1.Antenatal (in utero) - 80-96% of cases
Primary Maternal Infection
Recurrent Maternal Infection
1. Horizontal Transmission
CMV excreted in saliva, urine, stool, tears
2. Organ Transplantation
kidney, marrow, heart, liver, blood (leukocytes)
90% of infants with congenital CMV
infection are clinically silent.
70% - microcephaly.
60% - intellectual impairment.
35% - sensorineural hearing loss
22% - chorioretinitis.
Caused by the protozoan Toxoplasma gondii
ocular, central nervous system (CNS)
incidence: 0.3-1/1000 live births.
Routes of Transmission.
Neonatal (in utero).
Primary Maternal Infection.
acquired by the ingestion of raw or undercooked meat
( cattle), or of infectious oocysts in feces (cats, birds).
1st trimester - 17% - spontaneous abortion.
2nd trimester - 25% - spontaneous abortion or
3rd trimester - 65% - subclinical disease.
Congenital toxoplasmosis show the typical multifocal
periventricular and cortical/subcortical punctuate calcifications as
well as a moderate ventriculomegaly as complication of the infection.
Congenital toxoplasmosis shows bilateral microophthalmia and chorionic
calcifications as well as deformity of the lenses (white arrows).
Toxoplasmosis of immune compromised
patient with multiple ring enhancing lesions.
CONGENITAL RUBELLA(German measles).
Caused by an RNA Togavirus.
Routes of Transmission.
Antenatal (in utero).
1st trimester - 75-90%.
2nd trimester - 35-40%.
3rd trimester - 25-50%.
Congenital rubella infection show small calcifications within the basal ganglia,
along the intramedullary veins within both frontal lobes and within the deep
Layers of the overlying cerebral cortex and adjacent subcortical white matter
(white arrows on A). MRI shows ill-defined, multifocal regions of dysmyelination
within the periventricular white matter of both cerebral hemisphere.
Rubella. Unenhanced axial CT (a) in a 3-day-old with congenital
rubella demonstrates punctate calcifications of the basal ganglia
(arrow) and low attenuation of the white matter.
The classic clinical
picture of cytomegalic inclusion disease (CID) is characterized
by involvement of multiple organs, in particular the
reticuloendothelial and central nervous system, with or
without ocular and auditory damage. Obvious symptoms of
CID could be jaundice, Hepatosplenomegaly and petechiae in
a growth retarded often prematurely born baby. The
neurological involvement includes microcephaly, seizures,
hypotonia and lethargy. The most severely affected infants
have a mortality rate of about 30%. Deaths are usually due to
hepatic dysfunction, bleeding, disseminated intravascular
coagulation or secondary bacterial infections. Some 85- 90%
of children with a congenital CMV infection are asymptomatic
in the neonatal period.
Congenital cytomegalovirus infection.
Congenital CMV-infection show multifocal, predominantly periventricular
located calcifications within the supra- and infratentorial brain as well as a
thickened, smooth dysplastic cortex, moderate ventriculomegaly, a small
cerebellum and a CT-hypodense, T2-hyperintense dysmyelination of the
periventricular white matter. In addition, a mild microcephaly is noted.
Axial CT-images (A, D), T2-weighted images (B, E), and SWI images (C, F) of with congenital
cytomegalovirus infection presenting with moderate hydrocephalus and white matter
volume loss as well as subtle subependymal calcifications are seen on the CT study (white
arrow on D). The extent of calcium depositions is however much better appreciated on the
SWI images as SWI-hypointense signal abnormalities (C, F). In addition, cerebellar
hypoplasia (A, B) and high-grade loss of the hemispheric white matter (E), including a
more focal subcortical defect in the right parieto-occipital region are noted.
MENINGITIS & ENCEPHALITIS.
Meningitis – inflammation of
Encephalitis – infection of the
inflammation of brain +
Aseptic meningitis –
inflammation of meninges
with sterile CSF
Symptoms of encephalitis.
.Many encephalitides are mild and
.In a minority, serious illness develops with
high fever, headache, mood change and
drowsiness over hours or days.
Focal signs, seizures and coma ensue.
Death, or brain injury follows.
Axial T2-weighted (A), coronal FLAIR (B), axial DWI (C) MR images, and axial
ADC map (D) with encephalitis . MRI shows symmetrical, ill defined T2- and
FLAIR-hyperintense signal abnormalities in both thalami with matching
regions of restricted diffusion (DWI-hyperintense, ADC-hypointense) on
diffusion weighted imaging (white arrows on A-D) encephalitis.
Rasmussen's encephalitis with hemispheric volume loss.
Symptoms of meningitis.
.Altered consciousness, irritability, photophobia vomiting,
. Seizures 20 - 30%
. Bulging fontanel 30%
. Stiff neck or nuchal rigidity
. Meningismus (stiff neck + Brudzinski + Kernig signs).
• Infection of the meninges which may be pyogenic, viral or
• Inflammation of the leptomeninges can be divided into acute
pyogenic (bacterial), lymphocytic (viral), and chronic (TB)
meningitis. The diagnosis is usually clinical.
• The role of neuroimaging is to exclude complication of
meningitis(e. g, abscess, ventriculitis, empyema).
CT and MRI of meningitis with dense basal cistern
which is seen enhanced at MRI images.
Acute pyogenic meningitis with basal cistern
exudates with enhancement and hydrocephalus.
Meningitis with predominant leptomeningeal enhancement.
Post-meningitis sequale with epidural and subdural empyema.