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Micro/Immuno FINAL > Neisseria (G-) > Flashcards

Neisseria (G-) Flashcards

1
Q

what is the only genus of G- cocci that frequently causes disease?

A

neisseria sp.

  • usually diplococci
  • n. gonorrhoeae (gonorrhea)
  • n. meningitidis (bacterial meningitis and septicemia)
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2
Q

is the neisseria sp. motile?

A

non-motile (twitching motility from pili)

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3
Q

do neisseria sp. require oxygen?

A
  • aerobes (but can grown anaerobically)

- grow best on media supplemented with blood in presence of CO2

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4
Q

what type of host does neisseria spp. require to live?

A

-obligate human pathogens: fragile, do not survive long outside host, humans are ONLY reservoirs

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5
Q

how prevalent is gonorrhea among other STDs and the youth?

A

4th on list of amount of youth who get it

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6
Q

how is gonorrhea diagnosed?

A
  • culture on chocolate agar in presence of CO2
    • boiled blood, iron, vitamins
    • colonies = nonpigmented, mucoid, non-hemolytic
  • modified Thayer-Martin agar (MTM)
    • indicative of antibiotic resistance
  • catalase and oxidase reactions
    • both rxns positive->aerobic
  • sugar fermentations
    • meningococci:ferment glucose and maltose, but not sucrose or lactose
    • gonococci: ferment glucose, but not maltose or sucrose
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7
Q

what are the two major neisseria sp.?

A
  1. n. meningitidis (meningococcus)

2. n. gonorrhoeae (gonococcus)

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8
Q

in what habitat does n. meningitidis live?

A

-throat, human nasopharynx is the only known reservoir

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9
Q

how do we encounter n. meningitidis and how does it enter?

A
  • spread by airborne droplets, viral resp. infections (eg influenza) may enhance the spread
  • attach to nasopharyngeal epithelial cells and invade mucous membranes
    • asymptomatic carriage induces humoral antibody response
    • most individuals acquire immunity by age 20
  • invasion of the blood stream only occurs in individuals deficient in complement component (C5-C8)
  • type 4 pili: attach organism to meninges in CNS
  • lipooligosaccharide (LOS) damages host tissue: elicits host inflamm response, resulting in hemorrhaging of blood into skin and mucous membranes (purpuric rash)
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10
Q

what are the virulence factors for n. meningitidis?

A

LARGE CAPSULE, outer membrane blebs (LPS endotoxin), hemolysin

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11
Q

what is the habitat for n. gonorrheae?

A
  • mucosal epithelia of male urethra or female cervix

- asymptomatic carriers greater among women

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12
Q

how do we encounter n. gonorrhoeae and how does it enter?

A
  • contact with genital secretions
  • upon introduction, attach to columnar epithelia of cervix or urethra (gonococci)
    • pili and surface proteins
    • adhesins controlled by:
      1. phase variation-presence/absence
      2. antigenic variation-composition
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13
Q

what are n. gonorrheae’s virulence factors?

A
  • no capsule
  • pili and strong adhesins
  • LPS endotoxin
  • IgA 1 protease
  • phase/antigenic variation
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14
Q

describe the cell surface of n. gonorrhoeae.

A

classic diplococcus morphology

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15
Q

describe the cell surface of n. meningitidis.

A

membrane blebs are profuse

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16
Q

describe the phase variation of e. coli.

A
  • expression of gene product is turned on or off at high frequency
  • promoter inversion
    • promoter on -> fimbriae
    • promoter off - no fimbriae
17
Q

describe the phase variation of n. gonorrhoeae.

A
  • slipped strand mispairing: colony opacity-associated (Opa) genes (10+)-> constantly changing its color
    • encode outer membrane proteins
    • Opa’s presence results in neutrophil uptake
    • ***some gonococci lack Opa and avoid phagocytosis
    • *also controls other surf proteins, as well as LPS in gonococci and meningococci
18
Q

what is the antigenic variation of n. gonorrhoeae?

A
  • changes in composition or structure of surface molecules (eg. pili- host cell attachment)
  • reassortment and recombination of pilS loci
19
Q

**generally, how is gonococci spread and how does it multiply?

A
  • multply rapidly
    • shed in genital secretions
    • do not have flagella and are not motile
    • can enter epithelial cells
  • extracellular protease cleaves IgA1
    • removes Fc receptor end of antibody
    • enables escape from phagocytosis: haemophilus and streptococcis also posses
20
Q

what type of cells do gonococci attach to and where are they located?

A
  • non-ciliated cells
  • human fallopian tubes and columnar epithelial cells have ciliated and non-ciliated cells
    • non-ciliated cells have microvilli
21
Q

what happens once gonococci attached to the non-ciliated cells?

A
  • ciliary statsis: ciliary cell motility slows and ceases

- death of ciliary cells: slough from epithelial surf, can be elicited by LPS and peptidoglycan (G+/G-)

22
Q

what do the non-ciliated cells do once microvilli contact gonococci?

A
  • engulf bacteria: internalized by “parasite directed endocytosis”
  • intracellular replication (protection): gonococci may multiply within vacuoles
  • intracellular traffic: vacuoles fuse with basement membrane
  • exocytosis: vacuoles discharge bacteria into subepithelial connective tissue
23
Q

what damage do gonococci cause/do they secrete endotoxin?

A
  • do not secrete endotoxin
  • LPS (LOS- lipooliogsaccharide) and other cell wall components cause cell damage by inducing TNF-alpha
    • sloughing off of ciliated cells
    • non-ciliated cell lysis: release of factors that cause inflamm
24
Q

how do we fight gonococci?

A

-serum antibodies recognition that target LPS (LOS), Protein I of the outer membrane and other surf proteins

25
Q

how does gonococci evade human antibodies?

A
  • strains alter LPS with host-derived NAM (sialic acid)
  • surface component of RBCs (camouflage)
  • LOS is similar to antigens on human erythrocytes and may allow ‘self’ recognition
26
Q

gonococci causes what type of infection?

A
  • localized inflamm

- rarely lethal (even with spread to blood stream)

27
Q

what are the 3 general diseases from meningococci?

A
  1. uncomplicated bacteremic process
  2. metastatic infection of the meninges
  3. overwhelming systemic infection: circulatory collapse and disseminated intravascular coagulation (DIC)
    * individ. may lack IgG Abs that have specificity for capsular polysaccharide
    * highest known bacterial titers in blood
28
Q

which has a capsule? meningococci or gonococci?

A

meningococci is heavily encapsulated (polysaccharide) and produces hemolysin

29
Q

Pelvic Inflammatory Disease is an infection of which neisseria sp., and where does it infect?

A
  • gonococcal infection of female upper reproductive tract
    • inflamm of uterus and fallopian tubes (ciliated cells)
    • scarring of upper tract and adjacent organs: infertility, ectopic prego, chronic pelvic pain

-epididymitis: ascent of organism into upper reproducive tract of men

30
Q

what can disseminated gonococcal infections result from?

A
  • PID due to endotoxin
  • pustular lesions of skin
  • inflamm of tendons and joints
  • suppurative arthritis (pus)
  • more common in women
31
Q

what is purpura fulminanas-meningococcus?

A
  • disseminated intravascular coagulation (DIC) due to ability to survive in bloodstream
    • skin manifestations
    • meningitis
    • shock
    • death
  • response to LOS mediated by TNF-alpha and IL-1
  • the higher the response, the greater the damage and risk of death
32
Q

how are neisseria treated?

A
  • most are penicillin resistant
  • resistance to tetracycline
  • resistance to other antibiotics incr
  • antimicrobial chemoprophylaxis of close contacts is the primary means of preventing secondary cases of sporadic meningococcal disease
33
Q

how is contracting a neisseria sp. prevented?

A
  • behavioral: condom use, partner notification, early diagnosis and treatment
  • VACCINES TO GONOCOCCI DIFFICULT TO PRODUCE
    • antigenic and phase variation
    • protective intracellular components
  • vaccine to meningococci: quadrivalent-derived against capsular polysaccharide from 4 serotypes or tetravalent

Micro/Immuno FINAL (16 decks)

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