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NMSP 1 > CNS Infections > Flashcards

CNS Infections Flashcards

1
Q

What are the four principle routes of CNS infection?

A
  • hematogenous (most common, primarily arterial)
  • direct implantation (trauma, congenital malformations)
  • local extension (sinuses, teeth, osteomyelitis)
  • PNS (rabies, herpes zoster)
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2
Q

How does CSF contribute to brain infections?

A
  • a complete exchange of CSF every 3-4 hours means that soon after infection, the brain is bathed in bacteria
    note: 85% of the CSF is produced by the choroid plexus of the 3rd and 4th ventricles
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3
Q

How does TB meningitis occur?

A

-subepidural or submeningeal granulomas seed CSF

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4
Q

True or False: the CSF has lymphatics

A

False; but the epidural space has lymphatics.

Infections of the retropharyngeal space, posterior mediastinal space, or retroperitoneal space may produce spinal epidural abscesses.

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5
Q

How do HSV and herpes zoster infect the CNS?

A
  • they product latent infections of sensory ganglia
  • replicate in Schwann cells
  • ascend to the CNS within SENSORY nerves
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6
Q

How does rabies infect the CNS?

A

-virus bind at/near Ach receptors at the neuromuscular junction and ascend to the CNS via MOTOR nerves

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7
Q

What is the main way that molecules move across the capillary wall into the brain?

A
  • active transport

- lipid solubility

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8
Q

True or False: capillaries in the brain are permeable to immunoglobulins, complement and abx

A

False; capillaries are relatively IMpermeable

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9
Q

True or False: when referring to bacterial meningitis and many viral encephalidites, widespread infection involving all tissue elements is characteristic

A

True

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10
Q

What is the major determinant of the characteristic neurological symptoms associated with different infectious agents?

A

–which cell types and/or anatomic area is involved

–different cell populations and different neuro-anatomical regions have different functional specializations

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11
Q

What are the categories of meningitis and their cause?

A

Chemical Meningitis: nonbacterial irritant in subarachnoid space

Acute Pyogenic Meningitis: bacterial

Aspetic Meningitis: acute or subacute viral (you’ll see lymphocytes in the CSF)

Chronic: TB, spirochetes (neurosyphilis and neuroborreliosis), cryptococcus

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12
Q

What is meningoencephalitis?

A

inflammation of the meninges and brain parenchyma

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13
Q

What does pyogenic meningitis look like on gross exam, which organisms are commonly associated with it, and what might you see on PE?

A
  • suppurative exudate covering brainstem and cerebellum
  • TB and syphilis

-papilledema d/t thickened leptomeninges not letting CSF circulate properly

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14
Q

What is the cause of cerebral edema?

A

–infection/inflammation cause loss of capillary integrity and the blood-brain barrier

–transudation of intravascular fluid into brain and spinal cord

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15
Q

What accelerates cerebral edema and what is a possible treatment for cerebral edema?

A

–accelerated by products released by living bacteria and by abx-lysed bacteria

Tx: corticosteroids slow and reverse process

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16
Q

What are the symptoms of acute meningitis?

A
  • HA, +Kernig, +Brudzinski, high fever, confusion, coma

- can develop over several days or just a few hours

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17
Q

What is the most common location for exudate in Pneumococcal meningitis and a possible complication of the infection?

A

over convexities near sagittal sinus

possible complication: chronic adhesive arachnoiditis d/t capsular polysaccharides (“sticky”)

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18
Q

What is the most common location for exudate in H. flu meningitis?

A

basal location

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19
Q

What do you see on histology of acute suppurative meningitis?

A

PMN’s filling the subarachnoid space

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20
Q

What is focal cerebritis?

A

-when inflammatory cells infiltrate walls of the veins and extend into the brain substance

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21
Q

What is ventriculitis?

A

-fulminant infection w/ inflammation extending into the ventricles

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22
Q

What are possible complications of phlebitis in a neuro setting?

A

-can lead to venous thrombosis and hemorrhagic infarction of the underlying brain

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23
Q

What is a complication of leptomeningeal fibrosis?

A

hydrocephalus

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24
Q

What are possible complications of bacterial meningitis?

A
  • seizures
  • encephalitis
  • hearing loss
  • blindness
  • paralysis
  • fulminant rash
  • adrenal hemorrhage (Waterhouse-Friderichsen)
  • death
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25
Q

What are the symptoms of Waterhouse-Friderichsen Syndrome?

A
  • rapidly progressive hypotension leading to shock
  • DIC associated w/ widespread purpura of the skin
  • rapidly developing adrenocortical insufficiency

-more common in children

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26
Q

What tests should be performed when meningitis is suspected?

A
  • lumbar puncture w/ Gram stain of CSF
  • culture of CSF and blood
  • Ag detection in CSF and urine
  • PCR on CSF
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27
Q

What is the Gram stain of N. meningitidis?

A

Gram negative diplococci

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28
Q

What is the Gram stain of Strep pneumo?

A

Gram positive diplococci

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29
Q

What is the Gram stain of H. flu?

A

Gram negative pleomorphic (rods)

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30
Q

What is the Gram stain of Staph aureus and Staph epidermidis?

A

Gram positive cocci

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31
Q

What is the Gram stain of E. coli?

A

Gram negative bacilli

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32
Q

Where is the needle inserted in a lumbar puncture?

A

b/w the 3rd and 4th lumbar vertebrae

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33
Q

What are the characteristics of CSF in bacterial meningitis?

A
  • cloudy/turbid
  • neutrophils
  • markedly decreased glucose
  • moderately increased protein
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34
Q

What are the characteristics of CSF fluid in viral meningitis?

A
  • clear/colorless
  • lymphocytes/monocytes (early stage is PMN’s)
  • normal glucose
  • slightly elevated protein
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35
Q

What are risk factors for developing meningitis?

A
  • age <5yrs or >60yrs
  • DM
  • immunosuppression
  • contiguous infection (ex: sinusitis)
  • IV drug use
  • bacterial endocarditis
  • sickle cell
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36
Q

What are the most common pathogens for meningitis in neonates?

A
  • Group B Strep

- E. coli

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37
Q

What is the most common pathogen for unvaccinated young children?

A

H. flu

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38
Q

What is the most common pathogen for meningitis among adolescents and young adults?

A

Neisseria

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39
Q

What are the most common pathogens for meningitis in the elderly?

A
  • Strep pneumo

- Listeria

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40
Q

What are the most common pathogens for meningitis in immunocompromised patients?

A
  • Strep pneumo
  • Neisseria
  • Listeria
  • Pseudomonas
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41
Q

What are common pathogens for meningitis in a basilar skull fracture?

A
  • -Strep pneumo
  • -H. flu
  • -Group A beta-hemolytic Strep
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42
Q

What are common pathogens for meningitis post-surgery or w/ head trauma?

A
  • -Staph aureus and Staph epidermidis

- -aerobic Gram-negative bacilli (ex: Pseudomonas)

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43
Q

What are common pathogens for meningitis in pt’s w/ a CSF shunt?

A
  • -Staph epidermidis and Staph aureus
  • -aerobic Gram-negative bacilli ex: Pseudomonas)
  • -Proprionibacterium acnes
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44
Q

What conditions would put pt’s at risk of a brain abscess?

A
  • acute bacterial endocarditis (multiple abscesses)
  • chronic pulmonary sepsis (bronchiectasis)
  • systemic dz w/ immunosuppression
  • congenital heart dz
  • -ex: R to L shunt removes pulmonary filtration
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45
Q

What pathogens are the most common causes of brain abscesses in non-immunocompromised pt’s?

A
  • Strep

- Staph

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46
Q

How does a patient present with a brain abscess?

A
  • progressive focal neurological deficits
  • symptoms of increased intracranial pressure
  • -HA, vomiting, AMS, papilledema
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47
Q

What is the composition of the CSF when a pt has a brain abscess?

A
  • high WBC
  • high protein
  • normal glucose
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48
Q

What are possible complications of a brain abscess?

A
  • abscess rupture w/ ventriculitis or meningitis

- venous sinus thrombosis

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49
Q

What is the Tx for a brain abscess?

A
  • surgical drainage
  • abx

-<10% mortality w/ proper Tx

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50
Q

What is a subdural empyema?

A

-bacterial or fungal infection of skull bones or sinuses that spreads to the subdural space (arachnoid and subarachnoid usually not affected)

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51
Q

What is a complication of a subdural empyema?

A

thrombophlebitis of bridging vessels and infarction

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52
Q

What are the symptoms and CSF finding of a subdural empyema?

A
  • progressive focal neurological deficits
  • symptoms of increased intracranial pressure
  • -HA, vomiting, AMS, papilledema

CSF: high WBC, high protein, normal glucose

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53
Q

What is the Tx for a subdural empyema?

A
  • surgical drainage
  • thick dura is the only residual evidence

untreated: lethargy, coma

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54
Q

What is the common cause of an extradural abscess?

A

osteomyelitis

-an extradural abscess of the spine may cause spinal cord compression (neurosurgical emergency)

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55
Q

How is Neisseria meningitidis spread?

A
  • colonizes the oropharynx and rhinopharynx of asymptomatic carriers (colonization may be 2-3%, but may be higher in crowded populations like dorms)
  • direct contact w/ contaminated resp. secretions
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56
Q

What is the clinical presentation of a pt. w/ meningitis d/t N. meningitidis?

A
  • rapidly progressive septicemia
  • fever
  • hypotension
  • DIC
  • petechial and purpuric lesions
57
Q

How might the purpuric lesions of N. meningitidis progress?

A
  • purpura fulminans

- -hemorrhagic skin lesions which progress to gangrene, occurring in the distal portions of limbs

58
Q

What is the most serious condition associated with N. meningitidis?

A

Waterhouse-Friderichsen Syndrome

  • -hemorrhagic infarction of the adrenal glands
  • -rapidly progressive hypotension and shock
  • -DIC w/ widespread purpura of the skin
59
Q

What are the symptoms of chronic meningitis?

A
  • fever
  • HA
  • lethargy
  • confusion
  • N/V
  • stiff neck
60
Q

What is the composition of the CSF in cases of chronic meningitis?

A
  • elevated protein
  • low glucose
  • predominantly lymphocyte infiltrates
61
Q

When can a Dx of chronic meningitis be made?

A

-symptoms and CSF abnormalities persist/progress for at least 4wks

62
Q

What are common pathogens of chronic meningitis?

A
  • TB
  • T. pallidum
  • Borrelia burgdorferi
63
Q

Where does chronic meningitis d/t Mycobacterium tuberculosis typically affect?

A
  • subarachnoid space (gelatinous or fibrous exudate)
  • predilection for the base of the brain (arachnoiditis)
  • obliterates the cisterns (hydrocephalus)
  • encases CN’s (CN symptoms)
64
Q

What is obliterative (Heubner) endarteritis?

A
  • inflammation that infiltrates vessel walls
  • intimal thickening
  • arterial occlusion and infarction
65
Q

What is a tuberculoma?

A
  • -well-circumscribed intraparenchymal mass
  • -central caseous necrosis
  • -inactive lesions may calcify
66
Q

What kind of stain detects Mycobacterium tuberculosis?

A

acid-fast

67
Q

In chronic meningitis caused by Borrelia burgdorferi, how long after the rash do the neurological symptoms appear?

A

4wks

68
Q

What are the prominent characteristic symptoms of chronic meningitis d/t Borrelia burgdorferi?

A
  • CN palsies

- peripheral neuropathies

69
Q

What is seen in the CSF of pt’s w/ chronic meningitis d/t Borrelia burgdorferi?

A
  • Ab’s that can Xreact w/ mono, RA, SLE, and syphilis

- use PCR to detect

70
Q

What percentage of untreated pt’s w/ syphilis (caused by Treponema pallidum) develop neurosyphilis?

A

10%

71
Q

What is meningovascular neurosyphilis?

A
  • chronic meningitis involving base of the brain
  • -variable convexities and spinal leptomeninges
  • causes communicating hydrocephalus
  • causes obliterative endarteritis
  • -noted by perivascular plasma cells and lymphocytes
72
Q

What is paretic neurosyphilis?

A
  • insidious, progressive mental deficits
  • mood alterations
  • delusions of grandeur
  • severe dementia (general paresis of the insane)
73
Q

What is seen on histology of paretic neurosyphilis?

A
  • perivascular iron deposits
  • granular ependymitis
  • -proliferation of subependymal glia under damaged ependymal lining (causes hydrocephalus)
74
Q

What is tabes dorsalis and its symptoms?

A
  • dorsal root ganglion damage (sensory nn.)
  • orthopedic (joint) damage and pain (Charcot Joints)
  • reflexes diminished
  • sharp pain (“lightning pain”)
  • ataxia
  • loss of pain sensation
  • impaired joint proprioception
  • d/t syphyilis
75
Q

What is the characteristic patient presentation of someone with aseptic meningitis?

A
  • meningeal irritation
  • fever
  • alterations of consciousness
  • acute onset
  • absence of organisms in the CSF
76
Q

What causes the majority of cases of aseptic meningitis?

A

80% are caused by enteroviruses

77
Q

True or False: the clinical course of aseptic (viral) meningitis is more fulminant that pyogenic meningitis

A

False

78
Q

What is seen in the CSF of aseptic meningitis?

A
  • lymphocytic pleocytosis
  • moderate increase in protein
  • normal glucose
79
Q

What is the Tx for aseptic (viral) meningitis?

A

-treat the symptoms; it’s usually self-limiting

80
Q

True or False: viruses can infect the CNS via both hematogenous spread and through the nerves

A

True

-nn. examples are olfactory and trigeminal sensory nerves or motor nerves

81
Q

What type of cells comprise the inflammatory response?

A

lymphocytes

82
Q

What are some examples of arthropod-borne viruses that can cause encephalitis in the Western Hemisphere?

A
  • Eastern and Western Equine
  • West Nile (involves spinal cord; polio-ish paralysis)
  • Venezuelan
  • St. Louis
  • La Crosse
83
Q

True or False: in arthropod-borne viral encephalitis, there are multiple foci of necrosis in both grey and white matter

A

True

84
Q

What age groups are affected by HSV-1 to cause encephalitis?

A

children

young adults

85
Q

What types of damage does HSV-1 cause?

A

necrotizing

hemorrhagic

86
Q

What lobes of the brain are most commonly affected by HSV-1?

A
  • inferior/medial temporal lobes

- orbital gyri of the frontal lobes

87
Q

What is seen on histology of HSV-1?

A
  • Cowdry Type A

- -intranuclear viral inclusions in neurons and glia

88
Q

What age groups are affected by HSV-2 to cause encephalitis?

A

Neonates

-50% delivered vaginally to women w/ active primary HSV genital infection develop severe encephalitis

89
Q

Where does herpes zoster most commonly lie latent?

A

-trigeminal nerve

or

-sensory neurons of dorsal root

90
Q

What is shingles?

A

-reactivation of herpes zoster that results in painful vesicular skin eruptions limited to a single dermatome

91
Q

What is persistent post-herpetic neuralgia syndrome?

A

persistent pain as well as painful sensation following non-painful stimuli

92
Q

What types of individuals are most commonly affected by CMV?

A
  • fetuses

- immunosuppressed (opportunistic infection w/ AIDS)

93
Q

What damage does CMV cause in utero?

A
  • periventricular necrosis
  • microcephaly
  • periventricular calcification
94
Q

Where does CMV localize in the brain of non-neonates?

A

-paraventricular subependymal regions

95
Q

What damage does CMV cause in non-neonates?

A
  • severe hemorrhagic necrotizing ventriculoencephalitis
  • choroid plexitis
  • radiculoneuritis in lower spinal cord and roots
96
Q

What is seen on histology in CMV?

A

-prominent enlarged cells w/ intranuclear and intracytoplasmic inclusions

97
Q

What does poliomyelitis do to the brain and what major symptom does it produce?

A
  • mononuclear cell perivascular cuffs
  • neuronophagia of the anterior horn motor neurons
  • -flaccid paralysis

-may extend to posterior horns and occasionally produce cavitation

98
Q

What is post-polio syndrome?

A
  • develops 30yrs after resolution of initial illness

- progressive weakness w/ decrease muscle mass, pain

99
Q

What is the incubation period of rabies (lyssa virus genus in the rhabdoviridae family)?

A

-1 to 3 months, depending on distance of the wound from the brain

100
Q

How does rabies get from a wound to the brain?

A

-infection ascends along peripheral nerves

101
Q

What are the symptoms of rabies?

A
  • -non-specific (malaise, HA, fever)
  • extraordinary CNS excitability, violent motor response
  • convulsions
  • flaccid paralysis and resp. ctr failure
  • hydrophobia (“foaming at the mouth”) d/t ctx of pharyngeal muscles that produce an aversion to swallowing even water
  • local paresthesias (pins and needles) around wound
  • -diagnostic
102
Q

What types of intracellular inclusions are seen in rabies?

A

Negri bodies (cytoplasmic inclusions)

103
Q

What proportion of HIV+ pts experience aseptic meningitis and when does it occur?

A

-occurs in about 10% of patients within 1 to 2 wks of seroconversion

104
Q

What can be seen on histology of aseptic meningitis d/t HIV?

A

Vessels: prominent endothelial cells and perivascular foamy or pigment-laden macrophages

White Matter: multifocal or diffuse areas of MYELIN PALLOR, AXONAL SWELLING, and GLIOSIS

Acute - mild lymphocytes, PERIVASCULAR INFLAMMATION, myelin loss

Chronic - MICROGLIAL NODULES w/ MULTINUCLEATED GIANT CELLS

105
Q

What is Immune Reconstitution Inflammatory Syndrome (IRIS)?

A
  • paradoxical deterioration after starting antivirals
  • exuberant inflammatory response

-paradoxical exacerbation of symptoms from opportunistic infection

106
Q

What is HIV-associated dementia?

A
  • inflammatory activation of microglial cells

- no specific pathologic lesion

107
Q

What cancer has increased incidence among pts who are HIV+?

A

primary CNS lymphoma

108
Q

What virus causes Progressive Multifocal Leukoencephalopathy (PML)?

A

-JC Polyomavirus

  • the primary infection is asymptomatic
  • latency
  • reactivation during immunosuppression
109
Q

What types of cells does JC polyomavirus attack and what is the resulting pathology?

A
  • -oligodendrocytes
  • -demyelination is the primary pathological effect
  • -irregular, ill-defined white matter destruction
  • -subcortical demyelination w/ lipid-laden macrophages
110
Q

What are the symptoms of Progressive Multifocal Leukoencephalopathy (PML)?

A
  • loss of coordination

- weakness

111
Q

What is Subacute Sclerosing Panencephalitis (SSPE)?

A

–caused by a paramyxovirus in non-immunized children or young adults

–can occur months to years following early-age acute infection w/ measles (rubeola)

112
Q

What are the symptoms of Subacute Sclerosing Panencephalitis (SSPE)?

A
  • cognitive decline
  • spasticity of limbs
  • seizures
113
Q

What is seen on histology of Subacute Sclerosing Panencephalitis (SSPE)?

A
  • widespread gliosis
  • myelin degeneration
  • viral inclusions in nuclei of neurons and oligos
  • variable inflammation of white and grey matter
  • neurofibrillary tangles
114
Q

What type of patients are normally affected by fungal meningoencephalitis?

A

immunocompromised

115
Q

How is fungal meningitis spread?

A

hematogenously

116
Q

What are typical pathogens responsible for fungal meningoencephalitis?

A
  • candida albicans
  • mucor
  • aspergillis fumigatus
  • cryptococcus neoformans
117
Q

What fungal infection w/ neural involvement is commonly associated with diabetes patients?

A

mucormycosis

118
Q

What two fungal pathogens are most often responsible for vasculitis?

A
  • mucormycosis
  • aspergillosis
  • candida (occasionally)
119
Q

What is a complication of fungal vasculitis?

A

-thrombosis that causes a hemorrhagic infarction and becomes septic

120
Q

What are some examples of fungal endemic pathogens?

A
  • Histoplasma capsulatum (Mississippi River Valley)
  • Coccidioides immitis (SW US)
  • Blastomyces dermatitidis (Ohio River Valley)
121
Q

What fungal pathogens are most associated with parenchymal infections?

A
  • candida

- cryptococcus

122
Q

What fungal pathogen is most associated with meningitis?

A

Cryptococcus neoformans

123
Q

What patient population is most commonly affected by Cryptococcus meningitis and what is the prognosis of the disease?

A
  • AIDS pts
  • having an immune dysfunction predisposes
  • fulminant and fatal within 2wks (up to yrs, though)
124
Q

What is important in regards to the CSF in pts with Cryptococcus meningitis?

A
  • India Ink preparation
  • Cryptococcal polysaccharide antigen
  • culture the CSF

–Also culture urine, sputum, blood, and stool

125
Q

What are the neural implications of Toxoplasmosis gondii?

A
  • parasitic protozoa
  • opportunistic infection for HIV and immunosuppressed
  • also causes problems during pregnancy

-brain abscess near grey/white junction of cerebral cortex and DEEP GREY NUCLEI

126
Q

What do you see on histology of Toxoplasmosis?

A
  • CENTRAL FOCI OF NECROSIS (ring-enhancing lesion)
  • petechial hemorrhages surrounded by inflammation
  • macrophage infiltration
  • VASCULAR PROLIFERATION

-FREE TACHYZOITES and ENCYSTED BRADYZOITES at periphery of necrotic zones

127
Q

What is cerebral amebiasis?

A
  • caused by naegleria fowleri
  • found in warm freshwater and soil

-infects people when contaminated water enters the brain through the nose

128
Q

What is acanthamoeba?

A
  • an amoeba that causes chronic granulomatous meningoencephalitis
  • also can infect the eye and skin
129
Q

How does Plasmodium falciparum affect the CNS?

A
  • -cerebral malaria

- -results in long-term cognitive defects in survivors

130
Q

What is Creutzfeldt-Jakob Disease (CJD)?

A
  • prion disease
  • abnormal proteins (Prion Protein - PRP)
  • rapidly progressive neurodegenerative disorder
  • SPONGIFORM change w/ intracellular vacuoles
131
Q

True or False: prion disease can be sporadic, familial, or transmitted

A

True

132
Q

When do most cases of Creutzfeld-Jakob Disease appear?

A

-90% is the sporadic form that appears in the 60’s

133
Q

In addition to sporadic CJD, what is another mode of transmission?

A
  • iatrogenic
  • -corneal transplant
  • -brain implantation of electrodes
  • -contaminated preps of human growth hormone
134
Q

What are the symptoms of Creutzfeld-Jakob Disease?

A
  • rapidly progressive dementia
  • startle myoclonus
  • survive approx. 7 months after symptoms appear
135
Q

True or False: there is abundant gross evidence of brain atrophy in CJD pts.

A

False; the progression is so rapid that there is little (if any) grossly evident brain atrophy.

136
Q

What is the variant Creutzfeld-Jakob Disease?

A
  • in young adults in the UK in 1995
  • behavior changes early in the disease
  • slower progression
  • exposure to bovine spongiform encephalopathy
  • Kuru Plaque in the cerebellum
137
Q

What is seen on histology of Variant Creutzfeld-Jakob Disease?

A

Kuru Plaque

  • extracellular deposits of aggregated abnormal protein
  • Congo Red positive
  • PAS+
  • located in the cerebral cortex of vCJD
138
Q

What is Fatal Familial Insomnia (FFI)?

A
  • sleep disturbances initially
  • aspartate substituted for asparagine at codon 129
  • ataxia
  • autonomic disturbances
  • stupor (eventually coma)
  • death within 3yrs

NMSP 1 (9 decks)

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