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CMED 311 > Trans 040 Patho Infections of CNS > Flashcards

Trans 040 Patho Infections of CNS Flashcards

1
Q

MOST COMMONLY

IN PEDIATRICS referred to as Meningimus

A

non bacterial aspetic meningitis

There is reaction of meninges in systemic infection but it
is not in the brain it is just a reaction

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2
Q

in 3 mos to 2 y/o, what is the most common cuase of bacterial meningitis?

route?

A

N. Meningitidis

Route: respiratory tract

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3
Q

Acute Pyogenic Meningitis (Bacterial Meningitis)

• In neonates, common organisms are
In adolescents and young adults, most cmmon pathogen is?
In older adults,

A

Escherichia
coli and group B streptococci.

N. meningitidis

Strep Pneumoniae and Listeria Monocytogenes

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4
Q

Modifiable Risk Factors for Bacterial Meningitis

A 
• Not completing childhood vaccines**
• Median age of diagnosis 25 years
• Living in close quarters (meningococcal)**
• Pregnancy (listeriosis)
• Working with animals (listeriosis)
• Compromised immune system (from aids, spleen removal,
diabetes, use of immunosuppressant drugs
**Most common in our country
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5
Q

MOST COMMON ROUTE OF ENTRY, bacterial mening

A

Hematogenous route: through arterial and venous spread

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6
Q

Routes of infection in bacterial mening?

A

• Hematogenous route: through arterial and venous spread- MOST COMMON ROUTE OF ENTRY
 Mucosa → Upper respiratory tract → blood vessels (arteries) → choroid plexus →meninges
• Direct implantation
 If you do lumbar puncture to some disease
 Not working on sterile condition, you can introduce bacteria into CSF
o Maybe traumatic
o Rarely, iatrogenic i.e., through lumbar puncture needle
• Local extension: through air sinuses, infected tooth or surgical site
• Through peripheral nervous system as occurs with certain viruses

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7
Q

How does bacteria gain entry through meningitis?

A

 It is through the choroid plexus coz CSF is produce here and choroid plexus has blood supply
 CSF is a secretory product of Choroid plexus which is derived from blood circulation
 Once it gains entry to CSF → break into subarachnoid space → rapid multiplication in CSF

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8
Q

Pathophysio of bacterial meningitis?

A

 You get it through air that’s why easily transmissible in people who are living very close together
 Bacterial transport through air → Entry → implantation (at the site where it gains entry) → multiplication → nasopharyngeal colonization in epithelial cells → Local invasion into intravascular space (viremia) → bacteremia → artery that supplies part of brain → meningitis

 Suppuration in subarachnoid space → Inc. ICP → non-communicating hydrocephalus → cerebral herniation → death

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9
Q

Difference if bacterial invasion is via the artery vs via veins

A

 If the bacterial invasion is into the artery it will go into brain through choroid plexus
 If the bacterial invasion is venous it will drain into systemic circulation. If it drains there, you will produce a septicemic condition known as WFS or Waterhouse-Friderichsen syndrome

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10
Q

Complications of acute pyogenic miningitis

A

Phlebitis

Leptomeningeal infarction and consequent hydrocephalus
Septicemia with hemorrhagic infarction of the adrenal glands and cutaneous petechiae (known as

Waterhouse-Fridrichsen Syndrome particularly common with meningococcal meningitis)

Waterhouse-Friderichsen syndrome (WFS) syndrome or hemorrhagic adrenalitis or Fulminant meningococcemia

Focal cerebritis and seizures

Cerebral abscess

  • Cognitive deficit
  • Deafness
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11
Q

Adrenal gland failure due to bleeding into the adrenal glands

A

waterhouse Friderichsen syndrome

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12
Q

cause of waterhouse friderichsen syndrome

A

Caused by severe bacterial infection – most commonly the meningococcus Neisseria meningitidis

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13
Q

MC cause of DIC?

A

Septicemia

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14
Q

What are direct extension causes of cerebral abcess? (4)

A

Otitis
Paranasal Sinus
Mastoiditis
Calvarial or meningeal infection

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15
Q

most common cause of cerebral abcess?

A

septic embolization to the brain

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16
Q

MOST COMMON ROUTE OR SOURCE OF SEPTIC EMBOLIZATION?

A

congenital heart disease. Px with abnormal valves

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17
Q

most common source of direct extension to the brain causing cerebral abcess?

A

MOST COMMON SOURCE is otitis media

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18
Q

small subpial or subependymal foci of metastatic caseous lesion

A

Rich foci

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19
Q

complications of TB meningitis

A 
• Hydrocephalus
• Subdural effusion
• Hemiplegia/Paraplegia
• Late:
o Intellectual impairment
o Blindness
o Deafness
o Intracranial calcifications leading to hypothalamic and pituitary dysfunction
o Growth failure
o Diabetes insipidus
o Failure of development of secondary sexual characteristics
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20
Q

MOST COMMON INFECTION OF CNS ESPECIALLY IN <1 YR

bacterial or viral?

A

Viral

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21
Q

Common viral agents?

A 
Enterovirus
coxsackie virus A e B
Echovirus
Arbovirus
HIV
HSV - 2
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22
Q

Herpes simplex encephalitis pathophysiology?

A

Brain infection is thought to occur by means of direct neuronal transmission of the virus from a peripheral site to the brain via the trigeminal or olfactory nerve.

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23
Q

The Herpes virus preferentially involves what lobes?

A

the temporal lobe and orbital surfaces of the frontal lobes.

24
Q

why is HSV 1 more common than HSV 2?

A

The ability of HSV-1 to induce apoptosis in neuronal cells, a property not shared by HSV-2, might explain why the former causes virtually all cases of herpes simplex encephalitis in immunocompetent older children and adu

25
Q

HSV 1 vs HSV 2 ?

A

 HSV type-1 – causes cold sore on the lips and can infect the gasserian ganglion via the mandibular nerve trunk. CNS infection affects primarily affects the temporal lobes; infected neurons contain small, eosinophilic nuclear inclusions
 HSV type-2 – sexually transmitted disease-causing vesicular lesions in the penis and vagina; virus can be transmitted to the newborns during delivery and cause severe neonatal encephalitis.

26
Q
  • A viral disease that causes acute encephalitis (inflammation of the brain) in warm-blooded animals.
  • A zoonotic disease (a disease that is transmitted to humans from animals) that is caused by a virus.
A

Rabies

27
Q

how does the rabies gain entry into the brain?

A

It does not gain entry into the brain through the bloodstream but FROM THE PERIPHERAL NEURAL SYSTEM → SPINAL CORD → BRAIN

Virus travels along the peripheral nerves at the bite site and transported by retrograde axoplasmic flow to the spinal cord and brain

28
Q

specific cytoplasmic inclusion body in rabies?

A

Negri bodies

29
Q

Pathophysiology of Rabies Virus

A

I. Rabies Virus (RV) enters the peripheral nervous system at the bite site by binding to one or more specific neural receptors with or without local replication
II. Once inside neurons, RV is spread by retrograde transport to the spinal cord and then to the brain
III. Inflammatory reactions and other histological lesions are mild with relatively little neuronal loss
IV. Fatal rabies may result from neuronal dysfunction rather than neuronal damage
V. RV induces dysfunction of ion channels which could prevent infected neurons from firing action potentials and generating synaptic potentials resulting in functional impairment.
VI. Terminal stage of the disease, neurons are no longer capable of releasing neurotransmitters at the synaptic junctions

30
Q

are cytoplasmic, round to oval, eosinophilic inclusions that can be found in pyramidal neurons of the hippocampus and Purkinje cells of the cerebellum, sites usually devoid of inflammation

A

Negri bodies

31
Q

Clinical features of rabies

A

o Contracture of the pharyngeal musculature on swallowing produces foaming at the mouth, which may create an aversion to swallowing even water (hydrophobia).
o There are signs of meningeal irritation and, as the disease progresses, flaccid paralysis.
o Alternating periods of mania and stupor progress to coma and eventually death from respiratory failure

32
Q

prognosis of rabies?

A

• Nearly 100% treatable if exposure is known and post-exposure treatment begins before signs of disease
• Nearly 100% fatal once symptoms occur
• Only 6 people have ever survived (with brain damage) when treated after clinical signs began.
 I think this is an old article already. Maybe there are more.
• Once symptoms begin, death within 2 weeks
- Often within days
- Usually within 1 week

33
Q

A highly infectious viral disease, which destructs the motor neurons and damages brain and spinal cord and is characterized by muscle weakness and paralysis

A

Poliomyelitis

34
Q

• The virus is transmitted thru contaminated food and water, and multiplies in the intestine from where it can invade the nervous system.

Nonenveloped, single-stranded RNA enterovirus preferentially infects the anterior horn cells and bulbar motor nuclei of the spinal cord

Fecal-oral route transmission`

A

Poliomyelitis

35
Q

prognosis of poliomyelitis

A
  • Paralysis lasting >12 months tends to be permanent.
  • 50% of people with paralytic polio recover completely.
  • 25-50% of paralytic polio survivors develop post-polio syndrome.
36
Q

is a debilitating and frequently fatal central nervous system (CNS) demyelinating disease caused by JC virus (John Cunningham virus)

A

PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY

37
Q

PML patho?

A

• Lytic infection of oligodendrocytes in the brain leads to their eventual destruction and progressive demyelination, resulting in multiple foci of lesions in the white matter of the brain

38
Q

Poliomyelitis has a predilection to what neuron cell?

A

MOTOR NEURON

39
Q

PML has a predilection to what cell?

A

OLIGODENDROCYTES

40
Q

Clinical presentation of PML?

A

• Patchy demyelinization of the brain leading to:
- Weakness, sensory deficits, hemianopia, incoordination, aphasia
- Seizures (16%)
- Behavioral and cognitive dysfunction in 30 to 50%
• Optic nerves and spinal cord are usually spared
 Signs and symptoms will develop as to the predominant side where you have the neuronal death.

41
Q

most common viruses infecting the CNS in utero

A

CYTOMEGALOVIRUS & RUBELLA VIRUS

42
Q

Causes necrotizing encephalitis resulting in developmental malformations and microcephaly especially when infection occurs during the 1st trimester of pregnancy

A

CYTOMEGALOVIRUS & RUBELLA VIRUS

43
Q

caused by the measles virus persisting in the CNS for years and resulting in a chronic neurodegenerative process; primarily affects the cortex.

A

SUBACUTE SCLEROSING PANENCEPHALITIS

44
Q

CNS involvement commonly involved in AIDS and in pre-AIDS stages; directly infecting the macrophage and microglia; causes mild brain atrophy, diffuse demyelination.

A

AIDS ENCEPHALOPATHY

45
Q

Every cell has prion protein T or F?

A

T

46
Q

group of disorders involving conformational changes of the human prion proteins.

A

spongiform encephalopathies

47
Q

an infectious particle made up of misfolded prion protein

A

Prion

48
Q

Exact function these is not defined, but believed its involved in communication between neurons, cell death, and controlling sleep.

A

Prion protein

49
Q

The causative agents of Transmissible spongiform encephalopathy (TSEs) are believed to be

A

PRIONS

50
Q

usually presents in adult life as a rapidly progressive dementia often with pyramidal and extrapyramidal signs

A

Creutzfeldt-Jakob disease (CJD)

51
Q

most common prion disease?

A

CJD

52
Q

Sporadic human prion disease?

A

CJD

53
Q

Familial (genetic) human prion disease? (3)

A

Familial CJD
Gerstman-straussler-scheinker Syndrome (GSS)
Fatal familial insomnia

54
Q

Human prion disease acquired by transmission?

A

Kuru
Iatrogenic CJD
Variant CJD

55
Q

Contraindications to lumbar tap?

A 
Increased ICP
Coagulopathy
Prior lumbar surgery
Severe vertebral osteoarthritis/ DDD
Significant cardiorespiratory compromise
Infection near the puncture site
Space occupying lesion
56
Q

You can determine increased ICP by doing fundoscopic

examination, what finding?

A

Protruding optic disc

57
Q

Another site where chemotherapeutic agents cannot

cross are the

A

testicles

CMED 311 (47 decks)

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