Abstract
Animal models for the toxoplasmosis are scarce and have limitations. In this study, a neurological mouse model was developed in BALB/c mice infected intraperitoneally with 15 cysts of a Toxoplasma gondii isolate. The mice were monitored for 42 days and euthanized at different time points. Another group of mice were orally treated with dexamethasone (DXM: 2.66 mg/kg daily, 5.32 mg/kg daily) at 42 days after infection and monitored for a further 42 days. A mortality rate of 15% and 28.6% was observed in mice given 2.66 mg/kg/day and 5.32 mg/kg/day of DXM, respectively. The mean cyst numbers in the brain of DXM treated mice increased up to twofold compared with chronically infected untreated mice. Infections up to 42 days were associated with an increase in both IgM and IgG levels but following dexamethasone treatment, IgM levels declined but IgG levels continued on rising. The brain of toxoplasmosis infected mice showed mononuclear cellular infiltrations, neuronal necrosis, and cuffing. The severity of pathology was higher in mice treated with dexamethasone compared to the positive control groups. The findings of this study demonstrate that DXM-induced reactivation of chronic toxoplasmosis may be a useful development of laboratory animal model in outbred mice used for in vivo studies.
Highlights
Toxoplasmosis, caused by Toxoplasma gondii, is one of the most common parasitic infections of man and other warmblooded animals [1]
The infected mice treated with dexamethasone [2.66 mg/kg/day and 5.32 mg/kg/day] showed various clinical signs which increased with increase in dosage level
The results of this study show that BALB/c mice can be used to develop a good model for toxoplasmosis
Summary
Toxoplasmosis, caused by Toxoplasma gondii, is one of the most common parasitic infections of man and other warmblooded animals [1]. It is estimated that between 500 million to 2 billion people worldwide are chronically infected with this parasite [2]. The parasite can cause severe disease in people with immunodeficiencies and in fetuses infected in utero [2]. These two classes of patients present different challenges to health professionals in terms of diagnosis, case management, and drug treatment. There is brief acute stage characterized by the proliferative tachyzoite stage of the parasite, but thereafter the parasite undergoes latency, characterized by slowly growing bradyzoites within tissue cysts. The parasite invades a variety of immune cells and is subsequently disseminated throughout the body, traversing biological barriers to reach immunologically privileged sites
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