Journal of Postgraduate Medicine
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Year : 1987  |  Volume : 33  |  Issue : 3  |  Page : 158-61  

Congenital malaria (a report of 2 cases).

SV Kothare, SG Kallapur, SF Irani, SB Prabhu, PS Gangal, GJ Agarwal 

Correspondence Address:
S V Kothare

How to cite this article:
Kothare S V, Kallapur S G, Irani S F, Prabhu S B, Gangal P S, Agarwal G J. Congenital malaria (a report of 2 cases). J Postgrad Med 1987;33:158-61

How to cite this URL:
Kothare S V, Kallapur S G, Irani S F, Prabhu S B, Gangal P S, Agarwal G J. Congenital malaria (a report of 2 cases). J Postgrad Med [serial online] 1987 [cited 2023 Feb 5 ];33:158-61
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Congenital malaria is defined as malarial parasites demonstrated in the peripheral smear of the newborn from twenty four hours to seven days of life.[14] Clinically apparent congenital malaria is rare in areas in which malaria is endemic and levels of maternal antibody are high. Two cases of congenital malaria which were present in our neonatology unit are reviewed.


Case 1:

A 30 year old primipara with 32 weeks' amenorrhea came for delivery with history of pregnancy induced hypertension. She had no history of fever with chills or rigors any time during her pregnancy nor had she received any blood transfusions. She delivered normally at 34 weeks of gestation, a male child weighing 1450 gram. By Dubowitz' and clinical criteria stated by Illingwort[6] the child was preterm and small for gestational age. Clinical examination of the baby revealed coarse facial features and puffed up eyes. There was no pallor or jaundice but a just palpable spleen with mild hepatomegaly was present. On day 4, the child developed loose motion for which investigations were done. They were as follows: Hb 17 gm%, reticulocyte cound 2%, total WBC 5,900/mm3; polymorphs 50%, lymphocytes 36%, eosinophils 1%, basophils 2% and band forms 10%. Ring forms of P. vivax were seen. BUN and serum electrolytes were within normal limits. Blood culture showed no growth.

Liver function tests (LFT) were as follows: SGPT 42 IU/L (normal 5 to 40 IU/L); SGOT 35 IU/L (normal 5 to 40 IU/L). Total bilirubin 1.4 mg%--direct 0.4%. Serum IgM level was, 225 mg%, (normal 0-20 mg%).

DCT and cold agglutins were negative. Ring forms of P. vivax were demonstrated twice in the child and once in the mother.

VDRL test of the child was negative. The child was treated with syrup chloroquine 10 mg/ kg immediately followed by 5 mg/kg after 6 hours, followed by 5 mg/kg once a day for the next two days. Peripheral smear of the baby on day 3 and day 7 after therapy did not show any malarial parasites.

Case 2:

A 26 year old primipara with no history of fever during pregnancy delivered normally at 30 weeks of amenorrhea. The baby weighed 1.3 kg and by Dubowitz and clinical criteria (mentioned by Illingworth[6]) was of thirty weeks of gestation. This baby also belonged to the category of small for gestational age. On clinical examination, the child had no pallor, icterus or splenomegaly. Liver was just palpable. A routine blood count and periphal smear revealed the presence of malaria parasites. The following investigation were done: Hb 15.3gms% on day 3. Reticulocyte count 2%. Total WBCs 6800/mm3, polymorphs 52%, lymphocytes 36%, bandforms 10%, eosinophils 2%. Ring forms of P. vivax were seen on peripheral smear. Mother peripheral smear also showed ring forms of P. vivax. BUN, serum electrolytes, LFT of the child were within limits. DCT and cold agglutinis were absent. IgM was 175mg% normal being upto 20gm. The child was treated on similar lines as the first child. Repeat peripheral smear on day 3 and day 7 after therapy were negative for malarian parasites.


Two important facts may be noted form these two cases. Firstly malaria was detected accidentally in both; and they ware essentially asymptomatic. Thus we should suspect congenital malaria more often. Secondly we wish to emphasize that malaria in pregnancy is often associated with significant intra-uterine growth retardation. This was noted in both of our cases. Placental histology was not done, but they weighed 400 and 450gm respectively and were grossly normal. Jellife[7] has suggested a direct correlation between the intensity of placental infection and severity of fetal affection.

Malaria in the newborn is believed to be uncommon. More than 150 cases of congenital malaria have been reported in the world literature. The mechanism of transplacental passage of this infection is disputed. In 1941, Torpin[12] reviewed 27 cases of malaria in pregnant women where maternal mortality rate was 4% and fetal mortality was 60%. From Delhi, Dhatt et al[1] have reported 15 cases of malaria in the first 4 months of life, with positive history of malaria in mothers in 50% of cases. In malaria endemic areas the incidence of congenital malaria which is 0.3% rise to 1-4% following overt attacks of malaria in the mother. Santhanakrishnan et al[10] from Madras reported 2 cases of congenital malaria diagnosed in the first 4 months of life in a study of 221 children with malaria.[10]


1. Effect of pregnancy on malaria: Increased density of parasitemia has been documented in pregnant women as compared to non pregnant women.[14] This density reduce with increasing parity, correlating with an increase in immunity against malaria with age.[14]

2. Infection of the placenta: Infection of the placenta following an over attack was 20-30%, but only 1 to 4% of these had suffered from congenital malaria.[2],[8],[11] Hence placenta serves as a relatively effective barrier to the fetus against transport of parasites. The inflammatory response in the placenta is more severe following infection with P. falciparum.[5] Increased lymphocytes interfere with placental circulation and contribute to reduced oxygen and nutrient transport to the fetus.[4],[7],[13]

3. Influence of maternal antibody on risk of infection: Antimalarial antibodies detectable by complement fixation test or indirect haemaglutination assay, are passively transferred from the mother to the infant. Antibody levels fall from birth to 6 month of life and then rise due to endogenous production. Probably the amount of protective antibody transferred to the fetus is decreased with heavy infestation of placenta.[1]

4. Other factors influencing the risk of infection: Infants below 3 months have lesser incidence, severity, parasitemia and death from malaria.[9] This may be related to lesser exposure to mosquitoes, HbF in the blood, low PABA content of breast milk and high titres of transferred maternal antibodies.

Clinical features

Onset may be as early as 14 hours to as late as 8 weeks of age but on an average it is between 10 to 28 days of life.[1],[4],[5],[13],[14] Fever, anaemia, splenomegaly occur in 80% cases. Reticulocytosis occurs in 50% cases and jaundice in 33% cases. Other features include hepatomegaly, poor feeding, loose motions and failure to thrive.[13]

Prevention and treatment

Prevention of malaria during pregnancy in non-endemic areas involves the use of chloroquine in the dose of 300 mg base/ week. Its use in pregnancy may not be entirely safe as is demonstrated by the occurrence of severe vestibulo-cochlear paresis and posterior column defects in two babies born to a mother suffering from SLE and who was on chloroquine.[3] The dose of chloroquine was four times higher than that recommended for antimalarial prophylaxis and may be the cause of teratogenecity.[3] However, despite widespread use of chloroquine in pregnancy, teratogenic effects of the same have not been confirmed in controlled trials. Administration of pyrimethamine and primaquine for resistant cases and eradicating exo-erythrocytic phase respectively is not advised in view of the teratogenic potentials of these.[9]

Chloroquine given in the dose of 10 mg/ kg body weight of base, followed by 5 mg/ kg after 6 hours and 5 mg/kg once a day for the next two days is the accepted regimen for treating congenital malaria. Primaquine is not required for treatment as the tissue phase is absent in congenital malaria.[14]

As malaria contributes significantly to fetal losses, still births and premature births in endemic areas, its effective control can lead to an increase in mean birth weights of babies in these areas.[8]


We are grateful to Dr. G. B. Parulkar, Dean, K. E. M. Hospital and Seth G. S. Medical College for allowing us to publish this case report.


1Dhatt, P. S., Singh, H., Singhal, S. C., and Madan, Sushama: A clinicopathological study of malaria in early infancy. Ind. Pediatr., 6: 331-336, 1979.
2Ghosh, Shanti, Patwari, A., Mohan, M. and Berry, A. M.: Clinical and hematological peculiarities of malaria in pregnancy. Clin. Pediatr., 17: 369-371, 1978.
3Hart, C. W. and Naunton, R. F.: The ototoxicity of chloroquine phosphate. Arch. Otolaryngol., 80: 407-412, 1964.
4Harvey, B., Remington, J. S. and Sulzer, A. J.: IgM malaria antibodies in a case of congenital malaria in the United States. Lancet, 1: 333-335, 1969.
5Hindi, R. D. and Azmi, P. H.: Congenital malaria due to P. falciparum Pediatrics, 66: 977-979, 1980.
6Illingworth, R. S.: The assessment of maturity. In, "The Development of Infant and Young Child-Normal and Abnormal". 8th edition. Churchill Livingstone, London, 1985, p. 87.
7Jelliffe, E. F. P.: Low birth weight and infection of placenta. Bull. WHO, 38: 69-72, 1968.
8Mac-Gregor, 7. D. and Avery, J. G.: Malaria transmission and fetal growth Brit. Med. J., 3: 433-436, 1974.
9Morley, D., Woodland, Margaret and Cuthbertson, W. F. J.: Controlled trial of pyrimethamine in pregnant women in an African village. Brit. Med. J., 1: 667-668, 1964.
10Santhanakrishnan, B. R., Parthasarthy, A., Bhawani, C. R. and Ramesh, S.: Profile of malaria in Madras. Ind. J. Pediatr., 52: 249-252, 1985.
11Spitz, A. J.: Malaria infection of placenta and its influence on prematurity in East Nigeria. Bull. WHO, 21: 242-246, 1959.
12Torpin, R.: Malaria complicating pregnancy-with report of 27 cases. Amer. J Obstet. & Gynecol., 41: 882-885, 1941.
13Woods, W. G., Mills, E. and Ferrieri, P.: Neonatal malaria due to P. Vivax. J. Pediatr., 85: 669-671, 1974.
14Yeager, A. S.: Protozoan and helminth infections, in "Infectious Diseases of the Fetus and Newborn Infant". Editors: J. S, Remington and J. O. Klein, 2nd edition, W. B. Saunders Company, Philadelphia, 1983, pp. 563-569.

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