Page 37 - Haematologica Atlas of Hematologic Cytology

CHAPTER 4 - Viral infections
Chapter 4. VIRAL INFECTIONS
Viral infections can lead to alterations of all hematopoietic lineages, but they cannot be definitively classified on cytological preparations because of their lack of specific features. The most frequent finding is an increase in the number of circulating lymphocytes that may present morphological features identical to those of normal lymphocytes (such as in infections due to Coxsackie virus, various adenoviruses, influenza virus) or may be atypi- cal (as in infectious mononucleosis, IM). Atypical or reactive lymphocytosis is characterized by a high degree of cellular polymorphism with a morphological spectrum ranging from the small lymphocyte to the immunoblast or plasma cell (Zini et al., 2010; Palmer L et al., 2015). In IM, Epstein-Barr virus (EBV) infects B lymphocytes that may show a basophilic and vacuolated cytoplasm; the characteristic atypical lymphocytes observed in the blo- od smear are a reactive population of T cells. Reactive lymphocytes are usually large in size, and have eccentric nucleus, basophilic cytoplasm, rather loose chromatin and evident nucleolus. Other conditions may present the mononucleosis syndrome pattern, i.e. lymphocytosis with a high number of reactive lymphocytes: acute viral hepatitis, cytomegalovirus (CMV) and adenovirus infection, mumps, rubella, roseola, toxoplasmosis and drug re- actions. In the bone marrow, an increase in typical and atypical lymphoid cells similar to those of the peripheral blood is usually observed.
As for the erythroid series, viral infections may be associated with hemolytic anemia due to red cell auto- antibody production, usually of the warm type, although cold-antibody syndromes have been reported in me- asles, influenza, IM and mumps. In such cases, reticulocytosis, occasional peripheral spherocytes or red cell agglutinates and bone marrow erythroblastic hyperplasia are observed. During viral infections, non-immune microangiopathic hemolytic anemia may also occur, in association with thrombotic thrombocytopenic purpura or disseminated intravascular coagulation. The finding of fragmented red cells and leuko-erythroblastic anemia is useful for diagnosis.
Anemia occurs with pancytopenia (as a result of bone marrow suppression by a range of cytokines) in virus-as- sociated bone marrow aplasia in infections due to hepatitis viruses, CMV, herpes viruses, especially in immuno- suppressed hosts. It occurs as an isolated finding in parvovirus B19-induced pure red cell aplasia and in transient erythroblastopenia of childhood caused by human herpesvirus 6 (HHV6) (See Chapter “Pure red cell aplasia”).
Both thrombocytopenia and thrombocytosis can be observed in response to viral infections. Children with idiopathic thrombocytopenic purpura frequently have a history of a preceding viral illness and anti-platelet auto- antibody production is reported in IM, rubella and CMV infections. In the case of peripheral platelet destruction, bone marrow megakaryocytes are well represented or increased in number. In the course of viral infections, a reduction in bone marrow thrombopoiesis is frequently subclinical, but it can be clinically relevant in virus-asso- ciated aplasia.
Viral infections, especially herpetic infections, may be associated with hemophagocytic syndrome with conse- quent pancytopenia (See Chapter “Hemophagocytic syndrome”).
Finally, it is important to mention the important pathogenetic role of some viruses, in particular hepatitis C virus (HCV), EBV and HHV8, in various types of lymphoproliferative disorders (see Chapter “Mature B-cell neo- plasms”).
Table 1. Human immunode ciency virus (HI ) infec on peripheral blood and bone marrow morphological featu- res.
Peripheral blood
Reac ve lymphocytes and dysplas c neutrophils Macrocytosis
Isolated thrombocytopenia
Pancytopenia
one marrow
Increased lymphocytes, plasma cells, macrophages, eosinophils Dyserythropoiesis and dysgranulopoiesis
Increased re culin bers
Hemophagocytosis
Infec ous granulomas
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