1. Perivascular cuffing

2. neuronophagia -- inflam cells eating up neural tissue

Herpes Simplex Infection of the CNS

Describe HSV1 and HSV2 in terms of their affects on the CNS;  What clinical findings indicate HSV CNS infection?

What if you initially expect its a tumor, and not HSV inf?

HSV2:  causes recurrent viral meningitis (every month or so)

HSV1 is much more deadly;  Patient presents w/ headaches (possible fever), and MRI shows temporal lobe hemorrhage (around the insula) and/or CSF shows hemorrhage 

Treat instantly w/ antivirals, very time-sensitive just like acute bact meningitis

Does NOT matter if you think its a tumor, the tumor probably wont kill them in the next few hours, but the HSV encephalitis could; be safe and treat it like an HSV1 infection

HIV Leukoencephalopathy

2 gross pathological findings?

Histopath finding?

1. Loss of myelin, this area shows up white on an otherwise blue/purple myelin-stained brain (why its called leuko (white) encephalopathy)

2. Dilated ventricle, rounded edges rather than sharp --> due to hydrocephalus

Histopath:  Multinucleated giant cell (carries virus to the brain from another body location)

Pediatric HIV

Characteristic MRI finding?

Why does this limit your Dx to HIV?

Angiocentric Mineralization Deposits - abundant mineralization around BV's, visible by MRI

Because kids arent nearly as likely to have an opportunistic inf (much less exposure), this is a pretty clear sign of HIV

Cytomegalovirus (CMV, HSV5)

Affects CNS/PNS/both?

Give 6 possible infections of the NS by CMV

Affects both

CNS:

Disseminated Meningo-encephalitis

Ependymitis

Choriod Plexitis

PNS:

Polyradiculitis (inflam of the nerve roots)

Polyneuritis

Sensory Ganglionitis

CMV Ventriculitis

Describe;

How does the name cytomegalovirus help you remember the histopathology?

Infection and inflammation cause the ventricles to become swollen and hemmorhagic w/ reddish irregular borders

Histopath features large inclusions, infection increases the size of cells, think cyto-MEGAlo-virus

CMV Encephalitis 

How does CMV get into the CNS?

Does CMV always involve the ventricles?

CMV gets in the blood, then infects the choroid plexus cells, which are subsequently shed into the ventricle

CMV doesn't exclusively affect the ventricles, could cause aggressive necrotizing lesions

CMV in the PNS

2 characteristics of PNS inf

1. Cytoplasmic inclusions

2. Schwan cells infected

Congenital CMV Infection

How does this happen?

3 symptoms/clinical presentations (2 neuro, 1 non)

This is a CMV infection through the placenta; different from HIV compromised kids contracting a primary infection

Sx:

Hepatosplenomegaly

Mental Retardation

Microcephaly

Amebic Meningoencephalitis

Seen in immunocompetent/compromised?

What type of pathogen causes this?

Give the 3 specific Amoebae causing this disease

Can equally affect the immuno-complement

A protozoan infection disease:

Naegleria fowleri

Acanthamoeba

Balamuthia mandrillaris

Naegleria fowleri-associated Disease

Where is this protoza found, and how does it infect the CNS?

Progression of 9 symptoms.

What is the severity/time course of the disease following infection?

Found in warm lakes, it crawls into your nose and burrows thru the cribriform plate, follows olfactory nerves then invades the brain

Symptoms:  Headache, sore throat, runny nose, olfactory problems

then vomiting, stiff neck, lethargy, confusion

then coma and death

Meningoencephalitis (acute, suppurative infection of the CNS) is very deadly and causes death rapidly, 5-7 days

Its the most deadly CNS infection apart from rabies

Acanthamoeba

3 diseases caused by this protozoan

Time course/severity?

Granulomatous encephalitis

Uveitis (inflam of uvea area of eye)

Keratitis (inflam of cornea)

if encephalitis, patient will die in 6 weeks

1. pyogenic abscesses formed throughout the brain

2. Hemorrhage

3. Protozoa themselves are round w/ central nuclei, look somewhat like MP's

4. Perivascular inflammation 

Granulomatous Encephalitis

(but we have know idea where its found in the environment!)

Granulomatous Encephalitis

How does its progression compare w/ Meningoencephalitis?

4 associated, non neural symptoms?

4 CNS gross pathology identifiers?

Can you examine CSF to aide your diagnosis?

Status of many patients that increase their susceptibility (3)

Time course/prognosis?

More slowly progressive infection

Non-neuro Sx's:

Subcutaneous nodules

eye or skin inf

progressive nasal congestion

headache

CNS:

Multiple ring enhancing lesions

Granulomatous inflammation

hemorrhagic necrosis

vasculitis

Ameba are rarely seen in the CSF

Many patients are either alcoholic, debilitated, or immunocompromised

Death within 6-8 weeks of diagnosis (but symptoms may date back several months)

Give anti-Toxoplasma meds first, check to see if lesions get smaller

If not, it could be lymphoma, you need a biopsy

Toxoplasma Gondii

What are histopath findings in toxo inf?

they are obligate intracellular parasites, must be very infective in order to stay alive

Perivascular lymphocytic cuffing, inflam w/ possible necrosis

Cysticercosis

Caused by what parasite?

What must you additionally do to a patient while attempting to rid them of this infection?

Taeniae Solium

Must add corticosteroids to treatment regimen;  treatment to kill orgs can cause an allergic reaction in patients, can be very dangerous, we want to limit allergic response