NEISSERIA!!! MICROM 442 Deck 15 Flashcards

1
Q

2 pathogenic species?

A
  • N. gonorrhoeae
  • N. meningitidis
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2
Q

what GM and shapre are these? -> c’mon literally loops like a pair of balls

A

GM- diplococci, kidney bean shaped

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3
Q

these are non-motile and??

A

non-sporeforming

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4
Q

Fastidious, requires enriched
medium like

A

chocolate agar

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5
Q

primary selective media used to culture

A

Modified Thayer Martin Agar

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6
Q

fast or slow growth?

A

fast -> 24 to 48 hours

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7
Q

oxidase???

A

positive

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8
Q

gonococus uses which sugar?

A

glucose

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9
Q

meningococcus uses what sugar?

A

theres two, maltose and glucose

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10
Q

what type of spectrometer is used to identify it?

A

MALDI-TOF

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11
Q

host range of pathogenic neisseria?

A

-obligate for human
-mouse for n. gonorrheae

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12
Q

what about commensal nessieria species?

A

usually just stay in the pharynx

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13
Q

what are the major antigens?

A

-pili
-outer membrane proteins
-lipoogliosaccharides (LOS)

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14
Q

outer membrane proteins

A

Por, Opa

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15
Q

LOS

A

in place of
lipopolysaccharides for other Gram-
negative bacteria

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16
Q

these are masters of???

A

disguise -> immune evasion

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17
Q

pili

A
  • Function in initial attachment to host cells
  • Variable in sequence
  • Host receptors:
    -CD46 on male urogenital epithelial cells
    -CR3 on female cervical epithelium
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18
Q

pili phase variation

A

transcriptional regulation

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19
Q

pili antigenic variation = different sequences

A

Contains conserved regions and 6
immunodominant variable regions

20
Q

Por (OMP I) -> most abundant structural surface proteins

A
  • Mediates attachment to mucosal cell surface
  • Invasion of host cells by binding to
    complement receptor 3 (CR3) on cervical
    epithelial cells in women
21
Q

por (OMP I) can be used for serological classification because it has two distinct

A

structural classes -> PorA & PorB

22
Q

Opa (OMP II) expression determines?

A

colony phenotype:
opaque or transparent

23
Q

OMP II also functions in??

A

close attachment to host cells

24
Q

LOS

A
  • Major role in production of inflammatory
    mediators
  • Plays a role in attachment to some host cells
  • Sialylated LOS – confers serum resistance and
    attenuates the inflammatory response
25
Q

male infx often causes

A

urethritis

26
Q

female infx is often

A

asymptomatic

27
Q

male genitalia pathogenesis

A

-Initial attachment via pili to urethral epithelium
-Cell receptor is CD46
-Not sufficient to trigger internalization
-Opa expression results in closer adhesion between
gonococci and host cells
-Opa receptors are varied: tissue tropism?
-Internalization occurs

28
Q

pathogenesis male urthrea

A
  • Gonococcus enters and multiply within
    epithelial cells, reach the submucosa
  • Triggers inflammatory response
  • Hematogenous spread can occur
    ➢ Symptomatic infection
29
Q

Pathogenesis—Female genitalia

A
  • Pili and Por bind to CR3 on cervical
    epithelial cells
  • iC3b deposits on LOS, binds to CR3
  • Internalization via CR3 does not trigger
    an inflammatory response
    ➢ Asymptomatic infection
30
Q

Clinical Spectrum and Manifestations

A
  • Urethritis
  • Rectal
  • Pharyngeal
  • Cervicitis
  • Salpingitis
  • Disseminated Infection
  • Conjunctivitis (infants)
31
Q

Urogenital infection in Females

A
  • Asymptomatic in many
  • Symptoms range from minimal to severe
  • Increased vaginal discharge due to
    endocervical infection
  • Dysuria – urethral colonization
32
Q

Salpingitis

A
  • Symptoms: lower abdominal pain, abnormal
    menses
  • Can result in inflammation of fallopian tube, with
    scarring
  • Important cause of infertility, ectopic pregnancy
33
Q

Disseminated Gonococcal Infection (DGI)

A

causes minor lesions on the skin

34
Q

Predominant test for GC diagnosis

A

NAAT

35
Q

abx-R is an issue so what drug is reccomended?

A

ceftriaxone

36
Q

Neisseria meningitidis

A
  • Semi-typical Gram-
    negative cell wall
  • Same as N.
    gonorrhoeae except
    that N. meningitidis
    has a polysaccharide
    capsule
37
Q

Neisseria meningitidis Antigens

A
  • Major antigens are capsular polysaccharide
    (CPS), LOS, pili, OMP’s
  • N. meningitidis has fewer Opa genes, but has
    another similar family Opc
  • Antigenic diversity is due partly to
    interspecies genetic exchange with closely
    related Neisseria species
38
Q

NM capsule expression is

A

down-regulated during
carriage; up-regulated during invasion into
bloodstream

39
Q

Asymptomatic carriage

A
  • More common in adolescents, young adults
  • Usually transient: 75% clear within a few months
  • Is primary reservoir of infection
  • Transmission via respiratory droplets and throat
    secretions (saliva or spit)
  • Carriage is immunizing
40
Q

NM pathogenesis

A
  • Attachment to oropharynx – via pili
  • Most organisms remain as extracellular
    adherent pathogens
  • Dissemination from pharynx is via blood
    stream; invasion through blood-brain barrier
41
Q

Meningitis

A
  • Seen primarily in children 6 months – 10 years
  • Fever, vomiting, headache, confusion
42
Q

Meningococcemia

A

Abrupt onset of illness: spiking fever, chills,
arthralgias, myalgias

43
Q

Dx NM

A
  • Real-time PCR for N. meningitidis most sensitive
  • Gram stain of CSF (85% sensitivity)
  • Culture from blood (50-60% sensitivity) for CSF;
    less commonly from skin lesions, joints
44
Q

Treatment & Vaccination

A
  • Penicillin G has been drug of choice, but some
    resistance has been identified
  • IDSA now recommends ceftriaxone or cefotaxime
  • Adjunct steroid therapy is beneficial in children
45
Q

“New” Meningococcal Vaccines

A
  • Protein-based
  • Bivalent vaccine (Trumenba, Pfizer)
  • fHbp variants
  • 4 Component MenB vaccine (GSK)
  • 3 conserved proteins mixed with OMV
  • Approved for use in Europe and US
  • GET THIS IMMUNIZATION!!!!
  • Some protection against gonorrhea