CNS and STDs Flashcards

1
Q
  1. What is the reservoir for Neisseria meningitidis?
  2. How is it spread?
A
  1. Nasopharynx of humans only
  2. Spread by respiratory transmission
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2
Q

What is the characteristic structure/physiology of Neisseria meningitidis?

A

Gram negative diplococci with a LipoOligoSaccharide capsule

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3
Q
  1. Does Neisseria meningitidis possess pili?
  2. What is the general process of a N. meningitidis infection?
A
  1. Yes
  2. Attach to non-cilia columnar epithelia → Internalized into phagocytic vacuoles → Transcytosis to subepithelial space → LOS induces vascular damage, vessel inflammation, thrombosis
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4
Q
  1. What does an acute *N. meningitidis *infection look like?
  2. What does infantile meningitis look like?
  3. How is N. meningitidis infection diagnosed?
A
  1. Abrupt and insidious onset w/ symptoms of a general meningitis (Nuchal rigidity etc.)
  2. Irritable, Decreased PO, Seizures, Disturbed tone, Coma
  3. Oxidase positive, Gram negative diplococci gram stain of CSF.
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5
Q
  1. What is the demographic with the highest incidence of N. meningitidis infection?
A
  1. School-age children and young adults
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6
Q
  1. How many and which serogroups does the N. meningitidis vaccine cover?
  2. What is added to make the vaccine effective?
A
  1. It is tetravalent for A, C, Y, W135
  2. It is a conjugate vaccine with Diptheria toxin.
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7
Q

What is the treatment for N. meningitidis infection?

A

Cefotaxime
Ceftriaxone
Penicillin G

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8
Q

What is used for prophylaxis if someone is exposed to the disease for >8 hours?

A

Rifampin
Cipro
Ceftriaxone

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9
Q

At what age are neonates most at risk/susceptible to N. meningitidis?

A

6 to 24 months

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10
Q

What two sugars does N. meningitidis metabolize?

A

Maltose and Glucose which can be remembered because meningitis has an M and a G in it.

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11
Q
  1. What is different about the structure of N. gonorrhea compared to N. meningitidis?
  2. How are they similar in structure?
A
  1. It has NO polysaccharide capsule
  2. They both possess pili
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12
Q

What does N. gonorrhea express that interferes with neutrophil degranulation and resists complement?

A

PorB

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13
Q
  1. What do Opa proteins do to promote N. gonorrhea virulence?
  2. What portion of N. gonorrhea causes cellular damage?
A
  1. They mediate binding to non-ciliated epithelial cells
  2. Core LOS damages urethral and vaginal epithelium
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14
Q

How does N. gonorrhea escape antibodies produced by the immune system?

A
  1. Pili frequently alter epitopes
  2. PorB has significant serological variation
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15
Q

What organism is responsible for the presence of Oxidase positive, gram negative diplococci within PMNLs?

A

Neisseria gonorrhea

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16
Q

What are the special needs of N. gonorrhea when attempting to culture?

A

It requires a complex medium (chocolate agar) and is sensitive to cold

17
Q

Why isn’t there a vaccine for gonorrhea?

A

No capsule + High variability

18
Q
  1. What age group is the peak incidence for gonorrhea?
  2. What is the major reservoir?
  3. Are symptoms more common in women or men?
A
  1. 15-24 year olds
  2. Asymptomatic individuals
  3. Men
19
Q
  1. How is Chlamydia trachomatis structure similar/different than N. gonorrhea?
  2. What implication does this have on clinical treatment?
A
  1. It is gram negative but does not have a PDG cell wall
  2. Beta lactam antibiotics won’t work
20
Q

There are two structural forms for Chlamydia trachomatis, the elementary body and the reticulate body. What is the purpose of each?

A
  1. Elementary body is the infectious form and is environment stable.
  2. Reticulate body is the replicative form, is metabolically active, and is NOT environment stable.
21
Q
  1. Where does Chlamydia trachomatis replication take place?
  2. *Chlamydia trachomatis *is an obligate intracellular parasite. How does it manage to survive inside of inclusion body?
A
  1. Within an inclusion body.
  2. It interferes with normal endocytic trafficking.
22
Q
  1. How is Chlamydia trachomatis acquired?
A
  1. It is acquired through abrasions or lesions at a sexual site. It attached to non-ciliated **columnar cuboidal ** or transitional epithelia cells.
23
Q
  1. What is the more invasive form of Chlamydia trachomatis that can develop into proctitis in women?
  2. What happens with untreated Chlamydia trachomatis?
A
  1. Lymphogranuloma venereum
  2. It enters a chronic ulcerative phase.
24
Q
  1. How/where is a specimen collected for women concerning for Chlamydia trachomatis?
    * 2. Chlamydia trachomatis* cannot be grown in artificial media. What is the best way to test the specimen collected?
A
  1. Endocervical specimen
  2. Nucleic acid amplification test.
25
Q
  1. What is Reiter syndrome and what organism causes it?
  2. What is trachoma?
A
  1. It is urethritis, conjunctivitis, polyarthritis and mucocutaneous lesions. It is caused by Chlamydia trachomatis.
  2. It is keratoconjunctivitis by serotypes A,B,Ba, and C. It is endemic to everywhwere except North America and Europe.
26
Q

Who is more likely to be asymptomatic with urogenital *Chlamydia trachomatis *infection, Men or Women?

A

Women are asymptomatic 80%

Men are asymptomatic 25%

27
Q

What antibiotics are used for Chlamydia trachomatis?

A

Doxycycline, Erythromycin, or Azythromycin

28
Q

Chlamydia psittaci is primarily an infection of birds and poultry, how can humans acquire it and what kind of illness does it create?

A

Inhalation of desicated feces particles which causes a viral-like atypical pneumonia.

29
Q
A