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52 Cards in this Set

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What are the 3 causes of genital ulcers?
1. Treponema pallidum: syphilis
2. Haemophilus ducrei-chancroid
3. HSV-genital herpes
What are the causes of genital warts?
HPV
What are the general characteristics of Treponema Pallidum (cause of Syphilis)?
-Spirochetes
-Gram -, spiral shaped bacteria;
-hard to see w/ LM b/c thin cell wall
-other spirochetes: Leptospira (disseminated dz can get meningitis), Borrelia (lyme dz), Treponema.
What is the role of virulence factors in path of syphilis?
sex-->outer membrane proteins of organism adhere to host mucosal cells-->hyaluronidase secreted which lets organism migrate into tissues & into blood stream-->org coats itself w/ host fibronectin to avoid phagocytosis-->lesions & clinical dz's from HOST IMMUNE RESPONSE to bacterial antigens;
What are the epidemiological factors assoc w/ Syphilis?
-Since 1990, infection rate dec (b/c of safer gay men sex), but currently inc;
-Infection rates vary in US:GA one of highest states 3/100,000.
-Rates of syphillis vary w/ race/ethnic group; highest in blacks.
-Rates of syphilis vary w/ age and gender, most common group: MEN 30-44
Describe the stages of syphilis.
1. Primary Syphilis: regional lymphadenopathy, ulcer (chancre) formation @ initial infection site (painless ulcer, has abundant T. Pallidum, chancres on penis, anal canal, mouth, cervix, labia, or external genitalia); heals w/o tx in 2-6 wks.
2. Secondary syphilis (tissue replication from widespread dissemination of T. Pallidum-fever, generalized rash incl PALMS & SOLES, highly variable rash, lesions contain organisms, malaise, myalgias, arthralgias, lymphadenopathy. 30% spontaneously clear body of organism. Condyloma lata.
3. Latent syphilis
-Early phase: primary or secondary syphilis acquired or diagnosed during preceding yr.
-Late phase: defined as seroreactivity, in absence of sx's, >2 yrs post infection.
4. Tertiary syphilis
-uncommon in US b/c of tx. result of chronic, progressive inflam process producing clinical manifestatopms yrs-decades to post infection.
-wide spread tissue destruction secondary to host response to organism.
Describe the characteristics of Condylomata lata.
-type of rash assoc w/ secondary syphilis.
-knob-like or warty papular lesions.
-on folds of moist intertriginous areas esp around genitalia & anus.
-typically 1-3 cm in diameter.
-highly infectious: T. pallidum orgs can be seen by exam of surface exudate under darkfield micro.
What diseases are associated w/ Tertiary syphilis
1. Inflammatory lesions w/ gumma-->gumma is coalescent granulomatous lesions (T cell macrophages leading to local destruction) that usually affect skin, bone, mucus membranes, but can involve any organ system, cause local destruction of affected organ system;
2. Organ systems most affected: cardio, musculoskeleta, CNS
3. Vascular dz: endarteritis of aorta, subsequent medial necrosis, aortitis, aneurysm formation;
4. Musculoskeltal: CHARCOT jt--> bone overgrowth & instability of hts.
5. Neurosyphilis: syphilitic meningitis, meningovascular syphilis, or parenchymatous neurosyphilis, tabes dorsalis.
When does local replication & dissemination of syphilis begin?
incubation period (3 wks)
How is Syphilis diagnosed?
-won't grow in culture-too thin;
-microscopy of exudates to look for organisms: darkfield, direct fluorescent Ab.
-Serology: non-treponemal Ab's, treponemal Abx.
What are the non-treponemal serologic tests (VDRL & RPR)?
-Pts w/ syphilis make Ab's that react w/ lipid (cardiolipin) found on mitochondrial membranes but also + in SLE, pregnancy, so need further testing.
2 tests available:
a) VDRL (venereal dz reference laboratory) test
b) RPR (rapid plasma reagin) test.
-these are non-specific but cost-effective, can't rule in dz: sensitivity of tests: 80% in pts w/ symptomatic primary syphilis & virtually 100% in pts w/ secondary syphilis.
-Must be followed by specific tests to look Ab's to T. pallidum.
What are the TREPONEMAL Serologic Tests: FTA-ABS & MHA-TP?
-tests for Ab's to T. Pallidum in pt's serum.
-Commercially available tests incl:
-->FTA-ABS-fluorescent treponemal Ab absorption
-->MHA-TP: microhemagglutination
What is the tx for primary and secondary syphilis?
Benzathine PCN IM in single dose.
What is the tx for Latent Syphilis?
-Early Latent Syphilis: Benzathine PCN IM in single dose;
-Late Latent Syphilis or Latent Syphilis of Unknown Duration: Benzathine PCN 3 doses IM at 1 wk intervals.
What are the 3 causes of genital ulcers?
1. Treponema pallidum: syphilis
2. Haemophilus ducrei-chancroid
3. HSV-genital herpes
What are the causes of genital warts?
HPV
What are the general characteristics of Treponema Pallidum (cause of Syphilis)?
-Spirochetes
-Gram -, spiral shaped bacteria;
-hard to see w/ LM b/c thin cell wall
-other spirochetes: Leptospira (disseminated dz can get meningitis), Borrelia (lyme dz), Treponema.
What is the role of virulence factors in path of syphilis?
sex-->outer membrane proteins of organism adhere to host mucosal cells-->hyaluronidase secreted which lets organism migrate into tissues & into blood stream-->org coats itself w/ host fibronectin to avoid phagocytosis-->lesions & clinical dz's from HOST IMMUNE RESPONSE to bacterial antigens;
What are the epidemiological factors assoc w/ Syphilis?
-Since 1990, infection rate dec (b/c of safer gay men sex), but currently inc;
-Infection rates vary in US:GA one of highest states 3/100,000.
-Rates of syphillis vary w/ race/ethnic group; highest in blacks.
-Rates of syphilis vary w/ age and gender, most common group: MEN 30-44
Describe the stages of syphilis.
1. Primary Syphilis: regional lymphadenopathy, ulcer (chancre) formation @ initial infection site (painless ulcer, has abundant T. Pallidum, chancres on penis, anal canal, mouth, cervix, labia, or external genitalia); heals w/o tx in 2-6 wks.
2. Secondary syphilis (tissue replication from widespread dissemination of T. Pallidum-fever, generalized rash incl PALMS & SOLES, highly variable rash, lesions contain organisms, malaise, myalgias, arthralgias, lymphadenopathy. 30% spontaneously clear body of organism. Condyloma lata.
3. Latent syphilis
-Early phase: primary or secondary syphilis acquired or diagnosed during preceding yr.
-Late phase: defined as seroreactivity, in absence of sx's, >2 yrs post infection.
4. Tertiary syphilis
-uncommon in US b/c of tx. result of chronic, progressive inflam process producing clinical manifestatopms yrs-decades to post infection.
-wide spread tissue destruction secondary to host response to organism.
Describe the characteristics of Condylomata lata.
-type of rash assoc w/ secondary syphilis.
-knob-like or warty papular lesions.
-on folds of moist intertriginous areas esp around genitalia & anus.
-typically 1-3 cm in diameter.
-highly infectious: T. pallidum orgs can be seen by exam of surface exudate under darkfield micro.
What diseases are associated w/ Tertiary syphilis
1. Inflammatory lesions w/ gumma-->gumma is coalescent granulomatous lesions (T cell macrophages leading to local destruction) that usually affect skin, bone, mucus membranes, but can involve any organ system, cause local destruction of affected organ system;
2. Organ systems most affected: cardio, musculoskeleta, CNS
3. Vascular dz: endarteritis of aorta, subsequent medial necrosis, aortitis, aneurysm formation;
4. Musculoskeltal: CHARCOT jt--> bone overgrowth & instability of hts.
5. Neurosyphilis: syphilitic meningitis, meningovascular syphilis, or parenchymatous neurosyphilis, tabes dorsalis.
When does local replication & dissemination of syphilis begin?
incubation period (3 wks)
How is Syphilis diagnosed?
-won't grow in culture-too thin;
-microscopy of exudates to look for organisms: darkfield, direct fluorescent Ab.
-Serology: non-treponemal Ab's, treponemal Abx.
What are the non-treponemal serologic tests (VDRL & RPR)?
-Pts w/ syphilis make Ab's that react w/ lipid (cardiolipin) found on mitochondrial membranes but also + in SLE, pregnancy, so need further testing.
2 tests available:
a) VDRL (venereal dz reference laboratory) test
b) RPR (rapid plasma reagin) test.
-these are non-specific but cost-effective, can't rule in dz: sensitivity of tests: 80% in pts w/ symptomatic primary syphilis & virtually 100% in pts w/ secondary syphilis.
-Must be followed by specific tests to look Ab's to T. pallidum.
What are the TREPONEMAL Serologic Tests: FTA-ABS & MHA-TP?
-tests for Ab's to T. Pallidum in pt's serum.
-Commercially available tests incl:
-->FTA-ABS-fluorescent treponemal Ab absorption
-->MHA-TP: microhemagglutination
What is the tx for primary and secondary syphilis?
Benzathine PCN IM in single dose.
What is the tx for Latent Syphilis?
-Early Latent Syphilis: Benzathine PCN IM in single dose;
-Late Latent Syphilis or Latent Syphilis of Unknown Duration: Benzathine PCN 3 doses IM at 1 wk intervals.
What is the follow to tx for Syphilis?
-Repeat VDRL or RPR should be done @ 3, 6, & 12 months.
-If adequately treated, VDRL & RPR becomes non-reactive.
-Tx failure can occur & may be b/c of lack of penetration of drug into CNS (organisms enter CNS early in infection)
If pt has a sustained 4x inc in nontreponemal test titer (ie compared w/ max or baseline titer @ time of tx) or have sx's recur or persist what does this mean?
They probably failed tx or were reinfected. These pts should be retreated & reevalauted for HIV infection
Describe the characteristics of HSV.
-DNA virus, replicating in nucleus
-they have an envelope that they get from nuclear membrane.
-HSV-1: oral> genital
-HSV-2: genital.
-Latent in ganglia.
Describe the epidemiology of HSV-1.
-70% of adults in US infected.
-Get virus from saliva contact--kissing, sharing toys, eating utensils.
-Can cause genital infections-oral-genital contact.
Describe the epidemiology of HSV-2.
-20-35% of adults in US are infected.
-transmitted by contact w/ sexual secretions containing virus.
-infection rate inc especially among teens.
-many not aware of infection.
Describe the pathogenesis of HSV infections.
Virus get in-->replicates in epithelial cells (may or may not cause lesion but still have virus replication & shedding in latent pt)-->ascend to ganglia-->latent in ganglia-->descends to skin, mucous membranes.
What are the results of primary genital infection w/ HSV?
-Asymptomatic infection
-Symptomatic infection (Constitutional signs: pain, urethral, vaginal discharge, fever, meningitis (more HSV2 in women; Genital lesions;
Does one get recurrences of Herpes?
-Recurrences prevented by strong cellular immune response by CD4 & CD 8 cells;
-High Ab titer does NOT prevent recurrences
Is HSV-1 or 2 more likely to be recurrent?
HSV-2
What changes from primary to non-primary to recurrent syphilis?
-# of lesions (multiple-->several-->absent)
-Sx's (present, mild, absent)
-Days/lesion: 21-->14-->7
-Days/shedding: 15-20, 10, 5.
How is genital HSV diagnosed?
Clinical appearance (ulcers), virus isolation w/ typingYPE A INCLUSION BODIES & PYKNOTIC NUCLEUS), viral antigen detection, serology w/ typing.
What is the tx for HSV?
-Antiviral drugs won't prevent latency, recurrences or transmission, but they will dec them.
-Antivirals: Acyclovir, Valacyclovir, Famciclovir-->can be given for 1st episorde or to tx or suppress recurrences.
Whats the recommended tx of first clinical episode of genital herpes?
Acyclovir, Famciclovir, Valacyclovir (about a week, extend w/ incomplete therapy)
What are the suppressive therapies for HSV w/ by how much will these recurrences be reduced post treatment?
-Acyclovir, Famiciclovir, Valacyclovir, dec frequency of genital herpes recurrences by 70-80%.
If someone presents w/ a chancroid (painful papule w/ erythematous base) w/ tender inguinal lymphadenopathy, what do you need to rule out? What do you think it is?
Its STD from Haemophilus ducreyi-->need to rule out syphilis & genital herpes
What are the general characteristics of the Human Papilloma virus?
Family Papovavirus, genera papillomavirus (30 types cause genital infection); double stranded DNA, nonenveloped, cause CHRONIC infection. Causative agents of benign squamous cell lesions that can progress to carcinomas.
Are chronic infections always replicating?
Yes, they are always replicating even if in small amts.
Whats the epidemiology of HPV?
-very common ST in US.
-20 million people inUS have genital papillomavirus infection.
-5.5 million new infections/yr
-by 50, 80% of women get HPV infection
-Spread by direct contact.
Describe the pathogenesis of Genital HPV infection?
-Virus infects epithelial cells-->Benign lesion (6, 11)-->condyloma to regression or persistence or Potentially malignant (16,18)-->premalignant lesion-->regression or progression-->malignant lesion
What are the clinical manifestations of HPV?
-Benign lesions (Condyloma accuminatum)
-Pre-Malignant lesions (Flat condyloma, CIN)
-Malignant lesions (cervical CA)
How is HPV diagnosed?
-Genital warts-->clinical appearance.
-Pre-Cancerous lesions: initially dx w/ Pap; HPV DNA can determine if hi risk HPV type is present (nucleic acid hybridization done on cells collected from cervix, detects DNA of high-risk HPV type, doesn't detect individual types or low risk types)
What on a pap smear would indicated HPV infection?
Koilocytes
What is the tx for HPV?
-Topical: podophyllin, salicylic acid, trichloroacetic acid.
-Surgery: laser, cryosurgery, cauterization, traditional.
-Immunomodulation:Imiquimod: stimulates IFN secretion, promotes Th1 cell inflamm response
-alpha-interferon injected.
How can HPV be prevented?
Quadrivalent vaccine 6, 11, 16, 18: these are responsible for 70% of cervical Ca's and 90% of genital warts.