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Flashcards in UGI Deck (145):
1

UTIs in children

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

2

Proteus mirabilis

Virulence factors

• Proteases

• Haemolysins

• Biofilm formation

• Urease production

Increase in alkalization will cause stones to form 

3

Lactobacilli characteristics 

• Gram + rods, non-spore forming

• Facultative or strict anaerobes, produce lactic acid

• Rarely cause UTIs  do not grow in urine well

4

Psuedomonas biofilm development

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Diagnosis of UTIs

• 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

5

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

Proteus mirabilis

6

Serotypes of E. coli in UTI

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

7

Uncomplicated vs Complicated UTIs

• 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

7

Pathogenesis of UTI pic

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8

Clinical Outcomes of UTIs 

• 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

9

Chronic UTI associated with which bacteria 

E. coli 

10

Sx and location of infection of UGT

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Virulence factors contributing to UTIs

– Adhesins (pili, fimbriae, etc.)

– Ig proteases

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

– Siderophore expression

– Factors promoting colonization and movement

10

Tamm-Horsfall Protein

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

UTI Treatment

• Usually antibiotics

• Drug and length depends on patient’s history and infecting microbe

• Sensitivity tests useful in selecting most effective drug

11

Protective components of UGT

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

12

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

UT infections due to catheterization

13

Asymptomatic Bacteriuria

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

15

Recurrent UTIs

• 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

16

UTI vs. STI

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

17

Normal microflora of vagina 

– More diverse, influenced by hormones

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

– Lactobacilli  become more prominent at puberty

19

Epidemiology of UTIs

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

20

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

What bacteria 

• Escherichia coli • Klebsiella pneumoniae

• S. saprophyticus • Proteus mirabilis

21

Complicated urinary tract infection bacteria 

• E. coli

• Enterococcus species

• K. pneumoniae

• Pseudomonas aeruginosa

• P. mirabilis

22

Normal Microflora

• Urethra

– Lactobacilli

– Streptococci

– Coagulase-negative Staphlococci

24

Staphylococcus saprophyticus seasonality

Summer

(summer time sex) 

26

Ascending vs Descending UTIs

• Descending is far less common

• Ascending – microorganisms may travel from urethra  bladder  kidney

27

What allows for organisms to stick to catheters 

Biofilms

28

UPEC serotypes

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Pregnant women w/UTIs

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

– Smooth muscle relaxation

– Urethral dilation

– Greater chance to progress to pyelonephritis

30

UPEC (Uropathogenic E. coli)

Characteristics 

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

31

UTI Risk Factors

• being female

• recent sexual intercourse

– abrasions, etc.

• recent use of a diaphragm with spermicide • history of recurrent infection

• urinary catheter

32

Abbreviated work-ups for UTIs 

 

• 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

33

Catheterization predisposes you to 

– obstruction -> bacterial glycocalyx

– encourages formation of encrustations and infection

stones consisting of urea, other complex substances

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

34

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

– Staphylococcus saprophyticus

– Proteus mirabilis

– Klebsiella species 

– Mycoplasma and Ureaplasma 

– Candida 

35

Primary cause of UTIs pathogen

UPEC (Uropathogenic E. coli)

36

• Cause of UTIs (usually young, sexually active women)

• Infrequent asymptomatic colonizer of UT

• Infections have been on the increase

Staphylococcus saprophyticus

37

Adhesion support for differnt types of organisms 

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39

Uropathogenic E. coli (UPEC)

Key virulence features

• Type I (cystitis)

• P pili (pyelonephritis)

Additional:

• α-hemolysin

• Siderophore

• Pathogenicity islands

40

Biofilms

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

41

Lactobacilli

• In addition to genitourinary tract also found in

– mouth, intestines, stomach

42

uropathogenicity of Staphylococcus saprophyticus

– novel cell wall-anchored adhesin

– redundant uro-adaptive transport systems

– urease

43

Summary 1 of STDs 

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44

STD summary 2

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45

STI epi

• 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

46

“New” STIs

– Giardia lamblia - Protozoan

– Amoeba sp. - Protozoan

– Shigella sp., E. coli – True Bacteria

47

Vaginal discharge seen in

VAGINITIS:

– Trichomoniasis

– Candidiasis

CERVICITIS:

– Gonorrhoea

– Chlamydia

48

Urethral discharge seen in

Gonorrhoea

Chlamydia

49

Genital ulcer caues 

Syphilis

Chancroid

Genital herpes

50

Lower abdominal pain seen in what STI

Gonorrhoea

Chlamydia

Mixed anaerobes

51

Scrotal swelling seen in which STDs

Gonorrhoea

Chlamydia

52

Inguinal bubo what is it/ seen in what stds

what is it:

Painful enlarged

inguinal lymph nodes

seen in:

LGV

Chancroid

53

Neonatal conjunctivitis in what stds

Gonorrhoea

Chlamydia

54

Anaerobic Gram negative bacteria and GYN Infections includes what organisms

Prevotella bivia and disiens,

Bacteriodes fragilis (common in abscesses)

• Virulence factors: capsules, etc. (adherence)

55

Gonorrhea: Epidemiology

• occurs only in humans (no other known reservoir)

• transmittedprimarilybysexualcontact,veryrare fomite transmission

• major reservoir is the asymptomatically infected individual

• infectionincreaseslikelihoodofHIVinfection

56

Gonhrea age relation

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• 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

Gonorrhea

58

Neisseria gonorrhoeae: Characteristics

• Neisseria gonorrhoeae: Gram – diplococci

• non-motile, non-spore forming

• Fastidious

• oxidase +

• outer surface w/ multiple antigens

59

Neisseria gonorrhoeae: Pathogensis

• 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

Neisseria gonorrhoeae microbe movement

• 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

Gonorrhea: Diagnosis

• 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

Three Paths of Neisseria gonorrhoea Infections

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Gonorrhea: Prevention, Control and Treatment

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

since resistance is prominent 

64

Resistance of N. Gonorrhoeae 

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65

Chlamydia: Epidemiology

• 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

Chlamydia sex/age rates 

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

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68

Chlamydia complications for women

– Infertility

– ectopic pregnancy

– chronic pelvic pain

69

Chlamydia: Characteristics

 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

Chlamydia trachomatis is not visible w/

Gram stain!

71

Chlamydia should be suspected with cervicitis when

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

72

Chlamydia: Pathogenesis

Receptors for EBs: restricted to certain epithelial cells

– mucous membranes of the urethra

– endocervix, endometrium, fallopian tubes

– anorectum

– respiratory tract and conjunctivae

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Chlamydia: Diagnosis

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

74

Chlamydia: Prevention, Control and Treatment

• 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

Syphilis: Epidemiology

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

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

Primary Syphilis 

77

most common STds 

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• Lesionsoftenhavethin, greyish crust (easily removed  crater w/ viscous fluid containing living T. pallidum cells

• Multiple lesions are quite common

Hard painless chancre 

Primary syphilis 

79

Wet, mucous patches are contagious

The inflammatory reaction is similar to but less intense

than that of the primary chancre

Condylomata Lata of Secondary Syphilis

80

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

Secondary syph

81

Primary/ secondary syph epi 

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82

Where in the US has the highest syph incidence 

South 

West 

83

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

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84

– 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

Tertiary syph

85

INfective organism for congenital syph

T. pallidum 

86

Effects of Tertiary syph

Most cases  spontaneous, septic abortion

• Occasionally a live birth takes place; infants

are actively infected with the organism

• Teratogenic effects usually seen

87

Stromal haze syphilitic interstitial keratitis

due to late-staged congenital syph

88

saddle nose

Congenital syph

89

Hutchinson’s teeth

Congenital syph 

90

Treponema pallidum: Characteristics

• 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

Treponema pallidum: Pathogenesis

• 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

Syphilis: Pathogenesis primary

 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

Syphilis: Pathogenesis secondary

2 – evasion of the immune system poorly understood

• Inflammatory response may be responsible for some symptoms

94

Syphilis: Pathogenesis tertiary

diffuse chronic inflammation, damage to CNS

95

Syphilis: Diagnosis

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

• Definitive for diagnosing early syphilis

• Direct fluorescent antibody test

96

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

– 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

Syphilis: Prevention, Control and Treatment

• 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

Chancroid: Epidemiology

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

pathogen for Chancroid

 Obligate human pathogen Haemophilus ducreyi

• Chancroid (ulcer of the genital region)

100

• Soft chancre or chancroid

• Painful genital ulcer (5-10 days incubation period)

• spontaneously rupturing buboes occur in approximately 25% of cases

Chancroid

101

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

Inguinal bubo along w/ penile ulceration

Chancroid

102

Chancroid ulcer where on vagina

posterior wall 

103

Haemophilus ducreyi: Characteristics

• Fastidious

• Gram – anaerobic rods (sometimes called “coccobacilli”)

• Pleomorphic

• Related to H. influenzae

104

Haemophilus ducreyi stain

Gentian Violet Simple Stain

105

Haemophilus ducreyi: Pathogenesis

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

Chancroid: Diagnosis

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

Chancroid: Prevention, Control and Treatment

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

Chancroid vs Syphilis

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109

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

Bacterial Vaginosis/Vaginitis

110

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

Bacterial Vaginosis/Vaginitis

111

Vaginal infection that can increase HIV transmission

Bacterial Vaginosis/Vaginitis

112

can help distinguish BV from Candidiasis and Trichomonas

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

Candida albicans: Characteristics

 Oval, yeastlike forms

site of colonization is GI tract • Normal microflora

• Commensuals:

– vagina

– urethra

– skin, under the nails

114

Candidiasis: Source of infection patient

• ~ 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

Clinical Manifestations of Candidiasis

Candidiasis of the fingernail

2ndary oral pseudomembraneous candidiasis infection,

116

 Common curable STD in young, sexually active women

Trichomoniasis

117

Trichomoniasis most common site of infection in women/men

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

118

primary mode of transmission Trichomoniasis

Sexual intercourse is primary mode of transmission; fomite transmission possible

119

Trichomoniasis increases risk for 

• Genital inflammation,  risk of HIV transmission

120

Parasite with 4 flagella and short undulating

membrane responsible for motility

Trichomoniasis

121

Trichomoniasis: Clinical Presentation

Vulvovaginal trichomoniasis

Cervical trichomoniasis

Vaginal pH > 4.5  can also be suggestive of Trich

122

Most genital herpes type

HHV-2

123

HHV-1 and -2 is transmitted by

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

 

124

When are viruses released with ulcers 

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

HHV1/2

125

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

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

126

What do you test for in reinfection of syph

Nontreponemal RPR levels 

127

Clinical Manifestations of HHV-2

Primary genital herpes of the vulva

 

vesiculopapular herpes genitalis lesions

128

HHV-1 and -2: Characteristics

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

HHV-1 and -2: Pathogenesis

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

HSV infection sites 

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131

HHV-1 and -2: Diagnosis

– 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

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

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

Human Papillomavirus (HPV): Epidemiology

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

134

Spectrum of HPV

• Condyloma Acuminata (low-risk HPVs)

• Cervical Dysplasia (high-risk HPVs)

• Cervical Cancer (high-risk HPVs)

135

Estimated Contribution of

HR-Mucosal HPVs to

Various Cancers

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136

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

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137

Cervical Cancer International Incidence Patterns

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138

HPV: Clinical Presentation, Anogenital Warts

 

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

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

HPV 6 and 11

140

HPV – Oral sex causes throat cancer

HPV16 present in the tumors of 72% of cancer patients

141

HPV: Pathogenesis

HPV lifecycle tightly coupled to differentiation process of the epithelium

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142

Mechanisms of Human Papillomavirus-Associated Carcinogenesis

HPV genome integration during malignant progression

Integration terminates life cycle

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

 

 

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143

Mechanisms of HPV-Associated Carcinogenesis

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144

HPV: Diagnosis

• Genital warts  diagnosed by visual inspection

• Cervical cell changes: 1) routine Pap tests, 2) HPV testing / typing

145

HPV: Prevention, Control and Treatment

• 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)