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Toxoplasma gondii. T.gondii causes Toxoplasmosis. Recently, due to the emergence of several outbreaks, prevalence of AIDS and the improvement of diagnostic measures, gradually it is realized to be an important opportunistic protozoan, which may be lethal.
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T.gondii causes Toxoplasmosis. Recently, due to the emergence of several outbreaks, prevalence of AIDS and the improvement of diagnostic measures, gradually it is realized to be an important opportunistic protozoan, which may be lethal.
There are 5 morphologically different stages: Trophozoite: or Tachyzoite is crescent or banana shaped with a pointed end and a bluntly round end. In the acute stage of the disease, trophozoites are usually scattered in the blood, cerebrospinal fluid and various pathological exudates arranged in pairs or singly. The trophozoite community is within a host cell parasitophorous vacuole not surrounded by a cystic wall. Hence they are also known as a pseudocyst (usually a swelling macrophage with a several parasites). The trophozoites within a pseudocyst are Tachyzoites.
Tissue cyst: is round and oval in appearance and the cystic wall created by the parasite is thin, but firm and elastic. The protozoa multiply in the tissue cyst slowly and repeatedly. The trophozoites in the cyst are called Bradyzoites, which are similar to the Tachyzoites, but smaller than them.
Schizont: can be found in the small intestinal mucosa of the infected cat. Schizonts contain about 4-40 merozoites. Gametocytes are also found in the small intestinal mucosa of the cat. Male gametocytes produce 12-32 male gametes, crescent in shape. The female gametocyte develops into a female gamete.
Male and female gametes fertilize to form a zygote that dvelops into an oocyst. An oocyst is round or elleptic and covered with a smooth transparent cystic wall consisting of two layers. Each mature oocyst contains two sporocysts with each sporocyst containing 4 sporozoites.
Two different kinds of host are needed in the sexual and asexual generations present in the life cycle of T.gondii. Sexual development or Gametogony and only the schizogony of the asexual development occurs in the epithelial cells of the small intestine of cats(intra-intestinal phase). The binary fission and endodyogeny ( process of internal budding in which two daughter cells are formed within the body of the mother cell that dies when the progeny are released) of the asexual development takes place in various nucleated cells outside the intestine of many spp. Of mammals and birds.
The extra-intestinal phase begins when the oocyst or the meat or animal viscera containing cyst or pseudocyst are ingested by an intermediate host (man, pig, cattle, cheep. Mouse etc…), sporozoites bradyzoites or tachyzoites are released in the host intestine. Parasites penetrate the intestinal wall. They actively invade or are ingested by the mononuclear phagocytes and develop and inhabit them. The ability and effeciency of the cell invasion is varied in different strains of T.gondii with high or low virulence. Binary fission and endodyogeny results in the production of Tachyzoite bearing Trophozoites, encircled by the host cell membrane called Pseudocysts.
When Tachyzoites increase more than 10 per cell, the host cell breaks and parasites released, that in turn invade new cells , develop and multiply. In an immuno competent host, these Tachyzoites develop into cysts especially in the cells of the brain, eye and skeletal muscles and can survive for several years. Several hundred bradyzoites can be observed a cyst. Under immuno suppressed conditions, cysts rupture, deliver many bradyzoites which infect more cells. The ability of invasion and multiplication of T.gondii and the host immune status are in a dynamic equilibrium, and as a result, tachyzoites can transform into bradyzoites and vice versa.
When food or water contaminated with T.gondii oocyst or animal body containing cysts, pseudocyst ingested by a feline, sporozoites, bradyxoites or Tachyzoites are released in the small intestine. These parasites invade the epithelial cells, and 3-7 days later transform into multinucleated schizont. On maturation, merozoites are released, in turn they invade new epithelial cells and repeat schizogony.
Several generations later, some merozoites develop into micro and macro gametes . Fertilization results into a zygote which develops into an oocyst. OOcyst leaves the host lumen, finally mixed with feca and expelled. Under favorable conditions, each oocyst devlops into infectious stage with 2 sporocysts and each containing 4 sporozoites.
Pathogenesis: Tachyzoite is the principle stage responsible for the pathological changes. After entering the host cell, trophozoites multiply, break the cell and the released tachyzoites invade new cells once again. The process repeats itself and a foci of edema and necrosis surrounded by lymphocytes monocytes and plasma cells are formed.
The pathological changes can be divided into 3 categories: A) Necrotic foci result from cell destruction by the quickly multiplying tachyzoites. These foci, later form the fibrosis scars with the cysts present all around. B) Cysts normally do not induce inflammation, but if it breaks, the released bradyzoites , although cleared by the host immune system, some will survive and cause delayed hypersensitive reaction, which results in the formation of granuloma and scar. C) Secondary pathological changes initiated by focal damage can result in blood vessel blockage induced by inflammation of these vessels and further results in tissue infarction, usually in the brain.
After infection of the intestinal epithelium, the organisms can spread to other organs like brain, lungs liver and eyes. This spread controlled by cell-mediated immunity, but circulating antibodies enhance killing of the parasite.
Congenital Toxoplasmosis: Congenital infection occurs when mother is infected during pregnancy. Infection during First trimester, the outcome is often severe. Second trimester infection, some babies will show symptoms months or years after birth. Third trimester infection is usually non-significant. Congenital toxoplasmosis occurs only in babies of primigravida. If mother infected before pregnancy, parasites will be in cyst form and no trophozoites to cross the placenta. If mother having previous infection, reinfected during pregnancy, will have antibodies and will not transmit parasites to the child.
Clinical findings: Immuno competent adults asymptomatic, or may resemble Infectious mononucleosis., but heterophil antibody test is negative. Congenital infection can result in abortion, still birth or neonatal disease with encephalitis, chorioretinitis and hepatosplenomegaly. Fever, jaundice and intra-cranial calcifications are also seen. Mental retardation may develop in children, months to years later. Congenital infection is the leading cause of blindness in children. Toxoplasmosis, is one of the most severe complications of AIDS, leading primarily to encephalitis.
Laboratory diagnosis: Involves an Immunofluoroscens assay for IgM antibody during acute and congenital infections. High IgG antibody titres may be useful, but could be of the mother. Giemsa stained crescent shaped trophozoites in acute infections. Cysts may be seen in tissue.
Treatment: For Congenital toxoplasmosis (symptomatic or non-symptomatic and disseminated disease in immuno- compromised individuals: Combination of Sulfadiazine and pyrimethamine. Prevention: Cook meat thoroughly to kill the cysts. Avoid proximity to cats.
