GUM/HIV Flashcards
How long after exposure do symptoms of gonorrhoea/chlamydia develop?
Gonorrhoea - symptoms develop within 2-5 days Chlamydia within 1-2 weeks
Causes of Urethritis in men?
Common: - Gonorrhoea - Chlamydia - Non-specific urethritis Less common: - Mycoplasma genitalium - Trichomoniasis - HSV - Adenovirus - E.coli - UTI - Trauma - Foreign body - Urethritis associated with reactive arthritis and allied conditions
Mx of Urethritis in males?
1) Hx + Ex (discharge) 2) Take urethral swab + test first pass urine (NAAT) 3) Treat for gonorrhoea + chlamydia if urethral gram stain is positive for gram-negative intracellular diplococci 4) Treat Chlamydia if smear shows 5 or more polymorphs per HPF & Gram stain does not suggest gonorrhoea 5) explain diagnosis, tx and methods of prevention 6) Advice to avoid sex until treatment and F/U completed 7) Advice partner Tx
Abx of choice for pts with non-gonococcal urethritis?
- Azithromycin 1g single dose - Doxycycline 100mg BD for 1/52 –> Active against chlamydial infection and other pathogens associated with NGU If persistent sx, investigate for treatment failure, reinfection or infection by less common pathogens Eg. trichomonas vaginalis, mycoplasma genitalium
Chlamydia - symptoms in men/women
Men Main: Urethral discharge, dysuria Less common: Proctitis, conjunctivits, epididymo-orchitis & reactive arthritis Women Main: Dysuria, vaginal discharge, intermenstrual bleeding Less common: PID, peri-hepatitis (Fitz-Hugh-Curtis), conjunctivitis, reactive arthritis.
Gonorrhoea - symptoms in men/women
Men Main: Urethral discharge, dysuria, tender inguinal lymph nodes Less common: epididymo-orchitis, abscesses of paraurethral glands and urethral stricture Women Main: discharge, dysuria, bleeding Less common: Lower abdo pain, bartholinits and vulvu-vaginitis (pre-pubertal girls) Ix: Cervical gram stain + culture
Gonorhhoea extragenital symptoms
Pharngitis, rectal pain + discharge, conjunctivitis Disseminated infection involving skin, joints + heart valves Secondary infertility after dmg to fallopian tubes or epididymis
Causes of scrotal swelling and pain?
Infections of testis & epididymis: Gonorrhoea, chlamydia, TB, mumps, virus, Gram -VE bacteria Torsion Hydrocoele, spermatocoele varicocoele Vasculitis: HSP, kawasaki’s, Buerger’s Amiodarone Tumour Hernia Trauma
Acute epididymo-orchitis organism
Young men: Gonorrhoea or chlamydia Men >35: E.coli, Klebsiella, Pseudomonas & Protein
Prostatis Organisms Mx?
Most acute infections: - E.coli, Proteus, Strep faecalis, Klebsiella, Pseudomonas - STIs (Gon/Chlam) account for less but can also cause it Mx: 28 day course of quinolone or tetracycline, which have better prostatic penetration than other ABx
Causes of painful prostate?
NIH classification of prostatis syndromes: I Acute bacterial prostatitis II Chronic Bacterial prostatitis III Chronic prostatis (inflammatory and non-inflammatory) IV - asymptomatic inflammatory prostatitis Other causes: - Pudendal neuralgia - BOO - Bladder tumour - Urinary stone disease - Ejaculatory duct obstruction - Seminal vesicle calculi - IBS
Anorectal STI symptoms ?
Asymptomatic Ulceration (herpes/syphilis) Warts Proctitis Pain Tenesmus Bleeding Discharge Diarrhoea (rare)
Mx Males with symptomatic non-gonoccal proctitis?
3 week courses of Abx recommended to eliminate LGV
Chlamydia complications?
Prostatitis Epididymitis Bartholinitis Endometritis PID Cervical neoplasia Perihepatitis (Fitz-Hugh-Curtis - liver capsule inflammation leaving to creation of adhesions) Conjunctivitis Reactive arthritis
Chlamydia in pregnancy: complications:
Preterm delivery Low birth weight PROM Neonates: Chlamydia opthalmia neonatorum Conjuncitivits RTI
Gonorrhoea Abx?
Uncomplicated Genital/Rectal: - Ceftriaxone 250mg IM or Cipro 500mg oral Adult gonococcal conjunctivitis: - Ceftriaxone 1g IM
Chronic Prostatis/Chronic Pelvic pain syndrome
Most common form of prostatitis Cause: ?AI Sx: Chronic unilateral testicular pain (provoked by coitus), urinary obstruction, sexual dysfunction Ix: Exclude other causes including bladder or prostate infectionn
NGU causes & Mx
Mycoplasma genitalium, TV, HSV, adenovirus mainly. Mx: Avoid sexual intercourse until tx completed and symptoms resolved Doxycycline 100mg BD for 7 days + Azithromycin 1g single dose Partner notification
What is PID?
Inflammation of upper female GUT and supporting structuers. Usually a result of infection: - Ascending from endocervix - Less commonly spread from other abdo organs
PID causative organisms?
STIs N.gonorrhoea in 5-75% Chlamydia in 5-45% Other: - BV associated organisms - Viridian group strep - E.coli - M.genitalium
PID DDx?
Acute PID: - Ectopic - Acute appendicitis/pylonephritis - Ruptured ovarian/endometrial cyst - Ovarian neoplasms - IBD - Adnexal torsion Chronic: - Endometriosis - Ovarian cysts - Ovarian/uterine neoplasms - Interstitial cystitis - IBD/IBS - Previous surgery –> Adhesions - Psychosocial –> Somatisation disorder
Acute PID Sx & signs?
Sx: - Onset within 7 days of 1st day of menstruation correlates with gonococcal/chlamydial infection - Lower abdo pain - menstrual irregularity - Abdo bleeding - Dysmeorrhoea - Vag discharge - N+V Signs: - Lower abdo tenderness + guarding (rebound if severe) - Adnexal & cervical motion tenderness - Fever > 38 - Adnexal mass in 50% of women with gonococcal PID - Abdo distention due to paralytic ileus if very severe
Signs & Sx of chronic PID
Asymptomatic Constant/intermittent pain/ discomfort in lower abdo, groin or back Dyspareunia Malaise Frequent menstrual periods
PID Complications
Tubo-ovarian and pelvis abscess Peri-appendicitis Infertility Ectopics Chronic pelvis pain Fitz Hugh Curtis
PID Ix
swabs for N.gonorrhoeae & C.trichomatis (NAAT) Gram stain of cervical smear Bloods: WBC, ESR, CRP Chlamydial antibody Pregnancy test Urine analysis & MSU Endometrial histology/microbiology Pelvic imaging Laparoscopy
PID Abx?
Outpt: - Ceftriaxone 250mg IM single dose + Doxy 100mg BD PO 14days + Metronidazole 400mg BD for 7-14 days Inpt: consider IV Cefoxitin 2g + Doxy 100mg oral/IV
Primary Syphilis?
9-90 days after infection (Avg 3/52) Painless papule at inoculiation site Expands & ulcerates –> Painless round/oval chancre 1-2cm with an indurated margin and clear moist base Exudes serum without blood on pressure Typically solitary, though multiple lesinos may occur Bilateral painless regional lymphadenopathy May also present with multiple painful ulcers with little induration, mimicking genital herpes Sites: transmitted sexually to and from mucosal skin through small abraisons - Genitals: Mucosal services eg. glans, labia, fourchette & cervix - Extra-genital: Oral: Lips, mouth, tongue, tonsils, pharynx anal margin Rectum
Secondary syphilis
4-8 weeks after infection until 6mo, from haematogenous dissemination PC: Constitutional: Malaise, fever, headache, anorexia, myalgia Skin lesions: Polymorphic (80%), pruritic (40%), Maculopapular. condylomata lata - hypertrophied wart like lesions on moist areas; especially around vulva and anus Hyper or hypogmented lesions (Leucoderma) Lymphadenopathy (75% inguinal, 60% generalised) Mucus membrane lesions in 30% - may coalesce with others forming snail track ulcers Other: Alopecia, periostitis, arthralgia, hepatitis, rarely GN
Latent syphilis?
Serological proof of infection without symptoms Warly latent: within first 2 years of infection Late latent:: >2 yrs after acquisition
Tertiary syphilis features?
Occurs approx 3-15 yrs after initial infection and is divided into several groups: Gummatous Cardiovascular - Condution defects eg. Stokes-Adams syndrome - Aortitis leading to: Aortic aneurysm, Aortic regurg and coronary ostial stenosis Neurosyphilis - Including Tabes Dorsalis
Gummatous syphilis?
Gumma formation (syphilitic granulation tissue) due to reaction of residual treponemes in sensitised host. Gummata - nodules or nodulo-ulcers, indurated and indolent (painless) - Commonly heal with central scarring while peripherally still active - ‘punched out’ ulcers - Not contagious - Sites: Skin, bones, mouth, throat, liver, testis, oesophagus, stomach, intestine, cerebrum, spunal cord, aortic wall, myocardium
Neurosyphilis features?
1) Asymptomatic - just CSF findings 2) Meningovascular - focal arteritis causing infarction and meningeal inflammation. Most common neurosyphilitic presentation. Consider if cerebrovascular accident in a young adult. - Often sudden onset preceded by prodromal headache, insomnia, emotional lability - Hemiplegia/paresis, aphasia & Seizures typical features, but ocular palsy and trigeminal neuralgia may occur 3) Pupillary abnormalities frequent, full argyll robertson (prostitutes pupil - accommodates but doesn’t react to light) 4) General paralysis of the insane: Cortical neuronal loss: psychiatric symptoms 5) Tabes dorsalis
What is Tabes dorsalis?
Selective inflammation and degeneration of the spinal dorsal columns + nerve roots (proprioception, vibration + Fine touch) + lightning pains - Sensory ataxia with stamping gait - Positive Romberg sign - Diminished or absent reflexes - Trophic changes lead to neuropathic joitns (charcot) - Argyll robertson pupil seen most commonly in tabes dorsalis
Syphilis Ix
- Dark ground microscopy - Direct Fluourescent antibody stain - PCR for T.pallidum - CSF for neurosyphilis - Biopsy & histology of gummata - Serology
What is Dark Ground microscopy?
Test used to identify T.pallidum Clean lesion with a guaze soaked in normal saline and squeeze it to encourage a serum exudate. Serum then scaped off lsion and placed on 3 slides . T.pallidum is bluish white, closed coiled and 6-20um long. 3 characteristic movements: watch spring, corkscrew and angular
Syphilis serological tests?
1) Non-specific (Non-treponemal) - Useful to monitor response to Tx and diagnosis of reinfection fo syphilis. - May also give false +se 2) Specific (treponemal) - Useful for confirming diagnosis at first presentation - Usually remain +ve throughout a pts life, even after successful treatment
Non-Specific syphilis tests?
Rapid plasma reagin (RPR) - Appearance of cardiolipin Abd in the serum and usually become +ve 3-5 weeks after infection VDRL (Venereal disease research lab) Quantitative tests - useful in assessing stage + activity - decreasing titres associated with treatment response. - High titre (>1:16) indicative of active infection
Non-specific syphilis test false +ves?
NB. VDRL/RPR may also decay naturally without treatment - Both yield false +ve results to acute infections (eg. HSV, Measles, mumps) or after immunisation with typhoid/yellow fever Chronic causes of false +ve: - AI disease - RA Both specific/non-specific also false +ve in other conditions that are similar to syphilis eg. Yaws, Bejel, and pinta Yaws - Treponema pallidum subsp pertenue - usually an infection acquired in childhood and characterised by skin ulceration, of lower limbs.
Specific syphilis test?
1) Treponema enzyme immunoassay (EIA) - Become +ve early in course of infection - Combined IgG/IgM EIA +ve within 2-4 weeks after infection - +ve in 85-90% of primary syphilis. In early syphilis, may be only +ve sero test 2) Flourescent treponemal antibody test (FTA) 3) T.pallidum haemagglutination assay (TPHA)
Neurosyphilis lumbar puncture findings?
Most will have a CSF: - WCC> 5x10^6/L - Protein > 40g/L
Syphilis Mx. Complications?
Primary/Secondary/Early Latent: Ben-Pen single dose IV - 10 days procaine Ben Pen IV If Pen allergic: doxycycline Complication: - Jarisch-Herxheimer : non-specific fever + Flu like symptoms occuring 3-12 hrs after first injectino of penicillin. Mx: Reassurance, antipyretics eg. paracetamol/NSAIDs
Syphilis contact tracing?
pt with early infectious syphilis: Contact tracing on all sexual contacts in previous 3-6 mo Late syphilis - pt no longer infection, serological testing only in pts regular partners.
Syphilis and HIV co-infection?
Primary syphilis: Larger, painful, multiple ulcers Secondary: Genital Ulcers (slow healing), Higher titres of RPR/VDRL Possibly more rapid progression onto neurosyphilis
Cervicitis causes?
Gonorrhoea Chlamydia Mycoplasma genitalium
Vagina - normal predominant organism. Normal pH?
At puberty, oestrogen causes development of stratified squamous epithelium - Lactobacilli (gram-positive rods) become predominant organism - pH falls to 3.5-4.5 - After menopause, atrophic changes occur - pH rises again to 7 with return to normal skin flora
Vag discharge diagnostic test?
Microscopy of a saline wet mount + gram-stained vaginal smear allows immediate diagnosis. Subsequent lab culture + NAAT as needed. - Also test for gonorrhoea + chlamydia Vaginal pH can also be measured with pH paper: - BV/TV excluded if pH
Vaginal discharge: Candidiasis?
Itchy Yeast White discharge Curdy consistency pH
BV discharge?
Offensive fishy grey/white/yellow discharge Thin, homogenous ph 4.5 - 7 (Excluded if
TV discharge?
Very itchy May be offensive, yellow or green, thin homogenous DC pH 4.5-7 MC+S
Cervicitis discharge?
No itch or smell May have white/green , Mucoid DC - MC + test for chlamydia and gonorrhoea - may be caused by chlamydia, gonorrhoea , mycoplasma genitalium. - Mucopurulent DC seen and cervix s friable with contact bleeding
Factors predisposing to vaginal candidiasis?
Broad spectrum Abx Increased oestrogen (Oestrogen dependent) - Pregnancy - COCP DM Underlying dermatosis (Eczema) Immunosuppression - HIV/ Steroids Vaginal douching, bubble bath, shower gel, tight clothing, tights
Vaginal candidiasis Mx + complications?
- Single dose topical azole eg. clotrimazole pessary 500mg - Oral fluconazole 150mg tablet single dose Longer course of tx (eg. clotrimazole 100mg/day for 6-7days) indicated: - In pregnancy - When predisposing factors cannot be eliminated, eg. steroid therapy Complications - Azoles not recommended in pregnancy - Rare: severe episode of candida can trigger long term vulvodynia
BV organisms? BV complications?
Gardnerella Bacterioides sp. Mycoplasma hominis A.vaginae Atopobium vaginae (predominately anaeorbes) - overwhelm the lactobacilli - pH rises to 4.5-7 During pregnancy, women with BV have greater risk of second trimester miscarriage & preterm delivery
BV criteria?
Atleast 3 of Amsel criteria: - Vaginal pH >4.5 - Release of a fishy smell on addition of alkali (KOH 10%) - Characteristic DC O/E - Presence of ‘clue cells’ - vaginal epithelial cells so heavily coated with bacteria, the border is obscured. Dx: Gram-stained vag smear OR micrscopic examination of gram-stained vaginal smear using Hay-Ison Criteria: 1) Normal: Dominance of lactobacillus 2) Intermediate: Mixed flora 3) BV: Dominance of garnerella and/or mobiluncus
BV Mx?
Metronidazole 400mg BD for 5 days
TV clinical features
- Vulvo-vaginitis - Purulent green/yellow DC - Punctate haemorrhage –> Strawberry cervix Dx: - MC + S of Vaginal secretions in specific medium eg. Fineberg-Whittington: - Numerous polymorphonuclear cells seen - Motile organism identified from its shape + 4 moving flagellae - Can also use microscopy of a wet-mount smear (less sensitive, but more easily available)
TV Mx Complications?
Mx: - Metro 2g single dose or 400mg BD for 5 days - Partner notification (NGU) & should not resume sex until partner treated. Complications - ?PID - Risk factor for preterm birth
Vaginal DC in children causes?
- Strep infection - Shigella - chronic haemorrhagic vaginitis (Often with no history of D) - Recurrent: ?Foreign body? - Pinworms - ?Sexual abuse
Atrophic vaginitis: Sx + Mx?
Common in post-menopausal women - Superficial dyspareunia + vaginal soreness Mx: Oestrogen replacement with topical dienoestrol cream effective. Occasional bacterial vaginitis caused by strep –> Co-amoxiclav
Toxic shock syndrome
Rare condition associated with retention of tampons / FB in vagina - Overgrowth of staph producing a toxin causes systemic shock + fever + D+V + erythematous rash
Gonorrhoea gold standard diagnosis?
Culture + Identification of colonies, as sensitivity can be tested too. - Newly available NAATs for gonorrhoea and chlamydia are increasing in popularity
Advantages and disadvantages of POCT?
Advantages: - Specific clinical scenarios eg. HIV POCT for late presentation labour) - Community outreach - Ease of use - Destimatises testing - Small volume of blood/ perceived as more confidential Disadvantages: - High burden of training - Second sample required for confirmation of positives - May reduce testing for other STIs - Loss of epidemiological data
Most common cause of sexually acquired genital ulceration
Genital herpes - HSV-1 Infection most common cause of first episode ulceration in young - Most pts with HSV-2 will have recurrent disease Other causes: - Primary syphilis - Lymphogranuloma venereum Rare: - Donovanosis - Chancroid
HSV incubation period? Location for virus?
5-14 days -
Primary herpes infection characteristic features? Duration
- Vesicles which then become superficial exquisitely painful ulcers - Ulcers coalesce to form larger superficial lesions with characteristic serpiginous edges. - Often associated tender local lymphadenopathy - Muscle aches involving lower limbs - Systemic features (headache, malaise, photophobia) in 10% - May have dysuria - Typical episode lasts 3 weeks
HSV infection complications?
Local: - Superinfection of lesions with strep/strap - Adhesion - Candida - External dysuria –> ?Retention Distant: - Myalgia - Dissemination (rare outside neonate & pregnancy) - Erythema multiforme Neuro: - Headaches - Enchephalitis, radiculitis, transverse myelitis - Autonomic neuropathy Psych: - Anxiety, depression
Primary HSV infection course?
1) Vesticular phase - Day 0-6 - day 2 lesions noted 2) Wet ulcer 3) Dry crusts - Day 12 - lesions start to heal - Day 15 - symptoms generally gone - Day 20: Lesions healed
Factors associated with increased risk of frequent symptomatic recurrent disease?
- Genital HSV2 - No previous infection with any other HSV - Gender (Male > Female) - First year following infection - Symptomatic acquisition episode - Prolonged acquisiton episode - Dmgd immune system
HSV Mx?
Tx of first episode (for 5-10 days): - Aciclovir 400mg TDS Episodic Tx: - Aciclovir 800mg TDS for 2 days - Short course of Tx early in recurrence during prodrome or in first 24-48 hrs has been shown to abort lesions and hasten healing suppressive therapy (severe, frequent or complicated disease/ specific concerns) - Aciclovir 400mg BD Counselling to ‘normalise’ condition –> Transmission occurs when HSV present on skin is inocculated onto broken skin/mucous membranes. - viral shedding can occur in absence of any genital symptoms or signs
HSV counselling?
- Possible source - Possible duration - Natural course of illness - must include risks of asymptomatic shedding - Future Tx options - Options for reducing transmission to sexual partners - Reassurance around risks of transmission to a fetus in pregnancy - advise informing midwife/obstetric team –> Acquisition in third trimester associated with an unacceptable high risk fo HSV transmission to neonate if vaginal delivery - Importance for men to avoid new transmissions to partners during pregnancy - Role and value of partner notification Managing transmission anxiety: - Avoid sex when symptoms/signs suggestive of HSV present - Use condoms (reduces transmission by 50%) - Suppressive antiviral reduces transmission by 50% - Sharing diagnosis with partner allows couple to work together to avoid transmission
LGV epidemiology?
AKA tropical.climatic bubo - STI caused by chlamydia trachomatis serovars L1, L2 and L3 (Normal strain Serovars A-K) which invade and destroy lymphatic tissue - In developing countries acquired heterosexually. - In Europe/N.America - L2 now among MSM, presenting with anorectal sx –> Proctitis –> Proctocolitis
LGV clinical features
3 stages: 1) Primary genital ulceration 2) Secondary inguinal/anorectal syndrome 3) Tertiary genito-anorectal syndrome
LGV primary stage
Primary: Genital ulceration - 3-30 days after infection - Transient papules / ulcers at site of inoculation - Lesion usually a single non-indurated ulcer, occasionally pain, heals rapidly without scarring
LGV secondary stage
2) Secondary inguinal/anorectal syndrome - 2-6weeks after primary - Iguinal/femoral lymphadenopathy + buboes (enlarged painful glands in groin) - 1/3 have characteristic groove sign - groove like depression caused by femoral and inguinal lymph node enlargement above and below inguinal ligament - Inguinal buboes may suppurate and rupture
LGV tertiary stage?
Follows chronic untreated infection May occur any number of years after infection - Resultant fibrosis leads to lymphatic obstruction and genital lymphoedema - Women may develop oedema (elephantiasis) of the vulva and scarring (esthiomene) - Late complications include rectal strictures, proctitis, colitis, perianal abscess, perineal fistular rectovaginal fistulae and urethral fistulae. - Intestinal obstruction may result from stricture formation.
LGV Dx and Mx
Dx - Consider in anyone presenting with genital ulceration, regional lymphadenopathy and/or anorectal manifestations - Confirmed by detecting L.serovar of C.trachomatis by PCR from lesional samples Mx: - Avoid sexual intercourse until they and partners have finished Tx - Doxycycline 100mg BD or erythromycine 500mg QDS for 3 weeks
What is chancroid?
Single non-indurated (Soft sore) painful anogenital ulcers with a purulent base - Contact bleeding - Painful unilateral inguinal lymphadenopathy - Caused by H.ducreyi, incubation period 3-10 days dx: MC+S or PCR –> Reveals typical bacilli running in parallel in a ‘shoal of fish’ formation Tx: - Azithromycin 1g single dose
What is Donovanosis?
Granuloma inguinale - Caused by Klebsiella granulomatis - Occurs in S.America, India, S.africa & Aboriginal aus Slow growing, PAINLESS, friable genital/inguinal lesions which are typically granulomatous, beefy-red and haemorrhagic. Complications: - destruction fo genital tissue - genital lymphoedema (elephantiasis) - Stenosis (Anus, urethra, vagina) Dx: Demonstation of intracellular Donovan bodies (bipolar, closed safety pin like organisms) Tx: Azithromycin 1g week daily
Most common virally acquired STI?
Genital Warts –> HPV –> Small DNA virus that infects cutaneous or mucosal epithelium - Majority caused by low risk HPV 6 & HPV 11 - Spread by direct skin-skin contact - Autoinoculation as HPV site specific
Genital warts features
Incubation period 3 months (2wks-9mo) - Most never develop visible warts but can still transmit the virus - Asymptomatic lumps associated with mild itch/irritations - Tend to occur in areas traumatised during sexual intercourse
Genital warts Dx DDX?
- Visual insepction with a bright light - Biopsy when Dx uncertain, especially with immunocompromised pts to ensure recognition of pre-malignant lesions Other infections: - Molluscum/ Condylomata lata of syphilis Acquired derm conditions: - Seborrheic keratosis - Lichen planus - Fibro-epithelial polp - Melanocytic naevus - Neoplastic lesions Normal anatomical variants: - Pearly penile papules/coronal papillae - Fordyce spots - Vestibular papillae - Skin tags
Genital warts appearnce
1) Condylomata acuminata - cauliflower like 2) Smooth papules - dome shaped/skin coloured 3) Flat papules - Macular to slightly raised, flesh coloured with smooth surface. - More commonly found on internal structures (eg. cervix) 4) Keratotic warts Without Tx, warts may disappear (30%), stay the same (20%) or grow (50%) at 3 months - Most HPV infections will clear within 2 yrs in immunocompetent pts, leaving 10% with subclinical HPV
Genital warts Mx
Inform pt of diagnosis, transmission and Mx options. - Offer full STI screen - Use condoms/ stop smoking Options: Cryotherapy Electrosurgery Laser Ablation Imiquimoid Non-keratinised: - Podophylllotoxin 0.5% - imiquimoid Keratinised: - Cryotherapy - Imiquimoid - If large/extensive, surgery? - If partial/no Tx response at 4-6 weeks (16 for imiquimod, consider switching Tx
Molluscum?
Pox virus - large DNA virus which replicates in cytoplasm of epithelial cells - Incubation 3-12 weeks - Genital infection: papules found in pubic hair, thighs, buttocks and lower abdomen - Tend to SPARE mucous membranes - Small smooth pearly coloured papules with central umbilication Dx: Visual inspection. If unsure, central punctum can be extracted and viewed under EM for pox like praticles, or histology will reveal enlarged epithelial cells with intracytoplasmic molluscum bodies
Molluscum Mx?
- Spontaneos resolution within 3mo common , but 35% pts may experience recurrence within 8-24 mo Tx for cosmetic reasons: - Cryotherapy - Extraction of central core - Piecing with orange stick that has been dipped in iodine or phenol
Scabies incubation? Pathognomonic lesion?
First infection, sx caused by hypersensitivity reaction which may take 4-6 weeks to develop With reinfection, sx develop within 24-48 hrs because of previous sensitisation Pathognomonic: burrow - a small raised greyish wavy channel on the skin surface extending from an erythematous papule.
Scabies Tx
General advice; Avoid close body contact until pt & partner have completed tx - Full STI screen Topical: Permethrin or malathion. –> Applied to whole body from neck downwards and washed off after 12 hrs (most convenient is to apply, leave overnight, wash off next morning. Pts should be warned that itch may persist for several weeks following treatment –> effect of antigenic material in skin. Contaminated clothes and bed linen should be wahed at 50 degrees
Pubic lice? Tx:
Caused by Phtiris pubic Incubation period 5 days-several weeks Topical Tx: - Malathion - Permethrin Phenothrin second application after 3-7 days advice - Fine toothed comb to remove dead eggs
Hep A: Spread Incubation period Sx? MX?
Faeco-oral, Sexual in MSM, parenteral spread in IVDU/transfusions Incubation period 2-6 weeks Sx: Acute hepatitis starts with a flu like prodrome illness lasting up to 2 weeks. Normally followed by jaundice for a few weeks - Age related, rare for children below 5 to show symptoms, where as 75-90% of adults will. Mx: most with acute hepatitis will recover uneventfully with sx control, rest and hydration. - Isolation may be require dto prevent spread,eg. in pts with faecal incontinence
HAV prevention?
HAV vaccine - >90% effective at preventing infection - Should be offered to MSM with at risk lifestyle, non-immune travellers to endemic countries, men with haemophilia, IVDU, pts with CLD and sewage workers. - If non-immune person exposed - should be offered vaccination - Human normal immunoglobulin (HNIG) should be given within 1 week of exposure in pts with high risk (immunosuppressed)
Features of acute viral hepatitis
Serum ALT: 500-10000 Serum bili: 30-100: Mixed conjugated/unconjugated Serum ALP: usually normal/mildly raised (5 s suggests impending hepatic failure
HBV transmission?
Heterosexual transmission 40% vaginally with acute HBV - Vertical (90% of infants become carriers) - Parenteral - Sexual Incubation period 8-12 weeks
HBV mx? Prevention?
Acute mx - conservative, as with HAV - Antivirals given for fulminant HBV infection Chronic HBeAg +ve infectino can be cured in 30-50% of pts with: - Pegylated IFN-a - Lamivudine - Entecavir/ adefovir / tenofovir Vaccination and consistent condom use will prevent most cases of sexually transmitted Hep B if advised to those at risk such as MSM, sex workers or IVDU
Hep D?
RNA virus which can only exist as co-infection with HBV –> Fulminant hepatitis is 10x more likely than with other types of viral hepatitis with an 80% rate of fatality. - HDV superinfection: 80% rate of chronicity - 3x rate of liver cancer/cirrhosis Mx: no effective antiviral therapy, but infection largely preventable through HBV vaccination, condom use, sterile medical equipment and avoidance of equipment sharing in IVDU
HCV transmission
Predominantly parenterally transmission Vertical transmission - 1% rate in HIV -ve women, but >9% in HIV co-infection Sexual transmission: 0.5-2% per year of relationship
HVC: features & MX
- Jaundice only occurs in 20% of acute infections, rest asymptomatic - Fulminant hepatitis rare - 60-80% of pts develop chronic HCV. Symptoms mild until cirrhosis which is seen in 20% ater 20 years. - 5% develop HCC - Cirrhosis develps more rapidly if there is high alcohol ntake, HIV or HBV coinfection Mx Pegylated interferon and ribavirin for 6mo cures 50-90% of carriers, depending on viral genotype. - Cure rate lower if pt also HIV +ve NO effective vaccine
EBV disease associations?
Burkitt’s lymphoma Hodgkin’s lymphoma Nasopharyngeal carcinoma Lymphoproliferative diseaes In HIV: Oral hairy leukoplakia and som non-Hodkin’s lymphomas
CMV Ix?
4 fold increase in IgG Abd from paired samples taken 10-14 days apart
HHV8 associations?
Kaposi’s sarcoma (with immunosuppression) Associated with Castleman’s disease
HIV prevalence recommended for screening?
2/1000
What portion of HIV +ve individuals in the UK are undiagnosed
25% - 30% diagnosed very late (CD4 More prevalent in older age groups, heterosexual men and BME
Who to test for HIV?
Recommended HIV test offered on an opt-out basis to all patients presenting for care: - in a number of specific settings - Who are members of specific higher risk groups - Who have certain meical condition Specific settings: - GUM/sexual health clinics - Antenatal services - TOP services - Drug dependency programmes - Healthcare services for those diagnosed with TB, HBV , HCV and lymphoma
Groups of people who should be offered a routine HIV test?
1) Pts where HIV is a differential 2) Pts with STI 3) Sexual partners of HIV +Ve 4) MSM 5) Female sexual contacts of MSM 6) ever IVDU 7) pts from countries of high prevalence (>1%) 8) Pts who had sexual contact abroad or in UK with individuals from countries of high HIV prevalence 9) Following groups: Blood donors, dialysis pts, organ transplant donors and recipients
AIDS defining conditions
Resp: TB, PCP Neuro: Toxo, primary cerebral lymphoma, Cryptococcal meningitis, progressive multifocal leucoencephalopathy Derm: Kaposi Gastro: Persistant crypto Onco: Non-Hodgkin’s lymphoma Gyne: Cervical cancer Opth: CMV retinitis
Which pt groups should be HIV tested more frequently
MSM - atleast annually or more frequently if Sx/High risk behaviour IVDU - Anually or more frequent if Sx Pregnant women: If ongoing high risk or become unwell with seroconversion like symptoms during pregnancy, repeat test at 34-36 weeks.
How should a positive HIV test result be given?
BY the team/clinician who consented the pt Face to face In a confidential environment Using clear language - use translation service rather than family member is not english Make sure you understand what positive result means (not good news) HIV team should then see pt as soon as possible to assess disease stage, consider the need for treatment and to carry out partner notification
Primary HIV infection features:
Time between initial infection and development of antibodies against HIV. During this period, pt develops symptoms compatible with an acute viral infection ‘HIV seroconversion illness’ - ranges from mild glandular fever like illness with a rash to encephalopathy - Onset of PHI within 3/52, lasting longer than 2/52 and CNS involvement are associated with rapid progression to AIDs Sx: - Fever - Lymphadenopathy - Pharyngitis - Erythematous maculopapular rash, mainly on face and trunk - Myalgia - D + N + V - Hepatosplenomegaly
HIV infection categories?
Category A: - Asymptomatic HIV infection, persistant generalised lymphadenopathy or PHI Category B: - Symptomatic conditions eg. orophayngeal candidiasis, OHL, HZV Category C: - Clinical conditions listed in AIDS surveillance eg. oesophageal candidiasis, burkitts, PCP, toxo etc
AIDs defining HIV wasting syndrome
10% weight loss from baseline + one of: - Fever - Diarrhoea Lasting atleast 1 month
What is AIDS
‘persistent and profound selective in the function and number of CD4 T lymphocytes of the helper/inducer subset, and a possible activation of the suppressor/cytotoxic subset.
Factors affecting HIV disease progression?
1) Older age 2) PHI: Early onset 2 weeks 3) Higher HIV Viral load 4) Baseline albumin
CD4 count & Disease associations?
AIDs defining Cancers?
Kaposi Sarcoma High grade B-cell non-Hodgkin’s lymphoma (including primary cerebral lymphoma) Invasive cervical cancer
AIDs-related systemic lymphoma
60-100x in HIV than matched general pop 1/3: Burkitt/Burkitt-like 2/3: Diffuse large cell lymphoma Mx: Combination anthracycine based chemo + Intrathecal chemo for those at risk of meningeal relapse + concomitant cART & opportunistic infection prophylaxis
AIDs related cerebral lymphoma
primary cerebral lymphoma - NHL that’s confined to the craniospinal axis without systemic involvement - Associated with advanced immunosuppression and has a particularly poor prognosis Both this and toxo PC: Headaches and focal neuro deficits - PCL: More gradual onset over 2-8 weeks and absence of fever CT/MRI: solitary or multiple ring enhancing lesions with prominent mass effect and oedema - PCL tend to be periventricular where as toxo affects basal ganglia Main way of differentiating: - More than 85% of pts with cerebral toxo will respond clinically/radiologically to 2 weeks of anti-toxo therapy - Detection of EBV DNA in CSF by PCR in pts has high sensitivity and specificity for PCL - FDG PET can also help Mx: Whole brain irradiation + cART
AIDs related Kaposi? 1) Cause 2) Histology 3) PC
KSHV/HHV8 - Transmitted horizontally (kissing)/vertically Histologically: Proliferation of spindle shaped cells accompanied by endothelial cells, fibroblasts and inflammatory cells that form slit-like vascular channels that resemble neo-angiogenesis. PC: Multiple pigmented raised painless skin lesions - Frequent oral lesions Nodular KS more frequently seen in Africans
Most common sites for visceral KS?
Lungs & Stomach. Pulmonary KS: life threatening, PCL dyspnoea, dry cough +- fever +- haemoptysis CXR: reticulonodular infiltrate and pleural effusion
KS management?
Clinical Mx determined by clinical staging: - T0 - commence cART - for most, KS will respond to cART alone in 6-12mo - In view of delay, cosmetically significant local lesions may be treated with either intralesional vinblastine or localised radio - Advanced visceral/cutaneous KS: chemo + cART
AIDs related cervical cancer
HIV associated with high prevalence of HPV in cervix, multiple HPV genotypes and persistence of HPV in cervix
Non - AIDs defining malignancies
cancers 2-3x more common in HIV +ve than age/gender matched Viral associated: - Anal cancer (HPV) - Hodgkin’s lymphoma (10x) - EBV implicated - HCC - Multicentric Castleman’s disease (MCD) - KSHV No known viral aetiology: - Seminoma - NSC lung cancer
Multicentric Castleman’s disease?
Rare lymphoproliferative disorder related to KSHV. Diagnosed histologically PC: Fever, lymphadenopathy, hepatosplenomegaly + atleast 3 systemic symptoms eg oedema, ascites, rash, xerostomia, jaundice + CRP >20 High lvels of HHV8 DNA almost always present in blood. Mx: NO definitive gold standard therapy. Rituximab + cART
HIV associated respiratory disease?
Infections: Acute bronchitis Acute /chronic sinusitis Bronchiectasis Bacterial pneumonia (10x background rate) TB PCP Cryptococcus neoformans pneumonia Histoplasma capsulatum Influenza A Malignancy: Lung Cancer (2-4x as common) Kaposi sarcoma Non-Malignant conditions: Non-specific pneumonitis COPD Pulmonary arterial (6-12x) hypertension Pneumothorax
Bacterial pneumonia in HIV Commonest organism?
6-10x if not on cART than in general population - Especially in HIV IVDU Commonest: S.pneumonia, H.influenza CXR frequently atypical, mimicking PCP (diffuse bilateral infiltrates Immunisation with 23-valent pneumococcal vaccine recommended in all adults and adolescents (at diagnosis of HIV infection and after 5 yrs)
PCP diagnosis?
Tx usually started empirically in pts with typical clinical and radiological features and a CD4 count of
Factors associated with a poor outcome from PCP?
Factors at PC: - Older age - 2nd/3rd episode of PCP - Hypoxaemia (Low PaO2) - Anaemia - Low albumin - Raised SBR - Raised CRP - Coexistant KS - Coexistant Medical comorbidity eg. lymphoma/pregnancy Once hospitalised: - Development of pneumothorax - Admission for ICU - Need for mechanical ventilation
PCP stratification + Mx
Mild: Pa02 > 11kPta Moderate: Pa02 = 8-11 Sever: Pa02
Indications for PCP prophylaxis?
Primary prophylaxis -CD4 200 and undetectable HIV RNA , both for >3 months Drugs: Cotrimoxazole 2nd: Nebulised pentamidine 3rd : Atovaquone
Cryptoccal infection: Dx & Mx?
Diagnosis of pulmonary infection is by identification of cryptococcus neoformans in resp secretions or lung tissue Tx: - Fluconazole - Liposomal amphotericin + Flycytosine
Histoplasmosis PC?
subacute presentation with fever + wt loss - 50% have non-productive cough + dyspnoea O/E: Hepatosplenomegaly CXR: normal / bilateral widespread
Influenza A in HIV?
- Not more common, but more severe disease - In those with low CD4, may deteriorate rapidly/ complicate with 2ndry bacterial pneumonia Tx: Like general population, if suspected influenza A + duration of Sx
HIV: TB reactivation risk?
HIV uninfected individual has 10% lifetime chance of latent TB reactivation, whereas HIV individual has approx 10% per annum - Overall, HIV co-infected person is 20-40x more likely to develop active TB - TB is cause of around 1/4 of all adult AIDs deaths
TB HIV PC?
As blood CD4 count falls,the typical CXR upper zone cavitatory disease is replaced by pulmonary infiltrates, mediastinal lymphadenopathy and pleural effusions. - Non-pulmonary disseminated and multi-organ involvement is also more common - May also have near normal CXR and minimal systemic symptoms to suggest active disease.
HIV TB Ix?
- HIV +ve TB are more likely to be AFB sputum smear negative making this inexpensive and rapid test less sensitive. - High rate of non-pulmonary disease makes culture of other samples (blood/urine) useful - Microscopic oberservation drug susceptibility assay (MODS) - sputum inoculated in specific assay is sensitive, specific and largely unaffected by HIV status as well as providing info on drug resistance
HIV TB drug resistance?
- prevalence of drug resistant TB is 2-3x higher –> eg. XDR (extensively drug resistant) TB linked to HIV co-infection in SA, where mortality was around 50% within 1 month of diagnostic suspicion of disease
Monoresistant TB in HIV?
Most commonly isoniazid resistance. HIV associated also with increased incidence of rifampicin resistance
TB HIV Mx?
HIV doesn’t alter standard anti-TB regimes: Pulmonary/extra-pulmonary TB with no cerebral TB: RIPE for 2/12 followed by RI for further 4 months (pending sensitivity info)
TB/HIV drug interactions?
Rifampicin - Potent Cyp450 inducer –> Numerous Drug-drug interactions with other agents particularly cART: –> Subtherapeutic levels of these drugs can lead to treatment failure and HIV drug resistance –> Alternative to R with less cyp inh = Rifabutin. Avoid Rifampicin + Protease inhibitors eg. ritonavir (Subtherapeutic levels) –> Nucleoside reverse transcriptase inhibitors better
Starting cART in pts on TB treatments - risks of early and delayed therapy?
Early (within 2 weeks) concomitant use: - Drug-drug interactions - Overlapping toxicities and additive adverse effets - High pill burden - Risk of reduced pt adherence - IRIS Delay: - Risk of other major opportunistic infections and death nb. Subjects with very low CD4 (
Stavudine SE ?
peripheral neuropathy, particularly with isoniazid
What is IRIS?
Immune reconstitution inflammatory syndrome (IRIS) is a condition seen in some cases of AIDS or immunosuppression, in which the immune system begins to recover, but then responds to a previously acquired opportunistic infection with an overwhelming inflammatory response that paradoxically makes the symptoms of infection worse
TB IRIS case definition?
A) Antecent requirements - TB before cART + initial response to TB tx B) Clinical criteria: - onset of TB IRIS within 3/12 of cART initiation. Atleast 1 major: - Enlarging lymph nodes/ focal tissue involvement - Worsening radiological features - Worsening CNS TB/serositis or 2 Minor: - worsening constitutional Sx/ resp sx/ abdo pain caused by peritonitis, hepatosplenomegaly to abdominal adenopathy C) Alternative explanations for clinical deterioration must be excluded if possible: - TB drug resistance - Poor adherence - another opportunistic infection or neoplasm - drug toxicity
IRIS Ix + Mx?
Ix - no specific test - diagnosis of exclusion Mx: Generally managed without interrupt of either anti-TB or cART. Less severe forms will often resolve without any additional therapy - More serious/prolonged events, especially when associated with worsening cerebral or mediastinal disease likely to cause compression of vital structures should be treated with systemic corticosteroids
Neuro complications in HIV infection?
Opportunistic: - Toxo: Abscesses and encephalitis - Crytococcus neoformans: Meningitis - JC virus - Progressive multifocal leucoencephalopathy (PML) - CMV - Retinitis, encephalitis, cauda equina , vasculitis neuropathy Tumours: - Primary CNS lymphoma - Metastatic systemic lymphoma HIV-related disorders: - HIV associated neurocognitive disorders (HAND) - Peripheral neuropathy - Polymyositis Drug-induced complications: - Neuropathy (didanosine, stavudine, isoniazid) - Myalgia, myopathy (NRTIs) IRIS: - cryptococcys - PML - TB
Efavirenz neuro SE?
Headaches Drowsiness agitation Insomnia Cognitive dysfunction
Neurological syndromes at HIV seroconversion?
Aseptic meningitis Meningoencephalitis Acute disseminated encephalomyelitis (ADEM) Transverse myelitis Cauda equina syndrome Acute demyelinating polyradiculoneuropathy (Guillian barre syndrome - only difference is pleocytosis > 20cells/uL) - Brachial neuritis - Mononeuritis multiplex - Acute polymyositis
CD4 count and neuro complications?
CD4
Meningitis in HIV infection?
Fungal: Cryptococcus (commenest cause of meningitis) Bacterial: - Strep pneumo - TB VIral: HSV VZV
Cryptococcal meningitis PC?
General malaise, headache, confusion or seizures that have an acute or insidious onset over days or weeks - Classical meningism often absent Brain Imaging: - Hydrocephalus - Cryptococcomas (dilated virchow-robin spaces filled with fungal organism) Dx: Detection of cryptoccal antigen in CSF in >95% - India ink staining positive in 75% - Perform manometry at LP as opening pressure frequently up –> due to blockage of CSF resorption across the ventricular arachnoid villi by cryptococcus
Poor prognostic factors in HIV associated cryptococcal meningitis
Altered mental status: Obtundation/coma CSF WCC 25cm CSF CrAg >1:1000 Positive india ink Hyponatraemia Culture of extrameningeal cryptococcus eg. in blood or from skin Relapse episode
Cryptococcal Meningitis Mx?
Mx: 2 week induction period with liposomal amphotericin B,usually combined with flucytosine , followed by 5 weeks of fluconazole - Mx of raised ICP: repeated Lumbar puncture
Investigating HIV neuro mass lesions?
Commonest causes of mass lesions in Neuro HIV?
1) Toxo
2) PCNSL (Primary CNS lymphoma)
3) TB
HIV Toxo presentation?
Usually reactivation of latent infection in invididuals previously exposed
Headache, with rapidly evolving focal neuro over 1-2 wks:
hemiparesis, dysphasia, visual field defects, movement disorders (chorea/ athetosis, parkinsonism) & Seizures
May rarely affect spinal cord
–> Bood serology only useful if negative, since this makes the diagnosis less likely - pts should have heir toxo serology documented at first diagnosis of HIV infection
CT/MRI shows multiple ring enhancing lesions with mass effect in the region of the basal ganglia and at the grey-white interface
IF significant mass effect - dexo
Progessive multifocal leucoencephalopathy?
- Reactivation of JC virus in AIDs (over 80% exposed to virus in childhood)
PC: Slowly evolving focal neuro eg. hemiparesis, visual field defects, language problems
Cranial MRI shows non-enhancing areas of low attentiuation in the white matter on T1 weighted images and hyper intense lesions on T2 with typical areas of ‘scalloping’ at the grey/white interface.
- Usually no associated oedema.
Diagnosis confirmed by isolating JC virus DNA by PCR in CSF
CMV encephalitis in HIV?
reactivation when CD4<50
Should be considered in pts presenting with rapidly evolving encephalitis involving brain stem with cranial nerve palsies and seizures
CMV DNA may be isolated from CSF using PCR
Tx: Ganciclovir +- foscarnet
HIV HAND?
HIV associated neurocognitive disorder
Since cART: Incidence of severe HAND declined, but prevalence of less severe increased
- Represents a group of syndromes of varying severity affecting cognition, behaviour and motor function
Ranges from:
- Asymptomatic neuropsycholical impairment (ANI) - cognitive impairment atleast 1 SD below mean in 2 or more cognitive domains without difficulties in ADLs
NExt is HIV associated mild neurocog disorder (MND)
Most severe is HAD - HIV associated demendtia - marked cognitive decline atleast 2SD below mean in two or more cognitive domains causing moderate to severe difficulties in ADLs
DDx among pts presenting with cognitive symptoms
Substance abuse, including alcohol / opiods
Iatrogenic: Antidepressant, ARTs eg. efavirenz
Psychiatric disorders: Depression/anxiety
Dementia: AD, LBD
metabolic or systemic : Vit b12 / Folate , hypothyroid, renal/hepatic failure
Infectinos: Pneumonia, UTI, sepsis
CNS infections: Cryptococcal meningitis, toxo, PML, TB, encephalitis
Tumours: PCNSL, primary/secondary brain tumours
Other: Neurosyphilis, hydrocephalus, dementia due to CVA
Risk factors for HAND
Older age
Female
Current/previous low CD4 (<100)
High plasma viral load
Comorbid conditions (Anaemia)
Coinfection with hep C
Hx of drug use
Cranial MRI shows variable cortical atrophy and diffuse or patchy white matter signal abnormalities on T2 weighted images
Peripheral nerve disorders in HIV?
before cART upto 40% of pts developed distal sensory peripheral neuropathy (DSPN)
Tx: Symptomatic with anticonvulsants (gabapentin, pregabalin, lamotrigine) Antidepressants (amitriptyline) and opiates (oxycodone)
Symptoms and Signs of DSPN:
- Numb, burning feet
- Sharp, stabbing pains
- Contact hypersensitivity
- Little or no weakness
- Impaired pain and temperature sensation
- Normal, depressed or absent ankle reflexes
What is antiretroviral toxic neuropathy?
Neuropathy primarily due to nucleoside analogue drugs Didanosine and stavudine
Dose dependents
PC like DSPN, but more PAINFUL
60% improve on stopping drug
Workup of HIV neuropathy?
Consider neurotoxic drugs, including excess vit B6
Consider excess alcohol/poor diet
Bloods: B12, glucose, HBa1c, Bence jones
Nerve conduction studies
Nerve biopsy (usually sural nerve looking for vasculitis, DILS, CIDP, malignant infiltration
HIV compartmentalisation syndrome?
CSF HIV viral load much higher than plasma viral load
Pts may present acutely/ sub acutely with increasing confusion, ataxia and cognitive decline
HIV and the eye?
HIV infected individuals - cotton wool spots, retinal microaneurysms and retinal haemorrhages can occur in the absence of opportunistic infections
CD4> 500 - asymptomatic/ inflammatory eye conditions eg. allergic conjunctivitis
CD4: 200-500: Ocular bacterial infections
<200: Opportunistic eye infections/malignancy
Most common ocular opportunistic infection in HIV?
CMV retinitis: 20% annual risk when CD4<50
If CMV retinitis is close to macula/optic nerve, risk of visual loss high
Mx: Intraocular injections of ganciclovir/foscarnet
Ganciclovir implant placed within pts affected eye released drug over a 6 month period and reduces need for repeated intraocular injections
- Anti- CMV systemic therapy (oral valganciclovir) to prevent disease in uninvolved eye
- Risk of retinal detachment continues for months after retinal disease has been controlled.
Ocular VZV in HIV?
In pts with very low CD4 Counts <10, an aggressive rapidly progressive retinitis (previously known as progressive outer retinal necrosis PORN) may occur. Multiple discrete retinal lesions rapidly coalesce and cause very rapid total retinal destruction with little associated ocular inflammation
Tx: Intravitreal foscarnet at the time of vitreous sampling, followed by IV high dose aciclovir
Incidence of retinal detachment high + prognosis for vision very poor
Ocular TB
TB can present with uveitis, or less commonly ocular granulomas
Characteristic appearance of choroidal granulomata in TB
Ocular TB granulomas requires no specific Tx and will respond to standard systemic anti TB Therapy.
Ocular TV uveitis requires topical (for anterior uveitis) or systemic (for intermediate/posterior uveitis) steroid therapy
Ocular malignancies associated with HIV?
Kaposi sarcoma (eyelid/conjunctiva)
Lymphoma (PCNSL)
Squamous cell carcinoma of the conjunctiva - associated with sun exposure and B-HPV infection - Exisional biopsy usually recommended
NB. rogue point but rifabutin may accumulate within eye, leading to marked intraocular inflammation, which settles with topical steroids and drug dose reduction.
