TOXO Presentation ENGL[2]
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Transcript of 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.
Obtain a new specimen for IgG and 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.
Obtain a new specimen for IgG and IgM.
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.