Numerous concerns regarding the potential for misdiagnosis of Lyme disease using commercial assays have been voiced by the US Food and Drug Administration (FDA). We attempted to clarify the clinical value of serologic testing for Lyme disease using the results of commonly marketed assays for detecting antibody to Borrelia burgdorferi, the organism that causes Lyme disease. We reviewed published studies on B burgdorferi test performance published through 1998, package insert labeling from FDA-cleared test kits for B burgdorferi, and Lyme Disease Survey Set LY-A from the College of American Pathologists. We assessed the sensitivity and specificity of commercial serologic tests (enzyme-linked immunosorbent assay [ELISA], immunofluorescence antibody [IFA], and immunodot) for diagnosis of Lyme disease. To reduce this risk of misdiagnosis, it is important that clinicians understand the performance characteristics and limitations of these tests. These tests, in common use in clinical or commercial laboratories, should be used only to support a clinical diagnosis of Lyme disease, not as the primary basis for making diagnostic or treatment decisions. Serologic testing is not useful early in the course of Lyme disease because of the low sensitivity of tests in early disease. Serologic testing may be more useful in later disease, at which time sensitivity and specificity of the test are improved. Positive or equivocal results on an ELISA, IFA, or immunodot assay requires supplemental testing with a Western blot assay. A negative result on the Western blot or ELISA indicates that there is no serologic evidence of infection by B burgdorferi at the time the sample was drawn.
A prospective microbiological surveillance (PMS) program was developed in a comprehensive hospital-wide effort for control of nosocomial methicillin-resistant Staphylococcus aureus (MRSA). This PMS program entailed: 1) active identification of colonized and infected patients; 2) application of a screening microbiologic system for MRSA; 3) isolation of colonized and infected patients; 4) antibiotic decolonization of MRSA; and 5) educational efforts. The PMS program was studied over three and one half years for its contribution to infection control of MRSA, early identification of nosocomial MRSA outbreaks, use of the highest yield surveillance culture sites, and cost effectiveness. Following initiation of the PMS program in December 1982, during an MRSA outbreak, the frequency of new MRSA cases declined from 14 to none by the end of a 3-month pilot study. The frequency of new MRSA cases stabilized at approximately 2 per month until October 1983, when the PMS system allowed prompt detection of a new outbreak of 11 cases. Following isolation and antibiotic decolonization, the frequency of cases again declined to 3 per month. A third outbreak in December 1985 again was promptly detected and controlled. Infection to colonization ratio decreased from a maximum of 1.5 during outbreaks to a minimum of 0.17 after outbreaks. Wounds and tracheostomy sites provided the greatest yield of detection of new cases of MRSA. During one 15-month period, 35 of the 43 new cases were detected initially at wounds and tracheostomy sites. No new MRSA cases were detected by a positive axillary or nares site alone. The estimated quarterly cost of outbreaks and infection paralleled the quarterly frequency of new MRSA cases. The cost of managing MRSA outbreaks and treating MRSA infections versus the cost of implementing the PMS program suggested that the PMS program may be cost effective. This prospective microbiological surveillance program may be applicable to other institutions for hospital-wide infection control of MRSA.
The abilities of commercial MIC, automated, and reference methods for in vitro detection of methicillinresistant Staphylococcus aureus were determined on 49 strains from eight hospitals. Micro-Media, MicroScan, Sensititre, Sceptor, API Uniscept KB, Abbott MS-2, Vitek AMS, Autobac MTS, NCCLS disk diffusion, and broth microdilution antimicrobial susceptibility testing procedures were evaluated. All testing was performed by using manufacturers' or reference procedures, and results were determined at no later than 24 h of incubation at 35°C. With NCCLS disk diffusion, all strains were resistant to oxacillin (1 ,ug), 47 (96%) were resistant to methicillin (4 jig), and 48 (98%) were resistant to nafcillin (1 ,ug). The percentages of strains resistant to methicillin (>8 ,ug/mI) were 98% with API Uniscept KB, 86% with Sceptor, MicroScan, and Autobac MTS, 84% with Sensititre, 71% with Micro-Media, and 70% with NCCLS MIC. Abbott MS-2 detected 86% of strains resistant to methicillin (>5,ug/ml). With oxacillin (>2 ,ug/mI), 90% were detected with Vitek AMS and 70% were detected with NCCLS MIC. With nafcillin (>2 ,Ig), 82% were resistant with Micro-Media, 57% were resistant by NCCLS MIC, and 50% (three of six) were resistant by MicroScan. Two strains from one hospital and one strain from another gave susceptible results with all automated and commercial methods. All strains from three centers were detected by all methods. Variability also occurred among the systems with cephalothin, clindamycin, gentamicin, chloramphenicol, and trimethoprim sulfamethoxazole.
As infections due to methicillin-resistant Staphylococcus aureus become increasingly prevalent, newer alternative antibiotics, especially those which are orally administered, will be required. In order to provide an in-vitro basis for selecting alternative antibiotics, we studied the susceptibility of 103 strains of methicillin-resistant Staph. aureus from seven institutions to oral antimicrobial agents. Novobiocin, rifampicin, and trimethoprim-sulphamethoxazole had excellent in-vitro activity against virtually all strains of methicillin-resistant Staph. aureus. The MIC90 and MBC90 of novobiocin against methicillin-resistant Staph. aureus were 0.25 mg/l. Since previously reported achievable serum levels with oral novobiocin are 100 to 200 times its MIC90 against methicillin-resistant Staph. aureus, novobiocin should be evaluated further for combination therapy with rifampicin or trimethoprim-sulphamethoxazole.
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