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PT2 B1 > Lecture 11 - Pathology of CNS Infections > Flashcards

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
Q

Poliomyelitis — where does the disease damage? how does this manifest /

A

Anterior horn neuronal damage
LMN

Flaccid paralysis

26
Q

What are the parasitic CNS infections we discussed in lecture?

A

Toxoplasmosis gondii –
Malaria
Amebiasis
Neurocysticercosis

27
Q

Toxoplasmosis gondii –

who gets this disease? how is it acquired ?

what is the typical presentatin?

what is the differential?

A

IC patients; cat feces contact

HIV patient with motor signs; weakness, seizure

lymphoma vs toxoplasmosis

28
Q

Malaria

  • which organism can cause cerebral malaria?

presentation?

pathologenseis?
gross path
micro path

A

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
Q

Amebiasis: PAM vs GAE

PAM –organism? how is it acquired? prgoression of disease?

GAE – organisms? how do they spread to the brain? from where?

A

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
Q

Neurocysticercosis
Organism?

briefly describe lifecycle

common presenting symptom?

A

taenia solium

human ingest the larvae and matures into the adult tape worm

Most common worldwide cause of seizures

PT2 B1 (38 decks)

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