Sexually Transmitted Infections Flashcards

1
Q

Names of three important bacterial causes of STIs

A

Chlamydia trachomatis
Neisseria gonorrhoeae
Treponema pallidum

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2
Q

Main cause of damage in chlamydia, gonorrhoea and syphilis

A

Immune response

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3
Q

Serovars

A

Serotypes

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4
Q

Serovars of Chlamydia trachomatis that cause trachoma

A

A, B, C

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5
Q

Serovars of Chlamydia trachomatis that cause conjunctivitis, uro-genital tract infections, reactive arthritis, pneumonitis

A

D - K

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6
Q

Serovars of Chlamydia trachomatis that cause lymphogranuloma venereum

A

L1, L2, L3

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7
Q

Disease caused by Chlamydophila pneumoniae

A

Atypical pneumonia

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8
Q

Disease caused by Chlamydophila psittaci

A

Acute respiratory disease in humans

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9
Q

Most common STI in developed countries

A

Chlamydia trachomatis serovars D-K

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10
Q

Common sites of Chlamydia trachomatis infections (D-K)

A

Cervix, urethra, pharynx, rectum, conjunctiva

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11
Q

Chlamydial infection that results in penile and vaginal discharge

A

Urethritis, cervicitis

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12
Q

Can Chlamydia trachomatis cause pelvic inflammatory disease?

A

Yes

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13
Q

Diseases that newborns can develop from contact with maternal Chlamydia trachomatis

A

Conjunctivitis, pneumonia

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14
Q

Features of Chlamydiae

A

Gram negative

Small (0.25-0.8micrometers)

Peptidoglycan not detected in cell wall (not detected by Gram stain)

Weakly endotoxic, truncated LPS

An energy parasite (obligate intracellular, uses host mitochondria)

Slow replication (2-3 days)

Damage mostly caused by host immune response

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15
Q

Elementary body of Chlamydia trachomatis

A

Infectious, extracellular particle

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16
Q

Reticulate body of Chlamydia trachomatis

A

Replicative, intracellular particle

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17
Q
Chlamydia trachomatis infection
1)
2)
3)
4)
5)
6)
7)
A

1) EB binds columnar epithelial cells with adhesins
2) Enters cell via cell-mediated endocytosis
3) Prevents endosome fusion with lysosome.
4) Endosomes clump together to form an ‘inclusion’
5) EB transforms into RB in inclusion
6) RB replicate in inclusion (200-1000RBs), feed with ‘drinking straws’ inserted into cytoplasm
7) RB converted to EB, released from cell

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18
Q

Target of antimicrobials directed against Chlamydia trachomatis

A

Reticulate bodies

Therefore antimicrobial has to be able to penetrate tissues and cells

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19
Q

Effect of interferon gamma on Chlamydia

A

RB phase is prolonged

Leads to low-level chronic inflammation

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20
Q

Cells that release interferon gamma

A

Activated CD4, CD8, macrophages

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21
Q

Damage caused by the immune response to a Chlamydial infection

1)
2)
3)
4)

A

1) Infected epithelial cells release chemokines, leading to an influx of neutophils, monocytes, DCs, NKs
2) T and B cells activated, T cells lead to a persistence of RB stage (IFN gamma). These cells and macrophages form follicles
3) Chlamydial heat shock protein 60 (hsp60) also contributes to chronic inflammation
4) Inflammation leads to scarring

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22
Q

Preferred method of testing for Chlamydia

A

PCR of samples (discharge, first-pass urine)

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23
Q

Treatment of Chlamydia

A

Tetracycline or macrolide antibiotics, given over a long period (good tissue penetration)

Single, long-acting dose of azithromycin

24
Q

Neisseria gonorrhoeae features

A
Gram negative
Diplococcus
Often intracellular
Extremely fastidious, doesn't survive drying, disinfectants
Grows best in high-CO2 environment
25
Q

Symptoms of Neisseria gonorrhoea infection

A

Similar to Chlamydia trachomatis

Presents as urethritis

26
Q

Possible complications of gonorrhoea in females

A

Can ascend the genital tract, cause pelvic inflammatory disease

27
Q

Main demographic infected with gonorrhoea in Australia

A

Men who have sex with men

28
Q

Neisseria gonorrhoea infection and spread

A

Target columnar epithelial cells
Attach using adhesins
Replicate at cell surface, spread in mucus (aided by twitching pili)
Can invade some cells and translocate to systemic tissue

29
Q

Neisseria gonorrhoea adhesins

A

PIli
Outer membrane proteins
Lipo-oligosaccharides (LPS without O antigen)

30
Q

Neisseria gonorrhoea pathogenesis

A

No exotoxins
Inflammatory response stimulated by LPS and peptidoglycan
TNF secretion results in loss of ciliated epithelial cells

31
Q

Gonococcal evasion of the immune system

A

Invasive strains can avoid the complement cascade and neutrophils
Antigenic variation of pili helps avoid antibody response
Efficiently acquires genetic material form other bacteria –> rapid antibiotic resistance

32
Q

Neisseria gonorrhoea identificaiton

A

Culture of discharge or urethral, cervical swab
PCR of urine, vaginal swab
Intracellular and extracellular
Gram negative diplococci, polymorphonuclear neutrophils

33
Q

GC medium

A

Horse blood agar, presented as a biplate, lysed blood cells
One side has antibiotics included
Grow in capnophilic environment

34
Q

Capnophilic

A

LIkes high carbon dioxide environment

35
Q

Reason for biplate of GC medium

A

Gonorrhoea samples are with normal flora

This allows for selection of gonorrhoea

36
Q

Treatment of N. gonorrhoeae infections

A

Injectable beta-lactamase-resistant cephalosporin (EG: ceftriaxone)

37
Q

Comorbidity of chlamydia and gonorrhoea

A

40%

38
Q

Treponema pallidum characteristics

A
A spirochete
Slender, spiral rod (0.1-0.2micrometers)
Motile
Very labile
Can't be cultured (can be grown in rabbit testes, doesn't cause syphilis)
39
Q

Stages of syphilis timeframe

A
Infection
3 weeks
Primary syphilis - 2 - 6 weeks
2-24 weeks asymptomatic
Secondary syphilis - 2 - 6 weeks
3 - 30 years asymptomatic
Tertiary syphilis
40
Q

Primary syphilis characteristics

A

Chancre or asymptomatic

41
Q

Secondary syphilis characteristics

A

Rash
Warty genital lesions
Lymphadenopathy

42
Q

Tertiary syphilis characteristics

A

Targets eyes, ears, heart, brain

Gummas

43
Q

What is occurring in the asymptomatic period between stages of syphilis?

A

Control of infection by Th, MF, B cells

44
Q

What is a chancre sore?

A

Local ulcer

45
Q

What is occurring during secondary syphilis?

A

Disseminated bacteria localise in tissues, causing symptoms

46
Q

What is occurring during tertiary syphilis?

A

Multiplication of bacteria

Hypersensitivity response

47
Q

Diagnosis of syphilis

A

Dark-ground microscopy of droplet from primary (or rarely secondary) genital lesion

PCR of the same specimen

Rapid tests that test for cross-reactive antibodies with cardiolipin (Rapid plasma reagin RPR test)

EIA for treponemal antigens

48
Q

Rapid plasma reagin test

A

Detects antibodies directed against components of damaged cells - Cardiolipin
Highly sensitive (few false negatives)
Not very specific (some false positives)
Cheap
Must be confirmed with specific tests for anti-treponemal antibodies (EIA)

49
Q

Syphilis treatment

A

Penicillin - no resistance detected

Treatment needed to prevent mothers giving syphilis to babies

50
Q

How is Chlamydia trachomatis cultured?

A

Using live cells, as Chlamydia is an energy parasite

51
Q

Discharge associated with Chlamydia serovars D-K

A

Watery

Intracellular parasite, therefore there is a T-cell response, not purulent

52
Q

Feature of Chlamydial or Gonococcal infections that leads to infertility

A

Scarring of Fallopian tubes

53
Q

Discharge associated with Neisseria gonorrhoea infection

A

Purulent

54
Q

DIfference in ID of gonococcal infection between males and females

A

In males, detection of gonococcus in a urethral swab is a positive ID

In females, normal commensal gonococci. Ned more testing for a positive ID

55
Q

Gumma

A

Soft, non-malignant growth