VERY DESCRIPTIVE AND COMPREHENSIVE SLIDES ON TORCH AND OTHER INFECTIONS (TAKING INDIAN SCENERIO IN ACCOUNT)

1. MODERATORs-
PROF. S.M. ALI
DR. UZMA FIRDAUS
PRESENTED BY-
DR. KUMAR VASU
DCH-II (2017 Batch)
INTRAUTERINE INFECTIONS

2. INTRODUCTION
 The TORCH pneumonic typically comprises
toxoplasmosis, Treponema pallidum, rubella,
cytomegalovirus, herpesvirus, hepatitis B virus,
hepatitis C virus, human immunodeficiency virus and
other viruses, including varicella, parvovirus B19.
 Vertically transmitted from mother to baby
 Divided into 3 categories :
 CONGENITAL,
 PERIPARTUM &
 POSTNATAL
 CMV is the most common congenital infection

3.  Significant causes of stillbirth and may account
for up to half of all perinatal deaths globally.
 Burden is especially great in developing
countries.
 Stigmata of disease may be seen at birth, in the
early neonatal period, or later.
 Treatment strategies are available for many of the
TORCH infections.
 Early recognition, including maternal prenatal
screening and treatment when available, are key
aspects in management of TORCH infections.

4.  Account for 2% - 3% of birth defects which arise
form a spectrum of organisms.
 The first trimester is usually the most dangerous
time for fetus being affected
 Fetus becomes immunologically competent from
the 14th week
 The most important risk factor for severe
congenital defects is the stage of gestation at the
time of infection

5. DIAGNOSIS REQUIRES HIGH
INDEX OF SUSPICION
 IUGR infants
 HSM
 Thrombocytopenia
 Unusual rash
 Concerning maternal history
 Microcephaly
 “Classic” findings of any specific infection

6. TOXOPLASMA

7. INTRODUCTION
 Toxoplasmosis is a disease caused by an intracellular
parasite TOXOPLASMA GONDII.
 Human acquisition of the infection occurs by:
1. Ingestion of raw or undercooked meat containing tissue cysts
(Sheep, pigs and rabbits are the most common meat
sources).
2. Oocyst from contact with cat feces, contaminated soil, salads,
vegetables.
 Congenital infection results most commonly from the
transplacental transmission of T gondii after maternal
primary infection during pregnancy, during a time of high
parasite burden
 Reactivation of toxoplasmosis in immunocompromised
women (ie, women with HIV) may also lead to congenital

8.  Risk of transmission increases with the date of
maternal infection, from less than 15% at 13
weeks of gestation to greater than 70% at 36
weeks.
Late trimester-
increase
infection
Early
trimester-
increase
mortaLity!

9. LIFE CYCLE

11. Maternal disease
 Most often, maternal infection is asymptomatic or
without specific symptoms or signs.
 As with other adults with acute toxoplasmosis,
lymphadenopathy is the most common symptom.

12. CLINICAL FEATURES
 The signs and symptoms of T gondii overlap
other TORCH infections;
 More severe manifestations usually indicate
infection earlier in gestation, whereas
 Fetal infections occurring in the third trimester are
usually subclinical at birth.

13.  Most (70%–90%) infected infants are
asymptomatic at birth
 Classical triad of symptoms (chorioretinitis,
hydrocephalus, and intracranial calcifications) is
rare!
 More common manifestations include
 Anemia
 Seizures
 Jaundice
 Splenomegaly
 Hepatomegaly
 Thrombocytopenia

14.  Newborns with mild or no S/S are still at high risk
for late manifestations and sequelae of the
disease
 Chorioretinitis
 Motor and cerebellar dysfunction
 Microcephaly
 Seizures
 Intellectual disability (mental retardation)
 Sensorineural hearing loss

16. DIAGNOSIS
 No 1 universally endorsed screening protocol for T
gondii in pregnant women!
 risk factor–based approach on suspicious findings (ie,
hydrocephalus, cerebral, hepatic, or splenic
calcifications) on ultrasonography.
Maternal screening comprises
 T gondii IgM -High false-positive rate and may persist
for up to 2 years after acute infection
 T gondii IgG More sensitive - IgG avidity testing
 Polymerase chain reaction (PCR) - Amniotic fluid
PCR at 18 weeks’ gestation can determine fetal
infection and guide medical therapy

17. TREATMENT
 Treatment for pregnant mother – Spiramycin (1 g
every 8 hr PO without food) is recommended for
prevention of fetal infection if the mother
develops acute toxoplasmosis during pregnancy
till reports (PCR and USG) are available.
 Pyrimethamine (50 mg once daily PO),
sulfadiazine (1.5-2 g bid PO), and Folinic acid (10
mg once daily PO) are recommended for
treatment of the pregnant woman whose fetus
has confirmed or probable fetal infection
 In the 1st trimester when there is definite
infection, sulfadiazine alone is recommended
because pyrimethamine is potentially teratogenic
at that time.

18.  Postnatal Infant with stigmata of congenital
toxoplasmosis:
 IgG, IgM, and IgA (more sensitive than IgM)
 Serum and CSF PCR should be obtained.
 Testing only at experienced reference laboratories.
 Ophthalmologic, auditory, and neurologic
examinations
 CT head for intracranial calcifications.

19.  For infants diagnosed prenatally with
toxoplasmosis, either symptomatic or
asymptomatic, as well as infants diagnosed
postnatally
 12 months TT with pyrimethamine and
sulfadiazine
 Folinic acid is also given to minimize
pyrimethamine-associated hematologic toxicity

20. CYTOMEGALOVIRUS

21. INTRODUCTION
 CMV is a doubles stranded DNA herpes virus
 The most common congenital viral infection
 The CMV seropositivity rate increases with age
 CMV infection requires intimate contact through
saliva, urine, and/ or other body fluids

22.  Primary,reactivation,or recurrent CMV infection
can occur in pregnancy and can lead to
congenital CMV infection.
 Approximately 85 percent of newborns with
congenital CMV infection can be asymptomatic at
birth.
 15 percent will develop progressive hearing loss
and visual impairment .
 Vertical transmission of CMV can occur at any
stage of pregnancy
 Severe sequelae are more common with infection
in the 1st trimester.
 The overall risk of infection is greatest in the 3rd
trimester.

23. ROUTES OF TRANSMISSION
 Transplacental Transmission
 Transmission Via Breastmilk
 Blood Transfusion(rare)
 Organ Transplant

24. CLINICAL FEATURES
 Hepatomegaly
 Spleenomegaly
 Jaundice
 Thrombocytopenia
 Petechiae
 Microcephaly
 Intrauterine growth retardation
 SNHL
TRIAD

25. Late features
 Venticulomegaly
 Cerebral atrophy
 Mental retardation
 Psychomotor delay
 Seizures
 Learning difficulties and language delay
 Chorioretinitis / Optic atrophy
 Intracranial calcifications (perivenricular)
 Long bone radiolucencies
 dental abnormalities
 Pneumonitis
 Enteritis
BREAST
MILK
assosciated

27. DIAGNOSIS
 CMV Polymerase chain reaction
 Spin enhanced or SHELL VIAL culture
 CMV antigen
 CMV IgG/ IgM detection

28. TREATMENT
 Ganciclovir 5mg/kg IV every 12 hours for 14 days
 Valganciclovir 900mg PO daily for 3-6 months
 CMV-specific hyperimmune globulin (200 units/kg
of body weight)

29. HERPES SIMPLEX VIRUS

30. INTRODUCTION
 Herpes simplex virus (HSV) infection during
pregnancy can pose a serious threat to the
developing fetus and the newborn infant.
 HSV is a member of the Herpesviridae family of
viruses.
 Enters the host through the inoculation of oral,
genital, or conjunctival mucosa.
 Inoculation also can occur through breaks in the
skin.
 Dissemination of the virus eventually allows the
virus to reach the dorsal root ganglia, where it
remains dormant for the rest of the host’s life.

31.  Antiviral drugs do not affect latent HSV infection
and therefore infection is life-long .
 Intrauterine HSV is a rare occurrence and most
likely is caused by maternal viremia associated
with primary infection during pregnancy.
 Transmission typically occurs via direct contact
between the neonate and an infected maternal
genital tract.
 If the primary HSV infection was acquired during
pregnancy, then the risk of transmission is
greater as compared with reactivation of a
previous infection.

32. ROUTES OF TRANSMISSION
 Antenatal Transmission(very rare)
 Postnatal Transmission(approx.10%)
 Intrap[artum Transmission(90%)

33. CLINICAL FEATURES
 Skin lesions
( vesicles, ulcerations or scarring)
 Eye damage
(conjunctivitis, cataract, retinopathy)
 CNS abnormalities
( hydranencephaly, microcephaly)
Triad @
BIRTH

34.  Diseminated Infecions :
 Most severe
 Incidence -22%(1 in 4!), mortality about 60%
 Manifestations - Pneumonitis, fulminant hepatitis,
DIC, seizure, shock, resp. distress & resp.
failure(within 1st week).

37. DIAGNOSIS
 Isolation of HSV in culture
 Detection of DNA via PCR assays
 Detection of HSV specific antigens using rapid direct
immunofluorescence or enzyme immunoassays
 Classical findings in CSF Testing(a mononuclear cell
pleocytosis, normal or slightly low glucose
concentration and moderately elevated protein level)
 On EEG(focal or multifocal periodic epileptic form
discharges )
 On neuroimaging(parenchymal brain edema,
hemorrhage or destructive lesions in the temporal,
frontal, parietal or brainstem regions in the brain)

38. TREATMENT
 Suppressive viral therapy from 36 weeks until
delivery (Valacyclovir 500 mg orally BD OR
Acyclovir 400 mg orallyTDS. Cesarean section is
recommended for all women in labor with active
genital lesions or prodromal symptoms such as
vulvar pain )
 For SEM envolvement(Acyclovir 20 mg/ kg every
8 hrs x 14 days)
 For CNS / Disseminated Disease(give Acyclovir
for 21 days)

39. RUBELLA

40. INTRODUCTION
 Rubella (German measles or 3-day measles).
 Single-stranded RNA virus.( rubivirus genus and
family Togaviridae)
 Vaccine-preventable disease.
 mild, self-limiting often exanthematous disease of
infants and children.
 In the pre vaccine era, rubella appeared to occur
in major epidemics every 6-9 yr, with smaller
peaks interspersed every 3-4 yr, was most
common in preschool and school-aged children.

41.  Intrauterine infection with rubella virus is referred
to as congenital rubella infection (CRI) or
syndrome.
 Infection with rubella earlier in pregnancy(1st
trimester ) cause worse prognosis and neonatal
complications.
 The virus can be transmitted to the fetus through
the placenta and is capable of causing serious
congenital defects, abortions, and stillbirths.
 Infection in weeks 8-10 of pregnancy results in
damage in up to 90% of surviving infants. Multiple
defects are then common.
 The risk of damage reduces to 10-20% if the
infection is in weeks 11-16 of pregnancy.
 Fetal damage is rare over 18-20 weeks of

42.  Transmission to the fetus occurs via maternal
hematogenous spread to the placenta..
 It typically occurs 5-7 days after maternal
inoculation.
 After the virus invades the placental barrier, it
spreads throughout the fetus via their vascular
system.
 The congenital defects that result from infection is
secondary to the cytopathical damage ensued to
the blood vessels.
 This in turn results in ischemia of the affected
organs.
 cardiac and eye defects typically resulting when
maternal infection occurs prior to 8 week.
 Hearing loss is typically observed in infections up

43. CLINICAL FEATURES
 TRANSIENT: Intrauterine growth restriction,
Thrombocytopenic purpura (25% - 'blueberry
skin'), Haemolytic anaemia,
Hepatosplenomegaly, Jaundice (common),
Radiolucent bone disease (20%),
Meningoencephalitis (25%) +/- neurological
sequelae .
 DEVELOPMENTAL:Sensorineural deafness
(80%), General learning disability (55%), Insulin-
dependent diabetes (20%, immune- mediated but
often delayed to adolescence or adulthood),

44.  PERMANENT:Congenital heart disease
(commonly patent ductus arteriosus or peripheral
pulmonary artery stenosis), Eye defects including
cataracts, congenital glaucoma, pigmentary
retinopathy (50% - so- called 'salt and pepper'),
severe myopia, microphthalmia, Microcephaly.
TRIAD

45. PCKD
THYROID & THYMUS
ABNORMALITIES
CRYPTOR-
CHIDISM

47. DIAGNOSIS
 Isolation of the rubella virus in culture.
 Demonstration of rubella-specific IgM antibodies.
 Demonstration of rubella-specific IgG antibodies
that persist at a higher concentration or longer
duration than expected from mere passive
transfer of maternal antibodies.
 Detection of rubella virus RNA by reverse-
transcriptase polymerase chain reaction

48. PREVENTION
 NO treatment available till now.
 Supportive care and surveillance is the only
recommended option available at this time.
 Close monitoring within the first 6 to 12 months of life
is recommended; particularly for the evaluation of
hearing impairment .
 Prevention is considered the most important aspect
as far as the management of CRI concerned.
 Preventive measures include recommended
immunizations, testing of pregnant women for
rubella immunity and proper
counseling regarding avoiding exposure.

49. HIV

50. INTRODUCTION
 HIV pandemic is one of the most serious health
crises the world faces today.
 “Human Immunodeficiency Virus”
H = Infects only Human beings
I = Immunodeficiency virus weakens the
immune system and increases the risk of
infection
V = Virus that attacks the body

51.  Acquired Immune Deficiency Syndrome”
A = Acquired, not inherited
I = Weakens the Immune system
D = Creates a Deficiency of CD4+ cells in the
immune system
S = Syndrome, or a group of illnesses taking
place at the same time
 H.I.V (Human Immunodeficiency Virus) is a
unique type of virus (i.e. a retrovirus) that invades
the T- helper cells (CD4 cells) in the body of the
host (defense mechanism of a person).

52. • There are two types of HIV. 1. HIV-1 2. HIV-2
HIV-1
1. HIV-1 is more common
worldwide.
2. HIV-1 is easily
transmitted.
3. HIV-1 is pathogenic in
nature
4. Duration of HIV-1
infection is quite long.
5. HIV-1 is commonly seen
in India.
HIV-2
1. HIV-2 is found in West
Africa, Mozambique,
and Angola.
2. HIV-2 is less easily
transmitted.
3. HIV-2 is less
pathogenic
4. . Duration of HIV-2
infection is shorter .
5. HIV-2 is relatively rare
and has not been
reported from India.

53.  AIDS:acquired immunodeficiency syndrome is a
disease of the human immune system caused by
infection with human immunodeficiency virus.In
children it is acquired perinatally or by vertical –
maternal- infant trasmission.
 In, 2010 an estimated 3,90,000 children were
newly infected with HIV with majority of
transmission being perinatal.
 In INDIA , estimated 2.1 million people are living
with HIV infection as on year 2012.
 Adult prevelance of HIV infection in INDIA is
0.3%.

54. MODES OF TRANSMISSION
 From mother to featus i.e during pregnancy,labor
and delivery and breast feeding,
 Blood trasfusion.
 Sexual trasmission

55. RISK FACTORS
 Advanced maternal disease.
 High maternal viral load.
 Prolonged rupture of membranes(>4Hrs).
 Vaginal bleeding.
 During breast feeding.

57. CLINICAL FEATURES
 WHO clinical staging system for HIV infection and
related disease in children:
1. Category-N
2. Category-A
3. Category-B
4. Category-C

60. STAGE OF AIDS
 AIDS defining opportunistic infections.
 Severe failure to thrive.
 Progressive encephalopathy.
 Malignancy.
 Recurrent septicemia or meningitis

61. OPPORTUNISTIC INFECTIONS
CD4 <500 CD4<200 CD4<50
Bacterial infections Pneumocystic carinii Disseminated
mycobacterium avium
complex (MAC)
Tuberculosis (TB) Toxoplasmosis Histoplasmosis
Herpes Simplex Cryptococcosis CMV retinitis
Herpes Zoster Coccidiodomycosis CNS lymphoma
Vaginal candidiasis Cryptosporiosis Progressive multifocal
leukoencephalopathy
Hairy leukoplakia
Kaposi’s sarcoma
Non hodgkin’s
lymphoma
HIV dementia

62. CLINICAL DIAGNOSIS
 The WHO clinical case defines pediatric
AIDS if the existence of at least two
major signs associated with at least one
minor sign in the absence of other
known cases of immunosupression such
as cancer or severe malnutrition or other
recognized etiologies.

63. MAJOR SIGNS MINOR SIGNS
Weight loss (10% of body wt) • Persistent cough over a month
Chronic diarrhoea Generalized dermatitis
Prolonged fever OR Recurrent herpes zoster
Intermittent fever for over a month Oropharyngeal candidiasis
Generalised lymphadenopathy
OTHER SIGNS AND SYMPTOMS
Persistant thrush
Lymphadenopathy
Hepatosplenomegaly
Chronic diarrhoea
Parotid gland enlargement
Leukopenia
Hepatitis
Cardiomyopathy Nephopathy

64. DIAGNOSIS

65. PREVENTION
 Give ART to women during pregnancy & labor.
 Give NVP to infant in first 6 weeks.
 Prefer elective LSCS(before onset of labor &
rupture of membrane)
 Completre avoidance of DBF from inflammed
breast.
 Avoid suctioning of new born unless liquor is
meconium stained.
 Not give mixed feeding.
 Not give bottle feed.
 Give TOP FEED (if AFASS fulfilled)

66. TREATMENT
 First line Regimens for Pregnant Women Eligible
for ART
AZT/3TC/NVP is the preferred regimen
• Stavudine to be given in the place of
Zidovudine in those having low haemoglobin
(<9G%)
• Women with contraindications to NVP
(hepatotoxicity and rash) can be given EFV
• Avoid Efavirenz during First Trimester of
Pregnancy (teratogenic in first trimester)
• Efavirenz to be used with caution and with
“thorough” counselling of the risks to foetus

67.  If mother received adequate treatment(atleast 24
wks): Daily NEVIRAPINE prophylaxis @ birth and
continue for 6 weeks
 If mother not received adequate treatment :
continue NVP for 12 wks.
 Give first dose of NVP within 6-12 hrs of delivery.
BIRTH WEIGHT NVP DAILY
DOSE(mg)
NVP DAILY
DOSE(ml)
<2000gm 2mg/kg 0.2ml/kg
2000-2500gm 10mg daily 1ml daily
>2500gm 15mg daily 1.5ml daily

68. SYPHILIS

69. INTRODUCTION
 Causative Organism – Treponema pallidum
 Transmission –Transplacental , Sexual activity

70. CLINICAL FEATURES
 Majority are symptomatic at birth
 Early Congenital Syphilis (symptoms at 1-2
months of age) :Maculopapular rash, “snuffles,”
maculopapular rash, lymphadenopathy,
hepatomegaly, thrombocytopenia, anemia,
meningitis, chorioretinitis, osteochondritis

71.  Late congenital Syphilis (symptoms after 2 years
of age)
a. Hutchinson Teeth
b. Mulberry Molars
c. Perforated hard palate
d. Rhagades (cracks or fissures in the skin
around the mouth)
e. Saber Shins
f. Sensorineural hearing loss (CN VIII)
g. Interstitial Keratitis
h. Saddle Nose

73. DIAGNOSIS
 Dark field microscopy
 FTA-Abs
 RPR
 VDRL

74. TREATMENT
 Routine serological testing for syphilis(STS) must
be undertaken in all women @ first prenatal visit.
 It shoulb repeated @ 28 wks & delivery.
 If mother with SYPHILIS(reactive VDRL/RPR &
confirmed by reactive TPHA/FTA-ABS)
Evaluate the 5 things

75. 1. Adequacy of MATERNAL Treatment
2. Examination of placenta or umblical cord for any
gross/microscopic pathology.
3. Dark field microscopy of suspecious lesions or
body fluids.
4. Clinical examination of infant for evidence of
syphilis
5. Quantitative VDRL/ RPR on infant serum

76.  SCENERIO :1
-physical abnormalities present
-VDRL/ RPR positive in 4X titre than mother
-positive dark field microscopy
PenicillinG (1 to 1.5 lakh units/kg/day)X IV X
10days
(BD for 0-7 days & then TDS thereafter)
OR Procaine Penicillin (50,000 units/kg/day)X IM X
10days
OR Benzathine Penicillin (50,000units/kg/day)X IM X
single dose

77.  SCENERIO:2
-normal physical examination
-mother not take treatment or take incomplete
treatment(<4 wks)
-VDRL/ RPR titre >4X
SAME AS SCENERIO :1

78.  SCENERIO:3
-normal physical examinatio
-titre <4x
-mother adequately treated DURING pregnancy
no treatment required OR
consider single dose of Benzathine Penicillin
if followup is uncertain

79.  SCENERIO:4
-normal physical examination
-titre <4X
-mother complete treatment BEFORE
pregnancy
no treatment required

80. Contd…

81. HEPATITIS B

82. INTRODUCTION
 Cause by Hepatitis B virus
 It is double stranded DNA virus.
 Member of the Hepadnaviridae family of viruses.
 Mother with Hepatitis B infection is no
contraindication for breastfeeding.
 HepatitisB vaccine gives 90% immunity and Ig
give only 5-10% immunity.
 90% of infected infants become chronic carriers.

83.  RISK of VERTICAL TRANSMISSION:
 1. Mother HBsAg +ve but HBeAg –ve = 5-20%
 2. Mother HBsAg +ve but HBeAg +ve = 70-90%

84. TRANSMISSION

85. TREATMENT
 Neonate born to mother with Hepatitis B infection
 @birth give Hepatitis B vaccine with HBIG (200
IU IM)
 In followup complete Hepatitis B vaccination.
 In followup @ 9-18m test for antiHBs and HbsAg
 1.if anti Hbs >/=10mIU and HbsAg negative: NO
action
 2.if anti Hbs <10 and HbsAg negative :

86. MALARIA

87. INTRODUCTION
 Congenital malaria is defined as malarial
parasites demonstrated in the peripheral smear of
the newborn from 24 hours to 72 days of life.
 Clinically apparent congenital malaria is rare in
areas in which malaria is endemic and levels of
maternal antibody are high.
 Symptoms occur 10 to 30 days postpartum

88. TRANSMISSION
 Congenital
 Intrapartum(ask about abruption)

89. CLINICAL FEATURES
 Fever
 Anaemia
 spleenomegaly
 hepatomegaly
 Jaundice
 Regurgitation
 loose stools
 poor feeding.
 Occasionally, drowsiness, restlessness, and
cyanosis may be seen.

90. TREATMENT
 Chloroquin is the drug of choice for treatment.(10
mg/kg stat followed by 5 mg /kg after 6, 24 and
48hours of the first dose)
 Primaquin is not required for congenital malaria,
because there is no persistent liver phase in
congenitally acquired infections.

91. TUBERCULOSIS

92. INTRODUCTION
 Congenital TB is defined as Tuberculosis in a new
born due to infection with MycobacteriumTB
during intrauterine stay or before complete
passage through birth canal.
 It is a very rare variant of TB
 Infection can be acquired through hematogenous
route through Umblical Vein to liver and lungs OR
aspiration of infected amniotic fluid inutero or
during delivery.
 Primary envolve organs are: GIT & LUNGS.
 Reassure mother that DBF is safe.(except if
mother is sick, non compliant to treatment, or has

93.  BEITZKE CRITERIA is use for diagnosing
Congenital TB which includes :
1. prescence of TB lesion in first week of life
2. demonstration of primary hepatic complex or
caseating hepatic granulomas.
3. confirm TB in placenta or maternal genital tract
4.Exclusion of post natal transmission after contact
investigation.

94. CLINICAL FEATURES
 Non specific
 Fever
 Lethargy/ irritability
 Not able to feed
 Respiratory distress
 Abdominal distention
 Scrotal swelling
 Ear discharge
 Lymphadenopathy
 Hepaospleenomegaly
 Skin papules

95. TREATMENT
 SCENERIO:1
 Mother diagnosed TB during or after delivery +
active infection is present + still taking ATT OR
non compliant OR treatment not yet started
Assess clinical evidence of
congenital TB
Absent
Present

96. CXR and GA X3 CXR, GA x3
and
Lumbar
Puncture
No evidence evidence present
Start INHx6 mnths Start HRZE
+ follow up
Every 4-6wks+
MTX @ 3 mnths+

97.  Scenerio : 2
 Mother diagnosed TB during or after delivery +
mother completed treatment+ no clinical evidence
of congenital TB
follow up for 6 months &
w/f clinical evidence for 4-6 wks

98. VARICELLA

99. INTRODUCTION
 Chickenpox, also known as varicella, is a highly
contagious disease caused by the initial infection
with varicella zoster virus (VZV)
 Incubation period of Varicella is 10-21 days.
 Usually rash appears on mother 5 days before
and 2 days after delivery.

101. CONGENITAL VARICELLA
SYNDROME
 Damage to BRAIN: encephalitis, microcephaly,
hydrocephaly,[24] aplasia of brain
 Damage to the EYE: optic stalk, optic cup, and
lens vesicles, microphthalmia, cataracts,
chorioretinitis, optic atrophy
 Other NEUROLOGICAL DISORDER: damage to
cervical and lumbosacral spinal cord,
motor/sensory deficits, absent deep tendon
reflexes, anisocoria/Horner's syndrome
 Damage to BODY: hypoplasia of upper/lower
extremities, anal and bladder sphincter
dysfunction

103. NEONATAL VARICELLA
 The disease results in a characteristic skin rash
that forms small, itchy blisters, which eventually
scab over.[1] It usually starts on the chest, back,
and face then spreads to the rest of the body.
 Complications may occasionally include
pneumonia, inflammation of the brain, and
bacterial skin infections.

105. DIAGNOSIS
 Clinically (characteristic appearance and site of
rash)
 Vesicular fluid can be examined with a Tzanck
smear, or by testing for direct fluorescent
antibody.
 A PCR (DNA) test of the mother's amniotic fluid
 Prenatal diagnosis of fetal varicella infection can
be performed using ultrasound

106. PREVENTION
 Hygeine Measures
 Vaccine

107. TREATMENT
 SCENERIO : 1
Chances of Developing Neonatal Disease is less
If baby is infected before rash period
As Infant has protective antibodies +
Likelihood of severe disease is low
Do not separate baby from mother +
continue DBF +
Isolate dyad from other infants
No VZIG, give acyclovir if
Baby develops rash.

108.  SCENERIO : 2
Baby develop Neonatal Disease if
infected during the rash period
in this case baby not has protective Ig +
Likelihood of severe Neonatal Disease Is high
Separate mother and baby till
maternal lesions get crusted
Give VZIg within 72Hrs of exposure
+ Acyclovir

109.  SCENERIO : 3
Chances of developing Neonatal Disease is less
If baby get infected after rash phase
Infant does not have protective Ig but likelihood of
severe neonatal disease is low
Separate mother and baby until maternal lesions
dried up
NO VZIg
Give Acyclovir if baby develops rash

110.  Give EBM if baby is separated from mother
(during phase of active lesions)
 Baby not get separated from mother if too
develops rashes.
 Separate infected DYAD from others.

111. RECAP

112. RECAP