Aminoglycosides often are employed for empiric therapy of nosocomial infection because of their activity against a wide spectrum of gram-negative aerobic bacilli (GNAB). New beta-lactam antimicrobials also are active against many GNAB. As toxicity appears less likely for the beta-lactams than for aminoglycosides, their use might be preferable if susceptibility profiles were equivalent.

We studied susceptibility of 90 GNAB recovered from blood culture during a three-month period. All were susceptible to aminoglycosides; 93% were susceptible to at least one of the following: ampicillin, carbenicillin, ticarcillin, cephalothin, chloramphenicol or trimethoprim-sulfamethoxazole. All were susceptible to at least one of our newer beta-lactams (cefamandole, cefoxitin, cefotaxime, moxalactam, piperacillin), but the percentage susceptible to any single beta-lactam was lower than that for any of the aminoglycosides tested. All of the isolates were susceptible to combinations of two beta-lactam drugs.

In our hospital, beta-lactams may be reasonable alternatives to aminoglycosides in selected cases where susceptibility has been demonstrated. However, aminoglycosides continue to provide the broadest single-drug coverage for empiric therapy of known or suspected sepsis with GNAB. The utility of combinations of beta-lactam drugs for empiric therapy requires further assessment by clinical trials.

The dissemination of resistance determinants among bacterial populations depends on ecological and epidemiological properties as well as additional factors: 1) the mechanism of resistance or its specificity toward a certain drug, and 2) the genetic basis in relation to the mobility of the genetic material and its survival in bacteria. From two resistance mechanisms directed toward old-fashioned drugs, namely sulfonamides (Su) and streptomycin (Sin), we can deduce that a resistance mechanism is encoded by a special sort of genetic material. Thus the linked SmSu resistance mediated by a sulfonamide-resistant dihydropteroatsynthetase II and the aminoglycoside phosphotransferase APH-(3") is always located on very small pBPl-like plasmids. Such plasmids survive without selective pressure of drugs in Enterobacteriaceae in the bowel flora of humans and animals. Both resistance determinants can be mediated by a transposon which codes for the production of a dihydropteroatsynthetase I in connection with an aminoglycoside adenylyltransferase AAD-(3"). These two mechanisms are genetically linked as well. The basic structure is a transposon designated Tn2411, which belongs to a whole family of transposons, all including the basic structure; however, their genetic exchange and substitution leads to structures coding for many different enzymatic characters: ANT-(2") (Gentamicin resistance), CAT (Chlo-ramphenicol resistance), AAC-(6') (resistance to all modern aminoglycosides), TEM-1, OXA-1, OXA-2, or PSE (β-lactam resistance). Resistance to the modern (β-lactamase-stable antibiotics is mediated by mutation in the regulatory genes of chromosomally-determined (β-lactamases. A spread of these resistance mechanisms can be avoided as long as the responsible genes are not located on sufficient structures like small plasmids or efficient transposons.

The genetic determinants of antibiotic resistance originate as a result of random events, affected only by those physical and chemical agents that stimulate mutation. It is the selection and spread, within and between species, of new genetic material that is influenced by environmental factors, though the intrinsic antibiotic resistance of many opportunistic pathogens remains to be explained.

Depending on the frequency of genetic change, the biochemical resistance mechanism, the efficiency of selection (including access of antibiotic to relevant bacteria), and the opportunity for person-to-person spread, resistance may present in a number of ways. The use of an antibiotic in any individual may give rise to resistance, among pathogens or normal flora, to that antibiotic alone, to some or all members of its class, or to additional unrelated antibacterials, or to the acquisition of new bacteria, from a variety of sources (humans, animals, inanimate environment). A resistant organism may occasionally have other advantages that enable it to spread in the absence of the initial selective agents.

In the absence of controlled experiments, which are difficult or perhaps impossible, the only evidence of the truth of these hypotheses comes from the clinical use of antibiotics. A wise observer will conclude that the emergence of resistance is a rare event in an individual patient, but is commoner but by no means universal in populations, especially those that are closed. He will note the reports of diminished resistance in the presence of increased usage.

The role of academic infection control is to explain all the phenomena observed, and to formulate methods for identifying and countering the actual as opposed to the imagined hazards.

Much has been written recently concerning the new and growing occurrence of infections in compromised hosts. During the almost four decades since the end of World War II scientific investigation has produced extraordinary advances in diagnosis and treatment. This has resulted in two changes which have implications for this discussion. First, the classical acute community-acquired infections now are recognized quickly and treated effectively with antibiotics. Indeed, many such infections are managed quite effectively by physicians in the office or clinic and no longer require admission to the hospital. (For example, it has been years since I have seen mastoiditis or streptococcal erysipelas in my hospital consulting practice.) We have abandoned our “pneumonia ward” which once housed patients in various stages of life-threatening pneumococcal infection. Similarly, intensive immunization of our population has virtually eliminated poliomyelitis, diphtheria, tetanus, and measles; once common, these classical infectious diseases now are absent from our hospital.

The second effect of medical progress has been the opportunity to offer patients with certain diseases, previously untreatable, the hope of increased survival and even cure. The list here is long and includes premature infants, children with congenital immune deficiency disorders, individuals with leukemia, lymphoma, aplastic anemia, burns, renal and other organ failure, and many others. Thus, the numbers of such patients in our hospitals have increased. These patients are at an increased risk of acquiring a complicating infection because of their underlying disease or because of our diagnostic and therapeutic interventions.

Prevention and treatment of burn wound infection requires knowledge of the epidemiology of such infections. Prevention of infection rests on removal of reservoirs or sources of microorganisms from the burn patient's environment and interruption of transfer of microorganisms to the surface of the wound. When prevention fails and burn wound infection develops, successful therapy may depend on an understanding of the epidemiology of the burn wound during therapy. Contrary to the oft stated concept that antibiotics penetrate the avascular burn wound poorly, our study demonstrated that gentamicin and tobramycin achieved therapeutic concentrations in burn wound tissue. As in other types of infections, susceptible microorganisms were eradicated and resistant microorganisms persisted. Of most importance was the observation that resistant microorganisms may repopulate the wound within four days of starting therapy. It would appear that failure of therapy is not due to failure of antibiotics to penetrate the burn wound but rather to rapid development of superinfection during therapy.

Since the introduction and widespread performance of transplant surgery in the 1950s and 1960s, infectious complications have been a major cause of morbidity and mortality. The risks of infection are directly related to the potency and duration of immunosuppressive therapies, organ-donor selection, surgical techniques, and postoperative exposures to invasive procedures or treatments.

Despite impressive advancements to decrease the risks of infection, between 40% and 80% of renal transplant patients become infected within the first two or three postoperative years. Infections that occur during the first month following transplantation are often caused by common nosocomial pathogens and are secondary to invasive procedures or therapies. Infections that occur between one and six months post-surgery are often caused by opportunistic pathogens. Symptomatic and subclinical cytomegalovirus (CMV) infections are common during this time and may contribute to a further impairment of host defenses. Late infections involve both opportunistic and conventional pathogens; opportunistic infections occur in patients with poor transplant function who require high levels of immunosuppression and conventional infections occur in patients who require little immunosuppression.

During the past two decades, there has been a significant decrease in deaths from infectious complications among renal transplant recipients. Further reductions in morbidity and mortality will occur with the development of more specific approaches for immunosuppressive therapy, new strategies to prevent CMV infections and methods to eliminate sources of nosocomial infections.

The primary objectives of nurses caring for the immunosuppressed patient are to create a safe, peaceful environment and to promote the quality of the patient's life. Strengthening the patient's defense mechanisms is inherent in these nursing objectives, and the nurse must have certain competencies to reinforce these defense mechanisms. One competency is a thorough understanding of the immunosuppressed patient. The infection control practitioner (ICP) should assist the nurse in understanding what an immunosuppressed patient is, what his risk of infection is, what his reaction to infection might be, and what isolation practices are appropriate. Another necessary nursing skill is proficiency in patient assessment, not only when the patient is admitted, but on a continuous basis since the patient's status can change so rapidly.

Finally the nurse must have the ability to implement appropriate nursing measures. The nurse must use the principles of asepsis in all patient care activities, recognize risk factors of infection, and understand the importance of such details as proper nutrition, oral hygiene, and skin care. Psychological support is also an essential part of the nursing care plan.

Nursing care affects the well-being of the immunosuppressed patient and infection control practitioners have a role in ascertaining that nurses know how to treat such patients appropriately.

Serratia marcescens has an interesting and many-faceted history. The presence of the red pigmented organism on starchy food products long had been noted and was thought to be blood; its presence on consecrated wafers was thought to be the blood of Christ. It was not until 1819 that Bizio, a pharmacist, demonstrated that a microorganism was responsible for the red pigment. He named this microorganism Serratia marcescens; Serratia in honor of Serafino Serrati, an Italian physicist who invented the steamboat and marcescens from the Latin, “to decay.”

Because of the pigment production and because Serratia marcescens was believed to be a benign, saprophytic organism, it was used widely as a biological marker from 1906 to 1968. This use has been controversial in regard to experiments conducted by the US Army involving biological warfare techniques. In addition, the recognition in the 1950s of the ability of this organism to cause nosocomial infections has curtailed its use as a biological marker. Serratia marcescens is now recognized as a cause of serious infections in man. It has been implicated in practically every kind of infection and is a particularly serious problem with nosocomial infections.