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Toxoplasmosis in immunoglobulin M-suppressed mice
Infection and Immunity
|October 1, 1982
Summary
Sulfadiazine treatment enables mice to develop immunity to Toxoplasma gondii. While antibodies are not crucial for acute infections, they play a role in controlling long-term toxoplasmosis.
Area of Science:
- Immunology
- Parasitology
- Infectious Diseases
Background:
- Toxoplasma gondii infections are fatal in mice without treatment.
- Sulfadiazine (SD) treatment can induce immunity and survival.
- The role of antibodies (Ab) in protective immunity requires further investigation.
Purpose of the Study:
- To investigate the role of antibody (Ab) in protective immunity against acute Toxoplasma gondii infections.
- To determine the importance of Ab in maintaining chronic toxoplasmosis.
- To compare the effects of SD treatment and Ab in different immunodeficient mouse models.
Main Methods:
- Utilized B-cell-deficient (immunoglobulin M-suppressed) and T-cell-deficient (athymic) mice, alongside normal BALB/c mice.
- Administered sulfadiazine (SD) treatment to some mice before challenging with T. gondii.
- Assessed survival rates, parasite loads, and histopathological changes in various tissues.
Main Results:
- Untreated mice rapidly died from infection.
- SD treatment led to immunity and long-term survival in most intact mice.
- Athymic mice had reduced survival after SD withdrawal.
- Immunoglobulin M-suppressed mice, lacking Ab, survived longer with SD treatment than without, but eventually died.
- Antibody transfer improved parasite clearance in immunoglobulin M-suppressed mice.
Conclusions:
- Antibodies may not be critical for acute Toxoplasma gondii infections.
- Antibodies appear important for controlling chronic toxoplasmosis.
- Sulfadiazine treatment combined with antibody presence enhances control of T. gondii infections.