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Microbio Exam 1 > Sexually transmitted agents > Flashcards

Sexually transmitted agents Flashcards

1
Q

STDs are a large cause of morbidity and mortality across the world. Complications include:

A
  • congenital infection, infertility, ectopic pregnancy, cancers, enhanced transmission of HIV
  • When other STDs are present, transmission of HIV is 2-5x higher
  • if we better control STDs, can decrease HIV transmission
  • HIV also makes one more likely to get other STDs
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2
Q

There _________ new STD infections int he US annually and nearly half of these will occur in what age group?

A
  • 20 million

- adolescents/young adults (15-24)

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3
Q

Why haven’t STDs disappeared in the US despite better treatments and screening?

A
  • people still have unprotected sex
  • clinicians dont keep up with treatment guidelines
  • asymptomatic nature= not diagnosed
  • gender and sex differences
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4
Q

Gender differences in STDs

A
  • women are biologically more susceptible, often asymptomatic or minimally so
  • so more difficult to diagnose and more likely to suffer from more frequent and more serious health complications
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5
Q

Adolescent women and STDs

A

-younger females do not have full cervical maturity that can lead to enhanced risk of infection with gonorrhea and chlamydia

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6
Q

What are the 2 most common bacterial STDs? What type of STDs do they cause?

A
  • gonorrhea and chlamydia

- both cause clinically indistinguishable inflammatory STDs, but are bacteriologically very different

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7
Q

Gonorrhea and chlamydia symptoms in women, men, or both.

A

-Women: mucopurulent cervicitis, PID, tubo-ovarian abscess, peritonitis, dysuria-pyuria syndrome, Fitzhugh-Curtis syndrome (inflammation of Glisson’s capsule of liver)

  • Men: urethritis and epididymitis
  • Both: conjunctivitis and anorectal infection
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8
Q

Only gonorrhea can cause ______ and only chlamydia can cause _________.

A
  • pharyngitis
  • neonatal pneumonia
  • *these occur in both men and women**
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9
Q

Sequelae of chlamydia vs. gonorrhea

A
  • C: reactive arthritis (Reiter’s Syndrome)

- G: Disseminated Gonococcal infection (DGI) and reactive arthritis

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10
Q

Gonorrhea’s genus and species

A
  • Neisseria Gonorrhoeae

- “flow of seed”

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11
Q

Physiology and structure of Gonorrhea

A
  • gram negative
  • diplococcus with adjacent sides flattened like coffee beans
  • no capsule
  • very fastidious and requires special media and 5% CO2 for isolation in culture
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12
Q

Gonorrhea virulence factors

A
  1. pili that allow for attachment to host cells
  2. Por protein
  3. Opa protein
  4. Lipooligosaccharide
  5. Beta Lactamase enzymes which promote penicillin resistance
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13
Q

Antigenic variation and pili of Gonorrhea

A

-allows for no significant immunity to develop and re infection can occur

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14
Q

Por Protein function

A
  • virulence factor of gonorrhea

- promotes intracellular survival of organism allowing it to evade destruction by phagolysosome

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15
Q

Opa protein function

A
  • VF of gonorrhea

- mediates binding to epithelial cells

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16
Q

Pathogenesis of Gonorrhea

A
  • organism attaches to mucosal cells via pili and penetrates into the cells where it establishes infections in the subepithelial space
  • lipooligosaccharide stimulates an inflammatory response that includes release of TNF and other cytokines
  • WBCs are called in and this response results in inflammatory process and clinical findings of an “itis” and discharge
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17
Q

Where does gonorrhea establish infection?

A

-subepithelial space

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18
Q

Natural hosts of Neisseria gonorrhoeae

A

-only humans

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19
Q

Route of transmission of Neisseria Gonorrhoeae

A

-direct mucosal contact with infected mucous membranes or fluids

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20
Q

Can you get gonorrhea from a toilet seat?

A

-no, it does not survive well outside the body

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21
Q

Neisseria Gonorrhoeae epidemic exists in what age group?

A

-adolescents where case rates 6-7 times higher than the general population

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22
Q

Is Neisseria Gonorrhoeae symptomatic?

A
  • 90% of males infected become symptomatic in 5-7 days
  • 50% of women become symptomatic within 2 weeks
  • SCREENING IS ESSENTIAL
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23
Q

Gonorrhea lab diagnosis

A
  • in men, gram stain of urethritis
  • culture is weaning out due to weird conditions required to grow on (Thayer-martin media); make sure to swab all exposed sites
  • Non-culture based diagnostics have become gold standard over last 2 decades
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24
Q

What are examples of non-culture based diagnostics used in gonorrhea and chlamydia diagnoses?

A
  • PCR
  • Nucleic acid amplification tests (NAATs)
  • non invasive urine tests and NAATS
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25
Q

Treatment for uncomplicated Gonococcal infections

A
  • intramuscular Ceftriaxone PLUS oral azithromycin
  • single dose regimen
  • ALWAYS treat for chlamydia co-infection
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26
Q

_______ in men and ________ in women can infect other mucousal sites and cause invasive disease (disseminated gonococcal infection)

A
  • urethritis

- cervicitis

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27
Q

Physiology and structure of Chlamydia trachomatis

A
  • obligate intracellular bacterium
  • small, gram negative bacillus
  • requires living tissues or cells for culture, which is labor intensive and insensitive
  • exists in 2 forms
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28
Q

Transitions of cervical maturity

A
  • prepuberty: cervical entrance is squamous and columnar cells
  • Puberty: squamous, squamous-columnar junction (transitioning cells), columnar cells
  • Postmenarche: 100% squamous cells
  • *STDs target columnar cells, so younger girls are more at risk
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29
Q

What types of diagnostics are gold standard for Chlamydia?

A

-non-culture based diagnostics

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30
Q

Chlamydia has many serotypes: what are they and what do they cause?

A
  • A,B,C: endemic trachoma of the eyes
  • D-K: GU syndromes
  • L1-L3: lymphogranuloma venereum (LGV)
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31
Q

What are the 2 forms C. trachomatis exists in? Are they both infectious?

A
  • elementary body (EB); infectious form

- Reticulate body (RB): noninfectious, intracellular form that promotes replication

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32
Q

What life form is C. trachomatis transmitted in?

A

-elementary body

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33
Q

Describe the Chlamydia life cycle

A
  • elementary body access epithelial cell
  • forms reticulate bodies which multiple and form an inclusion
  • Inclusion matures into RB and EB
  • EBs multiple, lyse cell and spread
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34
Q

Pathogenesis of Chlamydia: receptors for the EB are only found on mucous membranes of…

A
  • urethra
  • endocervix, endometrium, fallopian tubes
  • anorectum
  • respiratory tract (pneumonia in children)
  • conjunctiva
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35
Q

Why is re-infection problematic in Chlamydia?

A
  • it causes cellular destruction and an inflammatory host immune response
  • inflammatory response with re-infection is strong and can lead to end organ damage (sterility and blindness)
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36
Q

What are the hosts of chlamydia and how is it spread?

A
  • humans are only natural host

- spread by direct mucosal contact with infected mucous membranes or fluids

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37
Q

Is chlamydia or gonorrea more widespread?

A
  • chlamydia

- most commonly reported infectious disease in the US

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38
Q

Chlamydia rates in women appear to be increasing at a much higher rate than in men…why?

A
  • better diagnostic tests in women because they have greater side effects
  • so this discrepancy is due to greater diagnostic criteria for women
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39
Q

3 risk factors for chlamydial infection

A
  • young age (adolescent)
  • heterosexual
  • increased sexual partners (2 or more)
40
Q

Why is chlamydia called the silent epidemic?

A
  • 75% of females and up to 50% of male infections are asymptomatic
  • C. trachomatis can persist for 2 years in female genital tract (silent PID)
41
Q

Asymptomatic chlamydial infection is the primary reason for __________.

A
  • tubal infertility

- and PID in women

42
Q

Laboratory diagnostics for chlamydia

A
  • nonculture based diagnostics are preferred, as in GC
  • PCR tests
  • Single swab for both GC and CT
43
Q

Treatment of uncomplicated Chlamydia

A
  • azithromycin single dose (macrolide)
  • doxycycline (7 day regimen)(tetracycline)
  • both are equally efficacious
44
Q

urethritis in males: signs/symptoms; exam; diagnosis

A
  • signs: dysuria, discharge, burning
  • exam: discharge varies in color/amount
  • Diagnosis: gram stain
45
Q

When a gram stain is performed, how would you tell if it was due to GC?

A
  • intracellular, gram negative diplococci

* confirm GC with cultures and tests (NAATs)

46
Q

Urine-based diagnostics for Chlamydia and Gonorrhea benefits and drawbacks

A
  • benefits: no pelvic exam, no urethral swab, accuracy, enhances screening opportunities, enables data collection on asymptomatic population
  • Drawback: no substitute for sexual history-taking, no detection of resistance, cannot test rectal/oropharyngeal specimens, and amplification inhibitors can lead to false negatives
47
Q

If on a urethritis gram stain, there are no gram negative diplococci, but there are 5 or more PMNs/oil field, then the clinical diagnosis is __________. What is the most common cause of this?

A
  • NGU: non-gonococcal urethritis
  • Chlamydia is most common cause
  • Diagnosis: discharge, + gram stain, + leukocyte esterase on urine dip, or U/A with >10 PMNs/hpf
48
Q

How does epididymitis present?

A
  • presents as pain, swelling, and erythema of the scrotal sac
  • usually unilateral
  • on exam, there is tenderness and swelling and erythema
  • may not have concurrent discharge
49
Q

In young (<35) sexually active men, epididymitis is almost always caused by _______________. Occasionally what else can cause it and in what population?

A
  • GC or CT

- E. coli in men who practice insertive anal sex

50
Q

Mucopurulent cervicitis in women is often asymptomatic, but when symptoms are present, what are they?

A
  • discharge
  • dyspareunia
  • bleeding
  • dyuria
  • lower abdominal pain
51
Q

What symptoms of mucopurulent cervicitis are seen upon a clinical exam?

A
  • cervical friability (bleeds easily with swab)
  • edema
  • erythema
  • and/or endocervical discharge
  • sometimes it is normal but still tests positive for GC or CT
52
Q

What can cause mucopurulent cervicitis?

A
  • GC
  • CT
  • Both
  • rarely, neither
53
Q

If a physician swabs the endocervix and their is a yellow discharge on the tip, what is that indicative of?

A

-mucopurulent cervicitis

54
Q

Gram stains and mucopurulent cervicitis

A

-low sensitivity and is not routinely recommended

55
Q

PID induces inflammation of the upper genital tract and may manifest as what 4 things?

A
  • salpingitis
  • tuboovarian abscess
  • endometriosis
  • peritonitis
56
Q

25% of women with PID will develop chronic sequelae. What are the chronic sequelae of PID?

A
  • ectopic pregnancy
  • chronic pelvic pain
  • infertility
57
Q

Antimicrobials and PID sequele

A
  • data suggest that antimicrobial therapy has NO EFFECT on subsequent rates of sequelae. Therefore, the only way to impact these chronic sequelae is to find the woman and diagnose her before she developed symptomatic PID
  • Thus, screening for GC and CT are essential!!
58
Q

3 other sides of GC infections

A
  • phayngeal GC: often asymptomatic, non-exudative, and may be difficult to eradicate
  • Conjunctivitis: pain, erythema, eye discharge
  • Perirectal: tenesmus, pain, anal discharge and friability
59
Q

Disseminated gonococcal infection is the result of _________.

A
  • gonococcal bacteremia

- organism disseminated from GU tract into the blood stream

60
Q

2 ways patients may present with DGI

A
  1. Dermatitis-Arthritis Syndrome: 10-20 pustular, hemorrhagic lesions around small joints and have small joint tenosynovitis
  2. septic, monoarticular arthritis, usually of the knee
    * rare complication is gonococcal endocarditis*
61
Q

Patients with DGI are treated with ______________.

A

-IV ceftriaxone initially and changed to oral therapy after improvement

62
Q

Chlamydia infections at other sides include:

A
  1. perirectal
  2. conjunctivitis
  3. dysuria-pyuria syndrome**
  4. sexually active women with UTI symptoms and pyuria (WBC in urine) but sterile urine cultures usually due to CT and CG, less commonly
63
Q

Is conjunctivitis level better or worse in GC or CT?

A

-always less symptomatic in CT patient than GC

64
Q

Lymphogranuloma venereum presentation

A
  • inguinal lymphadenopathy with or without proctitis
  • pelvic and lumbar nodes are involves
  • fever, tenesmus, bleeding and rectal pain
  • due to L1-L3 serovars of CT
65
Q

Reactive arthritis is a post-inflammatory syndrome that is seen more commonly after_______ than ______, and can also be seen after ________.

A
  • CT than GC

- bacterial gastroenteritis

66
Q

Classic triad of symptoms of Reactive arthritis

A
  • arthritis
  • conjunctivitis
  • urethritis
  • skin lesions can also be seen and include keratoderma blenorrhagicum and a circinate balantis
67
Q

What is the etiologic agent of syphilis?

A

-Treponema pallidum

68
Q

Physiology and structure of Treponema pallidum

A
  • corkscrew-shaped, helical, motile bacterium (spirochete)
  • cannot be cultures in vitro
  • cannot be seen under LM
69
Q

Pathogenesis of SyphilisL Treponema pallidum

A
  • organism penetrates and enters via skin or mucous membranes
  • smaller the inoculum, longer the incubation period
  • before any symptoms occur, the organism has traveled via the lymphatic system to region LN and then through the body via blood streams
70
Q

What appears at the site of syphilis inoculation?

A

-chancre

some spirochetes lodge at entry site, proliferate, sensitize lymphocytes and activate macrophages

71
Q

Syphillis immunity

A

-immunity is present with chronic infection but lost after treatment

72
Q

Invasion of the ______ occurs in >30-40% of patients with primary or secondary syphillis

A

-CNS; permanent in some people

73
Q

Syphillis routes of transmission

A
  • direct contact with active lesions or infectious mucous membranes (usually sexual contact)
  • congenital
  • bloodborne (rare)
74
Q

When are patients with syphillis more infectious?

A

-1st year of infection

75
Q

MSM or MSW have higher rates of syphillis?

A
  • MSM

- men more likely to have it than women

76
Q

Primary syphillis

A
  • incubation period 9-90 days depending on inoculum size
  • primary chancre: single painless ulcer at site of inoculation; smooth clear ulcer base, borders raised, rolled, indurated
  • painless region adenopathy
  • no constitutional symptoms (dont feel sick)
77
Q

If you see oral lesions on buccal, pharyngeal mucosa, on tongue or lips/perioral area, you should have a high index of suspicion of ______.

A

-syphillis primary chancre

78
Q

Secondary syphilis

A
  • the great imitator
  • manifests occur 2-8 weeks after chancre
  • spirochetes disseminated, meninges seeded
  • skin manifestations
  • constitutional symptoms: fever, malaise, anorexia, wt loss, pharyngitis, myalgias
  • mucous patches
  • painless, generalized adenopathy
  • CNS disease
  • arthritis, hepatitis, osteitis
79
Q

What are the skin manifestations of secondary syphillis?

A
  • rash: macular, papular, maculopapular, papulosquamous; diffuse; palmar-plantar
  • condylomata lata: grey-whitge or pink moist plaques found in intertriginous areas
  • alopecia
80
Q

CNS disease of secondary syphillis

A
  • headaches
  • 1-2% get aseptic meningitis
  • rarely can see CN involvement
81
Q

Latent syphillis

A
  • no clinical manifestations
  • only evidence is positive serology
  • early vs. late latent syphilis
82
Q

Early vs. Late latent syphilis

A
  • early: asymptomatic infection of 1 year in duration, or of unknown duration
  • 25% of early latent cases may relapse into secondary
83
Q

3 types of tertiary syphillis

A
  • gummatous
  • cardiovascular
  • neurosyphilis
84
Q

Gummatous syphillis

A
  • characterized by gummatous lesions in the skeletal, spinal, and mucosal areas
  • eye and viscera (lung, stomach, liver, genitals, breasts, brain, heart) can also be affected
  • gummas are granuloma-like lesions
  • spirochetes often not seen in biopsies
85
Q

Cardviovascular syphillis

A
  • presence of thoracic aortic aneurysm due to endarteritis of aortic vasovarum
  • rarely rupture but often track back into the heart leading to aortic insufficiency
86
Q

Neurosyphilis (5)

A
  • most common manifestation of tertiary syphilis
  • earliest to occur is meningovascular (5010 years)
  • parenchymatous neurosyphilis presents as personality changes, dementia, delusions of grandeur, paranoia (20 years post infection)
  • Tabes dorsalis (25-35 years/latest) presents with lightning pain down legs, neuropathy characteristic gait due to demyelination of dorsal spinal columns and incontinence
  • less commonly: eye disease and syphilitic otitis
87
Q

Meningovascular syphilis usually presents as ______.

A

-stroke in young person

88
Q

Laboratory diagnosis of syphilis

A
  • cannot culture in vivo
  • darkfield microscopy: scrapings of active lesions examined under darkfield scope
  • serologic tests
89
Q

Serologic testing for syphilis is done in 2 steps:

A
  1. screening test performed using nontreponemal test; if positive, confirmatory test is ordered
  2. Confirmatory test are specific treponemal tests; will be positive for life
90
Q

Nontreponemal tests

A
  • not specific for T. pallidum
  • measures antibodies developed against lipids released from damaged cells
  • rapid, cheap, quantitative, but insensitive to certain stages, biological false positives
91
Q

2 tests of nontreponemal testing

A
  1. RPR card test: read directly

2. VDRL test: read via microscope

92
Q

Specific treponemal tests for syphilis

A
  • immunofluorescence: FTA-Abs
  • HemagglutinationL TPPA and TPHA
  • tests depend on serum dilution and absorption for specificity
93
Q

Can specific treponemal tests be used to determine reinfection or adequacy of treatment?

A

-no, once treated, these remain positive for life

94
Q

Newer “reverse screening” for Specific treponemal tests

A
  • enzyme immunoassats
  • chemiluminescence immunoassays
  • microbead immunoassays
95
Q

Treatment of syphilis

A
  • Penicillin G is drug of choice for ALL stages
  • it is the only therapy with documents efficacy for neurosyphillis or for syphilis during pregnancy
  • doxycycline is allergic to PG, non pregnant, and non HIV infected

Microbio Exam 1 (13 decks)

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