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DNB pediatric
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ATYPICAL INFECTIONS
DR. ATUL KULKARNI(MD)DR. MANDAR HAVAL(DCH DNB FELLOW
in NEONATOLOGY)
Definitions
• congenital – contracted in utero
• perinatal– from completion of 28 weeks gestation until 1-4
weeks after birth• postnatal
Common Infecting Agents
• Bacteria
• Viruses
• Protozoa
• Chlamydiae/Mycoplasma/Rickettsia
• Fungi
CASE 1
• 10 day FTND with fever, respiratory distress with cynosis.
• Had a history of conjuntivitis on day 5 and is on topical treatment
• Examination – tacypnea, cynosis • RS- bilat –crepts no wheese• Investigation –CBC – Eosinophilia• Xray –pnemonia
Chlamydia trachomatis
• Acquisition occurs in some 50% of infants born vaginally
to infected mothers and in some delivered by CS with
intact membranes
• The nasopharynx is the common site of primary
multiplication in the infant
– conjunctivitis in 15-50%
– pneumonia in 5 - 20%
Chlamydia trachomatis
• Pneumonia occurs between 1-3 months of the age and is
always insidious with persistent cough, tachypnea and
absence of fever
• Absence of fever and wheezing helps to distinguish
Chlamydia trachomatis from RSV.
DIAGNOSIS TREATMENT• Isolation of Chlamydia
in conjunctival and Nasopharynx
• Direct fluorescent antibody
• PCR
• Oral erethromycin 40mg/kg/day divided into 4 divided dose for 14 days
CASE 2
• 30wks Preterm on ventilator 10 days O2 dependent even
after 3wk x-ray bilat opacities
• Vaginal delivery
• Mother had history of chorioamniotis
• Baby required reintubation
• ?BPD
• CBC –N / BLOOD C/S Serile
Ureaplasma Urealyticum
• M.hominis and Ureaplasma Urealyticum have also been described to cause
- neonatal conjunctivitis
- lymphadenitis
- pharyngitis
- pneumonitis
- osteomyelitis
- brain abcess
- intraventricular hemorrhage and hydrocephalus
Ureaplasma Urealyticum
• Ureaplasma urealyticum has been recoverd from the
cervical culture of the pregnant women and implicated as
a possible cause of chorioamniotis, preterm, BPD
• PCR is diagnostic
• ERETHROMYCIN to prevent BPD
CASE 3
• 1 day preterm child had genaralised swelling, pale,
tacypnea
• Examination – generalized edema , pallor, tachycardia,
hypotension,hepatomegaly.
• Investigation –Hb 6.2 g/dl , Retic – 0.8%
USG – ascitis & pleural effusion
HYDROPS FETALIS
Parvovirus B19
• When acquired by a non-immune pregnant woman the transmission rate to the foetus is about 33%
• Anaemia , cardiomyopathy, hepatic dysfunction, hydrops foetalis - foetal death may occur
• Diagnosis by specific IgM
• Exchange transfusion in utero is appropriate therapy in severe cases
• IVIG (limited success)
CASE 4
• 3 days old IUGR came with a complain of jaundice , and convulsion.
• Mother having an 1 abortion history.
• On examination - icteric , hepatosplenomegaly, macrocephaly. Chorioretinitis
• Investigation – TLC – 3800 (E – 14% ) PLAT- 102000/cumm CRP – neg Blood culture – negative
CT HEAD- calcifications
INTRACRANIAL CALCIFICATION
Chorioretinitis of congenital toxo
Toxoplasmosis Clinical Manifestations
• Most (70-90%) are asymptomatic at birth• Classic triad of symptoms:• Chorioretinitis
– Hydrocephalus– Intracranial calcifications
• Other symptoms include fever, rash, HSM, microcephaly, seizures, jaundice, thrombocytopenia, lymphadenopathy
• Initially asymptomatic infants are still at high risk of developing abnormalities, especially chorioretinitis
Diagnosis Treatment• Maternal IgG testing• Culture from placenta,
umbilical cord, infant serum
• PCR testing on WBC, CSF, placenta– Not standardized
• Newborn serologies with IgM/IgA
• Symptomatic infants– Pyrimethamine
and sulfadiazine Treatment for 12 months total
CASE 5
• 7th day preterm baby came with rash, jaundice, abdominal distention , pallor ,the child had convulsion next day
• On examination- 2kg ictric , hepatosplenomegaly, purpura over face and abdomen.
• Investigation – CBC (HB 9.2gm/dl; PLAT- 89000) SGPT – 486; Bilirubin 17.6 D- 8.4 CRP – NEG BLOOD CUL – NO GROWTH CSF – few lymoho
CMV Clinical Manifestations• Early Congenital Acute fulminant infection involving multiple organ
system - petechiae and purpura(79%) - HSM (74%) - jaundice(63%) & prematurity
• Early onset symptomatic without life threatening - IUGR or disproportionate microcephaly(48%) - Intracranial calcification - ventricular dilatation, cortical atrophy,
lissencephaly, pachygyria (RARE)
• Asymptomatic Congenital (commonest)
• Perinatally Acquired
• Cmv Pneumonitis
• Transfusion Acquired Cmv Infection
Ventriculomegaly and calcifications of congenital CMV
Diagnosis
• CMV PCR from urine or saliva in 1st 3weeks of life– Afterwards may
represent post-natal infection
• Cmv IgG IgM – limited success
• Ganciclovir x6wks in symptomatic infants
• Treatment currently not recommended in asymptomatic infants due to side effects
• Valgancyclovir
CASE 6
• 8TH day IUGR had rash, refusal to feed
• Examination – , Pale, purpuric spots all over, cataract ,
continuous murmur in pul. Area
• Investigation – Hb – 10.5gm/dl, PLAT – 55000/cumm,
2D echo – PDA , CRP/BLOOD CULTURE - WNL
Clinical Manifestations
• Sensorineural hearing loss (50-75%)
• Cataracts and glaucoma (20-50%)
• Cardiac malformations (20-50%)
• Neurologic (10-20%)
• Others to include growth retardation, bone disease, HSM,
thrombocytopenia, “blueberry muffin” lesions
Rash Cataracts CHD (PDA) Blindness Neurosensory
deafness Microcephaly &
mental retardation
CONGENITAL RUBELLA
“Blueberry muffin” spots representing
extramedullary hematopoesis
Diagnosis Treatment• Can isolate virus from
nasal secretions– Less frequently from
throat, blood, urine, CSF
• Serologic testing– IgM = recent postnatal
or congenital infection– Rising monthly IgG
titers suggest congenital infection
• Prevention…immunize, immunize, immunize!
• Supportive care only with parent education
CASE 7
• 21 days old newborn – not moving both LL.• H/O 2 SB ,1 Neonatal death• Home delivery.• O/E - 2.5 KG ,Pallor ++,hepatospleenomegaly,• LL –Swelling of both knee joints• CBC -HB 8gm ,CRP –neg ,Blood c/s –sterile,• X –ray - periostitis• Diagnosis -
Periostitis
Clinical Manifestations
• Fetal:– Stillbirth– Neonatal death– Hydrops fetalis
• Intrauterine death in 25%
• Perinatal mortality in 25-30% if untreated
Clinical Manifestations
• Early congenital (typically 1st 5 weeks):
– Cutaneous lesions (palms/soles)
– HSM
– Jaundice
– Anemia
– Snuffles
– Periostitis and metaphysial dystrophy
– Funisitis (umbilical cord vasculitis)
Clinical Manifestations
• Late congenital:– Frontal bossing– Short maxilla– High palatal arch– Hutchinson teeth– 8th nerve deafness– Saddle nose – Perioral fissures
• Can be prevented with appropriate treatment
CASE 8
• 25 days baby had presented with severe respiratory distress with cyanosis
• h/o contact with family member with resp infection.
• Examination –febrile, resp.ditress, cyanosis
R/S –bilat crepts &wheese• Investigation – CBC(lymphocytosis)
CRP/BC- Wnl
X-ray- B/l infiltrate• Baby required intubation.
RSV Bronchiolitis
• DIAGNOSIS – Immunoflorocence Antigen testing of resp secretion.
• Viral Culture (3-5)
• Prevention avoid crowds and handling!!
• Treatment • RIBAVIRIN
nebulisation• RSV IG
CASE 9
• 9th day full term home delivery had rash started from
presenting part face and trunk with tachypnea and refusal
of feed, this baby later had temperature instability and
seizure
• Examination- vesicular rash,
• Investigation – thrombocytopenia and nutropenia.
SGPT/CSF/ CRP/ BC all are WNL
HSV Clinical Manifestations• Most are asymptomatic at birth• 3 patterns of ~ equal frequency with symptoms
between birth and 4wks:– Skin, eyes, mouth (SEM)– CNS disease– Disseminated disease (present earliest)
• Initial manifestations very nonspecific with skin lesions NOT necessarily present
Presentations of congenital HSV
Diagnosis
• Culture of maternal lesions if present at delivery
• Cultures in infant:– Skin lesions,
oro/nasopharynx, eyes, urine, blood, rectum/stool, CSF
• CSF PCR
• High dose acyclovir 60mg/kg/day divided q8hrs– X21days for
disseminated, CNS disease
– X14days for SEM– Ocular involvement
requires topical therapy as well
CASE 10
• 7 days FTND had fever, rash all over body, respiratory
distress
• Mother had a history of chickenpox 3 days before delivery
• Examination – Febrile , Vesicular pleomorphic rash all over
body, tachepnea
• Investigation – TLC – 15,000,
Crp/Bc/Csf –Wnl,
X RAY – Pneumonia
Varicella / Chickenpox
Complications
Congénital infection (2%, 18-22 w of
gestation) Small size, cutaneous scarring,
limb hyplasia, microcephaly,
cortical atrophy, chorioretinitis, cataracts
Perinatal infection
5 days before to 2 days after birth
(high mortality without treatment 30%)
Treatment
• VZIG -125 U as soon as possible
• Isolation
• Iv acyclovir 20mg/kg/day 8hry for 7-10
days
CASE 11
• 16 days old baby had fever, restlessness, pallor, poor
feeding.
• Mother had fever before delivery
• Examination - pallor, jaundice and hepatosplenomegaly
• Investigation – cbc -Hb -5gm, Plt 40,000/cumm
• P/S falciparam
• Congenital malaria is acquired from the mother prenatally or perinatally and is a serious problem in endemic area
• In endemic areas, congenital malaria is an important cause of abortions, miscarriages, stillbirths, premature births, intrauterine growth retardation, and neonatal deaths
Treatment
• Chloroquin is the drug of choice for treatment. Primaquin
is not required for congenital malaria, because there is no
persistent liver phase in congenitally acquired infections.This
case highlights the fact that even in endemic regions malaria
can afflict the neonates with its varied presentation.
• Prompt treatment should be instituted to avoid associated
morbidity and mortality
Which TORCH Infection Presents With…• Snuffles?
– syphilis• Chorioretinitis, hydrocephalus, and intracranial
calcifications? – toxo
• Blueberry muffin lesions?– rubella
• Periventricular calcifications?– CMV
• No symptoms?– All of them
CASE 12
• 10 days baby – high fever, refusal to feed, excessive irritablity, rash
• Examination – Febrile 103 F, tacycardia (180)
flushing, CRT>3sec,
• Investigation – Hb-11.7g/dL, TLC-4,800/mm3
platelet 89,000/cumm
Neonatal Chikungunya
• The clinical features noticed in the chikungunya
confirmed infants were having foetal death,high fever,
seizures, loose stools, peripheral cyanosis and
dermatological manifestations like generalized
erythema,maculopapular rash, vesiculobullous lesions
and skin peeling.pigmentation over nose ,face ,limb.
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