Consequently, other unknown mechanisms also account for the thromboembolic phenomena observed in the setting of PVB19 infection. Conclusions Splenic infarcts may be an atypical presentation of PVB19 infection. occurence of splenic infarction. These events were attributed to the development of a transient antiphospholipid antibody syndrome. In contrast, LOXO-101 (ARRY-470, Larotrectinib) our patient did not have elevated titers of antiphospholipid antibodies. Conclusions Splenic infarcts can be an atypical presentation of B19 contamination. Parvovirus B19 may induce thromboembolic events, even in the absence of antiphospholipid antibodies. were negative, as was real-time reverse transcriptase PCR for H1N1 influenza A computer virus. Antibody assessments for EpsteinCBarr computer virus (EBV), coxsackie B computer virus, and showed evidence of past contamination. Parvovirus B19 IgM antibodies were positive, while parvovirus B19 immunoglobulin G (IgG) antibodies were unfavorable, indicating an acute contamination. Titers of anticardiolipin and anti-2-glycoprotein I antibodies were within normal limits. The patient received symptomatic treatment with antipyretic and analgesic brokers. Over the following few days, his clinical and laboratory status gradually improved. On the fifth hospital day, his fever resolved. He was discharged home around 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. Discussion Splenic infarction occurs as a result of the occlusion of the splenic artery or its branches due to thrombosis or embolism [3]. The most LOXO-101 (ARRY-470, Larotrectinib) common etiologies are hematologic diseases, including myeloid disorders, lymphomas, hemoglobinopathies, and LOXO-101 (ARRY-470, Larotrectinib) hypercoagulable says; cardioembolic events; viral infections; and trauma [4], [5]. The majority of patients present with pain in the left upper quadrant or left flank or both. However, as in this case, a surprising percentage of patients have no symptoms localized to the splenic area. The most frequent laboratory abnormality is usually elevated lactate dehydrogenase levels, as seen in our patient [6]. A major concern, when evaluating a patient with fever accompanied by splenomegaly and splenic infarcts, is usually bacterial endocarditis. This diagnosis was ruled out by sterile blood cultures and BMP2 normal transesophageal echocardiography as well as recovery without antimicrobials. Additionally, the acuity of our patient’s illness, and his rapid and complete recovery argued against hematologic malignancies, being most consistent with a viral contamination. The viral infections that have been associated with splenic infarcts are infectious mononucleosis [7], [8] and acute CMV contamination [9]. Both conditions were excluded on the basis of negative serologic testing. Our patient did not present with any of the classic syndromes associated with PVB19 contamination. Nevertheless, he had a remarkably low reticulocyte count. Asymptomatic transient reticulocytopenia is usually a hallmark laboratory feature of PVB19 contamination. PVB19 replicates primarily in erythroid progenitors. Virus-induced cytotoxicity results in cessation of red cell production. In individuals without hemolytic anemia, this transient arrest of red cell production will lead to only a minimal drop in hemoglobin levels but in patients with increased destruction of red cells, who depend on continual rapid production of erythrocytes (hemoglobinopathies or hemolytic anemias), this suppression of erythropoiesis can cause a transient aplastic crisis with severe anemia [1], [10]. A wide range of unusual clinical manifestations have been reported in association with PVB19 contamination, including vasculitis, myocarditis, glomerulonephritis, peripheral neuropathy, meningitis and encephalitis, immune thrombocytopenia, and hemophagocytic syndrome [11]. Three cases of thromboembolism have also been described, to our knowledge; a man with a splenic infarct [12], a woman with multiple pulmonary emboli [13], and a woman with right pulmonary arterial and superior mesenteric venous thromboses [14]. Comparable to our case, all these occurrences involved young previously healthy patients who recovered fully. In regards to pathogenesis, they were attributed to the development of a transient antiphospholipid antibody syndrome. Our patient did not have elevated titers of antiphospholipid antibodies. Consequently, other unknown mechanisms also account for the thromboembolic phenomena observed in the setting of PVB19 contamination. Conclusions Splenic infarcts may be an atypical presentation of PVB19 contamination. PVB19 contamination should be considered in the differential diagnosis of fever accompanied by splenic infarcts in immunocompetent young adults. Clinicians must be aware of.