Toxoplasma gondii is an obligate intracellular parasite that causes the infectious disease toxoplasmosis. It is capable of infecting all warm-blooded animals. In humans, it commonly causes mild flu-like symptoms but can cause serious issues in those with weak immune systems or congenitally acquired infections. It has a complex lifecycle involving sexual reproduction in cats and asexual reproduction in other hosts. Acute infection may be asymptomatic while latent infection involves tissue cyst formation that can reactivate if immunity wanes.

1. TOXOPLASMA
GONDII

2. DEFINITION
Is an obligate intracellular parasitic one-celled eukaryote that causes the infectious
disease toxoplasmosis. Found worldwide, Toxoplasma gondii is capable of infecting
virtually all warm-blooded animals, but felids such as domestic cats are the only known
definitive hosts in which the parasite may undergo sexual reproduction. In humans,
Toxoplasma gondii is one of the most common parasites in developed countries.

3. DEFINITION
• Toxoplasma gondii is an obligate intracellular parasite that lives within its host cells
within a membrane-bound vacuole. The parasitophorous vacuole membrane is host-
derived, yet extensively modified by the parasite to facilitate nutrient acquisition and
avoid host defenses. Formation of the vacuole also is accompanied by extensive host
cell cytoskeletal rearrangement and organellar recruitment to the vacuole.

4. STRUCTURE

5. STRUCTURE
• The apicoplast and mitochondria are endosymbiotic organelles that are thought to
perform essential metabolic functions for the viability of Toxoplasma gondii.
• The functions of the apicoplast, the plastid remnant, have been investigated most
intensively as potential unique targets for anti-parasitic chemotherapy.
• As membrane bound organelles with prokaryotic genomes, the biogenesis and
replication of the apicoplast and mitochondrion poses interesting cell biology
questions.

6. LIFECYCLE
• T gondii has 2 distinct life cycles.
• The sexual cycle occurs only in cats, the definitive host.
• The asexual cycle occurs in other mammals (including humans) and various strains of
birds.
• It consists of 2 forms: tachyzoites (the rapidly dividing form observed in the acute
phase of infection) and bradyzoites (the slowly growing form observed in tissue cysts).

8. LIFECYCLE
• A cat becomes infected by eating contaminated raw meat, wild birds, or mice. The organism’s sexual
cycle then begins in the cat’s gastrointestinal tract. Macrogametocytes and microgametocytes
develop from ingested bradyzoites and fuse to form zygotes. The zygotes then become encapsulated
within a rigid wall and are shed as oocysts. The zygote sporulates and divides to form sporozoites
within the oocyst. Sporozoites become infectious 24 hours or more after the cat sheds the oocyst via
feces.
• During a primary infection, the cat can excrete millions of oocysts daily for 1-3 weeks. The oocysts are
very strong and may remain infectious for more than one year in warm humid environments.
• T gondii oocysts, tachyzoites, and bradyzoites can cause infection in humans. Infection can occur by
ingestion of oocysts following the handling of contaminated soil or cat litter or through the
consumption of contaminated water or food sources (eg, unwashed garden vegetables). Transmission
of tachyzoites to the fetus can occur via the placenta following primary maternal infection.

9. LIFECYCLE• Rarely, infection by tachyzoites occurs from ingestion of unpasteurized milk or by
direct entry into the bloodstream through a blood transfusion or laboratory accident.
• Transmission can also occur via ingestion of tissue cysts (bradyzoites) in undercooked
or uncooked meat or through transplantation of an organ that contains tissue cysts.
(Slaughterhouse workers and butchers may be at increased risk of infection.)
• In Europe and the United States, pork is the major source of T gondii infection in
humans.

10. CELLULAR STAGES
• During different periods of its life cycle, individual parasites convert into various
cellular stages, with each stage characterized by a distinct cellular morphology,
biochemistry, and behavior.
• These stages include the tachyzoites, merozoites, bradyzoites (found in tissue cysts),
and sporozoites (found in oocysts).
An unstained T. gondii tissue cyst, bradyzoites can be seen within Two tachyzoites, transmission electron microscopy

11. THREAT
• Toxoplasma gondii causes a variety of clinical diseases in humans. The parasite is
typically asymptomatic in immune competent individuals but can cause serious, even
fatal, disease in congenitally infected children. Due to T. gondii's ability to persist as
bradyzoites for the life of the host, toxoplasmosis frequently presents as an
opportunistic infection of the immune compromised, including AIDS patients. This
comprehensive chapter discusses the diagnosis, treatment and clinical manifestations
of human toxoplasmosis.

12. TOXOPLASMOSIS
• toxoplasmosis is a parasitic disease caused by Toxoplasma gondii.
• Infections with toxoplasmosis usually cause no obvious symptoms in adults.
Occasionally, people may have a few weeks or months of mild, flu-like illness such as
muscle aches and tender lymph nodes.
• In a small number of people, eye problems may develop. In those with a weak
immune system, severe symptoms such as seizures and poor coordination may occur.
• If infected during pregnancy, a condition known as congenital toxoplasmosis may
affect the child.

13. 3 STAGES OF TOXO INFECTION
1) Acute toxoplasmosis
2) Latent toxoplasmosis
3) Cutaneous toxoplasmosis

14. ACUTE TOXOPLASMOSIS
• Acute toxoplasmosis is often asymptomatic in healthy adults.
• However, symptoms may manifest and are often influenza-like
• People with weakened immune systems are likely to experience headache, confusion,
poor coordination, seizures, lung problems that may resemble tuberculosis
• people, such as those with HIV/AIDS, those taking certain types of chemotherapy, or
those who have recently received an organ transplant, may develop severe
toxoplasmosis. This can cause damage to the brain (encephalitis) or the eyes
(necrotizing retinochoroiditis).

15. LATENT TOXOPLASMOSIS
• In most immunocompetent people, the infection enters a latent phase, during which
only bradyzoites (in tissue cysts) are present
• these tissue cysts and even lesions can occur in the retinas, alveolar lining of the lungs,
heart, skeletal muscle, and the central nervous system, including the brain.
• Cysts form in the CNS (brain tissue) upon infection with T. gondii and persist for the
lifetime of the host.
• Most infants who are infected while in the womb have no symptoms at birth, but may
develop symptoms later in life!

16. CUTANEUS TOXOPLASMOSIS
• Rarely skin lesions may occur in the acquired form of the disease, including roseola
and erythema multiforme-like eruptions, prurigo-like nodules, urticaria, and
maculopapular lesions.
• Newborns may have punctate macules, ecchymoses, or "blueberry muffin" lesions.
• Diagnosis of cutaneous toxoplasmosis is based on the tachyzoite form of T. gondii
being found in the epidermis.
• It is found in all levels of the epidermis, is about 6 by 2 μm and bow-shaped, with the
nucleus being one-third of its size.
• It can be identified by electron microscopy or by Giemsa staining tissue where the
cytoplasm shows blue, the nucleus red.

17. CUTANEUS TOXOPLASMOSIS
MANIFESTATION

18. DIAGNOSIS
• Diagnosis of toxoplasmosis in humans is made by biological, serological, histological, or molecular
methods, or by some combination of the above.
• Toxoplasmosis can be difficult to distinguish from primary central nervous system lymphoma. It
mimics several other infectious diseases so clinical signs are non-specific and are not sufficiently
characteristic for a definite diagnosis.
• As a result, the diagnosis is made by a trial of therapy (pyrimethamine, sulfadiazine, and folinic acid
(USAN: leucovorin)), if the drugs produce no effect clinically and no improvement on repeat imaging.
• T. gondii may also be detected in blood, amniotic fluid, or cerebrospinal fluid by using polymerase
chain reaction.
• T. gondii may exist in a host as an inactive cyst that would likely evade detection.

19. TREATMENT
• Treatment is often only recommended for people with serious health problems, such
as people with HIV, because the disease is most serious when one's immune system is
weak.
• Trimethoprim/sulfamethoxazole is the drug of choice to prevent toxoplasmosis, but
not for treating active disease. A study shows a promising new way to treat the active
and latent form of this disease using two endochin-like quinolones.

20. CONGENITAL TOXOPLASMOSIS
• Approximately 10-20% of pregnant women infected with T gondii become symptomatic. The most
common signs of infection are lymphadenopathy and fever. If the mother was infected prior to
pregnancy, there is virtually no risk of fetal infection, as long as she remains immunocompetent.
• When a mother is infected with T gondii during gestation, the parasite may be disseminated
hematogenously to the placenta. When this occurs, infection may be transmitted to the fetus
transplacentally or during vaginal delivery.
• If the mother acquires the infection in the first trimester and it goes untreated, the risk of infection to
the fetus is approximately 14-17%, and toxoplasmosis in the infant is usually severe. If the mother is
infected in the third trimester and it goes untreated, the risk of fetal infection is approximately 59-65%,
and involvement is mild or not apparent at birth. These different rates of transmission are most likely
related to placental blood flow, the virulence and amount of T gondii acquired, and the immunologic
ability of the mother to restrict parasitemia.

21. MANIFESTATION OF TOXOPLASMOSIS
IN THE FETUS
• The most significant manifestation of toxoplasmosis in the fetus is encephalomyelitis,
which may have severe results.
• Approximately 10% of prenatal T gondii infections result in abortion or neonatal
death.
• In approximately 67-80% of prenatally infected infants, the infection is subclinical and
can be diagnosed using only serological and other laboratory methods.
• Although these infants appear healthy at birth, they may develop clinical symptoms
and deficiencies later in life.

22. PREGNANCY PRECAUTIONS
• Cat owners and women who are exposed to cats should follow these tips to reduce exposure to Toxoplasma.
• Avoid changing cat litter if possible. If no one else can perform the task, wear disposable gloves and wash
your hands with soap and water afterwards.
• Ensure that the cat litter box is changed daily. The Toxoplasma parasite does not become infectious until 1 to
5 days after it is shed in a cat’s feces.
• Feed your cat commercial dry or canned food, not raw or undercooked meats.
• Keep cats indoors.
• Avoid stray cats, especially kittens. Do not get a new cat while you are pregnant.
• Keep outdoor sandboxes covered.
• Wear gloves when gardening and during contact with soil or sand because it might be contaminated with cat
feces that contain Toxoplasma. Wash hands with soap and water after gardening or contact with soil or sand.

23. THANK YOU!