A 33-year old man was admitted to our hospital because of a 5-day history of continuous fever up to 39  C, and diffuse headache. He was unmarried and lived with his parents in Thirasia Island near Santorini, working as a builder, was sexually active and consistently used condoms. He did not smoke, use illicit drugs, or misuse alcohol, had no pets or exposures to animals, and had never traveled abroad. The man reported no recent tick or mosquito bites, no ingestion of unpasteurized milk or milk products, and no sick contacts and had received all routine childhood vaccinations, had no known medical problems, and did not take any medications. His family history was negative for tuberculosis, cancer or autoimmune disease.
On physical examination, the patient appeared well and was in no acute distress; he was alert and communicative. His temperature was 39  C, heart rate 73 beats per minute, blood pressure 120/80 mmHg, respiratory rate 16 breaths per minute, and oxygen saturation 99% while breathing ambient air. He had no synovitis, rash, photophobia, or nuchal rigidity. His abdomen was soft, with mild tenderness in the left upper quadrant on deep palpation. There was no hepatomegaly or splenomegaly, and no cervical, axillary, or femoral lymphadenopathy. Heart murmurs were not detected.
Laboratory analyses revealed normocytic, normochromic anemia (hemoglobin level, 12 g per deciliter), with a low reticulocyte count (0.3%), leukopenia (white-cell count, 3420 per cubic millimeter, with 68% neutrophils, 25% lymphocytes, 7% monocytes, and no eosinophils or band forms), thrombocytopenia (platelet count, 87,000 per cubic millimeter), and elevated levels of hepatic aminotransferases (aspartate transaminase 138 U per liter, alanine transaminase 111 U per liter), lactate dehydrogenase (1383 U per liter), creatine phosphokinase (1019 U per liter), and C-reactive protein (112 mg per liter). Clotting times (dilute prothrombin time and activated partial-thromboplastin time) were not prolonged. Urinalysis was normal. Multiple blood cultures were sterile.
An abdominal ultrasound examination revealed a mildly enlarged spleen, with two peripheral wedge-shaped hypoechoic lesions, which were characteristic of splenic infarcts. A computed tomography (CT) scan of the abdomen (Fig. 1), obtained after the administration of intravenous and oral contrast material, confirmed the results of ultrasonography, demonstrating splenomegaly (with the spleen measuring 15.4 cm in the craniocaudal dimension), and two wedge-shaped areas of hypoenhancement in the periphery of the spleen, features that were consistent with splenic infarcts. No other organ abnormality was observed. An electrocardiogram showed sinus rhythm. Transesophageal echocardiography showed no valvular vegetations.
Hepatitis A immunoglobulin M (IgM) antibody, hepatitis B surface antigen and core IgM antibody, a polymerase chain reaction (PCR) assay for hepatitis C viral RNA, and serologic tests for cytomegalovirus (CMV), herpes simplex virus, coxsackie A virus, echovirus, human immunodeficiency virus, Rickettsia species, Coxiella burnetii, Brucella melitensis, and Leishmania were negative, as was real-time reverse transcriptase PCR for H1N1 influenza A virus. Antibody tests for Epstein-Barr virus (EBV), coxsackie B virus, and Toxoplasma gondii showed evidence of past infection. Parvovirus B19 IgM antibodies were positive, while parvovirus B19 immunoglobulin G (IgG) antibodies were negative, indicating an acute infection. Titers of anticardiolipin and anti-beta2-glycoprotein I antibodies were within normal limits. The patient received symptomatic treatment with antipyretic and analgesic agents. Over the following few days, his clinical and laboratory status gradually improved. On the fifth hospital day, his fever resolved. He was discharged home on the tenth hospital day. Whether he developed parvovirus B19-specific IgG antibodies during the convalescent phase remained unknown, because the relevant test could not be performed in his island.