Sexually transmitted infections Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

what is the predominant colonising species of the vaginal microbiome

A

Lactobacillus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how does lactobacillus inhibit growth of pathogenic species in the vagina

A
  • Produce lactic acid – helps maintain low pH. (prevents growth of many invading species)
  • Adhere to vaginal epithelial cells (create biofilm) and prevent long-term colonisation by other species.
  • Produce hydrogen peroxide (antimicrobial compound)– inhibits growth of other microorganisms directly or via human myeloperoxidase
  • produce antimicrobial peptides - bacteriocins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what pathogens can be inactivated by lactobacillus in the vaginal microbiome

A

HIV-1, herpes simplex virus type 2, Trichomonas vaginalis, Gardnerella vaginalis, Peptostreptococcus bivia and E. coli.!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what antimicrobial components of semen

A
antibacterial peptides including: 
–	Lysozyme
–	Lactoferrin
–	Phospholipase A2
–	Secretory leukocyte protease inhibitor
–	Semenogelin 1-derived peptides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

give some features of gonorrhoea

A

caused by Neisseria gonorrhoeae. different manifestations, characterised by symptoms and disease profile. can be uncomplicated or disseminated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how is gonorrhoea transmitted

A

almost always transmitted sexually in adults:
– genital – genital; genital – anorectal; orogenital; oro – anal
– autoinoculation of the eye

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

where is the uncomplicated gonorrhoeal infection found

A

localised, affecting the mucous membranes of urethra, endocervix, rectum, pharynx and conjunctiva.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

whats the difference between uncomplicated and disseminated gonorrhoea

A
Uncomplicated infection is localised, usually affecting the mucous membranes of urethra, endocervix, rectum, pharynx and conjunctiva.
Less common (< 1% people) is disseminated gonorrhoea – (spreads to other areas of the body) can present as septic arthritis or dermatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the complications of gonorrhoea for men

A

epididymitis, penile lymphangitis, per-urethral abscess, acute prostatitis, seminal vesiculitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the complications of gonorrhoea for women

A

• Bartholin’s abscess
polymicrobial infection.
• 10 – 20% pelvic inflammatory disease.
• During pregnancy, can cause spontaneous abortion, premature labour, early rupture of fetal membranes, etc.
• Disseminated gonorrhoea
• Rare but serious – lead to arthritis-dermatitis syndrome, gonococcal bacteremia and gonococcal endocarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

give 5 features of Neisseria gonorrhoeae

A

Fastidious, Gram negative diplococci.

Facultatively intracellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the virulence factors of Neisseria gonorrhoeae

A

Pilus – attach to epithelium. Contain constant & hypervariable regions, contribute to antigenic diversity.
Por proteins – form pores in membrane. Antigenic properties.
Opa proteins – aid in attachment.
LOS – contains lipopolysaccharide, has endotoxin activity.
Rmp proteins – inhibit bacteriacidal action of semen.
IgA protease – destroys IgA1.
Capsule - can resist phagocytosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is used for the initial diagnosis of gonorrhoea

A

Nucleic acid amplification tests (NAATs) (gonorrhoea is hard to grow this is better than culture methods)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the current treatment for gonorrhoea

A

a single dose of 500 mg of intramuscular ceftriaxone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the most common curable STI in the UK

A

Chlamydia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is chlamydia caused by

A

obligate intracellular bacterium, Chlamydia trachomatis

17
Q

where does Chlamydia trachomatis infect in men

A

the urethra

18
Q

where does Chlamydia trachomatis infect in women

A

endocervix or urethra or both.

19
Q

what percentage of chlamydia infections are asymptomatic

A

At least 70% women/50% men

20
Q

what are the two types of chlamydia infection, how do they differ

A
  • Uncomplicated – if not ascended into upper genital tract.

* Complicated – if in upper genital tract, causing pelvic inflammatory disease (PID) (women), epididymo-orchitis (men).

21
Q

what complications can chlamydia cause

A
  • Epididymo-orchitis – pain, swelling or inflammation of the epididymous and/or testicles.
  • Adult conjunctivitis – mainly caused by autoinoculation.
  • Lymphogranuloma venereum (LGV) – infection of lymphatic system.
  • Sexually acquired reactive arthritis (SARA) – polyarthritis of weight-bearing joints.
  • Anxiety and distress.
  • In pregnancy, can result in increased risk of membrane rupture, pre-term delivery, low birth weight, etc.
22
Q

how is chlamydia diagnosed

A

Nucleic acid amplification tests (NAATs)

23
Q

what are the virulence factors of Chlamydia trachomatis

A
  • Outer LPS cell membrane contains cysteine-rich proteins, inhibit phagosome fusion.
  • Adhesion to sialic acid receptors on mucous membranes, presence at sites inaccessible to phagocytes, T cells and B cells.
  • Antigenic variation so many serotypes. – harder to target
  • Needle-like projection type III secretion apparatus – injects bacterial proteins into cell cytoplasm, avoids lysosomes. – so it isn’t registered as foreign as quickly
  • Infested vacuole can divert lipids to itself rather than another part of the host cell.
24
Q

describe the unique lifecycle of Chlamydia trachomatis

A

metabolically inert, spore-like elementary bodies (EBs) infect host cells and develop into metabolically active, replicative reticulate bodies (RBs) within a membrane-bound inclusion. RBs redifferentiate into EBs 24–48 hours after infection (once they reach a certain number) and the EBs are eventually released by lysis of the host cell and go on to infect other host cells

25
Q

how is syphilis transmitted

A

Person to person transmission via direct contact with infectious lesions

26
Q

what causes syphilis

A

Spirochete bacterium, Treponema palladium.

27
Q

what are the symptoms of primary syphilis

A

painless ulcer (chancre), commonly affecting genitals, and localised lymphadenopathy

28
Q

what are the symptoms of secondary syphilis

A
severe multisystem
–	Rash, commonly on palms or soles.
–	Moist, wart-like lesions, commonly in perianal and vulval regions, under breasts, axillae.
–	Patchy lesions on oral mucosa. 
–	Generalised lymphadenopathy.
–	Low grade fever, headaches.
29
Q

what are the stages of syphilis infection

A

• Primary - easily treated and cured with medication
• Secondary - symptoms will go away, even if you don’t get treated. But if you’re not treated, your infection will get worse
• Early latent – within 1st 2 yrs of infection but no clinical features.
• Late syphilis can progress through two stages:
Late latent stage – serological confirmation, 2 yrs after infection, no clinical features. (bale to confirm infection)
Tertiary – rare due to widespread antibiotic use. Divided into neurosyphilis, cardiovascular and gummatous syphilis. can cause death

30
Q

give some features of treponema palladium

A
  • Obligate, intracellular parasite.
  • Fastidious, Gram negative.
  • Helically coiled, corkscrew shaped.
  • 6 –10 μm long and 0. 15 μm – 0.2 μm wide.
  • Relies on host cells for nutrients, making it hard to culture in lab
31
Q

what is the structure of Treponema palladium

A
Outer sheath composed of glycosaminoglycan.
Outer membrane contains peptidoglycan and maintains structure.
Axial filament (endoflagella) – inside the inner membrane which provides osmotic stability and covers the protoplasmic cylinder and structure
32
Q

how do Treponema palladium replicate

A

transverse fission (binary fission along the transverse axis)

33
Q

what are the virulence factors of Treponema palladium

A
  • Outer membrane proteins associated with adherence.
  • Can produce hyaluronidase, may allow perivascular infiltration.
  • Coated with host cell produced fibronectin – protects against phagocytosis. -disguise
34
Q

what serological tests can be used to diagnose syphilis

A
  • Non-treponemal – detect IgG and IgM antibodies in early stages of disease.
  • Treponemal – specific antibody tests.
  • Fluorescent Treponemal Antibody Absorption (FTA-ABS) test.
  • Trepanomal Palladium Haemagglutinin test (TPPA, TPHA).
35
Q

how is syphilis diagnosed

A
Microscopy:
•	Dark field illumination.
•	Direct immunofluorescence antibody staining.
Culture:
•	Generally unsuccessful.
Serology
36
Q

when were the first written records of syphilis

A

• 1st written records of a European outbreak come from 1494/5.

37
Q

when was treponema palladium first identified

A

1905

38
Q

what were the Tuskegee & Guatemala studies

A

uninformed human subjects infected with syphilis
• Study by US Public Health Service, started in 1932.
• Widespread problem and no effective, safe treatment.
• Measure progression of untreated disease.
• By 1947, penicillin was being used but it wasn’t until 1960’s that it was found that many participants had not been given this.
• Predominantly black male participants and not until 1972 that study was stopped.