Five strains of mice commonly used in transgenic and knockout production were compared with regard to genetic background and behavior. These strains were: C57BL/6J, C57BL/6NTac, 129P3/J (formerly 129/J), 129S6/SvEvTac (formerly 129/SvEvTac) and FVB/NTac. Genotypes for 342 microsatellite markers and performance in three behavioral tests (rotorod, open field activity and habituation, and contextual and cued fear conditioning) were determined. C57BL/6J and C57BL/ 6NTac were found to be true substrains; there were only 12 microsatellite differences between them. Given the data on the genetic background, one might predict that the two C57BL/6 substrains should be very similar behaviorally. Indeed, there were no significant behavioral differences between C57BL/6J and C57BL/6NTac. Contrary to literature reports on other 129 strains, 129S6/ SvEvTac often performed similarly to C57BL/6 strains, except that it was less active. FVB/NTac showed impaired rotorod learning and cued fear conditioning. Therefore, both 129S6/SvEvTac and C57BL/6 are recommended as background strains for targeted mutations when researchers want to evaluate their mice in any of these three behavior tests. However, any transgene on the FVB/NTac background should be transferred to B6.Habituation to the open field was analyzed using the parameters: total distance, center distance, velocity and vertical activity. Contrary to earlier studies, we found that all strains habituated to the open field in at least two of these parameters (center distance and velocity).

Histopathologic evaluation combined with a period of immunosuppression has been the standard procedure for detection ofPneumocystis carinii in commercial rat colonies. Variation in induction regimens and in the sensitivity of detection methods may result in underreporting of the presence of P. cariniiin breeding colonies or delay its detection. In the present study, methylprednisolone and cyclophosphamide were evaluated for the ability to induce P. carinii infection in rats from an enzootically infected commercial barrier colony. The presence ofP. carinii was detected by histopathologic methods and by amplification of a targeted region of the P. carinii thymidylate synthase gene by PCR over the 8-week study period. Sera taken from rats prior to either induction regimen were evaluated for the presence of P. carinii-specific antibodies by the immunoblotting technique. Few significant differences in ability to induce organism burden or in histopathology were observed between the two immunosuppressive regimens. However, a dramatic loss of weight over the study period was observed in rats treated with methylprednisolone but not in rats treated with cyclophosphamide. Although histopathologic changes attributable toP. carinii did not appear before 2 weeks with either immunosuppressant, the presence of the organism in these animals was detected by immunoblotting and PCR. Cyst scores and the intensities of the histopathologic lesions increased during the study period, but the number of rats exhibiting evidence of P. cariniiinfection did not change after week 3. These results suggest that use of the PCR method on postmortem lung tissue of rats without prior induction regimens or identification of anti-P. carinii antibodies in antemortem serum samples is a sufficiently sensitive method for detection of the presence of a P. cariniicarrier state in rodent breeding colonies.

The strategies used to control or eliminate opportunistic microorganisms from an animal colony depend on these organisms' risk to institutional research programs. The research benefits of controlling or eliminating the microorganisms must be balanced against the control measures' cost, complexity, and probability of success. A nonessential control strategy may be so complicated, expensive, and time consuming that it is circumvented (intentionally or unintentionally) by those expected to use it. In this paper, we outline an approach for analyzing the risk associated with each organism and for developing a control strategy that includes consideration of the research requirements, numbers of animals at risk, and available facility resources. RISK ASSESSMENTFor this discussion, risk assessment is the process of analyzing the nature and relative importance of a microorganism to a research program. Certainly, all risks are relative. For example, a virus such as sialiodacryoadenitis virus (SDAV 1 ) produces clinical signs in naive animals and can affect various physiological and metabolic functions (Bhatt and Jacoby 1985). Such a virus is likely to be of concern for more research programs than a bacterium such as Corynebacterium bovis (otherwise known as hyperkeratosis-associated coryneform species), which may cause disease and research effects only in glabrous mice (Clifford and others 1995).In very general terms, microorganisms can be ranked according to their established potential to cause disease and research interactions. This ranking should be based on data in the peer-reviewed literature coupled with the organism's ability to cause disease or research interactions in the absence of predisposing factors. A simple ranking scheme is provided in Figure 1. To evaluate the risk imposed by a William J.

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