|Year : 2015 | Volume
| Issue : 3 | Page : 206-208
Congenital malaria with atypical presentation: A series of three case reports
Geeta Gathwala, Poonam Dalal, Mohit Gupta
Department of Pediatrics, Pt. B.D. Sharma, PGIMS, Rohtak, Haryana, India
|Date of Web Publication||2-Jul-2015|
Department of Pediatrics, Pt. B.D. Sharma, PGIMS, Rohtak - 124 001, Haryana
Source of Support: None, Conflict of Interest: None
Congenital malaria is among rare presentation of the disease. Neonatal malaria remains extremely rare both in endemic and non endemic areas. Herein, we report three cases of congenital malaria presenting with prolonged jaundice from a non endemic region of North-India. This may emphasize the need to consider congenital malaria as a differential diagnosis while evaluating the babies with atypical symptoms like prolonged conjugated hyperbilirubinemia.
Keywords: Congenital malaria, prolonged, conjugated hyperbilirubinemia
|How to cite this article:|
Gathwala G, Dalal P, Gupta M. Congenital malaria with atypical presentation: A series of three case reports. J Clin Neonatol 2015;4:206-8
|How to cite this URL:|
Gathwala G, Dalal P, Gupta M. Congenital malaria with atypical presentation: A series of three case reports. J Clin Neonatol [serial online] 2015 [cited 2019 Dec 5];4:206-8. Available from: http://www.jcnonweb.com/text.asp?2015/4/3/206/154128
| Introduction|| |
Malaria in the neonatal period may be acquired by transfusion of infected blood products to neonate, perinatal transmission from mother and in endemic areas by mosquito bite. Congenital malaria is defined as malaria acquired from the mother prenatally or perinatally. , The predominant clinical features are fever, anemia and splenomegaly, the triad reportedly seen in more than 80% of cases, presentation as prolonged conjugated hyperbilirubinemia is far less common.  Herein, we report three cases of congenital malaria presenting atypically.
| Case Reports|| |
A 17-day-old male baby was admitted with yellowish discoloration of skin and eyes noticed since 8 th day of life. There was no history of fever. The baby was born at term to a fourth gravida mother with a birth weight of 2.5 kg. There was a history of fever in the mother at 8 th month of gestation, which was high grade and associated with chills and rigors. Mother was given antimalarials for that and became asymptomatic. Baby did not receive any blood products prior to illness. Examination revealed the icterus up to soles, mild pallor and hepatosplenomegaly with liver palpable 3 cm and soft to firm spleen 3 cm below the costal margin. Laboratory evaluation showed anemia with hemoglobin (Hb) 11.0 g/dL, total leukocytes 8000/cmm with 70% polymorphs, 25% lymphocytes, 3% monocytes, 2% eosinophils and normal platelet count. Peripheral blood film revealed normocytic, normochromic picture and malarial parasite. Both mother's and baby's blood group was A +. The total serum bilirubin was 18.8 mg/dL with direct 9.0 mg/dL, and indirect 9.8 mg/dL. Direct coomb test (DCT) was negative, and G-6PD was normal. C-reactive protein (CRP) was positive, blood culture sterile and liver enzymes (transaminases) were in normal range. Ultrasound abdomen revealed hepatosplenomegaly. Baby was diagnosed as a case of congenital malaria and was treated with chloroquine. Spleen regressed and baby became anicteric after 1 week of treatment.
A 21-day-old male was admitted with yellowish discoloration of eyes and skin since day 10 of life and dark yellow urine and acholic stools since day 20 of life. There was no history of fever. The baby was born to a primigravida mother at full term with a birth weight of 3.2 kg. Mother was asymptomatic throughout the pregnancy. The baby did not receive any blood products in the neonatal period. Examination revealed pallor, icterus up to the upper abdomen, liver palpable 3 cm below the costal margin and a soft to firm spleen palpable 2 cm below the costal margin. A provisional diagnosis of prolonged jaundice was made. Investigations revealed Hb 7.5 g/dL, total white blood cell 8000/cmm, polymorphs 25%, lymphocytes 70%, monocytes 1%, eosinophils 4% and microcytic hypochromic picture on peripheral blood film. Serum bilirubin was 13.6 mg/dL with direct fraction 6.6 mg/dL and indirect 7.0 mg/dL. Thyroid function tests were normal. Mother's blood group was B -- ve and the baby's was B + ve. However, the DCT was negative and G-6PD was normal. Serum glutamic-oxaloacetic transaminase was 81.0 IU/L, serum glutamic pyruvic transaminase 29.0 IU/L and the serum alkaline phosphatase was 509 IU/L. Ultrasound abdomen revealed no abnormality of the hepatobiliary system. Peripheral blood film on 2 nd day of admission revealed Plasmodium vivax. A final diagnosis of congenital malaria was made. The baby was treated with chloroquine. Repeat blood smear at end of treatment was negative, and the baby responded with regression of spleen and decreased icterus by 4 th day of treatment.
A 38-day-old male was admitted with moderate grade intermittent fever since day 25 of life and yellowish staining of eyes, skin and urine. The baby was born at term to a first gravida mother with a birth weight of 3.0 kg. Mother had high-grade fever with chills 1 day prior to delivery and 3 days after delivery. The baby remained asymptomatic and was not investigated at that time. The mother was treated with antimalarials and became asymptomatic 2 days after treatment. Examination of the newborn revealed temperature 101°F, marked pallor and hepatosplenomegaly with liver 5 cm and spleen 4 cm below the costal margin, and icterus up to the upper abdomen. Investigations revealed a Hb of 6.0 g/dL, total leukocyte count 5000/cmm, with polymorphs 68%, lymphocytes 28%, monocytes 2%, eosinophils 2% and a platelet count of 90,000/cmm with dimorphic anemia on peripheral blood film. The total serum bilirubin was 12.5 mg/dL: Direct reacting 4.5 mg/dL, indirect 8.0 mg/dL. DCT and G6PD were negative. Mother and baby blood groups were O + and B + respectively. Serum transaminases were normal. The CRP was positive, and blood culture was sterile. Injectable antibiotics were started with the provisional diagnosis of late onset sepsis. Thick and thin blood smears revealed P. vivax on two consecutive days. Baby was diagnosed as congenital malaria and treated with chloroquine. Anemia was treated with packed cell transfusion. Baby became afebrile and peripheral smear became negative following treatment, spleen regressed by 4 th day of treatment and baby became anicteric after 1 week.
| Discussion|| |
Congenital malaria has been reported as a rare event with an incidence of 0.3% in malaria immune mothers to 7.4% in non immune mothers despite 1--3% incidence of cord blood parasitemia in endemic countries.  Congenital malaria is mainly caused by P. falciparum in endemic areas, whereas most cases in European countries are due to P. malariae and P. vivax. 
Clinical onset of disease in a congenitally infected infant can be delayed for weeks, most of them presenting between 10 and 28 days of life. , All the three index cases became symptomatic between 8 th and 25 th day of life. Vottier et al.  reviewed clinical characteristics of all the reported cases of congenital malaria over last 30 years from non endemic areas. The predominant clinical features reported were anemia (77%), fever (74%), hepatosplenomegaly (68%), poor feeding and lethargy (35%). Hemolytic anemia was reported as most common laboratory finding, although clinical jaundice was not reported in any of them. In the index case series, however, all three had conjugated hyperbilirubinemia, anemia, and splenomegaly, fever was present in only one of them. Clinical symptoms are rare in younger infants and absence of febrile episodes has been described. This has been attributed to transplacentally acquired antimalarial antibodies, which give transient protection to young infants. 
Del Punta et al.  reported a 22 days old neonate presenting with fever, listlessness, hepatosplenomegaly and thrombocytopenia, which was incidentally diagnosed with congenital malaria and responded well to antimalarials. Similar case was reported by Sankar et al.  from a non endemic area in India. In both the cases, there was a history of the mother traveling to the endemic area during pregnancy. In the index case series, one of the three cases was initially treated as neonatal sepsis and later on was incidentally diagnosed as congenital malaria. All the three cases came from a non endemic area (annual parasite incidence <2) of North-India.
Prolonged conjugated hyperbilirubinemia is mainly described with neonatal hepatitis and biliary atresia. Congenital malaria is not mentioned as a cause for prolonged jaundice in literature except two case reports. , Davenport  reported a case of transplacentally acquired malaria with prolonged conjugated hyperbilirubinemia and liver disease in a 3 weeks old neonate. However, icterus persisted despite antimalarial therapy in contrary to index cases where all three became asymptomatic following antimalarial therapy. Valecha et al.  reported atypical presentation of congenital malaria as jaundice and hemolytic anemia in a 6 weeks old infant and akin to the three index cases improved with antimalarial therapy.
The incidence of congenital malaria is 0.3% which rises to 4% following overt attack of malaria in the mother  in endemic areas. In the index case series, maternal fever was reported in perinatal period in two of the three cases and was successfully treated with antimalarials. Congenital malaria has been reported to occur even in the absence of evidence of active malarial infection in the mother during pregnancy. Out of 15 cases of malaria in first 4 months, Dhatt et al.  reported positive history of maternal malarial infection during pregnancy in 50% cases.
Chloroquine given in the dose of 10 mg/kg body weight of the base, followed by 5 mg/kg at 6 h and 5 mg/kg once a day for next 2 days is the accepted treatment regimen. All the three cases in the index series were successfully treated with this regimen. Primaquin is not required for treatment as the exoerythrocytic phase is absent in congenital malaria. ,
| Conclusion|| |
The index case series emphasizes the importance of considering congenital malaria as a differential diagnosis in neonates even in low transmission area who may present with atypical symptoms like prolonged conjugated hyperbilirubinemia rather than the typical triad.
| References|| |
Siriez JY, De Pontual L, Poilane I, Ledeur F, Haouchine D, Lacharsine E, et al.
Congenital malaria as a result of Plasmodium malariae
in an infant born to a HIV-seropositive woman. Med Trop (Mars). 2005;65:477-81.
Krause PJ. Malaria (Plasmodium
). In: Behrman RE, Kleigman RM, Jenson HB, editors.
Nelson Text Book of Pediatrics. 17 th
ed. Philadelphia: Saunders; 2004. p. 1139-43.
Edwards MS. Fungal and protozoal infections. In: Fanaroff AA, Martin RJ, editors. Neonatal-Perinatal Medicine. Diseases of Fetus and Infant. 7 th
ed. Philadelphia: Mosby; 2000. p. 751-2.
Hagmann S, Khanna K, Niazi M, Purswani M, Robins EB. Congenital malaria, an important differential diagnosis to consider when evaluating febrile infants of immigrant mothers. Pediatr Emerg Care 2007;23:326-9.
Vottier G, Arsac M, Farnoux C, Mariani-Kurkdjian P, Baud O, Aujard Y. Congenital malaria in neonates: Two case reports and review of the literature. Acta Paediatr 2008;97:505-8.
Del Punta V, Gulletta M, Matteelli A, Spinoni V, Regazzoli A, Castelli F. Congenital Plasmodium vivax
malaria mimicking neonatal sepsis: A case report. Malar J 2010;9:63.
Sankar J, Menon R, Kottarathara AJ. Congenital malaria - A case report from a non-endemic area. Trop Biomed 2010;27:326-9.
Davenport M. Neonatal malaria and obstructive jaundice. Arch Dis Child 1986;61:515-7.
Valecha N, Bhatia S, Mehta S, Biswas S, Dash AP. Congenital malaria with atypical presentation: A case report from low transmission area in India. Malar J 2007;6:43.
Dhatt PS, Singh H, Singhal SC, Madan S. A clinicopathological study of malaria in early infancy. Indian Pediatr 1979;16:331-6.