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Microm 442 > Lecture 16 Neisseria > Flashcards

Lecture 16 Neisseria Flashcards

1
Q

What are the different species of Neisseria?

A

pathogens:

  • N gonorrhoeae
  • N meningitidis

Commensals:
Many (eg N lactamica)

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2
Q

Neisseria are structurally identified by..?

A
  • gram negative diplococci

- non-motile, non- sporeforming

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3
Q

How is Neisseria grown in cx?

A

-requires enriched CO2 in medium
-oxidase-positive
-Pathogens utilize different sugars:
Gnonococcus: glucose
Meningococcus: maltose and glucose

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4
Q

What is the host range?

A
  • obligate human pathogens

- no good animal model to study

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5
Q

What are structures found in both pathogens?

A
  • G- cell wall

- Major antigens are pili, outer membrane proteins (Por, Opa), LOS (lipooligosaccharide)

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6
Q

What are two host receptors that are utilized by pili?

A
  • CD46 on male urogenital epithelial cells

- CR3 on female cervical epithelium

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7
Q

How is the expression of pili controlled?

A

Phase variation (transcriptional)

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8
Q

What is the antigenic variation in Pili?

A
  • conserved regions and 6 immunodominant variable regions
  • on antigenic type at a time, multiple present but are silent
  • expression occurs at one active site
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9
Q

What causes antigenic variation in pili?

A

-recombination (non-reciprocal) via intrachromosomal or via transformation.

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10
Q

What are two outer membrane protein?

A
  • Por

- Opa

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11
Q

What is Por?

A

(OMP I)

  • Por most abundant structural protein
  • Trimers: porin function
  • involved in attachment and invasion of host cells by binding to host CR3 receptor
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12
Q

Why is serotyping scheme based on Por?

A

-each strain has one antigenic type, but there is variation
among strains
Por 1A - (disseminated infection)
Por 1B - (local genital infection)

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13
Q

What is Opa?

A

(Omp II)

  • compromises group of 12 genes (3-4 in meningiditis)
  • 0-3 Opa proteins may be expressed in single strain
  • expression determines colony phenotype: opaque or transparent
  • functions in close attachment to host cells
  • Phase switch depending on environment
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14
Q

How is Opa genetically controlled?

A
  • Multiple gene copies, all with promoters
  • constitutively transcribed
  • translationally controlled
  • CTCTT repeats immediately proceeds genes, puts it in or out of phase
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15
Q

What is LOS?

A

Similar to LPS, but lacks repeating sugar subunit.

  • major role in production of inflammatory mediators
  • plays a role in attachment
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16
Q

What is Sialylated LOS?

A

confers serum resistance and attenuates the inflammatory response

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17
Q

What is the pathogenesis in Male vs Female GC?

A
  • infection of males leads to acute urethritis

- infection in females is asymptomatic

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18
Q

What is the mechanism of male pathogenesis of GC?

A
  • attachment to CD46 receptor in urethral epithelium
  • Opa expression results in closer adhesion in gonococci and host cells
  • GC multiply, reach submucosa, triggers inflammation, can have hematogenous extension.
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19
Q

What is the mechanism of pathogenesis of GC in females?

A

-Pili and por bind to CR3 in epithelial cells, does not trigger inflammatory response

20
Q

What is the host immune response to Neiserria G?

A
  • Natural abx develop from colonization with commensal Neisseria and other gram-negative organism
  • results in ability of NHS + C to kill many strains
  • Bactericidal abx (IgM, IgA, IgG).
  • opsonic abx
  • ingested, but not killed by neutrophils
21
Q

What is the epidemiology and transmission of GC?

A
  • Mostly through sexual transmission, male to female.
  • higher rates in non-whites
  • asymptomatic (more in females) make it hard to eradicate
22
Q

What is the clinical spectrum manifestations of GC?

A
  • Urethritis
  • Cervicitis
  • Salpingitis
  • Disseminated Infection • Conjunctivitis (infants)
  • Rectal
23
Q

What are the sx of Urethritis?

A
  • Incubation period: 1-14 days; majority develop symptoms in 2-5 days
  • Symptoms: dysuria and/or urethral discharge; variable degree of edema and erythema
24
Q

How does Urethritis affect males?

A

• Course: spontaneous resolution over several weeks without therapy; >95% are asymptomatic within 6 months.
• Complications:
–Epididymitis – unilateral testicular pain,
swelling
–Prostatitis – acute or chronic

25
Q

How does Urogenital infections affect women?

A
  • Asymptomatic in many
  • Symptoms range from minimal to severe
  • Increased vaginal discharge due to endocervical infection
  • Dysuria – urethral colonization is present in 70-90% of infected women
26
Q

What are the complications of Salpingitis?

A
  • 10-20% of infected women
  • Symptoms: lower abdominal pain, abnormal menses
  • Can result in inflammation of fallopian tube, with scarring
  • Important cause of infertility, ectopic pregnancy
27
Q

What is disseminated gonohrea?

A

• Occurs in 0.5-3% of untreated patients
• Manifested by acute arthritis –
dermatitis syndrome
• More common in females- may be associated with recent menstruation

28
Q

How is Gonorrhea dx?

A
  • NA amplification test in urine (w/ CT)
  • Gram stain (G-) sensitive in male. Diplococci
  • Cx using Thayer-Martin media
29
Q

How is gonorrhea treated?

A 
• Combination treatment: Ceftriaxone 250 mg IM
PLUS
Azithromycin 1g PO
or
Doxycycline 100 mg PO,
twice daily X 7 days
30
Q

What are some distinguishable features of N Meningitidis?

A
  • Commonly carried in nasopharynx as a commensal
  • Sometimes causes disease
  • Semi-typical gram negative cell wall
  • Same as N. gonorrhoeae except that N. meningitidis has a polysaccharide capsule
31
Q

What antigens are found on N meningitidis?

A

• Major antigens are capsular polysaccharide (CPS), LOS, pili, OMP’s
-Antigenic diversity due partly through interspecies gene exchange

32
Q

How are capsule regulated?

A

—Capsule expression is down-regulated during carriage; up-regulated during invasion into bloodstream

33
Q

Which serotypes of Meningitidis cause the most infections in industrialized countries?

A

-B and C, recent clustered outbreaks of Y

34
Q

What is the asymptomatic carriage of Meningococci?

A
  • 10-20% of individuals carry meningococci in throats
  • More common in adolescents, young adults
  • Usually transient: 75% clear within a few months
  • Serve as the primary reservoir of infection via droplets
  • Carriage is immunizing
35
Q

What is the immune response of MC?

A

-Maternal abx will protect you when you are born, but it will decrease and you will have to start to make your own.

36
Q

What is the pathogenesis of MC?

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.

37
Q

What is the pathogenesis and immune response of MC?

A
  • Susceptibility to infection is due to lack of bacteridical antibodies directed against Por, Opc, LOS.
  • Opsonic antibodies develop during carriage of N. lactamica and other cross-reactive organisms in childhood
  • Bactericidal antibodies develop during asymptomatic carriage of N. meningitidis.
38
Q

What is the meningitis belt?

A

-Region in Africa where there are seasonal outbreaks, 10 % of infected die. Usually form Type A.

39
Q

What are the type of vaccines for Meningococcus?

A
  • CPS vaccines -effective against A, C, Y and W
  • Group B CPS is poorly immunogenic
  • MenB OMV vaccines are effective, targets PorA.
40
Q

What are some clinical spectrum and manifestations of MC?

A

• Meningitis
• Meningococcemia
—Fulminant Meningococcemia

41
Q

What are sx of Meningitis?

A

– Seen primarily in children 6 months – 10 years
– Fever, vomiting, headache, confusion
-Maybe hearing loss

42
Q

What are sx of Meningococcemia?

A

– Abrupt onset of illness: spiking fever, chills, arthralgias, myalgias
– 75% develop petechial rash

43
Q

What are the sx of Fulminant Meningococcemia?

A

◦ Seen in 10-20% of patients (high levels of
endotoxin circulating)
◦ LOS induces TNF and interleukins, leading to shock, hemorrhages of skin and organs, and influx of leukocytes (meningitis)
◦ 40-60% mortality
◦ Dramatic: healthy death in 6 hours

44
Q

How is MC dx?

A

• Gram stain of CSF (85% sensitivity)
• Culture from blood, CSF; less
commonly from skin lesions, joints
• PCR for Neisseria meningitidis is most sensitive

45
Q

What is the treatment for MC?

A
  • Penicillin G is drug of choice; adjunct steroid therapy is beneficial in children
  • Alternatives include newer cephalosporins
  • Antibiotic treatment of carrier state not warranted
46
Q

What is the type of binding from Opa?

A

• Promiscuous binding
–Cell surface proteoglycans
–Extracellular matrix proteins
–Other cell surface adhesion molecules

Microm 442 (16 decks)

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