TOXO Presentation ENGL[2]

8/7/2019 TOXO Presentation ENGL[2]

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Toxoplasma gondii- intracellular

protozoan

Definitive host - Felidae cats itsrelatives

Intermediate hosts - humans & warm-

blooded animals

All continents (birds - role spread)

Common in warm climates, lower

altitudes

Seroprevalence is higher in:- Central America - France

- Turkey - Brazil


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Unsporulated

oocysts are

shed in the

cats feces

Oocysts shed

for 1-2 weeks

Oocysts in 1-5 days

sporulate in the

environment and

become infective

Cat owners are not

at risk from handling

cats or from contact

with fresh cat feces


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Humans may become infected :

eating undercooked meat of animals harboring tissuecysts

consuming food / water contaminated with cat feces or bycontaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat)

transplacentally from mother to fetus

blood transfusion or organ transplantation


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Pathogenesis

During digestion release of:

tissue cysts from bradyzoites or of oocysts from sporozoites

From the GI tract, parasites disseminate to a variety ofsites, particularly:

- Lymphatic tissue - Skeletal muscle

- Myocardium - Retina- Placenta - CNS

Activation of humoral and cellular immunity

Infection persists even in immunocompetent hosts

Lifelong infection usually remains subclinical

Compromised hosts cannot control infection; progressivefocal destruction and organ failure occur.


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Infection in pregnant women

Women who are seropositive beforepregnancy usually are protected against

acute infection and do not give birth toinfected neonates.

There is no risk if the mother becomes infected 6 monthsbefore conception.

1/3 women infected during pregnancy transmit the parasiteto the fetus.

In pregnancy

Only 20% of women infected with T. gondiidevelopclinical signs of infection.

Maternal infection during the first trimester:transplacental infection ~15%, severe neonatal disease

Maternal infection during the third trimester:

transplacental infection 65%, infant usuallyasymptomatic at birth.


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In immunocompetent patients

Acute disease - usually asymptomatic and self-limited.

unrecognized > 80%

Most common symptoms: Lymphadenopathy (> cervical), generalized 2030%

Headache

Malaise, fatigue

Fever, usually < 37- 38C Less common:

Myalgia

Sore throat

Abdominal pain Maculopapular rash

Meningoencephalitis

Symptoms resolve within several weeks,

Lymphadenopathy may persist for some months.


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In immunocompromised patients

reactivation of latent infection or from acquisition of new infection

Symptoms and signs principally involve the CNS:

insidious (several weeks) or acute altered mental status 75%

fever 1072%

seizures 33%

headaches 56%

focal neurologic findings 60%: motor deficits, movement disorders

cranial nerve palsies, visual field loss

aphasia

Rarely - respiratory involvement:

fever

dyspnea, nonproductive cough

may rapidly progress to ARDS

Rarely - infection of the heart

can be associated with cardiac tamponade orbiventricular failure


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Ocular toxoplasmosis:

Blurred vision

Photophobia

Scotoma, loss of central vision

Nystagmus

Disorders of convergence/strabismus

Ophthalmologic examination:

Yellow-white, cotton-like patches with indistinct

margins of hyperemia

As the lesions age, white plaques with distinct

borders and black spots appear within the retinal

pigment.

In patients with AIDS, retinal lesions are often large,

with diffuse retinal necrosis.


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When ordering and interpreting maternalserological screening tests, providers should not

assume quality testing and should question eachindividual lab regarding its methods of qualityassurance; in addition, providers should not relyon a single sample test but seek confirmatorytesting through a nationally recognizedreference laboratory if results are positive.

The polymerase chain reaction (PCR)amplification of toxoplasmosis DNA fromamniotic fluid has been deemed the most

reliable and safe method of prenatal diagnosis:- sensitivity (ability to find true positives) -64%

- specificity (ability to find true negatives) -100%


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Universal screening is mandatory in France and

Austria:

Seronegative women are tested monthly during pregnancy.

Bader et al. used decision analysis to compare

three screening methods:

no screening,

targeted screening based on prenatal history of maternalrisk factors,

universal maternal screening.

Universal screening reduced the total disease

incidence the most, but had an unacceptable fetal

loss ratio compared with both no screening and

targeting screening.


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Florescein angiogram (OS). Fluorescein angiogram showing areas of

hyperfluorescence (a) which increases at the late phase(b); window

defects as well as atrophic scars on the left macular region are seen.


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Hypopigmented atrophic scars and annular posterior vitreus

detachment OS


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IgG IgM Report/Interpretation for All Except Infants

Neg Neg No serological evidence of infection

Neg Equiv Possible early acute infection orfalse-positive IgM reaction.

Obtain a new specimen for IgG and IgM.

If new specimen result remains the same = pts

is probably not infected

Neg Pos Possible acute infection or false-positive IgM.


If results remain the same = IgM reaction is

probably a false-positive.

Equiv Neg Indeterminate: obtain a new specimen for

testing or retest this specimen for IgG in a

different assay.

Equiv

ocal

Equiv

ocal

Indeterminate: obtain a new specimen for both

IgG and IgM testing.


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IgG IgM Report/Interpretation for All Except Infants

Equiv Pos Possible acute infection.


If results with the new specimen remain the

same or the IgG becomes positive, both

specimens should be sent to a reference

laboratory.

Pos Neg Infected for more than 1 year.

Pos Equiv Infected with Toxoplasma gondiifor probably

more than 1 year or false-positive IgM reaction.

If second specimen remain the same, sent to a

reference laboratory

Pos Pos Possible recent infection within the last 12

months.

Send the specimen to a reference laboratory


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Treatment ofToxoplasmosis DuringPregnancy

usually spiramycin started when evidence of

maternal seroconversion is noted and while fetaldiagnosis is taking place (spiramycin is notapproved US).

If fetal testing confirms infection:pyrimethamine + sulfa-diazine + folic acid .

Pyrimethamine should not be used before 12weeks' gestation = teratogenic effects.

Treatment during pregnancy is associated with a50% decrease in fetal infection and reduce theseverity of disease manifestations.


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Primary orReactivation

Acute disease in immunocompetent, non-pregnant:

usually no treatment, unless visceral disease or symptoms severeor persistent.

Treatment (AIDS, preferred):

pyrimetamine 50-100mg/d +

leucovorin 10-20mg/d +

sulfadiasine 1.1.5g qid all PO x 3-6 weeks after resolution ofsigns/symptoms;

followed by pyrimetamine 25mg/d + leucovorin 15mg/d + sulfadiasine500mg PO qid indefinitely (or until immune reconstitution).

Folinic acid (leucovorin) 15-20mg PO daily

Alternatives: pyrimetamine 50-100mg/d + leucovorin 10-20mg/d +clindamycin 600mg qid (PO or IV).

Atovaquone 750mg PO q6h, azithromycin 1200-1500 mg PO daily, ordapsone 100 mg PO daily instead of sulfa when pt. is sulfa-intolerant.

TOXO Presentation ENGL[2]

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