Toxoplasmosis is caused by way of ...

Toxoplasmosis is caused by way of the protozoan parasite Toxoplasma gondii. A late serologic survey (1) conducted as part of the Third National Health and Nutrition scrutinize found that 23 percent of adolescents and adults and 15 percent of women of childbearing age in the United States present to view laboratory evidence of T. gondii infection. Although T gondii infection in adults is usually asymptomatic or associated with self-limited symptoms (eg agitation malaise, lymphadenopathy), infection in a pregnant woman may cause serious health moot points if the parasite is transmitted to the fetus.

Based forward extrapolation of data from regional studies, (2-4) 400 to 4000 cases of congenital toxoplasmosis present itself in the United States each year. Congenital toxoplasmosis can have inexorable sequelae, including mental retardation, blindness, and epilepsy in infancy or frequently later in life.

Family physicians may be bring face to faceed with a number of issues regarding toxoplasmosis. more [i]or[/i] less of these issues are related to clinical presentation, laboratory testing, and prevention.

Toxoplasma gondii

LIFE CYCLE

The T gondii life period has three stages: tachyzoite, bradyzoite, and sporozoite. (5) During the acute stage of T gondii infection, tachyzoites invade and replicate within solitary abode; squalids and are responsible for congenital infection. The tachyzoites invade all organs, especially the muscles (including the heart), liver, grudge lymph nodes, and central nervous order (CNS). During latent infection, bradyzoites are at hand in tissue cysts. Sporozoites are build in environmentally resistant oocysts formed after the sexual stage of the life cycle

Members of the Felidae family, including domestic and feral cats, are the definitive entertainers for the sexual stage of T gondii, which takes place in their intestinal mucosa. During acute infection, cats discharge unsporulated (i.e., noninfectious) oocysts in their fece Depending upon environmental conditions, the oocysts sporulate and become infectious after united day to several weeks. in subordination to favorable conditions (i.e., in warm, moist soil), oocyst remain infectious for a year or more.

TRANSMISSION

T gondii is transmitted to humans according to three principal routes (Figure 1) (6) First, humans can acquire T gondii by dint of eating raw or inadequately falsifyed infected meat, especially pork, mutton, and wild game, (7) or uncook aliments that have come in contact with infected meat. secondary humans can inadvertently ingest oocyst that cats have passed in their fece either from a litter chest or from soil (e.g., soil from gardening, upon unwashed fruits or vegetables, or in unfiltered water). Third, women can transmit the infection transplacentally to their unborn fetus. In adults, the incubation period for T gondii infection ranges from 10 to 23 days after the ingestion of undercook meat and from five to 20 days after the ingestion of oocyst from cat feces

A report (8) from the Economic Research Service of the U Department of Agriculture conclud that common half of toxoplasmosis cases in the United States are caused by the agency of eating contaminated meat. This conclusion is supported at the findings of a community-based epidemiologic application of mind (9)

Women infected with T gondii before conception rarely transmit the parasite to their fetus, moreover those who become acutely infected or have reactivation of T gondii during pregnancy (i.e., because of immunosuppression) can transmit the organism transplacentally. The risk of congenital disease is lowest (10 to 25 percent) when maternal infection arises during the first trimester and highest (60 to 90 percent) when maternal infection happens during the third trimester. (1011) However, congenital disease is more austere when infection is acquired in the first trimester. (10) The overall risk of congenital infection from acute T gondii infection during pregnancy ranges from approximately 20 to 50 percent (10)

Immunosuppression resulting from human immunodeficiency virus (HIV) infection or therapies for malignancies, organ transplantation, and lymphoproliferative disorders can terminate in the reactivation of latent T gondii infection. Reactivation greatest in number often involves the CNS, and symptoms may include those of meningoencephalitis or a mass lesion. Women with reactivated T gondii infection can transmit the organism transplacentally. (10)

RISK FACTORS

modern epidemiologic studies have identified the following risk factors for T gondii infection: owning a cat, (12) cleaning a cat litter driver's seat (13) eating raw or undercook pork, mutton, lamb, beef, or minced-meat harvests (12-14) gardening, (15) eating raw or unwashed vegetables or fruits, (12) eating raw vegetables outside the to one's home (12) having contact with soil, (14) washing kitchen knives infrequently, (13) having poor hand hygiene, (12) travelling outside of Europe Canada, or the United States, (14) and drinking municipal water from a contaminated reservoir. (16)

It is important to note that modern epidemiologic studies have not shown cat ownership to be a consistent risk factor for T gondii infection. The risk of infection is not related to owning a cat further to being exposed to fece from a cat that is shedding oocyst When cats become infected with T gondii, they generally shed oocyst and nothing else for a few weeks during their lifetime. Indoor cats that do not look and are not fed raw meat are unlikely to acquire T gondii infection and therefore posture little risk. Furthermore, a contemplation (17) of cats induced to shed oocyst ground no oocysts on the cats' fur after they shed the oocyst Therefore, the possibility of T gondii transmission [i]or[/i] part of to the other touching a cat is considered to be minimal or nonexistent. (7)