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A - Neuroinfectious Diseases 2 > Bacterial Infections 2 > Flashcards

Bacterial Infections 2 Flashcards

1
Q

TB meningitis is caused by

A

Mycobacterium tuberculosis (MTb)

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2
Q

MTb stanning

A

can’t be gram stained (b/c of nusual, waxy coating on its cell surface primarily due to the presence of mycolic acid)

test used - Acid-fast bacilli

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3
Q

MTb is a ____ pathogen

A

Facultative intracellular pathogen - lives inside and outside cells

Considered one of the most successful pathogens in history - only lives in humans - have been unable to find a resevar

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4
Q

Hallmark of MTb is its

A

very intricate and elaborated cell wall

very waxy - reason why had to diagnose and kill

layer of heavily modified lipids - cannot use gram staning

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5
Q

MT b Killed

A

1.6 million people in 2017
- mostly due to pneumonia and its complications
- ~5% of TB patients develop TB meningitis
- Mostly children, elderly, or HIV+ patients

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6
Q

TB meningitis is a result of

A

a bloodstream dissemination
- usually coming from the lung
- source site may be latent (lung granulomas)

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7
Q

TB meningitis First seeds the

A

meninges, usually around the base of the skull
- classic triad: headache/fever, malaise, and neck pain

May produce hydrocephalus and cranial nerve palsies

As disease progresses, the parenchyma can be seeded
- forms brain abscesses (can be known as tuberculomas- can be latent for years)

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8
Q

tuberculoma

A

(in brain) immune response - try to wall of to contain infection - but not clear it - later in life can break open

(granuloma - can also be in lungs)

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8
Q

TB entry into CNS

A

Multiple routes of entry

Expresses virulence factors that enable invasion of BMECs
- cross transcellularly [into SAS APCs in - pro inflammatory cytokines - activate endothelial (makes BBB more loose) - also attract immune to control infection into turbucluomas - immune can also already be infected (constant infltration of immune can also cause BBB breakdown)]

Can also survive inside phagocytes
- cross using Trojan horse

Once in parenchyma, recognition induces immune response - BBB breakdown

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9
Q

MTb is a ____ pathogen

A

NOT an opportunistic pathogen – will infect healthy individuals as well!

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10
Q

Risk factors for TB meningitis

A
  • Close contacts of a person with infectious TB disease
  • Persons who have immigrated from areas of the world with high rates of TB
  • Persons who work or reside with people who are at high risk for TB (i.e. hospitals, jails, nursing homes, etc.)
  • Immunocompromised individuals (i.e. HIV)
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11
Q

It is estimated ____ of the world has latent TB

A

1/4

No effective vaccine - high priority with rise in MDR [multi drug resistant] TB - treatment also involves months of antibiotics - causes other issues

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12
Q

Listeria monocytogenes acquired from

A

generally contaminated food - port of entry GI tract (mostly gastroenteritis - if healthy can contain it)

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13
Q

Treponema pallidum acquired from

A

generally sexually transmitted

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14
Q

Borrelia burgdorferi acquired from

A

tick-borne

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15
Q

Burkholderia pseudomallei acquired from

A

tropical climate, associated with water

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16
Q

L. monocytogenes morphology

A

Gram-positive bacillus

Facultative intracellular bacterium – can live both free or inside other cells

Has 12 recognized serotypes

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17
Q

L. monocytogenes serotypes

A

(based on presence of 2 antigens), three of which (1/2a, 1/2b, and 4b) cause most (95%) human illness

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18
Q

L. monocytogenes burden

A

Worldwide burden (2010) ~24,000 cases with 5,500 deaths

In US ~1,600 cases yearly with ~260 deaths

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19
Q

L. monocytogenes cycle food to brain

A

Gastroenteritis in healthy individuals

CNS infection in immunocompromised
individuals

Abortions in pregnant women

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20
Q

L. monocytogenes Expresses surface proteins that ____

No ___ BUT ____

A

promote invasion of non-phagocytic (end/epithelial) cells

No capsule, easily internalized by phagocytes

BUT Once intracellular, it escapes the vacuole (phagosome - into cytoplasm) and replicates in the cytosol

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21
Q

L. monocytogenes can disseminate from cell-to-cell using

A

actin comets

22
Q

L. monocytogenes invasive infection is a

A

slow process, involving an asymptomatic phase

Healthy individuals can control and clear infection

23
Q

Ways L. monocytogenes enters the brain

A

1) from the bloodstream – it can induce its own phagocytocis by BMECs, and once inside it induces immune signals and activation of BMECs

2) from infected contiguous tissue – once inside a cell, it can disseminate through actin comets that propel the bacterium from one cell into the neighboring cell

3) Trojan horse – not only can use phagocytes [survives inside phagocites] to move between organs and spread, but it can use them to cross as a passenger into the brain parenchyma

24
Q

Most common manifestation of L. monocytogenes

A

is ventriculitis, probably because ease to get in through choroid plexus - hydrocephalus

25
Q

What is the/a consequence of ventriculitis?

A

hydrosphelus

26
Q

L. monocytogenes vaccine

A

No vaccine – very low burden, but would be very useful for at-risk groups

27
Q

At risk groups for L. monocytogenes

A
  • Pregnant women and their newborns
  • Older adults (age >65)
  • People with weakened immune systems
28
Q

L. monocytogenes treatment

A

Easily treatable with antibiotics, but needs to be diagnosed early on

  • Infection is common, but disease is rare!
29
Q

T. pallidum morphology

A

Corkscrew-shaped (spirochete) bacterium

very obvious

30
Q

Spirochetes surface

A

is very different from other bacteria, hence aren’t classified as gram negative or positive

31
Q

T. pallidum host

A

only known hose - humans

(only recently found way to culture) Can’t be cultured on lab – hindered research into pathogenesis and in turn, into vaccine development

32
Q

T. pallidum neurological manifestations

A

Can cause multiple neurological manifestations – meningitis may not be of clinical significance (just low headache)

neurosyphilis - late manifestation of the disease

33
Q

T. pallidum gummas

A

infection can go on for a long time - resulting in gummas (if in bones) - immune system kicks in - severe inflation

34
Q

Neurosyphilis incedence rate

A

Usually very late manifestation of the disease

May occurs in 10% of infected and untreated individuals after 10 – 15 years

can ocour at any time - symptoms appear much later

35
Q

Neurosyphilis is clinically

A

chronic meningoencephalitis (meninges & parachama) , with formation of internal gummas

sometimes also affect the spinal cord (meningoencephalomyelitis)

36
Q

prior to Neurosyphilis

A

that infected persons may transiently develop meningitis

  • mainly base of skull, affecting cranial nerves (face palsies)
  • cause recurrent ischemic strokes (due to vascular inflammation)
37
Q

___ allows T. pallidum to penetrate cellular barriers

___ makes T. pallidum very difficult to be
recognized by phagocytes thus ____

turning point is when ___

A

Corkscrew-shape and movement

Lacks antigenic proteins (PAMPs) on the surface

thus Can move around the body without detection - little inflammation

when phagocytes ingest it: It remains extracellular, as phagocytes are able to kill it if they can ingest it – turning point when antibodies are develop
- inflammation goes overboard - gummas

38
Q

Evidence suggests T. pallidum can easily go into CNS by ____

A

disrupting cellular junctions, crossing between the endothelial cells (paracellular route)

Depending on the area it crosses (pia arterioles/venules vs BBB) it can reach different areas of the CNS

Once on the CSF, if it finds its way down the central canal, it can cross into the spinal cord

39
Q

T. pallidum treatment

A

Easily treatable with penicillin G (if diagnosed early on), and no cases of resistance have ever been reported

Ethics of the Tuskegee Study (not given penicillin - wanted to develop late stages to see late manifestations if the disease)

40
Q

At risk groups for T. pallidum/Neurosyphilis

A
  • Men who have sex with men
  • People who are HIV positive
  • Sex workers
41
Q

T. pallidum incidence

A

in US has increased in the last decade
- <3 cases/100,000 in 2000
- ~7 cases/100,000 in 2016
- inc. 4x in recent years sence pandemic

Pregnancy testing now routine (some states also require it for marriage certificates)

42
Q

Myelitis is

A

Infection of the nerves and/or glia of the spinal cord

The parenchyma of the spinal cord

results in inflammation of the spinal cord

43
Q

Types of Myelitis

A

acute - not side to side

transverse - all nerves from that area and down are effected

44
Q

infectious diseases that cause acute myelitis

A

bacteria - rare (B. burgdorferi, S. aureus, B. pseudomallei, M. leprae)

mainly viruses (Polio or Herpes)

most of the time cause is not known - is Idiopathic

45
Q

Burkholderia pseudomallei is the causative agent of

A

melioidosis, a life-threatening infection with multiple manifestations

46
Q

Burkholderia pseudomallei morphology

A

Gram-negative environmental bacteria (soil, water, etc.)

Shows complex antimicrobial interactions - resistant and if combine antibiotics - weird interactions

47
Q

Burkholderia pseudomallei location

A

A disease of tropical climates, especially in Southeast Asia and northern Australia [yousto be restricted of oceanea]

Research interest due to potential as a bioweapon

Incidence in Western Hemisphere unknown – recent cases identified in parts of the Caribbean, Central America, and South America, usually associated with extreme weather events (tropical storms or heavy rainfall)

48
Q

Burkholderia pseudomallei is a ___ pathogen

A

facultative intracellular pathogen

Large array of virulence factors (pilins, adhesins, actin-based motility, etc.)

49
Q

Burkholderia pseudomallei entrance into CNS

A

Enters and replicates in epithelial cells - Trigeminal Nerve (into CNS)

Once inside (also Can multiply within phagocytes), can lyse the cell and infect the next cell down, but can also propagate between adjacent cells through actin comets

prefered way - nerve hopping

50
Q

Burkholderia pseudomallei Preferred way to get into the CNS

A

nerve hoping

nasal or throat infection - encephalomyelitis

limbs infection - myelitis

51
Q

Burkholderia pseudomallei clinical manifestations

A

many

1 - 5% of cases affects the CNS [ Very rare - mainly cardiovascular or lungs]

Grossly underdiagnosed (lack of tools, training, etc.)

52
Q

Neuromelioidosis Risk factors

A

Exposure to soil or water in endemic areas (especially during the rainy season)

Diabetes mellitus

Liver disease, chronic lung disease, chronic kidney disease and thalassaemia (all of which would affect your immune system)

53
Q

Commonalities between Burkholderia pseudomallei; T. pallidum; L. monocytogenes; and MTb

A

They all have specialized surfaces

Can use multiple or unique ways to cross the CNS barriers
- L. monocytogenes can invade BMECs directly, then infect contiguous tissue, or use Trojan horse.
- The spirochetes use unique shape and motility to “drill” a hole between cellular barriers, including BBB
- B. pseudomallei can invade nerves peripherally and spread cell-to-cell back into the CNS.

Big challenge, diagnosis!

A - Neuroinfectious Diseases 2 (9 decks)

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