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Clinical Pathology > Pathogenesis of HIV and the major sexually transmitted infections > Flashcards

Pathogenesis of HIV and the major sexually transmitted infections Flashcards

1
Q

What is the difference between an STD and a genital infectious disease?

A

STD - sexually transmitted by definition

GID - not all are acquired by sexual transmission, though act my precipitate e.g. bacterial vaginosis (normal vaginal commensal flora or GI flora)

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2
Q

What are the common bacterial pathogens causing STIs in the UK?

A
  • N. gonorrhoea
  • C.trachomatis
  • Ureaplasma
  • Mycoplasma
  • G. Vaginalis
  • Anaerobes
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3
Q

What are the uncommon bacterial pathogens causing STIs in the UK?

A

T. pallidum
H. ducreyi
K. granulomatis
C. trachomatis (LGS)

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4
Q

What are the common viral pathogens causing STIs in the UK?

A
  • HSV
  • HPV
  • Molluscum (pox virus)
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5
Q

What are the uncommon viral pathogens causing STIs in the UK?

A
  • HIV

- Hep B

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6
Q

What are the common protozoan/fungal/ectoparasites pathogens causing STIs in the UK?

A
  • Trichomonas vaginalis
  • Candida albicans
  • Phthirus pubis (crabs)
    Saroptes scabiei
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7
Q

What is the most common STI in the UK?

A

Chlamydia

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8
Q

What is the route of transmission for STIs?

A
  • Mucous membrane contact

- Exchange of bodily fluids

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9
Q

Which STIs remain at local sites of infection?

A
  • T. vaginalis
  • Chlamydia
  • HSV
  • HPV
  • N.gonorrhoeae
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10
Q

Which STIs have mixed sites of infection?

A
  • T. pallidum (tertiary syphilis - brain)

- N. gonorrhoeae

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11
Q

Which STI’s have other (i.e. not genital) sites of infection?

A
  • HIV

- HBV

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12
Q

What are the various forms of vertical transmission?

A
  • In utero - trans placental
  • Perinatal - passage through infected birth canal
  • Eye mucous membrane - conjunctivitis/keratitis
  • Present in breast milk
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13
Q

What is the risk of transmission/acquisition related to?

A
  • Number of sexual partners

- Use of non-barrier or no contrception

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14
Q

Are patients with one STI likely to have another STI?

A

Yes - hence universal screening for HIV

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15
Q

Why is contact tracing very important?

A

Infection may be asymptomatic

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16
Q

Describe the morphology of N. gonorrhoeae.

A

Gram negative diplococci

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17
Q

Where do N.gonorrhoeae replicate?

A

Are phagocytosed and replicate intracellulary.

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18
Q

What virulence factor do some N.gonorrhoeae cells possess which makes them more infective, and how?

A
  • Pili on cell surface
  • ↑ ability to attach to mucosal epithelial cells
  • Primarily infect columnar / cuboidal epithelium
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19
Q

What is the incubation period for gonorrhoea?

A

2-5 days

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20
Q

What percentage of women are asymptomatic?

A

60%

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21
Q

What are the symptoms of gonorrhoea in women?

A
  • Urethral discharge

- Dysuria

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22
Q

What are the local complications of gonorrhoea?

A
  • epididymitis, prostatitis;
  • barthonilitis, salpingitis, PID, peritonitis
  • Fitz-Hugh-Curtis Syndrome (perihepatitis): Usually co-infected with C trachomatis
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23
Q

What are the systemic complications of gonorrhoea?

A

Metastatic: Disseminated Gonococcal Infection (DGI)

  • 0.5-3% of untreated – ↑ with specific strains
  • bacteraemia, arthritis, dermatitis (meningitis).
  • (up to 13% DGI: Complement deficiency)
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24
Q

What are the complications of gonorrhoea in pregnancy?

A
  • Spontaneous abortion

- Premature labour

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25
Q

How can conjunctivitis be caused by gonorrhoea?

A

Self-inoculation

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26
Q

What are the neonatal complications of gonorrhoea?

A
  • Ophthalmia neonatorum

- Acute purulent conjunctivitis,

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27
Q

How is microscopy used in the diagnosis of gonorrhoea?

A
  • urethral swab : GNID: high sensitivity / specificity

- (Other sites: commensal Neisseria spp)

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28
Q

How are cultures used in the diagnosis of gonorrhoea?

A
  • Selective plates, 48 hours, fastidious
  • Endocervical (not High Vaginal) [Sens: 80-90%]
  • (1o locus = columnar epithelial cells endocervix)
  • urethral swab [Sens >/ 95% in men]
  • High specificity (confirm not N meningitidis / other spp)
  • Antibiotic sensitivity testing, (typing).
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29
Q

What is the nucleic acid amplification test?

A
  • Multiplexed with C trachomatis

- Urine / vaginal swab: specificity > 99%;

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30
Q

What is the treatment for gonorrhoea?

A

β-lactams:

  • (BenzylPenicillin, amoxicillin)
  • 1970s – resistance: β-lactamase; PBP change

Cephalosporins:

  • cefixime (oral)
  • ceftriaxone (iv or im route)

Fluoroquinolones:
- Ciprofloxacin (↑ resistance)

Others:

  • Spectinomycin, azithromycin.
  • (Tetracycline – widespread resistance)
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31
Q

Which antibiotic has the least resistance to N.gonorrhoeae?

A

Ceftriaxone

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32
Q

What are the likely causes of non-gonococcal urethritis (NGU)?

A
  • Chlamydia trachomatis types D-K

- Ureaplasma urealyticum (Mycoplasma genitalium)

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33
Q

How is NGU diagnosed?

A

Currently: NAAT for chlamydia

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34
Q

How is NGU treated?

A

Doxycycline; macrolide: erythro- / azithro-mycin

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35
Q

What kind of pathogen is C.trachomatis?

A

Obligate intracellular pathogens.

Unique lifecycle:

  • extracellular infectious form: Elementary body
  • Intracellular replicative form: Reticulate body
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36
Q

What are the target cells for C.trachomatis?

A
  • squamocolumnar epithelial cells of
  • endocervix / upper genital tract in ♀;
  • Conjunctiva, urethra, rectum in ♀ & ♂
  • Also respiratory tract cells in infants
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37
Q

What is the national chlamydia screening programme?

A

Screen (i.e asymptomatic)

- All sexually active

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38
Q

What is the prevalence of of chlamydia in the UK?

A
  • 16-44 yr olds: 1.5% sexually experienced ♀, 1.1% ♂

- 16-24 yr olds: 3.1% ♀, 2.3% ♂

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39
Q

What are the features of chlamydia cervicitis?

A
  • cervical friability,
  • oedema
  • ectopy
  • mucopurulant discharge
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40
Q

Why is chlamydia often the cause of ‘acute urethral syndrome’?

A

May have dysuria / frequency but sterile pyuria on standard urinalysis.

41
Q

What are the adult complications of chlamydia infection?

A

PID (> 9.5% within one yr w/out Rx), perihepatitis
- Tubal infertility (10.6% PID),ectopic pregnancy, chronic pain

Epididymitis (2%)

Conjunctivitis

Reiter’s syndrome:
- arthritis, conjunctivitis, urethritis, skin lesions

42
Q

What are the neonatal complications of chlamydia infection?

A
  • conjunctivitis (later onset than with N gonorrhoeae, 5-12 days)
  • Infant Pneumonia: usually present at 4-11 weeks
43
Q

How is the diagnosis of chlamydia performed?

A

(Histology: Inclusion bodies)

(Cell culture)

NAAT (superseded EIA)

  • Sensitivity: cervix 81-100%, urine ♀: 80-96%, urine ♂: 90-96%
  • Specificity:99.7%

(Serology – limited value in most oculogenital infections)

44
Q

What is the treatment for chlamydia?

A
  • Azithromycin 1g PO single dose

- Doxycycline 100mg BD for 7 days

45
Q

What is the treatment for paediatric chlamydia?

A
  • conjunctivitis / pneumonia: erythromycin, 14 days.

- (Treat parents as well)

46
Q

What is the association between PID and infertility?

A

1st, 2nd, 3rd episode associated with 10%, 30%, 50% risk of infertility

47
Q

Which subtypes of HPV cause 90% of genital warts?

A

6 and 11

48
Q

Which subtypes of HPV cause 70% of cervical carcinomas?

A

16 and 18

49
Q

What are the treatments for genital warts?

A

Burn - podophyllin, salicylic acid, trichloracetic acid

Freeze - Liquid nitrogen

Cut

Imiquimod

50
Q

Which HSV is more common in women than men?

A

HSV - 2`

51
Q

What kind of virus is HSV?

A

dsDNA

52
Q

What are the symptoms of primary genital herpes?

A
  • pain, itching, dysuria, vaginal / urethral discharge –
  • bilateral vesicles / ulcers - viral shedding,
  • Accompanied by constitutional symptoms
53
Q

Where does HSV become latent?

A

Sensory neuron cells – sacral nerve ganglia

54
Q

Why does HSV reactive?

A
  • local trauma, menstruation, stress
  • may have asymptomatic shedding
    (more common in men)
55
Q

How is HSV diagnosed?

A
  • Clinica
  • PCR (HSV 1 or 2)
  • histology
56
Q

What is the treatment for HSV?

A
  • Aciclovir
57
Q

What are the

A
  • dissemination
  • meningitis
  • encephalitis
  • sacral nerve parasthesiae
  • urinary retention
58
Q

Describe the morphology of T.pallidum.

A
  • Slender, helical, tightly coiled cells

- 0.18 μ wide, 6 – 20 long (too thin for Light Microscopy)

59
Q

What is the mode of infection for T.pallidum?

A

Penetrates intact mucous membranes or via abraded skin
Disseminated within days via lymphatics / bloodstream
Subsequent clinical symptoms & signs

60
Q

What is the histology of T.pallidm infection?

A
  • obliterative endarteritis
  • Concentric endothelial / fibroblastic proliferation
  • microscopic vascular compromise
61
Q

What is the incubation period for T.pallidum?

A

Median - 21 days

62
Q

What are the clinical features of primary syphilis?

A

1°: chancre

  • site of inoculation, painless indurated lesion
  • Heals spontaneously, within 3 – 6 weeks.
63
Q

What are the clinical features of secondary syphilis?

A

Most florid phase 2-8 weeks post onset of chancre

Skin:

  • Rash: macular / maculopapular, trunk, limbs -palms / soles
  • Condylomata lata – as coalesce in warm body areas – grey
  • erythematous plaques, highly infectious
  • “mucous patches” – silvery-grey erosions, muc membranes

Constitutional symptoms – fever, malaise, weight loss

Generalised lymphadenopathy (may include epitrochlear)

CNS involvement (40%), headache, meningismus

Spontaneous resolution after 3-12 weeks.

Latent: No clinical manifestation, positive serology

Without treatment: ~ 30% will develop late / 3o syphilis

64
Q

What are the tertiary manifestations of syphilis?

A
  • Neurosyphilis
  • Aortitis
  • Late benign syphilis
65
Q

What is neurosyphilis?

A

Meningovascular: Hemiplegia, seizures

Parenchymatous:

  • general paresis (cortex): personality changes, Argyll Robertson pupils: accommodate to near vision, don’t react to light
  • tabes dorsalis (spinal cord): demyelinisation of posterior column / dorsal roots / dorsal root ganglia: ataxic wide–based gait, lightening pains in legs, loss of position / vibratory sense
66
Q

What are the clinical features of aortitis?

A
  • aortic regurgitation

- saccular aneurysm

67
Q

What is late benign syphilis?

A
  • non-specific granulomatous reaction,

- Any organ, most commonly bone / skin / soft tissue

68
Q

What are the signs and symptoms of congenital (in utero transmission) syphilis?

A
  • Greatest risk: Spirochaetaemia of early syphilis
  • Early signs: snuffles, rash, hepatosplenomegaly

Late: include frontal bosses, saddle nose, sabre shins
Hutchinson’s incisors.

69
Q

What tests are used in the diagnosis of syphilis?

A

(Lack of culture)

Direct detection:

  • Darkfield microscopy – 1o or 2o lesions
  • PCR – more sensitive than microscopy, Sensitivity 89-95% when compared to serology (..NOT necess “false” +ve)

Indirect tests – serology: mainstay – two groups of tests:

  • Specific: anti-treponemal antibodies: EIA, TPHA, FTA. Sensitive / specific, but won’t sero-convert post Rx
  • Non-specific: reaginic antibodies versus lipoidal antigens: VDRL, RPR (Rapid Plasma Reagin) tests. False positives, but usually sero-convert post
  • successful Rx – can monitor with titres
70
Q

How is syphilis treated?

A
  • Standard: Penicillin – based
  • Length / route (IM / IV) depends on stage / site

Alternatives (depend on stage / site):
amoxicillin, ceftriaxone, doxycycline,

71
Q

What is the Jarish-Herxheimer reaction?

A 
Commonest in 2o syphilis
Fever, chills, myalgia
Hypersensitivity reaction – organism lysis: 
release of heat stable protein.
Self-limiting.
72
Q

What is the cause of trichomoniasis?

A
  • Trichomonas vaginalis
  • Trophozoite transmitted, no known cyst.
  • Humans only natural host
73
Q

What are the symptoms of trichomoniasis?

A
  • profuse greenish frothy vaginal discharge
  • mucosal inflammation
  • males are usually asymptomatic but may have urethritis + be a source of re-infection
74
Q

How is the diagnosis of trichomoniasis performed?

A

Microscopy/culture (high vaginal swab):

75
Q

What is the treatment of trichomoniasis?

A

Metronidazole

76
Q

What is the cause of bacterial vaginosis (BV)?

A
  • reduced vaginal lactobacilli

- increased Gardnerella vaginalis & anaerobes

77
Q

What are the symptoms of BV?

A
  • watery discharge
  • +ve KOH test (10% KOH - fishy odour)
  • vaginal pH >4.5
  • clue cells on microscopy
78
Q

What is the treatment for BV?

A
  • metronidazole
  • amoxycillin
  • topical clindamycin
79
Q

What factors might contribute to thrush/balanitis?

A
  • oral contraceptives, poorly controlled diabetes,

- antibiotics – inhibition of normal flora

80
Q

What is the source of the Candida albicans?

A
  • bowel source

- (sexual transmission)

81
Q

What are the symptoms of candidiasis?

A
  • vulval, vaginal and penile erythema; itching / irritation
  • Classically: thick / adherent discharge; white plaques
  • maculopapular & fissuring lesions
82
Q

What is the treatment for uncomplicated C.albicans?

A
  • (C albicans, not recurrent, not severe)
  • Topical agent: e.g. clo-trimazole (Canesten™)
  • Fluconazole: single 150mg oral dose
83
Q

What is the treatment for complicated C.albicans?

A
  • Treatment for 10-14 days (topical or oral)
    (? Obtain in vitro sensitivities)
  • Consider treatment of partner(s)
  • (Longterm suppressive treatment if frequent recurrence)
84
Q

What is AIDS?

A

The end-stage manifestation of HIV infection?

85
Q

What are the features of HIV?

A

A retrovirus: possesses reverse transcriptase

  • RNA dependent DNA polymerase
    • converts viral RNA into linear ds DNA
    • subsequently incorporated into host genome
  • Error prone – high rate of mutability.

RNA – based:
- survival advantage - great genetic diversity

DNA intermediary –
- latency, & can incorporate into host genome

CD4 / macrophage tropic
- reduction of host immune response.

86
Q

What are the transmission routes for HIV?

A
  • Sexual – transmission at genital or colonic mucosa
  • Exposure to other infected fluids: blood / blood products
    (including accidental occupational exposure)
  • Mother to infant
87
Q

What is the role of viral glycoprotein gp120?

A

Interacts with cellular receptor CD4 and chemokine receptor CCR5 for virion to gain host cell entry.

88
Q

Where does reverse transcription occur?

A

In cytoplasm

89
Q

What happens to the dsDNA once reverse transcription has occured?

A
  • dsDNA imported into nucleus
  • Integration into cell genome
  • Latency / immune evasion
90
Q

What is produced by the complex interaction between virion production & T-cell turnover?

A

Rapid emergence of viral mutants
- may promote immune escape, drug resistance

Progressive / fluctuating T-cell depletion.

91
Q

What is the result of loss of CD4+ve T-cells?

A

Allows “opportunistic” infections
- Organisms not normally pathogenic in immune competent patient.

Risk of different infections related to degree of immune suppression (“CD4 count”)

92
Q

What are the stages of HIV infection?

A

Stage I: CD4 count > 500 cells / μL
Stage 2: 349 – 499;
Stage 3 (Advanced HIV): 200 – 349
Stage 4 (AIDS):

93
Q

What are characteristics of primary infection?

A

Acute retroviral Syndrome
- fever, pharyngitis, lymphadenopathy, rash et al

  • Then asymptomatic phase
94
Q

What are the signs of the early symptomatic phase of HIV?

A
  • Pulmonary TB
    consider HIV test in all new TB cases
  • Persistent oral candidiasis
  • Unexplained chronic diarrhoea (> one month)
  • Unexplained persistent fever (> 37.6, for > one month)
  • Severe bacterial infections (e.g. S pneumoniae bacteraemia)
95
Q

What are the opportunistic infections seen in AIDS?

A
  • HIV wasting syndrome, HIV encephalopathy.
  • Oesophageal candidiasis
  • Pneumocystis jirovecii (formerly carinii) pneumonia
  • CMV disease (including retinitis),
  • CNS toxoplasmosis;
  • Progressive multifocal leukoencephalopathy (PML)
  • extra-pulmonary cryptococcosis
  • Disseminated non-tuberculous mycobacterial disease
  • Extra-pulmonary tuberculosis
  • Chronic cryptosporidiosis; chronic isosporiasis
  • Kaposi’s sarcoma, lymphoma (cerebral or non-Hodgkin’s)
96
Q

What percentage of HIV in the UK is undiagnosed?

A
  • ~ 25% cases in UK undiagnosed
  • Account for approximately 70% of transmission
  • New case rates doubled in past 10 years
97
Q

Which patients are screened for HIV?

A
  • GUM
  • patients with TB or lymphoma
  • Ante-natal.
98
Q

What are the various test used in the diagnosis of HIV?

A 
Antibody testing (sero-conversion)
- Confirm with second sample.

Polymerase Chain Reaction (PCR)

  • Detects viral nucleic acid:
  • Quantitative: viral copy numbers - “viral load”- in blood / (other fluids)
  • Genotypic mutations conferring drug resistance

(Opportunistic infections)

CD4 cell count

Clinical Pathology (65 decks)

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