Toxoplasma gondii

Introduction

  • Toxoplasma gondii, the causative organism of toxoplasmosis, was first observed in 1927 in the gondi, a North African rodent. The first human case of toxoplasmosis was also reported that year. The organism is a coccidian protozoa belonging to the sub-phylum Apicomplexa and has a world wide distribution occurring in all warm-blooded animals.
  • Cats are the definitive hosts and they become infected by ingesting oocysts or cysts in tissues of paratenic hosts, such as mice, or transplacentally. Man becomes infected either by direct ingestion of oocysts from a cat or by eating raw or undercooked meat. Those who handle raw meat are particularly at risk. Infection can be transmitted transplacentally.
Toxoplasma gondii parasite

Toxoplasma gondii parasite


Life Cycle

  • The development of the enteroepithelial (sexual) cycle in a cats intestine is brought about by the ingestion of sporulated oocysts of a mouse with cysts. The pre-patent period up to the shedding of the oocysts varies with the stage of T. gondii ingested, for example only 3–10 days if the cat has ingested a mouse containing cysts, but about 19–20 days or longer after direct infection with oocysts or ingestion of a mouse containing only tachyzoites. Women most at risk of delivering an infected infant are those who acquire the infection just prior to gestation.

Humans can acquire infection by:

• Accidental ingestion of the oocyst shed in the cats feces
• Ingestion of the tachyzoite in infected milk or transplacentally
• Ingestion of the tissue cyst in undercooked or raw meat.
• Transplant of an infected organ in a seronegative recipient

Toxoplasma gondii Life Cycle

Toxoplasma gondii Life Cycle


Clinical Disease

  • Serological evidence has shown that approximately one third of the world’s population has Toxoplasma antibodies. This suggests that the majority of infections are benign with most people exhibiting few or no symptoms, but fever and swelling may be seen. However, Toxoplasma gondii can cause severe illness in congenital infections, acquired infections and in immunocompromised patients. This may lead to ocular toxoplasmosis and ultimately to fatal CNS disorders such as encephalitis.
Toxoplasma gondii tissue cyst containing 8–20 parasites (Giemsa stain)

Toxoplasma gondii tissue cyst containing 8–20 parasites (Giemsa stain)

Toxoplasma gondii parasite in brain tissue

Toxoplasma gondii parasite in brain tissue


Congenital Toxoplasmosis

  • This occurs approximately in 1 per 1000 pregnancies. It can cause severe damage to and even death of the fetus. Proliferation of tachyzoites leads to intracellular calcification, choroidoretinitis, hydrocephaly, psychomotor disturbances and convulsions. A small, proportion of babies who are asymptomatic at birth develop retinochoroiditis or mental retardation as children or young adults. When a mother is first exposed to the parasite in later pregnancy the infant is likely to be less severely damaged or asymptomatic.
Congenital Toxoplasmosis

Congenital Toxoplasmosis

Toxoplasma periventricular calcification

Toxoplasma periventricular calcification


Acquired Infections

  • Infections with T. gondii are often mild with flu-like symptoms thus they often go unnoticed. However lymphadenopathy is the most easily recognized symptom and it can be accompanied by fever, headache and myalgia. Toxoplasmosis may also produce infectious mononucleosis like symptoms. Ocular toxoplasmosis is also a common manifest however it is not yet proven whether this is due to congenital or acquired infections. Other manifestations of Toxoplasma infections are meningoencephalitis, hepatitis, pneumonitis and myocarditis.

Immunocompromised Patients

  • Toxoplasmosis has been shown to occur as an opportunistic pathogen in immunocompromised patients and can cause severe complications. Toxoplasmosis in immunocompromised patients almost always arises from a reactivation of latent infections. Conditions which can predispose to toxoplasmosis are malignancies, organ transplants, leukemias and patients with acquired immune deficiency syndrome (AIDS).
  • In immunocompromised patients, the central nervous system is primarily involved with diffuse encephalopathy, meningoencephalitis or cerebral mass lesions. Toxoplasma encephalitis has been reported as a life-threatening among patients with AIDS.

 Laboratory Diagnosis

1. Serological Techniques

The detection of toxoplasma specific antibodies is most commonly used in clinical laboratories. Specific IgG antibodies typically persist for life whereas specific IgM antibodies begin to decline after several months. Most laboratories carry out preliminary tests for IgG antibodies and more definitive tests including IgM and IgA are carried out in reference laboratories. The Sabin-Feldman Dye Test is the benchmark for detecting the presence of specific antibodies. It measures the total amount of specific antibody in a serum which is capable of participating in antibody-mediated killing of tachyzoites by complement. This test involves the use of live tachyzoites which are derived from infected mice or rats. Because of the use of live organisms, this test is not recommended in the use of routine laboratories and is thus only employed in reference centers.

2. Isolation Techniques

Culture of parasites in animals is the best overall method but it can take up to six weeks before the result is available and is thus a disadvantage. Tissue culture is more rapid taking three or four days to obtain a result, but is not as sensitive.

3. Antigen Detection

The direct detection of very small amounts of specific nucleic acid has been made possible by the introduction in 1985 of the polymerase chain reaction (PCR). This technique results in the amplification of a specific fragment of DNA from within the parasite genome which is detected by ethidium bromide staining, following gel electrophoresis. PCR is so sensitive it should detect Toxoplasma DNA in one cyst. However this may indicate a latent infection rather than an active infection. However its sensitivity may create problems since it will detect very small amounts of DNA from latent as well as active infections and it does not differentiate between cyst and tachyzoite DNA. Thus samples like blood, CSF, urine and amniotic fluid should be used as they do not contain the latent stages. PCR shows great promise but as yet is still labor intensive and expensive for routine use in the laboratory.

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