We describe a case of locally acquired Plasmodium ovale malaria in Spain. The patient was a Spanish woman who had never traveled out of Spain and had no other risk factors for malaria. Because patients with malaria may never have visited endemic areas, occasional transmission of malaria to European hosts is a diagnostic and clinical challenge.

ABSTRACT. Kikuchi's disease (KD), or histiocytic necrotizing lymphadenitis, was initially described in Japan in 1972. In the following years, several series of cases involving patients of different ages, races, and geographic origins were reported, but pediatric reports have been rare.The etiology of KD is unknown, although a viral or autoimmune hypothesis has been suggested. The most frequent clinical manifestation consists of local or generalized adenopathy, although in some cases, it is associated with more general symptoms, multiorganic involvement, and diverse analytic changes (leukopenia, elevated erythrocyte sedimentation rate, and C-reactive protein, as well as an increase of transaminases and serum lactic dehydrogenase).Diagnosis is based on characteristic pathologic findings that permit differentiation of this disease from lymphoma, systemic lupus erythematosus, and infectious lymphadenopathies.We CASE REPORTA 14-year-old white boy was admitted to our hospital after presenting with fever up to 39.8°C for 1 week, malaise, odynophagia, arthralgia, myalgia, abdominal pain, and pruritic skin eruption. Personal and family history was irrelevant. He did not recall any history of exposure to fleas, ticks, cats, or dogs, and there was no indication of animals scratches. On physical examination, several multiple peripheral adenopathies were detected (cervical, axillary, and inguinal), the sizes of which ranged from 0.5 to 2.5 cm in diameter. In general, these nodes were indurated, mobile, and relatively tender. Liver and spleen were palpable 4 cm and 2 cm, respectively, below the costal margin. Erythematous, flat-tipped papules were patent on the face, back, and extremities (Fig 1).Serial blood analyses during the first 2 weeks after admission revealed pancytopenia (2.7 ϫ 10 9 leukocytes/L with normal differential formula and atypical lymphocytes in peripheral blood; 9.3 g/dL hemoglobin; 107 ϫ 10 9 /L platelets). Erythrocyte sedimentation rate was 39 mm per hour, and C-reactive protein was 163 mg/dL. Biochemical analysis, coagulation, hepatic and renal functions, immunoglobulins, and complement count were normal (Tables 1, 2). Rheumatoid factor, antinuclear antibodies, direct Coombs test, and two Mantoux test results proved to be negative. Multiple blood, urine, feces, sputum, and tissue culture results also were negative. Antibody titers against Epstein-Barr, cytomegalovirus, hepatitis, HIV, and Parvovirus B 19 , and serum polymerase chain reaction for herpesvirus type 6 were negative as well, as were results of serologic tests for syphilis, Brucella, toxoplasmosis, Leishmania, Rickettsia, Borrelia, and Bartonella henselae and quintana.Results of chest roentgenography, echocardiography, and bone scan were normal; an abdominal ultrasound examination detected hepatosplenomegaly with uniform density and nephromegaly with increased cortical echogenicity.The patient was treated with ceftriaxone and nonsteroid antiinflammatory drugs during the second week of fever. with apparent lack of remission. Furthermore, the ...

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The use of ticlopidine as an antiplatelet drug has been associated with agranulocytosis (I-2%) and thrombocytopenia (O.l%), and in a few cases (8 cases have been described) with severe aplastic anemia (SAA) [ 1-31, Patients with aplastic anemia and residual myeloid progenitors can respond to pharmacologic doses of growth factors such as granulocyte colony-stimulating factor (G-CSF). However, all patients who show an increase in neutrophil counts with G-CSF return to baseline values 2-10 days after discontinuation of the drug [4]. We describe here the first case of sustained granulocyte recovery after G-CSF in a patient with ticlopidineinduced SAA.A 78-year-old-man was admitted with a 48-hr history of fever. He had been taking amiodarone for 1 year for supraventricular tachycardia, and ticlopidine 500 mg/day for 6 weeks for peripheral arteriopathy. He suffered from chronic renal failure due to obstructive uropathy and recurrent urinary tract infections. For months, he had presented a normocytic normochromic anemia with hemoglobin levels near 10 g/dl and a creatinine clearance of 30 mlhin. On admission, physical examination revealed a temperature of 39°C. The lungs were clear. No lymphadenopathy or hepatosplenomegaly were found. Peripheral blood counts were WBC 0.9 X 109/L (10% neutrophils, 90% lymphocytes), hemoglobin 8.3 g/dl, and platelets 12 X 109/L. Biochemical parameters (except from creatinine 3.2 mg/dl); immunoglobulin levels, complement, and autoantibodies were normal. Serological studies for hepatitis B and C viruses, human immunodeficiency virus (HIV), parvovirus, and Epstein-Ban virus (EBV) were negative.Serrutiu marcenses was identified in blood and urine cultures. A bone marrow biopsy showed a picture of SAA without cytogenetic abnormalities. Ticlopidine was stopped. Treatment included IV antibiotics, red cell and platelet support, and G-CSF at a daily dose of 5 p,g/kg subcutaneously. Twelve days after G-CSF was begun, WBC was 1.9 X 109/L with 32% of neutrophils. Two days later, WBC was 6.6 X 109/L with 70% neutrophils and remained within the normal range thereafter, although G-CSF was discontinued on day 14. Hemoglobin and platelet counts remained at admis-0 1995 Wiley-Liss, Inc.sion values with high transfusion requirements. High-dose immunoglobulins and recombinant erythropoietin were given without results. The clinical course was stormy, and death occurred 5 months later from massive gastrointestinal bleeding.In six of the eight reported cases of ticlopidine-related SAA bone marrow completely recovered in 15 days to 1 year after discontinuation of the drug. The sustained neutrophil recovery after G-CSF in our case and the persistence of low hemoglobin and platelet counts might suggest that ticlopidine-related SAA is not immunologically mediated, as described by other studies [5]. Thus a trial with myeloid growth factors such as G-CSF or GM-CSF is warranted.Aplastic anemia is one of the most dreaded adverse drug reactions. Monitoring of the blood counts during ticlopidine therapy should he performe...