Nancy L. Stitt, RN, BSN


April 03, 2003

Opportunistic Infection

The majority of infections that occur in organ transplant recipients are opportunistic and are a major cause of death in the immunocompromised patient. Opportunistic infections are caused by organisms that are ubiquitous in the environment, but that rarely cause disease in the immunocompetent host. Normal protection from opportunistic organisms in the human is from innate and acquired immune mechanisms and normal flora. Functions of the innate and acquired immune system are described and discussed in detail in Chapter 2 of this book, "Immunologic Aspects of Organ Transplantation."[1]

The immunosuppressed individual is vulnerable to both endogenous and external organisms. In general, opportunistic infections result from at least 1 of 3 basic mechanisms: (1) exogenous acquisition of a particularly virulent pathogen (eg, meningococcal meningitis or pneumococcal pneumonia), (2) reactivation of an endogenous latent organism (eg, herpes simplex virus [HSV], herpes zoster virus [HZV or shingles], or tuberculosis, and (3) endogenous invasion of a normally commensal or saprophytic organism (eg, bacteria, viruses, fungi, or protozoa/parasites). The exact type of opportunistic infection (bacterial, viral, fungal, or protozoal/parasitic) that occurs depends on the type and extent of immunologic alteration, whether it be cellular, humoral, phagocytic, or a combined defect; and on organisms present in the internal and external environments. The administration of corticosteroids and other immunotoxic drugs to transplant recipients can result in massive depression of all phases of host defense, including a breakdown of cutaneous and mucosal barriers.

Nosocomial infections normally occur in approximately one fourth to one half of patients admitted to an ICU. The most common nosocomial infections encountered in the ICU are pneumonia, vascular catheter-related bacteremias, and urinary tract infection (UTI). Historically, these infections were caused by gram-negative bacteria the majority of the time, but etiologies for nosocomial infections have undergone a striking change: the last decade has witnessed the emergence of gram-positive bacteria as the foremost cause of infection in hospitalized patients. Staphylococcus aureus is second only to coagulase-negative staphylococci as the leading source of nosocomial bloodstream infections in the United States, with an increasing prevalence of MRSA.[2] National and global trends in escalating rates of infection due to resistant gram-positive organisms have emerged, with a parallel dramatic increase in MRSA and VRE infections among liver transplant recipients.[3]

Nosocomial infections are directly related to the microflora that are abundant in the hospital environment, which quickly colonize patients' skin, oropharynx, and rectum, and it is these colonizing organisms that most often lead to infection. Normal protection from infection is provided by surface barriers such as the skin and mucous membranes, cellular immune mechanisms, and humoral factors. Very few organisms are capable of penetrating the keratin layer of the epidermis. Most organisms that reach the host through the skin do so after iatrogenic breaks in the skin, usually created during insertion of invasive devices. Although fomites such as equipment routinely used for assessing and treating patients are partially responsible for transmission of organisms, the major route of transmission of iatrogenic infection is direct hand contact.[4] Adherence to aseptic technique with procedures, equipment, and supplies and avoiding injury of tissue and mucous membranes are important measures in the prevention of infection in the immunocompromised patient. The primary infection control measure, though, is thorough, consistent hand washing, utilizing the 2002 Centers for Disease Control and Prevention (CDC) Guidelines for Hand Hygiene in Healthcare Settings.[4]

Although many infections are latent or reactivation infections, approximately 50% are acquired.[5] With the use of immunosuppression, shifts in the host's microbial flora occur as well as the characteristics of organisms that previously colonized the patient. More than 80% of acquired infections are caused by organisms that previously colonized the immunosuppressed host.[5] Organisms that normally colonize mucosa of the immunosuppressed host can become pathogenic and penetrate the injured mucosa, and establish local infection that may disseminate to distant organs.

The Respiratory Tract

The surface of the upper respiratory tract is covered by bacteria while the lower respiratory tract is sterile. The organism that most commonly colonizes the upper respiratory tract is S aureus. Responsible protective mechanisms in the respiratory tract include the cough reflex, ciliated respiratory epithelium, and the immunoglobulin secretory IgA. Patients in the ICU who have an endotracheal tube are at risk of developing respiratory tract infections as a result of translocation of bacteria to the lower respiratory tract through endotracheal suctioning and patient positioning while intubated.[6]

The Gastrointestinal (GI) Tract

The GI tract maintains a normal flora as a result of the acidic gastric pH and gastric motility. Intestinal bacterial flora can be roughly divided into 2 types: (1) large numbers of anaerobic organisms, which tend to peacefully coexist with the host, and (2) smaller numbers of potentially pathologic aerobic flora (mainly aerobic gram-negative E coli), whose growth rate tends to be controlled by the anaerobic flora. Alterations in the protective balance due to the use of antacids, histamine-2 receptor blocking agents, antibiotics, and stasis of the GI tract can lead to an overgrowth of pathogenic and resistant gram-negative and gram-positive bacteria as well as fungi.[7]

Endogenous pathogens, primarily aerobic enteric bacteria and Candida, are potential causes of infections in liver transplant recipients, occurring within the first and second month posttransplantation. The usual sites are the abdomen, bloodstream, lungs, and surgical wound. Selective bowel decontamination (SBD) was developed as a means to eliminate aerobic gram-negative bacilli and fungi from the GI tract in order to reduce the incidence of infection by these pathogens. Despite the use of SBD at various centers over the past 15 years, the efficacy of this treatment has not been shown.[7]

Enteral nutrition is frequently necessary to provide adequate nutrients to critically ill or debilitated patients in the posttransplant period and may be favored over parenteral nutrition in hopes of avoiding fungal sepsis.[8]Enteral formulas, however, are also superb microbiologic culture media and are easily contaminated, and can lead to gastroenteritis and sepsis.[9,10,11,12,13]Organisms that frequently contaminate enteral formulas include Enterobacter cloacae, Klebsiella pneumoniae, streptococci, Pseudomonas aeruginosa, Serratia spp, Citrobacter spp, and Bacillus spp. The use of closed delivery systems and institution-based nursing policies and procedures related to volume and hang time of enteral formulas should be designed to prevent the contamination of these formulas.

The Urinary Tract

The bladder, ureters, and kidneys are sterile, but bacteria colonizing the perineum extend a short distance into the urethra. The major offender in the sterile bladder environment is the indwelling urinary catheter.


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