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Types of Clinical Presentation:

  • subclinical infection
  • severe illness during the neonatal period
  • mild or severe form in the first few months of life
  • sequelae or relapses (usually ocular) to an undiagnosed congenital infection occurring during childhood or adolescence

Most newborns do not have clinical manifestations at routine examination. If additional investigations are performed – CSF analysis, ophthalmologic examination, cerebral imaging, changes may occur:

  • ophthalmologic examination: unilateral macular scarring
  • cerebral imaging: small focal cerebral calcifications, hydrocephalus, cortical atrophy

It is preferable CT without contrast because it is fast, cheaper compared to MRI and does not require sedation.

  • CSF analysis: proteinorachie (sometimes> 1g/dl), mononuclear dominant pleocytosis


Detection of T. gondii specific IgM in the CSF or isolation of T.gondii from the CSF confirms the diagnosis.

  • hearing testing

Laboratory investigations for assessing those with suspicion of congenital toxoplasmosis

1. Serological

Diagnosis of congenital toxoplasmosis in the newborn estestabilit serological, but the interpretation of results can be very complicated

Particular situations, difficult to interpret:

  • Anti-Toxoplasma IgG in the newborn – May relfecta an old or active infection to the mother because IgG crosses the placenta
  • Fetal Ac IgM may disappear before birth
  • Prenatal treatment may affect the serological profile of the newborn. Usually, in newborns who received treatment in utero with Pirimetamina and sulfadiazine IgM antibodies are not present
  • The immune response of the newborn, directed against T. Gondii may be delayed for several months
  • The placental leakage of IgM and IGA maternal antibodies can lead to the result of IgM and IGA-specific positives in small titre in the newborn shortly in childbirth

Diagnosis in newborn is based on the presence of IgM antibodies specific T. gondii – Detected by ELISA (enzyme-linked immunosorbent assay) or ISAGA (immunosorbent agglutination assay)

!!! However, the absence of antibodies does not preclude infection, as they may occur at a variable time interval after birth, depending on the time when the maternal infection occurred.

If IgG Ac is negative or ambiguous, you must determine the specific IgA antibodies by the ELISA technique, which have a higher sensitivity, but lower specificity. They have also been used to diagnose specific IgE antocorpii, but without aaduceinformatii supplimentare to the specific IgM and IgA combination.

Antibody testing should be repeated at 10 days of life.

For example, specific IgM and IgA titres will quickly drop to non-infected newborns (in case of placental transfer of maternal antibodies), while those infected in utero will remain positive for weeks to months after birth.

If the initial results are ambiguous, serial tests are required. The maternal IgG needle transplacental into the newborn blood will become undetectable between 6 and 12 months, unlike children with congenital infection who have high IgG titres specific after the age of 1 year.

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2. Identification of the parasite Toxoplasma gondii

  • PCR from amniotic fluid for diagnositcul fetal infection
  • PCR, vitreous fluid, urine, mother’s blood, bronchoalveolar lavage, umbilical cord blood, newborn blood, placenta
  • Parasitological studies from tissues or liquids – Demonstarea Chisturilo for example
  • Isolation of parasites from blood or other human fluids by inoculation in mice

* Tests available in reference laboratories

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3. Other tests required for initial evaluation of newborns with suspicion of congenital toxoplasmosis

  • Lumbar puncture – CSF will be determined: proteins, glucose, number of elements, PCR T. gondii, IgG and IgM-specific anti-Toxoplasma

* PCR and Serology in CSF are working in reference laboratories

  • Blood counts: Anaemia, thrombocytopenia, eosinophilia-non-specific manifestations in symptomatic
  • AST, ALT, Total and direct bilirubin
  • creatinine, urea, urine summary – prior to initiation of treatment with sulfadiazine, Sulfamerazina or sulfamethazine, because doses require adjustment in case of renal failure
  • Glucose-6-phosphate deficiency test-dehydrogenase-before initiation of treatment
  • Quantitative determinations of IgG, IgM and IgA serum immunoglobulins
  • Urinalysis for CMV – which may have clinical manifestations related or can be co-infection
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 Confirmation of the diagnosis of congenital toxoplasmosis

  • Anti-Toxoplasma antibodies specific to IgM, IgA or IgE in the newborn serum with compatible maternal serology

Or

  • Characteristic clinical signs: chorioretinitis, cerebral calcifications, and/or hydrocephalus – to a newborn born from a mother with first infection in pregnancy or with chronic infection if the mother is immunosuppressed

Or

  • Anti-Toxoplasma IgG titre growth in the first year of life

Or

  • Increase in comparative IgG titres with mother titre

Or

  • Persistent anti-Toxoplasma IgG needle at the age of 1 year – up to this age disappearing IgG antibodies acquired Tranplacentar

!!! The infant with congenital infection may synthesize IgG anti-Toxoplasma antibodies from the third month of life if not treated. In those treated, the synthesis is delayed until the age of 6-9 months.

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Exclusion of the diagnosis of congenital toxoplasmosis

To those untreated-repeated serological tests demonstrating the continuous decrease of the IgG titre in the absence of IgM antibodies or IgA-specific anti-Toxoplasma.

* * With the mention that the child’s IgG synthesis capacity should be proven (determination of serum immunoglobulin levels)

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O-Congenital syphilis

CDC Case Definition

A. Laboratory Criterion for Diagnosis

demonstrating the presence of Treponema pallidum by dark field microscopy, or by other methods of visualizing them from lesions, placenta, umbilical cord or autopsy


B. Classification of cases

I. Probable case

  • newborn mother-in-law with untreated syphilis or inappropriately treated at birth, regardless of clinical signs
  • newborn or baby with positive treponemal test plus one of the following:
  • evidence of congenital syphilis at clinical examination:

age 0 – 2 years:

hepatosplenomegaly

– eruption

– condyloma lata

jaundice

– pseudoparalysis

– edema

– rhinitis

over 2 years:

– Interstitial keratitis

– neurosensory deafness

– tibia in jatagan

– frontal bosses

– Hutchinson teeth

– molars in the form of “dude”

– Nose in saddle

– cracks / scars that start from the mouthpiece

– Clutton joints – Symmetrical joint swelling, usually at the knee level: synovitis and intracapsular fluid collection lasting up to 1 year

  • radiological evidence (long bone x-rays) of congenital syphilis
  • positive CRL VDRL test
  • protein rhythm or increased number of elements in the CSF without another known cause

II. Confirmed: case confirmed by laboratory investigations

Some experts consider congenital syphilis newborns from mothers who have had contact with a person with primary or secondary syphilis up to 90 days before birth and have not been treated or treated inadequately.

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