parasite

ToxoplasmosisObjective :

Describe the Life cycle Mention the Infective stages Define Congenital Toxoplasmosis List the Lab.Diagnosis Illustrate the Immunity to Toxoplasmosis Show the relationship between Toxoplasmosis & Pregnancy

Human Toxoplasmosis

Toxoplasmosis is a zoonotic disease Caused by Coccidian protozoan Toxoplasma gondii Infectes a wide range of animals, birds but does not appear to cause disease in them

Toxoplasmosis

A disease of the blood and lymphatic system. Cats are a critical part of the life cycle. It is usually acquired by eating undercooked meats but can also be acquired by contact with cat feces. Primary problem is a congenital infection of fetus, resulting in either a stillbirth or a child with severe brain damage or vision problems.

Toxoplasmosis

The normal final host is cat and relatives in the family Felidae, only hosts in which the Oocyst is produced & the sexual stage of Toxoplasma can be developed

Introduction

The intestinal phase occurs in cats only (wild as well as domesticated cats) and produces "oocysts." The extraintestinal phase occurs in all infected animals (including cats) and produces "tachyzoites" and, eventually, "bradyzoites" or "zoitocysts.“The disease toxoplasmosis can be transmitted by ingestion of oocysts (in cat feces) or bradyzoites (in raw or undercooked meat). Tachyzoites are less resistant to stomach secretions so less important sources of infection than the other stages

Cats

Cats are the only animal species to shed the infectious stage in their feces. All animals however,can disseminate Toxoplasmosis if their infected meat is eaten. cats get it by eating rodents, raw meat, cockroaches, flies, or by contacting infected cats, infected cat feces, or contaminated soil.

Spread from Rats – Cats to Humans

Events on Development in man
When man ingests Oocysts with eight Sporozoites excreted in Cats feces, can establish an infection in humans. Oocysts open in duodenum and releases eight Sporozoites which pass through the gut wall Circulate in body and invade various cells

Toxoplasmosis can also be transmitted transplacentally resulting in a spontaneous abortion, a still born, or a child that is severely handicapped mentally and/or physically.

Morphology

Invade Organs
In futher development they penetrate new cells especially Eye and Brain. Further development slows down in these organs called ad Bradyzoites to form a quiescent tissue cysts The event lead to chronic stage of disease Brain involvement carries higher Morbidity and Mortality if the immunity is low


A zoitocyst of Toxoplasma gondii filled with bradyzoites; this zoitocyst (true cyst) is in the muscle ,eye or brain

Fate of Tissue Cysts

The tissue cysts are infective when ingested by cats or eaten by other animals. In man it is a dead end of disease or change to acute stage (tachyzoites) when the Immunity is Low

Sources of infection

Source of all oocytes ...Domestic (cats) and wild (zoo) cats ( Cats are the only known full-life-cycle host of the protozoan) parasite Complete hostPersist in environment (soil) if moist > one yearreservoir of infective oocytesMany intermediate hostsreservoir of infective tissue cysts( farm animals—cattle,sheep,rabbit)Cycle in humans (an accidental host)Infected by ingesting infective oocytes (in >4 day old cat feces)by ingesting tachyzoites or bradyzoites in raw meatby receiving blood or tissues with “-zoites”CONGENITALLY by transplacental tachyzoitesProliferative stages in humanstachyzoites result from all infective stagesbradyzoites predominate within cysts

In immunocompetent adults, toxoplasmosis, may produce flu-like symptoms, sometimes associated with lymphadenopathy. In immunocompromised individuals, infection results in generalized parasitemia involvement of brain, liver lung and other organs, and often death.


Toxoplasmosis produces severe Human infections in patient with AIDS The chronic infection is altered to Acute manifestations


Toxoplasmosis – Immunosupressed patients Varying degrees of disease may occur in Immunosupressed indivudals results in Retinitis Chorioretinits Pneumonias severe neurological disorders Other non specific manifestions

Immunology

Both humoral and cell mediated immune responses are stimulated in normal individuals. Cell Mediated Immunity is protective and humoral response is of diagnostic value.

Immunity

Acquired immunity in women is particularly protective to the fetus. In Immunosupressed and AIDS patients changes the host resistance and causes the chronic infection becomes fulminating acute Toxoplasmosis


Premunition: a host may recover clinically & be resistant to specific challenge but some parasites may remain and reproduce slowly

Immunity to T. gondii

Active infection normally occurs only once in a lifetime. Although the parasite remains in the body indefinitely latent infections usually persist for life (the immune system reacts against the parasite, causing the parasite to hide in an inactive form (cyst) in tissues throughout the body (usually the skeletal muscles and the brain). . , True cyst generally is harmless and inactive unless the immune system is not functioning properly in immuno-compromised host -- the parasite can reactivate and cause serious illness, characterized by inflammation of the brain If a woman develops immunity to the infection at least six to nine months before pregnancy, there is a very rarely any danger of passing it on to her baby because immunity is developed to it

Toxoplasmosis in Pregnancy

In 1 st Trimester may lead to still birth major central nervous system anomalies In 2nd Trimester Less severe complications Transmission to the fetus is more frequent if the maternal infection occurs in the 3rd trimester

Congenital Toxoplasmosis

Congenital infection develop in fetus only when non immune mothers are infected during pregnancy Post natal Toxoplasmosis is less severe.


Congenital infections occur in about 1-5 per 1000 pregnancies of which 5-10% result in miscarriage, 8-10% result in serious brain and eye damage to the fetus, 10-13% of the babies will have visual handicaps. Although 58-70% of infected women will give a normal birth, a small proportion of babies will develop active retino-chorditis or mental retardation in childhood or young adulthood( Post natal Toxoplasmosis is less severe)

Congenital Infection

Prenatal toxoplasmosis Lead to Still Birth Or Sabin`s tetrad: Chorioretinits Intracellular calcification Psychomotor disturbances Hydrocephaly or Microcephaly Prenatal toxoplasmosis may manifest with blindness apart from congenital defects

5. congenital toxoplasmosis: transmission from mother to fetus when mother has developed acute toxoplasmosis during pregnancy - increased transmission rate in third trimester, but increased severity of fetal disease in first trimester. Presents as hydrocephalus, hepatomegaly, cerebral calcifications, mental retardation with death at one end of spectrum and mental retardation or just later choreoretinitis at the other end of spectrum.

Diagnosis of Toxoplasmosis

Desired specimens, Blood ( serum) Sputum CSF Lymphnodes Tonsil tissues Striated muscle biopsy


Diagnosis
Suspected toxoplasmosis can be confirmed by finding the organism from tonsil or lymph gland biopsy.
Pseudocyst seen in the acute stage

Microscopic Examination of Tissues

Smears and sections stained with Giemsa’s stainPeriodic acid Schiff method preferred. The densely packed cysts seen in the brain or other parts of nervous system suggest chronic infection

Immunological tests:

Tests which employ whole parasites include the dye test (Sabin-Feldman Dye Test (DT) , direct agglutination and the fluorescent antibody test, whilst tests that use disrupted parasites as an antigen source include ELISA, latex agglutination, indirect haemagglutination and complement fixation.

Serology

Sabin Feldman dye test based on principle that Antibodies to Toxoplasma appear in 2-3 weeks that will render the membrane of the laboratory cultured living T.gondii impermeable to Alkaline methylene blue ,So the organism are unstained in the presence of serum with antibodies

Newer Methods in Diagnosis

-Immuno florescent assay method.-ELISA for IgM and IgG detection-PCRFrankel’s intracutaneous test (Toxoplasmin skin test )useful for epidemiologcal purpose

fluorescent antibody test,

ELISA Test


Acute infection


Detectable levels of IgM antibody appear immediately before or soon after the onset of symptoms. IgM levels normally decline within 4 to 6 months. IgG levels begin to rise 1 or 2 weeks after infection. Peak levels are reached in 6 to 8 weeks, then gradually decline over a period of months or even years. Low levels of IgG are generally detectable for life. immunocompromised individuals may not produce any IgM. Antibody levels do not correlate with severity of illness

Serologic Diagnosis of Toxo

unreliable in immunodeficient (AIDS) ptsnormally IgM and IgG rise simultaneouslyIgG - persists for years IgM - undetectable after “cure”Elevated IgM titer is diagnostic of recent infection in persons with normal immunityA negative IgG or IgM test excludes Diagnosis a + IgM test confirms acute toxoplasmosis or current Toxoplasma infection (measure IgM antibodies, have low specificity )

in the United States, most pregnant women are not screened routinely for toxoplasmosis Only those with a high risk.

Polymerase Chain Reaction (PCR)

PCR amplification is used to detect T. gondii DNA in body fluids and tissues. It has been successfully used to diagnose congenital, ocular, cerebral and disseminated toxoplasmosis. PCR performed on amniotic fluid has revolutionized the diagnosis of fetal T. gondii infection by enabling an early diagnosis to be made, PCR has allowed detection of T. gondii DNA in brain tissue, cerebrospinal fluid (CSF), vitreous and aqueous fluid, bronchoalveolar lavage (BAL) fluid, urine, amniotic fluid and peripheral blood.

incidence

Seroconversion rate -----7.5% in Egypt 30% in canada ----- 50 % in USA ----->60% in France
Very common throughout the world; up to 50+% in other developed or developing countries.

Care of the Meat

Avoid eating raw or undercooked meat. Freezing < -200c Heating at 500c for 4-6 minutes destroys the cysts and sterilizes the meat.

Widespread phobia

Toxoplasmosis is a part of TORCH syndrome It is not a cause of habitual abortion Only pregnant with primary active infection with toxoplasmosis during pregnancy leads to congenital tox and after primary infection there is persistence of cysts of tox BUT development of active immunity protect subsequent pregnancy Very rarely reactivation of previously latent T. gondii infection induced by severe decrease of immunity(People on chemotherapy , People with congenital immune deficiencies , People with AIDS/HIV , long administration of corticosteroid drugs in the case of transplant patients)

Toxoplasmosis TTT

Drugs of choice for pregnant women or immunocompromised persons: Spiramycin or Pyrimethamine plus Sulfadiazine Prophylaxis –in the primary prevention of toxoplasmosis in persons with HIV who have dormant or latent infection - trimethoprim-sulfamethoxazolepyrimethamine plus folinic acid

Treatment of Infected Newborns

Infected babies should be treated as soon as possible after birth with pyrimethamine and sulfadiazine which, as mentioned earlier, can help prevent or reduce the disabilities associated with toxoplasmosis.

Figure-5- Girl with hydrocephalus due to congenital toxoplasmosis.

Under research
developing vaccines against Toxoplasma gondii .

Thank You