After allogeneic bone marrow transplantation certain patterns of infectious complications emerge that follow the clinical course, are correlated to the immunobiology of transplantation and are almost predictable in their character and expression. The preparative regimen, designed to generate complete aplasia, will be associated with severe and sometimes life-threatening bacterial infections, predominantly with Gram-negative organisms derived from bowel flora, but also Gram-positive skin saprophytes. In this early aplastic phase, life-threatening viral infections are less common, consisting mainly of herpes simplex and possibly Epstein-Barr stomatitis and BK papovavirus cystitis. Systemic infections with invasive filamentous fungi are rare and are seen only when the induced aplasia is markedly prolonged. Once early marrow recovery has been achieved, systemic infections will generally disappear unless acute graft-vs.-host disease develops. This complication, which will lead to the breakdown of natural barriers such as skin and gastrointestinal epithelium and the marked impairment of all systemic defense mechanisms, can cause polymicrobial infections as well as set the stage for life-threatening viral infections. Such opportunistic viral infections, leading to either interstitial pneumonia or hemorrhagic gastroenteritis, are the major threat in the early recovery phase after engraftment has taken place. Usually caused by cytomegalovirus and rotavirus, respectively, these infections are the primary expression of the severe combined immunodeficiency post transplant, statistically associated with the presence of acute graft-vs.-host disease and amenable to immunologic manipulations. With the recovery of cellular and humoral immune function derived from transplanted donor lymphoid cells, the third phase of infectious complications is reached, covering 3 months to 2 years post grafting. In this phase the patient is highly likely to develop sinupulmonary infections primarily with encapsulated Gram-positive organisms such as Streptococcus pneumoniae. Since in this phase the patient is prone to develop chronic graft-us.-host disease and associated functional hyposplenism, these infections are often thought to result from this immunologic compromise. However, these infections can occur in the absence of chronic graft-us.-host disease and are then clearly associated with an IgG2 and IgG4 subclass deficiency seen frequently at that time period after bone marrow transplantation. Associated with chronic graft-us.-host disease or the therapy of this complication are also opportunistic infections with herpes zoster virus and fungal organisms such as Aspergillus. The strategies to prevent these almost predictable infections are being developed. The introduction of less toxic preparative regimens combined with extensive gnotobiosis in protective environments has reduced early bacterial complications to a minimum. Effective prevention of graft-us.-host disease together with the use of virus-free blood products and passive serotherapy with immunoglobulin preparations has markedly improved the survival rate of viral infections. Lastly prolonged use of antibacterial antibiotics coupled with the supplementation of necessary antibodies can virtually abolish late bacterial infections. These strategies can effectively reduce the posttransplant mortality from infectious causes to less than 10%.
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P. J. Tutschka (1988) studied this question.