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Murine model of drug-induced reactivation of Toxoplasma gondii

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Authors
Đurković-Đaković, Olgica
Milenković, V
Article (Published version)
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Abstract
A murine model of recrudescence of chronic toxoplasmosis, mimicking this life-threatening condition in immunosuppressed humans, was developed in Swiss-Webster mice infected 6 weeks previously with 10 cysts of the Me49 strain of Toxoplasma gondii, by treatment with dexamethasone (DXM, 2.5 mg/kgBM/day in drinking water), alone or combined with cortisone-acetate (CA, 50 mg/kg by subcutaneous injection 3 times a week). Treatment was continued for 7 weeks. Both DXM and DXM+CA treatment significantly increased mortality, as compared to infected untreated mice (P=0.0002 and P lt 10(-4), respectively), and to uninfected DXM-treated mice (P=0.043 and P=0.001, respectively). In both treatment groups, mean cyst numbers were 2-9-fold increased compared with chronically infected untreated mice. Spleen/body mass ratios and numbers of splenocytes were significantly lower (P lt 10(-4)) than in untreated both infected and uninfected mice, indicating decreased immune reactivity in treated animals. Acqui...red immunity too was impaired by corticoids, as shown by lower resistance to challenge infection with the mouse-virulent RH strain of T. gondii in mice with established chronic infection treated with DXM than in those left untreated (P=0.038). Most importantly, 8 of the 56 treated animals (14.2%) developed clinical signs of toxoplasmic encephalitis, which was verified histologically. In these, survival was significantly shorter (P=0.009) and cyst numbers 6-fold augmented (P lt 10(-4)) as compared to treated animals, which did not develop neurological signs. This simple model of drug-induced recrudescence of chronic toxoplasmosis, in addition to its potential use for in vivo studies of the pathogenic mechanisms of T. gondii reactivation, may be particularly suitable for the evaluation of chemotherapeutics.

Keywords:
chronic infection / corticoid drugs / immunosuppression / Mus musculus / reactivation / Toxoplasma gondii / toxoplasmosis
Source:
Acta Protozoologica, 2001, 40, 2, 99-106
Publisher:
  • Jagiellonian Univ, Inst Environmental Sciences, Krakow

ISSN: 0065-1583

WoS: 000168934900002

[ Google Scholar ]
25
Handle
https://hdl.handle.net/21.15107/rcub_rimi_67
URI
http://rimi.imi.bg.ac.rs/handle/123456789/67
Collections
  • Radovi istraživača / Researchers' publications
Institution/Community
Institut za medicinska istraživanja
TY  - JOUR
AU  - Đurković-Đaković, Olgica
AU  - Milenković, V
PY  - 2001
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/67
AB  - A murine model of recrudescence of chronic toxoplasmosis, mimicking this life-threatening condition in immunosuppressed humans, was developed in Swiss-Webster mice infected 6 weeks previously with 10 cysts of the Me49 strain of Toxoplasma gondii, by treatment with dexamethasone (DXM, 2.5 mg/kgBM/day in drinking water), alone or combined with cortisone-acetate (CA, 50 mg/kg by subcutaneous injection 3 times a week). Treatment was continued for 7 weeks. Both DXM and DXM+CA treatment significantly increased mortality, as compared to infected untreated mice (P=0.0002 and P lt 10(-4), respectively), and to uninfected DXM-treated mice (P=0.043 and P=0.001, respectively). In both treatment groups, mean cyst numbers were 2-9-fold increased compared with chronically infected untreated mice. Spleen/body mass ratios and numbers of splenocytes were significantly lower (P lt 10(-4)) than in untreated both infected and uninfected mice, indicating decreased immune reactivity in treated animals. Acquired immunity too was impaired by corticoids, as shown by lower resistance to challenge infection with the mouse-virulent RH strain of T. gondii in mice with established chronic infection treated with DXM than in those left untreated (P=0.038). Most importantly, 8 of the 56 treated animals (14.2%) developed clinical signs of toxoplasmic encephalitis, which was verified histologically. In these, survival was significantly shorter (P=0.009) and cyst numbers 6-fold augmented (P lt 10(-4)) as compared to treated animals, which did not develop neurological signs. This simple model of drug-induced recrudescence of chronic toxoplasmosis, in addition to its potential use for in vivo studies of the pathogenic mechanisms of T. gondii reactivation, may be particularly suitable for the evaluation of chemotherapeutics.
PB  - Jagiellonian Univ, Inst Environmental Sciences, Krakow
T2  - Acta Protozoologica
T1  - Murine model of drug-induced reactivation of Toxoplasma gondii
EP  - 106
IS  - 2
SP  - 99
VL  - 40
UR  - conv_1389
ER  - 
@article{
author = "Đurković-Đaković, Olgica and Milenković, V",
year = "2001",
abstract = "A murine model of recrudescence of chronic toxoplasmosis, mimicking this life-threatening condition in immunosuppressed humans, was developed in Swiss-Webster mice infected 6 weeks previously with 10 cysts of the Me49 strain of Toxoplasma gondii, by treatment with dexamethasone (DXM, 2.5 mg/kgBM/day in drinking water), alone or combined with cortisone-acetate (CA, 50 mg/kg by subcutaneous injection 3 times a week). Treatment was continued for 7 weeks. Both DXM and DXM+CA treatment significantly increased mortality, as compared to infected untreated mice (P=0.0002 and P lt 10(-4), respectively), and to uninfected DXM-treated mice (P=0.043 and P=0.001, respectively). In both treatment groups, mean cyst numbers were 2-9-fold increased compared with chronically infected untreated mice. Spleen/body mass ratios and numbers of splenocytes were significantly lower (P lt 10(-4)) than in untreated both infected and uninfected mice, indicating decreased immune reactivity in treated animals. Acquired immunity too was impaired by corticoids, as shown by lower resistance to challenge infection with the mouse-virulent RH strain of T. gondii in mice with established chronic infection treated with DXM than in those left untreated (P=0.038). Most importantly, 8 of the 56 treated animals (14.2%) developed clinical signs of toxoplasmic encephalitis, which was verified histologically. In these, survival was significantly shorter (P=0.009) and cyst numbers 6-fold augmented (P lt 10(-4)) as compared to treated animals, which did not develop neurological signs. This simple model of drug-induced recrudescence of chronic toxoplasmosis, in addition to its potential use for in vivo studies of the pathogenic mechanisms of T. gondii reactivation, may be particularly suitable for the evaluation of chemotherapeutics.",
publisher = "Jagiellonian Univ, Inst Environmental Sciences, Krakow",
journal = "Acta Protozoologica",
title = "Murine model of drug-induced reactivation of Toxoplasma gondii",
pages = "106-99",
number = "2",
volume = "40",
url = "conv_1389"
}
Đurković-Đaković, O.,& Milenković, V.. (2001). Murine model of drug-induced reactivation of Toxoplasma gondii. in Acta Protozoologica
Jagiellonian Univ, Inst Environmental Sciences, Krakow., 40(2), 99-106.
conv_1389
Đurković-Đaković O, Milenković V. Murine model of drug-induced reactivation of Toxoplasma gondii. in Acta Protozoologica. 2001;40(2):99-106.
conv_1389 .
Đurković-Đaković, Olgica, Milenković, V, "Murine model of drug-induced reactivation of Toxoplasma gondii" in Acta Protozoologica, 40, no. 2 (2001):99-106,
conv_1389 .

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