Lecture 11 - Pathology of CNS Infections Flashcards

1
Q

Acute Pyogenic Meningitis (aka Purluent Leptomeningitis) –

Age vs Organism

Neonates:
Infants/Children
adolescents/young adults
Elderly

Most common organism overall?

A

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

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2
Q

Purluent Leptomeningitis

  • Gross path
  • Histopath
  • How does it kill you?
  • labs/appearance of the CSF
  • symptoms
A

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

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3
Q
• Brain Abscess -- 
what is it?
what are the bugs?
what is seen on imaging? 
presentation?
Treatment?
Predisposing conditions?
A

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

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4
Q

what/where is a subdural empyema?

A
  • Subdural Empyema
    • Usually from infection on the skull

Pus accumulation in the subdural space; similar mass effect to subdural hemorrhage/hematoma

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5
Q

what/where is an epidural abscess?

treatment?

A
  • Epidural Abscess –
    • Usually spinal epidural; not cranial
    • Neurosurgical Emergency
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6
Q

Three types of TB infections of the CNS?

A

Tuberculous Meningtis

Tuberculoma

Pott Disease

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7
Q

Tuberculous Meningitis – what is it? where is it typically? therefore what are the findings? histopath what is seen?

A

reactivation TB

Usually at the base of the brain
therefore Cranial nerve signs

Histopath – Granuloma, multinucleated histiocytes, AFB positive (Zeil Neilson)

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8
Q

Tuberculoma

Pott Disease

A

Tuberculoma – walled off TB infection; caseous necrosis;

Pott disease –
○ TB of the spinal leading to pathologic fracture and deformity
○ Neurological compromise

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9
Q

Neurosyphilis —
what form of the disease ?

what are the two subtypes?

A

Tertiary form of the disease

Meningovascular Neurosyphilis

Parenchmatous

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10
Q

Meningovascular Neurosyphilis

– what is it ?

A
  • Inflammation of the leptomeninges;
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11
Q

Parenchmatous neurosyphilis ?

what are the two forms? pathogenesis and manifestations of each?

A

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

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12
Q

Viral Meningoencephalitis

  • general histopathology?
  • what viruses cause these generalized changes
A

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)
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13
Q

HSV 1

    • gross path?
    • tyically involves which lobes?
A

§ Hemorrhagic/necrotizing encephalitis mostly involving the Temporal Lobes

most common form of sporadic encephalitis

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14
Q

what 2 diseases cause loss of dorsal columns?

A

B12 deficiency (dorsal and lateral columns)

Tabes dorsalis

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15
Q

Cytomegalovirus

A

Brain – periventricular necrosis —

Also periventricular calcifications; which can be seen on X-ray

Path – Promintent Cytomegalic cells

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16
Q

Primary HIV infection -

Micropathology?

A

□ Meningo-encephalitis – cognitive motor complex;
® Multinucleated microglial — pathognomonic for HIV

Vaculoar Myelopathy – myeline damage of the spinal cord;

17
Q

Progressive Multifocal Leukoencephalopathy –

caused by what virus?
what population?
Gross path ?
Micropath?

A

J-C Virus
IC individuals
Involves the Oligodendrocyte specifically

“Moth eaten” white matter

Viral Inclusions in Oligodendrocytes + bizarre astrocytes

18
Q

Subacute Sclerosing Panencephalaitis

what virus?

A

Mutated Measles Virus

19
Q

Rabies

path findings?

A

Negri Bodies

Bullet shaped viruses by EM

20
Q

Fungal infections of the CNS:

who gets them? how do they spread?
what are the ones discussed in lecture?

A

IC patients
Hematogenous route

Cryptococcus neoformans
Candida Albicans
Aspergilus
Mucormycosis

21
Q

Cryptococcus neoformans

where will the disease present?

Stains for?
Gross path?

A

Meningitis +/- Parenchymal disease

can invade into the Virchow Robins spaces (perivascular spaces)

Stains for Mucin(mucicarimine) = Capsule

Gross Path of parenchyma = “soap bubbles”

22
Q

• Candida Albicans

  • gross path presentatin?
  • stain?
A

Multiple micro-abscesses in “shotgun pattern”

	○ Stain -- Silver for hyphae
23
Q

Aspergilus

micropath appearance?

pathologic damage and patient presentation?

A

§ Septate hyphae
§ Acute angles branching

	○ hemorrhagic  -- -predilection to invade and destroy blood vessels 

Multiple hemorrhagic infarcts in the brain

24
Q
Mucormycosis 
- micropath apperance
- who is most at risk? 
-where does the fungus attack?
- initial patient complaints? 
- Pathologic damage? 
- treatment? 
-
A

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

25
Poliomyelitis --- where does the disease damage? how does this manifest /
Anterior horn neuronal damage LMN Flaccid paralysis
26
What are the parasitic CNS infections we discussed in lecture?
Toxoplasmosis gondii -- Malaria Amebiasis Neurocysticercosis
27
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
28
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
29
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
30
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