Acute infectious lymphocytosis: cell phenotype and etiology

Most cases of acute infectious lymphocytosis have been described in children under 10 years of age. The disease is characterized by hyperleukocytosis secondary to a sharp increase in the number of small lymphocytes. Although a viral etiology has been suspected, thus far the specific agent was largely ased on epidemiologic data suggesting a contagious process. Most cases are sporadic but multiple family members can be affected and epidemics may occur in institutions.unlike infectious mononucleosis, AIL has no characteristic clinical pattern and accordingly is never clinicall suspected. It is a laboratory finding. The nature of the lymphocyte subpopulation involved in AIL has recently aroused interest; previous studies yielded conflicting information. Dadash-Zadeh et al and Cassuto et al reported 50 and 17% 'null' cells in the peripheral blood of two children with AIL, respectively. In both studies, 'null' cells were defined by the absence of mature T- or B-cell markers. In both patients, 'null' cells may have represented immature and undifferentiated cells of B or T lineage that had not yet expressed mature surface markers. In contrast, Bertotto et al reported that 87% of peripheral blood lymphocys, in a child with AIL, were T-cells and showed that the majority of these cells were helper/inducer phenotype. Sulsbury reported increased B-cells in approximately 70% of peripheral blood lymphocytes and half of them were immature. In our two patients, absolute counts of all lymphocyte subsets were increased.
The cause of the sharp increase in the lymphocyte counts is unknown. In an epidemiologic study, different viruses were isolated from patients with AIL. The only virus appearing in a substantial proportion of the patients was similar to a coxsackie A virus . We demonstrated the presence of a rhinovirus in our two patients. This suggests that AIL may be a heterogeneous disorder, with predominantly T- or B-cell activation, according to the nature of the triggering infectious agent. Further studies of lymphocyte populations and etiological agents of AIL should provide insight into the pathogenesis of the illness and the heterogeneous expression of the lymphocyte lineage.