STD/STI Flashcards
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Treponema Pallidum
Non-culturable Organisms
Treponema Pallidum
Treponema Pallidum bacterial characteristics
GN, spirochete, motile, slow growing, sensitive to desiccation and temperature
Endarteritis
T. pallidum; inflammation causing proliferation of endothelial and fibroblast cells - > blocking lumen
Periarteritis
T. pallidum; inflammation causing proliferation of adventitial cells/pericytes & cuffing of vessel by monocytes, lymphocytes, & plasma cells
Treponema Pallidum Virulence Factors
No LPS (few OMPs), Lipoprotein (act spike endotoxin, immunomodulator), antigenic variation (Tpr)
Transmission of Treponema Pallidum
No fomites (unstable), rare during latency, direct contact, transplacentally, blood transfusions
Treponema Pallidum incubation period
~21d (3-90d)
IgM w/ Treponema Pallidum
Peaks in 2nd Syphilis, but rapidly declines and goes away
IgG w/ Treponema Pallidum
Peaks at the end of 2nd Syphilis, but never goes away
Immune response to Treponema Pallidum
Th1 during Primary Syphilis, agent drives conversion to Th2 during Secondary Syphilis
Treponema Pallidum Reservoir
Humans
Endarteritis and Periarteritis are results of
Inflammatory reaction to Treponema Pallidum
Primary Syphilis Manifestations
Chancre/Genital Ulcer: indurated, sharply demarcated, eroded center, serous discharge, painless, highly infectious + regional LAD 7-10d after chancre appearance
Primary Syphilis chancre is d/t
immune response to local replication
Primary Syphilis often occurs _______ on the male penis
in the sulcus
Regional LAD may appear when during Syphilis
7-10d after primary chancre appearance, & during Secondary Syphilis
Secondary Syphilis appears
6 weeks after exposure
Manifestations of Secondary Syphilis
VARY, but include: non-pruritic rash on palms/soles,mouth/anus & spreads, condylomata lata, alopecia, fever, HA, malaise, arthralgia, LAD
Primary Syphilis chancre lasts
2-6wks
Infectious periods during Syphilis
Primary Syphilis & all bouts of Secondary Syphilis; Early Latent Stage (w/in year 1)
Condylomata lata
occurs during Secondary Syphilis; highly infectious, raised, painless, central erosion & covered w/ a thin membrane – found on genital, oral, &/or rectal mucosa
Rash of Secondary Syphilis
b/l symmetrical, non-pruritic, infectious skin rash, starting on palms/soles/mouth/anus and spreads, fever, LAD
In utero Syphilis infection can occur
anytime during latent syphilis or active syphiis
Alopecia
Secondary Syphilis
Why is Syphilis a disease of 1/3
1/3 untreated secondary syphilis pts will spontaneously cure, 1/3 secondary syphilis pts remain infected, but asymptomatic, 1/3 will progress to tertiary syphilis
What additional Manifestations may be present during secondary syphilis
hepatitis, IC-glomerulonephritis, meningitis/encephalitis, arthritis, GI and eye problems
secondary syphilis resolves
w/ or w/o treatment
Latent Syphilis
Asymptomatic phase but w/ (+) serology
Early Syphilis
1st year after exposure, considered Infectious, Most secondary syphilis relapses occur in early phase of latent syphilis
Late Syphilis
Year 1-4, not considered infectious, low rate of relapse
Tertiary Syphilis
Slow, degenerative progressive inflammatory disease, refractory to Abx, ~10yrs after exposure
Tertiary Syphilis Manifestations
Cardiovascular/Aortitis, Neurosyphilis, Gumma
Syphilitic Aortitis
Endarteritis of vasa vasorum -> ischemia of aortic arch/ascending aorta -> aortic aneurysm, stenosis, regurgitation
Early Neurosyphilis
Asymptomatic (+ CSF), Meningitis, stroke w/ focal S/S
Late Neurosyphilis
General Paresis, Tabes Dorsalis, Argyll-Robertson Pupil
General Paresis
Dementing illness (personality, affect, reflexes, eyes, sensorum, intellect, speech)
Tabes Dorsalis
P.C. - loss of proprioception & sensation -> ataxia/wide-based gait
D.R. - loss of pain & temp sensation, areflexia
Argyll-Robertson Pupil
Constriction to accommodation, but not light
Gumma
chronic granulomas found in various tissues, benign unless affecting organ
Early Congenital Syphilis
most are born without clinical evidence of disease (but would be STORCH test positive) & develop Sx ~3-4mo old
Early Congenital Syphilis Sx typically begin
3-4mo of age
Early Congenital Syphilis Sx
persistent rhinitis -> maculopapular, desquamative rash, condylomata lata, diffuse rhinitis, lesions on any organ
Latency in Congenital Syphilis
occurs ~6-12mo of age and persists typically to 5-15y/o -> Late Syphilis
Late Syphilis/Stigmata Sx
Hutchinson’s Triad, frontal bossing, bulldog jaw, higoumenakia sign, saber shins, cluttons joints
Most common outcome w/ Congenital Syphilis
Stillbirth
Hutchinson’s Triad
saddle nose, skin rhagades (radial scars), corneal ulcers and opacities, Hutchinson’s teeth and mulberry molars
Microscopy for Treponema pallidum
Darkfield
Which Abs rise first in response to Treponema pallidum
Specific-Treponema Abs
What is the 1st diagnostic test that is (+) in syphilis?
Darkfield
What is the 1st serologic test that is (+) in syphilis?
Specific-Treponema Abs
Screening Test for Syphilis
Non-Specific Antibody Test
DFA-TP for Syphilis
Specific Fluorescent Ab test to T. pallidum
Non-Specific Treponema Antibody
anti-phospholipid Abs, used for screening tests, VDLR, RPR, monitor Tx
Diagnosis of Neurosyphilis
VDLR (non-specific)
Monitor Syphilis Tx
RPR (non-specific)
Confirmatory Tests for Syphilis
Specific-Treponema Abs, FTA-ABS, used to diagnose late syphilis or neurosyphilis
Treatment for Syphilis
Benzathine Penicillin G
Treatment for Syphilis in pregnant female
Benzathine Penicillin G; if HSN -> Azithromycin
Treatment for Syphilis in penicillin-hsn pt
Azithromycin, Doxycycline, Tetracycline
Syphilis resistance to Tx
rRNA mutation confers resistance to Azithromycin in strains spontaneously
Jarisch-Herxheimer Reaction
endotoxic shock-like response due to dying agents released into blood (fever, HA, myalgia, chills, tachycardia)
Tx for Jarisch-Herxheimer Reaction
NSAID, prednisone
Reportable diseases
Syphilis
Haemophilus Ducreyi bacterial characteristics
GNR pleomorphic, highly fastidious
Culture of Haemophilus Ducreyi on
Chocolate agar
Chancroid is found primarily in
3rd world countries, and under diagnosed in the US
Most commonly associated w/ HIV transmission
Chancroid
Chancroid or Syphilis has a immune response during the primary stage
Syphilis
Why is Chancroid so highly associated w/ HIV transmission?
CD4+ Tcells & Monocytes are attracted to primary site
Chancroid Incubation period
7 days
Primary Chancroid Manifestation
genital ulcer: 1 or more painful, pustule, erodes & ulcerates w/ ragged edges +/- Bubo
Bubo
painful inguinal LAD, U/L, reddened skin, may suppurate & rupture
Bubo occurs
7-10days after chancre or during
Microscopy of Chancroid
GNR in chains in or outside of PMNs “school of fish” appearance
Treatment of Chancroid
Azithromycin, Erythromycin, Ceftriaxone
Chancroid may be resistant to what Tx
TMP-SMX; plasmid-mediated
Chlamydia trachomatis bacterial charcteristics
GN, obligate intracellular, biphasic (elementary & reticular bodies), cytoplasmic inclusions
Which strains of Chlamydia trachomatis cause LGV?
L1, L2, L3
Chlamydia trachomatis L1, L2, L3 preferentially infect
Macrophages
Immune response to Chlamydia trachomatis L1, L2, L3
CMI: Th1 -> IFN-gamma -> activate macrophages
LGV Incubation period
3-30days
Primary LGV Manifestations
small, inconspicuous genital papule or herpetiform ulcer of short duration and few symptoms (may go unnoticed)
Secondary LGV incubation
2-6 weeks after exposure
Secondary LGV Manifestations
fever, extensive inguinal LAD (acute inflammation) w/ bubo formation, groove’s Sign
Groove’s Sign
Secondary LGV; bubo formation and may bisect the inguinal mass by Poupart’s ligament
Tertiary LGV
genital ulcers, fistulas, & rectal strictures; genital elephantiasis due to lymphatic obstruction
Diagnosis of LGV
detection of chlamydial antigens by EIA, PCR
Treatment of LGV
Macrolides
Klebsiella granulomatis bacterial characteristics
encapsulated GNR, fastidious
Klebsiella granulomatis can only be cultured with
human monocytes/macrophages
Klebsiella granulomatis: Granuloma Inguinale is found
in the tropics
Granuloma Inguinale is characterized by
Chronic ulcerative, degenerative and mutilating disease of the urogenital tissue and draining lymphatics
Stain for Klebsiella granulomatis
Giemsa or Wright
Microscopy for Klebsiella granulomatis would show
Donovan bodies: clusters of organism in the cytoplasm of monocytes and macrophages Bipolar staining (safety pin)
Treatment of Granuloma Inguinale
Ciprofloxacin, TMP-SMX, Macrolides, Doxycycline
Donovan Bodies
Klebsiella granulomatis
HSV-2 viral characteristics
dsDNA, enveloped, latent in sacral ganglia
Transmission of HSV-2
Asymptomatic sexual contact, in utero or parturition, autoinoculation
HSV-2 incubation period
2-7 days
Immunocompetent pts w/ HSV-2 Manifestations
mostly asymptomatic, classic S/S: clear, fluid-filled vesicles on erythematous base (vesicle -> pustule -> ulcer -> crust); inguinal LAD; aseptic meningitis if disseminated
Immunocompromised pts w/ HSV-2 Manifestations
perirectal herpetic lesions (AIDS), viremia -> hemorrhagic necrosis in affected organs
Recurrent HSV-2 infection
prodrome (pain & tingling), milder lesions ~4d & healing in 10d
Perinatal Herpes S/S appear
9-14d after birth (contracted during birth)
Perinatal Herpes S/S
SEM, Disseminated, Encephalitis (fatal)
Stain for HSV-2
Tzanck or Pap
Microscopy of HSV-2
Syncytia formation + Intra-nuclear inclusions (Cowdry A)
Serology test for HSV-2
EIA or NAAT
Treatment for HSV-2
Acyclovir
Acyclovir MOA
activated by thymidine kinase, nucleoside analogue that gets incorporated into the growing viral genome, causing chain termination
Acyclovir is not a cure for HSV but does
reduce duration of lesions, stops shedding, prevents Sx of recurrence
N. gonorrhoeae bacterial charcteristics
GN diplococci, facultative intracellular, oxidase (+), antigenic pili, IgA protease
N. gonorrhoeae transmission
while Sx or aSx, auto-inoculation, perinatally
N. gonorrhoeae Tx
Ceftriaxone (2nd or 3rd Cephalosporin)
C. trachomatis D-K causes
cervicitis, urethritis, PID
C. trachomatis D-K infects
the columnar epithelial cells of the mucosal surface
C. trachomatis D-K transmission
while Sx or aSx, auto-inoculation, perinatally
C. trachomatis D-K Tx
Tetracycline, Azithromycin, Doxycycline
Cervicitis Sx
“tender, friable cervix” mucopurulent exudate, vaginal discharge, erythema, edema, dyspareunia, dysuria
Gonococcal Cervicitis may involve
Infection may involve the Skene’s and Bartholin’s glands
Cervicitis is asymptomatic how often with each agent
60-85% for C. trachomatis & ~50% for N. gon
PID may spread to cause
produce acute peritonitis and acute perihepatitis
PID can lead to
Tubal factor infertility, ectopic pregnancy, chronic pelvic pain, Fitz-Hugh-Curtis Syndrome
PID Sx
asymptomatic, or fever, lower and pain, dysmenorrhea, irregular menses, cervical motion tenderness, adnexal tenderness/mass
Fitz-Hugh-Curtis Syndrome Sx
RUQ pain, jaundice, ascites, adhesions w/ perihepatitis
PID Tx
2nd or 3rd generation Cephalosporin (Gonorrhea)
Tetracycline, Doxycycline (Chlamydia)
Metronidazole (Anaerobes)
Urethritis asymptomatic by agent
C. trachomatis 50-60%; N. gonorrhoeae 5-10%
Sx of Urethritis
Painful urethritis, mucopurulent discharge &/or dysuria (esp w/ gonorrhea), “bonjour spots” discharge on under garments in morning
Incubation period for Urethritis
2-10d, longer for C. trachomatis
Disseminated Gonococcal Infection (DGI)
rare, several days after genital infection
Sx of Disseminated Gonococcal Infection (DGI)
fever, joint pain (septic arthritis), rash (variable – sparse pustular or hemorrhagic)
Reactive Arthritis after cervicitis/urethritis
no systemic signs, sterile, aseptic conjunctivitis & urethritis, arthralgia
Opthalmia neonatorum
hyperacute, mucopurulent conjunctivitis contracted by the neonate during birth d/t untreated gonococcal infection
Inclusion conjunctivitis
conjunctivitis contracted by the neonate during birth d/t untreated Chlamydia infection
Agar used for N. gonorrhoeae
Thayer-Martin
Diagnosis of N. gonorrhoeae
Gram stain: GN diplococci in PMNs
Diagnosis of Chlamydia trachomatis
DFA, NAAT, LCR
Non-gonococcal Urethritis
50-90% is C. trachomatis
Other agents of Cervicitis/Urethritis/PID
Ureaplasma, Mycoplasma, T. vaginalis
N. gonorrhoeae is resistant to
beta-lactams, tetracycline, fluoroquinolones, Cefixime
HPV characteristics
Small, non-enveloped, icosahedral dsDNA virus
Strains causing Dysplasia/Cervical Carcinoma
HPV-16 & 18
Strains causing Genital Warts
HPV-6 & 11
HPV has a tropism for
squamous mucosal epithelium (stratum granulosum & corneum)
HPV oncogenes MOA
E6, E7 bind & inactivate p53 & p105
HPV microscopy
koilocytosis: cells w/ large perinuclear cytoplasmic vacuoles surrounded by dense cytoplasm
Immune response to HPV
CMI, but it has limited access to the stratum granulosum and corneum
incubation period for HPV
3-4mo
Condyloma acuminatum
1 or more soft, fleshy cauliflower-like raised lesion of the squamous epithelium of the anogenital region
Cervical papillomas
dysplasia -> cancer (16, 18, 31, 33)
Diagnosis HPV dysplasia
Colposcopy - Actowhite test (acetic acid -> white patches)
Treatment for HPV
Wart removal, interferon Tx, antiviral cream, imiquimod
Imiquimod MOA
immune response modifier; binds TLR7 to promote Th1 CMI -> production of IFN, TNF, IL-6, IL-8 to induce an immune response at the infection site
HPV quadrivalent vaccine
Gardasil: HPV-16, 18, 6, 11 (capsid particles)
HPV bivalent vaccine
Cervavix: HPV-16, 18 (L1 proteins)
Vaginal NF
anaerobes > aerobes
Agents of Vaginal NF
Lactobacillus, Peptostreptococcus, Bacteroides, Staphylococcus, Streptococcus (GNR, GPR, GPC)
Lactobacillus’s role in protection of the urogenital tract
fermentation of glucose to lactic acid (pH ~4) & H2O2 production -> Cl- to kill pathogens
Normal cellular makeup of vagina
VEC:PMNs should be 1:1
Conditions that predispose to vaginal infections
menses, oral BC, diabetes, feminine products
Trichomonas vaginalis characteristics
Pear-shaped, flagellated, facultative anaerobic protozoan, w/ jerky motion
Signs of vaginitis or vaginosis
increased PMNs, clue cells, KOH (+)
Trichomonas vaginalis engulfs
bacteria, PMNs, RBCs
Trichomonas vaginalis pathogenesis
causes desquamation of mucosal epithelium, but not invasive
Trichomonas vaginalis Sx
profuse, watery or foamy leukorrheal discharge that is highly irritating to the vagina, labia, vulva, & perineum; desquamation + intense pruritis is common
Trichomonas vaginalis incubation period
5-28d
Trichomonas vaginalis Diagnosis
wet mount w/ motile protozoans
Labs for Trichomonas vaginalis
elevated vaginal pH, high PMNs, KOH (-)
Treatment for Trichomonas vaginalis
Metronidazole, vinegar (acid douche)
Only protozoan STD
Trichomonas vaginalis
Candida characteristics
Yeast, invasive in all 3 forms (yeast, pseudohyphae, hyphae)
Candida albicans is different from other candida bc
forms germ tubes at 37C
Immune response to Candida
CMI + Neutrophils
Sx of Candidiasis
Pseudomembranous patches on the vaginal mucosa, labia and perineum; Thick yellow-white cottage cheese-like discharge w/ inflammation of the vaginal mucosa, Intense pruritis
Diagnosis of Candidiasis
Wet mount -> KOH -> methylene blue stain showing budding yeast, hyphae, pseudohyphae
Treatment of Candidiasis
ketoconazole, nystatin, miconazole, gentian violet, boric acid capsule
Labs for Candidiasis
normal pH, high PMNs, KOH (-)
Refractory cases of Candidiasis
C. glabrata, Tx w/ Gentian violet
Gardnerella vaginalis characteristics
anaerobic, nonmotile, small rod w/ Gram (+) cell wall architecture, but gram variable staining; NF
Bacterial vaginosis Pathogenesis
Decreased lactobacillus -> increased pH & anaerobe growth
Anaerobes produce which enzymes
Proteolytic carboxylic enzyme -> malodours amines
Succinate -> inhibit infiltration of PMNs
Other agents causing Bacterial vaginosis
Mobiluncus: GP curved rod, motile, anaerobe, stains gram-variable
Atopobium vaginae: anaerobe
Sx of Bacterial vaginosis
Malodorous discharge (gray, off-white, thin, discharge), fishy-odor most noticeable after intercourse or during menses; no erythema, edema, itching, burning, pain, or dysuria
Diagnosis of Bacterial vaginosis
Wet mount: clue cells (>20% of VEC); KOH (+) fishy-smelling amines
Labs for Bacterial vaginosis
high pH, normal PMNs, KOH (+)
Treatment for Bacterial vaginosis
Metronidazole
Agents of Menstrual TSS
S. aureus, CoNS, Group A b-hemolytic Strep, Mycoplasma
Immune response to TSS
Neutralizing Ab
Risk factors for TSS
colonization w/ S. aureus producing TSST-1, lack of neutralizing Ab
Super absorbent tampons may favor TSS bc
Low Mg2+ (chelator), surfactants released, higher O2 tension,
Sx of Menstrual TSS
w/in 2 days of period: Fever, hypotensive shock, intense mucosal hyperemia/erythema, diarrhea, vomiting, myalgias, rash (diffuse macular) followed by desquamation 1-2wks after onset of illness
TSST-1 is acquired by
lysogenization
Treatment of Menstrual TSS
Supportive, Macrolides
TSS agents are often resistant d/t
penicillinases/beta-lactamases
Prevention of Menstrual TSS
abx prophylaxis to prevent colonization
Bacteriuria >10^5 CFU, w/o Sx, Tx
no Tx required, unless pregnant!!
Pyuria
> 10WBCs/HPF (sedimented) or 50-100WBC/mL
Agents of Acute Uncomplicated Cystitis in Females
E. coli S. saprophyticus K. pneumoniae Proteus mirabilis Enterococcus spp Mixed
Agents of Acute Uncomplicated Pyelonephritis in Females
E. coli
Proteus mirabilis
K. pneumoniae
Mixed
Agents of Complicated UTI
E. coli Enterococcus spp Pseudomonas spp S. epidermidis Mixed Proteus mirabilis K. pneumoniae Yeasts S. saprophyticus
Agents of Catheter-Associated UTI
Yeast – Candida E. coli Mixed Pseudomonas spp K. pneumoniae S. epidermidis Enterococcus spp
Tamm-Horsefall
Uromodulin; prevents attachment of uropathogens to the epithelium & prevents kidney stone formation
Immune response to UTI
PMNs, Neutralizing Abs
UTI in children < 2y/o Sx
failure to thrive, vomiting, irritability, suprapubic tenderness, fever
UTI in Elderly Sx
dehydration, vertigo, fever, loss of appetite
Acute Uncomplicated Cystitis Sx
Abrupt or insidious onset of micturition, urgency, dysuria (voiding small amts of turbid urine), hematuria, suprapubic pain/tenderness
Labs of Acute Uncomplicated Cystitis
bacteriuria, pyuria, hematuria
Acute Uncomplicated Pyelonephritis Sx
fever, chills, malaise, n/v, HA, dysuria, micturition, urgency, excruciating flank or low back pain
Nephrolithiasis – Complicated UTI Sx
Flank pain, hematuria, ammonia-smelling urine (pH 7)
Risk factors for UTI
females, BPH in males > 50, immune deficiency (IL-8R mutation, neutropenic, agammaglobulinemia), ABH non-secretors, catheters, diabetes
Labs of Acute Uncomplicated Pyelonephritis
bacteriuria, pyuria, hematuria, paralytic ileus
Agents that produce urease and cause Nephrolithiasis
Corynebacterium urealyticum, Proteus mirabilis, K. pneumoniae, S. saprophyticus
Urease role in Nephrolithiasis
cleaves urea, increasing pH, causing precipitation of struvite stones (MgNH3 + CaCO3-apatite)
Acute Prostatitis Sx
E.coli
Fever, chills, flank pain, dysuria, micturition, urgency
White Cast cells
suggestive of pyelonephritis
Diagnosis for UTI
Urine sample (bacteria, WBC, WBC, pH, NH3)
Culture: MacConkey or Blood agar
Urine Dipstick: Esterase, Nitrite
Treatment for UTI
TMP-SMX, however may be resistance
Ampicillin if resistance to beta-lactams is low
Fluoroquinolones (Cipro)
Nitrofurantoin for pregnant females
Diagnosis of Pyelonephritis
CT scan - hypodense regions; White cast cells
Normal Urine
pH ~5, mildly urea, clear/yellow