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35 Cards in this Set

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Syphilis serology
1. Screening: non-specific non-treponemal test (antibody to host cardiolipin): RPR, VDRL; sensitive but not totally specific
2. Confirmatory test: TPHA, TPPA; treponemal test (antibody to protein antigens)

Or...

1. Tp
2. Confirmatory test with RPR, VDRL
Cannot culture...
Syphilis
Do not readily form antibodies
Chlamydia
Gonorrhea

Cannot diagnose with serology
Demographics of syphilis
Peak is higher (in age) and broader for men
Trend for women looks like other STIs: peak is low and narrow
Majority of cases in US are MSM
Syphilis and HIV
Synergism
Genital ulcers caused by syphilis increase susceptibility to HIV infection
HIV+ individuals have higher viral load if infected with syphilis
If HIV+, greater risk of developing neurosyphilis
Stages of syphilis
1. Exposure (few weeks)
2. Primary infection: painless chancre on anogenital skin and/or mucus membranes; oral
3. Asymptomatic
4. Secondary: spread of spirochetes through blood; malaise, myalgia, fever, lymphadenopathy, headache, sore throat, hepatitis, hair loss, RASH, CONDYLOMA LATA
5. Latent syphilis (early and late)
6. Tertiary: breakdown of latent control: gummatous lesions, cardiovascular and neuro symptoms
Congenital syphilis
50% of pregnancies in infected women end in miscarriage
40-70% of infants born to infected mothers have congenital syphilis
Bone, eye, ear, brain damage
Moon shaped incisors: Hutchinson's incisors
Treponema pallidum: bacterial features
Spirochete
Very thin- does not gram stain
Has an inner and outer membrane
Outer membrane has NO LPS
Lipoproteins on surface (very few)
Flagella wraps around the organism in the periplasmic space for motility
Cannot be cultured; grown in rabbit testes for research
T. pallidum pathogenesis
"Attachment, invasion, dissemination"
Corkscrew motility and proteins that bind ECM proteins -- allow access to spaces between cells
Non-specific for particular cell type
Syphilis immune response
Innate: no TLR4 activation because no LPS; TLR2 instead: release of TNF and pro-inflammatory cytokines and chemokines cause ulcerations

Cellular: T infiltrates: CD4, CD8; INFgamma

Activated macrophages can clear infection

Humoral: Abs to protein antigens and cardiolipin; antibody activity is not protective

Some ability to form memory response; partial
Primary ulcers of syphilis clinically indistinguishable from...
Chancroid caused by H. ducreyi
Syphilis treatment
Penicillin - still effective

Azithromycin can be used but resistance is increasing
Prevalence of trich and age
Prevalence of trichomonas vaginalis increases with age

Contrast with chlamydia that decreases with age
Trich and HIV
Synergy
Higher HIV viral load in HIV+
Recruitment of HIV-susceptible cells to infected mucosa
TREATMENT of trich decreases HIV viral load in vaginal fluid
Clinical presentations of trichomoniasis: women
Vagina, urethra, endocervix susceptible
Frothy discharge
Strawberry cervix: punctate hemorrhages caused by inflammation on ectocervix; highly specific
Itching, odor, dysuria
Lower abdominal pain
Elevated vaginal pH, amines
Can be asymptomatic
Clinical presentation: trichomoniasis in men
Non-gonococcal, non-chlamydial urethritis
Urethral discharge: watery; not highly inflammatory
Dysuria
Lower abdominal pain
Commonly asymptomatic
Characteristics: T. vaginalis
Protozoan pathogen- related to giardia
Free-swimming: roughly size of WBC
Attached to epithelial cells: transforms into ameboid shape
4 flagella on top - motility
Lacks mitochondira; uses hydrogenosome for energy metabolism
Immune response: trichomoniasis
Inflammation, influx of PMNs
IL-8 --> TLR4 --> TNFalpha
Antibodies; not protective
Diagnostic: trichomoniasis
Wet mount, culture, antigen-detection, NAAT
Wet mount: vaginal swab or male urine sediment
Org must be motile and viable
Must be performed <15 min after collection
Diagnostic but not very sensitive
Treatment: trichomoniasis
Metranidazole: anti-protozoa, anti-amoeba, anti-anaerobic bacteria
Drugs are activated within hydrogenosomes
Generate toxic nitro radicals and damage parasite DNA proteins
Resistance infrequent but increasing
Neisseria gonorrhea: bacteria features
Gram negative diplococcus
Round with two halves like a kidney bean
Ability to transform: take up naked DNA
NO CAPSULE (N. meningititis does)
Pili - long range attachment
Opacity proteins - sponsor tight adherence
Porins - nutrient uptake (and identifying serotypes)
LOS (lipid A)
Gonorrhea pathogenesis
"Attachment, Antigenic variation, Antibiotic resistance"
Use of pili, opacity proteins, porins, LOS
Ability to transform: antigenic variation
Treatment: gonorrhea
Highly resistant to antibiotics
Penicillin, tetracyclines, fluoroquinolones no longer effective
Treat with ceph triaxone
Uncomplicated gonorrheal infection (UGI)
Anterior urethral (men)- urethritis
Cervical and urethral (women)- cervicitis
Pharyngeal
Rectal (usually MSM)
Differential: gonorrhea
Women/pharyngeal/rectal: typically asymptomatic; difficult to distinguish from other STIs

Urethritis (men): usually symptomatic; abrupt onset, dysuria, profuse, purulent discharge (the drop, the clap)

Cervicitis: analagous to urethritis in men: purulent discharge from os (neutrophils)

Gonococcal conjunctivitis: in newborns delivered vaginally in infected mothers
Prophylaxis is silver nitrate, antibiotic ointment
Complicated gonococcal infection
PID: tends to happen after symptomatic infection
Occurs within few days of menses: extra iron as nutritional factor for organism
Cervical mucus aids in ascension of bacteria into URT

Salpingitis; adhesions; swelling; tubal pregnancy

DGI: disseminated; invasion of the blood stream --> skin and large joints
Chlamydia species
Human pathogens:
Trachomatis (sexually transmitted)
Pneumoniae: respiratory, most common
Psittaci: zoonotic
Chlamydia epidemiology
Infections climbing
Women more likely to be infected than men
Chlamydia trachomatis disease
Ocular, genital, LGV strains
Ocular: trachoma; eyelashes curl in; blindness can occur
LGV: lymphogranuloma venereum: invasive lymphoid disease; looks like genital warts; misshapen skin tags
Genital:
Men: non-gonococcal urethritis (less common, less purulent); epididymitis, rectal
Women: cervicitis with copious clear, watery, less purulent discharge; urethritis; PID
PID and GC and Chlamydia
PID more severe in chlamydia
Local inflammation more severe in gonorrhea
Chlamydia trachomatis: life cycle
Elementary bodies extracellularly: infectious but not metabolically active
Attachment of EB at clathrin coated pits --> internalized
Conversion to reticulate body (RB) intracellular form: metabolically active but not infectious
Forms inclusions like cloaks that recruits host cell mitochondria for energy
Modifies inclusion membrane by inserting proteins with T3SS --> causes inflammation
RBs begin to transform back to EBs in preporation for lysis
Lyse apically or basolaterally
Chlamydia: bacteria features
Gram negative
LPS on outer leaflet
MOMP proteins: porins that designate serovar
Chlamydia pathogenesis
Infected cells produce pro-inflammatory cytokines and chemokines
PMNs, NK cells activate APCs, phagocytes
Chronic inflammation --> necrosis, cell proliferation, scarring
Diagnosis: GC and chlamydia
NAAT is gold standard- sensitive and specific
Becomes negative 10-14 days after successful treatment
Non-invasive specimens possible
Treatment: chlamydia
Azithromycin