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Cytomegalovirus Infection was discharged at 15 days of age and

followed in the neonatal follow up
Acquired Through Blood clinic. At 4 months of age the baby
Transfusions had jaundice, hepatosplenomegaly
and thrombocytopenia. Investigations
showed presence of TgM antibodies
against CMV in the infant's blood.
Swarna Rekha Maternal CMV IgM antibodies were
M.K. Chandrasekhara absent. At the age of 2.5 years the
Malathi Yeshwanth growth and development was normal.
There was no icterus or chorioretinitis
but splenomegaly and hepatomegaly
was present.
Cytomegalovirus (CMV) infection is Case 2: This neonate was born to a
found worldwide and is spread by close primigravida mother at 34 weeks gesta-
contact. The prevalence of congenital tion and weighed 1720 g at birth. The
CMV infection varies from 0.2-2.4%(l). baby had multiple problems in the neo-
Neonates may be infected transplacen- natal period including unconjugated
tally or during birth through a CMV hyperbilirubinemia, apnea, sepsis,
positive mother (congenital CMV infec- thrombocytopenia and anemia. The
tion) or may acquire infection in the baby received multiple blood and plate-
neonatal period through blood transfu- let transfusions. The patient was dis-
sions and breastmilk of infected moth- charged at 9 weeks of age and readmit-
ers(l-3). We report three infants with ted a week later with jaundice,
symptomatic CMV infection, presum- hepatosplenomegaly, thrombocytopenia
ably acquired through blood transfu- and central nervous system bleeds. The
sions in the neonatal period. infant showed IgM antibodies to CMV
and simultaneous maternal CMV IgM
Case Reports was negative. The baby was treated
Case 1: A premature baby (birth symptomatically and discharged after
weight 1890 g and gestation 33 weeks) 10 days. On follow up at 1 year 3
was admitted to the neonatal ward with months of age there was no icterus or
respiratory distress syndrome. The neo- choreoretinitis. Hepatosplenomegaly
nate received assisted ventilation for six was present and the developmental age
of the child was 1 year (not corrected for
days and blood/plasma transfusions for
gestational age).
a low hematocrit and shock. The patient
Case 3: This baby was born at 30
From the Department of Pediatrics, St. John's
Medical College Hospital, Bangalore.
weeks gestation with a birth weight of
1160g. The baby had unconjugated
Reprint requests: Dr. Swarna Rekha, Depart-
ment of Pediatrics, St. John's Medical
hyperbilirubinemia requiring exchange
College Hospital, Bangalore. transfusion on day 2. At 7 days of age
Received for publication: March 4, 1994;
the baby presented with features of
Accepted: November 1, 1994 sepsis, jaundice, hepatosplenomegaly

and thrombocytopenia. IgM antibodies titres of less than 1:4 do not result in
against CMV were positive in the neo- transfer of infection(3). Use of washed
nate and negative in the mother. Mater- packed cells and deglycerolized blood
nal CMV IgG was also negative. On has also been shown to reduce CMV
follow up at 6 months of age there was infection(ll).
no jaundice, choreoretinitis or hepato-
splenomegaly. The developmental age
was 3 months (uncorrected). 1. Baley JE, Goldforb J. Viral infections.
In: Neonatal—Perinatal Medicine: Dis
All our cases had received blood ease of the Fetus and Infant, 5th edn.
transfusions and CMV TgM was nega- Eds. Fanaroff AA, Martin RJ, Chicago
tive in the mothers. We feel that these Mosby Year Book, 1992, pp 666-667.
babies may have acquired it through 2. Cuerine NG. Viral infections in the
blood. All the babies were preterm and newborn. In: Manual of Neonatal
were symptomatic. Care, 3rd edn. Eds. Cloherty TP, Stark
A. Boston Little Brown, 1992.
3. Kim HC. Blood component therapy in
CMV infection is found worldwide the neonate. In: Developmental and
and CMV is known to be endemic in In- Neonatal Hematology. Eds. Stockman
dia also. Pal et al.(4) from Chandigarh JA, Pochedly C. New York Raven
reported a prevalence of CMV antibody Press, 1988, pp 169-193.
positivity in 90-100% of the population. 4. Pal SR, Chitkara NL, Krech V.
CMV infection has been reported in Seroepidemiology of cytorn egalovirus
India(5). One fifth of children with infection in and around Chandigarh.
intrauterine infections have GMV anti- Indian J Med Res 1972, 60: 973-978.
body positivity. However, transfusion 5. Broor S, Kapil A, Kishore J, Seth P.
acquired CMV has not been reported. Prevalance of rubella virus and cy-
CMV infection may be acquired tomegalovirus infection in suspected
cases of congenital infection. Indian J
perinatally through a CMV positive Pediatr 1991, 58: 75-76.
mother(6) or through breastmilk(7). One
study has shown that 13.5% of infants 6. Yeager AS, Palumbo PE, Malchowski
transfused with CMV positive blood de- N, Aragno RL, Stevenson DK.
veloped CMV infection of whom 50% Sequelae of maternally derived cy-
were symptomatic(8). Majority of the tomegalovirus infection in premature
infants. J Pediatr 1983,102: 918-922.
babies who develop CMV infection are
asymptomatic but may have sequelae, 7. Dworsky M, Yow M, Stagno S, Pass
the most common being deafness(9,10). RF, Alford C. Cytomegalovirus infec-
In contrast, preterm babies are usually tion of breastmilk and transmission in
symptomatic, symptoms include infancy. Pediatrics 1983, 72: 295-299.
jaundice, hepatosplenomegaly and 8. Yeager AS, Grumet C, Hafleigh EB,
thrombocytopenia. Arvin AM, Bradley JS, Prober CG.
Prevention of transfusion acquired
Transfusion acquired CMV can be cytomegalovirus infection in newborn
prevented by donor screening; donor infants. J Pediatr 1981, 98: 281-287.


9. Saigal S, Zunyk O, Larke B, Chernesky paired children. Indian Pediatr 1993,

M. The outcome of children with con- 30: 977-979.
genital cytomegalovirus infection—A 11. Brady MT, Milian JD, Anderson DC,
long term follow up study. Am J Dis et al. Use of deglycerolized RBC to
Child 1982,136: 896-901. prevent post-transfusion infection with
cytomegalovirus in neonates. J Inf Dis
10. Deka RC. Management of hearing im- 1984,150: 334-339.

Case Reports
Case I: Two and a half year old girl
presented with fever, weight loss and
cough of 5 months duration. The weight
S.K. Kabra and height were below the fifth percen-
A. Bagga tile for the age. Examination showed
Madhulika marked pallor. The liver and spleen
A. Chatterjee were palpable 5 cm and 3 cm, respec-
V. Seth -lively below the costal margin. Rest of
the systemic examination was normal.
Investigations showed a hemoglobin
level of 7 g/dl, total leucocyte count of
Sarcoidosis is a chronic multisystem 7800/cu mm with 60% polymorphonu-
disease of unkmbwn etiology, usually af- clear leucocytes, 30% lymphocytes and
fecting adults. Only a few reports de- 10% eosinophils. The blood levels of
scribing the clinical features and course transaminases, alkaline phosphatase, se-
of sarcoidosis in children have been rum proteins, creatinine, calcium and
published. Only one case in a child has phosphate were normal. The liver biop-
previously been reported from this sy showed non-caseating granulo-
country(1). The rarity of the condition matous lesions. An X-ray film of the
prompts us to report the clinical fea- chest showed bilateral enlarged hilar
tures in two such patients. lymph nodes. The Mantoux test (using 1
TU injected intradermally) and VDRL
From the Department of Pediatrics, All India test were negative.
Institute of Medical Sciences, New Delhi
U0 029. A diagnosis of disseminated tubercu-
Reprint requests: Dr. S.K. Kabra, Department of losis was made and the patient treated
Pediatrics, All India Institute of Medical with isoniazid (5 mg/kg), rifampicin (10
Sciences, Ansari Nagar, New Delhi 110 mg/kg) and pyrazinamide (30 mg/kg)
029. daily for 2 months. Subsequently
Received for publication: May 6, 1994; pyrazinamide was stopped and therapy
Accepted: October 4, 1994 continued with rifampicin and isoniazid.