Congenital, Acquired Pyogenic, and Acquired Viral Infection

1. Congenital, Acquired
Pyogenic, and Acquired Viral
Infection
DR PRIYANKA RANA
15/03/2017

2. Congenital
Infections
• TORCH infection
• Cytomegalovirus
• Toxoplasmosis
• HIV
• Herpes encephalitis
Acquired Pyogenic
Infections
• Meningitis
• Abscess
• Ventriculitis
• Empyemas
Acquired Viral
Infections
• Herpes simplex
virus
• HHV -6
encephalopathy
• Miscellaneous acute
encephalitides
• Chronic
encephalitides

3. TORCH
TOxoplasmosis
Rubella
Cytomegalovirus
Herpes.
If congenital syphilis
is included, the
grouping is called
TORCH(S) or
(S)TORCH.

4. Pathology
Timing of infection during fetal development
determines pathology of insult
Timing more important than specific agent
involved
Early insult → brain malformations
Late insult → encephaloclastic, destructive
changes

5. General Imaging Findings
Calcifications
Periventricular (especially CMV)
Parenchymal (especially toxo)
Microcephaly, ventriculomegaly
Migrational defects
Polymicrogyria
Schizencephaly
Volume loss
White matter hyperintensities

6. Etiology
In addition to the recognized "classic" TORCH infections, a
host of new organisms have been identified as causing
congenital and perinatal infections. These include HIV,
hepatitis B, varicella, and tuberculosis.
Imaging
Toxoplasmosis, rubella, CMV, and HIV all cause
parenchymal calcifications. CMV causes periventricular
cysts, clefts, schizencephaly, and migrational defects.
Rubella and herpes simplex virus (HSV) cause lobar
destruction and encephalomalacia. Congenital syphilis is
relatively rare but when it occurs, it causes basilar
meningitis.
TORCH infections should be considered in newborns and
infants with microcephaly, parenchymal calcifications,
chorioretinitis, and intrauterine growth restriction.

7. Congenital
Cytomegalovirus
CMV is the leading cause of nonhereditary deafness in
children and is the most common cause of congenital
infection in developed countries.
Terminology and Etiology
Congenital Cytomegalovirus infection is also called CMV
encephalitis. CMV is a ubiquitous DNA virus that belongs to
the human herpesvirus family.

8. Pathology
The timing of the
gestational infection
determines the brain
insult. Early gestational
CMV infection causes
germinal zone necrosis
with subependymal
dystrophic calcifications.
White matter volume
loss occurs at all
gestational ages and
can be diffuse or
multifocal. 12-1).
Vascular inflammation
and thrombosis are also

9. Imaging
General Features
Imaging features of congenital
CMV include microcephaly
with ventriculomegaly,
intracranial calcifications,
white matter disease, and
neuronal migration disorders.
As a general rule, the earlier
the infection, the more severe
the findings.
CT Findings
NECT scans show intracranial
calcifications and
ventriculomegaly in the
majority of symptomatic
infants. Calcifications are
predominantly periventricular,
with a predilection for the
germinal matrix zones.

10. MR Findings
CMV exhibits a broad
spectrum of MR
abnormalities including
microcephaly with
ventriculomegaly, white
matter volume loss,
delayed myelination, and
periventricular cysts.
Migrational abnormalities
are present in
approximately 10-50% of
cases. Cortical
abnormalities range from
minor dysgenesis with a
simplified gyral pattern
and "open" sylvian
fissures to a near-agyric
lissencephalic pattern.

11. T1 scans show
subependymal
hyperintense foci caused
by the periventricular
calcifications. Enlarged
ventricles with
germinolytic cysts in the
adjacent white matter are
common.
T2-weighted and FLAIR
images show myelin
delay or destruction and
white matter volume loss
with focal or confluent
hyperintensities in most
cases. Periventricular
cysts, especially in the
anterior temporal lobe,
are common

12. Ultrasound
Sonography shows enlarged ventricles. Focal periventricular
hyperechogenic foci that correspond to the subependymal
calcifications observed on NECT scans are common
Fetal MR is more sensitive than US in the early detection of
CMV-associated abnormalities.
Differential Diagnosis
The differential diagnosis of congenital CMV includes other
TORCH infections, especially toxoplasmosis. Toxoplasmosis is
much less common and typically causes scattered parenchymal
calcifications, not the dominant subependymal pattern observed
in CMV. Microcrania and cortical dysplasia are also significantly
less common in congenital toxoplasmosis.
Lymphocytic choriomeningitis (LCM) may mimic CMV on
NECT scans. LCM typically causes necrotizing ependymitis and
aqueductal obstruction with hydrocephalus and macrocephaly,
not microcephaly.

13. Congenital
Toxoplasmosis
Etiology and Pathology
Congenital toxoplasmosis (toxo) is caused by intrauterine
infection with Toxoplasma gondii, a ubiquitous obligate
intracellular parasite. Infected domestic cats are a major
source of infection, which is usually acquired from
undercooked meat or food products (usually fresh fruit
and vegetables) contaminated by cat feces.
Macrocephaly with hydrocephalus and ependymitis are
prominent gross features of congenital toxo. In contrast to
CMV, malformations of cortical development are rare

14. Clinical Issues
Toxoplasmosis is the second most
common congenital infection.
Approximately 5 in 1,000 pregnant
women are infected with toxo.
Congenital toxo causes
hepatosplenomegaly, growth
retardation, chorioretinitis, and
brain damage. Infants with
subclinical infection at birth are at
risk for delayed cognitive, motor,
and visual defects.
Imaging and Differential Diagnosis
With some exceptions, imaging
features of congenital toxo
resemble those of CMV. NECT
scans show extensive parenchymal
calcifications that are predominantly
cortical and subcortical. MR scans
show multiple subcortical cysts and
moderate to severe
ventriculomegaly.

15. Congenital Herpes
Encephalitis
Terminology
CNS involvement in herpes simplex virus (HSV) infection is
called congenital or neonatal HSV when it involves
neonates and herpes simplex encephalitis (HSE) in
individuals beyond the first postnatal month
Etiology
Approximately 75-80% of neonatal herpes encephalitis is
caused by HSV type 2. The remainder is caused by HSV1.
The morbidity and mortality in neonatal HSV2 encephalitis
are significantly worse compared to HSV1 encephalitis.

16. Pathology
Neonatal HSV encephalitis is a diffuse disease, without the
predilection for the temporal lobes and limbic system seen
in older children and adults.
Early changes include meningoencephalitis with necrosis,
hemorrhage, and microglial proliferation. Atrophy with
gross cystic encephalomalacia and parenchymal
calcifications is typical of late-stage HSV. Near-total loss of
brain substance with hydranencephaly is seen in severe
cases.

17. Clinical Issues
Epidemiology
HSV2 is one of the most prevalent sexually transmitted
infections worldwide.
The vast majority (85%) of neonatal HSV is acquired at
parturition, and 10% is contracted postnatally. Only 5% of
cases are due to in uterotransmission. The risk is
increased with primary maternal infection during the third
trimester and can be decreased by cesarean delivery.

18. Presentation
Neonatal HSV infection causes three disease patterns: (1)
skin, eye, and mouth disease, (2) encephalitis, and (3)
disseminated disease with or without CNS disease.
Approximately 50% of all infants with neonatal HSV will
have CNS involvement, either isolated or as part of
disseminated disease.
Lethargy, fever, poor feeding, seizures, and bulging
fontanelle are common. Typical onset of symptoms
secondary to peripartum HSV infection is two to four weeks
following delivery (peak = 16 days). The definitive
diagnosis is based on PCR or viral isolation from ulcerated
vesicles and/or scarifying mucocutaneous lesions.

19. Imaging
Unlike childhood or adult
herpes simplex encephalitis,
neonatal HSV CNS infection
is much more diffuse. Both
gray and white matter are
affected.
CT Findings
NECT scans may be normal
early in the disease course,
but widespread areas of
hypoattenuation involving
both cortex and subcortical
white matter soon appear.
Hemorrhages may develop
and are seen as multifocal
punctate and curvilinear
hyperdensities in the basal
ganglia and cortex.

20. MR Findings
MR is the imaging procedure of choice in suspected cases of
neonatal HSV although the watery, unmyelinated neonatal brain
makes it difficult to discriminate between infection and
unaffected brain.
In the early stages, T1WI may be normal or demonstrate mild
hypointensity in the affected areas. T2WI and FLAIR are more
sensitive. Hyperintensity in the cortex, subcortical white matter,
and basal ganglia is typical. Hemorrhagic foci are uncommon in
early stages but may develop later and are best seen on T2*
(GRE, SWI) sequences.
Foci of patchy enhancement, with or without meningeal
enhancement, are common on T1 C+ scans. In later stages, T1
shortening and T2 hypointensity with "blooming" on T2* GRE
secondary to hemorrhagic foci may develop.
DWI is key to the diagnosis of congenital HSV encephalitis. In
half of all patients, DWI demonstrates bilateral or significantly
more extensive disease than seen on conventional MR . Areas
of restricted diffusion may be the only positive imaging findings
in early cases. Late-stage disease shows severe volume loss
with enlarged ventricles and multicystic encephalomalacia .

22. Differential Diagnosis
The major differential diagnosis for neonatal HSV is other
TORCH infections. Neonates with HSV are usually normal for
the first few days after delivery. Brain scans are normal or
minimally abnormal early in the disease course. Calcifications
and migrational anomalies are absent.
In some cases, HSV causes watershed distribution ischemic
injury in areas remote from the primary herpetic lesions and may
be difficult to distinguish from hypoxic-ischemic injury (HII).
However, term infants withHII follow a different clinical course,
becoming symptomatic in the intrapartum or immediate postnatal
period. Profound HII preferentially affects the perirolandic cortex
and sulcal depths, white matter, hippocampi, and deep gray
nuclei including the ventrolateral thalami. Hemorrhage with
"blooming" on T2* GRE is uncommon.

23. Other Congenital
Infections
Rubella
Humans are the only reservoir for the rubella virus. Transmission
is via virus-contaminated respiratory secretions. With the advent
of measles-mumps-rubella vaccination, the worldwide
prevalence of congenital rubella syndrome (CRS) has declined
dramatically. Approximately 100,000 infants are born with CRS,
mostly in countries with low national vaccination rates.
Early in utero infection results in miscarriage, fetal death, or
congenital malformations in surviving infants. Late infection
causes generalized brain volume loss, dystrophic calcifications,
and regions of demyelination and/or gliosis.
The clinical spectrum of CRS includes ophthalmic, auditory,
cardiac, and craniofacial defects. Imaging findings are
nonspecific, varying from parenchymal calcifications on NECT
scans to multiple foci of T2/FLAIR hyperintensity and volume
loss with mildly enlarged ventricles and sulci .

25. Congenital Syphilis
Congenital syphilis (CS) is caused by transplacental
passage of the Treponema pallidum spirochete from
untreated mothers with syphilis. The prevalence of CS is
low in most of the developed world although there has
been a mild resurgence of the disease reported in several
European countries.
Up to 60% of infants infected with CS are asymptomatic at
birth. Symptoms typically develop later in infancy, are often
subtle and nonspecific, and include seizures, stroke, and
signs of increased intracranial pressure.
The most common imaging findings in CS are
hydrocephalus and meningitis with leptomeningeal

26. Acquired Pyogenic
Infections

27. Meningitis
Terminology
Meningitis is an acute or chronic inflammatory infiltrate of
meninges and CSF. Pachymeningitis involves the dura-
arachnoid; leptomeningitis affects the pia and
subarachnoid spaces.
Presentation
Presentation depends on patient age. In adults, headache,
fever, nuchal rigidity, and altered mental status are
common symptoms. Fever, lethargy, and irritability are
common in infants. Children with N. meningitidis infection
may develop a purpuric rash. Seizures occur in 30% of
patients.
CSF shows leukocytosis (mainly polymorphonuclear cells),
elevated protein, and decreased glucose.

28. Imaging
General Features
Imaging should be used in conjunction with—and not as a
substitute for—appropriate clinical and laboratory
evaluation. Imaging studies are best used to confirm the
diagnosis and assess possible complications. While CT is
commonly employed as a screening examination in cases
of suspected meningitis, both primary and acute
manifestations of meningitis as well as secondary
complications are best depicted on MR.

29. CT Findings
Initial NECT scans may be normal or show only mild
ventricular enlargement (12-17A). "Blurred" ventricular
margins indicate acute obstructive hydrocephalus with
accumulation of extracellular fluid in the deep white matter.
Bone CT should be carefully evaluated for sinusitis and
otomastoiditis.
As the cellular inflammatory exudate develops, it replaces
the normally clear CSF. The cisterns and sulci appear
effaced as they become almost isodense with brain CECT
shows intense enhancement of the inflammatory exudate
as it covers the brain surfaces, extending into and filling the
sulci

30. MR Findings
The purulent exudates of acute meningitis are isointense
with underlying brain on T1WI, giving the appearance of
"dirty" CSF. The exudates are isointense with CSF on T2WI
and do not suppress on FLAIR Hyperintensity in the
subarachnoid cisterns and superficial sulci on FLAIR is a
typical but nonspecific finding of meningitis.
DWI is especially helpful in meningitis, as the purulent
subarachnoid space exudates usually show restriction .
Meningitis enhances intensely and uniformly on T1 C+, . A
curvilinear pattern that follows the gyri and sulci (the "pial-
cisternal" pattern) is more common than dura-arachnoid
enhancement. Delayed contrast-enhanced FLAIR scans
may be a helpful addition in detecting subtle cases.

32. Ventriculitis
Primary intraventricular abscess is rare. A collection of
purulent material in the ventricle is more likely due to
intraventricular rupture of a brain abscess (IVRBA), a
catastrophic complication. Recognition and prompt
intervention are necessary to treat this highly lethal
condition.
Terminology
Ventriculitis is also called ependymitis, pyocephalus, and
(less commonly) ventricular empyema.

33. Imaging
Ventriculomegaly with a debris level in the dependent part
of the occipital horns together with periventricular
hypodensity is the classic finding on NECT scans (12-33A).
The ventricular walls enhance on CECT.
MR should be the first-line imaging modality in cases of
suspected IVRBA. Irregular ventricular debris that appears
hyperintense to CSF on T1WI and hypointense on T2WI
with layering in the dependent occipital horns is typical.
Enhancement varies from none to striking (12-32A), (12-
33C). Some degree of ependymal enhancement can be
identified in 60% of cases.
The most sensitive sequences are FLAIR and DWI. A
"halo" of periventricular hyperintensity is usually present on
both T2WI and FLAIR scans (12-33B). DWI shows
diffusion restriction of the layered debris (12-32B), (12-
33D).

34. ACQUIRED HERPES ENCEPHALITIS
Etiology of Herpes Simplex Encephalitis (HSE)
> 95% of HSE caused by HSV1
Reactivation of latent virus in trigeminal ganglion
Trauma, stress, immunosuppression can trigger
Pathology
HSE: Striking affinity for limbic system
Temporal lobes, insular cortex, subfrontal, cingulate
gyri
Hemorrhagic, necrotizing encephalitis
Clinical Issues
HSE is most common cause of nonepidemic viral
encephalitis
Bimodal age distribution (6 months to 3 years, > 50
years)

35. Imaging
Bilateral but asymmetric
temporal lobe, insular cortex
lesions
FLAIR most sensitive
Restricts on DWI
Differential Diagnosis of
HSE
Neoplasm (gliomatosis
cerebri)
Stroke (vascular distribution,
both GM, WM)
Postictal hyperemia

36. Thank you