TOXOPLASMOSIS IN IMMUNOGLOBULIN-M-SUPPRESSED MICE
TOXOPLASMOSIS IN IMMUNOGLOBULIN-M-SUPPRESSED MICE
复制标题
DOI:
10.1128/iai.38.1.360-367.1982
复制
发表时间:
1982-01-01
影响因子:
3.1
通讯作者:
TAYLOR, DW
中科院分区:
文献类型:
--
作者:
FRENKEL, JK;TAYLOR, DW
Mice challenged with a pathogenic strain of Toxoplasm gondii develop fatal infections. If such mice are initially treated with sulfadiazine (SD), they develop immunity and survive with chronic infections. The role of antibody (Ab) in establishing protective immunity against acute parasitemias and in maintaining chronic infections was investigated using B-cell-deficient (IgM-suppressed), T-cell-deficient (athymic), and normal BALB/c mice. All mice not receiving SD treatment rapidly died (mean 7.5 days) after infection, but the majority (80%) of intact mice developed immunity during SD treatment and survived for over 5 mo. with chronic toxoplasmosis. Athymic mice rapidly died (mean 6.0 days) after the removal of SD treatment. Although all SD-treated IgM-suppressed mice eventually died, they lived considerably longer (18-83 days) in the complete absence of antitoxoplasma Ab than unprotected mice (7-9 days). Histopathological sections of liver, lung, brain and other tissues showed that toxoplasma organisms gave rise to fatal lesions in all nonsurviving animals. The injection of Ab into acutely infected and athymic mice imparted no protection, but transfer of antitoxoplasma Ab (titer > 1:8000) to IgM-suppressed mice after SD treatment resulted in elimination of the parasites in 50% of the mice. Apparently, Ab may not be decisive in acute infections, but may be important in controlling long-term toxoplasmosis.