Unit 1 - Gonorrhea and Chlamydia Flashcards

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1
Q

Neisseria gonorrhoeae bacteriology

A

G- diplococci with LOS

  • human-restricted
  • oxidase positive, not encapsulated, needs chocolate agar (not blood agar) as growth inhibited by trace metals and fatty acids
  • very sensitive to dehydration, cold
  • plasmid-borne Ab resistance is more common than in meningococcus (cephalosporin resistance emerging)
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2
Q

how are N. gonorrhea and N. meningitidis the same and different?

A

both

  • human restricted, G- LOS diplococci
  • oxidative positive
  • cleared from bloodstream by immune complement
  • growth in vitro inhibited by trace metals and FA (need chocolate, not blood, agar)

N. g

  • not encapsulated
  • hundreds of serotypes
  • even more sensitive to dehydration, cold

N. m
-ferment maltose

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3
Q

N. gonorrhea pathogenesis

A

sexually transmitted or at birth

  • genital tract infections most common, anorectal and pharyngeal also occur
  • Ab, complement, and neutrophils are restricted to local infection site (vagina, urethra)
  • bacteremia occurs in certain strains, predispositions
  • extremely contagious sexually (single-exposure transmission)
  • symptoms develop quickly (no latency)
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4
Q

what is the usually N. gonorrhea pathogenesis/exam for neonates, males, and females?

A

neonate: bilateral purulent conjunctivitis; if untreated, permanent blindness
male: usually symptomatic anterior urethritis
female: usually asymptomatic, cervicitis, purulent vaginal discharge, but type IV pili confer “twitching motility” for progression to PID
both: coinfection of pharynx, rectum, eye

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5
Q

virulence factors of N. gonorrhoeae

A
  1. IgA protease: clears IgA from mucosal surfaces for colonization
  2. pili: attach to columnar and transitional epithelium of mucosal surfaces, antiphagocytic
  3. Opa: opacity-associated proteins enhance cell adherence and entry
  4. porin A and B channels: in outer membrane, confer serum resistance and enhance cell entry
  5. LOS: less immunogenic than LOS, but induces local inflammatory response (irritation, discharge, containment)
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6
Q

is N. gonorrhoeae dependent on host for replication?

A

no, it’s replication-competent, so intracellular penetration is for immune evasion

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7
Q

describe pelvic inflammatory disease

-what is Fitz-Hugh-Curtis syndrome?

A

spread of cervical infection to fallopian tubes creates pain, risks of infertility, and ectopic pregnancy

  • follows from mixing bacteria with refluxed menstrual blood or attachment to sperm (“twitching motility” by pili)
  • intermenstrual bleeding, dysurea
  • sonogram may show thick fallopian tubes or abscess
  • FHCS: bacteria (gonorrhea or chlamydia) jump from tubes to liver capsule to cause acute perihepatis
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8
Q

what happens if bacteremia (dissemination) of N. gonorrhoeae occurs? predisposition?

A
  1. lack of urogenital symptoms
  2. arthritis/dermatitis (joint pain and skin pustules)
    - septic asymmetric arthritis (knee common)
    - asymmetric tenosynovitis with pain in wrists and akles
  3. rarely meningitis, endocarditis

certain strains are more likely to disseminate
-more common in women, asymptomatic infection, menses, pregnancy, and C6-9 deficiency predispose

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9
Q

how common are gonococcal meningitis and endocarditis? info on them?

A

both are rare

  • meningitis: spinal tap
  • endocarditis: EKG, cardio consult (mostly in men)
  • -aortic valve more common site
  • -subacute onset of fever, chills, sweats, malaise, chest pain, cough
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10
Q

gonorrhea labs for males

A

urine and exudate testing for PMNs and intracellular diplococci

  • if negative: urethral swab for G-, oxidase+, culture on Thayer-Martin agar
  • most sensitive and specific method
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11
Q

gonorrhea labs for females

A

obtain endocervical smear (urethral sample if hysterectomy) but wife exudate off first
-culture on Thayer-Martin

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12
Q

gonorrhea labs for DGI (disseminated gonococcal infection)

A
  1. swab, gram stain, culture samples from all affected areas
  2. blood, joint fluid cultured on nonselective chocolate agar
    - immunofluorescence may give better results than G stain or pustule samples
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13
Q

N. gonorrhea treatment

A

prompt antibiotics, before labs come back

  • ceftriaxone, alternate cefixime, cephalosporin
  • add azithromycin or doxycycline for coinfection with chlamydia
  • aspirate septic joints
  • admit if pregnant, PID, DGI, endocarditis, meningitis, purulent joint infection
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14
Q

what is expedited partner treatment?

A

provides scripts without exam for sexual partners of gonorrhea patients

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15
Q

C. trachomatis bacteriology

A

elementary bodies: dense, rugged, attach to cell, endocytosed, survive, and “unpack” into reticulate bodies
reticulate bodies: larger, delicate G- membrane, replicate, metabolize, “pack” into EBs, escape host cell

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16
Q

immune response to chlamydia

A

inflammatory cascade causes swelling and discharge, but fails to clear infection or prevent reinfection
-no useful immune memory, so reinfection common

17
Q

types of urogenital chlamydia and where most common

A

18 serovars
A, B, Ba, and C: blinding trachoma (Africa)
L1-L3: lymphogranuloma venereum (Central America)
D-K: genital tract infections (United States)

18
Q

blinding trachoma

A

serovars A, B, Ba, C

  • leading cause of preventable blindness
  • spread by secretions, fomites
  • endemic to Africa, S. Asia
  • eyelids turn inward, so eyelashes damage cornea
19
Q

lymphogranuloma venereum

A

serovars L1-L3

  • small ulcer –> painfully swollen lymph nodes near genitals (buboes)
  • -aspiration of buboes and fistulas may speed healing
  • symptoms from bacterial replication in mononuclear phagocytes of local lymph nodes
  • endemic to S. and C. America, rare in US (get detailed travel sex history)
  • labwork and treatment the same for other genital chlamydia
20
Q

“reservoirs” for gonorrhea and chlamydia

A

gonorrhea is more likely to have symptoms in males, but asymptomatic females are “reservoirs”

the reverse is the case for chlamydia

21
Q

pathogenesis of genital chlamydia

A

most commonly local mucosal inflammation and discharge, urethritis, vaginitis, cervicitis

  • infection increases risk of getting HIV
  • risk of PID; doesn’t go away after treatment of infection
22
Q

what is Reiter syndrome? symptoms? treatment?

A

reactive arthritis secondary to immune-mediated response

  • conjunctivitis + urethritis + arthritis
  • 80% of patients are HLA-B27 positive
  • treat with NSAIDs for 6 mo to 2 years until resolved
23
Q

chlamydia diagnosis exam for female

A
  • easily induced endocervical bleeding
  • mucopurulent endocervical discharge
  • intermenstrual bleeding
  • dysuria
  • abdominal pain
24
Q

chlamydia diagnosis exam for male

A
  • urethral discharge
  • urinary frequency and/or urgency
  • dysuria
  • scrotal pain/tenderness
  • perineal fullness
25
Q

three options for chlamydia diagnosis

A
  1. cytologic diagnosis (mostly for infant ocular trachoma)
    - stain eye swab with Giemsa or IF
  2. isolation in cell culture
    - grows well in many lines, and must ALWAYS do culture if legal implications
  3. detection of chlamydial rRNA by hybridizing to DNA probe
    - simpler, less expensive
    - more likely to give false positive
26
Q

why is serology not useful for chlamydia diagnosis?

A

past infection is too common

27
Q

chlamydia treatment

A
  1. intracellular antibiotics as chlamydia is intracellular
    - doxycycline (contraindicated if pregnant or < 9 yo b/c dental problems) or azithromycin
    - erythromycin and amoxicillin must be checked for efficacy
    - infection can hide “behind” other STDs