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PATHOLOGY > CNS infections > Flashcards

CNS infections Flashcards

1
Q

what are the 4 routes of entry of CNS infections

A

Haematogenous

Direct implantation - via instruments

Local extension - secondary to established infections

PNS into CNS - virus

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2
Q

signs and sx of meningitis

A

fever

headache

stiff neck

some disturbance of brain function

vomiting

light aversion

drowsy

joint pain

fitting

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3
Q

agents that cause meningitis

A

neisseria meningitidis

streptococcus pneumoniae

Haemophilus influenzae

TB

various viruses

cryptococcus neoformans

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4
Q

pathophysiology of meningitis

A

Neuro damage by:

  • Direct bacterial toxicity - meningococcus in menignes -> infection
  • Indirect inflammatory process and cytokine release and oedema
  • Seizure, shock, and cerebral hypoperfusion
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5
Q

px of meningits

A

10% mortality

5% morbidity of survivors - neuro sequelae mainly sensineural deafness

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6
Q

signs and sx of encephalitis

A

disturbance of brain function

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7
Q

agents that cause encephalitis

A

rabies virus

arbovirus

trypanosoma species

prions

amoeba

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8
Q

signs and sx of myelities (affects spinal cord)

A

disturbance of nerve transmission

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9
Q

agent that causes myelitis

A

poliovirus

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10
Q

signs and sx of neurotoxin (affects CNS and PNS)

A

paralysis

rigid - tetanus

or flaccid - botulism

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11
Q

agents that cause neurotoxin

A

clostridium tetani

clostridium botulinum

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12
Q

what is meningitis

A

inflammatory process of
meninges and CSF

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13
Q

what is meningencephalitis

A

inflammation of meninges and
brain parenchyma

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14
Q

causes of acute meningitis in order of liklihood

A

Neisseria meningitidis
Streptococcus pneumoniae
Haemophilus influenzae
Listeria monocytogenes - old, poor immune system
GBS - colonise vagina, can go through microabrasions in baby head -> meningitis
E coli - vaginas -> neonatal sepsis

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15
Q

summarise neisseria meningitides

A

Infectious cause of childhood death in all countries.

Transmission is person-to-person, from asymptomatic carriers.

non-blanching rash in 80%

stains - A B C Y W135 - vaccines for all

1/2 present just as meningits
1/2 have some degree of septicaemia

Pathogenic strains are found in only 1% of carriers.

Cause infections in less than 10 days.

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16
Q

how can we reduce N meningitidis transmission

A

stop travel and contact

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17
Q

why is it important to differentiate between meningitis and septicaemia

A

patients who present with shock are treated differently than patients who present primarily with increased intracranial pressure (ICP).

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18
Q

pathophysiology of septicaemia

A

capillary leak:
* albumin and other plasma proteins -> hypovolaemia

coagulopathy -> bleeding and thrombosis
* Endothelial injury results in platelet-release reactions
* The protein C pathway.
* Plasma anticoagulants.
* no LP - because will clot - important to look at bloods before LP!!

metabolic derangement - esp acidosis

myocardial failure - multiorgan failure

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19
Q
A

severe meningococcal disease and purpura fulminans

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20
Q
A

meningococcal septicaemia

Amputation or skin grafting due to digital or limb ischemia is required in 2-5% of survivors

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21
Q

features of chronic TB meningitis

A

indolent
Week long presentation
Not associated with rash

more common immunocomp

involves meninges and basal cisterns of brain and spinal cord

Can become TB abscess/granulomas or cerebritis in brain

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22
Q

epidemiology of aseptic meningitis

A

most common infection of CNS

mostly children less than 1yr

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23
Q

sx of aseptic meningitis

A

headache

stiff neck

photophobia

nonspecific rash

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24
Q

causes of aseptic meningitis

A

by definition - absence of bacteria

Enteroviruses (e.g. Coxsackievirus group B and echoviruses) are responsible for 80-90% cases

herpes can spread haemtologically to meningitis

25
clinical course of aseptic meningitis
self-limited and resolves in 1-2 weeks.
25
viral causes of encephalitis
enterovirus herpes VZV
26
non-viral causes of encephalitis
Bacterial encephalitis - **Listeria monocytogenes** -worse mortality and morbidity than listeria meningitis **toxoplasmosis** Amoebic encephalitis * **Naegleria fowleri** fatal - Habitat: warm water * **Acanthamoeba** species, and **Balamuthia mandrillaris**, -> brain abscess, aseptic or chronic meningitis.
27
summarise toxoplasmosis as a cause of encephalitis
obligate intracellular protozoal parasite, **Toxoplasma gondii**. Via the **oral, transplacental route or organ transplantation**. Severe infection in **immunocompromised** patients. -> **brain parenchyma -> encephalitis** Affected organs include the **gray and white matter** of the brain, **retinas**, alveolar lining of the **lungs, heart, and skeletal muscle**.
28
what are the most fatal encephalitis(es)
virus and parasites are much worse than bacteria
29
transmission of viral meningitis
mosquitoes lice tics person to person
30
what is becoming the leading cause of encephalitis internationally
west nile virus
31
brain abscess
32
pathophysiology of brain abscess
Usually from **direct extension** mode of infection - ear, or mastoid process, or sinuses otitis media/mastoiditis/paranasal sinuses endocarditis/haematogenously Therefore it’s the **bugs that cause ear, mastoid or sinus infections**
33
microbes that cause brain abscesses
Streptococci (both aerobic and anaerobic) Staphylococci, Gram-negative organisms. (particularly in neonates) Mycobacterium tuberculosis fungi parasites Actinomyces and Nocardia species
34
summarise spinal infections
**Pyogenic vertebral osteomyelitis** common form of vertebral infection. transmission: * **Direct open spinal trauma**, * **infections in adjacent structures**, * **hematogenous spread** of bacteria to a vertebra. - IVDU staph aureus septicaemia spread to spine Px - Left untreated, it can lead to: * **permanent neurologic deficits**, * significant **spinal deformity**, * **death.** Finate space around spine - so even small abscess have bad sequaelae
35
RF for spinal infections
Advanced age Intravenous drug use Long-term systemic steroids Diabetes mellitus Organ transplantation Malnutrition Cancer
36
Ix for CNS infections
MRI (CT cant see meninges - just if SOL in parenchyma) CSF biopsy blood culture throat swab * strep pneumoniae - 1 in 5 carry in nasopharynx * meningococcus - 1 in 20 carry in nasopharynx
37
what do you comment on in CSF studies
Color/Clarity Cell counts Chemistry * (Protein/ Glucose) Stains * (Gram/ Auramine(ZN)/ India Ink) Cultures * (bacterial, fungal, TB) PCR
38
how many white cells in CSF is normal
less than 5
39
what does neutrophils in CSF mean
bacteria
40
what does lymphocytes (PMN) in CSF mean
viral
41
what is india A stain for
cryptococcus
42
main differentials for these:
43
gram +ve cocci - pneumococcus
44
Gram negative cocci- meningococcus
45
Gram positive rod- Listeria
46
Ziehl-Neelsen stain- TB
47
cryptococcus
48
Limitations of diagnostics for CNS infections
MRI oedema pattern and moderate mass effect cannot be differentiated from tumor or stroke or vasculitis in some patients. Infections in early stages and serological tests. Amount of CSF. PCR techniques. Methods to detect amoebic infections. Availability of good laboratory technique.
49
time frame for investigations for CNS infection
50
Mx of meningitis - need to know dose
**Ceftriaxone 2g iv bd** If >50yrs or immunocompromised add: **Amoxicillin 2g iv 4hourly** - cover listeria
51
mx for meningoencephalitis - need to know dose
**Aciclovir 10mg/kg** **iv** tds **Ceftriaxone 2g iv** bd If >50yrs or immunocompromised add: **Amoxicillin 2g iv 4hourly**
52
mx s pneumoniae
Pen G 18-24 mu/d or Amoxicillin 12 g/d or Ceftriaxone 4 g/d or Chloro 75-100 mg/kg/d
53
mx n meningitides
Pen G 18-24 mu/d or Amoxicillin 12 g/d or Ceftriaxone 4 g/d or Chloro 75-100 mg/kg/d
54
mx H influenzae
Cefotaxime 12 g/d or Ceftriaxone 4 g/d
55
mx GBS
Pen G or Amoxicillin [plus aminoglycoside]
56
mx listeria
Amoxicillin 12 g/d plus aminoglycoside
57
mx gram -ve bacilli
Cefotaxime 12 g/d or Ceftriaxone 4g/d
58
mx pseudomonas
Meropenem 6g/d or Ceftazidime 6g/d

PATHOLOGY (94 decks)

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