BACTERIAL AND PARASITIC CNS

INFXNS
Presenter: Dr Tarus
Outline
 Imaging modalities
 Classification
Imaging modalities
 Plain radiography- limited role.Poor sensitivity and
specificity
 US- Can be useful screening tool in newborn and infant
population. Has pitfall of operator-dependency
 Contrast studies- ventriculography, cisternography and
myelography have been superceded by cross-sectional
imaging
Imaging modalities cont
 CT Scan- gained popularity and cost is
declining
- recorded good accuracy
- can be used in emergency setting
and restless pts
- contrast resolution can be limited
thereby lowering its sensitivity
Imaging modalities cont
 MR- Modality of choice in CNS infections
- superior contrast resolution increases
sensitivity
- multiplanar, multisequential
- non-ionizing
- advanced studies- MRS,
ADC, DWI, MTR
- Pt inherent limitations
- Poor sensitivity Ca++ and bony involvement
- Availability and cost can be inhibiting
Imaging modalities cont
 RNI- Th-201, Tc-99 HMPAO SPECT and PET scans have
been used for perfusion evaluation.
 Angio- Conventional DSA, CTA, MRA have role in
infections that have vascular involvement
Classification of CNS Infections
Aetiological Location
 Pyogenic  Parenchymal
 Mycobacterial  Extra-axial
 Fungal
 Parasitic
 Spirochetes
 Rickettsial
 Viral
CNS Infections: Routes of Entry
 Local spread- Paranasal sinusitis, otomastoiditis,
dental,trauma, surgery

 Haematogeneous- cardiac, lung

CNS Infections: Clinical Presentation
 General – fever, generalised ache,lethargy
 Raised intracranial pressure- headache, vomiting,
papilloedema
 Meningeal irritation-headache,photophobia, neck stiffness,
kernig’s sign
 Focal neuro deficits
 Seizures
 Coma
Parenchymal Infections: Acquired
 Pyogenic cerebritis and abscess
 Mycobacterial
 Fungal
 Parasitic
 Spirochetes
 rickettsial
 Viral
Pyogenic Cerebritis and Abscess

 Bacterial infection – anerobes, strep. Staph, bacteroides

 Occur at any age: M>F more common
 Local spread- paranasal sinusitis, otomastoiditis,
trauma,surgery
 Haematogeneous – heart dx ( congenital, endocarditis),
lung dx ( abscess, bronchiectasis), immunosuppression.
These tend to occur at W-G junction – frontal or parietal
(CXR mandatory)
 Ventricular extension carries poor prognosis
Pyogenic Cerebritis and Abscess

 Stages:
1-early cerebritis 3-5 d
-poorly defined area of
necrosis- may be nl CT or
hypodense, mild mass effect
and patchy enhancement. MR
>CT nonspec hypo T1/hyper
T2, FLAIR,PD.
2-late cerebritis 1-2 wks
-thick, irregular wall
enhancement with vasogenic
edema.
Late Cerebritis
 Mass effect
 Zone of collagen and gliosis starts
developing peripherally; liquefied
necrosis intensifies centrally.
 Heterogeneous enhancement:
increased vascularization
 Increased T2, FLAIR, DWI at center.
No clear rim is noticed
 Surrounding vasogenic edema
Pyogenic Abscess
 3-early capsule
- capsule is made of
collagen and reticulins
-well defined rim
enhancement, low T2.
 4-late capsule
-better defined rim with
possible loculation,
- paramagnetic effect (hypo
T2, hyper T1)
-possible mesial thinning
- surrounding oedema
 DDx: Glioma, metastasis, TB
abscess, hematoma
Pyogenic abscess- MR Characteristics
 Capsule shows increased T1
intensity
 It is reduced inT2WI, FLAIR
 Abscess shows increased DWI
and dark in ADC
 Enhancing capsule on Gd
T1WI
 surrounding oedema
 MRS- acetate, lactate, alanine,
succinate,pyruvate in central
necrotic area
Parenchymal Tuberculosis

 Causative agent is Mycobacteria tuberculosis.

MAI(Mycobact Avium intracellulare) is also known to
cause tuberculous lesions.
 More common in setting of immunosuppresion
 Haematogeneous –mainly 2° to pulmonary infection
 Can present as caseating tuberculoma, non-caseating
tuberculoma or as TB abscess
 Parenchymal TB is less common than extra-axial and the
two co-exist frequently
 Supratentorial > infratentorial
Tuberculomas
 Can be single or multiple
 Start as form of cerebritis
then form granulomatous
complexes
 Caseating – solid or necrotic
center
 Mixed density
round/lobulated with mass
effect on CT.
 Solid or rim enhancing
 Can cause obstructive
hydrocephalus
Tuberculomas
MR Features
 Both T1 and T2 are prolonged
 Caseous centre may be of very
low signal on T2-weighted
images
 Enhancement is usually a thick
ring or solid
DDx- sarcoidosis, primary
neoplasms, metastases,
abscess
Tuberculous Abscess
 Rarely seen in immunocompentent
 Features resemble pyogenic abscess
 MRS- Prominent lipid, lactate but no amino acids

Cx- Hydrocephalus, ischaemia (TB can invade CNS vascular

structures)
Parasitic Infections
 Protozoal
 Cestodes
 Trematodes
 Nematodes
Protozoan
 Toxoplasmosis- as discussed under congenital infections
and AIDS.
 Amebic encephalitis – single/multiple multiple, focal
nodular or ring-enhancing. Diffuse edema is encountered
 Malaria- normal, diffuse cerebral oedema, focal infarcts
(cerebral, BG,thalami, cerebellar)
Cestodes (Tapeworms)
Cysticercosis
 Causative agent: T.solium (pork tapeworm)
 Man is usually definitive host in a complete life cycle
 Can also become intermediate host in case of ingestion
of eggs, whereby larvae (cysticerci) invade several body
tissues including the muscles and CNS.
 This is usually end stage for the developing larva.
Cysticercosis
cont
 Commonest CNS infection worldwide
 CNS involvement- cisterns> parenchyma>
ventricles(4th)
 Sellar, orbital and spinal cord involvement is also
documented
 Cysts- 5-20 mm with a scolex inside measures 1-4 mm
 4 stages of evolution/degeneration- vesicular, colloid
vesicular, granular -nodular and nodular(can occur
concurently)
Cysticercosis
cont
 Plain radiograph may show
Ca++ muscular cysts
 In the brain, imaging findings
depend on stage of evolution
 NCECT- vesicular: hyperdense
dot within cyst
- colloid vesicular: hyperdense
cyst fluid with surrounding
edema
-granular nodular: mild
edema
- granular calcified: small
Ca++ nodule
Cysticercosis
cont
 MR
 Protocols-T1,T2,FLAIR, Gd
enhanced, DWI,T2* GRE
 Vesicular – cyst isointense to
CSF, scolex is hyper
 Colloidal vesicular- cyst hyper
to CSF. Marked edema
 Granular nodular- thickened
retracted cyst wall
 Granular Ca++
Cysticercosis
cont
 Can be intravenricular
 When subarachnoid it can
form racemose (grape-
like) pattern
Hydatid cyst (dog tapeworm)
 Larval stage of dog tapeworm (E.granulosis)
 Sheep/cattle are intermediate hosts
 Human- feco-oral route: intestinal-portal-systemic
transport to organs like lung, omentum, muscles, CNS
forming trilaminal cyst.
 CNS cyst- solitary/multiple, unilocular, MCA territory.
Can be large (>6 cm)
Hydatid Cyst

 Plain radiograph may show

asymmetrical skull
enlargement
 Cross-sectional imaging shows
cyst – CSF density
 Mass effect
 Non-enhancing or mild
 May Ca++
 DDx- porencephalic cyst,
arachnoid cyst
Other Parasitic Infections
 Trematodes (flukes) eg.
Schistosomiasis,
paragonimiasis may form
granulomatous lesions within
the meninges and the
parenchyma.
 Nematodes (roundworms) eg
loa loa, Angiostrongylus
cantonensis and trichinosis
can also invade CNS with
granuloma formations and
sometimes larvae can be seen
 Spirochetes
Neurosyphilis
 Secondary / tertiary stages of infection with T.pallidum –
STD. 5% of untreated pts will develop CNS involvement
 Usually asymptomatic but may develop aseptic
meningitis, meningovascular disease, tabes dorsalis or
general paresis.
 CNS involvement favored in AIDS
 Meningovascular- Presents as acute stroke syndrome.
Thickening of meninges and medium to large vessel
arteritis. Gummas may also form in CNS.
Meningovascular Syphilis
 Infarcts of basal ganglia
 Can also affect WM,
Cerebral cortex ,
cerebellum
 Angiography shows
multiple occlusions
/constrictions and
aneurysm formation
Lyme Disease
 Spirochete: B. burgdorferi
 Transmitted by deer tick
 Skin (erythema
migrans),cardiac, arthritic,
neurologic involvement
 Multiple cranial nerve
involvement, VII commonest
 MR – Multiple small WM
lesions.
 DDx- MS, other
demyelinating diseases.
Rickettsial Diseases
 Zoonotic- squirrels, tick bite
 Rocky mountain spotted fever, Q-fever, typhus fever,
Mediterranean spotted fever
 Diagnostic clue: Ill-defined areas of low density on CT,
WM increased signal on T2WI with skin rash
 Diagnosis: histopathology, immunoflourescence.
 DDx- MS, Vasculitis, Sarcoidosis, Viral- HSE.
References
 www.radiopedia.org
 Diagnostic Imaging Brain- Osborn
 Grainger and Allisons Diagnostics
 Grainger & Allison’s Diagnostic Radiology 5th ED
 Thank you..