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patient 1 , a 36-year - old woman who worked as a technician in a clinical laboratory , was admitted to bordeaux hospital , france , on june 2 , 2009 . she had a 7-day history of high fever ( up to 395 c ) , rigors , headache , and jaundice .
hematologic tests showed decreased platelets ( 33,000  10 platelets / l ) and increased serum c - reactive protein ( 130 mg / l ; reference < 5 mg / l ) .
although the patient denied having traveled abroad in the past 5 years , she lived near an international airport , and her clinical signs were typical of malaria .
consequently , thick and thin blood smears were performed and indicated p. falciparum parasitemia of 0.1% .
mol / l ) . by 6 hours after hospital admission , her condition had dramatically worsened , with hemodynamic collapse ( blood pressure 60/32 mm hg ) associated with macroscopic hemoglobinuria ; parasitemia increased to 6% .
treatment was intravenous quinine formate ( loading dose 17 mg / kg , followed by maintenance dose of 8.3 mg / kg 3/d ) .
after 5 days , her medication was switched to oral quinine for another 2 days .
parasitemia was absent 6 days after starting quinine , and the patient was discharged 2 days later .
patient 1 later recalled that 2 weeks before hospital admission she had been injured by a broken , blood - contaminated , malaria diagnostic ( qbc ) test tube at work . because she considered the incident trivial
had she done so , the standard blood exposure protocol would have been automatically triggered .
the source of the blood was subsequently traced to a patient returning from the congo , for whom p. falciparum parasitemia of 4% had been diagnosed when the blood sample was taken .
falciparum isolates were genotyped at the 7a11 , c4m79 , pf2802 , and pf2689 microsatellite loci and at the highly polymorphic loci of the merozoite surface protein 1 and 2 antigen genes by fluorescent end - labeled nested pcr and restriction fragment length polymorphism analysis ( 57 ) .
results showed that the 2 infections had the same molecular signature and complete homology and were confirmed by genotypic analysis of resistance markers . a threonine variant on codon k76 t point mutation of p. falciparum chloroquine resistance transporter and an identical level of resistance to antifolate drugs ( p. falciparum dihydrofolate reductase 
thymidylate synthase point mutations at positions 51 , 59 , and 108 ) were found ( table ) ( 5,7 ) .
a diagnosis of severe malaria as a result of occupational percutaneous blood exposure was therefore retained . *
na , not applicable ; msp , merozoite surface protein ; pfcrt , p. falciparum chloroquine resistance transporter ; pfdhfr , p. falciparum dihydrofolate reductase . 
pfcrt codon 76 point mutation was genotyped by nested pcr and restriction fragment - length polymorphism analysis .
pfdhfr point mutations at positions 16 , 51 , 59 , 108 , and 164 were genotyped by nested pcr and primer expansion .
patient 2 was a 15-day - old girl who was referred from dakar , senegal , where she had been born on march 11 , 2009 .
she was the third child of a lebanese family who had no known genetic illness and who lived in an air - conditioned house .
blood testing indicated decreased hemoglobinemia ( 5.2 g / dl ; reference 914 g / dl ) and reticulocytosis ( 260,000 
serum c - reactive protein was < 5 mg / l . the patient received a 60-ml whole blood transfusion from a compatible donor in dakar on march 26 ; the next day , she was transferred to bordeaux hospital .
at the time of admission , hematologic testing confirmed severe regenerative hemolytic anemia ( hemoglobin 9.5 g / dl , reticulocytes 320,000  10 cells / l , and serum haptoglobin < 0.08
serologic testing for malaria , thick and thin blood smear , and specific pcr for p. falciparum pbrk114 in the newborn and her mother were negative .
screening of both parents and the newborn for inherited hemolysis excluded an erythrocyte membrane abnormality .
hemoglobinopathy and erythrocyte enzyme ( glucose 6-phosphate dehydrogenase , pyruvate kinase , and hexokinase ) deficiencies were also ruled out .
the newborn and her parents were followed up weekly ; no pertinent clinical findings or abnormal pcr and blood smear were found until 7 weeks after birth , when febrile thrombocytopenia ( 92,000  10 platelets / l ) and neutropenia ( 540 
treatment with intravenous quinine formate at 8.3 mg / kg 3/d for 4 days , followed by oral mefloquine ( 20 mg / kg ) for 1 day led to prompt improvement .
follow - up at 3 and 5 months of age showed resolution of anemia and no relapse of malaria .
test results for hemolysis remained negative , and glucose 6-phosphate deshydrogenase and erythrocyte pyruvate kinase levels 6 months after transfusion were within normal limits .
although it could not be confirmed , neonatal anemia was attributed to fetal  maternal hemorrhage .
we contacted the clinic in dakar , where the blood sample but not the donor could be traced .
however , a thick and thin blood smear examination subsequently performed in dakar was positive for p. falciparum , clearly supporting a diagnosis of transfusion - transmitted malaria .
in non  malaria - endemic countries , accidental blood - borne inoculation of p. falciparum after direct occupational exposure of health care or laboratory personnel has been rarely reported ( 810 ) .
the course of such occupationally acquired malaria may be critical if the inoculating injury is neglected or unrecognized , as it was by patient 1 .
this case emphasizes the need for laboratories handling blood to ensure that every accidental injury , however trivial it may seem , is declared and managed . as occurred with patient 1 , a delayed diagnosis may also delay delivery of appropriate care for preventing severe or complicated illness ( 9,10 ) . whereas most non  malaria - endemic countries , including france ,
are implementing selective screening strategies for blood product donors ( 11 ) , prevention of transfusion - transmitted malaria in endemic areas such as senegal remains a challenge because such screening is not routinely performed . for patients such as patient 2
, malaria is rarely diagnosed in non  malaria - endemic countries ( 12,13 ) . for this patient ,
the chronology of events and exposure to blood from a contaminated donor are highly suggestive of transfusion - transmitted malaria . in the absence of immunologic indicators that the mother had been exposed to p. falciparum ,
vertical transmission is extremely unlikely , and the risk for mosquito transmission is low because of the family s living environment and the time of year .
nevertheless , without gene sequencing of parasites from the donor , transfusion - transmitted malaria can not be demonstrated unequivocally .
neonates are assumed to be able to counteract natural infection with malaria because of the predominance of fetal hemoglobin , which is not suitable for complete erythrocyte schizogony of p. falciparum ( 14 ) .
for patient 2 , transfusion with infected adult blood may have compromised this capacity , enabling the infection to follow its natural course . in senegal , blood transfusion recipients are routinely given antimalaria treatment ( 15 ) .
unfortunately , such treatment can not be extended to neonates because of lack of a validated and convenient therapeutic antimalaria regimen for this age group .
however , in non  malaria - endemic countries , a recent history of blood transfusion or an episode of accidental inoculation of blood may account for malaria infection in persons who are not otherwise at risk .
plasmodium falciparum malaria is usually transmitted by mosquitoes . 
 we report 2 cases in france transmitted by other modes : occupational blood exposure and blood transfusion . even where malaria is not endemic , 
 it should be considered as a cause of unexplained acute fever .