Toxoplasmosis

Microbes and Infection 5 (2003) 457–462 www.elsevier.com/locate/micinf

Review

Development of a vaccine for toxoplasmosis: current status
Girish M. Bhopale *
Parasitology and Immunodiagnostic Laboratory, Research and Development Division, Hindustan Antibiotics Ltd., Pimpri, Pune 411018, India

Abstract The need for a vaccine for human toxoplasmosis is briefly discussed. Recent progress inknowledge of the protective immune response generated by Toxoplasma gondii and the current status of development of a vaccine for toxoplasmosis are highlighted. © 2003 Éditions scientifiques et médicales Elsevier SAS. All rights reserved.
Keywords: Toxoplasmosis; Vaccine

1. Introduction Toxoplasmosis, caused by an intracellular protozoan parasite, Toxoplasma gondii, is widespread throughoutthe world [1,2]. The disease is of major medical and veterinary importance, being a cause of congenital disease and abortion in humans and in domestic animals [1]. In addition, recently, it has gained importance due to toxoplasma encephalitis in AIDS patients [3]. Treatment of this disease is difficult due to toxic effects of available drugs, and reinfection occurs rapidly. Under the presentscenario, development of either new antitoxoplasma drugs or a vaccine is an attractive alternative. In the last few years, there has been considerable progress towards the development of a vaccine for toxoplasmosis, and a vaccine based on the live attenuated S48 strain was developed for veterinary uses [4]. However, this vaccine is expensive, causes side effects and has a short shelf life. Furthermore,this vaccine may revert to a pathogenic strain and therefore it is not suitable for human use. Various experimental studies have shown that it may be possible to develop a vaccine against human toxoplasmosis. This review highlights the protective immune response generated by T. gondii as well as the current status of development of a vaccine for toxoplasmosis.

in these hosts is characterized byintracellular growth of the rapidly dividing tachyzoite stage in many tissues. As the immune response controls the acute infection, some of the tachyzoites become encysted, particularly in the muscles and brain, in a dormant stage termed the bradyzoite. These cysts contain hundreds of bradyzoites which are retained for years. If the tissue that contains these cysts is eaten by a nonfelinecarnivore, the bradyzoites are released in the intestine and again yield infection, characterized initially by rapid growth of tachyzoites and ultimately by the persistence of encysted bradyzoites. However, when encysted bradyzoites are eaten by a member of the cat family, the sexual cycle occurs in the intestine, resulting in the production of oocysts. When a sporulated oocyst (ovoid and measuringapproximately 10 × 12 µm) is ingested by a mammal, the sporozoites are released and infect the intestinal epithelial cells. They become rapidly multiplying tachyzoites that first produce an acute and then a chronic infection with encysted bradyzoites, thereby completing the natural life cycle [1]. Tachyzoites are crescent shaped and about 6 µm long and 2 µm wide. They are coated with three unit membranes,which form the pellicle. The anterior end of the tachyzoite is marked by the presence of a conoid, a hollow, truncated cone of spirally wound fibres that are likely to be microtubules. The rhoptries are club shaped, densely osmophilic structures whose narrow ends terminate in the conoid. Micronemes are situated close to the rhoptries and are believed to have a secretory function. Dense organs aredistributed throughout the cytoplasma of tachyzoites. Proteins from the dense granules are released into the external environment as excreted/secreted antigens. Bradyzoites differ from ta-

2. T. gondii T. gondii infects a wide range of intermediate hosts that include different species of mammals. Acute toxoplasmosis
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