Infection in the compromised host

In spite of the development of successive generations of more powerful antibiotics, sepsis remains a common cause of death in the surgical patient. This fact is not surprising, since it is of little importance which organism is causing the infection if the patient's intrinsic antibacterial defenses cannot respond. Realization of the limitations of antibiotic therapy has prompted many investigators to study the immune and inflammatory systems with the ultimate goal of improving host defenses and increasing survival. In this article the local and systemic antibacterial defense systems have been reviewed. It is clear that the immunocompromised state is associated with multiple defects of the humoral and cellular components of both the nonspecific host defense system and the specific immune defense system. However, although consensus has not been reached on either the mediators responsible for the immunocompromised state or the prognostic and clinical significance of many of the described defects, work in this field is progressing rapidly. Nonetheless, knowledge that the host's antibacterial defense systems can be aided by good surgical technique, nutrition, appropriate use of antibiotics, and the sterile care of invasive catheters, lines, and tubes is critical in the prevention of fatal infections in the immunocompromised patient. When more information becomes available concerning the complex interrelations between the various cellular and humoral components of the host defense systems and their mediators and the symbiotic relations between man and his bacterial flora, it should be possible to develop specific strategies for the clinician to use to reduce the risk of infection in the high-risk surgical patient. Thus, in the future it may not be unusual for the clinician to alter the immunologic system of the host by the use of immunomodulators or vaccines to increase the host's resistance to infection. On the other hand, by manipulating the complex interrelations between the host and the indigenous bacterial flora, it may be possible to prevent the development of opportunistic infections originating from the gastrointestinal tract.