Ira Shah
Consultant Pediatrician, Mumbai

Address for Correspondence: Dr Ira Shah, 1/B Saguna, 271/B St. Francis Road, Vile Parle (W), Mumbai 400056.

A one and a half month old male child presented with fever (up to 102F) and abdominal distension since 15 days of life. Antenatally, his mother had vivax malaria at 6 months of gestation for which she was treated with chloroquine. Birth history was normal with birth weight being 2.3 kg. On examination, the child had severe pallor with heart rate of 130/minute. There was no edema. He had firm hepato-splenomegaly (liver span being 7 cms) without dysmorphic features. His weight gain was appropriate for his age and other systemic examination was normal. A differential diagnosis of congenital malaria, sepsis and congenital leukemia was considered. His hemoglobin was 5.2 gm% with white cell count being 9,000/cu mm, Reticulocyte count of 3.5% and platelet count of 1,70,000/cu mm. Peripheral smear did not show any malarial parasites or abnormal cells. His CRP and blood culture were negative. USG skull did not show any intracranial calcifications. His HIV ELISA was negative. Thus sepsis, intrauterine infections such as CMV, HIV, Toxoplasma and leukemia seemed unlikely. His liver enzymes were slightly deranged with SGOT of 62 IU/dl [Normal = 0 to 25 IU/dl] and SGPT of 81 IU/dl (Normal = 0 to 46 IU/dl]. In view of suspicion of congenital malaria, an OptiMAL test for P. falciparum & P. vivax was done, which was positive for P. vivax. The child was treated with chloroquine in initial dose of 10 mg/kg base followed by 5 mg/kg at 6, 24, 48 hours after 1st dose and started on hematinics. His fever subsided and repeat optimal test after 72 hours of therapy was negative. His hemoglobin was 5.9 gm% after 1 week of hematinics and reticulocyte count was 3.9% with normal liver enzymes. Thus a diagnosis of congenital malaria was established inspite of a negative peripheral smear for P. vivax but on basis of a positive OptiMAL test for P. vivax, which subsequently became negative following therapy.

In areas in which malaria is endemic, infants are exposed to mosquitoes at a very young age and may become infected making it difficult to distinguish between acquired and congenital cases. Studies have shown that though placenta may be frequently infected in pregnant mothers with malaria, it still serves as an effective barrier and prevents the parasites from reaching the fetus most of the times (2). Thus clinically apparent congenital infections are rare and rate is 1-4%. It is probable that IgG antibody transplacentally acquired from the mother is an important factor to determine whether parasites reaching the fetal circulation cause infection or not and may also lengthen the incubation period (3). Usually onset of symptom is between 10 to 28 days of age with a range from 14 hours of life to 8 weeks of age. Laboratory studies may demonstrate malaria parasite (P. falciparum, P. vivax and P. malarial are all known to cause congenital infections) with anemia and reticulocytosis. Thus clinical picture may not vary in congenital on acquired malaria. (4)

Chloroquine is the drug of choice in initial dose of 10 mg/kg base followed by 5 mg/kg at 6, 24, 48 hours after 1st dose. Administration of primaquine is not necessary as no exoerythrocytic phase is seen in congenital infections. In patients with chloroquine resistant strains of P. falciparum, quinine and trimethoprim sulfamethoxazole may be used. (1)