STI III Flashcards

1
Q

Syphilis epidemiology and transmission

A

Causative organism: Treponema pallidum subspecies pallidum (also written as Treponema pallidum subsp. pallidum):

  • does not grow in cell-free cultures so have to do PCR
  • often cultured in tissue culture using epithelial cells
  • they lack to ability to synthesise growth factors
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2
Q

Syphilis transmission

A
  • Sexually transmissible
  • Bacteria enter the skin via abrasions and can invade mucous membranes
  • Can also spread to the fetus (congenital syphilis) or by transfusion with contaminated blood*
  • Does not appear to be spread via fomites (inanimate objects like towels, etc)
  • Syphilis is characterised by three phases: *primary, secondary *and tertiary (late)
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3
Q

Primary syphilis

A
  • Generally only one lesion (papule) develops (10-90 days) after initial infection*
  • Lesion develops at the point of entry of bacteria
  • Papule soon after erodes into a painless ulcer with raised borders
  • If untreated, the ulcer generally heals spontaneously (2-8 weeks) but the disease is still progressive
  • Note: the patient is infectious
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4
Q

Secondary syphilis

A

This is the disseminated stage of the the disease. Patients typically show intiial flu-like syndrome:

  • Sore throat
  • Headache
  • Fever
  • Myalgias (muscle pain)
  • Anorexia (loss of apetite)
  • Lymphadenopathy (enlarged lymph nodes)
  • Mucocutaneous rash involving the entire body, including the palms and soles

​If untreated at this stage, rash and symptoms generally resolve in a few weeks and patient tners the ‘clinically inactive/asymptomatic/latent’ stage of the disease

  • Note: the patient is infectious in the second stage of the disease
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5
Q

Tertiary syphilis

A

‘Late’ syphilis

If disease is not treated earlier, a tertiary stage usually develops (after 5-30 years after initial infection) in about 30-40% of patients. In tertiary stage the disease symptoms and signs are grouped into:

  • Neurosyphilis: seizures, changes in personality, slurring speech, pupillary disturbances (Argyll Robertson pupils)
  • Cardiovascular syphilis: predilection for destruction of the ascending aorta
  • Gummatous syphilis: lesions on skin, bones, mucous membranes
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6
Q

Congenital syphilis

A

Fetus infected during pregnancy leading to multi-orgam malformations, or death.

Infants who survive initial stage of disease often present with:

  • Hutchinson’s teeth
  • Saddle nose
  • Sabre shins
  • Intellectual disabilities
  • Blindness
  • Cardiovascular syphilis
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7
Q

Laboratory diagnosis syphilis

A

Syphilis cannot be cultivated in vitro.

  • Dark-field microscopy of exudates from skin lesions - not really used in TAS.
  • PCR: swab from base of the lesion
  • Treponema-pallidum particle agglutination (TP-PA) test: gelatin particles containing *T. pallidum *antigens are mixed with patient serum; if antibodies are produced by patient, the particles agglutinate.
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8
Q

Bacterial vaginosis epidemiology

A
  • A phenomenon initially observed in sexually active women
  • Usually associated with new or multiple sex partners
  • Most noted in women who have sex with women; individuals (source/partner) eventually share the same cohort of vaginal flora.
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9
Q

Bacterial vaginosis pathophysiology

A
  • This is not well understood.
  • Microscopic examination of vaginal discharge reveals a predominant flora of coccobacilli (gram negative rods)
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10
Q

Causative organisms for bacterial vaginosis

A
  • Gardnerella vaginalis* (facultative G –ve anaerobe)
  • Prevotella
  • Megasphaera
  • Coriobacterineae
  • Lachnospira
  • Sneathia
  • Mycoplasma hominis*
  • Ureaplasma urealyticum*

It is not just one bacteria - it is a whole cohort of gram negative organisms. When pH changes during sexual intercourse, Lactobacilli die, and their place is taken over by these organisms.

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11
Q

Bacterial vaginosis differential diagnosis

A

Women with bacterial vaginosis are at increased risk of infection by HSV-2, N. gonorrhoeae, and C. trachomatis

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12
Q

Bacterial vaginosis clinical manifestations

A
  • Homogenous vaginal discharge
  • ‘Fishy’ vaginal odor, most notably
    • During menstruation
    • After sexual intercourse
  • Minimal itching or irritation
  • Associated with an increased ris of:
    • Salpangitis
    • Post partum fever and post partum endometritis
    • Premature labour and delivery
    • Chorioamnionitis
    • Increased risk fo UTI
    • PID
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13
Q

Diagnosis for bacterial vaginosis

A
  1. Homogenous vaginal discharge
  2. Vaginal pH greater than 4.6 (normally 3.5-4.5)
  3. Positive ‘whiff’ test (amines are volatile at increased pH); in the lab, odour is detected by mixing vaginal discharge samples with 10% KOH
  4. Presence of ‘clue’ cells (epithelial cells coated with bacteria)

At least 3 of the 4 criteria must be met for the diagnosis.

Gram stain: should show reduced numbers of lactobacilli.

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14
Q

Trichomonas vaginalis epidemiology

A

T. vaginalis, a parasitic protozoan is a common cause of vaginitis in women of all ages. WHO estimates infection by T. vaginalis accounts for 50% of all curable infections worldwide.

Its presence is often also seen as a marker of risky sexual behaviour, and is commonly found with other STIs, like gonorrhoea.

In men, it may cause urethritis BUT it is more often asymptomatic*

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15
Q

Trichomonas vaginalis clinical manifestations in women

A

In women, the squamous epithelium of the vagina is infected, resulting in micro-ulceratiosn via direct contact with the organism.

The incubation period is 4-28 days before:

  • ‘frothy’ vaginal discharge (50-75%)
  • Pruritis (23-82%)
  • Dysuria (30-50%)
  • Lower abdominal discomfort (5-12%)
  • Colpitis mascularis (strawberry cervix)

Possible complications: premature rupture of membranes; preterm delivery

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16
Q

trichomonas vaginalis clinical manifestations in men

A

This is becoming a recognised cause of NGU (non-gonococcal urethritis?).

Rarely causes:

  • Epididymitis
  • Prostatitis
  • Penile ulceration
17
Q

Trichomonas vaginalis laboratory diagnosis

A
  • Microscopic examination of the vaginal fluid
  • pH > 4.5
  • Positive ‘whiff’ test
  • PCR - useful to some degree but not necessary
18
Q

Klebsiella granulomatis epidemiology

A

K. granulomatis is an encapsulated, pleomorphic, gram negative bacillus (can be found in the cytoplasm of mononuclear cells - WBCs).

Causes Donovanosis. This is a chronic, progressive ulcerative disease of the genital region.

Notably a cause of genital ulceration in:

  • India
  • Papua New Guinea
  • Carribean
  • South America
  • Parts of Africa (Zambia, South Africa, Zimbabwe)
  • South East Asia
  • Amounst Aboriginal and Torres Strait Islander populations

Hence, it is important to take a travel history.

19
Q

Donovanosis clinical manifestations

A
  • Primary lesion is usually small, painless papule
  • After an incubation period of 8-80 days, the lesion ulcerated producing a ‘beefy’ red ulcer with rolled edges that bleeds on contact.
  • Disease then spreads subcutaneously resulting in tissue destruction*

In men, most common sites are:

  • Prepuce
  • Corona
  • Penile shaft

In women:

  • Labia
  • Rarely, vaginal wall and cervix
  • Oral lesions (?) - history of oral-genital contact
20
Q

Diagnosis of Donovanosis

A

Diagnosis is usually made on clinical manifestations. Confirmation is proven by:

  • Histological examination of biopsies/scrapings taken from the edge of the active lesion
  • Demonstration of ‘donovan’ bodies is the gold reference standard
  • Culture of K. granulomatis in monocytes and hep-2 cells
  • PCR and DNA extracted from the biopsy material (i.e. specific for the *phoE *gene of the organism)
21
Q

Candida albicans epidemiology and transmission

A
  • This is part of the norma flora of women
  • Is the cause of approximately 80-90% of vulvovaginal cadidiasis in patients
  • Estimated that 75% of adult women will suffer at least one episode of vulvovainal candidiasis during their lifetime
  • Carriage rates are higher in women using oral contraceptives
  • Imuno-insufficiency also predisposes to overgrowth/infection
  • Transmission is poorly understood. What we do know is that
    • Colonisation increases with onset of sexual activity
    • Having multiple partners does not appear to increase incidence of infection in women.
22
Q

Clinical manifestations of vulvovaginal candiditis

A
  • Perivaginal pruritis
  • Vulvar irritation
  • Dysuria
  • Abnormal (candidal) discharge is usually thick and adherent (‘cottage cheese’)
23
Q

Diagnosis of Candida albicans vulvovaginal cadidiasis

A
  • Vaginal pH is usually nromal (pH 3.8-4.5)
  • No odour on ‘whiff’ test
  • Microscopic examination of vaginal material show yeast cell or hyphal forms
  • Culture of vaginal material
24
Q

Classification of vulvovaginal cadidiasis

A

Uncomplicated infection

  • Sporadic or infrequent
  • Mild to moderate severity
  • Likely to be caused by Candida albicans
  • Patient is not immunocompromised

Complicated infection

  • Recurrent infection (4 or more episodes a year)
  • Severe infection
  • Caused by non-albicans species of Candida
  • Uncontrolled diabetes, debilitation, immunosuppression, or pregnancy