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UGI Flashcards

1
Q

UTIs in children

A

UTIs in children: more common in those under the age of 2

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2
Q

Proteus mirabilis

Virulence factors

A
  • Proteases
  • Haemolysins
  • Biofilm formation
  • Urease production

Increase in alkalization will cause stones to form

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3
Q

Lactobacilli characteristics

A
  • Gram + rods, non-spore forming
  • Facultative or strict anaerobes, produce lactic acid
  • Rarely cause UTIs  do not grow in urine well
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4
Q

Psuedomonas biofilm development

A
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4
Q

Diagnosis of UTIs

A
  • Clean catch urine specimen (unspun, midstream)
  • White and red blood cells, bacteria
  • Culture and sensitivity tests
  • ~20% of patients w/UTIs do not have pyuria
  • No simple test to distinguish between upper from lower UTIs
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5
Q

Urine -> smells like ammonia, toxic to kidneys (alkaline -> urine struvite crystals)

A

Proteus mirabilis

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6
Q

Serotypes of E. coli in UTI

A

~85% of community- acquired, ~50% of hospital acquired UTIs

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7
Q

Uncomplicated vs Complicated UTIs

A

• Uncomplicated UTI

– no specific pre-disposing factors

– no structural abnormalities, etc.

• predisposing anatomic, functional, or metabolic abnormalities -> Complicated UTI

– requires more aggressive evaluation and follow- up

– definition is often imprecise

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7
Q

Pathogenesis of UTI pic

A
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8
Q

Clinical Outcomes of UTIs

A

• Prostatitis: spectrum of disorders, some infections (E. coli most common)

– acute bacterial prostatitis is most serious but least common (chronic more common)

– reflux of urine from urethra into prostate ducts

• Epididymitis: microorganisms can enter from prostate via ejaculatory duct

– pathogens vary in younger men vs older

– predisposing factors include prostatitis, indwelling urinary catheters, urologic surgery

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9
Q

Chronic UTI associated with which bacteria

A

E. coli

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10
Q

Sx and location of infection of UGT

A
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10
Q

Virulence factors contributing to UTIs

A

– Adhesins (pili, fimbriae, etc.)

– Ig proteases

– Hemolysins (get cytokine release, inflammation) – Ureases (i.e. P. mirabilis)

– Siderophore expression

– Factors promoting colonization and movement

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10
Q

Tamm-Horsfall Protein

A

Bladder host defense

  • binds specifically to type 1 fimbriated E. coli
  • key urinary anti-adherence factor serving to prevent type 1 fimbriated E. coli from binding to the urothelial receptors
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10
Q

UTI Treatment

A
  • Usually antibiotics
  • Drug and length depends on patient’s history and infecting microbe
  • Sensitivity tests useful in selecting most effective drug
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11
Q

Protective components of UGT

A

– Antimicrobial properties of urine (high urea conc., immunoglobulins, etc.) – Presence of normal microflora

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12
Q

most common site of healthcare-associated infection, accounting for more than 40% of the total # reported

A

UT infections due to catheterization

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13
Q

Asymptomatic Bacteriuria

A

Relatively common finding

  • Present in ~5% of unselected medical outpatients, 10% pregnant patients at term, also in hypertensive and diabetic patients
  • Anatomic obstruction increases incidence
  • Nearly all patients with indwelling catheter w/open drainage for more than 48 hrs
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15
Q

Recurrent UTIs

A
  • 3 or more UTIs within a 12-month period
  • Relapse
  • Re-infection
  • New infection
  • Predisposing factors
  • 20 - 25% women w/acute uncomplicated cystitis have 2 or more infections/yr
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16
Q

UTI vs. STI

A

Juxtaposition of urinary and genital tracts in

vertebrates is a source of confusion

  • UTI = Urinary tract infection. May or may not be transmitted by sexual activity – the more general term
  • STI = Sexually transmitted infection –more narrowly specific
  • Not all UTIs are sexually transmitted, and not all STIs manifest their symptoms and/or pathology

in the urogenital tract

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17
Q

Normal microflora of vagina

A

– More diverse, influenced by hormones

– Newborn girls  colonized w/ Lactobacilli, vaginal flora becomes more diverse over time

– Lactobacilli  become more prominent at puberty

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19
Q

Epidemiology of UTIs

A

2nd most common type of infection in the body*

Women: especially prone to UTIs (20-40% develops a UTI during her lifetime)

  • Men: not as common as in women but can be very serious when they do occur
  • US women that develop a UTI: 20% will have a recurrence
  • Women who experience three or more UTIs are likely to continue experiencing them
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20
Q

Acute uncomplicated cystitis, Recurrent cystitis in young women, Acute cystitis in young men, Acute uncomplicated pyelonephritis, Asymptomatic bacteriuria in pregnancy

What bacteria

A
  • Escherichia coli • Klebsiella pneumoniae
  • S. saprophyticus • Proteus mirabilis
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21
Q

Complicated urinary tract infection bacteria

A
  • E. coli
  • Enterococcus species
  • K. pneumoniae
  • Pseudomonas aeruginosa
  • P. mirabilis
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22
Q

Normal Microflora

• Urethra

A

– Lactobacilli

– Streptococci

– Coagulase-negative Staphlococci

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24
Q

Staphylococcus saprophyticus seasonality

A

Summer

(summer time sex)

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26
Q

Ascending vs Descending UTIs

A
  • Descending is far less common
  • Ascending – microorganisms may travel from urethra  bladder  kidney
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27
Q

What allows for organisms to stick to catheters

A

Biofilms

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28
Q

UPEC serotypes

A
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29
Q

Pregnant women w/UTIs

A

untreated - increased risk of delivering low birth weight / premature infants

– Smooth muscle relaxation

– Urethral dilation

– Greater chance to progress to pyelonephritis

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30
Q

UPEC (Uropathogenic E. coli)

Characteristics

A

primary cause of UTIs

Gram – rods, normal habitat is gastrointestinal

tract of humans and animals

distinguished by acquired genes (iron acquisition, siderophores)  virulence-

distinct UPEC associated biosynthetic pathways

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31
Q

UTI Risk Factors

A
  • being female
  • recent sexual intercourse

– abrasions, etc.

  • recent use of a diaphragm with spermicide • history of recurrent infection
  • urinary catheter
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32
Q

Abbreviated work-ups for UTIs

A
  • Leukocyte-esterase test
  • Nitrates → nitrites: what does this mean?
  • UTI symptoms in the presence of leukocytes are considered adequate to make a diagnosis of UTI

Urine cultures w/ 105 CFUs have defined infection

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33
Q

Catheterization predisposes you to

A

– obstruction -> bacterial glycocalyx

– encourages formation of encrustations and infection

stones consisting of urea, other complex substances

– local infections (urethritis, periurethral abscess, epididymitis, and prostatitis)

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34
Q

Organisms predominately responsible for remaining UTIs (~15% community- acquired, ~50% of hospital-acquired)

A

– Staphylococcus saprophyticus

– Proteus mirabilis

– Klebsiella species

– Mycoplasma and Ureaplasma

– Candida

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35
Q

Primary cause of UTIs pathogen

A

UPEC (Uropathogenic E. coli)

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36
Q
  • Cause of UTIs (usually young, sexually active women)
  • Infrequent asymptomatic colonizer of UT
  • Infections have been on the increase
A

Staphylococcus saprophyticus

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37
Q

Adhesion support for differnt types of organisms

A
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39
Q

Uropathogenic E. coli (UPEC)

Key virulence features

A
  • Type I (cystitis)
  • P pili (pyelonephritis)

Additional:

  • α-hemolysin
  • Siderophore
  • Pathogenicity islands
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40
Q

Biofilms

A

are groups of microorganisms, often many species, growing on surfaces encased in “slime”

  • Inert and living substances can be destroyed
  • Multi-step process involving communication
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41
Q

Lactobacilli

• In addition to genitourinary tract also found in

A

– mouth, intestines, stomach

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42
Q

uropathogenicity of Staphylococcus saprophyticus

A

– novel cell wall-anchored adhesin

– redundant uro-adaptive transport systems

– urease

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43
Q

Summary 1 of STDs

A
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44
Q

STD summary 2

A
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45
Q

STI epi

A

• Affect both sexes, all socio-economic groups; Disproportionately affect:

– women, infants of infected mothers

– adolescents and young adults

– communities of color

– 15-24-year-olds represent ~ 1⁄4 of the sexually active population  nearly 1⁄2 of all new STDs

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46
Q

“New” STIs

A

– Giardia lamblia - Protozoan

– Amoeba sp. - Protozoan

– Shigella sp., E. coli – True Bacteria

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47
Q

Vaginal discharge seen in

A

VAGINITIS:

– Trichomoniasis

– Candidiasis

CERVICITIS:

– Gonorrhoea

– Chlamydia

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48
Q

Urethral discharge seen in

A

Gonorrhoea

Chlamydia

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49
Q

Genital ulcer caues

A

Syphilis

Chancroid

Genital herpes

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50
Q

Lower abdominal pain seen in what STI

A

Gonorrhoea

Chlamydia

Mixed anaerobes

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51
Q

Scrotal swelling seen in which STDs

A

Gonorrhoea

Chlamydia

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52
Q

Inguinal bubo what is it/ seen in what stds

A

what is it:

Painful enlarged

inguinal lymph nodes

seen in:

LGV

Chancroid

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53
Q

Neonatal conjunctivitis in what stds

A

Gonorrhoea

Chlamydia

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54
Q

Anaerobic Gram negative bacteria and GYN Infections includes what organisms

A

Prevotella bivia and disiens,

Bacteriodes fragilis (common in abscesses)

• Virulence factors: capsules, etc. (adherence)

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55
Q

Gonorrhea: Epidemiology

A
  • occurs only in humans (no other known reservoir)
  • transmittedprimarilybysexualcontact,veryrare fomite transmission
  • major reservoir is the asymptomatically infected individual
  • infectionincreaseslikelihoodofHIVinfection
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56
Q

Gonhrea age relation

A
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57
Q
  • Men (~95% have symptoms): generally restricted to the urethra – purulent urethral discharge, dysuria
  • Women: site of infection is cervix – vaginal discharge, dysuria and abdominal pain
A

Gonorrhea

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58
Q

Neisseria gonorrhoeae: Characteristics

A
  • Neisseria gonorrhoeae: Gram – diplococci
  • non-motile, non-spore forming
  • Fastidious
  • oxidase +
  • outer surface w/ multiple antigens
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59
Q

Neisseria gonorrhoeae: Pathogensis

A

• Attachment to columnar epithelium of

distal urethra or cervix

– Pili – unusual, specialized mechanism of antigenic variation by DNA rearrangement

– Opa

– por protein

– Lipooligosaccharide – induces TNF-alpha in some cells

– iron-binding proteins

60
Q

Neisseria gonorrhoeae microbe movement

A

• Gonococci spread  into the urethra or cervix (as far as the fallopian tubes, usually limited to urethra in males)

– Not motile (no flagella)

– urethral or uterine contractions may contribute to the ascending infection

  • Bloodstream can be seeded (most commonly in individuals with defects in Complement System)
  • Chronic infection can produce scarring and stricture of fallopian tubes or urethra
61
Q

Gonorrhea: Diagnosis

A
  • 1) Microscopic examination of smears for intracellular Gram – diplococci
  • 2) Non-culture lab test
  • 3) Isolation on appropriate media for confirmation

– 24 hrs: Thayer Martin (VCN agar, Chocolate II Agar w/ vancomycin, colistin, nystatin)

– oxidase + colonies

Thayer used for neisseria only

62
Q

Three Paths of Neisseria gonorrhoea Infections

A
63
Q

Gonorrhea: Prevention, Control and Treatment

A

• Recommended treatments are limited to a single class of antibiotics, cephalosporins (– Lactamase resistant)

since resistance is prominent

64
Q

Resistance of N. Gonorrhoeae

A
65
Q

Chlamydia: Epidemiology

A
  • Most commonly reported STI in the US
  • 1,244,180 diagnoses in 2009 (majority in women 15-24 yrs old)
  • Most cases still go undiagnosed
  • Presence may increase HIV transmission
  • Severe impact on women, especially young and minority women
66
Q

Chlamydia sex/age rates

A
67
Q

Chlamydia trachomatis: Divided into 3 biovars (biological variants), then subdivided into serovars

A
68
Q

Chlamydia complications for women

A

– Infertility

– ectopic pregnancy

– chronic pelvic pain

69
Q

Chlamydia: Characteristics

A

Atypical bacterium, **Gram - **(Chlamydia trachomatis) - unique developmental cycle

  • infectious form  elementary bodies (EB)
  • noninfectious form  reticulate bodies

(RB)

  • small obligate intracellular parasites
  • gain entry through abrasions/lacerations
70
Q

Chlamydia trachomatis is not visible w/

A

Gram stain!

71
Q

Chlamydia should be suspected with cervicitis when

A

should be suspected in absence of clue cells, yeasts and trichomonads

72
Q

Chlamydia: Pathogenesis

A

Receptors for EBs: restricted to certain epithelial cells

– mucous membranes of the urethra

– endocervix, endometrium, fallopian tubes

– anorectum

– respiratory tract and conjunctivae

73
Q

Chlamydia: Diagnosis

A

Appropriate specimens intracellular parasites, swabs, not exudate, must be submitted for analysis

74
Q

Chlamydia: Prevention, Control and Treatment

A
  • STI prevention
  • Can be cured w/antibiotics

– Azithromycin 1 g orally in a single dose

– Doxycycline 100 mg orally twice a day for 7 days

  • Data suggests screening and treatment can reduce PID by over 50%
  • Reducing the impact of Chlamydia

requires reducing/treating it in males

75
Q

Syphilis: Epidemiology

A

Generally a highly infectious (transmission via direct contact with 10 or 20 lesions), genital, ulcerative disease that is easily curable in its early Primary&Secondary stages

• Increased likelihood of HIV transmission

76
Q

hard, painless but sensitive ulcer develops 9-90 days post-infection (pi)

– Disappears w/in 1 week after proper treatment

– Disappears spontaneously w/out treatment after 4 to 12 weeks

– 75% of all untreated cases resolve here and do not progress past this stage

– Easy, definitive diagnosis by Darkfield

Microscopy: examine exudate from the lesion

A

Primary Syphilis

77
Q

most common STds

A
78
Q
  • Lesionsoftenhavethin, greyish crust (easily removed  crater w/ viscous fluid containing living T. pallidum cells
  • Multiple lesions are quite common

Hard painless chancre

A

Primary syphilis

79
Q

Wet, mucous patches are contagious

The inflammatory reaction is similar to but less intense

than that of the primary chancre

A

Condylomata Lata of Secondary Syphilis

80
Q

generalized maculopapular rash + multiple symptoms indicative of systemic infection

– flulike syndrome, 2-8 weeks after ulcer

– rarely concurrent with chancre

– 80% show the maculopapular rash (rash may extend over face, palms and soles)

– lesions are “swarming” with the organism

A

Secondary syph

81
Q

Primary/ secondary syph epi

A
82
Q

Where in the US has the highest syph incidence

A

South

West

83
Q

Primary and Secondary Syphilis—Rates by Age and Sex, United States, 2012

A
84
Q

– diffuse chronic inflammation

– neurosyphilis (damage to CNS including progressive dementia, meningitis, hallucinations, etc.)

– cardiovascular effects such as aortic aneurysm

– “Gummatous” - A hypersensitive granulomatous reaction - Can be destructive to viscera or mucocutaneous areas

A

Tertiary syph

85
Q

INfective organism for congenital syph

A

T. pallidum

86
Q

Effects of Tertiary syph

A

Most cases  spontaneous, septic abortion

• Occasionally a live birth takes place; infants

are actively infected with the organism

• Teratogenic effects usually seen

87
Q

Stromal haze syphilitic interstitial keratitis

A

due to late-staged congenital syph

88
Q

saddle nose

A

Congenital syph

89
Q

Hutchinson’s teeth

A

Congenital syph

90
Q

Treponema pallidum: Characteristics

A
  • Thin, tightly coiled spirochetes w/pointed straight ends
  • 3 flagella @ each end: MOTILE
  • Replication slow – no in vitro culture
  • Obligate human pathogen
  • Unusual outer membrane

(no LPS, no porins)

91
Q

Treponema pallidum: Pathogenesis

A

• Tissue destruction and lesions  patient’s

immune response to infection

  • Outer membrane proteins promote adherence
  • Hyaluronidase may facilitate perivascular infiltration: “spreading factor”
  • Coating of fibronectin may protect against phagocytosis
92
Q

Syphilis: Pathogenesis primary

A

1 – enters subepithelial tissues via skin breach

  • Slow replication, not a wide range of environmental conditions tolerated: Fastidious
  • Endarteritis and granulomas
  • Lesion heals but bacteria disseminate via lymph nodes and blood stream (latency poorly understood)
93
Q

Syphilis: Pathogenesis secondary

A

2 – evasion of the immune system poorly understood

• Inflammatory response may be responsible for some symptoms

94
Q

Syphilis: Pathogenesis tertiary

A

diffuse chronic inflammation, damage to CNS

95
Q

Syphilis: Diagnosis

A

Rapid with dark-field examination of exudate from skin lesions (however, organism HIGHLY SENSITIVE)

  • Definitive for diagnosing early syphilis
  • Direct fluorescent antibody test
96
Q

A presumptive diagnosis of syphilis is possible with the use of two types of serologic tests:

A

– 1) nontreponemal tests (e.g., Venereal Disease Research Laboratory [VDRL] and RPR)

– 2) treponemal tests (e.g., fluorescent treponemal antibody absorbed [FTA-ABS] tests, the T. pallidum passive particle agglutination [TP-PA] assay, various EIAs, and chemiluminescence immunoassays)

97
Q

Syphilis: Prevention, Control and Treatment

A
  • STI prevention
  • CDC recommends sexually active men having sex with men be tested annually
  • Pregnant women should be screened at first prenatal visit
  • Penicillin (generally used for all stages, is only treatment for neurosyphilis)
  • All persons who have syphilis should be

tested for HIV infection

98
Q

Chancroid: Epidemiology

A

Predominant in the tropics (commonly in Africa, Asia and Latin America (accounting for 20% to 60% of genital ulcer disease infections)

  • Sporadic in North America
  • Infection increases likelihood of HIV transmission
99
Q

pathogen for Chancroid

A

Obligate human pathogen Haemophilus ducreyi

• Chancroid (ulcer of the genital region)

100
Q
  • Soft chancre or chancroid
  • Painful genital ulcer (5-10 days incubation period)
  • spontaneously rupturing buboes occur in approximately 25% of cases
A

Chancroid

101
Q

Unilateral Painful Inguinal lymph- adenopathy (50% of infected)

Inguinal bubo along w/ penile ulceration

A

Chancroid

102
Q

Chancroid ulcer where on vagina

A

posterior wall

103
Q

Haemophilus ducreyi: Characteristics

A
  • Fastidious
  • Gram – anaerobic rods (sometimes called “coccobacilli”)
  • Pleomorphic
  • Related to H. influenzae
104
Q

Haemophilus ducreyi stain

A

Gentian Violet Simple Stain

105
Q

Haemophilus ducreyi: Pathogenesis

A

extracellular pathogen that

resists phagocytosis

• Virulence factors include:

– an outer membrane serum resistance protein

– two toxins: cytolethal distending toxin (CDT) and hemolysin, both of which contribute to tissue destruction

106
Q

Chancroid: Diagnosis

A

requires the identification of H. ducreyi on special culture media that is not widely available from commercial sources; even when these media are used, sensitivity is <80%

  • Antigen detection, serology and genetic amplification methods: reported for H. ducreyi, but are not easily available
  • Accuracy of clinical diagnosis for chancroid ranges from 30% to 80%
  • Exclude T. pallidum and HHV-1 & -2
107
Q

Chancroid: Prevention, Control and Treatment

A

Antibiotics used for treatment

– Azithromycin 1 g orally in a single dose

– Ceftriaxone 250 mg intramuscularly (IM) in a single dose

– Ciprofloxacin 500 mg orally twice a day for 3 days

– Erythromycin base 500 mg orally three times a day for 7 days

108
Q

Chancroid vs Syphilis

A
109
Q

Normal balance of bacteria in vagina is disrupted - replaced by certain overgrowth

– sometimes accompanied by discharge (unpleasant odor, may be thin, white or gray)

– pain, itching, or burning outside vagina

A

Bacterial Vaginosis/Vaginitis

110
Q

most common vaginal infection in childbearing aged women (sexual activity?)

A

Bacterial Vaginosis/Vaginitis

111
Q

Vaginal infection that can increase HIV transmission

A

Bacterial Vaginosis/Vaginitis

112
Q

can help distinguish BV from Candidiasis and Trichomonas

A

Examining the vaginal discharge under the microscope can help distinguish BV from Candidiasis and Trichomonas

  • A sign of BV: unusual vaginal cell called a clue cell
  • Women with BV (polymicrobial) have fewer than normal vaginal lactobacilli
  • Vaginal pH > 4.5  can be suggestive of BV
113
Q

Candida albicans: Characteristics

A

Oval, yeastlike forms

site of colonization is GI tract • Normal microflora

• Commensuals:

– vagina

– urethra

– skin, under the nails

114
Q

Candidiasis: Source of infection patient

A
  • ~ 75% of all adult women  at least one genital “yeast infection” in lifetime (people w/ weakened immune systems, more frequent and severe)
  • Rarely, men may also experience genital Candidiasis
  • Other conditions that may put a woman at risk for genital Candidiasis:

– Pregnancy

– Diabetes mellitus

– Use of broad-spectrum antibiotics and / or corticosteroid medications

115
Q

Clinical Manifestations of Candidiasis

A

Candidiasis of the fingernail

2ndary oral pseudomembraneous candidiasis infection,

116
Q

Common curable STD in young, sexually active women

A

Trichomoniasis

117
Q

Trichomoniasis most common site of infection in women/men

A

Vagina: most common site of infection in women, urethra: most common site in men

118
Q

primary mode of transmission Trichomoniasis

A

Sexual intercourse is primary mode of transmission; fomite transmission possible

119
Q

Trichomoniasis increases risk for

A

• Genital inflammation,  risk of HIV transmission

120
Q

Parasite with 4 flagella and short undulating

membrane responsible for motility

A

Trichomoniasis

121
Q

Trichomoniasis: Clinical Presentation

A

Vulvovaginal trichomoniasis

Cervical trichomoniasis

Vaginal pH > 4.5  can also be suggestive of Trich

122
Q

Most genital herpes type

A

HHV-2

123
Q

HHV-1 and -2 is transmitted by

A

by close and/or sexual contact through mucosal membranes, breaks in the skin

124
Q

When are viruses released with ulcers

A

released from these ulcers, but they are also released between outbreaks from skin

HHV1/2

125
Q

What is the sequence of tests you should do for syph?

A

Nontreponemal initially (this has a high false positive) treponemal is then used to confirm.

126
Q

What do you test for in reinfection of syph

A

Nontreponemal RPR levels

127
Q

Clinical Manifestations of HHV-2

A

Primary genital herpes of the vulva

vesiculopapular herpes genitalis lesions

128
Q

HHV-1 and -2: Characteristics

A

share DNA homology, antigenic determinants, tissue tropism and disease symptoms

  • Ubiquitous, large, ds DNA, enveloped icosahedral virus, can stay in the body indefinitely
  • Encode enzymes that are good antiviral targets
129
Q

HHV-1 and -2: Pathogenesis

A

initially infect and replicate in mucoepithelial cells – lytic (most cells: Cowdry type A inclusion bodies, syncytia)

– persistent (lymphocytes and macrophages)

– latent infections (neurons)

Virus blocks effects of interferon, prevents CD8 T-cell recognition of infected cells, escapes antibody neutralization and clearance by going into “hiding” during latent infection

• Recurrence occurs in response to various stimuli

130
Q

HSV infection sites

A
131
Q

HHV-1 and -2: Diagnosis

A

– visual inspection if the outbreak is typical

– test a sample from the ulcer(s)

– virologic (PCR, cell culture) and type-specific serologic tests (based on type-specific glycoprotein G) are available

– between outbreaks by the use of a blood test to detect antibodies (results are not always definitive)

132
Q

HHV-1 and -2: Prevention, Control and Treatment

A

antiviral medications – 1st occurrence:

– Acyclovir 400 mg orally three times a day for 7–10 days or 200 mg orally five times a day for 7–10 days

– Famciclovir 250 mg orally three times a day for 7–10 days

– Valacyclovir 1 g orally twice a day for 7–10 days

– shorten and prevent outbreaks with medication

• Daily suppressive therapy for symptomatic herpes can reduce transmission

133
Q

Human Papillomavirus (HPV): Epidemiology

A

cumulative risk of acquiring HPV in sexually active persons = 80%

134
Q

Spectrum of HPV

A
  • Condyloma Acuminata (low-risk HPVs)
  • Cervical Dysplasia (high-risk HPVs)
  • Cervical Cancer (high-risk HPVs)
135
Q

Estimated Contribution of

HR-Mucosal HPVs to

Various Cancers

A
136
Q

Human Papillomavirus—Prevalence of High-risk and Low-risk Types Among Females Aged 14–59 Years,

A
137
Q

Cervical Cancer International Incidence Patterns

A
138
Q

HPV: Clinical Presentation, Anogenital Warts

A

HPV infections are often asymptomatic (both low- and high-risk)

May take weeks, months, years for symptoms to appear

Untreated, genital warts (low-risk HPV infections) may regress or increase in size and/or #

139
Q

responsible for >90% of anogenital warts1

• Peakprevalence

– Women 20–24 years of age (6.2/1,000 person years)

– Men 25–29 years of age (5.0/1,000 person years)

• Clinically apparent in ~1% of sexually active US adult population3

A

HPV 6 and 11

140
Q

HPV – Oral sex causes throat cancer

A

HPV16 present in the tumors of 72% of cancer patients

141
Q

HPV: Pathogenesis

A

HPV lifecycle tightly coupled to differentiation process of the epithelium

142
Q

Mechanisms of Human Papillomavirus-Associated Carcinogenesis

A

HPV genome integration during malignant progression

Integration terminates life cycle

No evidence for insertional mutagenesis Expression of E6 and E7 is retained

143
Q

Mechanisms of HPV-Associated Carcinogenesis

A
144
Q

HPV: Diagnosis

A
  • Genital warts  diagnosed by visual inspection
  • Cervical cell changes: 1) routine Pap tests, 2) HPV testing / typing
145
Q

HPV: Prevention, Control and Treatment

A
  • Women 21 – 29: Pap test every 3 years
  • Women 30 and 65: both Pap test and HPV test every 5 years (preferred), OR Pap test alone every 3 years

HPV Vaccine – Gardasil ®

– Active against 16, 18, 6, 11

– FDA approved in US for girls & boys ages 9-26 (Cervarix ® targets only HPV 16 and 18)

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