Malaria is one of the commonest parasitic infections causing a large number of deaths throughout the World. Humans are infected by 5 species, but infection with more than one species is uncommon in a single patient. The case discussed here is a female patient presenting with fever and pain abdomen due to malaria. Diagnosis revealed co-infection with vivax and falciparum malaria with incidental detection of splenic infarct which usually has a good prognosis.

A 32 years old female, a housewife by occupation, residing in South 24 Parganas district presents with fever for the last 3 days with chill and rigour with pain abdomen for the last one day in the right hypochondrium with a history of nausea and vomiting for the last 2 days without any history of loose motions. The pain increased in severity particularly with the rise of temperature without any radiation or relation to food. There was no history of myalgia, arthralgia, skin rash or any bladder bowel complaints. LMP was 7 days ago and there was no history of bleeding from any site. There was no significant past history treatment history or travel history. On examination, the patient was alert, conscious and cooperative without any signs of meningeal irritation. Mild pallor was present without any icterus or lymphadenopathy. Temperature was 101⁰F with tachycardia and normal blood pressure without any pedal edema.

Systemic examination revealed tender hepatomegaly and splenomegaly (non-tender) with right hypochondrial pain and tenderness without any ascites or dilated abdominal veins. Respiratory system examination revealed tachypnea with bi basal crepitations. Examination of other systems was unremarkable. A provisional diagnosis of enteric fever was done with differentials of malaria and scrub typhus as the patient resided in a Scrub typhus endemic area with a recent visit to a nearby jungle 7 days before the onset of fever.

The patient was treated with injection Ceftriaxone, injection Doxycycline, IV fluid, injection PPI, Ondansetron along with oral Paracetamol and drotaverine injection. The malaria slide showed ring forms, schizonts and gametocides of both Plasmodium Vivax and Plasmodium Falciparum

Malaria is a parasitic infection caused by protozoa Plasmodium which is transmitted by the female Anopheles mosquito. The 5 species causing human infections are P vivax, P falciparum, P ovale, P malariae and P knowlesi [1,2,3]. Among malaria patients, 5-7 % of cases are infected with more than one species and is also known in mosquito vectors [2]. After a blood meal by the mosquito, sporozoites enter liver cells within minutes and after a few weeks reach the bloodstream. The merozoites enter RBC and develop into trophozoites and schizonts over some days.RBC s ruptures result in fever and release of merozoites which enter new RBCs and repeat the process and thus increase the parasite burden. Plasmodium falciparum causes cytoadherence and rosette formation and causes microvascular damage. This is the probable mechanism of splenic infarct in the case. Annually 300-500 million cases of malaria occur worldwide [4]. mostly occurring in rural tropics below 1000 m elevations.1-3 million deaths occur per year, mostly children less than 5 years and most of the deaths are in rural areas of Sub Saharan Africa [4]. Thalassemia, sickle cell trait and G6 PD deficiency protects from death due to falciparum. Splenic complications are splenic infarction, spontaneous rupture of the spleen, hypersplenism, hyper-reactive splenomegaly syndrome, ectopic spleen, cyst and torsion [5]. Splenic infarction is rare in malaria but may be missed due to underreporting and under-diagnosis [6,7]. Spleen rupture was more frequent with P. vivax according to some studies [8]. As patients are asymptomatic,