. flat affect). unresponsive to social situations (i. Does not respond when called and a lot of colds and ear infections e. no eye contact. Holding toys close to eyes. daily interactions between the infant/toddler caregiver and child. Red flags 273.. A red flag may be discovered during a standardized developmental screening or through the ongoing. Extreme irritability and unresponsive to social situations 2) 12 month of age 49 . Fine motor: Infant is unable to hold or grasp an adult finger or a toy/object for a short period of time.7 272.e. Emotional: Unresponsive to familiar caregivers. Cognitive : Unable to follow moving objects with his/her eyes and will not reach out to explore/touch objects f. 2. Vision: Turning or tilting head to use only one eye to look at things. In essence. or no interest in small objects and constant jiggling or moving of eyes side-to-side d. or uses one hand exclusively b. not smiling socially g. simply implies that some aspect of the child’s development has been noticed as at risk for falling outside the range deemed the level of the brainstem. a red flag is a signal to pay increased attention to the aspect of concern in a child’s development. a difference between two sides of body or body too stiff or too floppy) c. in this context.

a difference between two sides of body or body too stiff or too floppy) c. turning or tilting head to use only one eye to look at things. does not search for dropped or hidden objects and child does not respond to caregiver interactions f. Social : Will not show interest or participate in social situations. move independently. Speech and language: Lost vocalization e. Vision: Eyes that itch or burn. Gross motor: Baby is unable to hold head in the middle to turn and look left and right and asymmetry (i. eyes that cross. stiffens when approached g. twisting. will only look at you if he or she hears you. does not search for objects when moved from within sight to out of sight 50 .hard to console. Gross motor: Baby is unable to hold head in the middle to turn and look left and right and asymmetry (i. Fine motor: Consistently ignores or has difficulty using one side of body or uses one hand exclusively b.e. or uses one hand exclusively a. Cognitive: Does not imitate simple actions. turning or tilting head to use only one eye to look at things. Speech and language: Failure to do what they may to do d. Cognitive : Does not make sounds to get attention. does not show any understanding of cause and effect. Emotional: Will not seek comfort when upset 3) 18 month of age a. avoidance of tasks with small objects. and constant jiggling or moving of eyes side-to-side (roving) d. unusually short attention span. move independently. no interest in small objects and pictures. sensitivity to bright light and sun. and constant jiggling or moving of eyes side-to-side c. turning. will only look at you if he or she hears you. Vision: Unusually short attention span. Fine motor: Infant is unable to hold or grasp an adult finger or a toy/object for a short period of time.a. unable to use hands in a variety of ways. throwing. turn in or out. eyes that cross. turn in or out. etc and unconsistently ignores or has difficulty using one side of body. a difference between two sides of body or body too stiff or too floppy) b.not laughing in playful situations.e.

does not seek comfort in a person or object when distressed 4) 12 month of age a. 276. and throwing. Emotional: Failure to talk about feelings. 282. CHAPTER III CONCLUSION 279. avoids or is hostile with caregiver after separation. sensitive to bright light and sun. 9 275. avoidance of tasks with small objects. and shows little fear towards a new room or stranger f. 284. 280. show preferences of likes and dislikes. very passive responses. 278. and rocks back and forth g. does not show preferences and dislikes. child shows few emotions. Emotional: Facial expression shows little variation. turning. Social : Does not make face to face contact during play or any interactions. does not show affection for familiar people or objects. Speech and language: Lack of face to face or eye contact and loss of speech e. 277. child kicks. Fine motor: Unable to use hands in a variety of ways. Social : Does not explore the environment.e. twisting. Vision: Eyes that itch or burn. show pride and pleasure at new accomplishments and express negative feelings. The sign of the symptoms that are appeared on the infant indicates the suffered Congenital Rubella Syndrome which cause by the infection. bites and scream easily and without provocation. 281. 283. b. 51 . child ignores. Gross motor: Unable to walk with heels down c. turning or tilting head to use only one eye to look at things d. Cognitive : Misses small objects when reaching for them and does not use trial and error to solve problems f. ldgrowth. Fiebelkorn AP. accessed on September 17th 2015 7. 2010. 6. Screening. Twentieth Edition. Feldman M. and Assessment. Sarosa Gatot Irawan. Nelson Textbook of Pediatrics. 8. Richard. Prevention of TW. 290. Bonita. Usman Ali. congenital rubella syndrome. Pediatrics & Child Health. Inc . Penerbit Ikatan Dokter Anak Indonesia . Nature Genetics. Temte JL. Joseph. Kliegman M. 2010. Bernd. Canada : Elsevier. 5. Robert. 2013: summary recommendations of the advisory committee on immunization practices (ACIP) MMWR Recomm Rep. Medical Microbiology 25th Edition. a Wolter Kluwer Business 4.aspx. and mumps.16(5):301-305. Behrman E. Infant/Toddler Development. Kosim Sholeh. http://www. 2012. 2009 3. 289. Dewi Eizalya. Mc Graw Hill. 52 .285. International Edition. A Common Mechanism for Microcephaly. Jawetz. Stanton F. rubella. 2011. Sadier. Centers for Disease Control and Prevention. Buku Ajar Neonatologi. 287. p. Department of Maternal and Child Health. 62: 1–34. 9. REFERENCES 286. McLean HQ.42(11): 923-4. Langman’s Medical Embryology 12th Edition. 2013. 1. Patel H. Schor F.vic. St Geme III W. Wallace GS. Melnick & Adelberg’s. Universal newborn hearing screening. Lippincott Williams and Wilkins. Chapel Hill : The University of North Carolina Wollnik. Nina. 2015 2. Yunanto Ari.