Congenital vivax malaria: rare or underdiagnosed infection

Introduction

In addition to endemic areas, congenital malaria (CM) has been reported from areas of low or no transmission areas. In some cases the history of immigration or travel to endemic areas by the mother during her pregnancy was not mentioned. Similarly, any malarial symptoms or parasitaemia in the mother were not indicative of CM^1–3 as its presentation is very similar to neonatal sepsis (NNS) and, therefore, it will be undiagnosed and untreated.^1,4 We recommend that malaria should be considered as a differential diagnosis of a sick neonate and infant even in the absence of other clues, in order to reduce possible mortality.

Case report

An 8-day-old boy presented with fever, decreased oral intake and decreased activity of 2 days duration. There was no history of seizures, rash, loose motions, vomiting, cough or ear discharge. On examination he was alert and his vitals were stable but he had poor sucking. He had a temperature of 101°F, severe anaemia, jaundice and splenohepatomegaly (spleen 6 cm, liver 5 cm below costal margin (BCM)). There was no history of blood transfusion or bleeding from any site. His anthropometric, respiratory, cardiovascular and nervous system examinations were unremarkable.

A possibility of neonatal sepsis, toxoplasma, rubella, cytomegalourus or herpes virus (TORCH) infections and haemolytic anaemia was borne in mind and empirical antibiotic therapy (ampicillin and amikacin) was started.

Investigations showed: haemoglobin 5.8 mg/dL; total leucocytes count 11,590/cm³; and platelet count 41,000/cm³. His C-reactive protein (CRP) was negative and a blood culture was sterile. He was seronegative for TORCH. The blood smears showed a leukocyte shift to the left but were negative for atypical cells and malaria parasites. He continued to remain symptomatic. On the second day a repeat sepsis screen was negative but this time trophozoits of P. vivax could be identified on the peripheral smears. The mean corpuscular volume (MCV) was 94.4fl and a corrected reticulocyte count was 6.2%. His serum bilirubin was 2.3 mg/dL, serum glutamic oxalo-acetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT) and alkaline phosphatase (ALP) were in the normal range.

He was treated with oral chloroquine 25 mg/kg spread over 3 days, he became afebrile on the third day of treatment and his oral intake improved. The antibiotics were stopped. He recovered successfully and his repeat peripheral smear on days 3 and 7 after therapy were negative for malaria parasites. After 7 days he was discharged on haematinics. At the time of discharge, his haemoglobin was 6.0 mg/dL and platelets were 1.2 lacs/cm³. At a repeat follow up after 14 days, his haemoglobin increased to 7.5 mg/dL, he had no clinical jaundice and his spleen was 2 cm below costal margin. After 2 months of follow up, his spleen had regressed to normal size and haemoglobin was 9.5 mg/dL. Blood smears remained negative during the first 3 months of follow up and there were no subsequent complications.

His mother was a resident of Uttar Pradesh and could not recall any history of fever or rash during her pregnancy. She was asymptomatic and her peripheral blood films were negative for malaria parasites on three consecutive days, but she showed a positive test for malarial antibodies.

Discussion

CM is rare both in endemic and non-endemic areas. India has an unstable transmission of malaria and the bulk of cases are reported from Orissa, Jharkhand, Chhattisgarh, West Bengal and Madhya Pradesh. In this era – when the annual parasite index (API) has decreased to 1.3 in 2010 from 3.29 in 1995 along with a decrease in total deaths due to malaria (767 from 1151) and slide positivity rate (1.41 from 3.51) – the reports of CM have recently increased. ⁵ As in our case, in most of these cases malaria was diagnosed accidently.

NNS is the primary working diagnosis in an infant with fever who may often receive antibiotics but is not investigated for malaria or administered anti-malarial drugs. Recently, Del Punta et al. described a case from Italy who was being investigated for NNS but later accidently diagnosed with CM. ¹ Similarly a case from India was only diagnosed after a large battery of tests. ⁴ Studies by Okechukwu et al. and Ekanem et al. illustrate that CM was diagnosed in 28.9% and 35%, respectively, of neonates suspected to have NNS.^6,7 A coexistence of CM and NNS was also noted.

Although we could not find data from India, reports suggest that there could be other deaths in the community as a result of undiagnosed malaria as demonstrated by Dhingra et al. which suggests that CM is more common than is generally thought. ⁸ These observations suggest the need for studies defining the role of CM in causing sickness, especially in low endemicity areas where symptomatic malaria can occur even at low parasitaemia.

As CM has been detected in uncomplicated asymptomatic pregnancies and maternal aparasitemia, a history of maternal fever or travel to an endemic area may not, as in this case, be a helpful clue.^1–3,9 Hence, we suggest that CM in a sick baby should be ruled out even in the absence of maternal malaria episodes, travel history or parasites on smear.

The chloroquine treatment over 3 days appears to be adequate and effective. Since the infection is caused by the transmission of infected erythrocytes, treatment for the exo-erythrocytic stages is unnecessary.

Increasing reports of CM indicate that it is not very rare now and so its diagnosis should be planned and not a matter of chance. This especially holds true in areas such as Delhi where immigration from highly endemic areas is a major concern.

Conclusion

This unsought and underdiagnosed infection raises the question of whether a sick infant who is not responding to empirical antibiotics should be treated with antimalarials considering: increasing reports of congenital malaria in recent years; its nonspecific signs and symptoms; its occurrence in both endemic and non-endemic areas; maternal aparasitaemia and an unreliable history of travel or malarial episodes; the limitations of serological tests and subjectivity of smear examination; the coexistence of NNS and CM; and the low estimates of the malarial burden.