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6. HDS GI Repro > Sexually Transmitted Infections and Vaginitis > Flashcards

Sexually Transmitted Infections and Vaginitis Flashcards

1
Q

Sexually Transmitted Infections

Epidemiology

A
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2
Q

STI’s

Transmission Risk

A
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3
Q

Treponema pallidum

Morphology and General Characteristics

A
  • Slender, helical or coiled spirochete
  • Cannot be cultured in vitro
  • Visualized by silver stain or dark field microscopy
    • Too thin to be seen by Gram’s stain or Giemsa
  • Fresh wet mount ⇒ corkscrew movement and flexion
  • Microaerophilic or anaerobic
    • Extremely sensitive to oxygen
  • Sensitive to drying, disinfectants and heat
  • Subspecies of Treponema that cause tropical diseases: yaws, pinta and bejel
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4
Q

Treponema pallidum

Transmission / Epidemiology

A
  • Transmission 1° through sexual contact and congenital
  • Transmission via transfusion possible but rare
  • Treponemes cross the placenta from mother → fetus by unknown mech
  • Humans are the only host
  • Disease occurs worldwide w/ no seasonal incidence
  • Incidence is ↑, particularly in MSM
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5
Q

Treponema pallidum

Pathogenesis

A
  • Sexual exposure to ⊕ individual ⇒ high probability of acquisition w/ subsequent disease
  • Enters host via mucous membranes or small abrasions in the skin which commonly occur during sexual intercourse
  • Incubation is 4-6 wks
  • Initially replicate locally
  • Spread via lymphatic and circulatory systems
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6
Q

Treponema pallidum

Virulence Factors

A
  • Limited knowledge of virulence factors that promote disease
  • Lack of species-specific surface Ag helps organism evade the immune system
  • Resists phagocytosis
  • Binds fibronectin allowing them to bind cells
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7
Q

Primary Syphilis

A
  • Immune cells → site of entry where treponemes are replicating
  • Battle between immune cells and bacteria ⇒ lesion of primary syphilis (chancre)
    • Painless w/ a raised border
    • Heals spontaneously in ~ 6 months
  • Organisms that spread via bloodstream ⇒ 2° Syphilis
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8
Q

Secondary Syphilis

A
  • ~3-6 wks after chancre heals, 2°form of syphilis appears in ~50% of individuals
  • Systemic spread of treponemes ⇒ replication in LNs, tissues and skin
  • Lesions ass. w/ secondary syphilis varied ⇒ “the great imitator”
  • Rash may be maculopapular, pustular, or scaly
  • Raised lesions called condyloma lata may appear in skin folds and mucous membranes
  • Clinical signs of disseminated disease include HA, fever, myalgia, LAD
  • Rash and sx resolve within a few wks but may recur
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9
Q

Tertiary Syphilis

A
  • ~ ⅓ ⇒ organisms disappear and person is cured
  • ⅔ ⇒ remain latent for yrs or even decades after 1° infection
    • ~½ of these ⇒ manifestation of tertiary syphilis
  • Most sx due to immune destruction of tissue due to presence of treponemal Ag
  • Chronic inflammation may manifest as:
    • Gummas: soft masses composed of few organisms and many inflammatory cells, frequently granulomatous lesions
      • May destroy bone and soft tissue
      • May involve vital organs such as the liver, brain etc.
    • Neurosyphilis
      • Characterized by some or all of the following:
      • Tabes dorsalis: loss of positional sensation ⇒ staggering
      • Charcot joint: trauma to the knee and ankle joints
      • General paresis
      • Gradual loss of higher integrative functions and personality
      • Argll Robertson pupil: pupil does not react to light but contracts when object is moved from far to near
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10
Q

Congenital Syphilis

A
  • Premature birth, intrauterine growth retardation
  • Most infected
  • Infants don’t initially show sx until ~ 2 y/o
    • Facial and tooth deformities
    • Hutchinson incisors and mulberry molars
    • Deafness, arthritis and CV disease are common
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11
Q

Treponema pallidum

Diagnosis

A
  • Fragile & fastidious ⇒ cannot be cultured
  • Darkfield microscopy or special stains
    • Visualize organisms in wet mounts from chancre or skin lesions
    • No longer performed
  • Non-Treponemal Serological Tests
    • Reaginic Ab
      • Measure IgM and IgG vs cardiolipin from damaged cells
      • Inexpensive and easy to use but can result in false ⊕s
      • Recommended for screening
      • May be ⊖ in 1° syphilis
      • ⊕ at 2-3 wks after infection, 30% ⊕ after 1 wk
      • ⊕ in 2° disease
      • ⊖ or ⊕ during latent and 3° disease
      • Titers ∆ w/ disease activity
    • Most commonly used tests:
      • Venereal Disease Research Laboratory (VDRL)
        • Slide micro-flocculation, cardiolipin Ag suspension
        • Specimen: CSF
        • Qualitative or semi-quantitative
      • Rapid plasma regain (RPR)
        • IgG and IgM vs cardiolipin Ag-coated particles
        • Rapid dx in clinical settings
  • Treponemal Specific Tests
    • Use T. pallidum as Ag
    • Specific and sensitive
      • False ⊕ of 1-2%
    • ⊕ specific serology remains ⊕ for life
      • Cannot be used to track efficacy of tx
    • Most commonly used tests:
      • Fluorescent treponemal Ab-absorption test (FTA-ABS)
        • Indirect IF test
      • Treponema pallidum particle absorption test (TP-PA)
        • Agglutination assay
      • EIA/CIAs
  • Lumbar puncture
  • For pts w/ ocular or neurologic sx, treatment failure (non-treponemal titers not declining appropriately)
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12
Q

Treponema pallidum

Treatment

A
  • Penicillin G ⇒ abx of choice in all stages of syphilis
    • Spirochete exquisitely sensitive to PCN despite almost a century of use
  • Sex partner(s) should be evaluated and treated
  • Adults w/ primary, secondary and early latent (less than 1 year) syphilis:
    • Benzathine PCN G IM (single dose)
  • Latent syphilis over 1 year, unknown duration, or tertiary sx:
    • 3 wks of Benz. PCN G IM (once weekly)
  • Evidence of Neurosyphilis (including ocular syphilis):
    • Aqueous crystalline PCN G IV
      • Dosed q4 hrs or continuous infusion, for 10-14 days
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13
Q

Benzathine Penicillin G

A
  • Repository PCN: PCN G + ammonium base
  • Depot injections ⇒ low but detectable serum concentrations of PCN G for up to 1 month
  • Bicillin C-R: combo of benzathine and procaine PCN which is not appropriate for syphilis
  • Bicillin L-A: benzathine PCN alone which is appropriate
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14
Q

Aqueous Crystalline Penicillin G

A

Used for IV therapy

When given in large dose it can penetrate the CNS

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15
Q

Treponema pallidum

Treatment Reactions

A
  • Jarisch-Herxheimer reaction
    • Acute febrile rxn w/ headache and myalgia
    • Occurs within first 24 hrs after tx
    • Not a drug allergy or adverse event to PCN
  • PCN allergy
    • Pts w/ established PCN allergy may need to be desensitized to PCN if alternative drug (doxycycline) cannot be used
      • Ex. pregnant women w/ a true penicillin allergy
    • Takes ~ 4 hrs and should be done in a hospital setting
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16
Q

Treponema pallidum

Immunity and Prevention

A
  • Immune response is largely unknown
    • CMI important b/c HIV pts have a rate of tx failures
    • CMI also contributes to pathology ass. w/ disease manifestations
  • No vaccine
  • Condoms are effective barrier method
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17
Q

Neisseria gonorrhoeae

Morphology and General Characteristics

A
  • Gram ⊖ diplococci, coffee bean shaped
  • Frequently visualized by gram stain inside of neutrophils
  • Cell wall contains outer membrane proteins and lipooligosaccharide (LOS), not LPS
    • LOS acts like endotoxin
  • Fragile organisms and do not survive long outside the human host
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18
Q

Neisseria gonorrhoeae

Transmission / Epidemiology

A
  • Sexually transmitted in men and women
    • Both can have asymptomatic carriage
      • Greater in women ⇒ less likely to be dx and receive tx
  • Transmission from mother → infant during passage through birth canal
  • Disease is most common in 15-24 age group and those w/ multiple sexual partners
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19
Q

Neisseria gonorrhoeae

Pathogenesis

A
  • Gonococci enter the vaginal or urethral mucosa
  • Attach to epithelial cells of the cervix or distal urethra ⇒ local replication
  • Pili and other surface proteins ⇒ facilitate attachment to host cells
  • Exhibit both phase variation and Ag variation
    • Pili and OSPs recognized by immune system but highly variable in structure ⇒ immune responses do not protect vs repeated infections
  • Important OSPs are called colony opacity associated proteins (Opa)
    • Bacteria w/o these proteins are not engulfed by neutrophils
    • Commonly ass. w/ PID, disseminated gonococcal infections (DGI) and arthritis
  • Damage to tissues caused by LOS ⇒ ⊕ TNF-alpha and causes other inflammatory processes
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20
Q

Neisseria gonorrhoeae

Urethritis

A
  • Occurs after 2-5 day incubation
  • Purulent discharge, thick, greenish-yellow, accompanied by pain
  • Usually subsides within a few wks w/o tx
  • Repeated infections can lead to scarring and strictures of the urethra
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21
Q

Neisseria gonorrhoeae

Cervicitis

A
  • Frequently asymptomatic (30% of women)
  • Sx can include dysuria, dyspareunia, discharge and genital discomfort
  • Lack of tx ⇒ ± local spread and inflammation ⇒ fallopian tube inflammation ⇒ ± long term sequalae:
    • Chronic pain, ectopic pregnancy, infertility
    • Pelvic Inflammatory Disease (PID)
      • Disorder that includes cervix, uterus, fallopian tubes and adjacent pelvic structures
    • May spread to the abdomen
      • Most common chief complaint is lower abd pain
    • May also cause tubo-ovarian abscesses
    • Can spread and cause peritonitis and perihepatitis (Fitz-Hugh Syndrome)
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22
Q

Disseminated Gonococcal Infections (DGI)

A
  • Most gonococci killed by nl human serum (IgG, IgM, complement activation) ⇒ don’t spread via the bloodstream
  • Serum resistant strains can spread
    • Lack colony opacity associated proteins (Opa)
  • Cause pustular skin lesions, septicemia and septic arthritis
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23
Q

Ophthalmia Neonatorum

A

Conjunctivitis seen in the newborn delivered via the birth canal in an infected mother.

Caused by Neisseria gonorrhoeae.

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24
Q

Neisseria gonorrhoeae

Diagnosis

A
  • Smear and culture
    • Gram stain of gonococci in PMNs
    • Samples from cervical or urethral secretions
    • Very sensitive in men w/ purulent discharge but not in asymptomatic men or in women (w/ or w/o sx)
    • Organisms can be cultured on chocolate agar or Thayer Martin medium
  • Nucleic acid assays (NAA)
    • Direct detection of organisms in clinical specimens
    • Rapid, sensitive and specific
  • Combination tests are available for Gonococci and chlamydia to screen asymptomatic individuals
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25
Q

Neisseria gonorrhoeae

Resistance

A
  • Resistant to PCN
    • Due to beta lactamase or altered affinity of penicillin binding proteins
  • Resistant to tetracycline
    • Ass. w/ Tet-m ⇒ ∆ ability to block binding and/or displace tetracycline from 30S subunit of ribosome
  • Quinolone resistance also widespread
  • Gonorrhea has shown resistance to every single class of abx

Neisseria gonorrhoeae now 1 of 3 resistant organisms CDC has categorized as “Urgent”

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26
Q

Neisseria gonorrhoeae

Treatment

A
  • Uncomplicated gonococcal infections of the cervix, urethra, and rectum
  • Ceftriaxone 500 mg IM single dose
  • If Chlamydia infection has not been ruled out ⇒ dual therapy
    • Add Doxycycline 100 mg BID for 7 days
      • Azithromycin no longer recommended b/c of developing resistance
  • Sex partner(s) should also be evaluated and treated
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27
Q

Ceftriaxone

A
  • 3rd gen cephalosporin
    • Resistant to cephalosporinases
  • Binds transpeptidase & other binding proteins ⇒ ⊗ cell wall synthesis
  • All beta lactams can cause hypersensitivity reactions
  • At high doses, beta lactams can cause seizures
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28
Q

Doxycycline

A
  • Same class tetracycline
  • Binds 30S subunit ⇒ blocks AA-linked tRNA from binding to the “A” site of the ribosome ⇒ ⊗ protein synthesis
  • GI upset and photosensitivity are most common AEs
  • Can cause esophageal irritation
    • Should be administered w/ water
    • Pts instructed to sit upright for 30 mins after admin
  • All tetracyclines can cause discoloration of the teeth
    • Contraindicated in pregnant women and children under 8
  • Tetracyclines can chelate ions
    • Should not be administered w/ calcium, iron, antacids, or multivitamins
  • No dose ∆ for renal or hepatic function
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29
Q

Neisseria gonorrhoeae

Immunity and Prevention

A
  • Immune response is Ab mediated
  • PMNs effective at killing many strains
  • Long-term immunity and cross-reactive immunity to other strains does not exist
    • Reinfection is common
  • Condoms are effective barrier method
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30
Q

Chlamydia trachomatis

Morphology and General Characteristics

A
  • Intracellular bacteria w/ a complex lifecycle
  • Two biovars: trachoma and lymphogranuloma vereum
    • LGV w/ further subdivides into serovars based on Ag differences
  • Ass. w/ different clinical syndromes
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31
Q

Chlamydia trachomatis

Lifecycle

A

Elementary body (EB) and reticulate body (RB)

EB resistant to environmental conditions much like a spore.

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32
Q

Chlamydia trachomatis

Transmission / Epidemiology

A
  • Found worldwide w/ no seasonal incidence
    • Different serovars ⇒ different types of disease ⇒ different prevalence rates depending on region
  • Diseases include:
    • Trachoma
    • Urogenital infections (STDs)
      • 1.4 million infections in the US
    • Adult inclusion conjunctivitis
    • Newborn inclusion conjunctivitis
    • Lymphogranuloma venereum (LGV)
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33
Q

Chlamydia trachomatis

Pathogenesis

A
  • Bacteria target columnar epithelial cells ⇒ acute → chronic inflammatory response
    • Infection freq. remains sub-acute ⇒ unnoticed and untreated
    • Trachoma ⇒ limited health resources
  • Unique life cycle protects from immune response
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34
Q

Trachoma

(Chronic keratoconjunctivitis)

A
  • Caused by the trachoma biovar of Chlamydia trachomatis
  • Leading cause of preventable blindness in the world (60 mil cases)
  • Endemic in Africa, Middle East, South Asia and parts of South America
  • Eye to eye transmission via droplet, hands, flies, fomites
  • Repeated infections from childhood
  • Chronic inflammation → eyelids turn inward ⇒ eyelashes abrade cornea ⇒ scarring, pannus (vessel formation in cornea) and loss of vision
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35
Q

Acute Follicular Conjunctivitis

A
  • Occurring in adults w/ genital infections caused by C. trachomatis
  • Probably auto-inoculation
  • Muco-purulent discharge, keratitis
  • Can result in scarring if not treated
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36
Q

Newborn Inclusion Conjunctivitis

A
  • C. trachomatis acquired by passage through infected birth canal
  • Occurs 1-2 wks after birth
  • Swelling of eyelids, purulent discharge
  • Untreated may lead to interstitial PNA
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37
Q

Chlamydia trachomatis

Urogenital Infections

A
  • In woman, up to 80% asymptomatic
    • Can become symptomatic and include cervicitis, salpingitis, endometritis
  • In men, 25% are asymptomatic
    • Urethritis characterized by discharge not quite as mucopurulent as that of N. gonorrhoeae but cannot be distinguished from it
      • These Infections frequently occur together
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38
Q

Reiters Syndrome

A
  • Urethritis, conjunctivitis, arthritis and lesions
  • Occurs in some men
  • Probably initiated by sexual transmission of Chlamydia
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39
Q

Lymphogranuloma Venereum (LGV)

A
  • Chronic STD that occurs mostly in tropical, developing countries
  • Chlamydia trachomatis serovars L1-3
  • Primary lesion on genitals of man or woman, small painless, often unnoticed, heals spontaneously
  • Followed by inguinal lymphadenopathy w/ formation of “bubos” ⇒ inflamed painful LNs, inguinal most common, containing the organism
  • Bubos contain infected, purulent material that must be aspirated or they may rupture
  • Includes fever, myalgias, systemic sx
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40
Q

Chlamydia trachomatis

Diagnosis

A
  • Gram stain
    • In symptomatic pts, look for PMNs but no gonocci present (presumptive)
  • Ag detection
    • Usually EIA or immunofluorescence from direct specimen
    • Most effective w/ symptomatic urethral specimen in males
    • Also LGV, neonatal PNA
  • NAAT
    • Test of choice for STIs
    • First void urine or urethral or cervical specimens
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41
Q

Chlamydia trachomatis

Treatment, Immunity and Prevention

A
  • Intracellular organisms that require CMI
    • Also causes the pathology
  • No long-lasting immunity
    • Reinfection leads to more vigorous immune response and pathology
  • Need abx that penetrate cells
  • Macrolides
    • 7 day course of tetracycline or usu. doxycycline
    • Or a single dose of Azithromycin
    • Dual-therapy w/ Ceftriaxone for Gonorrhea
  • Condoms can protect against STD
  • ID sex partners and f/u
  • Screen high risk populations
42
Q

Haemophilis ducreyi

Morphology, Transmission, Epidemiology

A
  • Small pleomorphic gram ⊖ rods
  • Sexually transmitted
  • Usually dx in men because women are asymptomatic
  • Endemic in many parts of the world but uncommon in developed countries
  • Frequently seen in HIV infected men
43
Q

Haemophilis ducreyi

Pathogenesis and Clinical Disease

A

Chancroid

  • 5-10 days incubation
  • Tender raised lesion w/ erythematous base develops in the genital area
  • Lesion ulcerates and becomes painful within a few days
  • Has soft ragged margins in contrast to the lesion of syphilis
  • Lesion resolves in 1-3 months
44
Q

Haemophilis ducreyi

Diagnosis

A
  • Specimen from base of lesion
  • Visualized by gram stain and microscopy
  • Cultured on specialized agar, but organism is fastidious so not always successful
45
Q

Haemophilis ducreyi

Treatment, Immunity and Prevention

A

Several abx options including azithromycin or ceftriaxone

Drain involved nodes

46
Q

Herpes Simplex Virus

Epidemiology

A
  • Infection w/ HSV is life-long
  • HSV type 1
    • ~60% sero-prevalence overall
    • Close to 90-100% in middle-aged adults
  • HSV type 2
    • ~20% sero-prevalence
    • ↑ w/ higher number of sexual partners and hx of other STIs
    • ↑ w/ age
    • More common in women
  • > 50 mil in the US have genital HSV 1/2
47
Q

Herpes Simplex Virus

Morphology

A

HSV-1/2 are double-stranded DNA human herpesviruses

48
Q

Herpes Simplex Virus

Transmission

A
  • Direct contact w/ mucosal surfaces
    • Oropharynx, vagina, rectum, cervix, and conjunctivae
  • Asymptomatic transmission possible
49
Q

Herpes Simplex Virus

Clinical Diseases

A
  • HSV 1 and 2 cause a variety of clinical presentations and can have overlap:
  • Most people are asymptomatic
  • HSV-1 usually causes herpes labialis (cold sores)
    • However, increasingly seen in anogenital disease
  • HSV-2 usually causes genital herpes
  • Stages of HSV infection include: primary, latent, and recurrent
50
Q

Herpes Simplex Virus

Natural History

A
  • Primary genital HSV
    • Classic sx is painful genital ulcers or vesicles – generally multiple
    • Local lymphadenopathy
    • ± Fever and headache
  • Oral HSV can include gingivostomatitis and pharyngitis
    • Sx can range from very mild to severe
  • Latent HSV
    • Can have no further episodes after 1° infection
  • Recurrent HSV
    • Can have over 3 reactivations per year
    • Usually recurrence sx are milder than 1° infection sx
    • Complications can include meningitis and proctitis
51
Q

Herpes Simplex Virus

Diagnosis

A
  • Usually diagnosed clinically based on appearance of lesions
  • Can directly swab lesion for HSV-1/2
    • HSV DNA by PCR – sensitivity higher than culture and more rapid
    • Viral culture – only 50% sensitivity
    • ↓ Viral detection as lesion heals and lower in recurrence
    • HSV shedding can be intermittent
      • ⊖ PCR or culture does not mean HSV infection is not present
  • Serologic blood tests
    • Type-specific glycoprotein (gG) ⇒ assay of choice
    • ⊖ Serology w/ active HSV lesion ⇒ consistent w/ new infection
  • Serology not recommended for routine screening (helpful in specific settings)
    • HSV-1 serology can reflect oral or genital infection
    • HSV-2 serology is consistent w/ genital infection
52
Q

1° Herpes Simplex Virus

Treatment

A
  • Acyclovir 400 mg PO TID for 7-10 days
  • Acyclovir 200 mg PO 5x/day for 7-10 days
  • Valacyclovir 1 g PO BID for 7-10 days
  • Famciclovir 250 mg PO TID for 7-10 days
53
Q

HSV

Suppressive Therapy

A
  • Acyclovir 400 mg PO BID
  • Valacyclovir 500 mg or 1 g PO qDay
  • Famciclovir 250 mg PO BID
54
Q

Acyclovir, Valacyclovir, Famciclovir

A
  • Nucleoside analogues
  • ℗ by viral thymidine kinase
    • Affinity is 200x greater for viral thymidine kinase vs. mammalian thymidine kinase
  • After acyclovir-monophosphate formed, cellular kinases ℗ further → acyclovir triphosphate
  • Compound acts as a substrate and an inhibitor of viral DNA polymerase
    • Acyclovir-℗3 incorporated into DNA ⇒ terminates chain elongation
  • Generally safer drugs
  • Important to stay hydrated to avoid crystalluria
55
Q

Genital Ulcer Disease

A
  • Can be seen in multiple STIs
    • Syphilis, HSV, chancroid, lymphogranuloma venereum, (and Granuloma Inguinale [donovanosis])
  • Generally classify based on:
    • Pain
      • Painful ⇒ HSV or chancroid
      • Painless ⇒ syphilis
    • Number of lesions
      • Single ⇒ syphilis or chancroid
      • Multiple or grouped ⇒ HSV
56
Q

Urethritis / Cervicitis

A
  • Infections characterized by dysuria, burning, and urethral /cervical discharge
    • Discharge can range from minimal to frank pus
  • Usually categorized as:
    • Gonococcal ⇒ caused by Neisseria gonorrhoeae
    • Can be seen on Gram stain
    • Nongonococcal ⇒ Chlamydia trachomatis is a major one
    • Others: Mycoplasma genitalium, HSV, T. pallidum, adenovirus, Ureaplasma urealyticum
      • M. genitalium is 15-25% of cases of nongonococcal urethritis in men in U.S.
  • Generally treat symptomatic urethritis empirically (for gonorrhea and chlamydia) while waiting for results
57
Q

Pelvic Inflammatory Disease

Characteristics

A
  • Spectrum of inflammatory disorders of upper female genital tract
  • Endometritis, salpingitis, tubo-ovarian abscess, pelvic peritonitis
  • Basic pathogenesis is an ascending infection from cervix → uterus → fallopian tubes and ovaries
  • Can spread outside the reproductive organs ⇒ pelvic peritonitis and rarely inflammation of the liver capsule w/ development of adhesions (Fitz-Hugh-Curtis syndrome)
58
Q

Pelvic Inflammatory Disease

Etiologies

A

Implicated causes:

  • Gonorrhea and Chlamydia
  • Normal vaginal flora (anaerobes, G. vaginalis, H. influenzae, enteric GNRs, S. agalactiae)
  • CMV, M. hominis, U. urealyticum, M. genitalium
59
Q

Pelvic Inflammatory Disease

Diagnosis

A
  • All women w/ PID should have gonorrhea, Chlamydia and HIV testing
  • Dx can be difficult
    • Wide variation in sx
    • May have mild sx
  • Clinical dx depends on pre-test suspicion
    • Abnl bleeding, dyspareunia, vaginal d/c
    • Pelvic or lower abd pain
  • Laparoscopy may be helpful
  • Sexually active women at risk for PID should be treated empirically if they have:
    • Pelvic or lower abdominal pain w/ no other cause identified as one or more:
      • Cervical motion tenderness
      • Uterine TTP
      • Adnexal TTP
    • One or more of these ↑ specificity:
      • Fever > 101°F
      • Abnl cervical or vaginal mucopurulent d/c, ↑ WBCs in vaginal fluid
      • ↑ ESR or CRP
      • Cervical infection w/ gonorrhea or Chlamydia
60
Q

Pelvic Inflammatory Disease

Treatment

A
  • Sexually active women at risk for PID should be treated empirically
    • PID usu. caused by Gonorrhea, Chlamydia and bacterial vaginosis organisms predominantly
    • Treatment should cover Gonorrhea, Chlamydia, anaerobes, GNRs and strep
  • Parental tx recommended for emergencies, in pregnant women, pts unable to tolerate oral therapy
    • IV therapy used until sx abate then pt switched to PO therapy
      • Cefotetan 2 gram IV every 12 hours + Doxycycline 100 mg orally or IV every 12 hours
    • Or
      • Cefoxitin 2 gram IV every 6 hours + Doxycycline 100 mg orally or IV every 12 hours
  • Intramuscular and oral therapy
    • PO therapy can be considered for women w/ mild to moderately severe acute PID, or after sx abate w/ IV therapy
    • Several possibilities including:
      • Ceftriaxone 250 mg IM in a single dose PLUS
      • Doxycycline 100 mg PO BID for 14 days
      • ± Metronidazole 500 mg orally twice a day for 14 days
        • Add if you suspect anaerobes, but also good for bacterial vaginosis which very often accompanies PID
    • or
      • Cefoxitin 2 g IM in a single dose PLUS
      • Probenecid 1 g orally administered concurrently in a single dose
        • Prolongs action of cefoxitin by ⊗ secretion via renal anion transporter
      • Doxycycline 100 mg orally twice a day for 14 days
      • ± Metronidazole 500 mg orally twice a day for 14 days
61
Q

Cefotetan and Cefoxitin

A
  • 2nd gen cephalosporins
    • Categorized as cephamycins
      • Similar activity as 2nd gen cephalosporins except for activity vs anaerobes in the GI tract
    • Used for surgical prophylaxis in abd surgery and abd and pelvic infections
  • Adverse effects:
    • AE similar to the beta lactams
    • Thrombophlebitis after IV injection
    • Cefotetan has a methylthiotetrazole group
      • Disulfiram like reaction w/ ethanol
      • ⊗ Vitamin K production ⇒ prolonged bleeding time
62
Q

Vaginitis

Overview

A

Disorder of the vagina characterized by inflammation or irritation of the vulva w/ abnl vaginal discharge.

  • Frequent cross contamination of nl and pathogenic flora b/t vaginal, urinary, and GI tracts
  • In pregnant women, vaginitis ass. w/ ↑ risk of miscarriage, pre-term delivery, and infections post-delivery
    • ↑ Likelihood of acquiring a STI upon exposure including HIV
63
Q

Vaginal Tract

Innate Defenses

A
  • Vaginal tract lacks a cleansing mech. to flush out microbes
    • Mucus from cervix, cycle dependent
  • Main defense is low pH (4-4.5) and high numbers of normal flora
    • Predominant genus is Lactobacillus spp
      • Gram ⊕ rods, facultative or microaerophilic
      • Bacterial fermentation of glycogen → lactic acid ⇒ low pH
        • Glycogen deposited in vaginal epithelial cells in response to estrogen
      • Produce hydrogen peroxide
        • Defense vs pathogens
64
Q

Vaginal

Normal Flora

A
  • Pre-puberty and post-menopausal
    • Scant flora
    • Some lactobacilli and other orgnaisms derived from skin and GI tract
  • Child-bearing years
    • Predominantly lactobacilli
    • Some yeast
    • Bacteria that tolerate low pH
    • Some aneaerobes
65
Q

Vaginitis

Etiologies

A
  • Most common causes of vaginitis__:
    • Trichomonas vaginalis ⇒ Trichomoniasis
    • Candida albicans ⇒ Candida vulvovaginitis
  • Most common causes of bacterial vaginosis:
    • Gardnerella vaginalis
    • Mobiluncus spp (anaerobic)
    • Prevotella spp (anaerobic)
66
Q

Vaginitis

Clinical Manifestations

A
  • Vaginitis is the inflammation of the vagina
  • Ass. w/ itching, burning, painful urination, odor, and vaginal discharge
  • Odor and discharge vary in amount and type depending on etiologic agent
  • Discharge may consist of inflammatory cells, epithelial cells, cell debris, and microbes
  • Different from urethritis, but overlap of sx and micro
67
Q

Bacterial Vaginosis

Characteristics/Epidemiology/Transmission

A
  • Most common vaginal infection in women of child bearing age
    • ~ 29% of women in the US are affected
  • Results from overgrowth of normal flora in the vagina ⇒ polymicrobial
  • Risk factors: multiple or new sexual partners, IUD, recent abx use, vaginal douching, and cigarette smoking
  • Role of sexual intercourse is poorly understood
    • Not thought to be sexually transmitted and celibate women may contract it
    • While not contagious, there may be a spread of bacteria between sexual partners that may predispose to the condition
68
Q

Bacterial Vaginosis

Clinical Manifestations

A
  • ~85% of women are asymptomatic
  • Most common sx are fishy odor and thin gray-white discharge
    • Both are more noticeable after sexual intercourse
69
Q

Bacterial Vaginosis

Pathogenesis

A
  • ↓ Lactobacilli (gram ⊕ rods, aerobes)
    • Usually present in high numbers in vaginal flora
  • Concomitant ↑ in anaerobes
    • Previously ass. w/ ↑ Gardnerella spp (gram variable, facultative anaerobe)
    • Now ass. w/ overgrowth of multiple anaerobic organisms including Mobiluncus and Prevotella spp (gram ⊖)
70
Q

Bacterial Vaginosis

Diagnosis

A
  • Pelvic exam w/ ⊕ Whiff test
    • When KOH comes into contact w/ discharge fluid, a “fishy” or amine odor is detected
  • Laboratory detection of “Clue Cells” (epithelial cells covered w/ gram variable organisms)
71
Q

Bacterial Vaginosis

Treatment

A
  • Polymicrobial syndrome resulting from replacement of normal H2O2 producing bacteria in the vagina w/ high concentrations of anaerobic bacteria
  • Many cases resolve on their own
  • May be treated by metronidazole PO or clindamycin cream
    • Benefits of therapy include relief of sx, ↓ risk of infectious complications s/p abortion/hysterectomy, ↓ risk of other infections (HIV and other STIs)
  • 50% experience recurrent sx within 12 months and need a 2nd course of abx
  • Recommended regimen:
    • Metronidazole 500 mg PO BID for 7 days
  • Or
    • Metronidazole gel 0.75% one full applicator (5g) intravaginally for 5 days
  • Or
    • Clindamycin cream 2% one full applicator (5g) intravaginally for 7 days
72
Q

Clindamycin

A
  • Derivative of lincomycin
  • Effective against anaerobes that participate in mixed infections
  • MOA similar to erythromycin
  • Clindamycin cream tx may have fewer adverse effects vs metronidazole PO
  • Tx w/ creams is not recommended in pregnant women
73
Q

Bacterial Vaginosis

Summary

A
  • Clinical manifestations
    • Often asymptomatic
    • Minimal discharge; usually has a fishy odor
    • May have mild vulvar irritation
  • Risk factor
    • Most often occurs in sexually active women
  • Physical exam
    • Gray to white, adherent, thin discharge
    • May have minimal vulvar erythema
  • Vaginal pH
    • 4.5-6
  • Wet mount
    • Large number of clue cells
  • “Whiff test”
    • ⊕
  • Treatment
    • Metronidazole (7 days)
74
Q

Trichomonas vaginalis

Characteristics/Transmission/Epidemiology

A
  • Motile protozoan parasite
  • Exists in flagellated trophozoite form w/ short undulating membrane
  • Anaerobic
  • Multiplies by longitudinal binary fission
  • Placed in vagina or urethra primarily by sexual intercourse, transmission by fomites possible
  • Infects ~ 3.7 million but only ~30% are symptomatic
    • Presentation may be related to overall status of host
    • Older women more likely to be symptomatic
75
Q

Trichomonas vaginalis

Clinical Manifestations

A
  • Men
    • Primarily asymptomatic carriers
    • May experience urethritis or prostatitis
  • Women
    • May be asymptomatic
    • Can have a scant, watery discharge
    • ± Extensive inflammation ⇒ erosion of vaginal epithelial lining
      • Purulent discharge (white or yellow)
      • Vaginal itching and burning
      • Painful urination
      • Discomfort during intercourse
76
Q

Trichomonas vaginalis

Diagnosis

A

Organisms may be visualized in discharge fluid or in PAP smears

Nucleic acid probe assay is also available

77
Q

Trichomonas vaginalis

Treatment/Prevention

A
  • Metronidazole is drug of choice for male and females
  • Sex partners must be treated to avoid reinfection
  • Prevention achieved through good hygiene, safe sexual practices and avoiding sharing of intimate apparel
  • Recommended regimen:
    • Metronidazole 2 gram orally single dose
  • Or
    • Tinidazole 2 gram orally single dose
78
Q

Metronidazole and Tinidazole

A
  • Members of the nitroimidazole family
  • Nitro group is reduced in anaerobic bacteria and sensitive protozoans
    • Reactive products responsible for antimicrobial activity
  • The only useful drugs for trichomoniasis
  • No alcohol for 24 hrs after metronidazole and 72 hrs after tinidazole
  • Metronidazole AE: nausea, headache, anorexia, and metallic taste
    • Class B for pregnancy ⇒ no adverse events in animal studies
  • Tinidazole has fewer side effects
    • Class C ⇒ some adverse events
79
Q

Trichomoniasis

Summary

A
  • Clinical manifestations
    • Purulent vaginal discharge
    • Usually has a bad odor
    • Vulvar irritation
  • Risk factor
    • Sexually transmitted
  • Physical exam
    • Purulent discharge; can be yellow-green or frothy
    • Vulvar erythema
  • Vaginal pH
    • 4.5-6
  • Wet mount
    • Neutrophils
    • May see motile trichomonads
    • Can also do NAAT testing
  • “Whiff test”
    • May be ⊕
  • Treatment
    • Metronidazole (single or 7 day)
80
Q

Candida albicans

General Characteristics

A
  • Numerous species, most important is C. albicans
    • Long term fluconazole tx ⇒ appearance of other Candida species (especially C. glabrata and C. krusei)
  • Candida albicans:
    • Unicellular ovoid organism
    • Adheres well to mucosal surfaces
    • Reproduces asexually by budding
    • Forms pseudohyphae ⇒ new budding cells → filamentous elongated form → true hyphae
    • Can also form sprout-like hyphae called germ tubes (in the presence of serum) → hyphae
81
Q

Candida albicans

Transmission and Epidemiology

A
  • C. albicans are nl flora of the mouth, intertriginous skin folds, GI tract and vagina
  • Immunocompetent individuals have high resistance to Candida & other fungal infections
  • Mucosal infections, particularly of the vagina
  • Due to disruptions in the normal flora (abx use) ⇒ microbial imbalance ⇒ allows Candida to overgrow
82
Q

Vulvovaginal Candidiasis

A
  • Pruritis (burning and itching)
  • ± Cheesy discharge
  • Not a typical STD (endogenous transmission)
  • Often recurrent
  • More common in 3rd trimester of pregnancy and users of estrogen contraceptives
83
Q

Candida albicans

Diagnosis

A
  • Usually clinical dx
  • Confirmed by microscopic exam of tissue (w/ or w/o KOH) for yeast and pseudohyphae
    • Gram ⊕, size in between bacteria and host cell
  • C. albicans: germ tube formation in 1-2 hrs at 37__°__C in serum, chlamydospores on corn meal agar
84
Q

Candida albicans

Treatment/Prophylaxis

A

Eliminate predisposing factor(s)

Topical antifungals

85
Q

Candida Vulvovaginitis

Summary

A
  • Clinical manifestations
    • Vulvar pruritis/irritation
    • May have mild discharge
  • Risk factor
    • Immune suppression, DM, ↑ estrogen, abx
  • Physical exam
    • Vulvar erythema
    • Thick, white, “cottage-cheese” like discharge
  • Vaginal pH
    • 3.8-4.5 (normal)
  • Wet mount
    • Pseudohyphae (also seen w/ KOH exam)
  • “Whiff test”
    • ⊖
  • Treatment
    • Fluconazole or topical antifungal agents
86
Q

Human Papilloma Virus (HPV)

Characteristics

A
  • Papovavirus
  • Small non-enveloped, isosohedral capsid
  • dsDNA genome
  • ~70 types, classified into 16 groups
  • Classified as cutaneous or mucosal HPV based on target tissues
87
Q

Human Papilloma Virus (HPV)

Genome

A
  • Episomal genome
  • 8 early genes: E1 to E8
    • Expression of E1 and E2 important for lytic cycle
    • Expression of E6 and E7 important for oncogenesis
  • 2 late or structural genes: L1 and L2
88
Q

Human Papilloma Virus (HPV)

Epidemiology

A
  • Found worldwide, no seasonal incidence
  • 20 million individuals in the US
  • 10-20% of women may be infected
  • HPV 16 and 18 directly linked to cervical CA
    • 2nd leading cause of CA mortality in women
89
Q

Human Papilloma Virus (HPV)

Transmission

A
  • Requires close contact for transmission:
    • Direct contact (breaks in skin)
    • Sexual contact
    • Passage through the birth canal
  • ⊕ Asymptomatic transmission
  • Capsid confers environmental resistance
    • Survives on inanimate objects (fomites
90
Q

Human Papilloma Virus (HPV)

Pathogenesis

A
  • Enters via skin breaks
  • Incubation 3-4 months
  • Lytic infection in a permissive cell
    • Cutaneous and mucosal forms
      • Wart appearance related to HPV type and site of infection
    • Common, plantar and flat warts ⇒ children and young adults
      • Resulting acquired immunity may limit disease in adults
    • Genital warts ⇒ sexually active individuals
    • Wart resolution in ~ 2 yrs
    • Viral persistence, asymptomatic shedding
  • ± Oncogenic transformation of a non-permissive cell
    • Usu. by integrating viral genome into host genome
    • Some HPV types ass. w/ oral and genital cancers
91
Q

Human Papilloma Virus (HPV)

Wart Formation

A

Viral replication linked to skin cell differentiation:

  • Infection of basal cells
  • HPV early genes ⇒ ⊕ host cell growth & viral genome replication using host DNA polymerase
    • Expression of E1 and E2 important for lytic cycle
  • Cell division ⇒ basal and prickle layer thickens
  • Basal layer differentiation ⇒ ⊕ expression of nuclear factors ⇒ ⊕ transcription of viral proteins
  • HPV late genes expression in terminally differentiated keratin layer
  • Assembled virion shed along w/ dead cells
  • Warts usu. spontaneously regress after months to years
  • ± Persistent or latent viral infections in the basal layer
  • Virus remains in plasmid form
92
Q

Human Papilloma Virus (HPV)

Oncogenesis

A

Strain specific (HPV 16, 18)

  • Integration of viral genome into host DNA ass. w/ oncogenic events
    • ~85% of cervical CA contain HPV DNA in integrated form
  • Integration limits viral replication (inactivation of E1 and E2 genes)
  • Allows expression of viral oncogenes (E6 and E7)
  • E6 and E7 ⇒ ⊗ cellular growth suppressor proteins (p53 and p105 or pRb)
    • Uncontrolled cell proliferation
    • ↑ Susceptibility to mutations and other cancer-causing events
93
Q

Oncogenesis

Risk Factors

A
  • Tobacco use
  • OCPs
  • Other STIs, chronic inflammation
  • Certain HLD-DR alleles
94
Q

Human Papilloma Virus (HPV)

Skin Warts

A
  • Infection of keratinized surfaces
  • May result in common, flat or plantar wart
    • Depending on HPV type (HPV 1-4, 10) and site of infection
  • Usually results from infection in childhood or adolescence
95
Q

Human Papilloma Virus (HPV)

Head and Neck Tumors

A
  • Occurs in young children or adults > 40 y/o
    • In children, HPV acquired through birth canal
  • Ass. w/ HPV 6, 11
  • Two types:
    • Oral papillomas ⇒ benign epithelial tumors in the oral cavity,
      • Usually solitary and rarely recur
    • Laryngeal papillomas ⇒ benign epithelial tumors of the larynx
      • Frequently recur
96
Q

Human Papilloma Virus (HPV)

Anogenital Warts

A

“Condyloma acuminata”

  • Occurs on external genitalia and perianal areas as a result of sexual contact
  • 90% are caused by HPV 6 and 11
  • Rarely become malignant (10%)
  • Risk factors:
    • Sexual activity before 16 y/o
    • Multiple sexual partners
    • Partner w/ multiple sexual partners
97
Q

Human Papilloma Virus (HPV)

Cervical Dysplasia and Neoplasia

A

STI of female genital tract w/ HPV 16 or 18

± Progressive cellular changes: dysplasia → neoplasia → carcinoma

98
Q

Human Papilloma Virus (HPV)

Immune Response

A
  • Virus sequestered in skin cells ⇒ limits exposure to immune system
  • CMI important for wart regression
  • Persistent infection ass. w/ transformation
    • AIDS, lymphoproliferative d/o, immunosuppressive therapy ⇒ ↑ risk
99
Q

Genital Warts

Diagnosis

A
  • Visual dx by appearance
  • Confirmed by PAP smear
    • Koilocytes
    • Hyperplasia of prickle cells
    • Excessive production of keratin (hyperkeratosis)
  • Molecular probes and PCR
    • Used to ID virus in cervical swabs and tissue specimens
    • HPV 16, 18
100
Q

Cervical Dysplasia

Evaluation

A
  • Dx cervical changes by Papanicolaou smears
    • Koilocytotic squamous epithelial cells
      • Contain vacuolated cytoplasm and occur in rounded clumps
101
Q

Human Papilloma Virus (HPV)

Treatment

A
  • Warts usually spontaneously regress but are frequently surgically excised
    • Removal ass. w/ high recurrence rate
  • Papillomas and cervical dysplasia and neoplasia must be surgically removed
  • Pharmacologic agents:
    • Skin warts ⇒ salicylic acid
    • Anogenital warts ⇒ podophyllin, imiquimode (INF inducer) tricloracetic acid
    • Laryngeal warts ⇒ intralesion interferon
  • Condoms ↓ but cannot completely prevent sexual spread
102
Q

Human Papilloma Virus (HPV)

Vaccine

A
  • Quadrivalent vaccine
    • HPV 6, 11, 16, 18
  • Gardasil 9
    • HPV 6, 11, 16, 18, 31, 33, 45, 52, 58
  • 3 shot series
    • Targeted to adolescent girls
    • Recently approved and recommended for boys
  • Will not prevent all genital warts but provides significant (not complete) protection vs cervical cancer

6. HDS GI Repro (30 decks)

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