Sexual health Flashcards
Herpes simplex virus (HSV)
HSV-1 & HSV-2 infections generally manifest with oral, genital and ocular ulcers
seroprevalence for HSV is high with >90% of the population worldwide having detectable antibodies
NB HSV-1 usually oral, HSV-2 usually genital
transmission of Herpes simplex virus (HSV)
transmission via direct contact with mucosal tissue / secretions of infected individual or perinatal transmission (more common with HSV-2)
Presentation of Herpes labialis (cold sores)
prodrome (~24h) of tingling, burning or pain
recurring erythematous vesicles that turn into painful ulcerations on oral mucosa /lips
Presentation of genital herpes
painful genital ulceration ± dysuria & pruritis
usually presents as single/disseminated red bumps/white vesicles found around genitalia / anus
may have tender lymphadenopathy
NB primary infection is usually more severe and may present with systemic features such as fever, headache, malaise
Investigations for Herpes simplex virus (HSV) infection
cold sores are usually a clinical diagnosis
genital herpes usually requires nucleic acid amplification test (NAAT) or PCR
HSV serology may be used in asymptomatic pts, those with recurrent/atypical ulcers or to distinguish HSV types
Management of Cold sores
generally symptomatic management
consider topical choline salicylate gel or lidocaine or topical aciclovir (not recommended)
NB infection control is key e.g. don’t touch lesions, avoid kissing & oral sex
Management of genital herpes
Refer to GUM clinic
general:
saline bathing, analgesia, topical anaesthetics e.g. lidocaine
oral acyclovir/valaciclovir (within 5 days of symptom onset)
consider suppressive antiviral therapy with acyclovir daily if >6 attack per year)
Genital herpes in pregnancy
elective C-section if genital herpes at >28 weeks, & give suppressive therapy in the form of acyclovir if recurrent attacks
When to consider suppressive therapy for genital herpes
consider suppressive antiviral therapy with acyclovir daily if >6 attack per year)
Syphilis
A predominantly sexually transmitted infection caused by the spirochaete bacterium Treponema pallidum
more common in men especially those who have sex with men (MSM)
incubation period of 10-90 days
Window period for syphilis
12 weeks
Window period
the window period for a test designed to detect a specific disease (particularly infectious disease) is the time between first infection and when the test can reliably detect that infection. In antibody-based testing, the window period is dependent on the time taken for seroconversion.
Presentation of primary syphilis
local lesion at site of infection (NB often not seen in women as it may be on cervix)
small painless papule rapidly forms under and ulcer (the chancre), usually single, round/oval PAINLESS surrounded by bright red margins
resolves spontaneously within 3-6 weeks
may have regional (usually inguinal) non tender lymphadenopathy
Presentation of secondary syphilis
~6-10 weeks after primary infection
systemic symptoms of fever, malaise, lymphadenopathy, hight time headaches, aches
Rash: generalised polymorphic rash on palms/soles/trunk, reddish brown or copper colour, non pruritic
Buccal snail track ulcers
condylomata lata (board based, wart like smooth white papular erosions usually found in moist & warm areas e.g. genitalia)
NB rash on soles/palms = pathomemonic
Presentation of tertiary syphilis
3 distinct clinical syndromes that may co-exist
Cardiovascular syphilis:
characterised by aortitis (usually of aortic root), ascending aortic aneurysm
manifests with aortic regurgitation, angina & aortic aneurysms
Gummata:
chronic destructive granulomatous lesions with necrotic centres that tend to ulcerate, can occur in any organ
usually seen in skin/bones
Neurosyphilis:
dorsal column loss (tabes dorsalis = impaired proprioception, broad based gait, ataxia, absent reflexes), dementia (general paralysis of the insane), Argyll Robertson pupil (bilateral miosis, pupils accommodate but pupillary light reflex is absent)
Cardiovascular syphilis
characterised by aortitis (usually of aortic root), ascending aortic aneurysm
manifests with aortic regurgitation, angina & aortic aneurysms
Gummata
chronic destructive granulomatous lesions with necrotic centres that tend to ulcerate, can occur in any organ
usually seen in skin/bones
Tertiary syphilis
Neurosyphilis
CNS invasion causing inflammatory reaction of the meninges/cerebral parenchyma
dorsal column loss (tabes dorsalis = impaired proprioception, broad based gait, ataxia, absent reflexes)
dementia (general paralysis of the insane)
Argyll Robertson pupil (bilateral miosis, pupils accommodate but pupillary light reflex is absent)
managed with IM/IV benzathine pencillin for 10-14 days
Congenital syphilis presentation
blunted upper incisors (hutchinson's teeth) mulberry molars linear scars at angle of mouth keratitis saber shins saddle nose deafness hepatomegaly jaundice sensorineural hearing loss
Effects of in utero syphilis
miscarriage
stillbirth
hydrops fetalis
Investigating syphilis
Treponemal specific antibody tests:
e.g. treponema enzyme immune assay (EIA), T.pallidum particle agglutination test (TPPA), T.pallidum hem agglutination test (TPHA) etc
stay +ve after treatment
Non treponema specific:
anticardiolipin antibodies
-ve after treatment, insensitive for advanced syphilis
screen for other STIs
dark field microscopy (for T. pallidum)
Management of syphilis
1st line: single dose IM bezathine penicillin (alternatives = azithromycin / doxycycline)
Neurosyphilis = IM/IV benzathine pencillin for 10-14 days
Jarisch-Herxheimer reaction
ruction to treatment, after 1st dose
acute febrile illness with headache, myalgia, riggers, tachycardia
generally self resolved in 24h
Syphilis causative organism
spirochaete bacterium Treponema pallidum
Lymphogranuloma venereum
An STI caused by the L1/L2/L3 serovars of chlamydia trachomatis, its an infection of mononuclear phagocytes
generally endemic to the tropics but now appearing in local outbreaks in europe
NB majority of pts in the west are HIV +ve
Lymphogranuloma venereum causative organism
L1/L2/L3 serovars of chlamydia trachomatis
Lymphogranuloma venereum (LGV) vs Chlamydia causative organisms
LGV: L1/L2/L3 serovars of chlamydia trachomatis
Chlamydia: D-K serovars of chlamydia trachomatis
Risk factors for Lymphogranuloma venereum (LGV)
MSM
unprotected sex
receptive/insertive anal intercourse
multiple sexual partners
Presentation of Lymphogranuloma venereum (LGV)
Primary:
small painless genital pustules that form painless ulcers & heal in a couple of days
Secondary:
~3 weeks after exposure, painful inguinal/pelvic/perirectal lymphadenopathy (may form fistulating buboes)
Tertiary:
up to 20 yrs after infection, proctocolitis (anal itching, bloody mucopurulent anal discharge, rectal pain, constipation)
granuloma mucosa & enlarged nodes on DRE
Investigation of Lymphogranuloma venereum (LGV)
nuclear acid amplification tests (NAATs) with swabs from anogenital lesions/rectal mucosa/lymph node specimen
STI testing
colonoscopy/rectal biopsy may be needed for anal symptoms
Management of Lymphogranuloma venereum (LGV)
Doxycycline (100mg BD for 21 days)
Buboes may require surgical drainage)
Chlamydia
A common STI caused by chlamydia trachomatis servars D-K
refers to chlamydia genitourinary infections
Most prevalent STI in the UK
Chlamydia
most common in sexually active people <25y/o
Risk factors for chlamydia
age <25 ≥ 2 sexual partners in previous year recent change in sexual partners no barrier contraception infection with other STIs poor socioeconomic status
Presentation of chlamydia in females
70% asymptomatic
cervicitis (discharge, bleeding)
deep dyspareunia, dysuria, vague lower abdo pain
intermenstrual/postcoital bleeding
friable inflamed cervix
pelvic adnexal tenderness & cervical excitation
NB always consider chlamydia asa cause of sterile pyuria
Presentation of chlamydia in males
50% asymptomatic
urethritis (dysuria, urethral discharge)
epididymo-orchitis (unilateral testicular pain ± swelling)
proctitis (perianal fullness)
fever
Investigating chlamydia
NAAT of vulvovaginal swab (women) or first void urine sample (men)
2 week window period
Window period for chlamydia
2 weeks
Complications of chlamydia
Reactive arhtirits (common cause of post STI reactive arthritis)
PID
Infertility (especially in females)
Fitz-Hugh-Curtis syndrome (Perihepatitis i.e. inflammation of the liver capsule, due to transabdominal spread of PID which presents with RUQ pain, nausea, vomiting)
Human papillomavirus (HPV) (focus on genital warts)
Genital warts are the most common form of viral genital mucosal lesions and are caused by infection with HPV type 6 / 11
most common viral STI in UK
Human papillomavirus (HPV) serotypes causing warts
6 & 11
Fitz-Hugh-Curtis syndrome
Perihepatitis i.e. inflammation of the liver capsule, due to transabdominal spread of PID
violin string like adhesions from peritoneum to liver
presents with RUQ pain, nausea, vomiting
pain may refer to R shoulder
Most common viral STI in UK
Human papillomavirus (HPV)
Risk factors for genital warts
smoking multiple sexual partners history of STIs (20% of pts with warts have other STIs) unprotected intercourse immunosuppression
NB: consistent condom usage majorly ↓ risk fo warts
Presentation of Genital warts (HPV)
single or multiple lesions which may forma confluent mass
usually 1-5mm discrete smooth exophytic papillomas which may be slightly pigmented (broad based or pedunculated)
may bleed or itch
usually found in vulva/anal/cervical region in women
usually found around foreskin/glans/shaft/urethral/anal regions in men
Investigations for genital warts (HPV)
speculum exam in women
proctoscopy (if unreceptive sex)
biopsy & viral testing (if uncertain diagnosis or treatment resistance)
Genital warts in children
discovery of genital warts in children should prompt consideration of sexual abuse unless clear evidence of mother-to-child transmission at birth / non sexual transmission from another household memeber
Prevention of HPV
HPV vaccination with Gardasil (quadrivalent covering type 6,11,16,18)
given to all boys & girls aged 11-13
Management of genital warts (HPV)
education & STI screening
assess current partner + all partners in previous 6 months
1st line: Podophyllotoxin (topical) or cryotherapy
2nd line: topical imiquimod 5%
majority clear without treatment in 1-2 yrs
recurrence common, in 20-30%
Genital warts in children
discovery of genital warts in children should prompt consideration of sexual abuse unless clear evidence of mother-to-child transmission at birth / non sexual transmission from another household member
Prevention of HPV
HPV vaccination with Gardasil (quadrivalent covering type 6,11,16,18)
given to all boys & girls aged 11-13
Treatment of genital warts in pregnancy
Treatment of choice = cryotherapy
Imiquimod & Podophyllotoxin = contraindicated in pregnancy
Molluscum contagiosum
a common localised viral infection caused by the molluscum contagiosum virus a member of the poxviridae family
most often seen in children but if seen in adults often due to sexual contacts
spreads via close personal contact or indirectly via formites e.g. contaminated towel
Presentation of Molluscum contagiosum
characteristic pinkish/pearly white papule with a central umbilication, usually found in clusters (anywhere on body except palms & soles)
if sexually transmitted often seen in genitalia/pubis/thighs/lower abdomen
lesions on face/eyelids/oral mucosa rare (usually seen with immunosuppressed pts)
Investigation of Molluscum contagiosum
usually clinical diagnosis
consider HIV testing if widespread/facial/lesions in adults
Management of Molluscum contagiosum
generally no treatment needed, self limiting, usually resolves within 18month
self care advice ie.e. avoid scratching, don’t share towels, use condoms if genital lesions
if troublesome symptoms = imiquimod 5% or cryotherapy
refer to specialist if HIV+ve, widespread lesions, or if eyelid/occular infection
Scabies
a parasite skin infestation caused by sarcoptes scabiei mites which is primarily spread by close ski to skin contact
outbreaks are known to occur in hospitals, prisons, residential/nursing hoes
Risk factors for scabies
overcrowding poverty poor nutritional status homelessness poor personal hygiene institutionalisation dementia sexual contact immunosuppression children
Presentation of scabies
Infected contacts may be asymptomatic for 3-4weeks
intense widespread pruritis:
worse at night, may have history of itch in close contacts
excortication (scratching) marks are common
greyish/silvery linear burrow on side of fingers / interdigital webs / flexor aspects of wrist
± erythematous papules / vesicular lesions
Investigations for scabies
largely clinical diagnosis
histological examination of skin scrapping = confirmatory
Management of scabies
treat whole household & close physical contacts at same time even if asymptomatic
1st line: permethrin 5%
2nd line: malathion 0.5%
General:
avoid close with contacts with others until treatment complete
launder/iron/wash clothing/bedding to kill mites
NB pruritis may persist for 4-6 weeks post treatment
Crusted (Norwegian) scabies
hyper infestation with thousands of mites seen in those with immunosuppression e.g. HIV
presents with hyperkeratotic crusted lesions on hands/feet/scalp/nails ± lymphadenopathy
treatment of choice = Ivermectin & isolation of individual
Gonorrhoea
An STI caused by the bacteria Neisseria gonorrhoea that leads to genitourinary tract infections such as urethritis, cervicitis, PID, epididymitis
Gonorrhoea
An STI caused by the Gram-negative diplococcus Neisseria gonorrhoea that leads to genitourinary tract infections such as urethritis, cervicitis, PID, epididymitis
transmission is via direct inoculation of infected secretions from one mucous membrane to another usually via sexual contact
Window period for gonorrhoea
2 weeks
Risk factors for gonorrhoea
young age history of previous STI new/,multiple partners recent sexual activity abroad history of drug use commercial sex work MSM
Presentation of gonorrhoea in women
endocervical (asymptomatic or PV discharge ± lower abdo pain)
urethral (dysuria but no frequency)
Rectal (asymptomatic)
pharyngeal (asymptomatic)
Presentation of gonorrhoea in men
urethritis (discharge ± dysuria)
Rectal (usually asymptomatic or discharge ± perianal pain & pruritis)
pharyngeal (asymptomatic)
epididymal (unilateral scrotal pain & swelling)
Investigations for gonorrhoea
NAAT (endocervical smear in women, first pass urine in men)
2 week window period
other STI screen & GUM
Management of gonorrhoea
1st line: IM ceftriaxone 1g single dose
2nd line: 500mg ceftriaxone IM + oral azithromycin (NB this is 1st line inpregancy) or 400mg PO cefixine + azithromycin 2g (e.g. if needle phobic)
test of cure (NAAT) at 2 weeks post treatment + partner notification (STI screen + empirical Abx)
Complications of gonorrhoea
PID infertility Fitz-Hugh-Curtis syndrome septic arthritis (most common cause of optic arthritis in young sexual active people) Disseminated gonococcal infection
Disseminated gonococcal infection (DGI)
due to haematogenous spread of infection
rare (~1%)
characterised by tenosynovitis, migratory polyarthritis, dermatitis (maculopapular/vesicular rash on trunk & extremities), fever
later endocarditis, perihepatitis, septic arthritis
IV ceftriaxone for 7 days is treatment of choice
Vaginal candida (thrush)
A very common yeast infection of the lower female reproductive tract, ~80% are caused by candida albicans
peak incidence age 20-40
~80% of women have candida vulvovaginitis at some point in their life
Causative organism for thrush
~80% are caused by candida albicans
Risk factors for thrush
pregnancy diabetes mellitus vaginal foreign body immunosuppression (e.g. HIV) imbalance of local flora e.g. from Abs use steroid use
Presentation of thrush
erythematous vuvla & vagina pruritis vulvae vulval soreness white, crumbly, sticky vaginal discharge (like cottage cheese), typically non offensive / odourless superficial dyspareunia dysuria
Investigations for thrush
clinical examination / no swabs required vaginal pH (normal, i.e. <4.5)
NB if complicated infection then take swabs for culture/sensitivity/microscopy
Management fo thrush
1st line: clotrimazole pessary
2nd line: oral itraconazole / fluconazole
NB in pregnancy only local treatment (creams/pessaries) may be used
Management of recurrent vaginal candidiasis
i.e. if ≥4 episodes in a year
high vaginal swab to confirm diagnosis with MC&S
check for diabetes
consider maintenance treatment e.g. PO fluconazole
Vaginal candidiasis in pregnancy
Oral Treatments e.g. oral itraconazole / fluconazole are contraindicated
only pessaries or creams e.g. clotrimazole pessary may be used
Trichomonas vaginalis
a very common STI caused by trichomonad vaginalis, a flagellated protozoa parasite
in adults its almost exclusively sexually transmitted
MOST common curable STI worldwide
Presentation of trichomonas vaginalis in women
foul smelling frothy yellow/green purulent discharge with offensive odour
vulval pruritis
dysuria
offensive odour PV
lower abdo pain
cervicitis (strawberry cervix i.e. erythematous mucosa with petechiae)
Presentation of trichomonas vaginalis in men
usually asymptomatic
common cause of non-gonoccocal urethritis
dysuria & discharge
Investigations for trichomonas vaginalis
vaginal pH (↑, pH >4.5) high vaginal swab (NAAT if available = test of choice otherwise saline wet mount = mobile trophozoites & multiple flagella, if wet mount inconclusive = culture)
Management of trichomonas vaginalis
contact tracing & further STI screening
1st line: PO metronidazole for 5-7 days
2nd line: single dose PO metronidazole
NB treat both sexual partners at same time & avoid intercourse until 1 week after treatment
Bacterial vaginosis (BV)
describes an overgrowth of predominantly aerobic organisms such as Gardnerella vaginalis leading to a consequent fall in lactic acid producing lactobacilli leading to ↑ vaginal pH
almost exclusively seen in sexually active women (but not and STI, only sexually associated)
Risk factors for Bacterial vaginosis (BV)
sexual activity new sexual partner previous STIs afro-carribbean women use of IUD vaginal douching bubble baths receptie oral sex smoking
Presentation of Bacterial vaginosis (BV)
often asymptomatic
offensive, fishy smelling vaginal discharge, usually are/milky clear
pruritus & pain = uncommon
Protective factors for Bacterial vaginosis (BV)
circumcised partner
condom use
COCP (oestrogen encourages lactobacilli)
Investigations for Bacterial vaginosis (BV)
vaginal pH (↑, pH>4.5) whiff test (addition of KOH = fishy odour) microscopy of discharge (clue cells - epithelia cells with stippled appearance)
Amsel criteria for diagnosis (3/4 of the following)
- thin white homogenous discharge
- vaginal pH >4.5
- positive whiff test (addition of potassium hydroxide = fishy odour)
- clue cells in microscopy
Management of Bacterial vaginosis (BV)
advice on vaginal hygiene e.g. avoid douching
if asymptomatic:
no treatment unless pregnant
if symptomatic:
PO metronidazole for 5-7 days
Bacterial vaginosis (BV) in pregnancy
↑ risk of preterm labour, low birth weight, chorioamnionitis, later miscarriage
use oral metronidazole for 5-7 days even if asymptomatic
Amsel criteria
For diagnosis of bacterial vaginosis
3/4 of the following
- thin white homogenous discharge
- vaginal pH >4.5
- positive whiff test (addition of potassium hydroxide = fishy odour)
- clue cells in microscopy
Non gonococcal urethritis (NGU)
inflammation of urethral mucosa the can be caused by carious pathogens, this term is reserved for men
usually an STI
this is used to describe the presence of urethritis in the absence of gonococcal bacteria on the first swab
Causative organism for Non gonococcal urethritis (NGU)
chlamydia trachomatis (most common)
myelopsama genitalium
trichomonas vaginalis
Most common form of urethritis
Non gonococcal urethritis (NGU)
Presentation of urethritis
usually asymptomatic if gooccocal
mucopurulent discharge ± blood, urethral pruritus, dysuria, penile discomfort
burning/itching of urethral meatus
NB generalised symptoms are rare and should rase suspicions
Investigations for urethritis
first pass urine or urethral smear/swab NAAT
consider urine dipstick to exclude UTI
STI screening
Management of urethritis
NGU:
doxycycline BD for 5-7 days or 1g azithromycin stat
Gonococcal urethritis:
IM ceftriaxone ± azithromycin PO
Complications of urethritis
epididymitis/orchitis
prostatitis
systemic dissemination of gonorrhoea
reactive arthritis
Epididymo-orchitis
an infection/inflammation of the epididymis & the testes usually caused by local spread of a genitourinary tract infection or bladder infections
Aetiology of Epididymo-orchitis
Men <35yrs:
STI e.g. chlamydia & gonorrhoea
Men >35yrs:
UTIs e.g. E. coli & pseudomonas
Unvaccinated children:
mumps
Presentation of Epididymo-orchitis
unilateral scrotal pain & swelling
pain radiating to ipsilateral flank
if STI related may have urethritis or urethral discharge
NB mumps usually presents with headache, fever, unilateral/bilateral parotid swelling
Important differential for Epididymo-orchitis
Testicular torsion:
usually acute, severe unilateral testicular pain & swelling., absent cremaster reflex
usually pts <20y/o
treat Epididymo-orchitis as testicular torsion until proven otherwise
Investigations for Epididymo-orchitis
exclude STI (first pass urine NAAT)
if mumps suspected = IgG/IgM serology
urine MC&S
scrotal USS
Management of Epididymo-orchitis
If organism as per organism
e.g. ceftriaxone for gonorrhoea or doxycycline for chlamydia
if unknown organism:
500mg ceftriaxone IM + 100mg doxycycline PO
Chancroid
primarily sexually transmitted infection caused by fastidious gram-negative coccobacilus Haemophilus ducreyi, generally a tropical disease &more common in men
important co factor for HIV transmission
Causative organism of chancroid
Haemophilus ducreyi
Presentation of chancroid
4-10 days incubation period
small (1-2cm) painful, shapely demarcated genital ulcers with ragged, undermined edges & a greyish necrotic base
unilateral lymphadenopathy (usually inguinal)
Distinguishing chancroid from syphilis chancre
chancre in syphilis = not painful
chancroid = painful
Investigating chancroid
usually clinical diagnosis
gram stain / culture of ulcer swabs
Management of chancroid
azithromycin or ceftriaxone
Pelvic inflammatory disease (PID)
compromises a spectrum of inflammation & infection of the upper female genital tract including the uterus, fallopian tubes, ovaries, surrounding tissue
usually secondary to ascending infection from the endocervix
most common cause of infertility
Aetiology of pelvic inflammatory disease
often polymicrobial
most common causes include chlamydia trachomatis & Neisseria gonorrhoea
other causes include gardenella vaginalus, mycoplasma hominis
Risk factors for pelvic inflammatory disease
multiple sexual partners unprotected sex history of previous STIs IUD termination of pregnancy
Presentation of pelvic inflammatory disease
lower abdo pain deep dyspareunia cervical excitation dysuria menstrual irregularities vaginal discharge fever adnexal / cervical motion tenderness
Investigating pelvic inflammatory disease
pregnancy test to exclude ectopic pregnancy
high vaginal / cervical swab
Chlamydia & Gonorrhoea screen
ESR/CRP (↑)
Management of pelvic inflammatory disease
Oral ofloxacin + metronidazole / IM ceftriaxone + metronidazole
consider IUD removal
Complications of pelvic inflammatory disease
Perihepatitis (Fitz-Hugh-Curtis syndrome)
infertility
ectopic pregnancy
Infectious mononucleosis (glandular fever)
a usually self limiting infection caused by Epstein-Barr virus (EBV) which is a human herpes virus (HHV 4)
most frequently seen in teenagers & young adults
Presentation of Infectious mononucleosis
Classic triad of sore throat, pyrexia, lymphadenopathy (in anterior/posterior neck triangles)
malaise, headache, splenomegaly, hepatitis, lymphocytosis, haemolytic anaemia
maculopapular pruritic rash (in 99% of pts taking ampicillin/amoxicillin whilst having the disease)
Investigating Infectious mononucleosis
monospot antibody test (+ve, specific for EBV antibodies)
FBC (lymphocytosis, atypical lymphocytosis)
LFTs (AST & ALT ↑)
heterophiles antibody test (+ve)
Management of infectious mononucleosis
avoid contact sports for 8 weeks to ↓ risk of splenic rupture
simple analgesia e.g. paracetamol
avoid alcohol
generally self limiting in 2-4 weeks
Fraser competency
The Fraser guidelines are used to assess if patient who has not yet reached 16 years of age is competent to consent to treatment, for example with respect to contraception
The following points should be fulfilled:
1) the young person understands the professional’s advice
2) the young person cannot be persuaded to inform their parents or allow the professional to contact them on their behalf
3) the young person is likely to begin, or continue having, sexual intercourse with or without contraceptive treatment
4) unless the young person receives contraceptive treatment, their physical or mental health, or both, is likely to suffer
5) the young person’s best interests require them to receive contraceptive advice or treatment with or without parental consent
Important points about Fraser competency
its a legal obligation to discuss the value of parental support
children under the age of 13 are considered to be unable to consent for sexual intercourse & hence a consultation regarding this age group should automatically trigger child protection measures
Child <13y/o & contraception
children under the age of 13 are considered to be unable to consent for sexual intercourse & hence a consultation regarding this age group should automatically trigger child protection measures
Contraceptive of choice in young people
Progesterone only implant (Nexplanon)
Aims of partner notification
treatment of those infected / screening those at risk
↓ re-infection in your pt
preventing onward transmission (i.e. breaking chain of infection)
preventing complications of untreated infections
opportunity to educate & discuss behavioural change
Type of partner notification
Patient referral:
pt contacts partners themselves
Provider referral:
partner is contacted by clinic (usually health advisor), source pt is not identified
Contractual referral:
in complex situations there may be a mutual agreement of a timeline i.e. if the pt has not unformed the partner by a set date then the clinic will
Follow up after partner notification
generally pt & partner contacted 1-2 weeks later ti check if treatment was complete, sex has been abstained from, all contact have been accounted for
Look back period for partner notification
look back period generally 3-6 months
may be longer e.g. secondary syphilis
all contacts in look back period should be informed regardless of condom use
Hormone replacement therapy (HRT)
the use of low dose oestrogen + progesterone (in a women with a uterus) to alleviate menopausal symptoms
Indications for HRT
vasomotor symptoms e.g. flushing/insomnia/headaches
premature menopause (continue unti age 50, main aim to prevent osteoporosis)
Types of HRT
in women with uterus = oestrogen + progestogen
in women without uterus = only oestrogen
give continuous combined regime if amenorrhoea >12 months/sequential HRT received for >12 months
give sequential combined regimes if amenorrhoea <12 months
Compounds used in HRT
natural oestrogens e.g. estradiol / estrone are used over synthetic oestrogens e.g. ethinylestradiol
synthetic progesterones e.g. levonogestrel are generally used
Adverse effects of HRT
↑ Risk of breast cancer (further ↑ risk if taking progesterone)
↑ Risk of endometrial cancer (give progesterone in addition to oestrogen in women with a uterus to reduce this risk)
↑ risk of VTE (Transdermal route does not ↑ risk of VTE)
↑ risk of stroke
↑ risk of IHD (if taken >10yrs after menopause)
Side effects of HRT
nausea
breast tenderness
fluit retention
weight gain
Emergency contraception
forms of contraception that can be administered within a specific time period after unprotected sexual intercourse (UPSI) to prevent pregnancy
Intrauterine device / copper coil as emergency contraception
insert within 5 days of UPSI (or if >5 days post UPSI may be inserted up to 5 days after likely ovulation date)
can be left in for longer contraception, but if removal is wanted then wait until next menstrual period
Time window after UPSI the intrauterine device can be used as emergency contraception
insert within 5 days of UPSI
or if >5 days post UPSI may be inserted up to 5 days after likely ovulation date
Levornogestrel (Levonelle) emergency contraception
effective up to 72h post UPSI
single dose 1.5mg (double if BMI>26 / weight >70kg)
repeat dose if vomiting within 3h
can be used >1x per menstrual cycle
can commence hormonal contraception immediately after use
Time window after UPSI Levornogestrel (Levonelle) can be used as emergency contraception
effective up to 72h post UPSI
Ulipristal (EllaOne) emergency contraception
effective up to 120h post UPSI
single 30mg dose
may ↓ effectiveness of hormonal contraception (start/restart hormonal contraception 5 days after taking EllaOne)
repeat dose possible in same menstrual cycle
Time window after UPSI Ulipristal (EllaOne) can be used as emergency contraception
effective up to 120h post UPSI
Combined oral contraceptive pill (COCP)
Examples: Microgynon, Logynon, Qlaira and Zoely
MOA: inhibits ovulation
Risks include: ↑ VTE/stroke risk, ↑ risk of breast cancer, ↑ risk of cervical cancer
Advantages include: ↓risk of endometrial cancer, ↓ risk of ovarian cancer, ↓ risk of colorectal cancer
generally taken for 21 days then 7 day pill free window with withdrawal bleed but can tricycle i.e. take packets back to back to avoid bleeding
Combined oral contraceptive pill (COCP) contraindications
>35y/o + smoking >15 cigarettes/day migraine with aura breastfeeding <6 weeks postpartum current breast cancer previous VTE/thrombogenic mutation
starting the Combined oral contraceptive pill (COCP)
start within 5 days of start of cycle = no extra precautions needed
if started later in cycle = use additional contraception for 7 days
Missed pills Combined oral contraceptive pill (COCP)
1 pill missed:
take missed pill i.e. 2 pills in 1 day and continue as normal
≥ 2 pill missed:
take last missed pill i.e. 2 at the same time then continue as normal
missing pill in:
Week 1: consider emergency contraception if unprotected sex in pill free break/week 1
Week 2: no need for emergency contraception
Week 3: finish current packet & omit pill free window
Combined oral contraceptive pill (COCP) and surgery
discontinue 4 weeks before elective surgery, offer progestogen only contraceptive as alternative
NB does not apply to minor surgery
Advantages of Combined oral contraceptive pill (COCP)
↓risk of endometrial cancer
↓ risk of ovarian cancer
↓ risk of colorectal cancer
Disadvantages of Combined oral contraceptive pill (COCP)
↑ VTE/stroke risk
↑ risk of breast cancer
↑ risk of cervical cancer
Progesterone only pill (POP)
Examples: Desogestrel, Norethisterone
MOA: thickens cervical mucous (desogestrel also inhibits ovulation)
should be taken at same time everyday (>3h late = missed pill), no pill free interval
irregular vaginal bleeding = most common side effect
Starting Progesterone only pill (POP)
immediate protection if commenced within 5 days of starting cycle
if started after day 5 of cycle take 2 days of additional contraception
Missed pills Progesterone only pill (POP)
Missed pill = pill >3h late (>12h for Desogestrel)
if pill missed = take pill ASAP (i.e. 2 in one day) & continue with rest of packet, use additional contraception until regular pill taking reestablished for 48h
Injectable contraceptive
Examples: depo provera
MOA: inhibits ovulation & thickens cervical mucous
duration: 12 weeks (cannot be reversed once given)
contraindications: current breast cancer
side effects include irregular bleeding, ↑ weight*, ↑ risk of osteoporosis
Contraceptive method proven to cause weight gain
Injectable contraceptive (depo provera)
Implantable contraceptive
Examples: Implanon, Nexplanon
MOA: inhibits ovulation & thickens cervical mucous
Duration: 3 years
contraindications: current breast cancer
side effects: irregular bleeding or heavy bleeding
Implantable contraceptive implant site
subdermal implantation into proximal non-dominant arm just overlying the triceps
Intrauterine device (IUD)
Copper coil
MOA: prevent fertilisation & toxic to sperm (spermicidal)
Duration: 5-10 years (depends on type)
effective immediately after insertion
side effects: periods tend to be heavier, longer & more painful, ↑ risk of PID, expulsion
Intrauterine system (IUS)
Examples: Mirena coil, Jaydess, Kyleena
MOA: inhibits implantation & prevents endometrial proliferation
Duration: 5 years (Jaydess = 3 years)
effective 7 days after insertion
many pts have infrequent bleeding & spotting early on before menses becomes lighter or absent
NB can be used as endometrial protection (progesterone component) of HRT
Combined contraceptive patch
Examples: Evra patch
similar to COCP, 4 week cycle, wear patch every day for first 3 weeks and change weekly, then no patch during 4th week leading to withdrawal bleed
If patch changed delayed at end of week 1/2
if <48h: put on new patch immediately and continue
if >48h: change patch immediately + 7 days of barrier contraception, consider emergency contraception if sex during window where patch wasn’t changed or in last 5 days
forgetting patch at end of patch free week = 7 days of additional contraception
Post partum contraception time window
women require contraception from 21 days post partum
Lactational amenorhoea
contraceptive method in post partum period
if women fully breastfeed (no supplementary feeds), amenorrhoeic & <6 months post partum
Types of post partum contraception
Lactational amenorhoea
POP (can bed started any time post partum even if breastfeeding)
COCP (contraindicated in breast feeding & <6 weeks post partum)
IUD/IUS ( can be inserted within 48h of birth or at 4 weeks postpartum)
Epilepsy & contraception
UKMEC 3 for COCP & POP is people taking lamotrigine, phenytoin, carbamazepine, barbiturates, topiramate
Contraception in women aged >40
No method of contraception is solely contraindicated by age
Women aged <50yrs & contraception
Hormonal contraception can be continued till age 50
non hormonal contraception methods can be stopped after 2 yrs amenorrhoea
Women aged >50yrs & contraception
non hormonal methods can be stopped after 1yr of amenorrhoea
COCP (switch to non-hormonal or progestogen only contraceptive)
Depo-provera (switch to non hormonal method, stop after 2 yrs of amenorrhoea, or switch to progestogen only contraceptive)
Implant/POP/IUS (continue use, if amenorrhoeic check FSH & stop 1 year after if FSH ≥30u/L or stop at age 55)
Hepatits A virus (HAV)
virus spread by faecal oral route, may be sexually transmitted in MSM or seen in IVDU
2-4 week incubation period
Most common form of acute hepatitis
Presentation of Hep A
prodrome:
mild flu like symptoms (fever, malaise, joint pain) ± RUQ pain, tender hepatomegaly
Icteric phase:
jaundice, pruritus, dark urine, pale stools, abdo pain
Investigations for Hep A virus (HAV)
IgM antibody to HAV (+ve from symptoms onset to 3-6 months after)
IgG antibody to HAV (+ve for several years, if only IgG = post infection or vaccination)
LFTs (↑ AST, ↑ALT, ↑ALP)
Bilirubin (↑)
Management of Hep A
usually self limiting, only needing supportive care
Vaccination available for high risk individuals e.g. MSM or IVDU
Hepatits B virus (HBV)
viral infection spread by sexual contact, parentally or perinatally
incubation period 6-20 weeks
most common cause of hepatitis world wide
Presentation of Hep B
acute infection often subclinical with flu like symptoms
symptomatic hepatitis: fever, skin rash, nausea, jaundice, RUQ pain
chronic help B:
detectable surface antigen (HBsAg) >6 months
nausea, fatigue, poor ppetute, non specific abdo pain, ↑ risk of hepatocellular carcinoma
Hep B serology
Surface antigen (HBsAg): implies acute disease (present 1-6 months)
Anti-HBs: implies immunity (either due to exposure or chronic infection)
Anti-HBc:
previous / current infection (i.e. negative if immunised)
HBeAg:
marker if HBV replication & infectivity
Management of Hep B
notify health protection unit
1st line: pegylated interferon
Prevention:
Hep B vaccination at 2,3 & 4 months of age + at risk groups e.g. IVDU/healthcare workers/sex workers
Hep B & pregnancy
Hep B routinely screened for
if chronic/acute infection in mother = full vaccination course + Hep B immunoglobulin for Baby
Immunisation of Hep B on serology
anti-HBs +ve only
Previous Hep B infection but not carrier on serology
anti HBc +ve
HBsAg -ve
Previous Hep B infection now carrier on serology
anti HBc +ve
HBsAg +ve
Acute Hep B infection on serology
anti-HBc +ve (especially IgM kind)
Hepatitis C virus (HCV)
virus that may be transmitted via sexual intercourse, especially high risk of HIV confection
incidence rising in UK
no vaccine available
Hep C presentation
acute infection generally asymptomatic
chronic disease generally mild & unspecific but ↑ risk of HCC, cirrhosis, cryglobulinaemia
Hep C investigations
HCV RNA test (gold standard)
NB if +ve for >6months = chronic Hep C
anti-HCV antibodies to check for previous infection
Hep C management
combination of protease inhibitors ± ribavirin
Human Immunodeficiency virus (HIV)
a retrovirus that targets & destroys CD4 T cells and is the etiological agent of acquired immunodeficiency syndrome (AIDS)
Types: HIV 1 (responsible for global epidemic) HIV 2 (restricted to africa)
Epidemiology of HIV
HIV diagnosis peaked in 2014 in UK, has been declining since
affects ~38million people globally
Routes of transmission of HIV
sexual (~80% of infections worldwide)
parenteral
vertical transmission from mother to child (during birth/breastfeeding)
Risk factors for HIV infection
needle sharing for IVDU unprotected receptive anal intercourse unprotected receptive penile-vagnial intercourse needle stick injury high maternal vial loads MSM
Pathophysiology of HIV infection
HIV enters body & attaches to CD4 receptors on target cells with its gp120 glycoprotein
viral envelop fuses with host cell using coreceptor CCR5/CXCR4
viral RNA is transcribed into dsDNA by viral reverse transcriptase & then integrated into the DNA by viral integrase
genomic RNA is used to replicate virus
viron repurposes part of cell membrane as envelope & lead cell = cell death & release of virons to infect more cells
Window period for acute HIV infection
4 weeks
Acute primary HIV infection (seroconversion illness)
1-6 weeks post infection
presents with fever, malaise, myalgia, pharyngitis, headaches, diarrhoea, neuralgia, neuropathy, lymphadenopathy, fatigue
maculopapular rash
NB antibody test generally negative but viral P24 antigen & HIV RNA ↑
Time between infection with HIV & seroconversion illness
1-6 weeks
tests for HIV seroconversion illness
HIV antibody test -ve
Viral p24 antigen ↑
HIV RNA ↑
Clinical latency stage of HIV
asymptomatic stage after acute seroconversion illness
generally low viral loads & normal CD4/CD8 count
may persist for 8-10 yrs
Symptomatic HIV stage (latency stage)
non specific constitutional symptoms e.g. fever, night sweats, diarrhoea, weight loss
Non-AIDS defining conditions (CD4 count <500cells/mm3)
e.g. chronic subfebrile temperature, persistent generalised lymphadenopathy, chronic diarrhoea (>1 month)
localised opportunistic infection e.g. oral candida, oral hairy leukoplakia, HPV related lesion (warts, SCC of anus), tine infections
Acquired immunodeficiency syndrome (AIDS)
a person developing serious opportunistic infections or disease as a result their damaged immune system from advanced symptomatic HIV (stage 3)
severe immunodeficiency
CD4 count generally <200 cell/μL
Persistent generalised lymphadenopathy
enlargement of ≥2 non contigous lymph node groups for >6 months usually non tender
sign of symptomatic HIV infection
Oral candida
may be a sign of symptomatic HIV infection
creamy white patches in the mouth that can be scrapped off, may be tender, erythematous
pt may have cotton feeling in mouth
redness, soreness, fissuring may occur at angle of mouth
managed with topical solutions or oral fluconazole
Oral hair leukoplakia
may be a sign of symptomatic HIV infection
triggered by EBV, similar to oral candida, creamy white patches in mouth but unlike candida they cannot be scrapped off
CDC classification of HIV
1993 CDC classification of HIV in adults stages according to CD4 count & clinical category
CD4 count: normal: 500-1500 cells/mm3 category 1: ≥500 cells/mm3 category 2: 200-499 cells/mm3 category 3: <200 cells/mm3
Clinical category
Category A: asymptomatic infection, persistent generalised lymphadenopathy (PGL) or acute HIV infection
Category B: symptomatic HIV i.e. HIV indicator conditions
Category C: AIDS defining conditions
NB categories A3,B3,C1,C2,C3 has AIDS
Category A of CDC classification of HIV
asymptomatic infection, persistent generalised lymphadenopathy (PGL) or acute HIV infection
Category B of CDC classification of HIV
symptomatic HIV i.e. HIV indicator conditions e.g. oral candida/ oral hairy leukoplakia, chronic diarrhoea
Category C of CDC classification of HIV
AIDS defining conditions e.g. oesophageal candidiasis, Kaposi sarcoma etc
CD4 count ranges for CDC classification of HIV
normal: 500-1500 cells/mm3
category 1: ≥500 cells/mm3
category 2: 200-499 cells/mm3
category 3: <200 cells/mm3
AIDS defining conditions
- Candidiasis of the esophagus, bronchi, trachea, or lungs
- Cervical cancer, invasive
- Coccidioidomycosis, disseminated or extrapulmonary
- Cryptococcosis, extrapulmonary
- Cryptosporidiosis, chronic intestinal (greater than one month’s duration)
- Cytomegalovirus disease or CMV (other than liver, spleen, or nodes)
- Cytomegalovirus retinitis (with loss of vision)
- Encephalopathy, HIV related
- Herpes simplex: chronic ulcer(s) (more than 1 month in -duration); or bronchitis, pneumonitis, or esophagitis
- Histoplasmosis, disseminated or extrapulmonary
- Isosporiasis, chronic intestinal (more than 1 month in duration)
- Kaposi sarcoma
- Lymphoma, Burkitt’s (or equivalent term)
- Lymphoma, immunoblastic (or equivalent term)
- Lymphoma, primary, of brain
- Mycobacterium avium complex or M kansasii, disseminated or extrapulmonary
- Mycobacterium tuberculosis, any site (pulmonary or extrapulmonary)
- Mycobacterium, other species or unidentified species, disseminated or extrapulmonary
- Pneumocystis pneumonia (PCP)
- Pneumonia, recurrent
- Progressive multifocal leukoencephalopathy
- Salmonella septicemia, recurrent
- Toxoplasmosis of brain
- Wasting syndrome due to HIV
Investigations for HIV
HIV antibody detection (ELISA)
FBC (anaemia, thrombocytopenia, lymphocytopenia, ↓CD4 count)
check other infections (TB/Hep B/CMV/toxoplasma/syphillis/varicella)
STI screening
baseline CXR
cervical smear
Diagnosis of HIV
based on anti-HIV antibodies in serum (IgG/IgM antibodies against HIV virus)
should be positive
Diagnosis fo acute HIV infection
anti-HIV antibodies may not be present
HIV PCR & p24 antigen tests are used, these are positive before appearance of HIV antibodies
Testing recommendations for HIV
Test people at ↑ risk of HIV:
MSM, female partners of MSM, black african, people who inject drugs, sex workers, prisoner, trans women, people form countries with high HIV seroprevelance + their sexual partners
test people attending health services who’s users have associated risk of HIV:
e.g. GUM/TB/hepatitis/lymphoma clinics, antenatal clinics, TOP services, addiction/substance misuse services
all people with symptoms and/or signs consistent with HIV indicator conditions
people accessing healthcare in areas with high seroprevalence (>5/1000)
Oesophageal candidiasis
AIDS defining condition
resents with dysphagia, odynophagia of solids & fluids, retrosternal pain
often also concomitant oral candidiasis
diagnosed via endoscopy
management = 14-21 days of oral fluconazole (if severe IV fluconazole or IV echinocandin)
Systemic candidiasis (candidaemia / disseminated candidiasis)
live threatening (up to 40% mortality)
presents similar to bacterial sepsis i.e. fever, chills, fatigue, headache, myalgia, end organs infection e.g. pneumonia, meningitis or endocarditis
investigated with blood cultures, serology, imaging
Managed with IV fluconazole/echinocandia
Pneumocystis pneumonia (PCP)
Pneumocystis jirovecii penumonia is an infection of the lung caused by the fungal organism pneumocystis jirovecii
leading AIDS defining illness, in ~50% of pts PCP is the first manifestation of AIDS
most common opportunistic infection of AIDS
Risk factors for Pneumocystis pneumonia (PCP)
CD4 count <200 cells/mm3
other AIDS defining illnesses
poor compliance with PCP prophylaxis / retrovirals
malnutrition
Presentation of Pneumocystis pneumonia (PCP)
dyspnoea (especially exertional)
non productive cough
tachypnoea
low grade fever, malaise, fatigue, chills, weight loss
Very few chest sign on examination (often normal respiratory exam, may have ↓ sats at rest)
NB if extra pulmonary disease (rare) = hepatomegaly, lymphadenopathy, ocular disease
Investigating Pneumocystis pneumonia (PCP)
Induced sputum / bronchoscopy & bronchoalveolar lavage (+ve for pneumocystis, NB sputum is often negative)
Chest X-ray (bilateral interstitial pulmonary infiltrates, may show pneumothorax or bilateral perihilar shadowing)
LDH (↑)
ABG (↓O2)
CD4 count (<200cells/mm3)
Management of Pneumocystis pneumonia (PCP)
1st line: Co-trimoxazole
2nd line: IV pentamidine (severe cases)
NB Co-trimoxazole = trimethoprim + sulfamethoxazole
Prevention of Pneumocystis pneumonia (PCP)
PCP prophylaxis is given to all HIV pts with CD4 count <200cells/mm3
prophylaxis with oral co-trimoxazole
Common complication of Pneumocystis pneumonia (PCP)
pneumothorax
Cryptococcosis
opportunistic fungal infection with cryptococcus neoformans, common cause of HIV related meningitis
AIDS defining illness, associated with bird droppings (especially pigeons)
most often seen in pts with CD4 count <100cells/mm3
Presentation of Cryptococcosis
meningitis/menigoencephalitis:
headache, confusion, altered mental state, coma, seizures,
neurological signs (diplopia, ataxia, aphasia, signs of ↑ ICP)
Meningism (neck stiffness, photophobia, headache)
Investigations for Cryptococcosis
CSF/blood/urine cultures
cryptococcus antigen titres (from CSF/serum)
MRI brain (soap bubble lesions in brain, hydrocephalus, cysts)
Management of Cryptococcosis
Induction:
amphotericin B + flucytosine
consolidation:
PO fluconazole
Maintenance:
low dose fluconazole for several months
Cryptosporidosis
AIDS defining protozoal infection with cryptosporidium hominis & cryptosporidium pavuum
presents as water diarrhoea, abdo cramps, low grade fever, nausea lasting up to a month)
generally seen in CD4 count 200-500cells/mm3 but may be severe if CD4 count <50cells/mm3 (i.e. more chronic)
diagnosis with cryptosporidium oocytes (acid fast cysts) & +ve cryptosporidium antigen test
managed with HAART (as hard to eradicate if CD4 count<200cells/mm3) + nitazoxamide/paromocyin
Toxoplasmosis
AIDS defining infection caused by protozoal parasite toxoplasma gondii, one of the most common human parasites, leading to encephalitis
often seen if CD4 count <200cells/mm3
cerebral toxoplasmosis = most common neurological AIDS defining condition
Toxoplasmosis presentation
generally asymptomatic if immunocompetent
cerebral toxoplasmosis (toxoplasmosis encephalitis): fever, headache, seizures, focal neurological deficits, mental state changes, cerebellar sign usually a reactivation
ocular toxoplasmosis (chorioretinitis) yellow-white retinal lesions, marked vitreous retraction, visual field deficits, ↓ visual acuity usually cute infection
Toxoplasmosis investigations
serology (anti-toxoplasmosis IgM/IgG
contrast CT/MRI brain (multiple ring enhancing lesions = brain abscesses, often in basal ganglia)
Toxoplasmosis management
pyrimethamine +sulfadiazine + folinic acid
prevention with dapsone + pyrimethamine
Cytomegalovirus (CMV)
A member of the herpes virus family that will infect the majority of human, after primary infection establishes lifelong latency
HIV pts with CD4 count <50/mm3 are at risk of reactivation
Presentation of cytomegalovirus (CMV)
CMV retinitis:
most common CMV manifestation in HIV pts
floaters, photopsia, visual field deficits, painless visual loss
usually unilateral
yellow, white areas with perivascular exudates & haemorrhages on ophthalmoscopy
NB other presentations include CMV pneumonia (interstitial pneumonitis) & GI manifestations
Investigations for cytomegalovirus (CMV)
histopathology:
owls eye appearance, due to large intranuclear inclusion body
serology:
anti-CMV IgG/IgM (not useful if immunosuppressed)
PCR for CMV DNA
Management of cytomegalovirus (CMV)
treatment:
valganciclovir / ganciclovir / foscarnet
Cidofivir if resistant CMV
+ optimise antiretroviral therapy
Prophylaxis:
valganciclovir or ganciclovir
Tuberculosis in HIV
infection caused by mycobacterium tuberculosis, may occur at any CD4 count
↑ chance of extra pulmonary TB or atypical presentation
often due to reactivation of latent TB
TB in HIV presentation
generally disseminated TB with chest involvement & generalised lymph node involvement
fever, fatigue, night sweats, weight loss
productive cough, haemoptysis, SOB, pleuritic chest pain
lymphadenitis i.e. generalised lymphadenopathy with firm enlarged nodes
sterile pyuria
potential CNS involvement
Investigations for TB
CXR (usually apical lesion or millet seed like profile of biliary TB)
Sputum smear (acid fast bacilli on Ziehl-Nielsen stain)
sputum culture
Management of TB in HIV
Treatment:
2 months of Rifampicin + Isoniazid + Pyrazinamide + Ethambutol
Then 4 months of Rifampicin + Isoniazid
Prophylaxis:
isoniazid prophylaxis recommended for at risk HIV pts
NB drug resistant TB is an issue with HIV pts
Myobacterium avian complex (MAC) / Myobacterium avian intracellulare (MAI)
opportunistic infection of immunocompromised individuals usually with CD4 count <50cells/mm3
seen in up to 40% of AIDS pts
Presentation of Myobacterium avian complex (MAC)
3 syndromes: disseminated MAC, Pulmonary MAC, MAC lymphadenitis
Disseminated MAC*: (most commonly seen in HIV)
diarrhoea, malaise, fever, significant weight loss, wasting, fever, sweats, pallor, tender hepatosplenomegaly, generalised lymphadenopathy
Pulmonary MAC: cough, ↑sputum production, dyspnoea, haemoptysis, fever, night sweats
MAC lymphadenitis: cervicofacial lymphadenopathy
Investigations for Myobacterium avian complex (MAC)
FBC (↓Hb, ↓CD4) albumin (↓)
sputum/blood/bone marrow culture (+ve for MAC growth)
CT/USS abdo (lymphadenopathy + hepatosplenomegaly)
CT chest (thin walled cavitary lesions of upper lobes)
Management of Myobacterium avian complex (MAC)
Treatment:
12 months course of Abx (clarithromycin/erythromycin + ethambutol + rifabutin)
Prophylaxis:
macrolide (azithromycin / clarithromycin) until CD4 count >100cells/mm3
Microsporidiosis
caused by microsporidium (in HIV pts)
presents with low volume diarrhoea
diagnosed on immunofluorescent staining of stool
managed with HAART, erythromycin
Isosporiasis
caused by isosporiasis belli
causes watery diarrhoea, abdo pain, fatigue, weight loss
treat with co-trimoxazole
Aspergillosis
uncommon in HIV unless CD4 count <30
presents with cough, fever, dyspnoea
Cavitating lesions on CXR
treated with amphoteracin B or itraconazole
HIV wasting syndrome
unintentional weight loss ≥10%, fatigue, fever, diarrhoea
due to variety of factors
Histoplasmosis
infection caused by histoplasmosis capsulate, in HIV usually a reactivation of latent disease
usually seen in CD4 count <200
Histoplasmosis presentation
fever, weight loss, erythema nodosum, lymphadenopathy, hepatosplenomegaly, non productive cough, pleuritic chest pain, ulcerative oral lesions
Investigation & management of Histoplasmosis
CXR (diffuse nodular density, focal infiltrate/cavity)
fungal blood cultures
managed with itraconazole
Bacterial pneumonia in HIV
common causes include
- strep pneumoniae (characterised by rusty sputum, but can be prevent with pneumovax)
- H.influenzae
- mycoplasma pneumoniae
- Staph aureus (especially in IVDU/advanced HIV, may cause cavitating lesions)
presentation is often atypical
CXR often shows diffuse infiltrates
At what CD4 counts do vaccinations become ineffective
CD4 count <200 makes many vaccines ineffective
Progressive multifocal leukoencephalopathy (PML)
progressive demyelinating condition caused by Joh Cunningham virus (JC virus) due to oligodendrocytes being infected with JC virus
presents with seizures, behavioural change, speech/motor/visual impairment, other focal neurological deficits, impaired vigilance
MRI shows disseminated non enhancing white matter lesions without mass effect, scalloping at grey-white matter interface), CSF (+ve for JC virus DNA on PCR)
no treatment available
HIV associated neurocognitive disorders (HAND)
due to HIV virus directly infection nervous system i.e. AIDS dementia, typically seen in untreated pts with advanced HIV infections
leads to subcortical dementia presenting with memory loss, depression, movement disorders, bradykinesia, impaired vigilance, aphasia, gait disturbance
investigated with MRI/CT (cortical/subcortical atrophy + multiple subcortical non enchaining lesions)
managed with early use of antiretroviral therapy
Herpes simplex virus & HIV
usually atypical presentations in HIV pts
e.g. chronic oral/genital ulcers (>1 month) or may cause encephalitis or herpes simplex keratitis (blurry vision, painful watery eyes, dendritic corneal ulcer)
management with aciclovir
NB chronic mucocutaneous herpes (>4 weeks) = AIDS defining
Molluscum contagiosum & HIV
common skin infection causing pinkish/pearly white papules with central umbilication,
lesions on face/eyes indicate immunosuppression and may be seen in HIV pts
treatment is imiquimod
Human papilloma virus & HIV
HIV +ve women are advised to have yearly cervical cytology due to ↑ risk of developing cervical cancer
invasive cervical cancer = HIV defining diagnosis
presents as postcoital/intramenstrual/postmenopausal bleeding, vaginal discharge
Kaposi sarcoma
connective tissue cancer caused by human herpes virus 8 (HHV-8) also known as Kaposi’s sarcoma associated herpes virus (KSHV)
characterised by neoplastic cells & abnormally growing blood vessels
Presentation of kaposi sarcoma
multiple visceral / cutaneous elevated tumours with rapid growth
initial stage:
painless, non pruritic violet/red/brown/black papules or nodules on skin/mucosa usually moth/nose/throat/face/chest
lesions may also involve internal organs e.g. lungs (dyspnoea, haemoptysis, pleural effusion), GI tract (can cause fatal bleed)
Investigations of Kaposi sarcoma
skin biopsy (spindle cells*, angiogenesis, leukocyte infiltration) CXR/Abdo USS/bronchoscopy/endoscopy consider HHV-8 serology
Management of Kaposi sarcoma
HAART = vital (lesions may spontaneously resolve after immune reconstitution)
radio/chemo/cryotherapy
Non-Hodgkins lymphoma in HIV
high grade B cell lymphomas are common in HIV population
presents as rapidly growing, bulky, painless lymphadenopathy, easy bruising, hepatosplenomegaly, fever, night sweat, weight loss
FBC (thrombocytopenia, pancytopenia, lymphocytosis), blood smear (nucleated RBCs), lymph node/bone marrow biopsy (monomorphous lymphocytic proliferation)
treated with chemo & opportunistic infection prophylaxis as CD4 count will drop
Primary CNS lymphoma in HIV
extra nodes non Hodgkins lymphoma associated with EBV infection, usually seen with CD4 count <100
presents with symptoms of ↑ICP (seizures, papilloedema, headache), lethargy, focal neurological deficits, personality changes, confusion
CT contrast shows (solitary solid enhancing lesion with homogenous enhancement) Thalium SPECT (+ve), CSF (+ve for EBV DNA)
managed with wholegrain radiotherapy, dexamethasone (↓ tumour size)
even treated the survival is <1 year
Primary CNS lymphoma vs toxoplasmosis
Toxoplasmosis = multiple enhancing lesions on contrast CT & negative Thalium SPECT
Primary CNS lymphoma = single enhancing lesions on contrast CT & positive Thalium SPECT
HIV peripheral neuropathy
can occur at any stage of HIV infection but more common in advanced disease, due to direct infection of nerves by HIV
presents as symmetrical distal numbness & pain in lower limbs, usually strength is preserved, reflexes are absent or ↓, pain & temp sensation is impaired
may also cause autonomic symptoms such as postural hypotension, impotence, bladder dysfunction or diarrhoea
managed with gabapentin for neuropathic pain
HIV assoicated nephropathy (HIVAN)
classically a collapsing focal segmental glomerulosclerosis due to direct infection of kidneys with HIV
usually seen in pts with CD4 count<200 & detectable viral loads
causes nephrotic syndrome (Proteinuria (> 3g/24hr), Hypoalbuminaemia (< 30g/L), Oedema) & progressive kidney failure (↓ eGFR)
managed with HAART or transplant
NB black individuals with HIV are more commonly effected
Nucleoside reverse transcriptase inhibitors (NRTIs) examples
emtricitabine (FTC) Lamivudine (3TC) abacavir zidovudine (AZT) Stavudine (d4T) didanosine (ddI) tenofivir
NB Tenofivir alafenamide (TAF) = tenofivir pro drug
Class of drugs for emtricitabine (FTC), Lamivudine (3TC), abacavir , zodofivir (AZT), Stavudine (d4T), didanosine (ddI), tenofivir
Nucleoside reverse transcriptase inhibitors (NRTIs)
MOA of Nucleoside reverse transcriptase inhibitors (NRTIs)
act as nucleoside analogues = competitive blockage of nucleoside binding to reverse transcriptase leading too termination of the viral DNA chain and preventing viral RNA being transcribed into DNA
Zidovudine (NRTI) side effects
bone marrow suppression (anaemia, neutropenia) lipoatrophy peripheral neuropathy skin/nail pigmentation lactic acidosis hepatic stenosis
Stavudine (NRTI) side effects
lipoatrophy peripheral neuropathy pancreatitis lactic acidosis hepatic stenosis
Didanosine (NRTI) side effects
peripheral neuropathy
pancreatitis
Rarely used NRTIs in HIV
Zidovudine, stavudine, didanosine
Emtricitabine (NRTI) side effects
reversible skin pigmentations
Abacavir (NRTI) side effects
~5% of pts have life threatening hypersensitivity reaction associated with HLA-B5701
Tenofivir (NRTI) side effects
renal dysfunction (glycosuria, subnephrotic proteinuria, ↑ creatinine) ↓ bone mineral density
NB the prodrug TAF has ↓ nephrotoxicity
antiretroviral causing life threatening hypersensitivity reaction
Abacavir (NRTI)
~5% of pts have life threatening hypersensitivity reaction associated with HLA-B5701
Non-nucleoside reverse transcriptase inhibitors (NNRTIs) examples
nevirapine efavirenz etravarine rilpivirine doravirine
Non-nucleoside reverse transcriptase inhibitors (NNRTIs) MOA
noncompetitive inhibitors of viral reverse transcriptase that bind at separate location to NRTIs
Nevirapine (NNRTI) side effects
rash (potentially SJS)
hepatotoxicity (contraindicated in Hep B/C confection)
Efavirenz (NNRTI) side effects
CNS toxicity (confusion, vivid/disturbing dream/somnolence) teratogenic
Antiretroviral contraindicated in Hep B/C coinfection
Nevirapine as it is hepatotoxic
Protease inhibitors (PI) examples
darunavir atazanavir lopinavir ritonavir tipranavir
NB ritonavir, tipranavir are now rarely used
Protease inhibitors (PI) MOA
inhibition of viral HIV-1 protease =inability to cleave viral mRNA into functional units = synthesis of impaired viral proteins = production of immature (non-infective) visions
Protease inhibitors (PI) administration
PIs are always given with low dose ritonavir (as it inhibits cytochrome P450) to ↑ intracellular concentration of the drug
known as boosted PI
Fusion inhibitors examples
Enfuvirtide (T-20) (given BD via SC injection)
NB fusion inhibitors are reserved for those with highly drug resistant HIV
Fusion inhibitors MOA
competitively binds to viral protein gp41 & thereby prevents fusion with cells
Fusion inhibitors side effects
skin irritation at injection site (enfuvirtide)
Integrase inhibitors examples
raltegravir
elvitegravir
dolutegravir
bictegravir
Integrase inhibitors MOA
inhibit viral integers = blockade of viral DNA integration into hosts DNA = inhibition of viral replication
Integrase inhibitors side effects
↑ creatine kinase
raltegravir (muscle pain, rhabdomyolysis)
dolutegravir (mood/sleep disturbances)
Co-receptor antagonists examples (ART)
Maraviroc (CCR5)
Co-receptor antagonists MOA
blocks CCR5 co-receptor onT-cells & monocytes that is essential for cell infection = inhibits gp120 interaction = prevents irons docking to cell
Co-receptor antagonists side effects
hepatotoxicity
allergic reaction
Weight gain on antiretroviral therapy
Agents such as Tenofivir alafenamide (TAF)
Weight gain on antiretroviral therapy
Agents such as Tenofivir alafenamide (TAF) is more associated with weight gain that tenofivir
integers inhibitors especially raltegravir are associated with weight gain
Indications for anti retroviral therapy
all persons with HIV regardless of CD4 count should be started on ART
prioritise ART if:
CD4 count <350
high viral load
presence of AIDS defining illness
antiretroviral therapy regimes
2 NRTIs plus 1 ritonavir boosted PI / 1 NNRTI / 1 integrase inhibitors
Switching antiretroviral therapy
deterioration of condition may require switching of therapy or adding a further ART
virological failure = persistently detectable HIV viral load on ART
new regime should be guided by HIV resistance testing & previous ART
Drug interactions of Protease inhibitors
inhibit P450
Drug interactions of Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
potent liver enzyme inducer = ↓ levels of other drugs
Drug interactions of Nucleoside reverse transcriptase inhibitors (NRTIs)
exacerbate cytopenic effect of chemo
Indications for post exposure prophylaxis (PEP)
- needle stick injury especially with HIV contaminated instrument / needles
- contamination of open wound / mucous membrane with HIV contaminated fluid e.g. bites
- unprotected sexual activity with a known / potentially HIV infected person
- sexual assault (↑ risk of HIV transmission)
Timing of post exposure prophylaxis (PEP)
ASAP / within 1-2h of exposure = ideal
> 72h after exposure = ineffective / ↓effectivity
NB for non occupational exposure the timing is usually later (~23h)
When post exposure prophylaxis (PEP) is needed
receptive / insertive vaginal & anal sex
fellatio with ejaculation
splash of semen into eye with HIV +ve individual
receptive anal sex with a person of unknown status from a group with high HIV prevalence
NB PEP is not needed if fellatio without ejaculation or cunilingus even with HIV +ve individual
post exposure prophylaxis (PEP) follow up
HIV tests at 3 & 6 months post exposure
repeat Hep B/C & syphilis serology
monitor for drug toxicity (FBC/U&Es/LFTs)
Important to facilitate completion of PEP regime
Treatment as prevention (TAsP)
when HIV +ve individual pt takes ART it ↓ their oral load
when pt with undetectable viral load for >6months = virus cannot be passed on unisexual encounters
if undetectable viral load = untransmissable = TAsP
i.e,. treating pt with ART to reduce viral loads & ↓ rate of new HIV infections (essentially TAsP is too protect others)
Pre exposure prophylaxis (PrEP) eligibility
negative HIV test result & no signs/symptoms of acute HIB infection
normal renal function
indications met for PrEP
Pre exposure prophylaxis (PrEP) indications
MSM:
condomless anal sex in last 6 months / sex with HIV +ve partner (unless partner on TAsP)
heterosexual men & women:
sexually active with HIV +ve partner, inconsistent / no condom use with one/more sexual partners of unknown HIV status
MSM & heterosexual men & women who had STI in last 6 months
IVDU with high risk needle behaviour (e.g. needle sharing) or HIV +ve injection partner
Pre exposure prophylaxis (PrEP) indications
MSM:
condomless anal sex in last 6 months / sex with HIV +ve partner (unless partner on TAsP)
heterosexual men & women:
sexually active with HIV +ve partner, inconsistent / no condom use with one/more sexual partners of unknown HIV status
MSM & heterosexual men & women who had STI in last 6 months
IVDU with high risk needle behaviour (e.g. needle sharing) or HIV +ve injection partner
Pre exposure prophylaxis (PrEP) follow up
HIV test every 3 months
STI screening every 3 months
renal assessment at baseline & every 6 months
counselling on adherence & risk reduction
HIV & pregnancy
due to ↑ incidence of HIV infection amongst heterosexual population there are ↑ number of HIV +ve women giving birth
aim of treating pregnant HIV +ve women is to minimise harm to both mother & baby + ↓chance of vertical transmission
Interventions to reduce transmission of HIV in pregnancy
early HIV diagnosis (via testing at antenatal screening)
HAART to ↓ viral load during pregnancy (offered to all women regardless if they have taken it previously)
continue HAART after delivery
infant feeding (bottle feeding)
delivery via elective C-section at 38 weeks
AZT (zidovudine) monotherapy for 4 weeks post term for baby
AZT infusion started 4h before C-section
exclusive formula feeding (breastfeeding contraindicated)
HIV transmission in pregnancy
usually occurs late in pregnancy at time of deliver or via breastfeeding
without intervention mother-to-child transmission rate is 15-20%
Delaying planned C-section in HIV +ve pregnancies
preplanned C section should be delayed to 39 weeks if maternal viral loads <50 copies/ml to ↓ risk of Transient Tachypnea of the Newborn (TTN)
HIV mother-to-child transmission rate with intervention
rate is <1%
Considering vaginal delivery in HIV +ve pregnancy
if maternal viral load is <50 copies/ml at 36 weeks but the preferred method is still C-section
Pubic lice (crabs)
crab’-shaped, grey-brown in colour,and about 2 mm in length which transmitted by close body contact
presents as finding of lice / eggs, itchy red papules, itching usually worse at night
managed with two applications of malathion 0.5% aqueous lotion or permethrin 5% dermal cream, seven days apart.
