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Toxoplasma gondii

Morphology
• The actively multiplying asexual form
in the human host is an obligate,
intracellular, parasite, pyriform in
shape and approximately 3-6 µ
• This parasite called tachyzoite, has a
cell membrane, nucleus, and various
organelles

• A collection of tachyzoites can fillup
a host cell, develop a parasite
membrane around themselves and
become a cyst
• In the encysted stage the organism,
called a bradyzoite, becomes
metabolically quiescent but remains
viable
• There is evidence that tachyzoites
are antigenically distinguishable from

• The cysts contain 50 to several
thousand bradyzoites and measure
from 10-100 µ in diameter
• Within the intestinal epithelial cell of
the cat, a variety of morphologic
forms has been described, ultimately
leading to male and female
gametocytes

• The fertilized macrogametes develop into nearly spherical oocysts that rupture out of intestinal epithelial cells • When passed in cats’ feces. contain 4 sporozoites . but the content develop into two sporocyst within several days after being passed • Each sporocyst. the oocysts measure 10-13 µ in diameter • The oocysts wall has two layers and contain undifferentiated material. in turn.

Life Cycle • T. in which two daughter cells are formed within a mother cell • As the distended host cells fill up with parasites.gondii tachyzoites multiply within host cells by a specialized form of division called endodyogeny. releasing parasite that enter new cells . they rupture.

use dextrose and preformed as well as precursor of pyrimidines and evolved CO2 but cannot synthesize purines. their respiration is cyanidesensitive .• The infected host cell may swell up develop a membrane. and become a cyst • The tachyzoites consume oxygen.

releasing organisms (bradyzoites) that penetrate epithelial cells of the small . mice and rats containing infective cysts are eaten by the cat. eye and skeletal muscles • In the natural cycle. developing in the brain. which serve as definitive host for the sexual stage of the parasite • The cyst wall is digested.• Toxoplasma can grow in any mammalian or avian organs or tissues.

and macrogametes • Fertilization of the latter results in development of oocysts that are discharged into the intestinal lumen by rupture of infected intestinal epithelial cells . finally culminating in development of micro.• Several generations of intracellular multiplication occur.

after passage to sporulate • Ingestion of the sporulated oocyst initiates infection by sporozoites in the intermediate host. cats excrete toxoplasma oocysts as early as 4 days later. these increase and then taper off by 14 days • Oocysts require 1-5 days.• After eating cysts. which can be virtually any animal . depending upon aeration and temperature.

but the tachyzoites multiply and spread to more distant organs to form cysts that are again infective when ingested by susceptible animal • Thus. a wild variety of animals. although the domestic cat or some wild species of Felidae can produce the the oocyst. cattle.• The oocyst-induced infection also begins in the intestinal epithelium. including sheep. and pigs can become infected by ingestion of the oocyst .

• These infected animals will. harbor infected cysts within muscle tissue • Organism within the cysts remain viable for years . in turn.

human infections can result: – 1. by ingestion of material with infected cat feces . from eating raw or partially cooked beef. fork or mutton containing toxoplasma cyst – 2.Hence.

the presence of antibodies to Toxoplasma is high in children .Epidemiology • Toxoplasmosis is cosmopolitan. sanitation is poor. favoring long-term oocyst viability. and the climate is humid and mild. antibody survey indicate that from 25-75% various populations are chronically but asymptomatically infected • In areas where cats are numerous.

not from mothers who have already been infected before pregnancy .• The other mode of transmission. is probably more common in developed urban areas • Although infection is common disease is rare • The congenital infection is required by transplacental transmission from mothers who develop toxoplasmosis during pregnancy. via ingestion of partially cooked or raw meat.

well-adapted parasite. or the site of the parasite . T.Pathology and Symptomatology • Ordinarily. and its disease-producing properties have been attributed to virulent strains.gondii is relatively benign.

varying in degree of severity with the age of the fetus at infection and the antibody protection from the mother . it is often severe and even fatal.Congenital Toxoplasmosis • This occurs is in about 1-5% per 1000 pregnancies • Unlike in adults.

• The child may present the typical syndrome of intracerebral calcifictiona. hydrocephally. and there maybe complete recovery . psychomotor disturbances. chorioretinitis. microcephaly. and convulsion • Visceral and muscular lesions are also present • Occasionally the infection is milder.

and occasionally even the organisms • Milder cases show only slight increases in cells and protein • It is estimated that of the congenital infetions.• Spinal fluid findings are variable • In severe overt cases there are xantochromia. increased cells and protein. 5-15% of the babies will die • 8-10% will have severe brain and eye damage .

second congenital infections rarely.• 10-13% will have moderate to severe visual handicaps • 58-72% will be asymptomatic at birth. occur . with a small proportion developing active retinochoroiditis or mental retardation as children or young adult • Since transplacental transmission takes place during initial exposure to the parasite. if ever.

• The chorioretinal lesions in infants are severe. extensive and bilateral • There is an intense edema of the retina and various degrees of degeneration and necrotic inflammation. with perivascular and general cellular infiltration • There may be an optic neuritis • Milder forms of congenital infection are seen as ocular involvement in older children and young adult .

• This is manifested only as a retinochoroiditis of varying severity. but without other evidence of generalized disease • The exact cause of toxoplasmic retinochoroiditis of this late-onset type is not known • It may be due to localized proliferation of organism or an immunologic hypesensitivity reaction .

cysts form in various tissues • The patients are asymptomatic .Acquired or Reactivity Toxoplasmosis • After infection and regional lymph node invasion. and with the production of antibody. the parasite is bloodborne to many organs where intracellular multiplication takes place • Parasitemia persist for several weeks.

is characterized by cervical and axillary lymphadenophaty. Slight aemia. malaise. leukopenia. muscle pain and irregular low fever. lymphocytosis. resembling infectious mononucleosis. mild lymphatic form. and slightly altered liver function maybe present . low blood pressure. the more common.• There are 2 main clinical types of acquired postnatal toxoplasmosis: – 1.

– 2. often with skin rash. pneumonitis. chills. disseminated infections. and myocarditis may be present . and prostration. the other type is characterized by acute. hepatitis. Meningoencephalitis. high fever. fulminating.

toxoplasmic encephalitis as a complication of AIDS has emerged as one of the most common parasitic disease in AIDS patients .• Toxoplasmosis has long been known to occur as an opportunistic infection because of immunosuppression associated with organ transplantation and treatment of certain neoplastic disease • In 1980s.

lethargy. fever. with progression to focal neurologic deficits and convulsions . and altered mental status.• CNS involvement by toxoplasma may even appear as the first clinical manifestation of AIDS • Early symptoms can be headache.

single or multiple lesion with predilection for basal ganglia and junction of gray and white matter can be visualized • Even in the presence of extensive brain lesions the parasite remains confined to the CNS and does not spread to other organs .• By CT scans or MRI imaging.

• This syndrome represents reactivation of a latent infection. so the usual serial antibody determinations are not helpful in diagnosis of toxoplasmosis complicating AIDS . so virtually all patients will have demonstrable IgG antibodies to Toxoplasma from a acquired previously infection • Changes in antibody levels are unpredictable and IgM responses do not occur.

tha there are other causes of retinochoroiditis and uveitis. although the exact mechanism is unknown • It should be emphasized.• The ocular involvement that occurs in later life following an inapparent congenital infection is probably a reactivationtoxoplasmosis also. however. probably most of it not a result of .

although it may be a useful clue for further diagnostic measures .• Serologic tests are very important in the diagnosis of toxoplasmosis • Because of the common occurence of antibodies to the parasite in the general population. diagnosis by serologic means requires demonstration of a significant increase in antibody titers • A very high antibodi level is not sufficient evidence in itself for a diagnosis of active toxoplasmosis.

• Congenital infections may be difficult to diagnose serologically because maternal IgG crosses the placental barrier and will appear and persist for several months in the circulation of the newborn • But since IgM antibodies do not cross the placenta. demonstration of antitoxoplasma IgM at birth or up to several months of age is presumptive evidence of conenital toxoplasmosis .

it is necessary to show that antibodies persist or increase in titer during the first 6 months or so of life as evidence of congenital infection • For measurement of IgM antibodies. the double-sandwhich ELISA test is the most specific and sensitive .• If tests that measure only IgG are available.

• The indirect fluorescent antibody (IFA) test is also used for both IgM and IgG determinations • Other serologic test tests for IgG antibody include the ELISA and IHA • The Sabin-Feldman dye test that was first develop requires preparation and use of living Toxoplasma organisms. so it is rarely used now .

and the significance of the test for diagnostic purposes is nor clear .• A complement-fixation (CF) test which can identify recent infections because of a slow rise and rapid fall in CF antibody. but antigens are not commercially available. is not used because it is difficult to standardize and is technically demanding • A delayed-type skin test has been described in toxoplasmosis.

a supension of the material should be inoculated into mice or cell cultures • Laboratory mice are very susceptible to infection. or blood have often been positive. muscle. and specimens of biopsied lymph nodes. spinal fluid. especially in acute cases .• If tissue of fluid suspected of containing parasites is available.

is that the orgasnisms recovered may represent encysted parasites from a previous infection . especially muscle tissue.• A positive result in mice can be shown either by actual isolation of the organism or by their development of antibody • One problem in interpretation of a positive isolation from tissue.

• Detection of parasite DNA by polymerase chain reaction (PCR) is being evaluated as a diagnostic measure .

Treatment • Symptomatic infections should be treated with pyrimethamine • The adult dosage is 25-50 mg per day orallyfor 3-4 weeks. plus 2-6 g daily trisulfapyrimidines orally for the same period • The two drugs act synergistically to inhibit nucleic acid synthesis of microorganisms .

• The sulfa by preventing incorporation of paraaminobenzoic acid in the synthesis of folate • Pyrimethamine by inhibiting dihydrofolate reductase (DHFR). a later stage in the process .

should be treated • If the retinochoroiditis is considered to be an active process. without systemic involvement.• Mild lymphatic toxoplasmosis will often subside without requiring treatment • It is often difficult to decide wether ocular toxoplasmosis. most opthalmologists treat with both corticosteroids and combined sulfa and pyrimethamine as outlined .

it may still be possible to manage by restarting with smaller but slowly increasing doses after dexamethasone pretreatment .• AIDS patients are much more susceptible to sulfa allergies and bone marrow supression by pyrimethamine • If severe toxicity requires stopping sulfa therapy.

one alternative drug is spiramycin .• Folinic acid at 10 mg per day will prevent or reversethe bone marrow suppresionof pyrimethamine without inhibiting its action because parasite can not utilize exogenous folate • Pregnant women should not be treated with pyrimethamine • In this situation.

• Another drug that might be used in emergency situations is clindamycin • Atovaquone. appears to be one of the more promising new drugs for treatment of toxoplasmic encephalitis in AIDS . a hydroxynaphthoquinone.