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IN THE NAME OF GOD
Evaluation of toxoplasmosis in neonate
• Shirvani F MD• Pediatric infectious diseases subspecialist• Shaheed Beheshti University of Medical Sciences
Mother infection is asymptomatic and lymphadenopathy is the most
common manifestation
WHAT Is THE PROSCESS OF MOTHER INFANT EVALUATION
• IgG POSITIVE low avidity• IgM True POSITIVE
Mother screening
Mother treatment
Fetus evaluation
• IgG low positive, high avidity , AC/HS
• IgM Neg
Mother screening
Mother NOT
treated • Except HIV positive mother
PRIMARY evaluation Prenatal
Sonography in fetus(every 2 week)
Amnioic fluid PCR(17th-21th week)
PostnatalMaternal and
NEONATALIgG,IgM,IgA,
IgE
Injection of placenta specimen,amniotic fluid,cord blood to
mice
Paired neonate and maternal serology:IgG
Gold standard= Sabin feldman dye testIgG immunobloting test
Indirect Immunofluorescent antibody test, more than 1/1000IgG ELISA AC acetone fixed/HS formalin fixed direct agglutinationEnzyme linked immunofiltration assay ,discriminates mother and infant IgG
IgG avidity test , low avidity antibodies dissolve with urea , high avidity shows more than 3 months OR 16 WEEKS ago infection, low avidity may remain pos . For a long time
Paired neonate and maternal serology:IgM
Double sandwich ELISA IgM test is pos in 50% - 75% of cong inf
- IgM IFA is false neg. in 25% to 75% -IgM immunosurbant Agglutination assay highly sensitive(ISAGA)- IgM immunobloting testsensitive(ISAGA)
IgM immunoflourescent antibody assay lower sensitivity than ELISA and immunosurbant test
Paired neonate and maternal serology:IgA
Specific IgA ELISA IgA immunofiltration assayIgA ISAGA
IgA immunobloting testIgA EIA
Paired neonate and maternal serology:IgE
IgE ISAGA
IgE ELISA
The IgE-ELISA and IgE-ISAGA are also sometimes useful in establishing the diagnosis of congenital toxoplasmosis or acute acquired T. gondii infection
At present, the IgM-ISAGA, the IgA-ISAGA, and the IgA ELISA are the best tests for diagnosis of congenital infection in the newborn.
WHAT ARE THE CLINICAL MANIFESTATION IN NEWBORN:
characteristic triad of chorioretinitis, hydrocephalus, and cerebral calcifications.
WHAT ARE THE CLINICAL MANIFESTATION IN NEWBORN:
• OTHER Manifestations of congenital toxoplasmosis:
• 10% severe congenital toxoplasmosis with CNS involvement, eye lesions, and general systemic manifestations;
• 34% mild involvement with normal clinical examination results other than retinal scars or
isolated intracranial calcifications;• and 55% no detectable manifestations.
WHAT ARE THE CLINICAL MANIFESTATION IN NEWBORN:
• From 25% to >50% of infants with clinically apparent disease at birth are born prematurely.
Intrauterine growth retardation, low Apgar scores, and temperature instability are common.
Other manifestations include lymphadenopathy, hepatosplenomegaly, myocarditis, pneumonitis, nephrotic syndrome, vomiting, diarrhea, and feeding problems.
Bands of metaphyseal lucency and irregularity of the line of provisional calcification at the epiphyseal plate may occur without periosteal reaction in the ribs, femurs, and vertebrae.
WHAT ARE THE CLINICAL MANIFESTATION IN NEWBORN:
Interpretation of neonate Antibodies:IgM+ IgG+
Rulout FP with RF and ANA of IgM AC/HS,IgE EIA/ISAGA,IgA EIA,IgM ISAGA in reference LAB, Neonatal evaluation
IgM ± IgG +Repeat test , do IFA if ELISA and VISEVERSA
IF documented primary infection in mother or neonate= reference LAB
IgM- IgG+25% false Neg IgMRepeat test , do IFA if ELISA and VISEVERSA
IF documented primary infection in mother or neonate= reference LABIgM+ IgG –
NO infection in mother, probable false positive IgMdo IFA if ELISA and VISEVERSA , REPEAT TEST
IgM – IgG - No infection in neonate
Antibody interpretation:
1-Antibody demonstrated at3rd mo of life if the infant is untreated.,
2-synthesis may be delayed for as long as the 9th mo of life or, may not occur at all, If the infant is treated
3-increase in the ratio of specific serum IgG antibody titer to the total IgG WITH INCREASE OF ANTIBODY IN ANY SITUATION
Neonatal evaluation:• ABR• Ophthalmologic Examination
• CBC• LFT, Alk Phos., Bil
• CSF microscopic and total IgG• Csf specific IgG and IgM
• Brain CT and Sonography
• Neonatal serology IgG , IgM , IgA
• PCR of CSF , Urine , blood
• Mouse inoculation of specimen
• Lymphocyte blastogenesis to Toxoplasma antigens
Treatment:Infected pregnant mother is treated with spiramycin
If infection in fetus occurs, mother treatment does not alter the severity and evolution of disease in fetus
Thus PCR in amniotic fluid leads us to treat the fetus
Treatment:Condition medication dosage Lengh of therapy
Congenital infection Pyrimethamin plus 2 mg/kg/day for 2 day then 1 mg/kg/day/for 6 month then 3 times weekly for 6 month
1 year , monitor weekly complete blood count and platelet
Sulfadiazine plus 100 mg / kg/day divided twice daily
Folinic acid 5-10 mg three times weekly
Dose adjusted to maintain CBC
prednisone 1 mg/kg /divided twice daily
Until resolution of CSF protein to <1gr/dl or sight threatening
Spiramycin can be used for prophylaxis in children at risk at first 6 to 9 months of age
• Treatment does not eradicate all cysts bradizoits
• Antibodies rebound 3 to 4 months after treatment discontinuation
• New retinal lesion occur 3 to 10 years after treatment stop
Follow up
After one year treatment examine retina every month till 3 months and every
three months till ability to report their vision and then every 6 months
prevention
Screening of pregnant mother s or neonates with IgM measurement
Education in hygiene control
Decision for treatment in neonate
Infection not confirmed
IgG and IgM in cord blood Infection confirmed before or after birth
treatment
Follow up
complementary serologic series and neonatal evaluation
High risk neonate
Infection confirmed
treatment
Low risk neonate
complementary serologic series
Infection confirmed
neonatal evaluation and treatment
Follow up
Infection not confirmed
Decision for treatment
Follow up
Infection not confirmed
Serial serology
Infection confirmed Infection not confirmed
treatment Follow up
THANK YOU