Acute Bacterial Meningitis

How serious is it?

How does the patient present, and what do you need to do?

It's a medical emergency;  8-10% mortality even w/ rapid antimicrobial treatment

Patient presents w/ headaches, and classic sign of being unable to twist the neck without pain

1. Proceed w/ lumbar puncture below L2, discovery of purulent CSF

2. IMMEDIATELY start patient on broad spectrum Abs

3. Send CSF to culture to ID specific infection

Acute Bacterial Meningitis

What are the 3 most common pathogens responsible? Who are the primary targets for each of these pathogens?

ABM causes enhanced meinges at the top of the brain -- presents as headaches w/ no CN involvement and pus where CSF should be

Meningitis at the base of the brain is characteristic of TB: CN's leave thru base of brain, so a patient w/ headaches and deficits in CN IV, VI, or VII (facial nerve palsy) is more likely to have TB

The pia matter;  subarachnoid space filled w/ neutrophils indicates meningitis

But if inf goes untreated for too long, bact can breach the pia and cause permanent brain damage

via Secondary Vasculitis - infection damages BV's in the meninges over time, causing brain ischemia

Damage is almost always worse in meningeal encephalitis vs. just meningitis)

A. CNS:

• seizures
• altered mental status
• cerebral edema
  • due to vascular injury (blood)
  • hydrocephalus (CSF)
  • Swelling due to either can cause cerebral herniation!
• Cerebrovascular damage (infarcts, hemorrhage)
• CN deficits (deafness, weakness)

Meningococcal Septicemia

Characteristic clinical symptom? Then What?

Mortality?

Patients present w/ a petechial rash

Rapid progression to shock;  complete vascular collapse (BP hits the floor)

Mortality 40%

Waterhouse-Friderichsen Syndrome

What happens, and what is the physiologic cause?

What can you do for them?

Adrenal glands are undergoing hemorrhagic necrosis --> no corticosteroid prod/release --> complete BV dilation and complete vascular collapse

(no drug or amt of fluid you can give to restore BP)

Brain Abscess

What are 3 causes?

What sort of herniation may result from pressure caused by an abscess in the cerebellum

1. Contiguous infection

2. Hematogenous spread from a distant site

3. Cranial trauma or surgery

cerebellar abscess --> tonsillar herniation

(in general, abscesses --> increased ICP ---> Herniation ---> Death)

Contiguous infections resulting in Brain Abscess

4 locations infection can occur?

3 areas of the brain infection typically spreads to?

Infection in sinuses, teeth, middle ear, or mastoid --> mastoid cellar ruptures and inf enters CNS

Frontal lobe, temporal lobe, and cerebellum are most commonly affected

Hematogenous spread causing Brain Abscess

Where can inf spread from (example), and where does this inf spread to?

What are 3 things that happen during early Cerebritis (brain inf causing abscess formation)?

Describe the structure/contents of the abscess

Why does the abscess develop a very strong CT wall?

1. Vascular congestion

2. Infiltration of neutrophils

3. Edema

(gliosis is beginning)

Abscess is multi-layered, w/ edema and reactive astrocytes on the outside, granulation tissue 'capsule' w/ lymphocytes & plasma cells, then a pyogenic necrotic center

Angiogenesis originally occurs in response to necrosis (matrix deposition, collagen), but then the BV's regress and you're left w/ a firm CT wall

Neonatal Meningitis

How is inf usually aquired?

Name 5 potential pathogen culprits;  

How's the prognosis for neonatal meningitis, and why?

Inf usually comes from the maternal genital flora:

1. Group B strep

2. E. coli

3. Proteus

4. Listeria monocytogenes

5. Pseudomonas aeruginosa

Bad prognosis, because these gram negative bacteria are extremely destructive

Neurotuberculosis

How does it occur? Patient presents w/?

2 forms observed?

neuroTB is secondary to TB inf elsewhere in the body

Presents w/ CN defecits

Tuberculous meningitis

Tuberculoma

Neurotuberculosis

Gross pathology can display brain sections surrounded by exudate, hypoxic ischemic injury

Histo:  features Giant cells (granulomatous disease)

mycobacterium avium complex can infect CNS (occurs when co-infectedc w/ HIV)

Both MAC and TB can be visualized via acid-fast stain

Pott's Disease

Bony complication of TB;  affects spinal cord but not brain

REsults in kinking of the bony spinal column, causing paralysis over time

Whipple's Disease

Caused by what pathogen?

What is it/clinical characteristics

What other body system does it primarily infect, and affect?

CNS infection by a gram positive bacillus, Tropheryma whippelii

causes personality changes and dementia

Usually infects the GI tract and causes malabsorption

Neurosyphillis: Early

What happens?

Treponema pallidum invades CNS within first 2 years of inf

Results:  mild meningitis w/ lymphcytes & plasma cells

Meningovascular syphillis

General Paresis

Tabes Dorsalis

Characterisitcs of General Paresis Neurosyphillis

How long after inf does this occur?

Give 3 clinical symptoms, and 2 physiologic changes that cause these symptoms;

What is the 'hallmark' of general paresis?

usually occurs after 10-20 yrs of infection

Causes intellectual decline

irritability

seizures

Result of neuronal loss and microglial proliferation (the Hallmark)

Tabes Dorsalis Neurosyphillis

Physiologic changes in the CNS?

3 resulting symptoms (2 of which are directly related to one another)

Inflam in the dorsal roots and ganglia, w/ secondary degeneration of the posterior columns (for fine touch, vibration, proprioception)

Sx's

1. severe 'lightning pains' usually in the legs

2. Ataxia (loss of coordination) from loss of position sense --> damage to Charcot joints secondary to loss of sensation/proprioception (result of lumbering walk)

 Cryptococcus Neoformans 

How does it infect the CNS?

Where does it then reside in the CNS?

What type of lesion is common of cryptococcosis?

(Its the most common cause of fungal meningitis)

Organisms are inhaled -- most pulmonary infections are asymptomatic

Spreads from lungs -- blood -- brain, especially in immunocompromised

Infects the subarachnoid space,

and parenchymal tissue (brain tissue in this case)

Lesion is characteristically smooth and shiny

Candidiasis

Where are these found in the body?

Patients normally immunocompetent/compromised?

What pathology does it cause, and what does it look like histologically?

Candida spp are part of the normal intestinal flora

seen in immunocompromised

Causes microabscesses in the brain

Histologically, you can see the yeast & hyphae's in the brain (described as spaghetti and meatballs)

Aspergillosis

Infects immunocompetent/compromised?

Where are they found in the body?

What are 2 ways a person can become infected?

Aspergillus has a propensity to invade _____   _____ (body tissue);  What is the result?

How do you ID aspergillus histologically?

Can infect anyone, but infection becomes invasive when immunocompromised

Aspergillus are ubiquitous molds found in decaying vegetation

Patient either:

1. Inhales spores, producing primary infection

2. can occur thru direct inoculation in surgery or trauma

Apergillus has a propensity to invade blood vessels -- mechanical destruction as they move thru

Result: multifocal hemmorhage (visible in gross pathology)

Histologically, aspergillus is hyphae w/ septation at 45 degree angles

Mucormycosis

severity of inf?

What chronic disease do most infected patients have, and what is the associate predisposing factor to infection?

How does it spread to CNS? And in what areas surrounding the brain?

How does its appearance compare to aspergillus

Aggressive fungal inf

Most cases are in diabetics; ketoacidosis is the predisposing factor

fungus spreads along arteries behind nasal sinuses and into brain (also involves orbit, eye, and bone)

similar appearance to aspergillus, but hyphae are much larger and have no septation