STIs Flashcards
1
Q
First line treatment for gonorrhoea
A
- 500mg IM ceftriaxone plus 1g azithromycin
- Same for genital, rectal, and pharyngeal infections
- Azithromycin added for:
- Cover against chlamydia co-infection
- Increasing resistance against ceftriaxone monotherapy
2
Q
Microbiology, epidemiology, pathophysiology of syphilis:
A
- Bacteria Treponema pallidum
- Can be seen with darkfield microscopy - cork-screw shaped organism with tightly wound spirals
- Cases rising - MSM disproportionately affected (with high rate of HIV co-infection in MSM)
- Transmission → direct contact with an infectious lesion during sexual intercourse
- Readily crosses the placenta → foetal infection
Pathophysiology
- Can’t grow on culture
- Early local infection → gains access to SC tissues via microscopic abrasions, evades host immune responses to establish initial ulcerative lesion (chancre) and establish infection in local draining lymph nodes → dissemination
- Late infection → prolonged latent period, waning immunity with age may facilitate recrudescence of treponemes that survived in sequestered sites, or a partially immune hypersensitive host may react to the presence of treponemes, engendering a chronic inflammatory response. Gummas develop - granulomas (cellular hypersensitivity reaction). Cardiovascular syphilis → vasculitis of the vasa vasorum, small vessel vasculitis - affecting ascending arch of the aorta and aortic valve
3
Q
Stages of syphilis and clinical manifestations:
A
-
Early syphilis
- Primary and secondary syphilis (weeks to months after infections)
- Early latent syphilis (asymptomatic infection acquired within previous 12 months in USA (2 years everywhere else)
-
Late syphilis
- Late latent disease (untreated disease, asymptomatic) OR
- Tertiary syphilis - develop major complications of infection
- Can occur anytime from 2-30 years after initial infection. Neurosyphilis can manifest at anytime during course of infection
Clinical manifestations
- Primary → Chancre (incubation approx. 21 days) at site of innoculation, can get multiple in the setting of HIV - heal spontaneously within 3-6 weeks
- Secondary → weeks to months after initial infection, 25% develop systemic illness - constitutional symptoms, adenopathy, rash → (diffuse, symmetrical, macular/papular trunk/extremeties, palms and soles involved usually a clue), condylomata mata (see picture) - mouth, perineum and often proximate to primaru ulcer, alopecia, GI → hepatitis, GI ulceration, MSK → synovitis, Renal → albuminuria, nephrotic syndrome, acute nephritis, Neuro → headache, meningitis, cranial nerve defects, stroke, Visual → ocular syphilis → uveitis (underappreciated, more common with HIV)
-
Late syphilis → 25-40% patients with late syphilis
- Cardiovascular → ascending thoracic aorta - dilated aorta and AR - dissection of syphilitic aneursyms rare. Aortitis
- Gummatous syphilis → very uncommon, can occur anywhere, granulaoms - on skin may present as ulcers. Visceral gummas can present as a mass lesion
- CNS - meningovascular, parenchymatous, tabes dorsalis
4
Q
Transmission risk of syphilis
A
- Primary, secondary or early latent disease may be infectious to recent sexual partners (early latent disease may transmit through lesions that were recently active but no longer present)
- Late latent disease not considered infectious to recent sexual contacts - don’t have lesions that can transmit disease
- Pregnancy → can transmit to foetus for up to four years after acquisition
5
Q
Who should be tested for syphilis
A
- Symptomatic individuals (note wide range of presenting symptoms)
- Rash - diffuse symmetric macular or papular eruption involving trunk and extremeties or rash that involves the palms and soles
- Also neuro symptoms
- Asymptomatic patients:
- Pregnant women
- Patients with a sexual partner with early syphilis
- MSM
- HIV
- High risk sexual behaviours
- History of incarceration or commercial sex work
6
Q
Tests for syphilis:
A
- Screening → T. pallidum enzyme immunoassay (EIA) - detects both IgM and IgG antibodies. Once positive remains positive.
- Positive → TPHA/TPPA and VDRL/RPR to confirm diagnosis
- TPPA/TPHA → confirms infection. Remains positive longterm
- RPR - non-treponemal test → indicates disease activity. Semi quantitative → gives a titre which can be used to monitor response to treatment. Can get false +ve in HIV, pregnancy, SLE, malignancy. Equivalent to VDRL (used mostly for CSF now)
7
Q
Treatment of syphilis
A
- Early infection → Benpen IM once
- Late infection → 3x doses benpen weekly
- CNS involvement inc. otic/ocular → 2.4g benpen IV Q4H for 10-14 days
- Ceftriaxone or doxycycline alternatives with penicillin allergy
8
Q
Jarisch-Herxheimer reaction
A
- Acute febrile reaction within 24 hours of antibiotic commencement in patients with spirochetes infections
- Systemic symptoms - headache, myalgias, rigors, hypotension
- Uncommon: meningitis, respiratory distress, renal/hepatic dysfunction, mental status changes
- Thought to be inflammatory response to dying organisms
- Occurs in 10-35%, particularly secondary syphilis
- Usually self-limited
- Other infections: Lyme, leptospirosis
9
Q
Monitoring of syphilis post-treatment
A
- Early syphilis - monitor RPR at 6 and 12 months
- Late syphilis - monitor RPR at 6, 12, 24 months
Re-infection more common than treatment failure with penicillin based regimens
10
Q
Notes on syphilis in pregnancy
A
- Crosses placenta at all stages
- Early syphilis almost always 100% fatal to foetus - needs to be treated urgently
Congenital syphilis
- In-utero death or still birth
- Major organ failure
- Skin lesions
- Inflammation or deformed bones/teeth
- Developmental delay
11
Q
Syphilis and HIV co-infection
A
- CD4 < 350 and RPR > 32 predict CSF changes on LP
- ?LP - only if neuro/ocular symptoms
- No evidence for different treatment
- Follow up → note re-infection rate high
Prophylaxis
- Some evidence that doxycyline can reduce syphilis acquisition if taken with PREP following unprotected sexual intercourse
12
Q
HSV Virology and Epidemiology
A
Virology
- DNA virus
- Penetrates susceptible mucosa of broken skin - transported to sacral ganglia along peripheral nerve axons → latent phase. Lifelong reservoir, never clears
- DNA replicates → translation viral proteins → transport back down the axon to mucosa → ulcer or shedding blips
- Sheeding more frequent than previously recognised - at least 17 days of asymptomatic shedding, more frequent in 1st year following infection
Epidemiology
- Most common etiology of genital ulcers
- 1/5 infected NZ
- F>M
- Majority due to HSV2, trend over last few years of HSV1 causing genital infection
- Transmission → contact with mucosa/epithelial surface or person who is shedding or in genital/oral secretions
- Autotransmission to other sites is possible
13
Q
Clinical features of HSV
A
First episode
- 25% will have a positive HSV2 antibody test (= not true primary infection - previously asymptomatic acquisition)
Primary genital infection
- First infection with absence of antibody
- Severe, multiple bilateral genital ulcers, pain, itching, dysuria, vaginal or urethral discharge, tender inguinal lymphadenopathy
- Systemic symptoms - fevers, headaches, aseptic meningitis or symptoms of autonomic dysfunction (urinary retention) - peak within 3-5 days onset of lesions and gradually recede over 3-4 days
- Can last 14-21 days without antivirals
- Women: Cervicitis possible
- Herpes proctitis → severe anal ulceration, some develop symptoms of autonomic dysfunction including urinary retention
- Infection of urethra may cause clear mucoid discharge
Recurrent infection
- Usually shorter, milder, unilateral lesions resolve within 3-5 days.
- No systemic symptoms
- Most have prodromal symptoms (localised tingling, burning)
- HSV 2 - decreases after 1st year, 3-4 episodes/year
- HSV1 - 1 episode a year
- 80% seropositive for HSV2 never received a diagnosis of genital HSV (asymptomatic or very mild disease) → main source of propagating the infection
14
Q
Complications of HSV infection
A
- Aseptic meningitis
- Radicular pain
- Sacral paresthesias
- Transverse myelitis
- autonomic dysfunction
- Rectal pseudotumour
- Dissemintated viraemic infection
- Fulminant hepatitis
Associated with HIV acquisition - risk factor for acquiring and transmitting HSV
15
Q
Diagnosis of HSV
A
- Viral cell HSV culture or nucleic acid amplification methods (PCR assays for HSV DNA) - preferred for ulcers.
- Vesicles need to be deroofed and the base of the ulcer swabbed to obtain adequate cells for viral culture or PCR
- Serology - IgG only, no IgM role in HSV
