Whittum-Hudson: Sexually Transmitted Infections Flashcards
1
Q
What is the leading reported infectious disease in the US
A
Chlamydia trachomatis (Chlamydia)
2
Q
Chlamydia trachomatis (Chlamydia)
Symptomatic or asymptomatic?
F vs M:
A
Often asymptomatic
Affects more females than males
3
Q
What is an obligate intracellular bacteria?
A
Chlamydia trachomatis (Chlamydia)
4
Q
Chlamydia trachomatis (Chlamydia)
Cell wall similar to:
Is it an energy parasite?
A
Cell wall similar to Gram negative: but lacks peptidoglycan layer between membranes
Has its own ATP transporters: therefore, NOT an energy parasite (only requires host ATP during latent/persistent infection)
5
Q
Chlamydia trachomatis (Chlamydia)
Genome recently sequenced:
Disseminates from primary site of infection in what types of cells?
A
Genome recently sequenced: massive loss of genes involved in biosynthetic functions
Disseminates from primary site of infection: in mononuclear cells (ie. monocytes or dendritic cells)
6
Q
Chlamydia trachomatis (Chlamydia)
Complex life cycle with 2 morphologically distinct forms:
Which is infectious?
Which is metabolically active?
A
Elementary body: infectious
Reticulate body: non-infectious, metabolically active
7
Q
Chlamydia trachomatis (Chlamydia)
What is the reticulate body enclosed in?
What does it synthesize large amounts of?
Can stain with what?
A
Enclosed in inclusion bodies during replication in the host
Synthesize large amounts of glycogen (can therefore stain inclusion bodies with iodine)
8
Q
Chlamydia trachomatis (Chlamydia)
Inhibits what after Elementary Body (EB) entry?
When does the inclusion increase in size?
A
Inhibits endosome/lysosome fusion in host cell:
Chlamydia develops in membrane bound inclusions that increase in size during differentiation and development
9
Q
Chlamydia trachomatis (Chlamydia)
What fuse to form a single inclusion:
How many EB inside?
Exception due to mutation in what genes:
A
Multiple inclusions from more than 1 EB fuse to form a single inclusion:
Can have up to 500-1000 EB inside
Exception: mutations in lnc or other genes can result in multiple, nonfusing inclusions
10
Q
Chlamydia trachomatis (Chlamydia) What can happen under stressful conditions?
A
Can become persistent under stressful conditions
11
Q
Chlamydia trachomatis (Chlamydia)
What is persistence?
What happens to gene expression?
Reduced expression of what?
A
Persistence: organism is present and viable but non-culturable
Differential gene expression
Reduced expression of MOMP (major outer membrane protein), which is often used for clinical detection (hard to detect)
12
Q
Chlamydia trachomatis (Chlamydia)
What results in T and B cell responses that cause chronic inflammation?
Refractory to:
A
Increased production of stress response proteins (chlamydial hsp60, hsp10) and presence of LPS result in T and B cell responses that cause chronic inflammation
Refractory to antibiotic therapy!
13
Q
Chlamydia trachomatis (Chlamydia)
Persistence may be induced by:
Triggers what?
What can also induce resistance in a similar manner?
A
Persistence may be induced by IFN-gamma: inhibits chlamydial growth in cells
- Triggers depletion of tryptophan pools via activation of IDO
Penicillin can also induce resistance in a similar manner
14
Q
Chlamydia trachomatis (Chlamydia) Pathogenesis
What serotypes cause urogenital infection?
Associated with what types of infection?
What can neonates develop?
A
Serotypes D-K cause urogenital infection
Can also be associated with ocular and respiratory infections
Neonates born to infected mothers can develop conjunctivitis or pneumonia
15
Q
Chlamydia trachomatis (Chlamydia) How long do infections persist?
A
Infections can persist for long periods of time
16
Q
Chlamydia trachomatis (Chlamydia) Diseases in Men: (2)
A
Urethritis
Epipdidymitis
17
Q
Chlamydia trachomatis (Chlamydia) Diseases in Women
Conditions Caused: (4)
A
Cervicitis
Salpingitis (inflammation of Fallopian tubes)
Urethral syndrome
Chronic pelvic pain
Note: Often asymptomatic: but can produce a discharge
18
Q
Chlamydia trachomatis (Chlamydia) Diseases in Women
Ascending infections can lead to:
What results in chronic inflammation and tissue scarring (fibrosis)?
A
Ascending infections can lead to PID:
Exposure to hsp 60, hsp10, and LPS through reinfection and persistent infection results in chronic inflammation and tissue scarring (fibrosis)
19
Q
Chlamydia trachomatis (Chlamydia) Diseases in Women
What can fibrosis lead to?
What % of women with undetected infections develop PID?
A
In PID, this can lead to infertility and ectopic pregnancy
20-40% of women with undetected infections develop PID
20
Q
Chlamydia trachomatis (Chlamydia) Systemic Complications:
A
Reactive arthritis
Infertility
21
Q
Chlamydia trachomatis (Chlamydia) Lymphogranuloma Venereum (LGV)
Cause:
Local Symptoms: (3)
A
Cause: serotypes L1, L2 and L3
Local Symptoms:
- Small papule on external genitalia, anus or rectum (heals in a few days)
- Swollen, painful regional LNs
- Mucoid/purulent anal discharge
22
Q
Chlamydia trachomatis (Chlamydia) Lymphogranuloma Venereum (LGV)
Systemic Symptoms: (2)
A
- Fever, rashes, nausea
- Meningitis and arthritis also possible, but rare
23
Q
Chlamydia trachomatis (Chlamydia) Lymphogranuloma Venereum (LGV)
What can happen?
Increases risk of what?
A
Can become chronic as a serious systemic disease
Increases risk of HIV co-infection
24
Q
Chlamydia trachomatis (Chlamydia) Lymphogranuloma Venereum (LGV)
Treatment:
A
Doxycycline or erythromycin
No known treatment for systemic LGV infection
25
Chlamydia trachomatis (Chlamydia)
```
How are samples collected?
Females
Males
What is First catch urine?
For LGV:
```
Collection of epithelial cells from infected site
Cervical specimens for females
Urethral scrapings for males
First catch urine: urine first thing in the morning (will be from within infected urethra and more concentrated)
For LGV only: pus from genital lesions
26
Chlamydia trachomatis (Chlamydia)
Isolation can be done in what type of cell culture?
Cells stained with fluorescent Ab to what?
What does iodine staining detect?
When must culture confirmation be done?
Isolation can be done in epithelial or fibroblast cell culture (detect intracellular bacteria):
Cells stained with fluorescent Ab to chlamydial LPS or MOMP
Iodine staining to detect glycogen in inclusions
Culture confirmation MUST be done in cases of suspected child abuse
27
Chlamydia trachomatis (Chlamydia)
Which types of detection method are the most sensitive and routinely used now?
Direct Detection in Clinical Specimens: molecular detection methods are the most sensitive and routinely used now
28
Chlamydia trachomatis (Chlamydia)
Direct Detection in Clinical Specimens: (4)
Fluorescent Abs to MOMP or LPS
DNA or RNA hybridization and PCR
Ligase chain reaction (LCR)
*Often use multiplex reactions to detect more than 1 STD pathogen
29
```
Chlamydia trachomatis (Chlamydia)
Treatment
```
Sensitive to:
For pregnant women and infants:
What are not effective?
Sensitive to many antibiotics: typically tetracyclines (doxycycline) and erythromycin
Erythromycin for pregnant women and infants
B-lactams NOT effective (can drive infection into persistent state
30
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Chlamydia trachomatis (Chlamydia)
Treatment
```
What are more effective for intracellular chlamydial infection?
Effective in persistent infection?
Growing concerns about:
CDC recommendations:
```
New Macrolides (Azithromycin): more effective for intracellular chlamydial infection if the drugs reach the site of infection
- Unclear if they are effective in persistent infection
```
Growing concerns about resistant organisms (ie. some LGV strains)
New CDC Recommendation: essential that both partners get treated
31
Chlamydia trachomatis (Chlamydia)
Take Home Messages
Obligate intracellular bacterium
Complex biphasic life cycle (EBs and RBS) within an inclusion
Disseminates from initial mucosal infection site within mononuclear cells
Disease sequelae are due to inflammatory and immune responses to Chlamydia
No lasting protective immunity after infection
Reportable infectious disease (to CDC)
32
Neisseria gonorrhoeae (gonococcus)
M vs F:
Hosts:
Infection facilitates transmission of:
Effects men and women about equally
Humans are the only host
Infection facilitates transmission of HIV and/or C.trachomatis
33
Neisseria gonorrhoeae (gonococcus)
Motile?
G +/-?
Replicates in what types of cells/tissues
Non-motile, Gram negative, diplococci
Facultative intracellular bacterium: replicates in neutrophils, subepithelial tissues
34
Neisseria gonorrhoeae (gonococcus)
Growth Requirements:
Sensitive to:
Best agars: (2)
T and CO2:
Growth Requirements: fastidious with complex nutritional growth requirements
- Sensitive to fatty acids (inhibit growth)
- Grows best of chocolate agar or Thayer-Martin plates
- 37 degrees C, enriched CO2 environment
35
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Neisseria gonorrhoeae (gonococcus)
Virulence Factors: (6)
```
```
Pili
Opa Proteins
Lipooligosaccharide (LOS)
Outer Membrane Protein 1 (OMP1)
IgA Protease
Transferrin Receptor
```
36
Neisseria gonorrhoeae (gonococcus)
Virulence Factors
Pili
Definition:
Phase variation:
What acts as the receptor?
Pili: long, filamentous structures that are required for colonization
Phase Variation: variation between pilus + and pilus – phenotypes
Human CD 46 (membrane cofactor protein) acts as a receptor for gonococcal pili
37
Neisseria gonorrhoeae (gonococcus)
Virulence Factors
Pili
Antigenic Variation:
pilE:
pilS:
Antigenic Variation: variation in the pilus subunit expressed
pilE: encodes the pilus subunit and is the expression locus
pilS: several partial copies of the pilin gene that can recombine into the pilE locus and generate variant pili
38
Neisseria gonorrhoeae (gonococcus)
Virulence Factors
Opa Proteins
Definition:
Expression Color:
Phase Variation:
Opa Proteins: outer membrane proteins conferring an opaque appearance to the cells (OPA for opacity)
Expression: if expressed, colony will be white; if not
expressed, colony is clear
Phase Variation: variation between opa + (white colony) and opa – (clear colony)
39
Neisseria gonorrhoeae (gonococcus)
Virulence Factors
Opa Proteins
Function:
Function: involved in binding of host cells; pili anchor bacteria to host cells while the opa proteins facilitate close contact
Some may also facilitate bacterial invasion of host cells
40
Neisseria gonorrhoeae (gonococcus)
Virulence Factors
Opa Proteins
```
Encoding:
Expression is controlled by:
What type of repeat changes:
When does translation occur?
What controls the reading frame?
What can shift the ATG codon?
```
Encoding: Opa proteins encoded by several genes, but usually only a few or none are expressed
Expression controlled by translational frameshift involving CTCTT repeat changes
All 11 Opa gene loci are constitutively transcribed, but translation occurs only if the ATG start codon is in frame
Reading frame is controlled by a structural element with variable number of CTCTT repeats
Units can spontaneously be lost or added to shift the ATG codon in or out of frame
41
```
Neisseria gonorrhoeae (gonococcus)
Virulence Factors
Lipooligosaccharide (LOS)
```
Structure:
Variation Mechanism:
Causes release of what type of molecule?
Structure: Lipid A but no O antigen side chains (similar to LPS)
Variation: occurs by unknown mechanism; sialyation of LOS confers serum resistance on the bacteria, facilitating dissemination
Proinflammatory: causes release of proinflammatory molecules (ie. TNF)
42
Neisseria gonorrhoeae (gonococcus)
Virulence Factors
Outer Membrane Protein 1 (OMP1)
Use:
Major antigen used in serotyping gonococci (porin)
43
Neisseria gonorrhoeae (gonococcus)
Virulence Factors
IgA Protease
Cleaves and inactivates:
Result:
Function:
IgA Protease: cleaves and inactivates IgA1 molecules (both secretory and serum)
Result: allows adherence to mucosal surfaces even in the presence of secretory Ab
Function: thought to be involved in invasion, HOWEVER, loss of protease has no effect on infectivity of the bacteria
44
Neisseria gonorrhoeae (gonococcus)
Virulence Factors
Transferrin Receptor
Involved in:
What is the effect of Transferrin Receptor mutation?
Involved in iron acquisition; transferrin R mutants do not appear to cause infections in humans
45
Neisseria gonorrhoeae (gonococcus)
Sialyation of LOS confers:
Sialyation of LOS confers serum resistance on the bacteria which facilitates dissemination
46
Neisseria gonorrhoeae (gonococcus)
What do the bacteria adhere to? When?
What type of cell can they invade?
Adherence: bacteria adhere onto a mucosal surface following sexual contact with infected individual
- Non-sexual contact rare (children with disease usually victims of sexual abuse)
Invasion: can invade epithelial cells (but unclear if this is part of normal, uncomplicated infection)
47
Neisseria gonorrhoeae (gonococcus)
What is mucosal damage due to?
Where can it spread?
Mucosal damage: due to granulocyte response
Spread:
- Can spread to deeper structures
- Fallopian tubes and ovaries
- Prostate and epididymis
48
Disseminated gonococcal infection (uncommon)
Spread:
Can result in:
Bacteremia and hematogenous spread
Can result in arthritis, dermatitis, endocarditis
49
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Neisseria gonorrhoeae (gonococcus)
Disease in Males
```
Most common:
How many days after infection?
May have:
Urethritis most common; can also have epididymitis
Symptoms begin 2-7 days after infection
May have dysuria and purulent urethral discharge
50
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Neisseria gonorrhoeae (gonococcus)
Disease in Females
```
Most common:
Symptoms include:
Can result in:
Cervicitis is most common
Symptoms include vaginal discharge, urinary frequency, dysuria, chronic pelvic pain
Can result in infertility (~20% of the time in women with gonococcal salpingitis)
51
Neisseria gonorrhoeae (gonococcus)
When do you use Direct Gram smears?
Direct Gram smears: sensitive for symptomatic men, but not women
52
Neisseria gonorrhoeae (gonococcus)
Where is culture taken from?
Must specify:
Can identify:
What is diagnostic in men?
Culture: from urethral exudates (men) or cervical swabs (women)
Must specify suspicion of gonococci so appropriate media can be used
Can identify via Gram stain and oxidase test positive
Diplococci within PMN in urethral swabs diagnostic in men
53
Neisseria gonorrhoeae (gonococcus)
Direct Detection: (2)
What are these methods often multiplexed to detect?
Enzyme immunoassays
DNA/RNA hydbridization
These methods often multiplexed to detect Chlamydia as well
54
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Neisseria gonorrhoeae (gonococcus)
Treatment
```
What used to be the DOC:
What do many gonococci contain?
Why shouldn't it be used?
Penicillin used to be DOC (no more due to resistance)
- Many gonococci contain plasmid encoded B-lactamase
- Also should not be used since concomitant Chlamydial infections are common
55
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Neisseria gonorrhoeae (gonococcus)
Treatment
```
Current recommendation:
Dual therapy with ceftriaxone PLUS azithromycin or doxycycline
56
```
Neisseria gonorrhoeae (gonococcus)
Take Home Messages:
```
Gram negative diplococcic inside PMN are diagnostic
Multiple virulence factors contribute to pathogenesis (Pilin, Opa, LOS, IgA protease, transferrin receptor)
Antibodies helpful to control pathogenesis (bactericidal vs. opsonin)
Granulocyte response believed to contribute to mucosal tissue damage and scarring
Assume a chlamydial co-infection
No lasting protective immunity after infection
57
Treponema pallidum (Syphilis)
M vs F:
More men affected than women
58
Treponema pallidum (Syphilis)
Type of pathogen:
G+/-?
Shape:
Obligate human pathogen: therefore, no animal models so difficult to study
Gram negative spirochete: helical in shape
59
Treponema pallidum (Syphilis)
```
Sheath:
Motile?
What does it require to be seen?
Staining and culturing:
Metabolism:
```
Has an outer sheath or a glycosaminoglycan coating
Very motile (corkscrew motion)
Requires darkfield microscopy to be seen
Does not stain by routine methods
Difficult to culture
Little known about metabolism
60
Treponema pallidum (Syphilis)
Genome recently sequenced:
Metabolism:
Enzymes encoded for the building of complex molecules:
How much encodes transport proteins?
- Metabolically crippled organism
- Very few enzymes encoded for the building of complex molecules (ie. even nucleic acids)
- ~5% of genes encode for transport proteins
61
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Treponema pallidum (Syphilis)
Stability:
```
Highly unstable:
- Rapid death in environment
- High sensitivity to microbials (single dose penicillin)
62
Treponema pallidum (Syphilis)
Acquisition:
Placenta:
What are co-factors for the transmission of HIV?
Direct sexual contact with an individual with an active primary or secondary syphilitic lesion
Transplacental transmission can also occur
Chancres are co-factors for the transmission of HIV: genital ulcers caused by syphilis
63
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Treponema pallidum (Syphilis)
Virulence Factors
```
What is Hyaluronidase?
Outer membrane aids in:
Inhibits:
What do Tpr do?
Very simple organism: little is known due to difficulty in culturing and no animal models
Hyaluronidase: produced by pathogenic species (enhance invasion?)
Outer membrane: has few integral proteins
- Aids in evading host humoral responses
- Inhibits complement mediated killing
Tpr (T.pallidum repeat genes): may facilitate invasion
64
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Treponema pallidum (Syphilis)
Pathogenesis
```
Where is there disease?
What happens after organism invades?
When does organism spread to perivascular lymphatics and systemic circulation?
Disease of blood vessels and perivascular area
Organism rapidly multiplies and disseminates after invasion of mucous membranes or abrasions
Spread to perivascular lymphatics and systemic circulation occurs BEFORE development of primary lesion
65
Primary Syphilis
When does chancre develop? Where?
Usually located:
What are lesions filled with?
What happens after 4-6 weeks?
Chancre develops within 3-4 weeks at site of contact (round, hard, reddish and painless)
Usually located on the penis, external genitalia, anal area or lips (females can also have them on the cervix or vaginal walls)
- Primary lesions filled with bacteria
- Spontaneously heals after 4-6 weeks
66
Secondary Syphilis
When does it develop?
What symptoms develop?
What are lesions filled with?
What happens in 1/3 of the cases?
Can develop 2-10 weeks after primary lesion has healed
Fever, sore throat, rash or skin lesions (most often on palms, soles and face)
Skin lesions filled with bacteria
1/3 of untreated cases resolved by immune response; the rest go on to latent state
67
Latent Syphilis
Signs and symptoms:
What prevents progression to tertiary syphilis?
What % progress if untreated?
Symptoms in primary and secondary in respect to tertiary:
No signs or symptoms but seroreactive
Antimicrobial therapy to prevent progression to tertiary syphilis (~40% will progress to this if untreated in anywhere from 5-20 years)
Patient can be asymptomatic for primary and secondary stages, but still develop tertiary disease
68
Tertiary Syphilis
What does host immune response cause?
What can also cause this?
Rare to find:
Non-progressive granulomatous lesions of the skin, bone and joints (gummas) that are primarily due to the host immune response
These can also be cause by other spirochetes
Rare to find organism present in tertiary lesions
69
Tertiary Syphilis
Neurosyphilis
Manifestations: (5)
Neurosyphilis: many different manifestations
```
Paralytic dementia
Tabes dorsalis (odd gait)
Optic atrophy
Seizures
NF tangles post mortem (similar to AD)
```
70
Tertiary Syphilis
Cardiovascular syphilis
Involves what?
Cardiovascular syphilis: commonly involves aortic aneurysm
71
Congenital Syphilis
What indicates that infant is infected?
When is the fetus susceptible?
Anti-treponemal IgM: indicates infant is infected since maternal IgM does not cross placenta
Susceptibility: fetus susceptible at ANY time during gestation; mothers can transmit during any clinical stage of disease
72
Congenital Syphilis
Result:
Eventually develops:
What happens 25% of the time?
Treatment:
Result: can cause prematurity and low birth weight
- Often asymptomatic at birth
Eventually develop rhinitis, pneumonia and failure to thrive
Severe form of syphilis results that can be fatal (~25% of the time)
Treatment: of mother during pregnancy prevents spread and prevents late stage syphilis
73
Congenital syphilis definition
Congenital syphilis is syphilis present in utero and at birth, and occurs when a child is born to a mother with secondary syphilis.
74
Syphilis
| Diagnosis: (3)
Darkfield Microscopy: of fluid from primary or secondary lesions
Serological Tests:
Genetic probes
75
Syphilis
Darkfield Microscopy of fluid from what type of lesion?
Genetic probes availability:
Darkfield Microscopy: of fluid from primary or secondary lesions
Genetic probes: now available since genome has been sequenced
76
Syphilis
Serological Tests
What is non-specific and therefore indicates treatment?
What do titers reflect?
Depend on:
Positive during which stages?
False positives:
Non-treponemal cardiolipin Ag (VDRL and RPR): VDRL is non-specific and therefore a reduction in this indicates successful treatment
Titers reflect disease activity: depends on immune flocculation in the presence of lecithin and cholesterol; positive during primary and secondary stages
Many false positives: must confirm with treponemal tests
77
Syphilis
Serological Tests
What tests Ab to T.pallidum directly?
FTA-ABS:
NERA-TP:
Treponemal tests: direct detection of Ab to T.pallidum (levels unaffected by treatment)
FTA-ABS: fluorescent Ab absorption test (Ab present for life so cannot be used to follow treatment response)
NERA-TP: microhemagglutination test
78
Syphilis
Treatment:
DOC:
What is used recently?
Antibiotics: penicillin is very effective and DOC
Azithromycin has been used recently as a 4 treatment regimen
However, new isolates have been found to be resistant to azithromycin (if non-responsive, must return to penicillin or other therapy)
79
Syphilis
| Take Home Messages:
o Motile spirochete
o Darkfield microscopy of wet mounts used for diagnosis but fluorescent Ab more common (PCR coming)
o Few outer membrane proteins
o Virulence factors not well understood (hyaluronidase aids in penetration)
o Complex and lengthy course of disease (includes a variable latent phase)
o Cardiolipin based tests (VDRL and RPR) reflect infection and cure; FTA-Abs reflect infection but persist for life regardless of cure
o Primary and secondary stages highly infectious
o Congenital infection can occur at any stage of pregnancy (fetal anti-treponemal IgM diagnostic)
o Easy to cure with penicillin during primary and secondary stages
80
What causes chancroid?
Hemophilus ducreyi
81
Hemophilus ducreyi (Chancroid)
G+/-?
Hosts:
Pathogenesis:
Infects what type of skin?
Increases susceptibility to:
Fastidious Gram negative rod
o Strict human pathogen
Pathogenesis:
Painful genital ulcers with ragged edges appear 2-14 days after infection
Infects abraded non-genital skin, mucosal surfaces and stratified squamous epithelium
Increases susceptibility to HIV: possibly because CD4 T cells are found in chancroid lesions
82
Hemophilus ducreyi (Chancroid)
Diagnosis:
Diagnosis:
o Antibody base
o DNA probes or multiplex PCR best for sensitivity and specificity
83
Hemophilus ducreyi (Chancroid)
Treatment:
Antibiotics: azithromycin, ceftriaxone, erythromycin of ciprofloxacin
HIV co-infection: may alter response to treatment
84
Candida albicans
Normal flora of:
Forms in most conditions:
What forms are produced during tissue invasion?
Normal flora: of alimentary tract and mucocutaneous sites (mouth, vagina)
Multiple forms: grows as a yeast under most conditions, but can for pseudohypae
Hyphal forms produced during tissue invasion
Note: Not really classified as an STD pathogen!
85
Candida albicans
| Virulence Factors: (5)
Adhesins
Morphogenesis
Tissue invasion (proteases and phospholipases)
Biofilm formation
SAPs (proteinases only found in pathogenic yeast)
86
Candida albicans
Adhesins
Can bind to:
Adhesins
- Can bind structures found in human tissues (fibronectin, collagen, laminin)
- Adhere to vaginal epithelial cells
87
Candida albicans
Morphogenesis
Phenotype switching between:
Induced by:
Morphogenesis (phenotype switching between yeast and hyphae)
| - Induced by environmental/nutritional stimuli in vitro (not sure what signal is in vivo)
88
Candida albicans
| Tissue invasion is produced by what form?
```
Tissue invasion (proteases and phospholipases)
- Produced by hyphal form
```
89
Candida albicans
SAPs
Regulated by:
Determines level of:
Regulates:
SAPs (proteinases only found in pathogenic yeast)
- pH regulated activity
- Determines level of tissue invasion
- Regulates other virulence factors
90
Candida albicans
Cause:
Can be caused by:
Most often caused by:
Effect of immunodeficiency:
Cause most vulvovaginal yeast infections
Can be caused by sexual contact (direct mucosal contact with lesions)
However, most often caused by endogenous flora in women
Immunodeficiency: can result in progressive infection
91
Candida albicans
Predisposing Factors: (4)
Pregnancy
Diabetes
Oral contraceptives or hormones
Antibacterial antibiotics
92
Candida albicans
Infection requires:
Increase in local numbers of candida
Compromised integrity of epidermal or epithelial surface
93
Candida albicans
Normal immune response:
Can produce:
Possible susceptibility due to:
Normal immune response: phagocytosis by macrophages (bind mannan in cell wall)
Can produce recurrent infections (RCVC): even in apparently healthy women
- Possible susceptibility: due to defective macrophage function
94
Candida albicans
Diagnosis
White-gray pseudomembranes on the vaginal mucosa
Yellow-white discharge
Hyphal forms seen in skin scrapings and vaginal exudate
95
Candida albicans
| Treatment:
Topical Nystatin or miconazole
96
Candida albicans
| Take Home Messages:
```
o Fungus that is not a true STI
o Two growth forms: yeast and hyphal
o Normal inhabitant of mucosal tissues
o Overgrowth and biofilm can lead to symptoms and pathology (chronic vaginitis)
o Topical treatment
```
97
Trichomonas vaginalis
Motile?
Viability:
How long can it survive outside human host?
Highly motile flagellated protozoa
Viability: no cyst form, but
Can survive outside human host for 1-2 hours on moist surfaces
98
Trichomonas vaginalis
Can be grown:
How long can it survive in fluids?
Location:
Can be grown on artificial medium
Can survive for 24 hours in urine, semen and in water
Location: inhabits vagina (women) and urethra/prostate
99
Trichomonas vaginalis
Transmission:
What causes destruction of cells and PMN inflammatory response?
Transmission: mostly venereal, although nonvenereal can occur (rare)
Direct contact with squamous epithelium causes destruction of cells and PMN inflammatory response
100
Trichomonas vaginalis
| Surface structures:
Coated with host-derived macromolecules (α1 anti-trypsin, α2-macroglobulin, fibronectin, lipids)
101
Trichomonas vaginalis
| Phagocytosis:
Phagocytosis: capable of phagocytosing bacteria, viruses, RBC and PMN
102
Trichomonas vaginalis
Symptoms
Men:
Women:
Men: generally asymptomatic
Women: if symptomatic, exhibit dysuria, vaginal itching and burning; severe infections produce a foamy, malodorous yellow-green discharge
103
Trichomonas vaginalis
Persistence:
Ingests what in vaginal flora?
Persistence: organism can persist for up to 90 days; manifestations often worsen during menses and pregnancy
Upsets vaginal flora: ingests lactobacillus
104
Trichomonas vaginalis
| Diagnosis:
Microscopic examination of wet mount preparations from vaginal discharge or urethral exudates
Culture of urogenital specimens can increase number of detected cases
105
Trichomonas vaginalis
| Treatment:
Oral metronidazole (Flagyl)
Should not be used during pregnancy
Simultaneous treatment of sexual partners is also desirable
106
Trichomonas vaginalis
| Take Home Messages:
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o Motile, flagellated protozoan
o Most common STI worldwide
o Induces a PMN response
o Metronidazole standard treatment
o Foamy, malodorous yellow-green discharge
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SOCIAL DISPARITIES
| Just read over once
• CDC Division of STD Prevention Addresses:
- Personal barriers (language and low literacy levels)
- Concerns regarding confidentiality, discrimination and stigma
- Cultural differences (reluctance to seek care)
- Disease inducing behaviors:
o High risk sexual practices (heterosexual and MSM)
o High rates of unprotected sex
- Important social determinants in syphilis elimination campaign:
o Psychosocial risk factors
o Substance abuse and extreme alcohol use
o Mental stress associated with being a marginalized population
o Social discrimination related to racism, classism or homophobia
o Social isolation related to shame
o Public perceptions of decrease risk for STDs due to the availability of HIV treatment
o “Safer sex fatigue” related to HIV and other STDs
