Effect of Eimeria falciformis infection on the development of toxoplasmosis in mice

White mice previously infected with 10(2), 10(3) or 10(4) Eimeria falciformis oocysts on days 0, 5, 10 or 30 were inoculated per os with 10(1), 10(2), 10(3) or 10(4) Toxoplasma oocysts. While the results obtained for mice with higher Toxoplasma inocula were consistent, animals with 10(1) and 10(2) oocysts previous inoculation with Eimeria showed important differences related with those infected only with Toxoplasma. For example, survival time was higher in animals infected with both parasites, especially if inoculated with Eimeria 30 days before Toxoplasma infection. Furthermore the number of T. gondii cysts found in the animals previously infected with Eimeria was lower compared with mice inoculated with Toxoplasma only. Body weight of mice infected with Toxoplasma previous infection with Eimeria was almost normal in relation to those infected only with Toxoplasma, indicating a probable pathological effect due to the parasite, more evident in "non immunized" mice.     

Murine neonatal infection provides an efficient model for congenital ocular toxoplasmosis

Congenital infection is one of the most serious settings of infection with the apicomplexan parasite Toxoplasma gondii. Ocular diseases, such as retinochoroiditis, are the most common sequels of such infection in utero. However, while numerous studies have investigated the physiopathology of acquired toxoplasmosis, congenital infection has been largely neglected so far. Here, we establish a mouse model of congenital ocular toxoplasmosis. Parasite load and ocular pathology have been followed for the first 4 weeks of life. Ocular infection developed slowly compared to cerebral infection. Even after 4 weeks, not all eyes were infected and ocular parasite load was low. Therefore, we evaluated a scheme of neonatal infection to overcome problems associated with congenital infection. Development of infection and physiopathology was similar, but at a higher, more reliable rate. In summary, we have established a valuable model of neonatal ocular toxoplasmosis, which facilitates the research of the underlying physiopathological mechanisms and new diagnostic approaches of this pathology.     

Disseminated toxoplasmosis in a Mediterranean pregnant Risso's dolphin (Grampus griseus) with transplacental fetal infection

Fatal disseminated toxoplasmosis was diagnosed in a Risso's dolphin (Grampus griseus) dam and its fetus on the basis of pathologic findings, immunohistochemistry, and structure of the parasite. The dolphin was stranded alive on the Spanish Mediterranean coast and died a few hours later. At necropsy the dam was in good condition. From the standpoint of pathology, however, it had generalized lymphadenomegaly and splenomegaly, enlargement of and multifocal hemorrhage in the adrenal glands, diffuse mucosal hemorrhage of the glandular and pyloric stomach, ulcerative glossitis and stomatitis, focal erosions and reddening of the laryngeal appendix, and severe paraotic sinusitis with intralesional nematodes Crassicauda grampicola. The dolphin was pregnant, most probably in the first gestational trimester. The most prominent microscopic lesions were multifocal granulomatous encephalomyelitis, diffuse subacute interstitial pneumonia, mild multifocal necrotizing hepatitis and nonsuppurative cholangiohepatitis, gastritis and adrenalitis, mild lymphoid depletion, medullary sinus and follicular histyocitosis, and systemic hemosiderosis. The fetus had foci of coagulative and lytic necrosis in the kidneys, the lung, and the heart. Most lesions were associated with tachyzoites and tissue cysts of Toxoplasma gondii. The diagnosis was confirmed immunohistochemically. This is the first report on toxoplasmosis in a Risso's dolphin (G. griseus) and on transplacental transmission to an early-stage fetus in any cetaceans.     

Pathophysiology of toxoplasmosis

Toxoplasma infection in most adult animals and humans is asymptomatic because of effective protective immunity; this involves antibody acting extracellularly, and T-cell factors acting intracellularly. Whenever immunity is not acquired in a timely fashion, tachyzoites continue to multiply, destroying an excessive number of cells, producing lesions in several organs, with pneumonia and encephalitis the prominent causes of illness and death. However, immunity is insufficient to destroy the slowly multiplying bradyzoites persisting in tissue cysts in many organs - a parasite adaptation to await ingestion of one host by another. Toxoplasma cysts produce lesions when they disintegrate, because of the delayed type of hypersensitivity accompanying infections. In the presence of immunity, the released bradyzoites are destroyed, but when protective immunity fails, the bradyzoites can develop again into actively multiplying tachyzoites parasitizing and destroying cells in expanding foci, usually in the brain. In this review J.K. Frenkel discusses the complex interplay of immunological and parasite factors participating in the various lesions associated with acute and chronic Toxoplasma infections.     

A heterophile antigen associated with experimental toxoplasmosis

The biological characteristics of a heterophile protein (HP) in peritoneal exudate from mice, hamsters, rats, and guinea pigs infected with Toxoplasma gondii were studied by immunofluorescence, immunoelectrophoresis and immunodiffusion techniques using specific antisera raised in rabbits. HP of mice had the highest antigenicity, HP of hamsters and rats had intermediate antigenicity and HP of guinea pigs had the lowest antigenicity. HP was found in normal peritoneal exudates from mice, hamsters and rats inoculated with paraffin oil instead of T. gondii and in normal guinea pig serum. HP was detected by the fluorescent antibody technique on the surface of T. gondii in peritoneal exudates of mice, but not on mouse peritoneal cells, and by the indirect fluorescent antibody technique on L cells infected with T. gondii and on free Toxoplasma derived from them, but not on uninfected L cells. T. gondii could make host cells produce HP to cover its surface for protection. The relation between HP from host cells and T. gondii is discussed.     

Cellular responses of cats with primary toxoplasmosis.

The cellular responses of 8 kittens (4 inoculated orally with mouse brains containing Toxoplasma gondii cysts and 4 uninfected controls) were studied. Oocyst numbers, body weight, and rectal temperature were monitored daily. Blood was collected weekly for serology and mononuclear cell purification. At necropsy, peritoneal and alveolar macrophages, spleen, and lymph node cells were harvested. Infected cats shed oocysts 4-15 days postinfection, maintained normal body weight and rectal temperature, and developed anti-T. gondii immunoglobulin M and G. Infected cats had normal surface immunoglobulin-positive cell populations and peripheral blood lymphocyte functions. The infected cats differed in their responses from control cats in that they developed circulating T. gondii antigen-specific lymphocytes, had increased interleukin 1 secretion by monocytes, had spleen and lymph node cells with depressed mitogenic responses and interleukin 2 production, and had macrophages with enhanced abilities in preventing the intracellular proliferation of T. gondii. Overall, the primary response of the cat to an infection with T. gondii appeared similar to that of other hosts.