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Micro Exam 2 > Whittum-Hudson: Sexually Transmitted Infections > Flashcards

Whittum-Hudson: Sexually Transmitted Infections Flashcards

1
Q

What is the leading reported infectious disease in the US

A

Chlamydia trachomatis (Chlamydia)

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2
Q

Chlamydia trachomatis (Chlamydia)

Symptomatic or asymptomatic?
F vs M:

A

Often asymptomatic

Affects more females than males

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3
Q

What is an obligate intracellular bacteria?

A

Chlamydia trachomatis (Chlamydia)

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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)

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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)

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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

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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)

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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

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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

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10
Q 
Chlamydia trachomatis (Chlamydia)
What can happen under stressful conditions?
A

Can become persistent under stressful conditions

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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)

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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!

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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

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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

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15
Q 
Chlamydia trachomatis (Chlamydia)
How long do infections persist?
A

Infections can persist for long periods of time

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16
Q 
Chlamydia trachomatis (Chlamydia)
Diseases in Men: (2)
A

Urethritis

Epipdidymitis

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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

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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)

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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

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20
Q 
Chlamydia trachomatis (Chlamydia)
Systemic Complications:
A

Reactive arthritis

Infertility

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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
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22
Q 
Chlamydia trachomatis (Chlamydia)
Lymphogranuloma Venereum (LGV)

Systemic Symptoms: (2)

A
  • Fever, rashes, nausea

- Meningitis and arthritis also possible, but rare

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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

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24
Q 
Chlamydia trachomatis (Chlamydia)
Lymphogranuloma Venereum (LGV)

Treatment:

A

Doxycycline or erythromycin

No known treatment for systemic LGV infection

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25
Q

Chlamydia trachomatis (Chlamydia)

How are samples collected?
Females
Males
What is First catch urine?
For LGV:
A

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

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26
Q

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?

A

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

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27
Q

Chlamydia trachomatis (Chlamydia)

Which types of detection method are the most sensitive and routinely used now?

A

Direct Detection in Clinical Specimens: molecular detection methods are the most sensitive and routinely used now

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28
Q

Chlamydia trachomatis (Chlamydia)

Direct Detection in Clinical Specimens: (4)

A

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

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29
Q 
Chlamydia trachomatis (Chlamydia)
Treatment

Sensitive to:
For pregnant women and infants:
What are not effective?

A

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

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30
Q 
Chlamydia trachomatis (Chlamydia)
Treatment

What are more effective for intracellular chlamydial infection?

Effective in persistent infection?

Growing concerns about:

CDC recommendations:

A 
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

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31
Q

Chlamydia trachomatis (Chlamydia)

Take Home Messages

A

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)

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32
Q

Neisseria gonorrhoeae (gonococcus)

M vs F:
Hosts:
Infection facilitates transmission of:

A

Effects men and women about equally

Humans are the only host

Infection facilitates transmission of HIV and/or C.trachomatis

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33
Q

Neisseria gonorrhoeae (gonococcus)

Motile?
G +/-?
Replicates in what types of cells/tissues

A

Non-motile, Gram negative, diplococci

Facultative intracellular bacterium: replicates in neutrophils, subepithelial tissues

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34
Q

Neisseria gonorrhoeae (gonococcus)

Growth Requirements:
Sensitive to:
Best agars: (2)
T and CO2:

A

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
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35
Q 
Neisseria gonorrhoeae (gonococcus)
Virulence Factors: (6)
A 
Pili
Opa Proteins
Lipooligosaccharide (LOS)
Outer Membrane Protein 1 (OMP1)
IgA Protease
Transferrin Receptor
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36
Q

Neisseria gonorrhoeae (gonococcus)
Virulence Factors
Pili

Definition:
Phase variation:
What acts as the receptor?

A

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

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37
Q

Neisseria gonorrhoeae (gonococcus)
Virulence Factors
Pili

Antigenic Variation:
pilE:
pilS:

A

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

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38
Q

Neisseria gonorrhoeae (gonococcus)
Virulence Factors
Opa Proteins

Definition:
Expression Color:
Phase Variation:

A

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)

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39
Q

Neisseria gonorrhoeae (gonococcus)
Virulence Factors
Opa Proteins

Function:

A

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

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40
Q

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?
A

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

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41
Q 
Neisseria gonorrhoeae (gonococcus)
Virulence Factors
Lipooligosaccharide (LOS)

Structure:
Variation Mechanism:
Causes release of what type of molecule?

A

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)

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42
Q

Neisseria gonorrhoeae (gonococcus)
Virulence Factors
Outer Membrane Protein 1 (OMP1)

Use:

A

Major antigen used in serotyping gonococci (porin)

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43
Q

Neisseria gonorrhoeae (gonococcus)
Virulence Factors
IgA Protease

Cleaves and inactivates:
Result:
Function:

A

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
Q

Neisseria gonorrhoeae (gonococcus)
Virulence Factors
Transferrin Receptor

Involved in:
What is the effect of Transferrin Receptor mutation?

A

Involved in iron acquisition; transferrin R mutants do not appear to cause infections in humans

45
Q

Neisseria gonorrhoeae (gonococcus)

Sialyation of LOS confers:

A

Sialyation of LOS confers serum resistance on the bacteria which facilitates dissemination

46
Q

Neisseria gonorrhoeae (gonococcus)

What do the bacteria adhere to? When?
What type of cell can they invade?

A

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
Q

Neisseria gonorrhoeae (gonococcus)

What is mucosal damage due to?
Where can it spread?

A

Mucosal damage: due to granulocyte response

Spread:

  • Can spread to deeper structures
  • Fallopian tubes and ovaries
  • Prostate and epididymis
48
Q

Disseminated gonococcal infection (uncommon)

Spread:
Can result in:

A

Bacteremia and hematogenous spread

Can result in arthritis, dermatitis, endocarditis

49
Q 
Neisseria gonorrhoeae (gonococcus)
Disease in Males

Most common:
How many days after infection?
May have:

A

Urethritis most common; can also have epididymitis

Symptoms begin 2-7 days after infection

May have dysuria and purulent urethral discharge

50
Q 
Neisseria gonorrhoeae (gonococcus)
Disease in Females

Most common:
Symptoms include:
Can result in:

A

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
Q

Neisseria gonorrhoeae (gonococcus)

When do you use Direct Gram smears?

A

Direct Gram smears: sensitive for symptomatic men, but not women

52
Q

Neisseria gonorrhoeae (gonococcus)

Where is culture taken from?
Must specify:
Can identify:
What is diagnostic in men?

A

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
Q

Neisseria gonorrhoeae (gonococcus)

Direct Detection: (2)
What are these methods often multiplexed to detect?

A

Enzyme immunoassays
DNA/RNA hydbridization

These methods often multiplexed to detect Chlamydia as well

54
Q 
Neisseria gonorrhoeae (gonococcus)
Treatment

What used to be the DOC:
What do many gonococci contain?
Why shouldn’t it be used?

A

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
Q 
Neisseria gonorrhoeae (gonococcus)
Treatment

Current recommendation:

A

Dual therapy with ceftriaxone PLUS azithromycin or doxycycline

56
Q 
Neisseria gonorrhoeae (gonococcus)
Take Home Messages:
A

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
Q

Treponema pallidum (Syphilis)

M vs F:

A

More men affected than women

58
Q

Treponema pallidum (Syphilis)

Type of pathogen:
G+/-?
Shape:

A

Obligate human pathogen: therefore, no animal models so difficult to study

Gram negative spirochete: helical in shape

59
Q

Treponema pallidum (Syphilis)

Sheath:
Motile?
What does it require to be seen?
Staining and culturing:
Metabolism:
A

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
Q

Treponema pallidum (Syphilis)

Genome recently sequenced:
Metabolism:
Enzymes encoded for the building of complex molecules:
How much encodes transport proteins?

A
  • 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
Q 
Treponema pallidum (Syphilis)
Stability:
A

Highly unstable:

  • Rapid death in environment
  • High sensitivity to microbials (single dose penicillin)
62
Q

Treponema pallidum (Syphilis)

Acquisition:
Placenta:
What are co-factors for the transmission of HIV?

A

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
Q 
Treponema pallidum (Syphilis)
Virulence Factors

What is Hyaluronidase?

Outer membrane aids in:
Inhibits:

What do Tpr do?

A

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
Q 
Treponema pallidum (Syphilis)
Pathogenesis

Where is there disease?
What happens after organism invades?
When does organism spread to perivascular lymphatics and systemic circulation?

A

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
Q

Primary Syphilis

When does chancre develop? Where?
Usually located:
What are lesions filled with?
What happens after 4-6 weeks?

A

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
Q

Secondary Syphilis

When does it develop?
What symptoms develop?
What are lesions filled with?
What happens in 1/3 of the cases?

A

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
Q

Latent Syphilis

Signs and symptoms:
What prevents progression to tertiary syphilis?
What % progress if untreated?
Symptoms in primary and secondary in respect to tertiary:

A

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
Q

Tertiary Syphilis

What does host immune response cause?
What can also cause this?
Rare to find:

A

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
Q

Tertiary Syphilis
Neurosyphilis

Manifestations: (5)

A

Neurosyphilis: many different manifestations

Paralytic dementia 
Tabes dorsalis (odd gait)
Optic atrophy
Seizures
NF tangles post mortem (similar to AD)
70
Q

Tertiary Syphilis
Cardiovascular syphilis

Involves what?

A

Cardiovascular syphilis: commonly involves aortic aneurysm

71
Q

Congenital Syphilis

What indicates that infant is infected?
When is the fetus susceptible?

A

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
Q

Congenital Syphilis

Result:
Eventually develops:
What happens 25% of the time?
Treatment:

A

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
Q

Congenital syphilis definition

A

Congenital syphilis is syphilis present in utero and at birth, and occurs when a child is born to a mother with secondary syphilis.

74
Q

Syphilis

Diagnosis: (3)

A

Darkfield Microscopy: of fluid from primary or secondary lesions

Serological Tests:

Genetic probes

75
Q

Syphilis

Darkfield Microscopy of fluid from what type of lesion?

Genetic probes availability:

A

Darkfield Microscopy: of fluid from primary or secondary lesions

Genetic probes: now available since genome has been sequenced

76
Q

Syphilis
Serological Tests

What is non-specific and therefore indicates treatment?

What do titers reflect?
Depend on:
Positive during which stages?
False positives:

A

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
Q

Syphilis
Serological Tests

What tests Ab to T.pallidum directly?
FTA-ABS:
NERA-TP:

A

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
Q

Syphilis

Treatment:
DOC:
What is used recently?

A

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
Q

Syphilis

Take Home Messages:

A

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
Q

What causes chancroid?

A

Hemophilus ducreyi

81
Q

Hemophilus ducreyi (Chancroid)

G+/-?
Hosts:

Pathogenesis:
Infects what type of skin?
Increases susceptibility to:

A

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
Q

Hemophilus ducreyi (Chancroid)

Diagnosis:

A

Diagnosis:
o Antibody base
o DNA probes or multiplex PCR best for sensitivity and specificity

83
Q

Hemophilus ducreyi (Chancroid)

Treatment:

A

Antibiotics: azithromycin, ceftriaxone, erythromycin of ciprofloxacin

HIV co-infection: may alter response to treatment

84
Q

Candida albicans

Normal flora of:
Forms in most conditions:
What forms are produced during tissue invasion?

A

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
Q

Candida albicans

Virulence Factors: (5)

A

Adhesins
Morphogenesis
Tissue invasion (proteases and phospholipases)
Biofilm formation
SAPs (proteinases only found in pathogenic yeast)

86
Q

Candida albicans
Adhesins

Can bind to:

A

Adhesins

  • Can bind structures found in human tissues (fibronectin, collagen, laminin)
  • Adhere to vaginal epithelial cells
87
Q

Candida albicans
Morphogenesis

Phenotype switching between:
Induced by:

A

Morphogenesis (phenotype switching between yeast and hyphae)

- Induced by environmental/nutritional stimuli in vitro (not sure what signal is in vivo)

88
Q

Candida albicans

Tissue invasion is produced by what form?

A 
Tissue invasion (proteases and phospholipases)
-	Produced by hyphal form
89
Q

Candida albicans
SAPs

Regulated by:
Determines level of:
Regulates:

A

SAPs (proteinases only found in pathogenic yeast)

  • pH regulated activity
  • Determines level of tissue invasion
  • Regulates other virulence factors
90
Q

Candida albicans

Cause:
Can be caused by:
Most often caused by:
Effect of immunodeficiency:

A

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
Q

Candida albicans

Predisposing Factors: (4)

A

Pregnancy

Diabetes

Oral contraceptives or hormones

Antibacterial antibiotics

92
Q

Candida albicans

Infection requires:

A

Increase in local numbers of candida

Compromised integrity of epidermal or epithelial surface

93
Q

Candida albicans

Normal immune response:
Can produce:
Possible susceptibility due to:

A

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
Q

Candida albicans

Diagnosis

A

White-gray pseudomembranes on the vaginal mucosa

Yellow-white discharge

Hyphal forms seen in skin scrapings and vaginal exudate

95
Q

Candida albicans

Treatment:

A

Topical Nystatin or miconazole

96
Q

Candida albicans

Take Home Messages:

A 
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
Q

Trichomonas vaginalis

Motile?
Viability:
How long can it survive outside human host?

A

Highly motile flagellated protozoa

Viability: no cyst form, but

Can survive outside human host for 1-2 hours on moist surfaces

98
Q

Trichomonas vaginalis

Can be grown:
How long can it survive in fluids?
Location:

A

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
Q

Trichomonas vaginalis

Transmission:
What causes destruction of cells and PMN inflammatory response?

A

Transmission: mostly venereal, although nonvenereal can occur (rare)

Direct contact with squamous epithelium causes destruction of cells and PMN inflammatory response

100
Q

Trichomonas vaginalis

Surface structures:

A

Coated with host-derived macromolecules (α1 anti-trypsin, α2-macroglobulin, fibronectin, lipids)

101
Q

Trichomonas vaginalis

Phagocytosis:

A

Phagocytosis: capable of phagocytosing bacteria, viruses, RBC and PMN

102
Q

Trichomonas vaginalis
Symptoms

Men:
Women:

A

Men: generally asymptomatic

Women: if symptomatic, exhibit dysuria, vaginal itching and burning; severe infections produce a foamy, malodorous yellow-green discharge

103
Q

Trichomonas vaginalis

Persistence:
Ingests what in vaginal flora?

A

Persistence: organism can persist for up to 90 days; manifestations often worsen during menses and pregnancy

Upsets vaginal flora: ingests lactobacillus

104
Q

Trichomonas vaginalis

Diagnosis:

A

Microscopic examination of wet mount preparations from vaginal discharge or urethral exudates

Culture of urogenital specimens can increase number of detected cases

105
Q

Trichomonas vaginalis

Treatment:

A

Oral metronidazole (Flagyl)

Should not be used during pregnancy

Simultaneous treatment of sexual partners is also desirable

106
Q

Trichomonas vaginalis

Take Home Messages:

A 
o	Motile, flagellated protozoan
o	Most common STI worldwide
o	Induces a PMN response 
o	Metronidazole standard treatment
o	Foamy, malodorous yellow-green discharge
107
Q

SOCIAL DISPARITIES

Just read over once

A

• 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

Micro Exam 2 (18 decks)

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