Toxoplasmosis: Symptoms and Treatment

Symptoms and Treatment

Definition and Causes:
Toxoplasmosis, a parasitic disease caused by the protozoan Toxoplasma gondii, manifests as cysts or germ carriers. It affects various human tissues, including nerves, eyes, cardiovascular system, lymphatic system, and retina. Classified under the TORCH group, it poses hereditary risks.


  • Discovered in 1908 by French scientists S. Nicolle and L. Manceaux, Toxoplasma gondii earned its name from “taxon” meaning bow and “plasmon” referring to shape.
  • In 1923, Czech ophthalmologist I. Yanku linked Toxoplasma to human diseases by describing ocular toxoplasmosis symptoms in an infant.
  • In 1938-1939, American researchers confirmed mother-to-fetus transmission and isolated the parasite from an infected child.


  • Kingdom: Protozoa
  • Phylum: Apicomplexa
  • Class: Conoidasida
  • Order: Eucoccidiorida
  • Family: Sarcocystidae
  • Genus: Toxoplasma
  • Species: Toxoplasma gondii
Forms of presence of Toxoplasma

Life Cycle:

  • Toxoplasma exists in three forms: tachyzoites, bradyzoites (cysts), and oocysts.
  • Tachyzoites measure 4-7 µm and invade mammalian cells except red blood cells. They multiply through division and actively penetrate host cells.
  • Bradyzoites form cysts with a dense membrane, housing thousands of parasites. They persist in the host’s body, especially in muscles, cardiac muscles, and the central nervous system, without causing harm.
  • Oocysts, found in cat feces, facilitate disease transmission. They survive in the environment for extended periods, spreading infection through ingestion or contact.


  • Toxoplasmosis prevalence varies globally, with an estimated 1.5 billion infected individuals.
  • Approximately 200,000 infections occur annually in utero.
  • The parasite’s global presence is evident, with differing infection rates across countries, ranging from 85% in France to 15% in the USA and England.

Transmission Mechanisms:

  • Oral-fecal route: Contaminated water, food, or contact with cat feces.
  • Vertical transmission: From mother to fetus during pregnancy, particularly in HIV-infected mothers.
  • Artificial routes: Organ transplantation with cyst-containing tissues.
  • Airborne and dermal routes: Ingestion of dust contaminated with oocysts or skin abrasions.
  • Human-to-human transmission is rare except through consumption of human flesh.

Immunity and Recurrence:

  • Toxoplasma infection confers lifelong immunity but may reoccur with a different strain, especially in pregnant women consuming meat from other regions.

Understanding toxoplasmosis, its transmission routes, and immunity mechanisms is crucial for effective prevention and treatment strategies.

Symptoms of Toxoplasmosis:

The incubation period in initial forms (clear onset of symptoms) ranges from two weeks to two months. There are no specific symptoms that distinctly characterize toxoplasmosis. In most cases of acquired toxoplasmosis, the disease passes unnoticed or presents with mild symptoms resembling a cold: temporary fever, weakness, discomfort, temperature elevation up to 38.0 degrees Celsius, peripheral lymph node enlargement, slight increase in liver and spleen size.

It has been established that toxoplasmosis can affect the human mind. This manifests in increased risk-taking behaviors, decreased concentration, and increasing nervous tension, with individuals experiencing acute or long-term chronic toxoplasmosis being at increased risk of developing schizophrenia.

Occasionally, the disease appears in isolation in the form of eye problems – chronic eye infections, iritis and uveitis, and retinal detachment. These disturbances usually result from late recognition of a congenital process.

Ocular toxoplasmosis

The disease may progress in individuals with immune deficiency (such as human immunodeficiency virus, or following organ transplantation with immunosuppressive therapy) to a generalized process involving multiple organs (brain, heart, liver, kidneys, lungs), often manifesting as a severe syndrome of multiple organ failure.

Toxoplasmosis may affect pregnant women in various clinical forms and poses a risk not so much to the pregnant woman herself (except for severe complications that may occur in pregnant women with AIDS), but to the fetus.

In cases of primary infection of pregnant women with toxoplasmosis, the timing of pregnancy is of utmost importance:

  • When infection occurs in the first trimester of pregnancy, transmission to the fetus occurs in only 4% of cases (6% by week 13), but mostly resulting in fetal death and miscarriage in early stages. If the mother’s primary infection is confirmed in the first trimester of pregnancy but miscarriage has not occurred by week 13 of pregnancy, the likelihood is very high that intrauterine transmission has not occurred, and the child will be healthy.
  • When infection occurs in the second trimester (especially in weeks 24-26), the risk of intrauterine transmission increases sharply to 30-40%, accompanied by the development of severe disease symptoms – simultaneous splenomegaly and hepatomegaly, iritis and retinitis, central nervous system involvement such as hydrocephalus, calcifications, skin rash, myocarditis, pneumonia, and others.
  • When infection occurs in the third trimester of pregnancy, transmission of the infection to the fetus occurs in up to 90%, however, the disease symptoms remain latent or appear without clear symptoms, and may manifest years after birth (delayed development, vision problems).

Pathogenesis of Toxoplasmosis:

The path of infection with toxoplasmosis starts from the mouth, where it enters via oocysts into the human gastrointestinal tract. Then, during the parasite’s development (as its cells multiply), trophozoites are formed, which migrate to various parts of the body and tissues (primarily to the central nervous system and muscles). False cysts are formed – large aggregates of multiplying parasites – inside cells.

As the parasite develops and multiplies, the infected cells break down, causing injury to new healthy cells. When the parasite enters the bloodstream, it spreads throughout the body. Cysts are formed along with the formation of fibrous tissue and calcification (deposition of calcium salts in the body).

Under the influence of the immune system, non-encysted trophozoites transform into bradyzoites (encysted aggregates of Toxoplasma), that is, tissue cysts, which remain active for decades in a dormant state and when the immune system is significantly suppressed, they can revert with worsening disease progression.

In cases of primary infection in pregnant women, the parasite penetrates the fetal tissues and causes an inflammatory process. At different stages of development, different types of inflammation are observed: changes occur only in the fetus (necrosis and erosion of tissues without fibrosis), in early fetal life fibrous tissue formation (fibrosis) is added, and in late fetal life the vascular component is added. Hence, different types and severity of fetal injuries arise, depending on the timing of maternal infection.

Classification and Stages of Toxoplasmosis:

Toxoplasmosis is classified according to the progression of the condition into the following types:

  • Acute Toxoplasmosis:
  • Acute – lasts up to one month.
  • Subacute – 1-3 months.
  • Chronic – more than three months.

Based on clinical features, five forms of the disease are identified:

  • Congenital Acute Toxoplasmosis:
  • Clear form (with mention of main symptoms).
  • Mild form (with mention of diagnostic confirmation method).
  • Congenital Chronic Toxoplasmosis:
  • Exacerbation / remission.
  • With residual phenomena / without residual phenomena.
  • Latent Congenital Toxoplasmosis.
  • Acquired Acute Toxoplasmosis.
  • Acquired Chronic Toxoplasmosis.

Disease severity:

  • Mild.
  • Moderate.
  • Severe (congenital infection, toxoplasmosis in AIDS cases).

Based on the presence of complications:

  • Complicated Toxoplasmosis.
  • Uncomplicated Toxoplasmosis.

In the International Classification of Diseases, six types of the disease have been identified:

  • B58.0: Ocular toxoplasmosis.
  • B58.1: Hepatic toxoplasmosis.
  • B58.2: Cerebral toxoplasmosis.
  • B58.3: Pulmonary toxoplasmosis.
  • B58.8: Toxoplasmosis with involvement of other parts of the body.
  • B58.9: Unspecified toxoplasmosis.

Complications of Toxoplasmosis:
Complications of toxoplasmosis:
In the congenital form, hydrocephalus, microcephaly, developmental delay, and blindness may occur. These complications are accompanied by increased or decreased skull size, various neurological disorders such as chorioretinitis, seizures, difficulty sitting and holding the head, vomiting, and others.
In the ocular form of the disease, blindness, decreased visual acuity, and inflammatory phenomena in all parts of the eye occur. Severe visual defects may occur at birth, or inflammatory phenomena and visual disturbances may appear years after birth.
Toxoplasmosis complicates in individuals with immunodeficiency due to AIDS with schizophrenia, toxoplasmic encephalitis, and multiple organ failure – a severe medical condition affecting various organs in the presence of immune system weakness. In this condition, a severe pattern of encephalitis is typically observed, and prognosis is generally unfavorable.

Diagnosis of Toxoplasmosis:

Laboratory Diagnosis:

  • Clinical blood analysis: Decreased platelet count, increased lymphocytic and eosinophilic cell count.
  • Blood chemistry analysis: There may be an increase in liver enzymes and bilirubin levels.
  • Enzyme-linked immunosorbent assay (ELISA):
  • Detection of specific antibodies of class M – acute infection or reactivation.
  • Detection of specific antibodies of class G (memory cells) – during pregnancy, infection – typically appears after the second week of illness and peaks in the first to second month, remains present for life, except in AIDS-related diseases.
  • Weak response for IgG – temporal determination of the disease.
  • Polymerase Chain Reaction (PCR) diagnosis: Detection of Toxoplasma DNA in blood, other fluids, and human body tissues. This is particularly valuable in diagnosing congenital, ocular, and comprehensive toxoplasmosis, including prenatal detection through amniocentesis (after week 16) and cordocentesis (from week 18 of pregnancy).
  • Ultrasound diagnosis: Detection of hydrocephalus, microcephaly in utero, calcifications, hepatosplenomegaly, and prominent developmental delay.

Differential Diagnosis:
Toxoplasmosis presents with highly varied symptoms, thus differential diagnosis focuses on specific laboratory tests, particularly serological tests.
Diseases to be ruled out include:

  1. Infectious mononucleosis (Epstein-Barr virus infection) – sore throat, primary and posterior lymph node enlargement, distinctive blood changes (large number of atypical lymphocytes and no very pronounced changes in congenital cases), positive IgM and PCR tests in blood.
  2. Cytomegalovirus infection (Cytomegalovirus) – lymphocytic features in blood analysis, recurrent salivary gland involvement, positive IgM and PCR tests in blood.
  3. Tuberculosis – prolonged slow onset, low-grade fever (up to 38.0 degrees Celsius), night sweats, unhealthy redness on cheeks, cough, specific lung changes, positive tuberculosis tests, and detection of Koch bacillus in sputum.
  4. Proliferative lymphatic diseases (such as Hodgkin’s lymphoma and non-Hodgkin’s lymphocyte tumors) – specific tissue changes in affected tissues during histology (lymph nodes).
  5. Human Immunodeficiency Virus (HIV) infection – presence of a possible infection, increased in all lymph node groups, positive serum test.
  6. Sarcoidosis (Sarcoidosis) – specific lung changes, positive histological studies.

Treatment of Toxoplasmosis:
Most cases of acquired toxoplasmosis are mild or asymptomatic and go unrecorded, thus seeming to not require treatment.
Specific treatment is only required for certain patient groups:

  • Individuals experiencing exacerbation of chronic toxoplasmosis.
  • Pregnant women with confirmed congenital infection (in some cases upon reactivation of chronic infection).
  • Children with congenital toxoplasmosis (based on clear clinical and laboratory signs of the disease, partial and latent clinical forms) – the extent and scope of treatment depend on individual data.
  • Immunocompromised individuals suffering from toxoplasmosis (in acute or reactivation stage of chronic process) with prominent clinical and laboratory symptoms.

In cases of acquired toxoplasmosis in individuals with normal immune systems, the prognosis is positive, but in individuals with compromised immune systems (such as AIDS patients), the prognosis is serious, often resulting in death.

Primary preventive measures for acquired and congenital toxoplasmosis involve compliance with cleanliness and health rules, especially for pregnant women lacking class G antibodies against the parasites:

  1. Reduce contact with cats.
  2. Avoid consumption of raw meat, minced meat, and seafood.
  3. Wash vegetables and fruits thoroughly.
  4. Washing hands before eating is essential.
  5. Gardening should only be done while wearing gloves. For pregnant women, it’s necessary to undergo screening for Toxoplasma antibodies to determine if the infection is acute or potential, providing an opportunity for pharmacological prevention of acute toxoplasmosis during pregnancy, reducing the risk of congenital infection by 60%. If there are no IgG antibodies in the first three months of pregnancy, monitoring for IgM and IgG antibodies should occur not only in the last three months but also in the second trimester. No preventive measures are taken against toxoplasmosis in disease outbreak centers, and vaccines have not been developed for it so far.
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