• Toxoplasmosis cosmopolitan protozoan, parasite intracellulaire SRH : Toxoplasma gondii.
  • Congenital form responsible for very severe malformations compromises the vital prognosis in the & rsquo; immunocompromised. The acquired form benign 95%
  • L & rsquo; infestation in the & rsquo; adult is oral.
  • Toxoplasma cysts are located in meat, and oocysts in raw vegetables (and the fur of cats),
  • It depends on dietary factors, culinary and sociocultural.
  • Serology is the primary means of diagnosis of the disease
  • C & rsquo; is that its results depend on any action to be taken.
  • It also determines the date and time of the & rsquo; infestation and any seroconversion.


  • subphylum Apicomplexa (previous complex)
  • Class of Sporozoea
  • Subclass Coccidia
  • Order Eucoccidiidea
  • Under order of Eimeridea
  • Family Sarcocystidés
  • Genre Toxoplasma
  • Espèce Toxoplasma gondii



a) The vegetative form :

optical microscopy :

  • Tachyzdite has an arcuate shape (arc = Toxon in Greek) 5à8pX2à3de large.
  • The front end is tapered / to the rear wider part and rounded, responsible for sepsis and acute fetal contamination.
  • The parasite has a clear cytoplasm surrounded d & rsquo; a thin membrane and a large single core.
  • A big karyosome occupies the entire nuclear area.
  • The tachyzoite is endowed with lateral limits of the apical portion movements that allow it to penetrate the host cells reticulohistiocytic system.
Ultrastructure of a Toxoplasma gondii tachyzoite

Electron microscopy :

■ The divided cell membrane in three layers. Innermost surrounds anteriorly : & Lsquo; the fan '.

the fan, cone-shaped is constituted of fibrils spirally wound one upon the other.

Rhoptries are maces 1 at 4 microns meeting at the apex of the parasite.

  • Autres organs : endoplasmic reticulum a, Golgi apparatus and a branched mitochondria.
  • The apicoplast is a plastid derived d & rsquo; an ancestral chloroplast. Role poorly known.

b) Cyst :

  • This is a form of latency and parasite resistance, in nervous tissue and muscle throughout the life of the & rsquo; intermediate host.
  • spherical formations 10 to several tens of microns in diameter. thick wall surrounding a large number of bradyzo & rsquo; ites to slow metabolism and division.


c) Oocyste :

  • form of resistance in the A Ext. from 10 at 12 pm.
  • Non-spore forming it contains a mass of granular cells.
  • Mature oocyst has a double-layer enveloping wall 2 sporocysts, each containing 4 sporozoïtes.


As with all sporozoites is divided into two parts : gamogonique and schizogonic.

Indeed if the first is sexual and takes place entirely in the & rsquo; second is the definitive host and asexual begins in cats and ends at the & rsquo; intermediate host.

a) La obase schizognique :

C & rsquo; is during this phase that the production of Toxoplasma is the most important It takes place almost entirely in intermediate hosts homeothermic.

This step is the cause of acquired and congenital complications of the disease.

At the & rsquo; intermediate host :

After ingestion of infective sporozoites form or bradyzo & rsquo; ites become tachyzoites, cross the intestinal lamina propria to be spread through blood or lymph throughout the reticulohistiocytic system.

In cells, they actively multiply and cause septicemia. The penetration into the cells- hosts actively through the movement of the parasite requiring the & rsquo; énergie.Une times with & rsquo; interior Toxoplasma multiplies by endodyogénèse.

C & rsquo; is during this step that the contamination of the fetus occurs. The immune system responds by producing & rsquo; specific AC

The parasite s & rsquo; encysted in tissues poor immunoglobulin namely the nervous system and muscle. Bradyzoites multiplication is slowed.

Cysts formed remain quiescent in the body of the & rsquo; intermediate host for the duration of its existence.

This immune stimulant almost constant in the tissues is the & rsquo; origin & rsquo; d & rsquo rate, residual blood and protective antibody

At the & rsquo; final host :

The schizogonic asexual phase continues in cats.

Ingestion of cysts contained in tissues.

Digestion releases bradyzoites that transform into tachyzoites in the digestive tract of the cat. They then penetrate the intestinal cells where they will multiply. These cells eventually burst and reject tens of Toxoplasma parasites that d & rsquo; other enterocytes.

After several intestinal schizogonies, we observe the emergence of parasitic sexual forms : gametocytes

b) Phase Gamoaoniaue :

  • Macro female gametes 5 at 7p. and microgametes male 3p having sickle 3 flagella.
  • Training the oocyst non-spore forming in the environment with feces feline
  • The maturation of the oocysts requires oxygen and moisture.
  • Oocystes : forms of dissemination in the environment
  • A very important telluric reservoir, to & rsquo; origin of the contamination herbivores.


The man may be contaminated with all parasitic forms.

Apart from any congenital immunodeficiency contamination remains the most serious

mainly depends on the eating habits and culinary populations

A- oral infections :

They are made by the & rsquo; intermediate cysts and oocysts.

For cysts :

  • Infection occurs by ingestion or handling of meat infested with cysts.
  • D & rsquo; an epidemiological perspective : cysts remain alive at + 4 ° C for several months
  • Freezing at -20 ° C kills the bradyzoites after thirty minutes.
  • Cooking at + 70 ° or microwave sterilizes food infective forms.

by The oocystes :

  • Contamination & rsquo; man crudités herbivorous, fruit or d & rsquo; contaminated water. Contact with cats or their litter. L & rsquo; oocyst is the form of resistance in the environment infesting several months. Sensitive to drying and heat (50° for half an hour).
  • they restentvivants an hour in the & rsquo; absolute alcohol, l & rsquo; sulfuric acid 0.5N, soda 6% and a day in formalin 10%, which shows their resistance to harsh outdoor conditions.

B- congenital infestation :

It is done by the & rsquo; intermediate trophozoites, placental lesions, fetal malformations are d & rsquo; all the more serious that & rsquo; infestation occurs at an early stage of pregnancy.

C- Infestation Laboratory :

dermal and / or through the mucous.

L & rsquo; importance of clinical signs depends on the virulence of the strain and the amount of & rsquo; inoculum.

D- Re endogenous infestations :

E- Transplantation or transplantation :

The number of human tissue transplants has increased significantly.

The graft & rsquo; infested organs Toxoplasma inoculated one hand and immunosuppressants d & rsquo; other.



  • During toxoplasmosis acquired the response is primarily humoral.
  • Types & rsquo; immunoglobulin IgA, IgM, IgE, IgG
  • The kinetics of AC shows that after a latency 5 at 8 days an increase in serum IgA and IgM to the 10th day,
  • IgA concentration increases the maximum rate at the end of & rsquo; one month 45 days
  • IgM appear almost simultaneously with IgA their rate increasing faster
  • May persist in some cases years
  • IgA and IgM does not cross the placental barrier Fetal (molecular weight).
  • IgG are emerging around the second week, after & rsquo; infestation and exceed rates 2560 U.l. from the 8th week.
  • These concentrations can remain shelf for several weeks
  • Degressive n & rsquo phase is initiated that & rsquo; the 5ise month and lasts B 4 month.

The kinetics of these antibodies is required, even indispensable to specify the stage of the disease and especially to determine the exact date of the contamination that will dictate how to behave in pregnancy.


There are two major entities : acquired toxoplasmosis and congenital toxoplasmosis, differing total lies the & rsquo; one another, both diagnostically, prognostic, that prophylactically.


It is benign in most cases and can be even asymptomatic.

In general the evolution depends on & rsquo; s immune status of the individual strain Toxoplasma infective. Next clinical forms are distinguished : toxoplasmosis acquired benign and severe acquired toxoplasmosis.

1- Toxoplasmosis acquired benign :

In some cases mononucleosis is observed mainly with cervical lymphadenopathy, a fever, asthenia and cutaneous signs fickle.

Only persist firm lymphadenopathy, indolores, mobiles, extendable to other lymph channels.

2- Toxoplasmosis acquired serious :

It comes in several clinical forms, Life threatening the patient involved. The most common are :

Form meningoencephalitic .

The pseudo tumoral form ; generalized infectious forms,

Toxoplasmosis acquired eye.


  • Fetal contamination n & rsquo; that occurs during the primary phase of the disease, during sepsis.
  • The transmission of the protozoan through placental n & rsquo; is not mandatory.
  • The birth & rsquo; an apparently healthy child does not mean that & rsquo; it n & rsquo; there was no contamination.
  • Some late complications do arise that & rsquo; after several years.
  • The seriousness of these birth defects depends on & rsquo; infestation compared to the & rsquo; age pregnancy.

■ In fact the & rsquo; fetal damage is more severe than maternal contamination was early.


The diagnosis of toxoplasmosis is almost always indirect.

It must be early because of birth complications and the frequency of latent forms.

In pregnant women, it is placed in the majority of cases in a systematic review.


Acquired forms :

  • The blood count shows leukocytosis
  • Before any acquired or congenital toxoplasmosis a background & rsquo; s eye should be practiced systematically in search of retinal atrophy beaches, of chorioretinitis and other eye injuries.
  • The lymph node biopsy shows a mixed lymphoid hyperplasia predominantly histiocytic cells and basophils hyper.
  • Physical examinations contribute largely in the diagnosis of disease, especially in immunocompromised.
  • We mention primarily the examinations in cerebral localization namely: l & rsquo; electroencephalogram, CT or cerebral magnetic resonance.

Congenital forms :

  • Congenital toxoplasmosis can be diagnosed before birth, at d & rsquo; seroconversion or at d & rsquo; a routine physical examination
  • Physical examinations :

L & rsquo; ultrasound : highlights any malformation mainly central nervous system.

It objectively the presence of & rsquo; hepatosplenomegaly +/- d & rsquo; ascites ; these signs indicate a severe visceral involvement.


Staining Direct :

The highlighting of the parasite remains exceptional in different samples. Lymph node biopsies, bone marrow aspirates and bodily fluids sampling, l & rsquo; ana-path examination of tissues and parts & rsquo; excision.

The colors are mainly conducted : Hemalun-eosin and M.G.G

Molecular biology : la P.C.R.

The detection of parasites is tricky, However, the discovery of the molecular structures of the protozoan has become possible nowadays thanks to the P.C.R.(polymerase chain reaction ). C & rsquo; is a very sensitive technique. It detects the & rsquo; A.D.N. parasitic.


These techniques highlight antibodies and circulating antigens in various biological fluids.

Antibody Search :

Techniques for Antigens Figures :

The title Ac corresponds to the dilution which 50% parasites are lysed.

Technique Soluble Antigen :

L’hémagglutination passive

L’E.L.I.S.A. : (Enzyme Linked immunologie Sorbet Assay) routine technique.

Tests Latex :

Western-blot :

C & rsquo; is a test to highlight the toxoplasma antibody isotypes

Search & rsquo; Circulating Antigens :

These are very few reactions used in the diagnosis of toxoplasmosis current. They are to detect antigens & rsquo; excretion or secretion in biological fluids especially if low humoral response.

Example profiles mother – child
Interpretation of Toxoplasmosis Serology




Courses of Dr. Fendri – Faculty of Constantine