Microbiology of the Vagina and Penis - Skildum Flashcards

1
Q

What does the normal microbial communities of the vagina consist of?

A

In ~80% of healthy women, lactobacilli are the dominant microorganisms.

Lactobacilli are gram positive rods/bacilli, facultative anaerobes

*Lactobacilli iners, *L. gasseri, L. cripsatus and L. jensenii are the most common.

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2
Q

What are the three products of Lactobacilli that help maintain the microbiota of the vagina?

A
  1. Lactic acid: through anaerobic fermentation, decreases pH (lactic acid makes environment more hostile to other pathogens, lactate is substrate for immune system)
  2. Hydrogen peroxide; hydroxyl radicals (makes hostile environment)
  3. Bacteriocins proteins that depolarize pathogenic bacteria => kill bacteria
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3
Q

What does the vaginal microbial community depend on for maintaining healthy colonies of Lactobacilli?

A

Estrogen!

Estrogen causes vaginal epithelial expansion => vaginal epithelial glycogen production => epithelial cell sloughing => extracellular glycogen converted to glucose => Glucose taken up by lactobacilli

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4
Q

Why do pre-pubertal and post-menopausal women have different microbial communities with less robust pathogen defense activity?

A

decreased estrogen production

less glucose for lactobacilli to utilize

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5
Q

What are the two ways (enzymes) Lactobacilli can utilize to make hydrogen peroxide?

A
  1. From pyruvate via Pyruvate oxidase (requires oxygen)

2. From glucose via Glucose oxidase

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6
Q

Hydrogen peroxide does not inhibit the growth of what common vaginal pathogen?

A

Gardnerella vaginosis

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7
Q

What are Bacteriocins? Primary fxn?

A

proteins produced by bacteria that are lethal to other bacteria

***Bacteriocins form a pore in the target cell’s membrane, resulting in depolarization and outflow of cytoplasmic contents.

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8
Q

Which molecule has an inhibitory effect on other pro-inflammatory cytokines?

A

IL-10

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9
Q

What receptors recognize common molecular patterns in pathogens and mediate inate immune response such as cytokine and chemokine production?

A. Major Histocompatibility Complex I (MHC I)
B. Major Histocompatibility Complex II (MHC II)
C. T Cell receptors
D. Toll Like Receptors (TLR)

A

D. Toll Like Receptors (TLR)

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10
Q

Which pathogen is least likely to be sensitive to ceftriaxone?

A. Escherischia coli
B. Mycoplasma genitalium 
C. Neisseria gonorrheae
D. Staphylococcus aureus
E. Streptococcus pyogenes
A

B. Mycoplasma genitalium => has no cell wall

Ceftriaxone = cell wall inhibitor

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11
Q

After a bacteria is phagocytosed and digested by a macrophage, how are its antigens presented to cells of the immune system?

A. Between Va and Vb domains of the T cell receptor
B. On the B cell receptor (IgM)
C. On MHC I
D. On MHC II
E. On CD4
A

D. On MHC II

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12
Q

Bacteria are more harmful if they carry genomic pathogenicity islands, which often encode toxins. Transfer of the Staphylococcus aureus SAPI1 pathogenicity island depends on _______________.

A. Conjugation
B. Mutation
C. Transduction
D. Transformation

A

C. Transduction

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13
Q

What is different about the non-dominant lactobacilli microbiotos of healthy females?

A

pH slightly higher more basic (5.3 – 5.5)

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14
Q

What causes bacterial vaginosis?

A

Not caused by a single pathogen!!!!

***It is a DISRUPTION of the normal vaginal microflora!

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15
Q

What type of bacteria is typically most abundant in BV patients?

A

Gardnerella vaginalis

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16
Q

BV is associated with increasing concentrations of what bacteria?

A

Anaerobic:
***Gardnerella vaginalis (gram variable, facultative anaerobic bacilli)

Mycoplasma hominis (tiny, lack a cell wall, require cholesterol in growth media)

Mobiluncus sp.  (gram negative, anaerobic, motile curved rod)

Atopobium vaginae (gram positive, anaerobic, elliptical cocci or rod shaped)
17
Q

How does Metronidazole treat bacterial vaginosis?

A

Metronidazole can only be reduced to its active form in anaerobic organisms.

Once active it:

1) Interferes with bacteria’s fuel metabolism
2) Generates reactive nitrogen, damaging nucleic acids

18
Q

What damage does PID cause in the upper reproductive tract?

A

selective loss of ciliated epithelial cells in the fallopian tube

can result in infertility or ectopic pregnancy

19
Q

What does the microscopic examination of vaginal samples show in PID?

A

Clue cells

20
Q

What pathogens cause PID?

A

Most common: Neisseria gonorrhoeae
(gram negative diplococci, non-motile, not acid fast, oxidase positive)

Most common: Chlamydia trachomatis
(gram negative, obligate intracellular parasite)

Haemophilus influenza - often accompany Neisseria and Chlamydia
(gram negative coccobacilli)

Streptococcus pyogenes - often accompany Neisseria and Chlamydia
(gram positive chained cocci, facultative anaerobic)

Rare causes: Streptococcus pneumonia, Escherischia coli, Klebsiella sp., Proteus mirabilis

Emerging cause: Mycoplasma genitalium
(tiny, lack a cell wall, require cholesterol in growth media)

21
Q

What is the treatment for PID?

A

Ceftriaxone (or Cefoxitin): Cephalosporin derivatives that binds penicillin binding proteins and inhibits bacterial cell wall synthesis, resulting in osmotic imbalance and death of dividing cells. It is effective against bacteria that produce b-lactamase.

Doxycycline: Binds to bacteria’s 30S ribosome and prevents tRNA binding, preventing protein synthesis.

+/- Metronidazole: Action require a redox reaction only possible in anaerobes.

22
Q

What signs/symptoms characterize Toxic shock syndrome (TSS)?

A

fever
diffuse rash
hypotension
organ dysfunction: renal, hepatic, muscle, etc.

23
Q

90% of TSS cases are associated with what pathogen?

A

Staphyloccus aureus

Strep pyogenes accounts for the rest

24
Q

What is the pathogenesis of TSS?

A

Superantigens produced by bacteria bind both TCR and MHC II, creating an immunological synapse without any specific antigen.

This causes systemic activation of T cells regardless of the specificity of their TCR.

Th1 response: IL-2 and IFNg + Macrophage response: IL-1 and TNF

25
How does Staph aureus produce the Superantigen in TSS?
TSST-1 is encoded on the SaPI1 pathogenicity island spread by phage transduction. Thus a community of S. aureus that is in benign equilibrium with the vaginal microbiome can become pathologic quickly if SaPI1 spreads through the community.
26
Do patients with Toxic Shock Syndrome have positive S. aureus blood cultures?
Rarely
27
Do patients with S. aureus sepsis (bacteria present in blood) get Toxic Shock Syndrome?
Rarely
28
What does the normal microbiome of the penis consist of?
The penis microbiome in healthy males is similar to the vaginal microbiome in healthy reproductive age women: dominated by lactobacillus.
29
What may be a consequence of having reduced Lactobacillus in the penis microbiome?
Infection Infection with an STI is associated with a depletion of lactobacillus.
30
What effect does circumcision have on HIV-1 transmission?
Decreased potential for HIV-1 transmission Circumcission => alters microbiome/macrophages further from surface => less chance of HIV
31
How does circumcision shifting the normal microbial community towards aerobic bacteria help prevent infection?
reduces inflammation and reduces the number of CD4+/CCR5+ macrophages in the urethra
32
What are the common causes of Epididymitis in Prepubertal boys, men 35?
Prepubertal boys: Escherichia coli Men younger than 35 years: Chlamydia trachomatis, Neisseria gonorrheae Men 35 years and older: E coli, Pseudomonas species
33
What does the normal microbiome of the prostate consist of?
Trick question! It is not known whether there is a ‘prostate microbiome’ or ‘normal prostate microflora’.