Term
what are the 3 main bacterial causes of STD? |
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Definition
neisseria gonorrhea, treponema pallidum, and chlamydia trachomatis |
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Term
what is slang for neisseria gonorrhea infections? |
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Definition
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Term
what characterizes the physiology of neisseria gonorrhea? |
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Definition
it is a very fastidious organism - neisseria gonorrhea will not grow on dried out or fatty acid media and *requires media supplemented w/iron (may be difficult to recover from clinical specimens in acute cases). |
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Term
is neisseria gonorrhea easily transmitted p2p? |
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Definition
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Term
what is the structure of neisseria gonorrhea like? |
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Definition
neisseria gonorrhea is a *gram negative diplococci w/a thin peptidoglycan layer and a loose associated *capsule. neisseria gonorrhea also is covered in *pili - which organism is avirulent w/o. |
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Term
what is one of the key reasons that it is so hard to make a vaccine against neisseria gonorrhea or develop immunity after infection? |
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Definition
pili expression is controlled by the pil gene complex, which is activated in different *phase variations during infection. these phase (antigenic) variations lead to changes in the conserved region at the N-terminal end (the highly variable exposed carboxyl end) of the pili - leading to different proteins being expressed at different times. |
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Term
what are the other surface proteins found on neisseria gonorrhea? |
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Definition
Por proteins: porins which form channels in the outer membrane and also *allow for antigenic variation (allows for serotype classification). Opa proteins: opacity proteins which mediate binding to epithelial cells via stabilization of pili. Rmp proteins: reduction-modifiable proteins (associated with Por proteins) |
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Term
how does neisseria gonorrhea acquire iron? |
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Definition
iron binding is mediated by 3 proteins: Tbp1, Tbp2 (receptor for binding *transferrin), and Lbp (receptor for binding *lactoferrin). |
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Term
what is the characterizes lipooligosaccharide found on the surface of neisseria gonorrhea? |
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Definition
the lipooligosaccharide (LOS) is similar to the gram negative LPS, but *does not have the antigenically diverse, stain-specific O polysaccharide antigens found in LPS. |
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Term
what is the function of the protease and beta-lactamase which neisseria gonorrhea expresses? |
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Definition
the protease can cleave IgA and the beta-lactamase hydrolytically destroys PCN |
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Term
what are the general features of n. gonorrhea pathogenesis? |
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Definition
n. gonorrhea attaches to mucosal cell, penetrates then multiplies. it can move into the subepithelial space and then travel through lymphatics and blood = systemic |
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Term
what is the mechanism of n. gonorrhea infection? |
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Definition
pili are important for initial attachment, which the *Opa protein then directs further tightening of. the *Por protein prevents phagolysosome fusion and the *LOS stimulates an inflammatory response (via release of TNF alpha, which most symptoms are caused by) |
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Term
what is the predominant IgG antibody produced during infection? |
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Definition
*IgG3, which mainly responds to *Pilin, *Opa, and *LOS. IgG3 has a minimal response to Por. IgG3's response to LOS can *activate complement - releasing C5a, a chemotactic factor for neutrophils. people w/inherited complement deficiencies are at greater risk for systemic disease. |
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Term
what are the clinical symptoms in men of a n. gonorrhea infection? |
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Definition
typically the infection occurs in the *urethra. there is a 2-5 day incubation w/urethral discharge and *dysuria and then 95% of pts will present with the following acute symptoms: epididymitis, prostatitis, and periurethral abscesses. complications (disseminated infections) are rare |
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Term
what are the clinical symptoms in women of a n. gonorrhea infection? |
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Definition
the site of primary n. gonorrhea infection in women is the *cervix, where columnar epithelial cells are at risk (squamous cells in vagina = unable to infect). only symptomatic pts present with vaginal discharge, dysuria and abdominal pain. 10-20% have an ascending genital infection including salpingitis, tuboovarian abscesses, and pelvic inflammatory disease. 1-3% present w/disseminated infection - *generally to joints (possible suppurative arthralgia), septicemia, and skin infection. the increased risk of dissemination compared to men is due mainly to asymptomatic presentations. |
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Term
is n. gonorrhea one of the leading causes of suppurative arthritis in adults? |
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Definition
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Term
what are other diseases associated with n. gonorrhea? |
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Definition
*perihepatitis/fitz-hugh-curtis syndrome: inflammation of lining of the liver (RUQ pain). *opthalmia neonatorum: purulent conjunctivitis in newborns. *anorectal gonorrhea in homosexual men. *pharyngitis is also possible. |
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Term
what general lab diagnoses are run for suspected n. gonorrhea infections? |
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Definition
gram stain: very sensitive and specific with purulent infection, but <60% sensitivity in asymptomatic pts. cx: thayer-martin media (selective media w/vancomycin to control growth of contaminating organisms) and chocolate blood agar (non-selective, used if organism is sensitive to vancomycin) |
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Term
what happens if n. gonorrhea is plated on media containing fatty acids or trace metals? dry or cold media? |
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Definition
n. gonorrhea will die on all of those media |
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Term
in terms of disseminated disease, when are blood cx's vs joint fluid cx's positive? |
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Definition
blood cx's for n. gonorrhea infections are only positive during the first week of infection and joint fluid cx's are only positive at the time of arthritis onset |
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Term
what characterizes the preliminary identification of n. gonorrhea? |
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Definition
isolation of an **oxidase positive,** gram negative diplococci that grows on chocolate agar or thayer-martin media |
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Term
what characterizes the definitive identification of n. gonorrhea? |
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Definition
in addition to the preliminary identification, detection of acid produced from glucose - but not other sugars |
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Term
what characterizes genetic testing for n. gonorrhea? |
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Definition
PCR is sensitive, specific, and rapid - but cannot detect antibx resistance |
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Term
what characterizes serologic testing for n. gonorrhea? |
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Definition
serologic tests can detect antigens and antibodies - but are not sensitive or specific |
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Term
why is PCN not used against n. gonorrhea? |
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Definition
the required therapeutic dose is too high, PCN-resistant strains are increasing and PCN-sensitive strains are becoming resistant thanks to plasmid involvement. |
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Term
what is the etiologic agent of syphilis? |
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Definition
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Term
how does the infection rate of treponema pallidum compare to n. gonorrhea or c. trachomatis? |
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Definition
treponema pallidum infection rates are lower. |
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Term
which sex is more infected with treponema pallidum? |
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Definition
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Term
what generally characterizes treponema pallidum? |
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Definition
treponema pallidum is a gram negative spirochete (particularly thin and long spiral shape) |
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Term
what tests can be run for treponema pallidum? |
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Definition
venereal disease research laboratory test (VDRL), plasma reagent test, microhemagglutination test (MHA), and fluorescent antibody test (FTA-ABS) |
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Term
what are physiological characteristics of treponema pallidum? |
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Definition
treponema pallidum is a natural pathogen of humans which cannot be grown in a free cell cx. in rabbit epithelial cells, treponema pallidum has a *slow doubling time of >30 hrs = limited growth. |
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Term
can spirochetes like treponema pallidum use glucose? |
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Definition
yes, originally spirochetes were thought to be strict anaerobes, but they *can used glucose oxidatively |
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Term
are spirochetes found in normal oral flora? |
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Definition
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Term
since treponema pallidum is too thin to be seen by gram or giemsa staining, what can be used? |
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Definition
darkfield staining or attaching a fluorescent antibody probe to the organism |
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Term
what virulence factors does treponema pallidum possess? |
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Definition
*outer membrane proteins which are important for attachment to host cells. virulent spirochetes produce *hyaluronidase which allows organisms to go through extracellular matrix (facilitates perivascular invasion). the most virulent treponema pallidum is coated w/host cell fibronectin, which protects it from phagocytosis (hides). t. pallidum genes have been cloned in e. coli to be able to study outer membrane proteins. |
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Term
what are the tissue destruction and lesions associated w/syphilis really due to? |
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Definition
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Term
how many phases are there to a syphilis infection? |
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Definition
3 - progression to the 3rd is uncommon these days |
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Term
what characterizes the primary phase of syphilis? |
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Definition
skin lesions, typically a *chancre (*not painful) which is erosion of the surface layer of skin active w/spirochetes. neutrophils/macrophages are found in the chancre, but macrophages cannot kill treponema pallidum. the chancre will often self-resolve (leading the pt to thinking they are cured). the spirochetes then disseminate in blood, inflaming the vessels. regional lymphadenitis develops 1-2 wks after the chancre. |
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Term
what characterizes the secondary phase of syphilis? |
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Definition
prominent skin lesions appear over the entire host body and a *flu-like syndrome consisting of a sore throat, headache, fever, myalgias, anorexia, generalized lymphadenopathy, and *rash (may be macular, papular, pustular, *on palms* or over entire skin) sets in. spontaneous remission (latent phase) may occur after the primary or secondary phase, but the disease can reactivate. |
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Term
what characterizes the tertiary phase of syphilis? |
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Definition
chronic inflammation, and any organs may be involved. granulomatous lesions (*gummas) are found in bone, skin, and other organs. less pts progress to this. |
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Term
is there increased incidence of neurosyphilis in AIDS pts? |
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Definition
yes - despite adequate therapy |
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Term
what is the course of syphilis generally? |
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Definition
the primary and secondary phases are fairly quick, then the latent benign phase can last 10+ yrs. cardiovascular symptoms may show up in 15 yrs and CNS symptoms in 20. spontaneous cures are rare. |
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Term
what characterizes congenital syphilis? |
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Definition
in utero syphilis infections are a serious fetal disease consisting of multiple organ malformations and are often fatal. latent infections are possible, and if the infant is born, it is often w/o clinical disease but these infants do develop *rhinitis and widespread *desquamating maculopapular rash. if untreated, *late boney destruction and *cardiovascular syphilis occurs. |
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Term
what are lab diagnostics for treponema pallidum? |
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Definition
darkfield examination of exudates or direct fluorescent antibody will detect treponema pallidum. t. pallidum will not grow in artificial cx or show up on gram stain. *serology is used most often to dx, of which there are 2 general tests. |
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Term
what are the 2 serologic tests for treponema pallidum? |
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Definition
1) non-specific non treponemal test, which looks for regain IgG/IgM antibodies against lipids released from damaged cells. cardiolipin (from beef heart) is then put on a slide w/a sample from the pt and VDRL and RPR (rapid plasma reagin) then measure aggregation of antibodies. a positive test is not specific for t. pallidum. 2) specific treponemal test: specific antibody test (FTA-ABS and MHA-TP) to confirm VDRL and RPR. *these tests are run in succession* |
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Term
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Definition
PCN is the drug of choice. benzathine PCN (long acting) for early states, PCN G for congenital and late stages. tetracyclines can also be used except in neurosyphilis and pregnancy. |
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Term
what is the #1 most common bacterial cause of STD? |
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Definition
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Term
why was chlamydia trachomatis once thought to be a virus? |
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Definition
b/c of its size - only 0.2 microns in diameter |
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Term
what does it mean that chlamydia trachomatis is an obligate bacterial parasite? |
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Definition
it requires internal host cell ATP for growth |
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Term
what is unique about chlamydia trachomatis? |
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Definition
c. trachomatis does not have a peptidoglycan layer unlike any other bacteria. c. trachomatis does have inner/outer cell membranes like gram negative bacteria, though it doesn't stain well. |
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Term
are the rates of chlamydia infections increasing? |
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Definition
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Term
what are the 2 main forms of c. trachomatis? |
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Definition
the elementary body (EB, spore-like, infects cells) and the reticulate body (RB, vegetative form, osmotically fragile, grows inside cells and then reverts to EB to be released via exocytosis or killing cell) |
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Term
what are the 3 biovars (3 different infection locations, all sexually transmitted) of c. trachomatis? |
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Definition
1) trachoma: infects conjunctive which invert and cause eyelashes to scrape the cornea = blindness - more common in 3rd world countries. 2) lymphogranuloma venereum (LGV): STD form. 3) mouse pneuomonitis. |
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Term
how many serovars are there of the lymphogranuloma venereum (LGV) c. trachomatis (STD form)? |
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Definition
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Term
where are the receptors for the EB form of c. trachomatis? |
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Definition
the receptors for the EB form of c. trachomatis are restricted to non-ciliated columnar, cuboidal, or transitional epithelia, found on: mucous membranes of urethra, endocervix, endometrium, fallopian tubes, anorectum, respiratory tract, and conjunctiva |
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Term
can the lymphogranuloma venereum (LGV) biovar replicate in mononuclear phagocytes? |
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Definition
yes - macrophages take in but are unable to kill organism |
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Term
what are the clinical manifestations of chlamydia due to? |
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Definition
destruction of host cells and the inflammatory response |
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Term
how does the lymphogranuloma venereum (LGV) biovar of c. trachomatis affect lymph nodes draining the site of infection? |
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Definition
the LGV form of chlamydia can form granulomas in these lymph nodes - which may become necrotic and attract PMNs. if these lymph nodes rupture, abscesses or sinus tracts may form. arthralgia may result when infection goes past the lymph nodes. |
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Term
what kind of inflammation does infection w/non-LGV serotypes stimulate? |
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Definition
severe inflammation w/PMNs, lymphocytes, and plasma cells. infection does not confer long-lasting immunity due to antigenic variation. |
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Term
what clinical syndromes are associated with the trachoma biovar of c. trachomatis? |
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Definition
trachoma, adult inclusion conjunctivitis, neonatal conjunctivitis, infant pneumonia, and ocular lymphogranuloma venereum. |
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Term
what characterizes urogenital chlamydia infections in females? |
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Definition
80% asymptomatic. symptomatic pts usually show a mucopurulent discharge (less purulent than gonorrhea) and hypertrophic ectopy. possible infections: cervicitis, endometritis, urethritis, salpingitis, bartholinitis, and perihepatitis. |
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Term
what characterizes urogenital chlamydia infections in males? |
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Definition
generally symptomatic, and postgonococcal urethritis (coinfection of c. trachomatis and n. gonorrhoeae) is becoming more common (automatically tx for both). symptoms include: urethral discharge, dysuria, pyuria - *but these only last for about 3 weeks, even though the infection continues as latent* (therefore important to test when symptoms appear) |
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Term
what is reiter's syndrome? |
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Definition
c. trachomatis moves to joints, causing reactive arthralgia (polyarthritis). typically seen in young white men. |
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Term
what is lymphogranuloma venereum? |
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Definition
lesions or abscesses (erosion of lymph nodes) appearing at the site of c. trachomatis infection. it happens in 2 stages, 1st: patient unaware of lesion but has fever, headache, and myalgia (non-specific symptoms) and 2nd: *inflammation - lymph node swelling, proctitis, ulcers, fistulas, genital elephantitis |
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Term
what are lab diagnostics used for chlamydia trachomatis? |
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Definition
giemsa staining is not sensitive. cx is *most sensitive, but other cells have to be infected - so takes time. direct immunofluoresence, ELISA (against LPS or outer membrane protein), and PCR are also possible. |
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Term
what is tx for chlamydia trachomatis? |
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Definition
azithromycin and doxycycline - penetrate to kill organism. sulfisoxazole is used in pregnant women. |
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