1. Dr. Dilip Kumar Choudhary
Department of Pediatrics,
Mata Chanan Devi Hospital,
New Delhi

2. Diagnosing Congenital Infections
 Thorough examination of infant
 Good maternal/prenatal history
 Directed labs/studies based on most likely diagnosis

3. Suspect congenital infections in neonates with:
• IUGR/ SGA
• Hematological (anemia, neutropenia,
thrombocytopenia, petechiae, purpura).
• Ocular sign- cataract, chorioretinitis,
keratoconjunctivitis, glaucoma,
microphthalmos
• CNS- microcephaly, hydrocephaly,
intracranial calcification, aseptic meningitis.
• Liver- hepatitis, HSM, jaundice.
• Nonimmune hydrops.

4. Investigations helpful for diagnosis

5. 1.Fetal ultrasonography
• IUGR
• Hydrops
• Placentamegaly
• Hydrocephalus
• Microcephalus
• Intracranial calcifications
• Hepatosplenomegaly
• Echogenic bowel
• Hepatic calcifications
• Meconium peritonitis
• Ascites
• Limb reduction

6. 2.Lab tests-
• CBC, peripheral smear
• LFT (transaminase levels and bilirubin level- direct
and indirect)
• Cerebrospinal fluid examination (cells, protein,
microbiological)
• Maternal and infant sera for microbiological testing

7. 3.Ophthalmology & audiology assessments
-Chorioretinitis
-Cataract
-SNHL

8. 4. Imaging studies-
• Cranial ultrasound, CT scan, MRI
-CMV,
-Toxoplasmosis.
• Skeletal Survey
-Syphilis,
-Rubella

9. 5.Culture-
1. Rubella- isolation from nasal/ oropharungeal
secretions
2. CMV- urine culture +/-
3. HSV -viral culture(HSV 1 & 2) from vesicular
swab, CSF, whole blood.

10. 6.Molecular assay-
• CMV- PCR DNA
 rapidly replacing viral culture as the most sensitive and
efficient method for detection of CMV (urine, saliva, serum,
liver tissue)
 saliva PCR now considered the investigation of choice to
detect CMV
• HSV viral PCR-DNA and rapid immunofluorescence
assays (IFA)

11.  An attempt to diagnose TORCH infection with
single serum sample gives USELESS
information.
 Test for each potential etiology individually.
 IgM- New infection, produced in acute/ late phase
of primary infection, appear immediately
after infection and usually persist till 8-12
wks, may persist for 1-2 yrs.
 IgG- Old infection, appear 1-2 weeks after
infection, fall within 1-2 months,
persist lifelong.

12. Ig M Ig G
No exposure - -
Acute infection + +/-
Past infection - +

13. IgG Avidity
 Measures the functional affinity of the IgG antibody in the
response to infection.
 The maturation of antibody avidity over time can be used to
discriminate between primary/ acute and non-primary/
remote infection.
 Low avidity primary/ acute infection
 High avidity remote infection

14.  T- toxoplasmosis
 O- other infections
 R- rubella
 C- cytomegalovirus
 H- herpes simplex virus
 Other infections- syphilis, varicella zoster, Parvo
virus B19, HIV, HBV.

16.  Caused by Toxoplasma gondii- an obligate,
intracellular protozoan parasite.
 Cat is the only definitive host, usually asymptomatic.
During acute infection, millions of oocysts are shed
daily in stool for ≥2 wks, which remain viable in soil
for over 1 yr. other animals infected by ingesting
oocyst resulting in tissue cysts.
 Human and other animals are intermediate host.
 Women without antibodies are at risk for acute
toxoplasmosis during pregnancy.

17.  Transmission-
(a) Feco-oral route- food, water or soil contaminated with
oocysts or through ingestion of cysts in uncooked meat.
The meat products most often implicated are pork and
lamb.
(b) Congenital infection- through transplacental route.

19.  Normal and adults- susceptible for acute infection if they
lack antibody to the organism. After acute parasitemia,
the organism form tissue cysts, which probably persists
for life in multiple organs including muscle and brain.
 Human congenital infection-
• Parasite from maternal circulation invade and multiply
with in placental cells before reaching fetal circulation.
This delay in transmission from placenta to the fetus is
k/as prenatal incubation period range from 4-16 wks.
• Gestational age ∝
𝐼𝑛𝑓𝑒𝑐𝑡𝑖𝑜𝑛 𝑟𝑎𝑡𝑒
𝐷𝑖𝑠𝑒𝑎𝑠𝑒 𝑠𝑒𝑣𝑒𝑟𝑖𝑡𝑦

20.  Infection in 1st trimester without prenatal therapy, most
fetuses die in utero or in neonatal period or have severe CNS
and ophthalmological disease.
 Infection in 2nd and 3rd trimester most fetuses in 2nd
trimester and almost all infected in 3rd trimester have mild or
subclinical disease.
 So period of highest risk for severe congenital disease is
between 10-24 wks.
 Congenital infection due to serologic relapse in chronic
maternal infection is extremely rare. Maternal immune
dysfunction including HIV should be suspected.

21. Clinical manifestation-
 Asymptomatic in >90% women.
 Symptoms- painless lymphadenopathy and chorioretinits.
 Fetal finding on USG- hydrocephalus, brain or hepatic
calcification, hepatomegaly and ascites.
Diagnosis-
(A) Maternal tests:
(i) Screening- IgG and IgM
IgG- after acute infection detectable in 1-2 wks, peak in 3-6
months, and persists at low titre for life.
IgM- appear within 2wks, peak at 1 month and usually decline
within 6-9 moths. However may persist for 1yr, so doesn’t
necessarily indicate an acute infection.

22. (ii) Confirmatory test-
 A series of IgG tests can differentiate acute vs remote
infection.
 IgG Avidity testing- IgG produced in early infection
have low avidity but avidity increases with time. The
presence of high avidity antibodies indicates that
infection occurred 12-16 wks prior, thus helpful in early
pregnancy.
 Rising IgG titre indicates acute infection.
(B) Fetal tests-
(i) Ultrasound- monthly in suspected acute infection.
(ii) Amniotic fluid PCR- to diagnose fetal infection,
when there is serological evidence of acute infection.

23. Treatment:-
 In suspected or probable cases- antenatal maternal
therapy to prevent or prevent fetal infection should
extend until delivery, even with a negative PCR result.
(A) Infection <18 weeks:
• Spiramycin + monthly USG.
• Spiramycin prevent transplacental transmission of
Toxoplasma but doesn’t treat fetus. However if
transmission occurs, disease severity may be unaltered.
• In USG if any fetal anomaly detected, advise MTP.
• Amniocentesis in 2nd trimester-
if no infection detected- continue spiramycin and USG
if infection detected- offer MTP

24. (B) Infection >18 weeks
• Start Spiramycin
• USG and Amniocentesis for any evidence of fetal
infection / damage
• Sulfadiazine, Pyrimethamine and Folinic acid. These
also recommended if fetal infection is confirmed by
amniotic PCR.

25. CLINICAL MANIFESTIONS
4 Pattern of presentation:-
(a) Subclinical infection-
• In 80% - 90%
• Without overt signs of infection at birth but may have
retinal and CNS abnormalities.
(b) Neonatal symptomatic disease- usually severe,
generalized and neurological signs are present.
Generalized symptoms: fever, HSmegaly, jaundice.
CNS: hydrocephalus, microcephaly, seizures, cerebral
calcification, chorioretinitis.

26. (c) Delayed onset- seen in preterms, within 3 months of
age, behave like neonatal symptomatic disease.
(d) Sequelae or relapse- in infancy through adolescence of
a previously undiagnosed infection, in 24-85% of infected.
Most commonly Eye (chorioretinitis) or
Neurological (seizures, late CSF obstruction)
Peak presentation of chorioretinitis from congenital
infection occurs between 15 to 20 years of age.

27. SPECIFIC SYMPTOMS
classical triad
• Hydrocephalus
• Chorioretinitis and
• Intracranial calcification
Others- HSM, persistent
conjugated
hyperbilirubinemia,
thrombocytopenia,
maculopapular rash.

28. NEONATAL INFECTION DIAGNOSIS:
(A) Serological tests:
IgG- transplacental IgG disappear by 6 to 12 months of
age. For patient with seroconversion or 4 fold rise in IgG
titre perform IgM testing.
IgM and IgA- doesn’t cross placenta, they useful
determining congenital infection..
(B) Other diagnostic tests:
(i)Lab- CBC (TLC ↑/↓, Eosinophilia, Thrombocytopenia)
LFT, G6PD(prior to starting Sulfadiazine).
(ii) OAE/ Auditory brainstem response.
(iii) NCCT Head- calcification (periventricular, basal
ganglia, scattered in white matter), hydrocephalus due to
periaqueductal obstruction, cerebral atrophy.

29. TREATMENT OF NEONATAL INFECTION
Multidisciplinary approach
• Pediatrician for medical management
• Ophathalmologist for retinal evaluation
• Neurosurgery for hydrocephalus management
Medications:
• Regardless of symptoms to prevent high incidence of
sequelae.
• Improved outcome if treated in the first year of life. Don’t
eradicate T. gondii and primarily act against tachyzoite
form not tissue cyst (especially from neural tissue and the
eye).
• Extended therapy until 1yr of age.

30. Drug Doses Side effect
Pyrimethamine
(1mg/kg/dose)
BD for 2 days
OD for 2 to 6 months then
Alternate day for next 6 months
• Bone marrow suppression
(neutropenia >>
megaloblastic anemia,
thrombocytopenia).
• GI distress
• Convulsions
• Tremor
Sulfadiazine
(50 mg/kg/dose)
BD till 1 year of age • Bone marrow suppression
• Crystalluria, Hematuria
• Hypersensitivity
Folinic acid
(10mg)
Alternate day until one week
after stopping pyrimethamine
Prednisolone
(0.5 mg/kg/dose)
BD for active CNS disease or
active chorioretinitis.
Stop when symptoms resolve
• GI distress
• Infection
• Cushingoid face
• Easy bruisability

31. Monitor-
 CBC twice weekly
 Ophthalmologic examination- every 3 months till 18
months, and then yearly.
Outcome-
 Chorioretinitis: resolve within 1 to 2 wks, don’t relapse
during therapy, may relapse after treatment, often during
adolescence. Visual impairment at 5 yrs of age is a
prominent sequela.

32. Case Scenario
Term baby delivered to primigravida mother, no perinatal depression,
Birth wt 1.9 kg, Head circumference 29 cms (< 3rd centile), develops
purpuric rash all over face & body and jaundice on D1 of life.
O/E-
Eye- leucocoria, large cornea.
P/A- hepatosplenomegaly.
CVS- systolic murmur pulmonary area,
Course- started on phototherapy for jaundice, developed respiratory
distress since birth requiring oxygen, later on DOL3 developed
seizures multifocal clonic requiring anticonvulsants.
Investigations- CBC- platelet =60,000 and mild leucopenia.
Serum bilirubin- total of 16mg/dl with direct fraction 4mg/dl
Sepsis screen was negative, Blood culture showed no growth
Chest X - ray revealed patchy infiltrates s/o pneumonia
Echo showed pulmonary stenosis
OAE Test done – Bilateral SNHL
TORCH report - awaited

34.  Cause self limiting infection in adults and susceptible
children but effect on fetus can be devastating.
 Epidemic occur every 6 to 9 yrs.
 Fetal infection can occur at any time, but early gestation
infection results in multiple organ anomalies.
 Gestational age ∝
𝐼𝑛𝑓𝑒𝑐𝑡𝑖𝑜𝑛 𝑟𝑎𝑡𝑒
𝐷𝑖𝑠𝑒𝑎𝑠𝑒 𝑠𝑒𝑣𝑒𝑟𝑖𝑡𝑦
 Infection at 10 wks100% of infected have cardiac
defects and deafness
13-16 wks 33% deafness
after 20 wks no anomaly

35.  Clinical features of CRS (Cong. Rubella Syndrome)
Triad of
Ocular –cataract
SNHL
Cardiac- PDA> pulmonary artery stenosis

36. Maternal infection:
 Clinical features- within 2-3 wks of exposure prodromal
symptoms (eg. Low grade fever, malaise, myalgia,
coryza, conjunctivitis) and cervical lymphadenopathy
1-5 days later macular or maculopapular rashes, which
disappear within 5-7 days.
 Confirmation- by demonstration of ≥4 fold rise in serum
IgG titre when measured at the time of symptoms and
2wks later.
 Maternal disease is mild and self limiting.

37. Rubella exposure to pregnant woman(measure rubella IgG)
Already sero+ve known to be Immune status
(immunization/ sero-ve uncertain but
Prior infection) (non immune) exposure +nt
No risk to fetus Sr. titre 3-4wks Sr. titre ASAP
after exposure (within 7-10days)
+ve - ve +ve -ve
Infection No infection already Repeat
immune after 3wks
-ve +ve
No infection Infection

38. Congenital rubella infection:
i. Detection of rubella specific IgM in blood
ii. Persistent (no decline) rubella specific IgG over time
iii. Isolation of rubella virus from urine or oropharynx
secretion.
Treatment:
 No specific therapy to halt the progression of most of the
complication of CRS.
 Close follow up if early gestation infection is suspected
or the timing of infection is unknown.
 Maternal infection is confirmed
Gestation <20 wks Gestation >20wks
Discuss for MTP reassure parents, no risk of
abnormalities

40.  Reservoir only humans, lifelong infection.
 Present in saliva, urine, genital secretion, breast milk
and blood/ blood products.
 Primary infection (acute infection)- usually
asymptomatic in older infants, children, and adults, may
present with mononucleosis like symptoms eg.
prolonged fever and a mild hepatitis.
 Latent infection- asymptomatic unless host become
immunocompromised.
 Very common, with seroprevalence 50-85% by 40 yrs
age.

41.  Primary CMV infection occurs in 1-3% of pregnant
women, with a fetal attack rate of 30-40%.
 80% of infants with congenital CMV infection will
remain asymptomatic.
 Vertical transmission can occur at any time, infection
during early gestation carries higher risk of severe fetal
disease.
 More common among HIV-1 infected infants, so
screening for CMV in HIV exposed infants is advised.

42. CLINICAL FEATURES:
(A)Symptomatic congenital disease-
Acute fulminant infection- 30% mortality
 Signs- petechiae/ purpura, Hepatosplenomegaly, juandice,
prematurity(1/3), IUGR(1/3), and “blueberry muffin
spots” reflecting extra-medullary hematopoiesis.
 Lab- CBC(anemia, thrombocytopenia),
LFT(↑transaminases and bilirubin)

43. Without life-threatening complication-
 IUGR or disproportionate microcephaly with or without
intracranial calcification (periventricular area).
 Other CNS- ventricular dilation, cortical atrophy,
chorioretinitis, developmental abnormalities and
neurological dysfunction.
 SNHL most common sequela (60% symptomatic and
5% asymptomatic infants at birth), so any infant failing
newborn hearing screening should be screened for CMV
infection.

44. (B) Asymptomatic congenital infection-
• Present in later infancy
• Developmental abnormalities, hearing loss, MR, motor
spasticity and acquired microcephaly.
(C) Perinatally acquired CMV- can be acquired from-
• Intrapartum exposure within the maternal genital tract
• Postnatal exposure to infected breast milk
• Infected blood or blood products
• Nosocomially urine or saliva
Almost all fullterm remain asymptomatic
In preterm infants  acute infection syndrome
(neutropenia, anemia, HSM, lymphadenopathy, hearing
loss).
(D) CMV pneumonitis-
In preterm infants <4 months old.

45. Diagnosis-
 CMV infection diagnosis is made if CMV is identified in
urine, saliva, blood or respiratory secretion.
 Congenital infection- if found in first 2 wks
 Perinatal infection- if negative in first 2wks and positive after
4 wks of life.
 Blood is the earliest specimen to become positive and urine-
highest sensitivity for diagnosis of CMV (as CMV is
concentrated in urine).
 -ve blood can’t rule out CMV but –ve urine test in an
untreated symptomatic infant for 4 wks or more rule out
infection.

46. Diagnostic techniques:
1.CMV PCR- in urine or blood. Sensitivity is high for
urine, but –ve PCR in blood doesn’t rule out infection.
2. CMV IgG and IgM:- IgG -ve in both maternal and
infant sera, excludes congenital CMV infection.
If IgG +ve in infant sera
uninfected infant infected infant
IgG decline within continue to produce
1 month and no the IgG through out
detectable by 4-12 the same period
months
-CMV specific IgM have limited specificity

47. Treatment
 With ganciclovir has been studied in many clinical trial
 6 wks of ganciclovir therapy can limit hearing loss and
improve developmental outcome in symptomatic infants
(CMV retinitis, CMV pneumonitis, CMV Hepatitis)
 Infants with severe perinatal CMV infection following breast
milk ingestion have been treated with ganciclovir.
 Evidences suggest 6 months of oral valganciclovir more
effective and less toxic than iv ganciclovir in infants with
symptomatic infection.

48. Screening:
 Because only 1-3% of women acquire primary CMV
infection during pregnancy with overall risk of symptomatic
fetal infection is only 0.2%, so screening of women at risk
generally NOT recommended.
 CDC recommendations -
• Pregnant women practice hand washing with soap and water
after contact with diapers or oral secretions and not to share
food, utensils, toothbrushes, pacifiers with children.
• Women who develop mononucleosis like illness during
pregnancy should be screened for CMV infection and
counselled about fetal risk.
• Antibody testing confirms prior infection.
• The benefits of breastfeeding overweigh the minimal risk of
acquiring CMV.
• No need to screen for CMV or exclude CMV excreting
children from schools or institutions.

50.  Life long infection, two types of virus.
 HSV-2 is the predominant cause (75-80%) of neonatal
HSV (because most likely to recur in genital tract), but
both types produce clinically indistinguishable disease.
 HSV-2 the predominant cause of recurrent genital
disease, seroprevalence increases with age and number
of sexual partners.
 Infection in newborn- direct exposure, most commonly
in perinatal period from maternal genital disease.

51. Transmission:
(A) Intra-partum transmission-
• Most common cause of neonatal HSV(95%).
• Maternal antibodies- important and is associated with
decreased risk of fetal or neonatal transmission. When Ab
present, the risk of acquisition is very low (<1%).
(B) Antepartum transmission-
• Documented but uncommon, true risk of early trimester
infection is unknown
• If maternal primary infection occur –
-near delivery, 30-50% of infants will acquire HSV,
-prior to pregnancy (recurrent) or in first half of
pregnancy, <1% infants get infected.
(C) Postnatal transmission-
• Potential sources- symptomatic and asymptomatic oro-
pharyngeal shedding by parent, hospital personnel, and
maternal breast lesions.

52. Clinical manifestations:
(A)Localised SEM (skin, eye and mouth infection)- 50%
• Vesicles typically appear on the 6th to 9th day of life
• Cluster of vesicles on the presenting part of the body
(extended direct contact).
• Significant morbidity despite in the absence of signs of
disseminated disease.
• Up to 10% later shows neurologic impairment and infants
with keratoconjunctivitis can develop chorioretinitis,
cataract and retinopathy.
• So ophthalmologic and neurologic follow up
• ≥ 3 recurrences of vesicles, reflecting poor cellular or
humoral viral control, have increased risk of neurologic
complications

54. (B) CNS infection-
• 1/3 of neonates with HSV present with encephalitis in the
absence of disseminated disease.
• Symptomatic at 8-17 days of life
• Hematogenous spread to CNS
• lethargy, seizures, temperature instability, hypotonia.
• 2/3 have impaired nurodevelopment
(C) Disseminated disease-
• Most severe form of neonatal HSV, accounts for 22% of
all neonatal HSV.
• Mortality >50%, pneumonitis and fulminant hepatitis are
associated with greater mortality.
• Present with shock, seizures, respiratory distress,
respiratory failure, DIC.

55. Diagnosis-
 Viral isolation or DFA (Direct Fluorescent Antibody)-
• For muco-cutaneous lesions, tissue from vesicle
scrapping, placed appropriate culture medium.
• Disseminated disease with the absence of vesicular
rashes, virus can be isolated from oropharynx, naso-
pharynx, conjunctiva, stool, urine and CSF.
• HSV encephalitis-
(i) CSF examination (increased protein and pleocytosis).
(ii) Viral isolation from CSF is successful in 40% of
cases, and detection rate by PCR may be up to 100%.
(iii) EEG, CT/MRI also useful in diagnosis of HSV
encephalitis.

56. Treatment – Acyclovir
• The timing of therapy is critical.
• It is selective inhibitor of viral replication with minimal side effect
on the host.
• Disease limited to skin, eyes and mouth- 20 mg/kg 8 hrly for 14
days.
• For CNS or disseminated disease- 21 days or longer if CSF PCR
remains positive
• Ocular involvement- ophthalmologic evaluation and treatment with
topical agents + parenteral therapy.
Prevention-
• Known HSV-2 seronegative woman should avoid sexual intercourse
with known HSV-2 seropositive partner in the third trimester.
• HSV- 2 primary infection during pregnancy- 10 days course of
acyclovir to woman.
• Women with HSV-2- test for HIV (as HSV-2 seropositive person
have two fold greater risk for acquisition of HIV).
• Delivery- offer acyclovir near term until delivery to women with
clinical or serological evidence of HSV-2, establishing vaginal route
of delivery if no visible lesions.

58.  One of the most common cause of acute and chronic
hepatitis worldwide.
 Risk of chronic infection ∝
1
𝐴𝑔𝑒
90% carriage rate following infection in neonates.
 Incubation period- 120 days ( range 45 to 160 days).

59. Transmission from infected mother to newborn-
(i)Primarily from exposure to maternal blood at the time of
delivery.
(ii)Transplacental transfer appears to occurs in Taiwan
(high chronic carrier rate), hasn’t found in other parts of
world.
• When acute maternal infection occurs in the 1st and 2nd
trimester, little risk to the newborn (antigenemia is
cleared by term and anti- HBs is present).
• Acute maternal infection during late pregnancy or near
term, may result in 50% to 70% transmission rate.
(iii)Breast feeding- although HBsAg can be detected in
breast milk, but this mode is very uncommon in developed
countries. The risk is negligible in infants who have
received HBIG and hepatitis vaccine

60. Prevention
 Immunoprophylaxis for newborn at risk of infection.
 3 doses before the age of 18 months.
 The schedule begins during newborn period
2nd dose- 1-2 moths later
3rd dose at the age of 6 months for infants of mothers with
HBsAg +ve or unknown status and between 6-18months
for infants of mothers with –ve HBsAg status.
 Recommended that all pregnant women be screened for
HBsAg. Screening should be done in early gestation. If
the test result is negative, no further evaluation is needed.

62. Hepatitis B vaccine schedule for infants.
From: Pickering MD, FAAP LK, editors. Red book: 2012
report of the Committee on Infectious Diseases. American
Academy of Pediatrics; 2012.

64.  Virus causing varicella (chicken pox) is also responsible for
herpes zoster (shingles).
 Chicken pox results from primary infection of V-ZV infection,
following which virus may remain latent in sensory ganglia
(dorsal root ganglia).
 Zoster results from reactivation of latent virus later in life or if
the host become immunosuppressed.
 Primary mode of transmission- respiratory droplets, can spread
through contact with vesicular lesion.
 Contagious period 2 days before and 5 days after the onset of
rashes.
 Incubation period- 10-21 days

65.  Varicella as well as zoster are uncommon in pregnancy.
 Risk of congenital varicella syndrome (CVS) is
-0.4% if maternal infection in first 12 wks of pregnancy
- 2% for infection in 13-20 wks.
 If rashes develop in newborn within 10 days, it is
presumed to result from in utero transmission.
 Peripartum varicella infection in mother:
- 25% of newborn develop varicella
- Severe disease if maternal varicella occurs 5 days before
and 2 days after delivery.
- 30% mortality.

66. Clinical features:
(A)Congenital varicella
syndrome- cicatrical skin
scarring in a zoster like
distribution (cicatrix) , limb
hypoplasia, ocular defects,
CNS abnormalities (cortical
atrophy), IUGR, early death.
Most commonly occurs with
maternal V-ZV infection in 7-
20 wks of gestation.

67. (B) Postnatal varicella- post natal exposure in newborn
period, generally mild disease.
Varicella has been detected in breast milk, so it may be
prudent to defer breastfeeding at least during the period,
mother is likely viremic or infectious.

68. Treatment:
(A)Congenital infection before perinatal period-
unlikely to have active viral disease, so antiviral therapy is
NOT indicated.
(B)Perinatal varicella-
-VZIG 125 Units itramuscular, alternative if VZIG is
unavailable IVIG 400mg/kg within 96 hrs of exposure.
-Therapy with acyclovir (10mg/kg IV 8hrly) is
recommended when lesions develop

69. MCQs
Q1. Forchheimer spots is found in-
(a)Measles (b) German measles
(c) Herpes (d) toxoplasmosis

70. Explanation 1.
 In children first manifestation of rubella (German
measles or 3 day measles) is usually the rash.
 Begins on the face and neck as small, irregular, pink
macules that coalesce, and spread centrifugally to
involve the extremities, where it tends to occur as
discrete macules.
 About the time of onset of rash, examination of
oropharynnx may reveal tiny, rose- colored lesion
(Forchheimer spots) or petechial hemorrhages on the
soft palate.

71. Q2. “fever blisters” is most common manifestation of-
(a) Parvo virus
(b) Recurrent HSV-1
(c) Recurrent HSV-2
(d) Varicella
Q3.Herpes whitlow is-
(a) HSV infection of paronychia
(b) HSV infection of scalp
(c) Genital herpes
(d) None of the above

72. Explanation 2.
Fever blister (cold sores) are the most common
manifestation of recurrent HSV-1 infection, most common
site of herpes labialis is vermilion border of the lip, but
may occur on the nose, cheek, or oral mucosa.
Explanation 3.
Herpes Whitlow is HSV infection of fingers or toes,
strictly speaking it refers to HSV infection of the
paronychia.
Among children, most commonly seen in infants and
toddlers who suck the thumb or fingers and who are
experiencing either a symptomatic or a subclinical oral
HSV-1 infection

73. Q4. What is breakthrough varicella?
(a) Epidemic of varicella, due to wild type virus.
(b)Varicella rashes occurring 14-42 days after vaccination .
(c)Varicella disease in a person vaccinated more then 42
days before rash onset.
(d) Varicella disease in a person vaccinated within 14 days
before rash onset.
Q5. what are the indications of varicella-zoster
immunoglobulin (VZIG)?

74. Explanation4.
 One dose of varicella vaccine >97% effective in preventing
moderate and severe varicella and 85% effective in preventing
all disease after exposure to wild type V-ZV.
 Breakthrough varicella is disease that occurs in the person
vaccinated more than 42 days before onset of rashes and is
caused by wild type virus.
 About 1 of every 5 children who received one dose of vaccine
may experience breakthrough varicella.
 It is usually mild with atypical rash (predominantly
maculopapular, <50 lesions, shorter duration, little or no
fever).
 Less contagious, but contagiousness ∝ number of lesions.
Typical breakthrough case (<50 lesions) is 1/3 as contagious as
unvaccinated , whereas ≥50 lesions are as contagious as wild
type cases.
 So children with breakthrough disease should be considered
contagious and should be excluded from school.

75. Explanation 5.
Indications of VZIG (varicella-zoster Immunoglobulin)-
1.All premature infants born <28 wks of gestation to a
mother with active varicella at delivery (even if the
maternal rash has been present for >1 wk).
2.Newborn whose mother develop varicella during the
period of 5 days before to 2 days after delivery

76. Q6. Peak presentation of chorioretinitis from congenital
infection occurs at the age of ?
(a) 4-5 years
(b) 5-7 years
(c)7-10 years
(d) 15-20 years
Q7. Triad of congenital Toxoplasmosis infection is-
(a) Chorioretinitis, PDA, SNHL
(b) Chorioretinitis, PDA, hydrocephalus
(c) Chorioretinitis, hydrocephalus, Periventricular
calcification
(d) PDA, SNHL, Periventricular calcification

77. Q8. A full-term newborn, the physician notes mild hepatomegaly.
Other physical findings are normal, including head
circumference and appearance of the retinas. A urine culture
grows cytomegalovirus (CMV). Results of head ultrasonography
are normal. Subsequent testing discloses no metabolic disorders.
The deficit most likely to occur in the next year is:
(a) Visual loss
(b) Hearing loss
(c) Cirrhosis
(d) Patent ductus arteriosus
(e) Immunoglobulin deficiency

78. Explanation 8.
Asymptomatic congenital CMV infection is likely a
leading cause of sensorineural hearing loss, which occurs
in 7-10% of all infants with congenital CMV infection,
whether symptomatic at birth or not.

79. Q9. A pregnant woman, at 15 wk of gestation, brings her 5
yr old son for evaluation of fever and cervical
lymphadenopathy( nontender and non suppurated). They
have kitten at home. The child and the mother regularly
cleaned the kitten’s litter pan together. All of the following
diagnostic tests to identify family members with or at risk
for toxoplasmosis are indicated EXCEPT:
(a) Sabin-Feldman dye test to measure T. gondii-specific
IgG in the mother’s serum
(b) Sabin-Feldman dye test to measure T. gondii-specific
IgG in the 5 yr old boy’s serum
(c) IgM ELISAAC/HS and avidity tests to measure T.
gondii-specific antibodies in the mother’s serum
(d) Fetal ultrasound examination
(e) CT of head and neck for the 5 yr old boy

80. Explanation 9.
-The Sabin-Feldman dye test is sensitive and specific. It
measures primarily IgG antibodies.
-The differential agglutination test (HS/AC) compares
antibody titers obtained with formalin-fixed tachyzoites
(HS antigen) with titers obtained using acetone-or
methanol-fixed tachyzoites (AC antigen) to differentiate
recent and remote infections in adults and older children.
- Fetal ultrasound examination, performed every 2 wk
during gestation, beginning at the time acute acquired
infection is diagnosed in a pregnant woman.

81. TAKE HOME MESSAGE

82. Congenital infection Diagnosis
Toxoplasmosis - Seroconversion or 4 fold rise in IgG titre
- Toxo specific IgM +ve
Rubella - Detection of rubella specific IgM in blood
-Persistent (no decline) rubella specific IgG over time
-Isolation of rubella virus from urine or oropharynx
secretion
CMV CMV is identified in urine, saliva, blood or respiratory
secretion.
-Urine has the highest sensitivity for diagnosis of CMV
-CMV PCR- in urine or blood
-CMV specific IgM have limited specificity
HSV For mucocutaneous lesions- Viral isolation or DFA
(Direct Fluorescent Antibody
-HSV encephalitis- CSF examination and Viral isolation
from CSF

83. THANK YOU FOR THE
PATIENT HEARING !!!!