Toxoplasma gondii: Introduction, Classification, Morphology, Lifecycle, Pathogenicity, Lab Diagnosis, Treatment and Prevention

Toxoplasma gondii: Introduction, Classification, Morphology, Lifecycle, Pathogenicity, Lab Diagnosis, Treatment and Prevention

Introduction of Toxoplasma gondii

Toxoplasma gondii is a tissue parasite. It was discovered by Nicolle and a French physician, parasitologist,  Louis Herbert Manceaux in 1908.  It causes the most common parasitic of humans and warm-blooded animals.

Size of parasite: 4-6 μm

Site in host: All organs

Mode of infection

Portal of entry:   Mouth/ ingestion

Causative agent:  Oocyst ( sporozoites)

Medium: Cat’s stool, congenital ( Mother to baby)

Clinical symptoms: Asymptomatic infection

Disease: Choriorentinitis, Hydrocephalus

 Classification of Toxoplasma gondii

Phylum: Apicomplexa

Class: Sporozoa

Order:   Eucoccidiorida

Family:  Sarcocystidae

Genus: Toxoplasma

Species: T. gondii


Geographical Distribution of Toxoplasma gondii

This parasite is cosmopolitan in distribution.

Habitat of Toxoplasma gondii

T. gondii is found in animals like mice, rats, rabbits, cats, birds, and other animals. These organisms are found in exudates, free or intracellular ( mononuclear and endothelial cells), or in pseudocyst in the tissue of the host.

Morphology of Toxoplasma gonndii

Tachyzoit ( Sporozoite)

  1. The parasites are ovoid, pyriform, or crescent in shape, 4-6 ×2-3 μm in size with ends pointed or rounded.
  2. Cytoplasm: Blue with Romanowsky’s stain. It contains a red-stained rounded mass of chromatin (nucleus) located near one end.  At the other end, there is a small red mass (para nuclear body)
  3. Nucleus: The nucleus shows a membrane and a central karyosome.
  4. In exudates, the organism may appear extracellular, singly or in pairs, and crescent-shaped. When intracellular, the organism resembles amastigote of Leishmania but kinetoplast is lacking


Tissue cyst or extracellular form

  1. Toxoplasma gondii may lie free in exudates or may lie embedded in the central nervous system (CNS) and muscles surrounded by a membrane.
  2. The organism within the cyst is known as bradyzoites.
  3. Brandzyoites are crescent-shaped, slender, measuring 7×1.5 μm.
  4. Young tissue cysts of the brain rarely rich at 60μm but intramuscular cysts may reach 100 μm in diameter and may contain 100 bradyzoites.

Pseudocyst or intracellular form

  1. T. gondii lies inside RE cells and other nucleated cells.
  2. Group of proliferating tachyzoites the host cells are known as a pseudocyst.


  1. It contains sporozoite and present in cats but not in men.
  2. It is oval or spherical 10-12 μm in diameter.
  3. Its wall contains two layers.
  4. The oocyst is formed by sexual reproduction.

Life cycle of Toxoplasma gondii

The life cycle of T. gomdii is completed in two-phase, the enteric cycle and the extra enteric cycle. The enteric cycle is completed in the homologous host, e.g domestic cat. It includes both the asexual (schizogony cycle) and sexual cycle (gametogony). The Entraenteric cycle is completed in man and mouse.

Enteric cycle

  1. Cat acquires infection by tachyzoites by tachyzoites or bradyzoites from tissue cyst or sporozoites from oocyst.
  2. These parasites invade mucosal cells of the small intestine and multiply asexually for several generations. The schizogony cycle occurs and on rupture, merozoites are liberated. T. gondii ( Sporozoites) escape from the cyst and invade epithelial cells, especially of the ileum.
  3. After that, the sexual cycle begins the male and female gametocytes are formed and fertilization occurs then develops to oocyst in the gut lumen.
  4. Oocyst is passed out in the feces.
  5. Oocyst becomes an infection only after development in soil for a new day. During the development, the sporoblast of the oocyst divides into two.
  6. These then become sporocyst by acquiring a cyst wall.
  7. Four sporozoites develop inside each sporocyst.
  8. The mature cyst containing eight sporozoites in the infective form of the parasite.


Extraenteric Cycle

  1. Infection acquires by ingestion of food and water contaminated with cat’s feces containing sporulated oocysts and also by ingesting undercooked meat containing tissue cysts.
  2. In the duodenum the oocysts release sporozoites and tissue cysts release bradyzoites.
  3.  These pass through the gut wall, circulate in the body, and invade various cells, especially macrophages.
  4. They from tachyzoites, multiply, break out, and spread the infection to other organs.
  5. Subsequently, they enter into the neural and muscular tissues, such as the brain, eyes,  skeletal and cardiac muscle where they multiply slowly to form tissue cysts, initiating the chronic stage of the disease.
  6. Tissue cyst may also develop in other such as lungs, liver, and kidney.
  7. Tissue cysts, when ingested by both definitive and intermediate hosts, are infective.
  8. The cycle is prepared.

Pathogenicity of Toxoplasma gondii

The infection caused by Toxoplasma is known as toxoplasmosis. The illness is self-limited

Sources ad mode of infection

  • Infected cattle, pigs, birds are the sources of infection but more likely infection occurs by sheep and pigs. Infection occurs by:

a. Ingestion of undercooked meat,

b. Handling of infected meat,

c. Inhalation

d. Infected cat: Ingestion of oocyst while handling,

e. Laboratory infection:    i) Handling infected mice,   ii) Handling culture.

  • Infected mother

Transplacental: Congenital infection develops focal lesions in the placement and the fetus may be infected. It leads to stillbirths, chorioretinitis, intracerebral calcification, and hydrocephaly. Clinical manifestations of this infection may be delayed long after birth.  Postnatally acquired infection:  Postnatally acquired toxoplasmosis is much less severe than the congenitally acquired disease.  The common manifestation is lymphadenopathy and lymph nodes may be involved. This is associated with fever, malaise, headache, muscle pain,  fatigue, and sore throat.

  • Organisms spread widely by the bloodstream and localize in various organs, CNS, eye, liver, muscles ( cardiac and smooth), lymphoreticular system ( spleen, lymph node), and bone marrow.
  • The affected sites show necrosis and infiltration with reticuloendothelial (RE)cells as well as small round cells. The organisms are present in a large number inside the cells.
  • Clinically, the lesions are congenital or acquired, the latter being cerebrospinal, lymphatic, cutaneous, pulmonary, cardiac, etc.

Laboratory Diagnosis of Toxoplasmosis

Direct Method

Materials (samples)

  1. Bone marrow and spleen aspirate.
  2. Centrifuged deposit of CSF
  3. Lymph node and muscle biopsy.

Microscopic: Microscopic examination of stained smear.

Animal inoculation: Animal inoculation and demonstration of organisms in animals, mice, guinea pigs, and hamsters.

Indirect Method


  1. Complement Fixation Test (CFT)- antigen from the culture of Toxoplasma  gondii
  2. Neutralizing antibody
  3. Agglutination test
  4. Indirect haemagglutination reaction: Soluble antigens used and are now commercially available.
  5. Indirect fluorescent antibody test (IFAT)

Another method

  1. Polymerase chain reaction (PCR): It is used to identify T.  gondii tissue cysts or tachyzoites in tissue where Toxoplasma DNA can be detected.
  2. Skin test- a delayed-type of reaction with Toxoplasma
  3. Methylene blue dye test
  4. CT scan is also useful in the diagnosis of human cerebral toxoplasmosis.

Treatment of Toxoplasmosis

A combination of Pyrimethamine and sulphadiazine is widely used for the treatment of toxoplasmosis.

Prevention and Control of Toxoplasma

  1. Avoid human contact, particularly of pregnant women with cat faces and uncooked meat.
  2. Meat should be cooked properly.
  3. The hands of the people handing meat and all cutting instruments in contact with uncooked meat should be washed thoroughly with soap and water.


  • The most reliable test for antibodies detection of  T. gondii is the Sabin-Feldman dye test.
  • A sexual multiplication of T. gondii by cell division can occur in virtually any host cell.
  • Necrosis is due to intracellular multiplication of tachyzoites but not due to toxin since T. gondii does not produce a toxin.

Further Reading



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