Nancy L. Stitt, RN, BSN


April 03, 2003

Bacterial Infection

Gram-negative bacteria are ubiquitous in the environment. P aeruginosa, Serratia marcescens, Proteus rettgeri, and E cloacae are the 4 most common gram-negative organisms implicated in infection in the immunosuppressed host.[21] Most bacterial infections are caused by organisms that already colonize in the patient and originate at sites of mucosal damage, ciliary dysfunction, or integumentary damage. In other words, bacterial infections generally begin when bacteria are allowed to bypass local anatomic and mechanical defense mechanisms. In addition to the obvious example of a break in the skin as a result of tissue injury or the insertion of invasive catheters, loss of the gut mucosal barrier is another important mechanism of bacterial infection. The gut serves as a primary reservoir for life-threatening bacteria in immunosuppressed individuals.

Bacterial infections are generally seen within the first posttransplant month, vary with the organ transplanted, and continue to be a major cause of morbidity in solid organ transplant recipients. Prevention of bacterial infections begins in some centers preoperatively (eg, use of SBD 3 days prior to liver transplantation), and all programs utilize perioperative antibiotic prophylaxis. The goal of perioperative prophylaxis is to eliminate any active infection and to protect against skin transient flora as well as resident flora of the transplanted site.[7]

Antimicrobial-Resistant Organisms

The incidence of antimicrobial resistance has escalated and is a particularly important problem. The incidence of MRSA infection has increased during the past decade, and deep-seated bacteremic infections due to MRSA (ie, bacteremic pneumonia or abdominal infections) have a poor prognosis (mortality of up to 86%).[22] The nosocomial spread of other drug-resistant pathogens, such as linezolid-resistant VRE and gram-negative bacteria that produce extended spectrum beta-lactamases, has also been observed.

Burkholderia cepacia complex is a group of 7 genetically distinct organisms (genomovars I-VII) that are inherently resistant to many antimicrobial agents. B cepacia complex causes pulmonary infection in 5% of cystic fibrosis patients and is associated with poor outcome following lung transplantation. In some centers, B cepacia complex infection has precluded lung transplantation.


Legionella organisms are aerobic, gram-negative rods that are ubiquitous in nature. Legionella infection in transplant recipients can be community-acquired or iatrogenic. The exact mode of transmission is unclear, but most outbreaks can be traced to a contaminated water or soil source. Legionella infection after transplantation can occur at any time, but is most common during the first few posttransplant weeks and after treatment of acute rejection.

Signs and symptoms of legionellosis include high fever, chills, myalgias, malaise, headache, and diarrhea. Although upper respiratory infection is uncommon, dyspnea, mild productive cough, and pleuritic chest pain may occur. Legionella pneumophilia is associated, in the majority of cases, with pathologic conditions limited to the lungs, causing bilateral bronchopneumonia and consolidation. Signs and symptoms include tachypnea, dyspnea, dry nonproductive cough, pulmonary rales, alveolar infiltrates on chest x-ray, headache, chills, fever, diarrhea, myalgia, and arthralgia. Legionella infections are more severe in transplant recipients and are associated with a mortality rate of 25% to 50% in this population.[23,24,25]

The diagnosis of Legionella is difficult. The definitive diagnosis is a positive culture obtained by transbronchial or percutaneous needle biopsy or bronchial washing. Legionella does not respond to beta-lactam antibiotic therapy. Agents most active against Legionella include erythromycin, rifampin, tetracyclines, trimethoprim-sulfamethoxazole (TMP-SMX), and the fluoroquinolones. Erythromycin is the most commonly used agent for treatment of legionellosis, but doses as high as 4 g/day may be necessary.


Nocardia species (N asteroides, N caviae, N braziliensis) are often misclassified as either fungi or mycobacteria, but they are true bacteria. Nocardia is found in soil and decaying vegetable matter worldwide and, in most cases, the organism enters the body by inhalation. Norcardiosis is relatively uncommon in transplant recipients, and the incidence has decreased since the introduction of cyclosporine.

Nocardia infections frequently involve the lung. Typical symptoms include fever, productive cough, pleuritic chest pain, dyspnea, weight loss, and hemoptysis. Hematogenous spread is common, especially to the central nervous system (CNS). Dissemination also occurs to the skin, soft tissues, bones, and joints.

Diagnosis of Nocardia is by culture, and the organism is easily visualized on Gram's stain. Sulfonamides (particularly TMP-SMX) are the recommended agents for treatment for nocardiosis. The starting dose is in the range of 4-8 g/day, depending on renal function and body weight.


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