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356 Cards in this Set
- Front
- Back
|
Which STD am I?
- small vesicles on vulva that erode to ulcers - ds DNA virus - 1-3 wk. incubation period |
HSV
|
|
|
which three things are candida associated with?
|
1. diabetes mellitus
2. OCs 3. Pregnancy |
|
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which STD is a flagellated ovoid protozoa that has the hallmark symptom of a "strawberry cervix?"
|
Trichomonas vaginalis
|
|
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causative agent of syphilis?
|
Treponema pallidum (spirochete)
|
|
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mode of transmission of syphilis from mother to fetus?
|
transplacental
|
|
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describe the primary stage of syphilis
|
chancre (2-6 wks)
|
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describe the secondary stage of syphilis
|
- appears weeks to months later
- erythemous and macropapular rash - heals in 2-6 wks |
|
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describe the tertiary stage of syphilis
|
- CV/nervous system damage
- obliterative endocarditis - CNS damage (tabes dorsalis) |
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which stain is used to see Treponema pallidum spirochetes?
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Warthin-Starry stain
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Causative organism of gonorrhea?
|
Neisseria gonorrhoeae
(gram - diplococcus) |
|
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female acute symptoms of gonorrhea?
|
- salpingitis
- PID |
|
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four complications of PID?
|
1. peritonitis
2. adhesions 3. bacteremia 4. infertility |
|
|
causative agent of chancroid?
|
Haemophilus ducreyi
(gram neg. bacillus) |
|
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common complication of chancroid?
|
scar formation causing urethral stenosis
|
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|
causative agent of Lymphogranuloma venereum?
|
Chlamydia trachomatis
|
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describe the three stages of lymphogranuloma venereum
|
1. stage one: vesicle
2. stage two: enlarged lymph nodes: may form fistula 3. stage three: scarring, genital elephantiasis, rectal strictures (years later) |
|
|
causative agent of granuloma inguinale?
|
Calymatobacterium granulomatis
(gram neg. encapsulated rod) |
|
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presentation of granuloma inguinale?
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ulcerated painful nodules in genital, inguinal, perianal regions
|
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Gardnerella is caused by? and associated with?
|
Gardnerella vaginalis
associated with BV |
|
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what causes the fishy odor present in a gardnerella infection?
|
mixing of vaginal discharge with 10% KOH (alkalinizes)
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which STD is histologically associated with Clue cells?
|
Gardnerella (BV)
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What are Donovan bodies and which STD are they associated with?
|
- Donovan Bodies are macrophages that have "swallowed up" bacteria.
- associated with granuloma inguinale |
|
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a gynecological mycoplasma infection is associated with? (4)
|
spontaneous abortion
puerpural fever salpingitis PID |
|
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what type of bacteria is Chlamydia trachomatis?
|
Gram negative intracellular rickettsia
|
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symptoms seen in men with chlamydia?
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none (asymptomatic)
|
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common complication of Chlamydia?
|
PID
|
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describe TB as a female genital tract infection
|
salpingitis
pyosalpinx and hydrosalpinx TB endometritis in 1/2 of cases |
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What is actinomycosis associated with?
|
IUD
|
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causative agent of actinomycosis?
|
Actinomyces israelii
(gram pos rod) |
|
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histological characteristic of actinomycosis?
|
sulfur granules
|
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which parts of the female reproductive tract does actinomyces israelii infect? (3)
|
uterine tube
ovary broad ligament |
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which bacteria is responsible for TSS?
|
strains of Staph aureus
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TSS is connected with what 2 things?
|
tampon use
contraceptive sponge use |
|
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in the pathogenesis of PID, gonococcal inflammation begins where?
|
Bartholins glands
(then spreads up to tubes and ovaries) |
|
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How does a gonococcal infx. differ from a non-gonococcal infx. (3)
|
1. gonococcal infections spare the endometrium, non-gonococcal infections don't.
2. non-GC causes have less exudate but deeper inflammatory response 3. bacteremia more common with non-GC PID |
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pathogenesis of PID starting at acute suppurative salpingitis?
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acute suppurative saplingitis -> salpingo-oophoritis -> tubo-ovarian abcess -> pyosalpinx -> adhesions -> hydrosalpinx
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5 possible complications of PID?
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1. peritonitis
2. adhesions 3. obstruction 4. bacteremia 5. infertility |
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what causes a Bartholin cyst?
|
an obstructed Bartholin's duct
|
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which three bacteria are Bartholin cysts associated with?
|
1. Staph
2. Chlamydia 3. Anaerobes |
|
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in what age group is lichen sclerosis most common?
|
postmenopause
|
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what is lichen sclerosis associated with?
|
other autoimmune disorders
|
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which disorder is hyperplastic dystrophy and secondary to pruritis (itching and rubbing)?
|
Lichen Simplex Chronicus
|
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what is the site of origin in hidradenoma?
|
aprocrine sweat glands
|
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where do hidradenomas MC appear?
|
labia majora
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are hidradenomas benign or malignant?
|
benign
|
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what is condyloma acuminatum and what is the MCC?
|
wartlike lesions
HPV types 6 and 11 are MCC |
|
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is condyloma acuminatum precancerous?
|
NO
(they regress spontaneously) |
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Most common endometrial carcinoma?
|
endometriod adenocarcinoma
|
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in the vulva: nuclear atypia in epithelial cells forming a precancerous lesion is known as?
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VIN (Vulvar Intraepithelial Neoplasia)
|
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four characteristics of high-grade dysplasia?
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1. Increased N/C ratio
2. Loss of polarity (cells become crowded) 3. Mitoses 4. Hyperchromatic nuclei |
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which two strains of HPV are associated with VIN?
|
16,18
|
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gross presentation of VIN?
|
white or pigmented plaques on vulva, multicentric presentation
|
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two scary things about VIN?
|
1. 25% reoccur after excision
2. associated with other squamous neoplasms in lower reproductive tract |
|
|
in older women, VIN can progress to become?
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Squamous Cell Carcinoma (SCC)
|
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2/3 of genital SCCs occur in which age group?
|
over 60 yrs
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verrucous and basal cell carcinomas are variants of SCC: how often do they metastasize?
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Rarely
|
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what exactly is desmoplastic stroma?
|
reaction of the surrounding stroma to cancer. HARD and fibrinous
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extramammary Paget Disease is confined to which parts of the vulva and perianal area? (3)
|
epidermis
hair follicles sweat glands |
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How does extramammary Paget's differ from mammary Paget's?
|
mammary Paget's - due to an underlying malignancy
extramammary Paget's - confined |
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if you are considering a diagnosis of Paget's you also must consider which diagnosis?
|
melanoma
|
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prognosis of malignant melanoma?
|
POOR
very aggressive, prognosis is related to depth of invasion |
|
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what is the molecular difference between malignant melanoma and Paget's?
|
MALIGNANT MELANOMA IS:
1. S100 positive 2. CEA negative |
|
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Vaginal Adenosis is associated with?
|
1. in utero DES exposure
2. increased risk of Clear Cell Carcinoma |
|
|
where are the tumors of vaginal adenosis most often located?
|
on the anterior wall
|
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is vaginal adenosis benign or malignant?
|
benign
|
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treatment for vaginal adenosis?
|
surgery and radiation
|
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VAIN is associated with? (risk factors for VAIN)?
(5) |
1. HPV
2. immunosuppression 3. irradiation 4. in utero exposure to DES 5. squamous neoplasia elsewhere in the lower reproductive tract. |
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VAIN can progress to?
|
Vaginal Squamous Cell Carcinoma
|
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Vaginal Squamous cell carcinoma is most common in women of what age?
|
60-70 yrs
|
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what comprises 90% of malignant vaginal CA?
|
Squamous cell carcinoma
|
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what is a rare vaginal tumor of childhood that is a polypoid mass resembling a bunch of grapes?
|
Embryonal Rhabdomyosarcoma
|
|
|
other name for embryonal rhabdomysarcoma?
|
Sarcoma Boytroides
|
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Embryonal Rhabdomyosarcoma consists of what cell type?
|
primitive spindle rhabdomyoblasts
|
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Embryonal Rhabdomyosarcoma is seen in what age group?
|
girls less than 4yrs
|
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how is an Embryonal Rhabdomyosarcoma fatal?
|
can invade locally and cause death by penetrating the peritoneal cavity
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treatment for Embryonal Rhabdomyosarcoma?
|
surgery
AND chemotherapy |
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in the cervix: where does metaplastic transformation occur?
|
transformation zone
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Describe the Schiller iodine test
|
stains glycogen rich cells brown
glycogen poor cells don't stain (dysplasia doesn't stain) |
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describe the change in the location of the transformation zone as you age.
|
prepubertal - inside cervix
adolescent/early adult - moves outside cervix postmenopausal - moves back inside cervix |
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how does an endocervical polyp present?
|
vaginal bleeding or discharge
|
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are endocervical polyps common?
|
yes, they are the most common cervical growth
|
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describe the histology of microglandular hyperplasia
|
closely packed glands with no intervening stroma(a cluster of benign glands)
|
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microglandular hyperplasia is associated with an excess of which hormone?
|
progestins
|
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What are the risk factors for cervical neoplasia? (8)
|
1. early age of first intercourse
2. multiple sexual partners 3. increased parity 4. male partner with multiple previous partners 5. HPV 6. certain HLA and viral subtypes 7. OCs and nicotine 8. genital infections (chlamydia) |
|
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In what type of CIN are koilocytes most often present?
|
low grade CIN
|
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CIN may progress to?
|
carcinoma in situ
|
|
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what is the average time for all grades of dysplasia to progress to carcinoma in situ?
|
10 yrs
|
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CIN is classified as a?
|
STD
(because it is so strongly associated with HPV) |
|
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at what age does Squamous cell carcinoma of the cervix most often appear?
|
40-45 yrs
(younger age) |
|
|
in what 3 ways does SCC of the cervix present?
|
fungating
ulcerative infiltrative |
|
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what defines a microinvasive carcinoma?
|
no greater than 3mm and no wider than 7mm
|
|
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how does SCC of the cervix spread?
|
via lymphatics and direct spread
|
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what is the most common cause of death in SCC of the cervix?
|
renal failure
|
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are most cervical SCCs well or poorly differentiated?
|
most are well differentiated
(5% poorly diff./worst prognosis) |
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in the cervix - an intraepithelial proliferation of columnar (glandular) cells is called?
|
Adenocarcinoma in situ (AIS)
|
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in 40% of cases, AIS is associated with?
|
high grade CIN
|
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AIS can progress to?
|
Invasive adenocarcinoma
(worse prognosis) |
|
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Invasive adenocarcinoma looks like?
|
No stroma, back to back glands
|
|
|
what type of glands would you see in the uterine lining during the proliferative phase?
|
round glands
multiple layers of cells |
|
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what type of glands would you see in the uterine lining during the secretory phase?
|
coiled glands
single layer of cells |
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what is characteristic of the histology seen in the menstrual phase?
|
neutrophils in the stroma
|
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what is a characteristic feature of the uterine lining on day 3 post-ovulation?
|
subnuclear vacuolization
|
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what is the Arias-Stella reaction?
|
a benign exxagerated hypersecretory response associated with hCG.
|
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Histological characteristic of the Arias-Stella reaction?
|
Bulbous nuclei protrude into the gland lumen
|
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when is the Arias-Stella reaction seen?
|
1. intrauterine pregnancy
2. ectopic pregnancy 3. trophoblastic disease |
|
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5 Congenital anomalies of the uterus?
|
1. agenesis
2. uterus didelphys 3. uterus duplex bicornis 4. bicornate uterus 5. Uterus septus |
|
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4 congenital anomalies of the vagina?
|
1. atresia
2. septate or double vagina 3. Gartner duct cysts 4. imperforate hymen |
|
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MC cause of uterine bleeding?
|
anovulatory cycle
|
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what two times in a woman's life is DUB most common?
|
menarche
perimenopause |
|
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which hormone is DUB most often attributed to?
|
excess estrogen
(promotes building up of endometrium but no sloughing) |
|
|
DUB due to an inadequate luteal phase often manifests as?
|
infertility
|
|
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why is there DUB seen with OCs?
|
there is a discordance between glands and stroma.
(glands are small and round, stroma is decidualized) |
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a condition involving inflammation of the endometrium and inflammed endometrial glands is called?
|
endometritis
|
|
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Histologically, how can one differentiate between inflammed endometrium and menstrual endometrium?
|
menstrual endometrium has tortuous glands, whereas the glands seen in endometritis are most commonly proliferative (round).
|
|
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Histologically, how can one differentiate between acute endometritis and chronic endometritis?
|
acute - see neutrophils
chronic - see plasma cells |
|
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Acute endometritis usually results from?
|
ascending infection in the cervix (abortion, delivery, instrumentation)
|
|
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chronic endometritis usually results from/is associated with?
|
IUD
PID retained products of conception |
|
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in endometritis, pyometria is seen when what happens?
|
cervical stenosis (blocks drainage, get pus in uterus)
|
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define endometriosis
|
the presence of endometrial glands or stroma in abnormal locations outside the uterus.
|
|
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what are the top four locations of endometriosis in descending order of frequency?
|
ovaries
ligaments retrovaginal septum pelvic peritoneum |
|
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three hallmark s/s of endometriosis?
|
infertility
dysmenorrhea pelvic pain |
|
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what is the age group of women most afflicted with endometriosis?
|
3rd and 4th decade
(affects 10% of these women) |
|
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a benign overgrowth of endometrial glands and stroma is called?
|
endometrial polyp
|
|
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do endometrial polyps slough during menstruation?
|
NO
|
|
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hallmark presenting symptom of endometrial polys?
|
intermenstrual bleeding
|
|
|
two types of endometrial polyps?
|
1. functional (looks like surrounding endothelium)
2. hyperplastic (lots of glands) |
|
|
a benign polyp may progress to?
|
adenocarcinoma
|
|
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which drug have endometrial polyps been associated with?
|
tamoxifen (anti-estrogenic)
|
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|
define endometrial hyperplasia
|
hyperplasia of the endometrial glands
|
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endometrial hyperplasia may progress to?
|
endometrial carcinoma
|
|
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time frame of the progression of endometrial hyperplasia to endometrial carcinoma?
|
4-10 yrs
|
|
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what is the simple most prognostic feature used in endometrial hyperplasia?
|
cytologic atypia
|
|
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what do the glands look like in endometrial hyperplasia?
|
mostly proliferative (round)
|
|
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which hormone excess is endometrial hyperplasia linked to?
|
estrogen
|
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besides excess estrogen: endometrial hyperplasia is associated with what other conditions? (4)
|
1. menopause
2. PCOS 3. granulosa cell tumors 4. cortical stromal hyperplasia |
|
|
genetic link to endometrial hyperplasia and further progression to endometrial carcinoma?
|
inactivation of PTEN tumor suppressor gene
|
|
|
three categories of endometrial hyperplasia?
|
1. simple hyperplasia
2. complex hyperplasia 3. atypical hyperplasia |
|
|
describe the histological characteristics of:
1. simple hyperplasia 2. complex hyperplasia 3. atypical hyperplasia |
1. round glands, minimal complexity and crowding, no cytologic atypia
2. branching glands, more glandular crowding, no cytologic atypia 3. branching glands with nuclear atypia, crowded (little intervening stroma) |
|
|
about what % of patients with atypical endometrial hyperplasia develop adenocarcinoma?
|
25%
|
|
|
what are the two treatments for endometrial hyperplasia?
|
1. progestins
2. hysterectomy (esp. if atypical hyperplasia) |
|
|
what is the 4th most common cancer in women and the most common gynecological cancer?
|
endometrial adenocarcinoma
|
|
|
which age group of women are most afflicted by endometrial adenocarcinoma?
|
postmenopausal women
(median age 63 yrs) |
|
|
risk factors for endometrial adenocarcinoma?
|
1. obesity
2. diabetes 3. hypertension 4. infertility 5. prolonged estrogen stimulation (nulliparous, anovulatory cycle) |
|
|
endometrial adenocarcinoma is associated with an increased risk of what 2 other cancers?
|
breast
ovarian |
|
|
genetic influence in the development of endometrial adenocarcinoma?
|
inactivation of PTEN gene
|
|
|
describe the FIGO grading differentiation for endometrial adenocarcinoma.
|
Grade 1: well differentiated, minimal solid areas
Grade 2: moderately differentiated, <50% solid tumor Grade 3: poorly differentiated, >50% solid tumor *also, significant nuclear atypia increases grade* |
|
|
what are the two strains of endometrial adenocarcinoma that have a worse prognosis?
|
Papillary serous carcinomas and clear cell carcinomas
*automatically considered a grade 3* |
|
|
#1 presenting symptom of endometrial carcinoma?
|
vaginal bleeding
|
|
|
an endometrial cancer with malignant stroma AND glands is called?
|
carcinosarcoma
|
|
|
two former names for carcinosarcoma?
|
mixed mesodermal tumor
mullerian tumor |
|
|
carcinosarcomas are derived from what cell type?
|
multipotential stromal cells
(stroma may differentiate to muscle, cartilage, bone) |
|
|
when a carcinosarcoma metastasizes it becomes an?
|
adenocarcinoma
|
|
|
carcinosarcomas are associated with what environmental exposure?
|
previous radiation therapy
|
|
|
endometrial cancer characterized by benign glands and malignant stroma?
|
adenosarcoma
|
|
|
adenosarcomas are most commonly seen in which age group of women?
|
40-50
|
|
|
why is an oophorectomy a treatment for adenosarcomas?
|
tumor is estrogen sensitive
|
|
|
recurrence rate of adenosarcoma?
|
25%
|
|
|
are adenosarcomas benign or malignant?
|
low grade malignant
|
|
|
what is a stromal nodule?
|
a benign, well circumscribed lesion of endometrial stromal cells located in the myometrium
|
|
|
stromal nodules may progress to?
|
stromal sarcoma
(rare cancer) |
|
|
describe a stromal sarcoma
|
neoplastic endometrial stroma invading muscle bundles of myometrium
|
|
|
mode of metastases in stromal sarcoma?
|
lymphatic channels
(15% of cases die from metastases) |
|
|
genetics of stromal sarcoma?
|
1. translocation t(7;17)(p15;q21)
2. fusion of JAZF1 and JJAZ1 genes *produces fusion transcript and protein* |
|
|
what is the most common benign tumor of the female genital tract?
|
Leiomyomas (fibroids)
|
|
|
how common are leiomyomas?
|
seen in 75% of females at reproductive age
|
|
|
describe the genetics of leiomyomas
|
each leiomyoma is monoclonal
|
|
|
which hormone promotes leiomyoma growth?
|
estrogen
|
|
|
presenting s/s of a leiomyoma? (4)
|
1. abnormal bleeding
2. urinary frequency 3. pain 4. infertility |
|
|
can leiomyomas become malignant?
|
RARELY
(usually the benign variant metastasizes to the lung or peritoneum) |
|
|
treatment for leiomyomas?
|
myomectomy or hysterectomy
|
|
|
a uterine malignancy of smooth muscle origin is called?
|
leiomyosarcoma
|
|
|
histological characteristics of leiomyosarcoma?
|
necrosis
irregular borders cell atypia increased mitoses |
|
|
age group most commonly afflicted with leiomyosarcoma?
|
>50 yrs
|
|
|
5 year survival rate of leiomyosarcoma?
|
20%
|
|
|
inactivation of PTEN associated with?
|
endometrial hyperplasia
endometrial adenocarcinoma |
|
|
fusion of JAZF1 and JJAZ1 genes associated with?
|
Stromal Sarcoma
|
|
|
excluding HIV: acute manifestations/symptoms of STDs can be classified in to what three categories?
|
1. discharge
2. ulcers 3. warts |
|
|
which two STDs are notorious for causing cervicitis and urethritis?
|
chamydia
gonorrhea |
|
|
two STDs responsible for vaginal discharge?
|
Trichomonas vaginalis
Candidiasis |
|
|
STDs that cause genital ulcers? (5)
|
1. Syphilis
2. Genital Herpes 3. chancroid 4. lymphogranuloma venereum 5. granuloma inguinale |
|
|
STD causing warts or papillomas?
|
HPV
|
|
|
two STDs causing PID?
|
gonorrhea
chlamydia |
|
|
causative bacteria of chancroid?
|
Haemophilus ducreyi
|
|
|
causative bacteria of granuloma inguinale?
|
Calymmatobacterium granulomatis
|
|
|
what type of bacteria is Neisseria gonorrhoeae?
|
gram negative diplococci
|
|
|
besides N. gonorrhoeae, only other gram neg. diplococci?
|
Moraxella
|
|
|
major reservoir for gonorrhea?
|
mainly asymptomatic males
|
|
|
group at highest risk for contracting gonorrhea?
|
young females (teens and early 20s)
|
|
|
metabolism of N. gonorrhoeae?
|
aerobic
prefers increased levels of CO2 requires chocolate agar to grow |
|
|
2 lab diagnostic tests for N. gonorrhoeae?
|
1. nonmotile
2. oxidase positive |
|
|
Virulence factors of N. gonorrhoeae? (5)
|
1. endotoxin (lipooligosaccharide)
2. pili 3. peptidoglycan 4. binding of blocking antibodies 5. IgA1 protease |
|
|
describe the endotoxin found in N. gonorrhoeae
|
lopooligosaccharide (shorter saccharide chain than LPS)
still displays lipid A toxicity |
|
|
functions of pili as a virulence factor for N. gonorrhoeae? (2)
|
1. avoid phagocytosis
2. adhesion |
|
|
reason for binding of blocking antibodies as a virulence factor for N. gonorrhoeae?
|
block so that bactericidal antibodies can't bind
|
|
|
function of IgA1 protease as a virulence factor for N. gonorrhoeae?
|
degrades IgG, IgA1, IGA2 (Ig's found in genital secretions)
|
|
|
function of peptidoglycan as a virulence factor for N. gonorrhoeae?
|
induces TNF-a, leading to sloughing of ciliated cells
|
|
|
3 surface components changed by N. gonorrhoeae to evade the immune system?
|
1. lipooligosaccharide
2. Opa proteins 3. Surface pili |
|
|
how does lipooligosaccharide help N. gonorrhoeae to evade the immune system? (2)
|
1. has LOS instead of LPS, therefore compliment can't bind & kill
2. Neisseria binds to sialic acid on LOS. this blocks C3b deposition and makes bacteria look like a RBC |
|
|
what is notable about sialated strains of N. gonorrhoeae?
|
because they look like RBCs they are more likely to lead to disseminated gonococcal infections (DGI). called serum resistance
|
|
|
describe opa proteins in their relationship to helping N. gonorrhoeae evade the host immune system
|
opa (opacity related proteins) cause the bacteria to look opaque. They allow the bacteria to not get engulfed by neutrophils and make an infection more likely to lead to DGI and PID
|
|
|
in relation to genetics, how are opa proteins expressed on the surface of N. gonorrhoeae?
|
switching occurs. there is a phase variation that results in varied expression of the gene(and new protein expression)
|
|
|
how many opa genes are there total in N. gonorrhoeae?
|
10-12
(variable number are expressed) |
|
|
how is antigenic variation acheived in the surface pili of N. gonorrhoeae
|
recombinant exchange leads to formation of different pili allowing N. gonorrhoeae to evade the immune response.
|
|
|
two types of pili genes seen in N. gonorrhoeae?
|
1. pilE (expressed)
2. pilS (silent) |
|
|
pili and/or opa facilitate the attachment of N. gonorrhoeae to nonciliated columnar epithelial cells. What surfaces, specifically, do pili bind to? (5)
|
1. urethra
2. vagina 3. fallopian tube 4. sperm 5. neutrophils |
|
|
pili and/or opa facilitate the attachment of N. gonorrhoeae to nonciliated columnar epithelial cells. What surfaces, specifically, do opa proteins bind to?
|
1. cervix
2. urethra 3. adhesion to other gonococci |
|
|
association between gonorrhea and HIV?
|
gonorrhea associated with increased transmission of and susceptibility to HIV (incr. shedding of HIV particles in gonorrhea infx.)
|
|
|
Hallmark symptom of men with gonorrhea?
|
painful, purulent discharge
|
|
|
two locations of infections in a male with gonorrhea?
|
1. urethritis
2. epididymitis |
|
|
what is the primary site of a gonorrheal infection in a female?
|
endocervical canal
|
|
|
s/s of a female gonorrheal infection?
|
*most asymptomatic*
vaginal discharge urinary frequency dysuria abdominal pain menstrual abnormalities |
|
|
three other locations of local gonococcal infections?
|
1. rectal
2. pharyngeal 3. conjunctiva |
|
|
4 primary features of DGI?
|
1. fever
2. migratory polyarthralgia 3. rash 4. skin lesions |
|
|
four metastatic gonococcal infections?
|
1. purulent arthritis
2. perihepatitis 3. endocarditis 4. meningitis |
|
|
what is the most frequently reported STD in the US?
|
chlamydia
(~3 million cases annually) |
|
|
why are beta lactams ineffective in treating chlamydia?
|
chlamydia has no peptidoglycan
|
|
|
is chlamydia trachomatis intracellular or extracellular?
|
OBLIGATE intracellular pathogen
(unable to synthesize ATP) |
|
|
what are the two forms of Chlamydia in its replication cycle?
|
EB (elementary body) - nonreplicating, infectious
RB (reticulate body)- replicating, noninfectious |
|
|
5 steps in the developmental cycle of Chlamydia?
|
1. EB attaches to epithelial cell
2. EB enters via endocytosis 3. EB differentiates to RB 4. RB condenses and forms EB 5. cell ruptures, releases EB |
|
|
Describe the replication of the RB form of Chlamydia in the host cell.
|
- RB uses ATP from host
- replicates in vacuole - forms large cytoplasmic inclusions |
|
|
what virulence factor does chlamydia produce that induces cytokines?
|
toxic principle
|
|
|
function of the unique cell wall structure of Chlamydia trachomatis?
|
inhibits phagolysosome fusion
|
|
|
three main classes of serotypes of Chlamydia?
|
1. endemic trachoma (A and C)
2. STDs and inclusion conjunctivitis (D and K) 3. lymphogranuloma venereum (L1, L2, L3) |
|
|
perinatal transmission of chlamydia results in?
|
neonatal conjunctivitis
|
|
|
in men, a chlamydia infection most commonly presents as what?
|
asymptomatic
*MC symptom is non-gonococcal urethritis (NGU)* |
|
|
two common complications of chlamydia infections in men?
|
1. unilateral epididymitis
2. Reiter's Syndrome (post-inflammatory immune response following infection) |
|
|
does Reiter's syndrome occur in women?
|
Rarely
|
|
|
two most common manifestations of chlamydia in women?
|
cervicitis
urethritis *most women with these remain asymptomatic* |
|
|
which diagnostic test for Chlamydia also tests for gonorrhea?
|
Gen-Probe
(detect chlamydial ribosomal RNA - NA probe) |
|
|
advantage of using ligase chain reaction (LCR) in testing for chlamydia?
|
can detect in first void urine
|
|
|
which serovars of Chlamydia trachomatis cause lymphogranuloma venereum (LGV)?
|
the invasive serovars (L1, L2, L3)
|
|
|
compare the presentation of LGV in females vs. males.
|
females - mostly asymptomatic (can be reservoirs)
males - more likely to have clinically evident infection |
|
|
How does LGV spread?
|
spreads via lymphatics
|
|
|
describe the 3 stages of LGV
|
1. First - small, painless ulcer or papule
2. Second - painful regional lymphadenopathy (buboes), systemic sx. 3. Third - fever, chills, arthralgia, rectal pain, mucopurulent or bloody discharge |
|
|
in order to diagnose LGV, what must be excluded? (2)
|
syphilis
herpes |
|
|
which method is used to diagnose LGV?
|
serology (PCR most sensitive)
|
|
|
How is syphilis transmitted?
|
sexually - by direct contact with a primary or secondary lesion.
|
|
|
in what sex and age group is syphilis most common in?
|
middle aged men
|
|
|
what type of bacteria is treponema pallidum?
|
gram neg. spirochete
(but NO LPS) |
|
|
describe the culturing conditions of treponema pallidum
|
has never been grown on artificial medium
- motile - microaerophilic (1-4% O2) |
|
|
two virulence factors for treponema pallidum?
|
1. surface associated hyaluronidase (aids in tissue destruction and spread)
2. outer membrane weakly antigenic (b/c no LPS) |
|
|
where does syphilis migrate to and replicate?
|
subepithelial tissues
|
|
|
how does syphilis enter the systemic circulation?
|
via the lymphatics
|
|
|
what stage of syphilis is a chancre considered?
|
primary
|
|
|
what causes a chancre?
|
cellular defenses at the site of replicating treponemes
|
|
|
what causes secondary syphilis?
|
systemic spread (2-10wks after chancre)
|
|
|
what causes tertiary syphilis?
|
tissue destruction caused by host response to presence of treponemal antigens
|
|
|
are chancres infectious?
|
YES - highly infectious
|
|
|
in what stage of syphilis are condylomata lata seen and what are they?
|
seen in secondary syphilis
they are highly infectious grey, flattened, wartlike lesions |
|
|
what is unusual about the rash seen in secondary syphilis?
|
it is a whole body rash (even on palms and soles)
|
|
|
at what stage of syphilis is neurosyphilis seen?
|
can be seen at any stage
|
|
|
manifestations of early neurosyphilis?
|
meningitis
ocular sx (can occur months to years after infx) |
|
|
manifestations of late neurosyphilis?
|
general paresis
tabes dorsalis ocular sx (can occur decades after infx, rare) |
|
|
about what % of syphilis patients progress to tertiary syphilis?
|
~30%
|
|
|
two diagnostic tests for syphilis?
|
1. VDRL (Ab that cross-reacts with cardiolipin)
2. FTA (fluorescent treponemal antibody test), very specific |
|
|
what is a possible complication of syphilis treatment?
|
Jarisch-Herxheimer reaction:
systemic reaction to anti-treponemal therapy due to dead spirochetes in the CV system. (NOT an allergic rxn) |
|
|
Haemophilus ducreyi causes?
|
chancroid
|
|
|
describe the bacteria Haemophilus ducreyi
|
fastidious gram negative rod
|
|
|
describe the ulcer seen in Chancroid
|
tender papule develops into a painful ulcer with sharp margins.
- satellite lesions may develop ("kissing lesions") - regional lymphadenitis common) |
|
|
Diagnostic test for chancroid?
|
culture
(rule out syphilis/herpes) |
|
|
describe the bacterial characteristics of Calymmatobacterium granulomatis?
|
fastidious gram negative bacillus
|
|
|
Calymmatobacterium granulomatis causes?
|
Granuloma inguinale
|
|
|
describe the ulcer seen in Granuloma inguinale
|
small firm papule develops into painless ulcer, chronic
|
|
|
diagnosis of granuloma inguinale?
|
Donovan bodies seen in smears from biopsy specimens.
(D. bodies = encapsulated coccobacilli in the cytoplasm of mononuclear cells) |
|
|
3 STDs characterized by vaginal discharge?
|
1. Trichomonas vaginalis
2. Candida albicans 3. Bacterial vaginosis |
|
|
describe normal vaginal discharge
|
clear to white
colorless odorless high viscosity |
|
|
what is the dominant bacterial flora of the vagina?
|
lactobacillus
|
|
|
two actions of lactobacillus that are beneficial to the vaginal "ecosystem"
|
1. convert glucose to lactic acid, thereby maintaining an acidic pH
2. produce H2O2 (potential microbicide) |
|
|
Describe Garderella vaginalis and how it causes bacterial vaginosis
|
G. vaginalis is part of the normal flora of the vagina. BV happens when the normal flora is disrupted and overgrowth of G. vaginalis occurs.
|
|
|
what type of bacteria is Gardnerella vaginalis?
other characteristics? |
Gram negative coccobacillus
fastidious facultative anaerobe |
|
|
what is the diagnostic hallmark of BV?
|
CLUE cells
(adherence of G. vaginalis to exfoliated epithelial cells) >20% is of diagnostic significance |
|
|
how does BV alter the pH of the vagina?
|
raises it (>4.5)
|
|
|
Define the Amsel criteria needed for the diagnosis of BV. How many must be present?
|
1. vaginal pH >4.5
2. presence of >20% per HPF of clue cells 3. positive amine "whiff" test 4. non-viscous, milky-white discharge adherent to the vaginal walls must have three features to diagnose with BV |
|
|
40-80% of PID can be attributed to?
|
STDs
|
|
|
risk factors for PID?
|
1. young age
2. unmarried 3. risky sexual behavior 4. substance abuse 5. poor healthcare behavior 6. IUD insertion |
|
|
most common bacterial agents of PID?
|
Neisseria gonorrhoeae
Chlamydia trachomatis |
|
|
what is the pathway of an ascending PID infection?
|
cervicitis -> endometritis -> salpingitis/tubo-ovarian abscess -> peritonitis
|
|
|
compare the clinical features of PID caused by:
1. gonorrhea 2. chlamydia |
1. abrupt fulminant presentation w/i 1 wk of onset of menses
2. subacute, mild sx. (often described as dull pain) |
|
|
complications of PID?
|
1. ectopic pregnancy
2. tubal infertility 3. recurrent PID 4. chronic abdominal pain 5. tubo-ovarian abscess 6. pelvic adhesions |
|
|
what is the minimum criteria for diagnosis of PID?
|
lower abdominal tenderness
-or- adnexal tenderness -or- cervical motion tenderness |
|
|
implications of gonorrhea and/or chlamydia on pregnancy? (3)
|
1. opthalmia neonatorum
2. pre-term delivery 3. puerpural infections |
|
|
implications of BV, trichomonas vaginalis on pregnancy?
|
pre-term birth
|
|
|
list the 3 bacteria that infect the fetus transplacentally
|
1. Listeria monocytogenes
2. Mycobacterium tuberculosis 3. Treponema pallidum |
|
|
Three bacteria that infect the fetus via an ascending infection?
|
1. Group B strep
2. E. coli 3. Listeria monocytogenes |
|
|
four bacteria that infect the fetus natally?
|
1. Group B strep
2. E. coli 3. Listeria monocytogenes 4. Neisseria gonorrhoeae |
|
|
what are the recommendations for screening of group B strep in pregnant women?
|
screened at 35-37 wks by vaginal-rectal culture
(if positive give antibiotics) |
|
|
antibiotic resistance of which bacteria (causing an STD)is a very big problem?
|
N. gonorrhoeae
|
|
|
which family of viruses do the HSV-1 and HSV-2 viruses belong to?
|
Alphaherpesviruses
|
|
|
Does HSV have an envelope?
|
yes
|
|
|
in the HSV virion, what is the region between the envelope and the capsid called?
|
tegument
|
|
|
what is contained in the tegument of the HSV virion?
|
REGULATORS of gene expression and cell RNA/protein synthesis
|
|
|
regarding the viral glycoproteins of HSV, what are gB and gC required for?
|
attachment
|
|
|
regarding the viral glycoproteins of HSV, what is gD required for?
|
entry
|
|
|
describe the genome of HSV
|
linear dsDNA
|
|
|
are the genomes of HSV-1 and HSV-2 similar?
*significance? |
yes, they are "colinear"
(50% homology between them) *means they can exchange genetic information |
|
|
what two things are found in the electron dense core of the HSV virion?
|
protein
DNA |
|
|
regarding HSV: what are the three waves of viral gene expression?
|
1. immediate early
2. early 3. late |
|
|
regarding HSV: what type of proteins are synthesized in the immediate early phase?
|
regulatory proteins
|
|
|
regarding HSV: what type of proteins are synthesized in the early phase?
|
DNA replication proteins
|
|
|
regarding HSV: what type of proteins are synthesized in the late phase?
|
structural proteins
|
|
|
where in the host cell does HSV replicate?
|
nucleus
|
|
|
how does HSV acquire its envelope?
|
budding from the inner nuclear membrane
|
|
|
HSV has "virulence factors" that result in what four alterations?
|
1. shutting off of host cell protein synthesis
(via degrading cellular mRNA) 2. blocks MHC I translocation (cells not recognized by immune system) 3. blocks apoptosis 4. blocks antiviral effects of interferon |
|
|
how much of the world's population is estimated to have recurrent HSV infections?
|
1/3
|
|
|
why does HSV have such a big viral reservoir?
|
*establishes long term latent infections
*viral shedding is asymptomatic |
|
|
HSV-1 is associated with what kind of infections?
|
orolabial infections
(transmitted by close personal contact) |
|
|
HSV-2 is associated with what type of infections?
|
genital infections
|
|
|
in HSV - which is usually more severe: primary disease or recurrent disease?
|
primary
|
|
|
which disease is usually more severe: HSV-1 or HSV-2?
|
HSV-2
|
|
|
which is more likely to establish latency and have recurrent episodes, HSV-1 or HSV-2?
|
HSV-2
|
|
|
where does the HSV replicate?
|
epithelial cells
|
|
|
what causes the formation of the vessicles seen in HSV?
|
cell destruction and local inflammation
|
|
|
where does the HSV establish latency? Does the site of infection change the specific location of latency?
|
in the dorsal root ganglion
*orolabial infections - trigeminal ganglia *genital infections - sacral ganglia |
|
|
during latency, in what form is the HSV viral genome maintained?
|
multi-copy episome
(limited transcription) |
|
|
what are some stimuli for reactivation of HSV?
|
*any momentary compromise of the immune system*
1. certain foods 2. friction from sexual activity 3. fever 4. surgery 5. sunlight 6. stress 7. menstruation |
|
|
what is the most common manifestation of primary infection with HSV-1 called?
|
gingivostomatitis
|
|
|
describe gingivostomatitis (primary infection)
|
presence of painful vesicles of ulcerations on gums, buccal mucosa, tongue and lips
|
|
|
how much earlier than the "erruptions" does the prodrome of itching or burning appear?
|
1-2 days
|
|
|
ocular manifestations of HSV-1?
|
keratoconjunctivitis
(can be primary or secondary infection) |
|
|
what would be seen upon fluoroscein staining in HSV-1 induced keratoconjunctivitis?
|
dendritic ulcers
|
|
|
in a female with an HSV-2 infection: where can vesicular erruptions be found?
|
external genitalia
cervix vagina (also rectum, urethra, mucosa of bladder) |
|
|
treatment of choice for HSV?
|
acyclovir
|
|
|
besides being active against HSV, what other two viruses in the herpes family is acyclovir active against?
|
VZV
EBV |
|
|
MOA of acyclovir?
|
chain terminator of viral (but not cellular) DNA replication
*must be phosphorylated by viral TK (thymidine kinase)* |
|
|
which viral mutations are associated with acyvclovir resistance?
|
mutations in the viral TK gene
|
|
|
when the viral TK gene is mutated, what antivirals are they automatically resistant to as well? (2)
|
1. gancyclovir
2. famciclovir |
|
|
when the viral TK gene is mutated, what 3 antivirals are they susceptible to?
|
1. virabidine
2. foscarnet 3. cidofovir |
|
|
what effect does acyclovir have on the:
1. duration of primary episodes 2. suppression of recurrent episodes |
1. shortens duration of primary infection
2. supresses recurrent episodes |
|
|
MOA of foscarnet?
|
inhibits pyrophosphate exchange in viral DNA polymerase -> inhibits viral replication
|
|
|
what is the risk of transmission of HSV during asymptomatic periods?
|
7-10%
advise condom use during this period |
|
|
connection between HSV infection and susceptibility to HIV?
|
people with genital HSV have 2x increased risk of acquiring HIV
|
|
|
HPV belongs to which family of viruses?
|
papoviridae
(a group of viruses associated with tumors in their natural hosts) |
|
|
describe the genome of HPV
|
circular dsDNA
(viral DNA is complexed with cellular histones) |
|
|
is HPV classified according to genotype or serotype?
|
genotype
|
|
|
what are the two phases of HPV gene expression?
|
1. early
2. late |
|
|
which oncogenes are expressed in the early phase of HPV gene expression?
|
E6 and E7
|
|
|
oncogenic effects of E6 and E7 when expressed by HPV?
|
inactivate p53 and pRB
|
|
|
what has a very high chance of occuring once the viral HPV genome is integrated into the host genome?
|
progression to malignancy
|
|
|
how can HPV be transmitted?
|
sexual
fomites (clothing, floors) nosocomial (cryoprobes, inhalation of smoke generated by electrocautery and laser therapy) |
|
|
where does HPV establish infection?
|
basal cell layer of the epithelium
|
|
|
in regards to HPV: what activates viral replication and gene expression?
|
migration of the basal cells (and virus) to the epithelial surface
|
|
|
early HPV gene expression causes cell proliferation and thickening of what epidermal layer?
|
stratum spinosum (prickle cell layer)
|
|
|
in an HPV infection: what causes expression of late genes and production of virions?
|
differentiation of epidermal cells to keratinocytes
|
|
|
where are the following types of HPV induced warts found?
1. verruca vulgaris 2. verruca plana 3. verucca plantaris |
1. common warts of hands and other surfaces
2. flat or juvenile warts on face, knees or arms 3. plantar warts, found on feet, tend to be deeply implanted |
|
|
what are condyloma acuminata?
|
genital warts with a cauliflower-like appearance
|
|
|
where are flat papules MC found as a manifestation of HPV?
|
cervix
|
|
|
a genital wart that has a thick, horny layer that resembles common warts is called?
|
keratotic wart
|
|
|
which types of HPV are associated with a high risk of progression to cervical cancer?
|
HPV types 16, 18, 31, 35
|
|
|
regarding HPV and cancer: what type of cell proliferation defines dysplasias and cervical intraepithelial neoplasias?
|
abnormal proliferation of the basal cell layer in cervical warts
|
|
|
what must happen for cell proliferation to be called an invasive squamous cell carcinoma?
|
breach of basement membrane
|
|
|
what is the differential diagnosis of a genital wart?
|
1. HPV
2. condylomata lata (caused by treponema infection) 3. molluscum contagiosum 4. acquired dermatologic skin condition |
|
|
what is the advantage to treating genital warts caused by HPV?
|
destruction of warts enhances immune response (so untreated warts also regress)
|
|
|
molluscum contagiosum is what type of virus?
|
poxvirus
|
|
|
describe the genome of molluscum contagiosum
|
very large dsDNA genome
|
|
|
describe the lesions seen with molluscum contagiosum
|
small, pearly, raised, flesh colored nodules in epithelial layer of the skin
|
|
|
treatment for molluscum contagiosum?
|
cryotherapy
|
