acute non viral infections bacterial fungal parasitic

Acute non viral infections

• Bacterial

• Fungal

• Parasitic

Bacterial Infections of the CNS

• Neonatal bacterial meningitis– Common organisms

• Gram negative bacilli

• Streptococci

– 30-60% mortality– Significant long-term morbidity 35%

Common etiologic agents of bacterial meningitis

• Most common– Neisseria meningitidis– Group B Streptococcus

• Other Gram Positive– Listeria monocytogenes– Staphylococcus aureus

• Other Gram Negative– E. Coli– Citrobacter– Klebsiella– Pseudomonas– Proteus– Salmonella

Bacterial meningitis: Gross findings

• Edematous brain +/- herniation

• Hemorrhage and infarction• Opacity of meninges

– Subdural empyema

• Ventriculitis• Obstructive hydrocephalus

From: Neuropathology Illustrated 1.0

Meningitis


Vessels cuffed by leukocytes

Empyema


Skull

Pus

Bacterial meningitis: Microscopic findings

• Meningeal infiltrate with abundant neutrophils macrophages, fibrin and cell debris

• Extension into the Virchow-Robin space

• Vascular thrombosis and infarction (more common in neonates)


Brain Abscess: Clinical

• Increasing CNS pressure + localizing signs

• If direct spread: frontal or temporal lobes

• Hematogenous spread: gray-white junction

• 50% morbidity– 20% mortality

Brain Abscess: Pathogenesis

• Half result from direct spread from sinus– Etiology

• Streptococcus, Bacteroides, Actinomyces, aerobic gram negative bacilli

• 25% result from hematogenous spread– Children with congenital heart defects– Adults lung abcess or endocarditis

• Streptococcus

– Etiologies:• Toxoplasma, Nocardia, Listeria, Gram negative bacilli,

mycobacteria, fungi

CT: Ring enhancing mass

Well encapsulated abscess

From: Neuropathology Illustrated 1.0From: Neuropathology Illustrated 1.0

Brain Abscess: Microscopic progression

• 1-2 days: suppurative encephalitis

• 2-7 days: focal encephalitis with central necrosis

• 5-14 days: early encapsulation


Epidural abscess

• Mostly in spinal canal

• Biconvex shape on MRI

• Direct extension most common

• Staphylococcus aureus

Tuberculosis meningitis

• Diffuse symptoms over 2-3 weeks– Later cranial nerves involved or increased CSF pressure

– Decreased glucose and increased protein

– PCR of CSF is diagnostic

• Gelatinous subarachnoid exudate– Sylvian fissure and base of brain

– +/- tubercles with focal findings• Abundant macropahges and necrotizing granuloma


Fite stained mycobacteria

Leptomeningeal inflammation

Tuberculosis meningitis

Syphilis

• Asymptomatic CNS involvement– CSF pleocytosis

• Meningitis– 1-2 years post primary infection– Rarely symptomatic

• Meningovascular syphilis– Peak incidence 7 years post primary infection– Chronic meningitis and multifocal arteritis

• Parenchymatous neurosyphilis and Tabes Dorsalis– Peak incidence 10-20 years after initial infection– General paresis of the insane

• Gummatous neurosyphilis


Chronic infarcts secondary to end-arteritis

Plasmacytic infiltrate Spirochetes

Parenchymatous neurosyphilis

Lyme Disease

• Borrelia burgdorferi

• Stage 1: Days to weeks– Maculopapular rash

• Stage 2: Weeks to months– Meningitis with cranial nerve palsies

• Stage 3: Months to years– Axonopathy, encephalopathy, polyarthritis

Fungal Infections of the CNS• Usually associated with immunosuppression• Mostly hematogenous dissemination

– Rare direct extension (mucormycosis)

• Yeasts - Leptomeningitis• Hyphae - Hemorrhagic infarcts


Aspergillosis

• Airborne spores from soil– Hemtogenous from lung– Direct extension from paranasal sinuses

• Necrotizing angiitis

• Usually CSF without detectable bug

Aspergillosis

From: Neuropathology Illustrated 1.0Branched Hyphae

Grocott Stain

H&E

Mucormycosis• Most common form: Rhinocerebral

– Direct extension from sinuses

– Poorly controlled diabetic

• Hematogenous dissemination of Mucor is less common but usually from lung


Early Abscess

Broad Hyphae

Cryptococcosis• Primary infection is usually pulmonary• Meningitis versus abscess

– Dilation of Virchow-Robin Space


Cryptococcosis• Encapsulated organism

• Stains with PAS & Mucicarmine

Encapsulated organisms


Candidiasis• Usually systemic nidus

– Intestinal overgrowth secondary to antibiotics

– Catheterization or surgery

• Seldom in immunologically intact• Microabcesses with hematogenous dissemination


Grocott

Pseudo Hyphae

Coccidioidomycosis or Histoplasmosis

• Soil organisms

• Inhaltion leades to primary pulmonary nidus– Pregnancy, diabetes or other immunosuppression


Encapsulated 50 micron cyst

Parasitic Infections

• Amebic Infections– Cerebral amebic abscess– Primary amebic meningoencephalitis– Granulomatous amebic encephalitis

Cerebral amebic abscess

• Entamoeba histolytica– Common intestinal parasite– CNS abscess is rare and late complication– Hematogenous dissemination of trophozoites– Trophozoites identifiable in abscess wall

Primary amebic meningoencephalitis

• In immunocompetent host, etiologic agent– Naegleria fowleri– Ubiquitous environmental contaminant that

seeds nasal passages• Follows swimming in fresh water

– Ascends into CNS through cribiform plate– Acute fulminant presentation with death in 72

hours

Amoebic Encephalitis



Nucleated amoebae

Hemorrhagic encephalitis

Granulomatous amebic encephalitis

• In immunocompromised host– Acanthamoeba or Balamuthia madrillaris

• Hematogenous dissemination into CNS from lower respiratory tract or skin

– Subacute or chronic disease• Focal deficits or seizures

• Usually fatal

Cerebral Malaria• Any of four species of malaria• 1-10% of P. falciparum have CNS

involvement– Usually in children– Incubation period 1-3 weeks– Clinical presentation secondary to increased

intracerebral pressure

• Pathogenesis– Occlusion of CNS capillaries by infected

RBCs– Mortality 20-50%


Blood vessel with infected RBCs

Cerebral Toxoplasmosis: Postnatally-acquired

• Definitive host is cat• Infection of immunocompetent human is

asymptomatic– High seropositivity (20-40% in US)

• CNS disease associated with compromised cell mediated immunity

• Ring enhancing lesions• Pathology:

– Necrotizing abscesses with coagulative necrosis and PMNs

Cerebral Toxoplasmosis


CT Multiple abscesses

Basal ganglia abscess

Toxoplasmosis



Immunostained Tachyzoites

H&E Tachyzoites

Cerebral Toxoplasmosis: Congenital

• Only a minority of cases show classical triad– hydrocephalus, calcifications and chorioretinits

• Results from transplacental spread in primary maternal infection

• Pathology– Multifocal necrosis

• Periventricular and sub-pial

• tachyzoites

– Microcephaly

Cysticercosis

• Commonest parasitic infection of CNS– Larval form of pork tapeworm Taenia solium– Humans are usually definitive host– Pig intermediate host

• Cysts = Cysticerci most commonly in muscle– 1-2 cm in diameter with single scolex– Calcifies

Cysticercosis


H&E ScolexMRI Multiple cysts

Schistosomiasis

• Man definitive host– Adult schistosomes inhabit

blood vessels– Large numbers of ova in blood

• CNS involvement rare– Retrograde passage of ova

though pelvic veins– Spinal cord involvement


acute non viral infections bacterial fungal parasitic

Documents

base of brain

mortalitybrain abscess

skullpusbacterial meningitis

signsif direct spread

increased proteinpcr

pathogenesishalf result

hematogenous spreadchildren

microscopic progression1