Lecture 11 - Pathology of CNS Infections Flashcards
Acute Pyogenic Meningitis (aka Purluent Leptomeningitis) –
Age vs Organism
Neonates:
Infants/Children
adolescents/young adults
Elderly
Most common organism overall?
Neonates - Escherichia coli, group B streptococci (GBS)
Infants & children - Streptococcus pneumoniae
Adolescents & young adults (mini-epidemics, e.g. military recruits, dorms) - Neisseria meningitidis
Elderly - Streptococcus pneumoniae, Listeria monocytogenes
most common overall – Strep Pnmeumo
Purluent Leptomeningitis
- Gross path
- Histopath
- How does it kill you?
- labs/appearance of the CSF
- symptoms
Gross Path: purlence of the SA space; inflammatory reaction can lead to death
Neutrophils around blood vessles leading to obstruction and necrosis
Symptoms: HA, Photophobia, nuccal rigidity, irritabilibty
Labs of CSF: cloudy appearnace;
high proteins but low glucose
• Brain Abscess -- what is it? what are the bugs? what is seen on imaging? presentation? Treatment? Predisposing conditions?
Predisposing conditions – bacterial endocarditis, cyanotic congential heart disease (right to left shunt), chronic pulmonary sepsis; dental procedures
Bugs: Streptocci, Staphylococci
Variable Presenation – can be focal or global – depending on where the abscess is
Treatment – surgical if large enough — + abx
Path: Pus filled lesion; hyperemic margin
Imaging: Ring enhancement (vasogenic edema) on imaging
what/where is a subdural empyema?
- Subdural Empyema
- Usually from infection on the skull
Pus accumulation in the subdural space; similar mass effect to subdural hemorrhage/hematoma
what/where is an epidural abscess?
treatment?
- Epidural Abscess –
- Usually spinal epidural; not cranial
Three types of TB infections of the CNS?
Tuberculous Meningtis
Tuberculoma
Pott Disease
Tuberculous Meningitis – what is it? where is it typically? therefore what are the findings? histopath what is seen?
reactivation TB
Usually at the base of the brain
therefore Cranial nerve signs
Histopath – Granuloma, multinucleated histiocytes, AFB positive (Zeil Neilson)
Tuberculoma
Pott Disease
Tuberculoma – walled off TB infection; caseous necrosis;
Pott disease –
○ TB of the spinal leading to pathologic fracture and deformity
○ Neurological compromise
Neurosyphilis —
what form of the disease ?
what are the two subtypes?
Tertiary form of the disease
Meningovascular Neurosyphilis
Parenchmatous
Meningovascular Neurosyphilis
– what is it ?
- Inflammation of the leptomeninges;
Parenchmatous neurosyphilis ?
what are the two forms? pathogenesis and manifestations of each?
General paresis – infiltration of the brain by the spirochete itself, leading to dementia (very rare now)
Tabes Dorsalis – damage to the dorsal root sensory nerves with impaired sensation and absence of DTRs
Viral Meningoencephalitis
- general histopathology?
- what viruses cause these generalized changes
virus has invaded into the parenchyma;
Histopath – Viruses in General
perivascular and perenchymal mononuclear infiltrates, microglial nodules
- Arthropod borne viral encephalitis (equine, west nile virus, HSV2)
HSV 1
- gross path?
- tyically involves which lobes?
§ Hemorrhagic/necrotizing encephalitis mostly involving the Temporal Lobes
most common form of sporadic encephalitis
what 2 diseases cause loss of dorsal columns?
B12 deficiency (dorsal and lateral columns)
Tabes dorsalis
Cytomegalovirus
Brain – periventricular necrosis —
Also periventricular calcifications; which can be seen on X-ray
Path – Promintent Cytomegalic cells
Primary HIV infection -
Micropathology?
□ Meningo-encephalitis – cognitive motor complex;
® Multinucleated microglial — pathognomonic for HIV
Vaculoar Myelopathy – myeline damage of the spinal cord;
Progressive Multifocal Leukoencephalopathy –
caused by what virus?
what population?
Gross path ?
Micropath?
J-C Virus
IC individuals
Involves the Oligodendrocyte specifically
“Moth eaten” white matter
Viral Inclusions in Oligodendrocytes + bizarre astrocytes
Subacute Sclerosing Panencephalaitis
what virus?
Mutated Measles Virus
Rabies
path findings?
Negri Bodies
Bullet shaped viruses by EM
Fungal infections of the CNS:
who gets them? how do they spread?
what are the ones discussed in lecture?
IC patients
Hematogenous route
Cryptococcus neoformans
Candida Albicans
Aspergilus
Mucormycosis
Cryptococcus neoformans
where will the disease present?
Stains for?
Gross path?
Meningitis +/- Parenchymal disease
can invade into the Virchow Robins spaces (perivascular spaces)
Stains for Mucin(mucicarimine) = Capsule
Gross Path of parenchyma = “soap bubbles”
• Candida Albicans
- gross path presentatin?
- stain?
Multiple micro-abscesses in “shotgun pattern”
○ Stain -- Silver for hyphae
Aspergilus
micropath appearance?
pathologic damage and patient presentation?
§ Septate hyphae
§ Acute angles branching
○ hemorrhagic -- -predilection to invade and destroy blood vessels
Multiple hemorrhagic infarcts in the brain
Mucormycosis - micropath apperance - who is most at risk? -where does the fungus attack? - initial patient complaints? - Pathologic damage? - treatment? -
No septated hyphae; branch at 90 degree
Multiple hemorrhagic infarcts in the brain
Dm patients in DKA
Rhinocerebral Mucomycosis
patients present with vague orbital complaints. Rapidly progresses
Requires Urgent radical resection
Poliomyelitis — where does the disease damage? how does this manifest /
Anterior horn neuronal damage
LMN
Flaccid paralysis
What are the parasitic CNS infections we discussed in lecture?
Toxoplasmosis gondii –
Malaria
Amebiasis
Neurocysticercosis
Toxoplasmosis gondii –
who gets this disease? how is it acquired ?
what is the typical presentatin?
what is the differential?
IC patients; cat feces contact
HIV patient with motor signs; weakness, seizure
lymphoma vs toxoplasmosis
Malaria
- which organism can cause cerebral malaria?
presentation?
pathologenseis?
gross path
micro path
P. Falciarium
Brain swelling, mass effect;
Malarial organisms induce molecular adhesion of the RBC to the endothelium
Gross path: Peteical lesions
MIcro path: infected RBCs
Amebiasis: PAM vs GAE
PAM –organism? how is it acquired? prgoression of disease?
GAE – organisms? how do they spread to the brain? from where?
Primary Amebic Meningoencephalitis (PAM)– Naegleria Fowleri –
Warm water; enters through nose –> cribriform plate –> death in 2 days
Granulomatous encephalitis (GAE)
- acanthameba, B. mandrillaris);
spreads hematogenously to brain from lung
Neurocysticercosis
Organism?
briefly describe lifecycle
common presenting symptom?
taenia solium
human ingest the larvae and matures into the adult tape worm
Most common worldwide cause of seizures
