Financial resources for health care have been restricted. Constraints demand that physicians and administrators get the most for their money, yet the myriad of diagnostic tests and antibiotics available today can easily boggle the minds of those who must choose among them. This situation is particularly true of infection control where active research continually produces new products. Each hospital must choose among disinfectants, detergents, antibiotics, protective clothing, immunizations, dressing supplies, respiratory therapies, and many other products. At every point, questions arise. Is a new product worth the extra money? Alternatively, is a less expensive product really more cost-effective? How many additional infections must be prevented before a product “pays” for itself?

Patient blood is recognized as a dangerous substance because it may contain infectious agents. While the practice of gloving provides some protection to hospital personnel exposed to instruments contaminated with patient blood, frequent breaks in techniques occur in which personnel inadvertently touch surfaces and objects in the environment with the potentially contaminated gloves. Also, “cleaned” instruments are placed on environmental surfaces to which other personnel are exposed. The purpose of this study was to determine the frequency of blood contamination of “cleaned” instruments used for patient procedures in the hospital, and on the gloved hands of central sterile supply (CSS) personnel handling those instruments.

The genus Capnocytophaga includes three bacterial species: Capnocytophaga ochracea, Capnocytophaga sputigena, and Capnocytophaga gingivalis. Although occasionally found in soil and water, the predominant natural habitat of Capnocytophaga species is the human oropharynx. These organisms are also found throughout the human gastrointestinal tract as well as in the vagina. Initially implicated only in the pathogenesis of periodontal disease, Capnocytophaga has recently been recognized both as an opportunistic pathogen in the immunocompromised host and also as a pathogen associated with a variety of infections in the immunocompetent host. The protean manifestations of infection and the enlarging pathogenic spectrum of Capnocytophaga. disease mandate a high index of diagnostic suspicion on the part of the clinician.

The issue of tuberculin skin testing in pregnant health care workers of third-world ethnicity who may have previously received bacille Calmette-Guerin (BCG) immunization is complex and multifaceted. The relevant issues are:

• Is tuberculin skin testing safe in the pregnant female?

• Is tuberculin skin testing indicated in the pregnant female?

• Is tuberculin skin testing accurate and reliable in the pregnant female?

• Does previous BCG vaccination alter the diagnostic utility of tuberculin skin testing?

• Finally, is tuberculin skin testing safe in the BCG-immunized pregnant female?

Is tuberculin skin testing safe in the pregnant female?

When purified protein derivative (PPD) tuberculin is injected locally into the skin, most of it is removed within hours by lymphocytes. The remainder is engulfed by macrophages, and a mild brief local inflammatory reaction develops in both nonsensitive and hypersensitive patients. The reaction goes no further in the nonsen-sitized patient. In the sensitized patient-who has had Mycobacterium tuberculosis infection in the past-the area becomes heavily infiltrated by mononuclear cells, and an inflammatory reaction continues to increase for several days.

Sulbactam/ampicillin was recently marketed for use in several infections caused by beta-lactamase-producing organisms. Sulbactam is the second beta-lactamase inhibitor to become available in the United States. Interest in inhibition of beta-lactamases arose in the late 1960s when a combination consisting of an antibacterial agent and an enzyme inhibitor was found effective in the treatment of certain resistant gram-negative infections. It is now well accepted that the addition of a beta-lactamase inhibitor to a beta-lactam antibiotic may expand its usefulness in a variety of infections.

The penicillin derivatives, known as beta-lactam antibiotics, possess a four-membered ring (beta-lactam ring) fused to a second ring (Figure). It is the beta-lactam ring that is essential for the inhibition of bacterial cell wall synthesis and subsequent bactericidal activity of these agents. The development of resistance to beta-lactam antibiotics may occur by a number of mechanisms, although the most important is bacterial production of enzymes (beta-lactamases) that are capable of beta-lactam ring hydrolysis and inactivation.

Sulbactam resembles the penicillin derivatives in structure (Figure) and is able to preserve their activity by its ability to inhibit the action of beta-lactamases, particularly those of the Richmond classes II-V (gram-negative) and the group A beta-lactamases (gram-positive). Sulbactam is referred to as a “suicide inhibitor” because while forming an irreversible complex with the enzyme, it is destroyed in the process. By virtue of its ability to render the beta-lactamases inactive, sulbactam has been combined with ampicillin in an effort to restore its activity against a number of pathogens that have developed resistance by this mechanism.

Sulbactam/ampicillin was recently marketed for use in several infections caused by beta-lactamase-producing organisms. Sulbactam is the second beta-lactamase inhibitor to become available in the United States. Interest in inhibition of beta-lactamases arose in the late 1960s when a combination consisting of an antibacterial agent and an enzyme inhibitor was found effective in the treatment of certain resistant gram-negative infections. It is now well accepted that the addition of a beta-lactamase inhibitor to a beta-lactam antibiotic may expand its usefulness in a variety of infections.

The penicillin derivatives, known as beta-lactam antibiotics, possess a four-membered ring (beta-lactam ring) fused to a second ring (Figure). It is the beta-lactam ring that is essential for the inhibition of bacterial cell wall synthesis and subsequent bactericidal activity of these agents. The development of resistance to beta-lactam antibiotics may occur by a number of mechanisms, although the most important is bacterial production of enzymes (beta-lactamases) that are capable of beta-lactam ring hydrolysis and inactivation.

Sulbactam resembles the penicillin derivatives in structure (Figure) and is able to preserve their activity by its ability to inhibit the action of beta-lactamases, particularly those of the Richmond classes II-V (gram-negative) and the group A beta-lactamases (gram-positive). Sulbactam is referred to as a “suicide inhibitor” because while forming an irreversible complex with the enzyme, it is destroyed in the process. By virtue of its ability to render the beta-lactamases inactive, sulbactam has been combined with ampicillin in an effort to restore its activity against a number of pathogens that have developed resistance by this mechanism.