Failure of chloroquine therapy in a splenectomized child infected with Plasmodium vivax

The district of Jabalpur, which lies in the 29.6%. His blood-group was A+. A sample of his blood gave a dark band, indicating centre of central India (23 ß 9 3⁄4 N, 79 ß 58 3⁄4 E), is highly malarious (Shukla et al., 1995) because a fairly high P. vivax parasitaemia, when tested with an OptiMAL dipstick, and all of the presence of three eYcient vector species: Anopheles culicifacies, An.  uviatilis stages of P. vivax infection were revealed by microscopical examination of a bloodsmear, and An. stephensi (Singh et al., 1999). Both Plasmodium vivax and P. falciparum are with 6400 asexual parasites/ml. The boy was given oral CQ (25 mg/kg), along with common, and resistance to chloroquine (CQ) has been detected in the local P. falciparum supporting treatment for his anaemia, by the attending physician. However, when a fresh since 1987 (Ghosh et al., 1989). Although there has been no previous evidence of blood sample was collected 48 h posttreatment and investigated by OptiMAL and CQ-resistant P. vivax in the district, a splenectomized child infected with P. vivax microscopy, the dipstick immediately gave a positive reaction (albeit with a relatively light recently failed to be cured with a standard dose of CQ. This unusual case is described band) and the smear revealed a P. vivax parasitaemia of 400 asexual parasites/ml. At below. Since 1991, the Indian Malaria Research this time the boy’s Hb concentration was found to have slipped even lower than it had Centre (supported by the Indian Council of Medical Research) has run a malaria been on admission (to 5.0 g/dl). Study of the boy’s medical history and records revealed clinic in the Medicine Department of the Government Medical College at Jabalpur. that he had hereditary anaemia (i.e. sickle/ b-thalassaemia), with 11.66% of his Hb as Here, bloodsmears are routinely prepared, from all the fever cases who present, and HbF and 4.36% 2 and that he had been splenectomized in 1996. Subsequent examexamined for malarial parasites under the microscope (Singh et al., 1999). Recently, ination of the medical records of the boy’s parents revealed that, as then expected, one such microscopy has been supplemented with a commercial rapid diagnostic test: parent (his father) had b-thalassaemia (with 0.4% of his Hb as HbF and 5.9% 2 OptiMAL (Flow Inc., Portland, OR; Moody et al., 2000). while the other (his mother) had the sicklecell trait (with HbAS, and 1.4% of her Hb On 6 September 2000, a Hindu (Brahamin) boy aged 11 years presented as HbF). The boy was then given an exchange at the clinic in Jabalpur, with a history of high-grade fever. The boy, who was weak, transfusion of two units of blood and another dose of CQ (again at 25 mg/kg ). thin (21 kg), severely anaemic and suVering from hepatomegaly, had 5.3 g haemoglobin Further examinations on days 2 and 7 posttransfusion, by both OptiMAL and blood(Hb)/dl, a packed-cell volume of 17.9%, a mean corpuscular Hb content of 22.7 pg, smear, revealed complete clearance of parasitaemia. By day 7 post-transfusion, a mean corpuscular volume of 76.8  and a mean corpuscular Hb concentration of the boy’s Hb concentration had increased