isolators and repeatedly testing them by the ELISA over many months (e.g., monthly until 12 months of age). Stocks found to be consistently negative could then be used for establishment of breeder production populations under barrier programs.

Definitive information on the elimination of M. pulmonis from clinically or subclinically infected stocks is lacking but the following suggestions might prove useful. For cesarean derivations, use only dams that are several months old and have been repeatedly found to be ELISA negative. Candidate stocks for rederivation may be maintained for a few months on tetracycline or other antibiotics for the purpose of suppressing the mycoplasma flora as much as possible prior to cesarean operation. A separate isolator should be used for the pups of each donor female and a single foster female (from a stock known to be free of mycoplasmas and other pathogens). The placental membranes from each donor female should be cultured for mycoplasmas using a variety of media (Tram et al., 1970; Cassell et al., 1983a).

Control of environmental factors that favor MRM may be helpful in preventing clinical disease or ameliorating outbreaks (e.g., more frequent cage sanitation and reduction of cage population density to reduce intracage ammonia concentrations, and prevention of Sendai and sialodacryoadenitis virus infections). While administration of antimicrobials such as tetracyclines may help to control clinical signs, such agents are not curative and may introduce variables if animals on experiment are treated.

MRM can cause morbidity and mortality, particularly in long term studies (Lindsey et al., 1971, 1982).

M. pulmonis respiratory infection can alter results of many experimental responses of the respiratory tract, including: carcinogenesis (Schrieber et al., 1972), ciliary function (Irvani and van As, 1972; Westerberg et al., 1972), cell kinetics (Wells, 1970), and immunity (Cole et al., 1975; Naot et al., 1979a,b; Davis et al., 1982).

M. pulmonis infection of the genital tract can alter histology (Cassell et al., 1979) and reproductive efficiency (Leader et al., 1970; Goeth and Appel, 1974; Fraser and Taylor-Robinson, 1977; Lal et al., 1980; Cassell, 1982).

M. pulmonis infection in LEW rats has been found to delay onset and reduce the severity of adjuvant arthritis, reduce the incidence of experimental collagen-induced arthritis, and reduce antibody response to collagen (Taurog et al., 1984).

M. pulmonis infection has been found to increase natural killer cell activity in mice (Lai et al., 1987), and suppress humoral antibody response to sheep red blood cells in rats (Aguila et al., 1988).