Differences in susceptibilities of the lymphogranuloma venereum and trachoma biovars of Chlamydia trachomatis to neutralization by immune sera.

Sera from seven patients from whom a C. trachomatis serovar L2 strain was isolated were tested in vitro for their ability to neutralize the infectivity of this organism. In one patient an inguinal lymph node was culture positive, whereas the remaining six patients had positive rectal biopsies. Sera from four of the patients, including the patient with the lymph node isolate, failed to neutralize serovar L2(434). In addition, the homologous strain recovered from the inguinal lymph node was available and was resistant to neutralization by the homologous sera. However, the same sera effectively neutralized a trachoma serovar, E(Bour). All four sera had inclusion immunofluorescent-antibody titers to C. trachomatis serovar L2 of 2,048 to 16,384 and microimmunofluorescent-antibody titers to the lymphogranuloma venereum biovar were equal or higher in all cases than to the 12 serovars of the trachoma biovar. The three remaining sera, while neutralizing the infectivity of the L2 strains tested, neutralized serovar E to a greater extent. These sera had the same inclusion immunofluorescent antibody titers as the sera that failed to neutralize serovar L2. To see whether this difference in the sensitivity of the biovars toward neutralization could be characterized, sera were obtained from mice immunized with different doses of both serovars L2 and E. Sera obtained from mice immunized with serovar E were able to effectively neutralize the homologous strain. In contrast, neutralization of the immunizing strain, L2(UCI-20), was not seen with sera obtained on days 7, 14, and 21 after immunization from animals receiving 8 x 10(5) and 8 x 10(4) inclusion-forming units of L2(UCI-20); however, these same sera neutralized serovar E. However, with a higher immunizing dose of L2 (10(7) IFUs), both E and L2 were neutralized with sera obtained 7 and 14 days after immunization. Therefore, the relative resistance to neutralization by serovar L2 compared with that of serovar E in the mouse model was inoculum dependent.