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SCIENTIFIC LETTER Congenital Plasmodium Vivax Malaria and Intracranial Hemorrhage Sushama Sahoo & Arindam Bandyopadhyay Received: 4 June 2013 /Accepted: 12 September 2013 # Dr. K C Chaudhuri Foundation 2013 To the Editor : Congenital malaria is extremely rare, both in endemic and non-endemic countries. A case of congenital malaria due to Plasmodium vivax , who presented with un- common features of recurrent seizures and intracranial hem- orrhage is described. A 12-d-old boy was admitted with fever of 7 d, poor feeding and occasional vomiting. The baby developed recur- rent seizures and pallor one day prior to referral. On admis- sion, he had a body temperature of 38.7 °C, pallor, mild icterus and hepatosplenomegaly. Blood sugar and serum electrolytes were normal. Hb% - 6.7 g/dL, Hct 20.3 %, reticulocyte count 3 %, TLC 4,800/cmm, N 34 %, L 62 %, M 2 %, E 2 % and platelets 120,000/cmm, ESR 35 mm/h. Total serum bilirubin 6.5 mg/dL, CRP 1.6 mg/dL. PT and aPTT were normal. Blood and urine cultures as well as CSF study and chest radiograph were normal. One unit of packed RBC was transfused on the day of admission. Seizures recurred, for which midazolam infusion was started along with maintenance doses of inj. phenobarbi- tone and phenytoin. CT scan of brain was done which showed intracranial hemorrhage in left parietal region. For persistence of fever and pallor, complete blood count was repeated along with peripheral blood smear which revealed Plasmodium vivax . His mother was positive for P. vivax as well. The baby was treated with injection quinine and the mother was treated with oral chloroquinine and primaquine. Both the baby and the mother had negative blood smears after 3 d of antimalarials. Before discharge, one more transfusion with packed RBC was required and all anticon- vulsants were stopped. Repeat CT scan of brain was done 3 mo after the discharge and it was normal. At one year follow-up, there was no recrudescence of fever or recur- rence of seizure. Growth and neurodevelopment of the infant is normal. Malaria contributes significantly to perinatal disease bur- den and information on congenital malaria, in terms of prev- alence and outcome is not well described in literature [1]. Clinical features of congenital malaria include fever, anemia, hepatosplenomegaly, poor feeding, lethargy, irritability and jaundice. This case showed additional features like recurrent seizures and intracranial hemorrhage [2, 3]. Postulated mechanisms for congenital transmission of malaria include maternal transfusion into fetal circula- tion either during pregnancy or at delivery, direct pene- tration through chorionic villi or penetration through premature separation of placenta [4]. Exact mechanism of intracranial hemorrhage in congenital malaria is not known but literature supports the view that malaria- associated cerebral vasculitis can cause small, punctate brain hemorrhages [5]. We conclude that congenital malaria can present with atyp- ical features like seizures and intracranial hemorrhage. More studies are needed to know the mechanism of pathogenesis of these atypical features of congenital malaria. S. Sahoo Department of Pediatric Medicine, Dr B. C. Roy Postgraduate Institute of Pediatric Sciences, 111, Narkeldanga Main Road, Kolkata, India A. Bandyopadhyay Department of Pediatric Medicine, College of Medicine and Sagar Dutta Hospital, Kolkata, India S. Sahoo (*) 8/4 Santoshpur East Road, Kolkata 700 075, India e-mail: [email protected] Indian J Pediatr DOI 10.1007/s12098-013-1252-z

Congenital Plasmodium Vivax Malaria and Intracranial Hemorrhage

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SCIENTIFIC LETTER

Congenital Plasmodium Vivax Malaria and IntracranialHemorrhage

Sushama Sahoo & Arindam Bandyopadhyay

Received: 4 June 2013 /Accepted: 12 September 2013# Dr. K C Chaudhuri Foundation 2013

To the Editor : Congenital malaria is extremely rare, both inendemic and non-endemic countries. A case of congenitalmalaria due to Plasmodium vivax , who presented with un-common features of recurrent seizures and intracranial hem-orrhage is described.

A 12-d-old boy was admitted with fever of 7 d, poorfeeding and occasional vomiting. The baby developed recur-rent seizures and pallor one day prior to referral. On admis-sion, he had a body temperature of 38.7 °C, pallor, mild icterusand hepatosplenomegaly. Blood sugar and serum electrolyteswere normal. Hb% - 6.7 g/dL, Hct – 20.3 %, reticulocytecount – 3 %, TLC – 4,800/cmm, N – 34 %, L – 62 %, M –2 %, E – 2 % and platelets – 120,000/cmm, ESR – 35 mm/h.Total serum bilirubin – 6.5 mg/dL, CRP – 1.6 mg/dL. PT andaPTT were normal. Blood and urine cultures as well as CSFstudy and chest radiograph were normal.

One unit of packed RBC was transfused on the day ofadmission. Seizures recurred, for which midazolam infusionwas started along with maintenance doses of inj. phenobarbi-tone and phenytoin. CT scan of brain was done which showedintracranial hemorrhage in left parietal region. For persistence

of fever and pallor, complete blood count was repeated alongwith peripheral blood smear which revealed Plasmodiumvivax . His mother was positive for P. vivax as well.

The baby was treated with injection quinine and themother was treated with oral chloroquinine and primaquine.Both the baby and the mother had negative blood smearsafter 3 d of antimalarials. Before discharge, one moretransfusion with packed RBC was required and all anticon-vulsants were stopped. Repeat CT scan of brain was done3 mo after the discharge and it was normal. At one yearfollow-up, there was no recrudescence of fever or recur-rence of seizure. Growth and neurodevelopment of theinfant is normal.

Malaria contributes significantly to perinatal disease bur-den and information on congenital malaria, in terms of prev-alence and outcome is not well described in literature [1].Clinical features of congenital malaria include fever, anemia,hepatosplenomegaly, poor feeding, lethargy, irritability andjaundice. This case showed additional features like recurrentseizures and intracranial hemorrhage [2, 3].

Postulated mechanisms for congenital transmission ofmalaria include maternal transfusion into fetal circula-tion either during pregnancy or at delivery, direct pene-tration through chorionic villi or penetration throughpremature separation of placenta [4]. Exact mechanismof intracranial hemorrhage in congenital malaria is notknown but literature supports the view that malaria-associated cerebral vasculitis can cause small, punctate brainhemorrhages [5].

We conclude that congenital malaria can present with atyp-ical features like seizures and intracranial hemorrhage. Morestudies are needed to know the mechanism of pathogenesis ofthese atypical features of congenital malaria.

S. SahooDepartment of Pediatric Medicine, Dr B. C. Roy PostgraduateInstitute of Pediatric Sciences, 111, Narkeldanga Main Road,Kolkata, India

A. BandyopadhyayDepartment of Pediatric Medicine, College of Medicine and SagarDutta Hospital, Kolkata, India

S. Sahoo (*)8/4 Santoshpur East Road, Kolkata 700 075, Indiae-mail: [email protected]

Indian J PediatrDOI 10.1007/s12098-013-1252-z

Conflict of Interest None.

Role of Funding Source None.

References

1. Nosten F, McGready R, Simpson JA, Thwai KL, Balkan S, Cho T,et al. Effects of Plasmodium vivax malaria in pregnancy. Lancet.1999;354:546–9.

2. Ibhanesebhor SE. Clinical characteristics of neonatal malaria. J TropPediatr. 2005;65:477–81.

3. Yadav D, Chandra J, Aneja S, Kumar V, Kumar P, Dutta AK. Chang-ing profile of severe malaria in north Indian children. Indian J Pediatr.2012;79:483–7.

4. Del Punta V,GullettaM,Matteelli A, Spinoni V, Regazzoli A, Castelli F.Congenital Plasmodium vivax malaria mimicking neonatal sepsis: Acase report. Malar J. 2010;9:63.

5. Roach ES, Golomb MR, Adams R, Biller J, Daniels S, DeveberG, et al; American Heart Association Stroke Council; Council onCardiovascular Disease in the Young. Management of stroke ininfants and children: A scientific statement from a Special Writ-ing Group of the American Heart Association Stroke Council andthe Council on Cardiovascular Disease in the Young. Stroke.2008;39:2644–91.

Indian J Pediatr