The Effects of Cortisone Treatment on Natural Resistance and Acquired Responses of the White Rat to Infection with Litomosoides carinii

Abstract

The near absolute resistance of the mature white rat to infection with Litomosoides carinii has been confirmed. Although more than 90% of the infective larvae do not complete migration in this host and cannot be recovered, some of the larvae do persist long enough to elicit a serological response detectable by the in vitro test. Antibody was suppressed by preinfection treatment with cortisone acetate. Cortisone treatment also suppressed the natural resistance of the mature white rat to infection, but preinfection treatment with cortisone was not required to produce this effect. As a result of this change in susceptibility, worms were recovered in numbers approximating those recovered from the normal host, the cotton rat. A residual resistance, however, was manifested by the delay of worm migration to the pleural cavities and the stunting of growth and development of worms in cortisone-treated white rats. Third-stage larvae of Litomosoides carinii introduced subcutaneously into the normal host, the cotton rat, migrate to the body cavities within 7 days, enter the adult stage in 25 days (Scott, 1959), and live for years. That the mature white rat is an abnormal host for this parasite is shown by the failure to infect this animal by exposure to either infected mites (Scott et al., 1946; Bertram, 1946) or to infective larvae introduced subcutaneously by artificial methods (Olson, 1959a). Using quantitative methods, Olson (1959b) has shown that manifestations of this host resistance depend upon the age of the host. In mature white rats resistance is expressed early in the course of infection, i.e., larvae are prevented from completing migration, but in younger white rats larvae complete migration in large numbers. In these young white rats, however, resistance is expressed later in the course of infection, i.e., worms developing in the pleural cavities are stunted and frequently encapsulated by an inflammatory response of the host. Olson (ibid.) also showed that cortisone (30 mg/kg) suppressed this inflammatory response and concomitantly eliminated encapsulation of postmigratory worms. He suggested that encapsulation of postmigratory worms noted by the 10th day of infection had been facilitated by an acquired response of the host. Although cortisone suppressed this encapsulation of postmigratory worms in rats of all ages, it did not, however, suppress the early resistance of mature white rats to migrating larvae. An in vitro test was used by Sarles (1938) to demonstrate antibodies elicited by Nippostrongylus braziliensis in its normal host and since that time has been used to evaluate acquired responses of highly susceptible hosts to their parasites. The list of examples includes responses to L. carinii by its normal host, the cotton rat (Scott, 1952). It was of interest, therefore, to determine whether such a serological reaction to L. carinii could be detected in the highly resistant mature white rat and, if so, what effects cortisone treatment would have on this response. MATERIALS AND METHODS Mature Carworth strain white rats and cotton rats were exposed to infection according to the method of Macdonald and Scott (1953). Thirdstage infective larvae of L. carinii were dissected from mites, Ornithonyssus bacoti, which had been Received for publication 26 July 1962. * Contribution from the Laboratory of Helminth Research, Department of Preventive Medicine and Public Health, The University of Texas Medical Branch, Galveston, Texas. This work was supported by a predoctoral fellowship awarded by the James W. McLaughlin Committee of The University of Texas Medical Branch and by National Institutes of Health Research Grant (E-64) directed by Dr. J. Allen Scott.