Mice chronically infected with Toxoplasma gondii were treated with cyc
lophosphamide, obiopeptide-1 (Obi-1) and/or anti-CD4 monoclonal antibo
dy to determine the effect of these immunosuppressive agents on the cy
sts in the brain. In the brain of non-treated, and infected cyclophosp
hamide-Obi-1 treated mice, with hematoxylin-eosin, and anti-Toxoplasma
avidin-biotin-conjugate labelling techniques, large typically rounded
tissue cysts were mostly detected, and sometimes with dividing microc
ysts. In contrast, brain tissue from cyclophosphamide only or anti-CD4
treated infected mice had multiple degenerate cysts of varied size in
some brain regions, as well as clusters of microcysts, however, such
change was more striking in the anti-CD4 treated group. Infected mice
treated with a combination of cyclophosphamide and Obi-1 showed a sign
ificantly higher survival of 80% compared to 20% survival in mice trea
ted with cyclophosphamide only. Percent neutrophilic leucocytes, monoc
ytes and lymphocytes in mice treated with a combination of Obi-1 and a
nti-CDL4, or Obi-1 and cyclophosphamide were higher compared to those
groups treated with anti-CD4 antibody, or cyclophosphamide only. The i
ncrease in neutrophilic leucocyte and lymphocyte counts after a combin
ed cyclophosphamide and Obi-1 treatment may, likewise, contribute to t
he induction of resistance in mice against T. gondii. Furthermore, the
se results seem to suggest that the reactivation or rupture of tissue
cysts in mice chronically infected with T. gondii is not principally c
orrelated with the death of cyclophosphamide treated mice.