Toxoplasma gondii laboratory diagnosis

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Toxoplasma gondii laboratory diagnosis

Toxoplasma gondii is found worldwide, mainly because so many animals can harbor the organism.Information collected to date indicates that no population is exempt from the possibility of contracting Toxoplasmosis.One of the most important populations at risk of contracting this parasite are AIDS patients.Several epidemiological considerations are worth noting. First, it was documented that Toxoplasma gondii infections occur in 15 to 20 percent of the population in the United States. Second, infection caused by undercooked meat consumption and its juices by women and their children in Paris was reported in 93% (the highest recorded rate) and 50%, respectively, of the local population. Third, there have been an estimated 4000 infants born with transplacentally acquired Toxoplasma gondii infections in the United States each year. Fourth, the Toxoplasma gondii mature oocysts are incredibly hardy and can survive for long periods under less than optimal conditions. In the state of Kansas, it was documented that these oocysts survived up to 18 months in the outside environment, withstanding two winter seasons. Finally, human infections in the United States are usually acquired by hand-to-mouth contamination of infected oocysts in cat feces, ingesting contaminated meat, or transplacentally during pregnancy. As noted, transfusion-acquired Toxoplasma gondii may also occur; however, it is extremely rare.

Morphology of Toxoplasma gondii

There are only two morphological forms of trophozoites, tachyzoites and bradyzoites, seen in humans. The infectious form for humans is the  Oocyst. This form can be found at times, especially when parasitological veterinary techniques are used.

Bradyzoites and tachyzoites of toxoplasma gondii
Bradyzoites and tachyzoites of toxoplasma gondii


The typical infectious form of Toxoplasma gondii, the oocyst, appears to be similar to Isospora belli. The most significant difference between these two organisms is that toxoplasma gondii is smaller.The round to slightly oval form is 10 to 15 μm in length and 8 to 12 μm in width. There are two sporocysts in the transparent oocyst, each with four sporozoites. The organism is bounded by a clear, colorless cell wall with two layers.

Toxoplasma gondii Oocyst from a stool wet mount
Toxoplasma gondii Oocyst from a stool wet mount


The active multiplication of crescent-shaped tachyzoites varies in size from 3 to 7 μm to 2 to 4 μm. One end of the organism is often more circular than the other.Each tachyzoite has a single central nucleus, surrounded By a cell membrane. A variety of other organelles, including a mitochondrion and a Golgi apparatus, are present, but these structures are not readily visible.

crescent-shaped tachyzoites of toxoplasma gondii
crescent-shaped tachyzoites of toxoplasma gondii


Although there is evidence to support an antigenic difference, the typical bradyzoite appears essentially the same physical as the tachyzoite, only smaller.These slowly growing viable forms gather in clusters inside a host cell, develop a surrounding membrane and form a cyst outside the intestinal tract in a variety of host tissues and muscles.Such cysts can contain up to 50 bradyzoites and up to several thousand.A typical cyst has a diameter of between 12 and 100 μm.

toxoplasma cyst full of bradyzoite
toxoplasma cyst full of bradyzoite

Life Cycle of Toxoplasma gondii

While the natural life cycle of Toxoplasma gondii is relatively simple, a number of animals and humans may be involved in the accidental cycle.The cat (or other felines) is the definitive host in the Toxoplasma gondii life cycle.When Toxoplasma gondii cysts are ingested in the brain or muscle tissue of contaminated mice or rats, the bradyzoites in the cat are released and quickly converted into tachyzoites.Sexual and asexual reproduction takes place in the cat’s gut.The sexual cycle leads to the production of immature oocysts, which are eventually shed in the stool.The oocysts complete their maturation in the outdoor environment, which usually takes between 1 and 5 days.Rodents, especially mice and rats, serve as intermediate hosts to feed the infected mature Toxoplasma gondii oocysts.Sporozoites emerge from the mature oocyst and quickly become active tachyzoites in the rodent’s intestinal epithelium.These tachyzoites migrate into the brain or muscle of the intermediate host, where they form bradyzoite-filled cysts.The cat gets infected when the contaminated rodent is ingested and the cycle repeats itself.

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Human Toxoplasma gondii infection is accidental and can be initiated in four ways.One route occurs when people come into contact with infected cat feces and subsequently ingest the mature oocysts that are present through transmission from hand to mouth.Boxes for cat litters and sandboxes for children are the primary sources of this infected fecal matter.

The second route involves the ingestion of undercooked contaminated meat from bovine animals, pigs or sheep.These and a wide variety of other animals can contract Toxoplasma gondii during feeding by ingestion of infective oocysts in cat feces.After ingestion, infectious sporozoites are released and follow the same cycle in these animals as in the natural intermediate hosts.The resulting cysts can remain sustainable for years in the animal muscle and the parasites in them.

The third means of human transmission of toxoplasma gondii is transplacental infection.This happens when an asymptomatic infection in a mother is passed on to her unborn fetus unknowingly.In response to the parasite, the mother produces IgG, which also crosses the placenta and can appear in the circulation of the newborn fetus for several months.The mother also produces IgM that doesn’t cross the placenta. The infant can however show anti-toxoplasma gondii IgM from birth to several months of age.

The fourth route of human infection, though extremely rare, occurs when contaminated blood is transfused into an uninfected person. Once in human beings, toxoplasma gondii tachyzoites emerge from the ingested cyst and quickly grow and divide.The form of tachyzoite causes tissue damage and initial infection. The tachyzoites migrate to several tissues and organs, including the brain,where cysts filled with bradyzoites then form.

life cycle of toxoplasma gondii
life cycle of toxoplasma gondii

Clinical symptoms of Toxoplasmosis


Many toxoplasma gondii infected patients remain asymptomatic, especially children who have gone through the neonatal stage of their lives. Although well adapted to its environment, Toxoplasma gondii appears to cause human disease only if one or more of the following conditions are met:

  1. A virulent strain of the organism has entered the body
  2. The host is in a particularly susceptible state (e.g., those suffering from AIDS)
  3. the specific site of the parasite in the human body is such that tissue destruction is likely to occur.
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Toxoplasmosis: General Symptoms

Although serious symptoms can be observed, the typical symptoms experienced by people infected with Toxoplasma gondii are mild and similar to those seen in infectious mononucleosis cases. The acute form of the disease has fatigue, lymphadenitis, chills, fever, headache and myalgia.In addition to the above symptoms, chronic disease patients may develop a maculopapular rash and demonstrate encephalomyelitis, myocarditis and/or hepatitis evidence. It was known that retinochoroiditis with subsequent blindness occurs rarely.

Congenital Toxoplasmosis

This severe and often fatal condition occurs in about 1 to 5 of 1000 pregnancies.The transmission of the disease occurs when the fetus is unknowingly infected by the asymptomatic infected mother (by transplacental means).The severity of the resulting disease varies and depends on two factors:

  • The mother’s antibody protection
  • The age of the fetus when infected.

Mild infections occur from time to time and result in a complete recovery.Unfortunately, after the initial infection, these patients may develop retinochoroiditis years later.Hydrocephalus, microcephalus, intracerebral calcification, chorioretinitis, convulsions and psychomotor disorders are the typical symptoms of an infected child.Most of these infections lead to mental retardation, severe visual impairment or blindness.

There are a number of important documented statistics on the symptoms that infants born with Toxoplasma gondii are likely to experience. 5 to 15 percent of infected infants are estimated to die as a result of toxoplasmosis. Another 10 to 13 percent of infected infants will most likely develop moderate to severe disabilities.Severe eye and brain damage occurs in about 8% to 10% of infants infected. The rest of 58% to 72% of infected infants are most likely to be asymptomatic at birth.Although the mechanism for this reactivation of the infection is unknown, a small percentage of these infants develop later mental retardation or retinochoroiditis, usually in children or young adults.

Toxoplasmosis in Immunocompromised Patients.

Patients immunosuppressed as an opportunistic infection due to organ transplantation or the presence of neoplastic disease, such as Hodgkin’s lymphoma, have long been known to contract toxoplasmosis.It is important to note the importance of screening for potential donor units for toxoplasmosis before transfusion, especially in patients who need blood transfusions.

Cerebral Toxoplasmosis in AIDS Patients.

The association of Toxoplasma gondii and AIDS patients has been a point of attention.Since the 1980s, toxoplasmic encephalitis in these individuals has been considered a major complication.Indeed, one of the first obvious clinical symptoms of AIDS patients may be the involvement of the central nervous system (CNS) of toxoplasma gondii.AIDS patients with Toxoplasma gondii infection may have early headache, fever, altered mental status (including confusion) and lethargy symptoms. There are generally subsequent focal neurological deficits, brain lesions and convulsions.

The Toxoplasma gondii organisms do not spread to other body organs but remain confined within the CNS.An increase in the IgG level of the spinal fluid is diagnosed, as is the demonstration of tachyzoites in the cerebrospinal fluid (CSF) during microscopic testing.In these patients, the serum IgG level does not respond or the CSF level.Most infected patients have no IgM antibodies in their serum levels.The lack of serum IgM combined with the lack of change in serum IgG levels in these patients indicates that their infections occurred due to a chronic latent infection reactivation and not due to a primary infection acquired.

Treatment of Toxoplasmosis

The combination of trisulfapyrimidines and pyrimethamine (Daraprim) is the treatment of choice for symptomatic cases of Toxoplasma gondii infection. It is important to note that pyrimethamine should not be given to infected pregnant women. Spiramycin is an acceptable alternative drug.Spiramycin is used in Europe, Canada and Mexico, but in the United States it is still considered an experimental drug.However, it can be obtained by the FDA in the first trimester of pregnancy with special permission for toxoplasmosis.Also valuable may be corticosteroids used as an anti – inflammatory agent.Folinic acid (leucovorin) may be given to infected patients with AIDS to counteract the suppression of the bone marrow caused by pyrimethamine. Atovaquone is an effective drug, especially for the treatment of toxoplasmic encephalitis in patients with AIDS.

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Prevention and Control of Toxoplasmosis

A number of measures need to be taken and implemented to prevent the spread of Toxoplasma gondii infections. One of these is to avoid contact with cat feces.This can be achieved by wearing protective gloves when a cat litter box is cleaned, the litter box is disinfected with boiling water and washed thoroughly afterwards.Furthermore, the placement of a protective cover over children’s sandboxes when not in use prevents cats from using them as litter boxes.

Infections with toxoplasma gondii can also be prevented by the intake of contaminated meat. This can be achieved by thorough hand washing after handling contaminated meat and also by preventing raw meat from being tasted.Furthermore, all meat must be cooked thoroughly before consumption. Additional prevention and control measures for toxoplasma gondii include keeping cats away from potentially infectious rodents, feeding cats only with dry or cooked canned cat food and/or not having cats.

All humans should put these preventive measures into practice. However, pregnant women should be particularly cautious about cat feces and contaminated meat because toxoplasmosis can be contracted and the disease transferred to their unborn children.

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About the Author: Arthur Westmann

DEFFE ARTHUR (AMOEBAMANN) is the founder and author of MLTGEEKS and MLTEXPO.He’s from Cameroon and is currently a Final year State Medical Laboratory Technician (MLT MA). Beyond lab works, he’s a passionate internet user with a keen interest in web design and blogging. Furthermore He likes traveling, hanging around with friends and social networking to do in his spare time.

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