Sexually transmitted infections Flashcards

1
Q

what is the predominant colonising species of the vaginal microbiome

A

Lactobacillus

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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
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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.!!!

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4
Q

what antimicrobial components of semen

A
antibacterial peptides including: 
–	Lysozyme
–	Lactoferrin
–	Phospholipase A2
–	Secretory leukocyte protease inhibitor
–	Semenogelin 1-derived peptides
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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.

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6
Q

how is gonorrhoea transmitted

A

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

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7
Q

where is the uncomplicated gonorrhoeal infection found

A

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

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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
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9
Q

what are the complications of gonorrhoea for men

A

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

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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

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11
Q

give 5 features of Neisseria gonorrhoeae

A

Fastidious, Gram negative diplococci.

Facultatively intracellular

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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.

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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)

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14
Q

what is the current treatment for gonorrhoea

A

a single dose of 500 mg of intramuscular ceftriaxone.

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15
Q

what is the most common curable STI in the UK

A

Chlamydia

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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
how is syphilis transmitted
Person to person transmission via direct contact with infectious lesions
26
what causes syphilis
Spirochete bacterium, Treponema palladium.
27
what are the symptoms of primary syphilis
painless ulcer (chancre), commonly affecting genitals, and localised lymphadenopathy
28
what are the symptoms of secondary syphilis
``` 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
what are the stages of syphilis infection
• 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
give some features of treponema palladium
* 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
what is the structure of Treponema palladium
``` 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
how do Treponema palladium replicate
transverse fission (binary fission along the transverse axis)
33
what are the virulence factors of Treponema palladium
* Outer membrane proteins associated with adherence. * Can produce hyaluronidase, may allow perivascular infiltration. * Coated with host cell produced fibronectin – protects against phagocytosis. -disguise
34
what serological tests can be used to diagnose syphilis
* 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
how is syphilis diagnosed
``` Microscopy: • Dark field illumination. • Direct immunofluorescence antibody staining. Culture: • Generally unsuccessful. Serology ```
36
when were the first written records of syphilis
• 1st written records of a European outbreak come from 1494/5.
37
when was treponema palladium first identified
1905
38
what were the Tuskegee & Guatemala studies
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.