The incidence of
P. vivax infection is rising in Sudan and has increased from about 5% in 2013 to 26% of the total malaria cases [
3]. Although severe
P. vivax cases were reported from many endemic areas in South East Asia, the Pacific islands and South America, a few cases were reported in Africa reflecting the neglected status of
P. vivax in Africa [
2].
The patient described in the report was living in Khartoum the capital city of Sudan where malaria transmission is seasonal and non-endemic of
P. vivax until recently. The fact that he was a known type 2 diabetic patients, presenting with high grade fever, chills, vomiting, sweating and confusion lead to suspicion of serious infections, including meningitis and falciparum malaria, which is the common cause of severe malaria in Sudan [
5]. The rapid deterioration of the patient into coma and stiffness within 48 h of his admission increased the suspicion of meningitis and cerebral malaria and required his admission to the Intensive Care Unit (ICU). Cases of bacterial and viral meningitis were previously reported in Khartoum [
6]. Lumbar puncture was recommended but the procedure was not performed since the patient had spinal cord disc making it a risky procedure. The negative finding of the CT scan excluded the possibility of central nervous system disease. The normal results of laboratory investigations including renal and liver parameters excluded renal and liver diseases. The lack of GIT and respiratory complain make the possibility of enteric infection and pulmonary TB less likely. On the other hand, the slight increase of the WBC suggested inflammatory reaction, while the low platelet counts increased the suspicion of severe infection including cerebral malaria. The finding of the blood film was decisive and demonstrated malaria parasite with high parasitaemia (+++), close examination of the thin films identified
P. vivax infection which was confirmed by the positive result of Plasmodium multi species PCR [
7]. Interestingly, most of the severe
P. vivax malaria reported in other endemic areas including those in children in eastern Sudan were accompanied by low parasitaemia contrary to the findings of this study [
8]. The fact that the patient was a known type 2 diabetes patient might had impaired his immune response leading to the increase in the parasite replication. It is worth noting that, this patient had an attack of severe
P. vivax malaria 3 months before his current illness. He presented with fever, chills and confusion. He was successfully treated with quinine 10 mg/kg body weight IV for 10 days, ceftazidime 1G IV 8 hourly for 7 days followed by primaquine 15 mg/days PO for 2 weeks evident by the negative blood film at the end of the treatment course. The recent attack could be a recurrent attack since
P. vivax prevails at low parasitaemia making its detection difficult [
9]. It is worth noting that no previous report on
P. vivax drug resistance in Sudan, however the possibility of noncompliance to primaquine treatment could be excluded strengthening the possibility of the persistent of the parasite from the first infection [
10].