The host immune response to cutaneous leishmaniasis has been considered to be predominately cell mediated (Bryceson et al., 1970, Clin. Exp. Immunol. 7: 301-341; Turk and Bryceson, 1971, Adv. Immunol. 13: 209266), although antileishmanial antibody can be detected in serum (Allain and Kagan, 1975, Am. J. Trop. Med. Hyg. 24: 232-236; Luzzio et al., 1979, J. Infect. Dis. 140: 370-377). Using the indirect immunofluorescence test, Behforouz et al. (1976, Ann. Trop. Med. Parasitol. 70: 293-301) have shown that antibody titers correlate well with the duration of active infection and the kind of cutaneous lesion in Leishmania tropica-infected mice and L. enriettii-infected guinea pigs. Since little is known about the kinetics of the antibody response in American cutaneous leishmaniasis, we have employed a radioimmunoassay to measure specific antibody during primary L. mexicana infections in the African whitetailed rat, Mystromys albicaudatus. Mystromys albicaudatus, originally described as experimental hosts for L. donovani (Mikhail and Mansour, 1973, J. Parasitol. 59: 1085-1087), and recently for L. braziliensis (McKinney and Hendricks, Am. J. Trop. Med. Hyg. 29: 753-760) was chosen for study since the clinical course of infection and cutaneous lesions in this animal model are nearly indistinguishable from those seen in humans infected with L. mexicana (Hendricks et al., manuscript in preparation). Rats were housed individually and given food and water ad lib. Leishmania mexicana (WR-201) amastigotes (round, nonflagellated culture forms) and promastigotes were propagated in vitro according to Hendricks et al. (1978, Parasitology 76: 309-316). Rats were infected by intradermal injection of 0.1 ml containing 5.0 x 106 culture-derived promastigotes into a shaved area just above the tail. A solid phase radioimmunoassay similar to that described previously (Hunter et al., 1979, J. Immunol. 123: 133-137) was employed to measure the specific antileishmanial antibody response. An antiserum to M. albicaudatus immunoglobulins was prepared by immunization of a rabbit with proteins insoluble in 50% saturated (NH4)2SO4 and emulsified in Freund's complete adjuvant. The rabbit was boosted every week for 2 mo with Mystromys immunoglobulins in Freund's incomplete adjuvant. An IgG fraction of the rabbit antiserum was prepared by chromatography on DE-52 cellulose; the IgG fraction showed two precipitin lines in agar when reacted against M. albicaudatus, but did not react with either mouse or rat (Norway) serum. Antigen was prepared by sonication of amastigotes or promastigotes on ice for 5 min at 30 kHz. The disrupted parasite preparations were centrifuged at 5,000 g for 15 min and the supernate used as antigen. Polyvinyl microtiter plates w re coated with 100 /g/ml of amastigote or promastigote antigen protein. Details of the assay, the procedure for radiolabelling the rabbit IgG, and the method for data analysis were published earlier (Hunter et al., 1979, loc. cit.). Twenty of 22 animals with proven infections (visible papules or ulcers) developed serum antileishmanial antibody titers of >1:10 (range 1:10 to 1:157), while two animals which failed to develop lesions and all unchallenged controls never had titers higher than 1:6. When mean antibody titers were plotted against day postinfection it was apparent that the specific antibody response increased over time (Fig. la). Moreover, when mean antibody titers were plotted against the type of cutaneous lesion (regardless of the time postinfection), animals without lesions had very low titers and those with papules,