Disseminated Pathogenesis

Cytomegalovirus (CMV) is a ubiquitous beta-herpesvirus that has the distinguishing characteristic of all herpesviruses, the ability to persist in the host. Persistent CMV causes serious infections such as interstitial pneumonia, gastrointestinal mucosal ulceration, retinitis, and hepatitis in immunosuppressed patients. Elucidating mechanisms of CMV persistence is critical to a complete model of pathogenesis as CMV infection, morbidity, and mortality often are the result of dissemination of virus acquired before the onset of immunosuppression. 

Shock is a constant finding in all cases of disseminated coagulation. In animal experiments, heparin injection prevents clotting and shock, and therefore it is generally accepted that shock is a direct consequence of the disseminated thrombosis. The drop in blood pressure may be slight and reversible, or it may develop into an irreversible state and lead to death. The pathogenesis of shock has been explained as follows. Sudden obstruction of liver and lung capillaries impairs the venous return to the heart, and the cardiac output is reduced. 

We have already pointed out that the local pathology of the heart and lungs may be important in determining the intensity of the symptoms. It seems that endothelial or vasomotor changes may determine the localization of the thrombi. The pathogenesis of disseminated coagulation is summarized in Fig. 7-10. 

Based on the understanding of the pathogenesis of colorectal liver metastasis via portal dissemination, intraportal chemotherapy after primary tumor resection was tested in several phase III trials. Neither a reduction of hepatic progression nor a survival benefit could be unanimously observed, so... 

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