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9. CP - Diseases of the Reproductive System > (50) HIV and STIs > Flashcards

(50) HIV and STIs Flashcards

1
Q

What is an STI?

A

Infections which are transmitted person-person by sexual contact - may be asymptomatic (men and women)

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2
Q

What is an STD?

A

STI but with evidence of disease (signs and symptoms)

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3
Q

Are gentile infectious diseases always sexually transmitted?

A

No, not all are acquired by sexual transmission (act may precipitate)

  • normal vaginal commensal flora
  • gasto-intestinal flora
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4
Q

What are the common bacteria causing STIs in the UK?

A
  • N. gonorrhoea
  • C. trachomatis
  • ureaplasma
  • mycoplasma
  • (G. vaginalis)
  • (anaerobes)

() = not STIs per se

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5
Q

What are the uncommon bacteria causing STIs in the UK?

A
  • T. pallidum
  • H. ducreyi
  • K. granulomatis
  • C. trachomatic (LGV)
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6
Q

What are the common viruses causing STIs in the UK?

A
  • herpes simplex virus (HSV)
  • human papilloma virus (HPV)
  • pox virus (molluscum)
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7
Q

What are the uncommon viruses causing STIs in the UK?

A
  • HIV

- Hepatitis B

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8
Q

Name a protozoa causing STIs in the UK?

A
  • trichomonas vaginalis
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9
Q

Name a fungus causing STIs in UK?

A

(-candida albicans)

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10
Q

Name an ectoparasite causing STIs in UK?

A
  • phthirus pubis (crabs)

- sarcoptes scabiei

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11
Q

Name 5 common STIs diagnosed at GUM clinics in England and Wales?

A
  • chlamydia (44%)
  • warts (35%)
  • gonorrhoea (11%)
  • herpes (9%)
  • syphilis (1%)
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12
Q

Who are most at risk of being diagnosed with an STI?

A

Age group 16-24

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13
Q

How are STIs transmitted?

A

Mucous membrane contact/exchange of bodily fluids

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14
Q

STI organisms are often fastidious. What does this mean?

A

A fastidious organism is any organism that has a complex nutritional requirement - in this cases, don’t survive well out in the environment

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15
Q

In which infections are the sites of infection/disease predominantly local?

A
  • T. vaginalis
  • Chlamydia trachomatis
  • HSV
  • HPV
  • Neisseria Gonorrhoea
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16
Q

In which infections are the sites of infection/disease mixed?

A
  • syphilis (treponema pallidum)
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17
Q

In which infections are the sites of infection/disease not local?

A
  • HIV

- HBV

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18
Q

Give the 2 way which STIs can spread

A
  • sexual contact

- vertical transmission = mother to baby

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19
Q

How can STIs spread through sexual contact?

A
  • male-female genitalia
  • oro-genital
  • male-male
  • female-female
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20
Q

How can STIs spread vertically from mother to baby?

A
  • in utero = transplacental
  • peri-natal = passage through infected birth canal
  • eye mucous membrane - conjunctivitis/keratitis
  • present in breast milk
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21
Q

Give through common concepts concerning STIs/STDS

A
  • risk of transmission/acquisition related to number of sexual partners (increased risk with use of non-barrier or no contraception)
  • patients with one STD likely to have other STIs/STDs
  • contract tracing very important (may be asymptomatic)
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22
Q

What is the cause of gonorrhoea (the clap)?

A

Neisseria gonorrhoeae

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23
Q

Why type of organism is neisseria gonorrhoeae?

A

Gram negative coccus - diploccocus - in pairs (resemble coffee beans)

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24
Q

What are the other Neisseria species?

A
  • N. meningitidis

- non-pathogenic neisseria species (normal commensal flora in throat and genital tract)

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25
Q

Neisseria gonorrhoea have pili on cell surface. Why?

A

Piliated cells more virulent

  • increased ability to attach to mucosal epithelial cells
  • primarily infect junction between columnar and cuboidal epithelium

(intracellular, phagocytosis, intracellular-multiplication)

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26
Q

Describe the structure of the neisseria gonorrhoea cell envelope

A

Has 3 layers like all gram negative bacteria

  • inner cytoplasmic membrane
  • thin peptidoglycan wall
  • outer cytoplasmic membrane (lipo-oligosaccharides)
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27
Q

Where do gonorrhoea affect?

A
  • GU tract
  • rectum
  • oropharynx
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28
Q

What is the incubation period of gonorrhoea?

A

2-5 days (short)

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29
Q

How often is gonorrhoea asymptomatic?

A

60% of women asymptomatic

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30
Q

What is a symptom of gonorrhoea?

A
  • urethral discharge

- dysuria (stinging on passing urine)

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31
Q

What are the local complications of gonorrhoea?

A
  • epididymitis
  • prostatitis
  • barthonilitis
  • salpingitis
  • PID
  • peritonitis
  • Fitz-Hugh-Curtis syndrome (perihepatitis)
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32
Q

If a gonorrhoea patients has perihepatitis, they are usually co-infected with what?

A

C. trachomatis

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33
Q

What is barthonilitis?

A

Inflammation of one or both of the two Bartholin’s glands, which are located one on either side of the opening of the vagina

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34
Q

What is salpingitis?

A

Inflammation of the fallopian tubes

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35
Q

What is DGI?

A

Disseminated gonococcal infection - more widespread metastatic disease caused by gonorrhoea

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36
Q

How often does DGI occur?

A

0.5-3% of untreated cases - increased with certain strains

Up to 13% of DGI is due to complement deficiency

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37
Q

What are the complications of disseminated gonococcal infection?

A
  • bacteraemia
  • arthritis
  • dermatitis
  • (meningitis)
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38
Q

What can gonorrhoea in pregnancy cause?

A
  • spontaneous abortion

- premature labour

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39
Q

What can gonorrhoea cause in the neonate?

A
  • ophthalmia neonatorum
  • acute purulent conjunctivitis less than 5 days post-delivery
  • can cause blindness if not treated appropriately
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40
Q

Name 3 methods of gonorrhoea diagnosis

A
  • microscopy
  • culture
  • nucleic acid amplification test (NAAT) eg. PCR
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41
Q

How is gonorrhoea diagnosed by microscopy?

A
  • urethral swab (male)
  • GNID = gram-negative intracellular diplococci
  • high sensitivity/specificity
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42
Q

How is gonorrhoea diagnosed by culture?

A
  • selective plates (because fastidious) for 48 hours
  • endocervical (columnar epithelial cells) (not high vaginal) - sens = 80-90%
  • OR urethral swab, sens over 95% in men
  • high specificity (confirm no n. meningitidis/other spp)
  • antibiotic sensitivity testing (typing)
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43
Q

How is NAAT e.g. PCR used in gonorrhoea diagnosing?

A
  • multiplexed with C. trachomatis
  • urine/vaginal swab
  • specificity over 99%
  • positive predictive value over 95% if prevalence 0.5%
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44
Q

What is multiplex PCR?

A

A modification of polymerase chain reaction in order to rapidly detect deletions or duplications in a large gene. This process amplifies genomic DNA samples using multiple primers and a temperature-mediated DNA polymerase in a thermal cycler

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45
Q

Give 3 antibiotic types used in the treatment of gonorrhoea

A
  • B-lactams
  • cephalosporins
  • fluoroquinolones
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46
Q

Give examples of B-lactams used in the treatment of gonorrhoea

A
  • benzylpenicillin

- amoxicillin

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47
Q

How did gonorrhoea develop resistance to B-lactams in the 1970s?

A
  • B-lactamase

- PBP change (penicillin-binding proteins)

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48
Q

Name 2 cephalosporins used in the treatment of gonorrhoea

A
  • cefixime (oral)

- ceftriaxone (IV or IM route)

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49
Q

Name a fluoroquinolone used in the treatment of gonorrhoea

A
  • ciprofloxacin (but increased resistance)
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50
Q

Name 3 other antibiotics used in the treatment of gonorrhoea (other than B-lactams, cephalosporins, fluoroquinolones)

A
  • spectinomycin
  • azithromycin
  • tetracycline (but widespread resistance)
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51
Q

Name 2 antibiotics used in the treatment of gonorrhoea, that as of 2007 had 0% total resistance

A
  • ceftriaxone

- spectinomycin

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52
Q

What is the recommend treatment of gonorrhoea according to BASHH 2011?

A
  • Std: ceftriaxone 0.5mg IM
  • and azithromycin 1g PO
  • and all cases “test of cure”
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53
Q

What is a problem with cefixime/ceftriaxone?

A

Decreased susceptibility. High level of resistant strains in some areas recently, eg. Japan, France 2011

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54
Q

What is NGU?

A

Non-gonococcal urethritis

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55
Q

What organisms can cause non-gonococcal urethritis?

A
  • mostly chlamydia trachomatis types D-K
  • ureaplasma urealyticum (mycoplasma genitalium)
  • trichomonas vaginalis
    etc.
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56
Q

What is the incubation period in NGU?

A

1-2 weeks

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57
Q

How is NGU diagnosed?

A
  • currently NAAT for chlamydia

formerly enzyme immunoassay:EIA/ELISA

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58
Q

How is NGU treated?

A
  • doxycycline

- macrolides eg. erythromycin, azithromycin

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59
Q

Describe the chlamydia trachomatis bacteria

A
  • obligate intracellular pathogen
  • gram-negative
  • ovoid in shape and non-motile
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60
Q

Chlamydia trachomatis has a unique lifestyle that includes which 2 stages?

A
  • extracellular infectious form = elementary body

- intracellular replicative form = reticulate body

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61
Q

What are the target cells for chlamydia trachomatis?

A
  • squamo-columnar epithelial cells of endocervix/upper genital tract in females
  • conjunctiva, urethra and rectum in males and females
  • also respiratory tract cells in infants
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62
Q

Which age groups have highest rates of chlamydia?

A
  • women = 16-19

- men = 20-24

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63
Q

What is the prevalence of chlamydia in the UK?

A
  • 16-44yr olds: 1.5% of sexually experiences females, 1.1% males
  • 16-24yr olds: 3.1% of females, 2.3% males
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64
Q

Who is screened (ie. asymptomatic) for chlamydia in the National Chlamydia Screening Programme?

A

All sexually active under 25 year olds, annually, or on change of partner

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65
Q

What happens if somebody tests positive for chlamydia?

A

They are treated and then re-tested 3 months post-treatment (10-15% will be positive due to new/re-acquisition or very rarely, treatment failure)

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66
Q

What else is important in positive chlamydia tests?

A

Partner notification

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67
Q

What are the symptoms of chlamydia?

A
  • often asymptomatic (female more than male)
  • urethritis (but less purulent discharge than gonococcal)
  • cervicitis (mucopurulent)
  • dysuria/frequency (a cause of “acute urethral syndrome” - sterile pyuria on standard urinalysis)
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68
Q

What do you see at the cervix in chlamydia cervicitis?

A
  • cervical friability (easily irritated and inflamed and can bleed)
  • oedema
  • ectopy
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69
Q

What are the complications associated with chlamydial infection?

A
  • pelvic inflammatory disease (PID)
  • epididymitis (2%)
  • complications in neonate/infant
  • conjunctivitis
  • Reiter’s syndrome
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70
Q

How often does PID occur in chlamydia?

A

Over 9.5% within one year, without treatment

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71
Q

When PID occurs in chlamydia, what other complications can it be related to?

A
  • perihepatitis (spread of infection from PID)
  • tubal infertility (10.6% of PID)
  • ectopic pregnancy
  • chronic pain
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72
Q

What problems in the neonate/infant can chlamydia cause?

A
  • conjunctivitis (later onset than with N. gonorrhoeae - 5-12 days)
  • infant pneumonia (usually present at 4-11 weeks)
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73
Q

Chlamydia can cause Reiter’s syndrome. What is this characterised by?

A
  • arthritis
  • conjunctivitis
  • urethritis
  • skin lesions
74
Q

How is chlamydia diagnosed?

A
  • histology: inclusion bodes (elementary bodies)
  • cell culture
  • NAAT (superseded EIA)
  • serology (limited value in most oculogenital infections)
75
Q

What is the sensitivity and specificity in NAAT for chlamydia?

A

Sensitivity: - cervix = 81-100%

  • urine female = 80-96%
  • urine male = 90-96%

Specificity = 99.7%

76
Q

How is chlamydia usually treated?

A
  • azithromycin 1g PO single dose
    OR
  • doxycycline 100mg BD for 7 days
77
Q

How is paediatric chlamydia treated?

A

Conjunctivitis/pneumonia: erythromycin for 14 days

Treat parents as well

78
Q

What is pelvic inflammatory disease (PID)?

A

An infection of the female upper genital tract, including the uterus, fallopian tubes and ovaries

79
Q

How does PID affect fertility?

A

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

80
Q

What is used in PID diagnosis?

A
  • diagnostic difficulties

- laparascopy

81
Q

Name 2 most common infective agents causing pelvic inflammatory disease

A
  • N. gonorrhoeae (30% of patients also have chlamydia)

- C. trachomatis

82
Q

There are over 100 HPV types. How many ‘high-risk’ types are there?

83
Q

The 12 high-risk HPV types are causally associated with what?

A

Cervical cancer - causing 1000 death in UK each year

84
Q

What are the low-risk HPV types associated with?

A

Not associated with cancer but cause warts (genital and other)

85
Q

Name 2 low-risk HPV types and what they cause

A

HPV 6, HPV 11 - 90% genital warts

86
Q

Name 2 high-risk HPV types and what they cause

A

HPV 16, HPV 18 - 70% cervical carcinomas (also some oesophageal cancers)

87
Q

What does cervarix (GSK) vaccinate against?

A

Bivalent vaccine (HPV 16 and 18)

88
Q

What does gardasil (MSD) vaccinate against?

A

Quadrivalent vaccine (HPV 6, 11, 16, 18)

89
Q

What is condylomata accuminata?

A

An epidermal manifestation attributed to HPV eg. warts

90
Q

How are genital warts treated?

A
  • burning, freezing or cutting
  • imiquimod cream
  • podophyllin
  • salicylic acid
  • trichloracetic acid
  • liquid nitrogen
91
Q

What causes genital herpes?

A

Herpes simplex types 2 and 1

  • double-stranded DNA viruses
  • HSV-2 more common in women than men
92
Q

What are the symptoms of genital herpes?

A
  • pain
  • itching
  • dysuria
  • vaginal/urethral discharge
  • bilateral vesicles/ulcers - viral shedding
  • accompanied by constitutional symptoms
93
Q

What can cause reactivation of latent HSV infection?

A
  • local trauma
  • menstruation
  • stress
94
Q

How is genital herpes diagnosed?

A
  • clinical
  • PCR (HSV 1 or 2)
  • histology
95
Q

How is genital herpes treated?

A
  • acyclovir

- consider suppression if frequent recurrence

96
Q

What are the complications associated with genital herpes?

A
  • dissemination
  • meningitis
  • encephalitis
  • sacral nerve parasthesiae
  • urinary retention
97
Q

Where does HSV reside when latent?

A
  • sensory neurone cells - sacral nerve ganglia
98
Q

Which organism causes syphilis?

A

Treponema pallidum (a spirochaete - helically coiled, thin)

99
Q

Describe treponema pallidum (cause of syphilis)

A

Slender, helical, tightly coiled cells

  • too thin for light microscopy
  • cannot be readily culture in vivo
100
Q

How does treponema palladium penetrate?

A

Through intact mucous membranes of via abraded skin

101
Q

How does treponema palladium disseminate?

A

Disseminated within days via lymphatics/bloodstream - causing subsequent clinical symptoms and signs

102
Q

What is the characteristic sign of syphilis on histology?

A

Obliterative endarteritis - severe proliferating inflammation of intima causing occlusion of lumen

  • concentric endothelial/fibroblastic proliferation
  • microscopic vascular compromise
103
Q

What is obliterative endarteritis caused be?

A

Radiation poisoning, TB meningitis or a syphilis infection

104
Q

What is the incubation period for syphilis?

A

Median 21 days

105
Q

What is usually the first sign/symptom of syphilis?

A

A chancre - a painless indurated lesion that occurs at the site of inoculation - heals spontaneously within 3-6 weeks

106
Q

What is the secondary phase of syphilis?

A

Most florid phase - 2-8 weeks post onset of chancre

107
Q

What are the skin symptoms in syphilis?

A
  • rash
  • condylomata lata
  • mucous patches
108
Q

Describe the rash in syphilis

A
  • macular/maculopapular

- on the trunk, limbs - palms and soles

109
Q

Describe condylomata lata in syphilis

A

Wart-like lesions - tend to occur in warm body areas

  • erythematous plaques
  • highly infectious
110
Q

What are “mucous patches” that occur in the secondary phase of syphilis?

A

Silvery-grey erosions on mucous membranes

111
Q

What are the constitutional symptoms that occur in syphilis?

A
  • fever
  • malaise
  • weight loss
112
Q

Other than skin manifestations and constitutional symptoms, what are the other symptoms of the secondary phase of syphilis?

A
  • generalised lymphadenopathy (may include epitrochlear)

- CNS involvement (40%) - headache and meningismus

113
Q

What is meningism?

A

Triad of:

  • nuchal rigidity
  • photophobia
  • headache
114
Q

What happens after the secondary phase of syphilis?

A
  • spontaneous resolution after 3-12 weeks
  • latent = no clinical manifestation but positive serology
  • without treatment, 30% will develop tertiary syphilis (late syphilis)
115
Q

Tertiary (late) syphilis may present as neurosyphilis which includes what symptoms?

A
  • meningovascular (hemiplegia, seizures)

- parenchymatous: general paresis (cortex) and tabes dorsalis (spinal cord)

116
Q

What does general paresis in tertiary syphilis cause?

A
  • personality changes

- Argyll Robertson pupils: accomodate to near vision by reducing in size, but don’t react to light (don’t constrict)

117
Q

What is tabes dorsalis? (happens in tertiary/late syphilis)

A

Demyelinsation of the posterior column, dorsal roots, dorsal root ganglia. Therefore loss of sense in proprioception, vibration and discriminative touch

  • ataxic wide-based gait
  • lightening pains in legs
118
Q

What are the cardiovascular manifestations of tertiary/late syphilis?

A
  • aortitis
  • aortic regurgitation
  • saccular aneurysm
119
Q

What is a gumma?

A

Soft, non-cancerous growth resulting from the tertiary stage of syphilis. It is a form of granuloma (late benign syphilis)

  • non-specific granulomatous reaction
120
Q

Where do gummas affect?

A

Any organ eg. liver. Most commonly bone/skin/soft tissue

121
Q

What is congenital syphilis caused by?

A

In-utero transmission

122
Q

What is the greatest risk congenital of syphilis?

A

Spirochaetaemia of early syphilis

123
Q

What are the early signs of congenital syphilis?

A
  • snuffles
  • rash
  • hepatosplenomegaly
124
Q

What are the late signs of congenital syphilis?

A
  • frontal bosses
  • saddle nose
  • sabre shins
  • Hutchinson’s incisors
125
Q

How is syphilis diagnosed?

A

Direct detection:

  • dark field microscopy
  • PCR (more sensitive than microscopy)

Indirect tests: serology

126
Q

What is dark field microscopy? (used in the diagnosis of syphilis)

A

Excludes the unscattered beam from the image. As a result, the field around the specimen (i.e., where there is no specimen to scatter the beam) is generally dark

127
Q

What are the 2 groups of serology tests used in syphilis diagnosis?

A
  • specific

- non-specific

128
Q

Describe the specific serology test for syphilis

A
  • anti-treponemal antibodies (EIA, TPHA, FTA)
  • sensitive and specific
  • but won’t zero-convert post treatment
129
Q

Describe the non-specific serology test for syphilis

A
  • reaginic antibodies versus lipoidal antigens
  • VDRL, RPR (rapid plasma reagin) tests
  • false positives, but usually sero-convert post successful treatment - can monitor with titres
130
Q

How is syphilis treated?

A

Penicillin-based antibiotics

- length and route (IM/IV) depends on stage and site

131
Q

What is the Jarish-Herxheimer reaction? (classical in penicillin treatment of syphilis)

A

A reaction to endotoxin-like products released by the death of harmful microorganisms within the body during antibiotic treatment - commonest in secondary stage syphilis

  • release of heat-stable protein
132
Q

What are the symptoms of the Jarish-Herxheimer reaction?

A
  • fever
  • chills
  • myalgia

Usually self-limiting

133
Q

What are the alternative antibiotics that can be used in syphilis treatment?

A
  • amoxicillin
  • ceftriaxone
  • doxycycline
134
Q

What is trichomoniasis caused by?

A

Trichomonas vaginalis

135
Q

What type of organism is trichomonas vaginalis?

A

Anaerobic, flagellated protozoan parasite

- lacks mitochondria (has hydrogenosome)

136
Q

How is trichomonas vaginalis transmitted?

A

Trophozoite transmitted, no known cyst

Humans are the only natural host

137
Q

What are the symptoms of trichomoniasis?

A

Profuse greenish frothy vaginal discharge and mucosal inflammation

138
Q

How is trichomoniasis diagnosed?

A

Microscopy/culture (high vaginal swab)

139
Q

What is used to treat trichomoniasis?

A

Metronidazole

140
Q

Can males get trichomoniasis?

A

Yes but usually asymptomatic, but may have urethritis, and may be a source of re-infection

141
Q

What is BV?

A

Bacterial (anaerobic) vaginosis

142
Q

In what way is the balance of bacteria inside the vagina disrupted in bacterial vaginosis?

A
  • reduced vaginal lactobacilli

- increased gardnerella vaginalis and anaerobes

143
Q

What are the signs and symptoms of bacterial vaginosis?

A
  • watery discharge
  • positive KOH test (10% KOH - fishy odour)
  • clue cells on microscopy
144
Q

What are clue cells?

A

Epithelial cells of the vagina that get their distinctive stippled appearance by being covered with bacteria - seen in bacterial vaginosis

145
Q

How is bacterial vaginosis treated?

A
  • metronidazole
  • amoxicillin
  • topical clindamycin
146
Q

What is candidiasis? eg. thrush, balanitis

A

A fungal infection due to any type of candida (a type of yeast)

147
Q

What factors can cause candidiasis?

A
  • oral contraceptives
  • poorly controlled diabetes-
  • antibiotics (inhibition of normal flora)
  • bowel source
  • sexual transmission
148
Q

What are the signs and symptoms of candidiasis? (thrush/balanitis)

A
  • vulval, vaginal and penile erythema - itching and irritation
  • thick/adherent discharge, white plaques
  • maculopapular and fissuring lesions
149
Q

How is candidiasis diagnosed?

A
  • clinical

- microscopy (10% KOH) and/or culture

150
Q

Which candida causes 80-90% of cases of candidiasis?

A

Candida albicans

151
Q

How is uncomplicated candidiasis treated? (C. albicans, not recurrent, not severe)

A
  • topical agents eg. clo-trimazole (Canesten)

- fluconazole: single 150mg oral dose

152
Q

How is complicated candidiasis treated?

A
  • treatment for 10-14 days (topical or oral)
  • obtain in vitro sensitivities
  • consider treatment of partner(s)
  • long-term suppressive treatment if frequent recurrence
153
Q

AIDS was first recognised in the US how and in what year?

A

1981

  • unexplained opportunistic infections, including pneumocystis jirovecii pneumonia (PcP) and Kaposi’s syndrome in homosexual men
  • loss of CD4 lymphocytes/immunosuppression
154
Q

HIV is what type of virus?

A

Retrovirus - possesses reverse transcriptase

155
Q

What is the role of RNA dependent DNA polymerase in HIV?

A

Converts viral RNA into linear ds DNA

- subsequently incorporated into host genome

156
Q

Formation of DNA from RNA in HIV is error prone. What does this mean?

A

High rate of mutability

157
Q

What do the different characteristics of the HIV virus allow it to do?

A
  • RNA-based = survival advantage, great genetic diversity
  • DNA intermediary = latency and can incorporate into host genome
  • CD4/macrophage tropic = reduction of host immune response
158
Q

What are the routes of HIV transmission?

A
  • sexual-transmission at genital or colonic mucosa
  • exposure to infected fluids (blood/blood products), including accidental occupational exposure
  • mother to infant
159
Q

Describe the process of HIV viral entry and incorporation into genome

A
  • viral glycoprotein gp120 interacts with cellular receptor CD4 and chemokine receptor CCR5 for virion to gain host cell entry
  • reverse transcription occurs in the cytoplasm
  • dsDNA imported into nucleus = integration into cell genome, and latency/immune evasion
160
Q

Which glycoprotein on HIV is important for viral entry into the host cell?

161
Q

Which receptors on the host cell are important for HIV entry into the cell?

A
  • CD4 cellular receptor

- CCR5 chemokine receptor

162
Q

dsDNA from HIV is imported into the host cell nucleus. What advantages does this have for the virus?

A
  • integration into cell genome

- latency and immune evasion

163
Q

What is there a loss of in HIV infection?

A

CD4+ve T cells

164
Q

What does the depletion of CD4+ve T cells in HIV allow?

A

Opportunistic infections = organisms not normally pathogenic in immune competent patients

  • risk of different infections related to degree of immune suppression (CD4 count)
165
Q

In HIV, there is rapid emergence of viral mutants. What does this result in?

A
  • may promote immune evasion

- drug resistance

166
Q

What are the clinical effects of HIV infection?

A

Very wide range from asymptomatic carriage to life-threatening opportunistic infection

Either directly due to virus or indirectly due to opportunistic infection/malignancy

167
Q

The WHO classification of HIV is based on what?

A

CD4 cell count

168
Q

Describe the classification system for HIV

A 
stage 1 = less than 500 cells/μL
stage 2 = 349-499 
stage 3 = 200-349
stage 4 (AIDS) = less than 200
169
Q

AIDS is defined as having a CD4+ T cells count of what?

A

Less than 200 cells/μL

170
Q

What is acute retroviral syndrome?

A 
Occurs in primary HIV infection
- fever
- pharyngitis
- lymphadenopathy 
- rash
etc.
171
Q

What are the early symptomatic signs of HIV?

A
  • pulmonary TB
  • persistent oral candidiasis
  • unexplained chronic diarrhoea for more than 1 month
  • unexplained persistent fever over 37.6 for more than one month
  • severe bacterial infections eg. S pneumoniae bacteraemia
172
Q

What should you do in all new TB cases?

A

Consider HIV test

173
Q

What are some of the opportunistic infections/conditions that occur in AIDS?

A
  • HIV wasting syndrome, HIV encephalopathy
  • oesophageal candidiasis
  • pneumocystis jirovecii penumonia
  • CMV disease
  • CNS toxoplasmosis
  • progressive multifocal leukoencephalopathy (PML)
  • extra-pulmonary cryptococcosis
  • disseminated non-tuberculosis mycobacterial disease-
  • extra-pulmonary tuberculosis
  • chronic cryptosporidiosis; chronic isosporiasis
  • Kaposi’s sarcoma
  • lymphoma (cerebral or non-Hodgkin’s)
174
Q

How do undiagnosed cases of HIV affect transmission?

A
  • 25% of cases in UK undiagnosed
  • account for approximately 70% of transmission
  • new case rates doubled in past 10 years
175
Q

When should you suspect HIV?

A
  • in the case of risk factors

- unusual/recurrent/recalcitrant infections

176
Q

How is HIV diagnosed?

A
  • antibody testing (sero-conversion) - confirm with second sample
  • PCR
  • CD4 cell count
177
Q

Why is PCR used in diagnosing HIV?

A
  • detects viral nucleic acid
  • quantitative: viral copy numbers “viral loads” in blood and other fluids
  • genotypic mutations conferring drug resistance
178
Q

Which different drugs are used in HIV treatment? (that target critical steps in viral replication cycle)

A
  • nucleoside/nucleotide reverse transcriptase inhibitors eg. zidovudine, lamivudine
  • non-nuceloside reverse transcriptase inhibitors eg. efavirenz
  • protease inhibitors eg. ritonavir, saquinavir
  • viral entry inhibitors
  • integrase strand transfer inhibitors
179
Q

Why are combinations of drugs used in HIV?

A
  • to prevent resistance mutations emerging

Be careful of drug interactions and side effects

180
Q

What is HAART?

A

Highly active antiretroviral therapy

9. CP - Diseases of the Reproductive System (5 decks)

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