Toxoplasma gondii

1. T x plasma g ndii

2. Outlines
• Taxonomy
• Prevalence
• Clinical importance
• Morphology
• Life cycle
• Prevention of infection
• Diagnosis
• Treatment

3. Taxonomy
Ctenodactylus gondi
Phylum: Apicomplixa
Class: Sporozoa
Definitive host: cats
Intermediate host: almost any
mammal
Prevalence: one third of the
world population

6. • Acute disease in adults:
• the majority are asymptomatic
or unrecognized.
Clinical Importance

7. • Immunocompromised Patients:
• Most frequently results from reactivation of latent
infection
• it can cause serious pathology including:
hepatitis, pneumonia, blindness, myocarditis
• 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.
Clinical Importance

8. • Congenital Toxoplasmosis:
• Total maternal-fetal transmission is about 30% throughout all of
gestation, but varies from 6% at 13 weeks to 72% at 36 weeks
• If the fetus is exposed during the first trimester, death nearly
always occurs as a result of CNS damage.
• Infection during the second trimester may result in hydrocephaly,
blindness, or other nervous system damage.
• Later infection may result in blindness or mild CNS defects.
• However, women who are exposed to this parasite before
pregnancy do not transmit the infection to the fetus.
Clinical Importance

10. - Ocular disease (toxoplasmic retinochoroiditis)
• the most common sequelae of congenital
toxoplasmosis
• up to 2% of adults newly infected with T. gondii
develop ocular lesions
Clinical Importance

11. Morphology
Tachyzoites,
trophozoites,
or endozoites
or
Cystozoite

12. Morphology
Tachyzoites
or
Cystozoite
oocyst
Sporulated
oocyst
Bradyzoites
within
tissue cyst
Tachyzoites

13. Tachyzoites vs bradyzoites
Tachyzoites
 rapidly dividing stage
 seen in body fluids in early,
acute infection
 directly destroy cells,
particularly parenchymal
and reticuloendothelial cells
Bradyzoites
 slowly dividing stage
 contained in cysts in muscle
and brain tissue and in the eye
 Released from ruptured tissue
cysts cause local inflammation
with blockage of blood vessels
and necrosis

15. Life cycle
sexual asexual
• Intestinal
(enteroepithelial)
phases
• occurs in cats only (wild
as well as domesticated
cats)
• produces "oocysts."
• Extraintestinal phases
• occurs in all infected
animals (including cats)
• produces "tachyzoites"
and,eventually,"bradyzi
tes“ or "zoitocysts."

17. Prevention measuresAction situation
Wash hands carefully after stroking a cat
Wear gloves when changing cat litter
Change litter frequently and wash the tray with hot water (> 60° C)
Avoid litter in the kitchen
Cat contact
Cook the meat well-done or stew
Avoid microwave cooking for meat
Avoid raw vegetables at restaurants
Avoid raw shellfish
Avoid raw goat milk
Meals
Wash vegetables, fruits and herbs thoroughly, especially if they grow
close to the ground
Wash hands, knives, any containers and table thoroughly after meat
manipulation or cutting
Preparation of
meals
Prefer mineral water to tap waterWater
Wash hands thoroughly and brush nails after any outdoor activities in
contact with soil
Wear gloves for gardening
Avoid ingestion of water during recreation activities in lakes or rivers
Gardening or
outdoor activities
Prevention of Toxoplasma infection

18. control
• It is difficult to control toxoplasmosis because of wide range
of animal reservoirs.
• Currently, there is no effective vaccine available for humans.
• A genetically engineered vaccine is under development for
use in cats.

20. Microscopy
• Tachyzoites and tissue cysts can be detected
• Specimens: blood, sputum, bone marrow aspirate,
cerebrospinal fluid (CSF), aminiotic fluid, and biopsy
material from lymphnode, spleen, and brain.
 Smear made from above specimens is stained by: Giemsa,
PAS, or Gomori methanamine silver (GMS) stain
 Tachyzoites or cyst can also be demonstrated effectively by
fluroscent conjugated antibody technique in tissue biopsy
or impression smear.
 Presence of only tissue cysts does not differentiate
between active and chronic infection.
 The presence of cysts in placenta or tissues of newborn
establishes congenital toxoplasma infection.

21. Serodiagnosis
Antibody detection
Diagnosis of acute infection with T. gondii can be made by detection of the
simultaneous presence of IgM and IgG antibodies.
 Tests for detecting IgG antibody include:
o Enzyme-linked immunosorbent assay (ELISA)
o Indirect fluorescent antibody test (IFAT)
o Latex agglutination test
o Sabin-Feldman dye test.
 Positive IgG can be detected as early as 2–3 weeks after infection.
Peak level of antibody is observed in blood 4–8 weeks after infection.
 Positive IgM antibody titer indicates an early primary infection. The serum IgM
titer can be measured by:
o sandwich IgM ELISA
o IgM immunosorbent assay (IgM-ISAGA).
Both assays are equally specific and sensitive.
Negative IgM titer and positive IgG titer indicate distant infection.
 Sandwich IgA-ELISA test is used for detecting congenital infection in newborns.

22. Serodiagnosis
Antigen detection
Detection of antigen by ELISA indicates recent
Toxoplasma infection.
In AIDS and other immunocompromised
patients, antigen detection is very useful.
Detection of antigen in amniotic fluid is helpful
to diagnose congenital toxoplasmosis.

23. Molecular Methods
• DNA hybridization techniques and polymerase
chain reaction (PCR) are increasingly used to
detect Toxoplasma from different tissues and body
fluids.
 B1 gene of T. gondii can be detected by PCR of the
amniotic fluid in case of congenital toxoplasmosis

24. Imaging
• Magnetic resonance imaging (MRI) and
computed tomography (CT) scan are used to
diagnose toxoplasmosis with central nervous
system involvement.
Ultrasonography (USG) of the fetus in utero at
20–24 weeks of pregnancy is useful for
diagnosis of congenital toxoplasmosis.

25. Animal Inoculation
• Toxoplasma can be isolated by
inoculating body fluids, blood, or
tissue specimens by intraperitoneal
inoculation in mice or in tissue culture.
• Mice should be examined for
Toxoplasma in their peritoneal
exudate after 7–10 days of inoculation.

26. Skin test of Frenkel
• Diluted toxoplasmin is injected intradermally and
delayed positive reaction appears after 48 hours.
• This test is not very reliable for diagnosis

27. Treatment
 Congenital Toxoplasmosis:
• Oral pyrimethamine (1 mg/kg) daily and sulfadiazine (100 mg/ kg) with folinic
acid for 1 year. Systemic corticostoriod may be added to reduce chorioretinitis.
 Immunocompetent Patients
who have only lymphadenopathy, do not require specific therapy unless they have
persistent, severe symptoms.
• Patients with ocular toxoplasmosis are treated for 1 month with pyrimethamine
plus either sulfadiazine or clindamycin
 Immunocompromised Patients
AIDS patients who are seropositive for T. gondii and have a CD4+ Tlymphocyte
count below <100/μL, should receive primary prophylaxis against toxoplasma
encephalitis.
 Trimethoprimsulfamethoxazole is the drug of choice. If
trimethoprimsulfamethoxazole cannot be tolerated by patients,
dapsonepyrimethamine is the recommended alternative drug of choice.
 Prophylaxis against toxoplasma encephalitis should be discontionued in patients
who have responded to antiretroviral therapy (ART) and whose CD4+ T
lymphocyte count has been above 200/μL for 3 months.

28. References
 MEDICAL AND CLINICAL LABORATORY PROFESSIONALS- John
W. Ridley, Ph.D.
 DIAGNOSING MEDICAL PARASITES- A Public Health Officers
Guide to Assisting Laboratory and Medical Officers
 MICROBIOLOGY DEMYSTIFIED- TOM BETSY, D.C.JIM KEOGH
 Lippincott’s Illustrated Reviews: Microbiology Third Edition
 Chapter 14 Toxoplasmosis: A Widespread Zoonosis Diversely
Affecting Humans and Animals-Florence Robert-Gangneux,
Dominique Aubert and Isabelle Villena
 Paniker’s Textbook of Medical Parasitology-SEVEnth EDition

29. THANK YOU