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LETTERS: Harald M Lipman Preventing severe infection after splenectomy: Risk of malaria and meningitis increases with asplenia BMJ 2005; 331: 576-b [Full text]

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Lethal malaria caused by Plasmodium malariae in an asplenic patient in Brazil.

Karin Kirchgatter, Simone L. Nogueira, Alexandre Padilha, Izilda Curado, Marcos Boulos, and Silvia M. Di Santi.   (5 December 2005)

Lethal malaria caused by Plasmodium malariae in an asplenic patient in Brazil. 5 December 2005
Karin Kirchgatter, research associate Superintendência de Controle de Endemias (SUCEN), São Paulo, SP, 05403-000, Brazil, Simone L. Nogueira, Alexandre Padilha, Izilda Curado, Marcos Boulos, and Silvia M. Di Santi. Send response to journal: Re: Lethal malaria caused by Plasmodium malariae in an asplenic patient in Brazil.	EDITOR - The letter by Harald M Lipman on preventing severe malaria infection after splenectomy deals mainly with the risks of falciparum infection in asplenic travellers to high risk malarial areas.1 Here we describe lethal quartan malaria in an asplenic patient in Brazil. Infection was confirmed by hemoscopic and molecular diagnosis. Plasmodium malariae was transmited by blood transfusion during surgery. The donor was asymptomatic and did not travel to high risk malaria areas. P. malariae usually causes low parasitemia and discreet symptoms and can persist lifelong in the blood. However, an asplenic woman that developed high parasitemia and cerebral malaria after infection with P. malariae during a blood transfusion has been described.2 The spleen influences the immunological defense against Plasmodium asexual stages because it contributes to innate resistance, limits the magnitude of the parasitemia in acute and chronic infections, and is important for clinical tolerance in the initial phases of infection. The spleen is the main organ where independent T cell immune response occurs, and where B cells, monocytes and macrophages prevail. Our patient, a 41-year-old man, has always lived in areas of São Paulo State without malaria transmission. The investigation discarded displacement to malarious areas or previous infection. In 1984 the patient presented diagnosis of Hodgkin’s lymphoma and was submitted to a splenectomy and chemotherapy. In 1991, due to reactivation of the disease, the patient received another cycle of chemotherapy, and the symptoms ceased. In July 2000 the patient suffered myocardial revascularization, developing constrictive pericarditis. A pericardectomy was accomplished and the patient was medicated with amicacin and cephalothin. During surgery the patient received two units of erythrocytes and 2 units of plasma from 4 different donors. During hospitalization the patient presented no fever and was discharged from hospital on July 16. On August 17, he was referred with a headache and nausea, presenting fever on August 26. Laboratory exams carried out on August 29 revealed 54% hematocrit, 17.7g% hemoglobin and erythrocytes containing Plasmodium. On the same day the patient was transferred to a hospital in São Paulo, with dyspnea and jaundice. Laboratory diagnosis accomplished by SUCEN confirmed the presence of Plasmodium, whose morphology resembled P. malariae, despite the high parasitemia (8.7%), uncommon for this species. Intravenous artesunate was used for treatment, but even with rapid decrease of the parasitemia to 0.3% after 24 hours, the patient developed delirium, multiple organ failure, shock and death on September 01. It is important to note that the Hodgkin’s disease was controlled for 9 years without immunosuppressive therapeutics, and thus there is no indication that this pathology might have contributed to the aggravation of the malaria. All 4 blood donors, resident in a city of São Paulo State without malaria transmission, referred no symptoms or travel to high endemic malaria areas. However, one donor (named here as 4) related a trip two years ago to Iguape, a city located in Atlantic forest area of São Paulo State, where sporadic cases of assymptomatic autochthonous malaria are described. Thick blood smears performed in all donors presented negative results. Indirect fluorescent antibody (IFA) test was carried out with antigens of asexual forms of P. vivax, P. malariae and P. falciparum to detect IgG and IgM antibodies. No IgM was detected in any donors. For donor 4, the IFA result using P. malariae antigens showed IgG antibodies titres of 1:2,560, the other donors being negative. Blood from donor 4 was collected on June 30 and transfused to the patient on July 11. On August 31 the same donor provided a second blood donation, for another patient. IFA using P. malariae antigen with serum from this second recipient revealed title of 1:80 for IgM antibodies and was negative for IgG. PCR was performed and confirmed the presence of the P. malariae species in blood from the patient, from donor 4 and from the second recipient, amplifying a fragment of ~150 bp.3 The case presented here, with acute and fatal evolution of P. malariae in an asplenic patient, emphasizes the importance of considering malaria infection even in the absence of symptoms and the possibility of high parasitemias with serious evolution in asplenic patients, even when the disease is caused by P. malariae. Furthermore, it seems opportune to review the criteria used in the clinical-epidemiological trials of the hemotherapy services located out with malaria endemic areas, especially in transfusions destined for immunodepressed or splenectomized individuals. Serological trials for malaria in low endemic areas should be done. Attention should also be given to displacement of donors to areas of sporadic transmission, where human cases of P. malariae are described4 and where primates, natural reservoirs for P. brasilianum/P. malariae, are present.5 References 1. Lipman HM. Preventing severe infection after splenectomy: risk of malaria and meningitis increases with asplenia. BMJ 2005;331: 576. (10 September.) 2. Tapper ML, Armstrong D. Malaria complicating neoplastic disease. Arch Intern Med 1976;136: 807-10. 3. Snounou G, Viriyakosol S, Zhu XP, Jarra W, Pinheiro L, do Rosario VE, Thaithong S, Brown KN. High sensitivity of detection of human malaria parasites by the use of nested polymerase chain reaction. Mol Biochem Parasitol 1993;61: 315-20. 4. Curado I, Duarte AM, Lal AA, Oliveira SG, Kloetzel JK. Antibodies anti bloodstream and circumsporozoite antigens (Plasmodium vivax and Plasmodium malariae/P. brasilianum) in areas of very low malaria endemicity in Brazil. Mem Inst Oswaldo Cruz 1997;92: 235-43. 5. Deane DM. Malaria studies and control in Brazil. Am J Trop Med Hyg 1988;38: 223-30. Competing interests: None declared Editorial note We have signed informed consent to publish the details of this case.